REPORT OF THE

UNITED-NAXI-ONS .

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EFFECTS OF !iit}ifffHiADIATION.. : . . .

·'GENERAL ASSEMBLY
OFFICIAL RECORDS : SEVENTEENTH SESSIONSUPPLEMENT No. 16 {A/5216}

New York, 1962

NOTE
Throughout the present report and the annexes thereto, references to theannexes are indicated by a letter followed by a number: the letter denotes the relevant
annex and the number the paragraph therein. Within each annex, references to its
scientific bibliography are indicated by numbers.
Symbols of United Nations documents are composed of capital letters combined with figures. Mention of such a symbol indicates a reference to a United
Nations document.

h we ut··m,.

CONTENTS
Page

Abbreviations. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

1v

ChapterI.

Introduction...... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

1II.

~hysi<?ll and biological aspects of the interaction of ionizing radiatlon with matter. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

4

III.

Somatic effects..... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

9IV.

Hereditary effects. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

14

V.

Sources of irradiation.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

20

VI.

Comparison of doses and estimates of risks....................

29

VII.

Evaluations and conclusions..... . . . . . . . . . . . . . . . . . . . . . . . . . . . .

31

ANNEXESA.

Definitions of quantities, units and symbols. . . . . . . . . . . . . . . . . . .

39

B.

Fundamental radio-biology..................................

41

C. The hereditary effects of radiation........... . . . . . . . . . . . . . . . . .

84

D. Somatic effects of radiation....... . . . . . . . . . . . . . . . . . . . . . . . . . . .

118

E.

Radiation from natural sources. . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

207

F.

Environmental contamination
I. Production and transport of nuclear weapon debris........
II. Transfer of radio-active material through food chains into
the human body. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
III. Exposure data...... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
IV. Disposal of radio-active wastes and releases from accidents
in nuclear reactors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

365

G.

Medical, occupational and other exposures....................

375

H.

Comparison of doses and estimates of risks ................ : . . .

414

I.

List of offers to assist with measurements of samples. . . . . . . . . . .

421

J.

List of reports submitted to the Committee...................

422

K.

Letter sent at the request of the Committee by its Secretary toState Members of the United Nations and members of the specialized agencies and of the IAEA on 7 April 1960..............

438

Appendix I. List of scientific experts, members of national delegations. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Appendix II. List of scientific experts who have co-operated ·with
the Committee in the preparation of the report. . . . . . . . . . . . . .

iii

233

287
347

441
442

ABBREVIATIONSFAOFood and Agriculture Organization of the United Nations

IAEA

International Atomic Energy Agency

ICRP

International Commission on Radiological Protection

ICRU

International Commission on Radiological Units andMeasurements'WHO

World Health Organization

WMO

World Meteorological Organization

*

*

CNS

Central nervous system

DNA

Deoxyribonucleic acid

ERG

Electroretinogram

ESR

Electron spin resonanceGI
LET

Gastro-intestinal
Linear energy transfer

OR

Observed ratio

RBE

Relative biological effectiveness

RES

Reticulo-endothelial system

RNA

Ribonucleic acid

TBR

Total body radiation

TNT

Trinitrotolueneiv*CHAPTER IINTRODUCTION
Constitution and terms of reference of
the Committee
1. The Scientific Committee on the Effects of Atomic
Radiation was established by the General Assembly at
its tenth session on 3 December 1955, under resolution
913 (X), as a result of debates held in the First Committee from 31 October to 10 November 1955. The termsof reference of the Committee were set out in paragraph
2 of the above-mentioned resolution by which the
General Assembly requested the Committee:"(a) To receive and assemble in an appropriate
and useful form the following radiological infonnation furnished by States Members of the United
Nations or members of the specialized agencies:"(i) Reports on observed levels of ionizing radiation and radio-activity in the environment ;"(ii) Reports on scientific observations and experiments relevant to the effects of ionizing radiation upon
man and his environment already under way or later
undertaken by national scientific bodies or by authorities of national Governments;·" ( b) To recommend uniform standards with respect to procedures for sample collection and instrumentation, and radiation counting procedures to be
used in analyses of samples;" ( c) To compile and assemble in an integrated
manner the various reports, referred to in sub-paragraph (a) ( i) above, on observed radiological levels ;" ( d) To review and collate national reports, referred to in sub-paragraph. (a) (ii) above, evaluatingeach report to determine its usefulness for the purposes of the Committee;"(e) To make yearly progress reports and to develop by 1 July 1958, or earlier if the assembled facts
warrant, a summary of the reports received on radition levels and radiation effects on man and his environment together with the evaluations provided forin sub-paragraph (d) above and indications ofresearch projects which might require further study;"(f) To transmit from time to time, as it deems
appropriate, the documents and evaluations referred
to above to the Secretary-General for publication anddissemination to States Members of the United
Nations or members of the specialized agencies."
2. The Committee consists of Argentina, Australia,
Belgium, Brazil, Canada, Czechoslovakia, France, India,
Japan, Mexico, Sweden, the Union of Soviet Socialist
Republics, the United Arab Republic, the United Kingdom of Great Britain and Northern Ireland and theUnited States of America.

proved on 13 June 1958 during its fifth session, andwhich the General Assembly noted with satisfaction
during its thirteenth session, on 13 December 1958
under resolution 1347 (XIII). In that resolution th~General Assembly: ( 1) commended the Scientific Committee on the Effects of Atomic Radiation for its workand for the valuable report which it had presented;(2) e.."<pressed its appreciation to the United Nations
agencies, to the international non-governmental and thenational scientific organizations, and to the individual
scientists who had assisted the Committee in its work;( 3) urged all concerned to take note of the suggestions
made and the views e."<pressed in the report of the Committee; ( 4) decided to request the Committee to continue its useful work, and to report to the General
Assembly as appropriate; (5) requested the Committee
to consult with the other agencies and organizations concerned on projects within its sphere of activities so as to
avoid the duplication of work and ensure effective
co-ordination; ( 6) called upon all concerned to assist theCommittee by making available to it reports and studies
relating to the short-term and long-term effects of ionizing radiation upon man and his environment and radiological data collected by them, and by pursuing suchinvestigations as might broaden world scientific knowledge in that sphere and by transmitting their results to
the Committee; (7) requested the Secretary-General tocontinue to provide the Committee with the assistancenecessary for the conduct of its work.
4. In conformity with this resolution, the Committee
continued its technical deliberations, based both on information obtained from the current scientific literature andon data made available to the Committee by :Member
States and by the specialized agencies, the International
Atomic Energy Agency (IAEA) and various non-governmental bodies, in particular the International Commission on Radiological Protection (ICRP) and theInternational Commission on Radiological Units andMeasurements (ICRU). The Committee also pursued
its activity in the field of standardization of reference
samples of various materials containing strontium-90,
which was initiated in 1957.
SECOND COMPREHENSIVE REPORT

5. At its sixth session, the Committee considered its
future work within the terms of reference set out by
the General Assembly, expressed its intention to submit
a further comprehensive report to the General Assemblyin 1962 and invited the Food and Agriculture Organization of the United Nations (FAO), the World HealthOrganization (WHO), the ICRP and ICRU to undertake, each within its own competence, such specifiedstudies as the Committee felt were relevant to the problem of the effects of radiation on man.

Activities of the Committee
FIRST cmrPREHENSIVE REPORT

3. In the course of its first four sessions, the Committee prepared a comprehensive report,* which it ap-

6. The Committee also suggested that a seminar on
use of vital and health statistics for genetic and radiation
studies be held under the joint sponsorship of the United
Nations and WHO. This Seminar was held in Geneva*Official Records of the General Assembly, Thirteenth Session, Supplement No. 17 (A/3838).

1from 5 to 9 September 1960, and was attended by sixtyfive scientists. Its proceedings are being published andthe Committee notes with appreciation that WHO, cosponsor of the Seminar, greatly contributed to its
success.

erating the completion of the present report, which it
adopted at its eleventh session on 23 March 1962.
11. In response to a request from the Secretary-General of the World Meteorological Organization(WMO), the Committee at its eleventh session gave
consideration to a draft plan proposed by WMO for the
implementation of part II of General Assembly resolution 1629 (XVI). The Committee requested its Secretary to transmit to the Secretary-General of WMO ageneral statement, which it had adopted, in reply to his
request for consultation.

7. At its seventh and eighth sessions, the Committee
discussed:(a) The physical aspects of fall-out;( b) Physical and biological problems concerning thetransmission of fission products through food chains;( c) The relationships between radiation doses andeffects, particularly at low doses;( d) Physical and biological problems concerned withcarbon-14;( e) Genetic problems ;(f) Dosimetric problems;(g) Content and preparation of the Committee's second comprehensive report;(h) Results of the Seminar on Use of Vital and
Health Statistics for Genetic and Radiation Studies.
In connexion with topic (h) above, the Committee expressed its support of the consensus of the participantsin the Seminar. on ways in which greater use might bemade of existing information. This consensus wasappended to its annual progress report to the General
Assembly for 1960 (A/4528).

12. Since its 1958 report, the Committee, following
the recommendation contained in paragraph 2 of resolution 913 (X) and in paragraph 4 of resolution 1347
(XIII) of the General Assembly, has submitted yearlyprogress reports to the General Assembly.
Sources of information

13. The reports submitted before 10 March 1962 by
and through States Members of the United Nations andmembers of the specialized agencies and of the IAEA, as
well as reports of the agencies themselves and of various
other non-governmental bodies, are listed in anne.'I: J.
These reports were supplemented by a number of otherreports and publications contributed by various individual scientists and laboratories. The information received or collected was evaluated and interpreted in thecontext of the current scientific literature.

8. In response to sections I and III of General
Assembly resolution 1376 (XIV), the Committee, at its
seventh session, requested its Secretary to address a
letter to States Members of the United Nations andmembers of the specialized agencies and of the IAEA,
outlining the type of data on environmental contamination needed from certain areas, and mentioning those
fields of biological research in which large-scale collaborative investigations are required. In pursuance of
the Committee's request a letter, dated 7 April 1960,
was sent to the above-mentioned States by the Secretary(see anne.."li: K).
9. In further response to sections II and III of resolution 1376 (XIV) 9f the General Assembly, the Committee also discussed, at the following session, appropriate arrangements for the purpose of stimulating theflow of information and data of the type already contained in its comprehensive report and for encouraging
genetic, biological and other studies, including thoseconcerned with carbon-14, that would elucidate theeffects of radiation exposure on the health of humanpopulations. The results of its discussions were submitted to the General Assembly in a report which was
also appended to the Committee's annual progress reportfor 1960. The report suggested ways and means whereby
the Committee's requests for relevant information could
best be channelled, in the respective countries, to theappropriate national scientific organizations and committees, as well as to individual scientists.
10. During its ninth and tenth sessions the Committee considered preliminary drafts of the present report. Between its tenth and eleventh sessions, as requested by the General Assembly in part I of resolution
1629 (XVI), the Committee gave its attention to thepossibility of submitting an interim report to the General
Assembly but considered that the facts at its disposal did
not call for such a report. The Committee did, however,meet the urgency expressed in the resolution by accel-

14. The Committee is gratified that, in response tosection IV of General Assembly resolution 1376 (XIV),
Governments of a number of Member States, IAEA and
WHO informed the Committee that they had madeknown to other Governments the extent to which they
were prepared, at the request of other Governments, toreceive and analyse samples in accordance with the programme of the Committee. The offers of assistancewhich were communicated to the Committee before 10
March 1962 are listed in annex I.
Organization of the work of the Committee

15. The officers serving prior to the sixth session arelisted in the first comprehensive report. Dr. R. M. Sievert of Sweden and Dr. V. R. Khanolkar of India
served as Chairman and Vice-Chairman, respectively, ofthe sixth and seventh sessions. Dr. M. Martinez Baez of
Mexico and Dr. F. Hercik of Czechoslovakia served as
Chairman and Vice-Chairman, respectively, of theeighth and ninth sessions, and Dr. F. Hercik and Dr. K
Tsukamoto of Ja pan served as Chairman and ViceChairman, respectively, at the tenth and eleventh sessions of the Committee. The scientists who have taken
part in the preparation of the report as members ofnational delegations are listed in appendix I. During theeleventh session Dr. D. J. Beninson of Argentina andDr. M. E. A. El Kharadly of the United Arab Republic
were elected Chairman and Vice-Chairman, respectively,of the Committee.
16. As in the past, the Committee set up ad hoe groupsof specialists to deal with topics falling within their
specific competence. The technical discussions and theevaluation of the information submitted to the Committee were informal and no detailed record of these discussions was taken.
2Relations with agencies of the United Nations andother international organizations

Preparation of the report

21. In its first comprehensive report, the Committeeemphasized that, as knowledge in its field of inquiry
increased, modifications and amplifications of that report would become necessary. Since 1958, new factors
have emerged and many experimental results have beenobtained. Rather than issue a revised version of thereport, the Committee decided, at its eighth session, toprepare an entirely new and self-contained document.
At that session, the Committee agreed on the broad outline of the report and requested the Secretariat to prepare first drafts of the annexes of the report under theguidance of groups of delegates nominated by the Committee itself. It also requested the Secretariat to prepare
subsequently a first draft of the report, which would
be based on the text of the annexes. The ninth and tenthsessions of the Committee were entirely devoted to theconsideration of these drafts, the final form of which
was adopted at the eleventh session.

17. The Committee wishes to acknowledge the valuable contributions made to its deliberations and to the
preparation of the present report by the agencies of theUnited Nations and various non-governmental organizations. In response to an invitation by the Committee,
FAO submitted a report on the radio-active contamination of the food chain, WHO a report on questions
relating to the hereditary burden of human populations,while ICRP and ICRU prepared, at the request of theCommittee, under a special service agreement with theUnited Nations, a report on the exposure of man toionizing radiations arising from medical procedures,with special reference to radiation-induced diseases, and
WMO organized a panel discussion with a number ofleading meteorologists on the factors governing the distribution of nuclear debris in the atmosphere, which
was held during the seventh session of the Committee;
IAEA submitted a series of reports dealing with the
problem of disposal of radio-active wastes.

Scope of the report
22. The present report is intended to review the current knowledge of the effects of radiation on man andhis environment and to emphasize the future investigations that are most urgently needed. Chapter II summarizes the background information in physics, biology
and fundamental radio-biology, which is needed to understand the following chapters. Chapters III and IV
describe the effects of irradiation on the individual(somatic effects) and on the progeny of irradiatedindividuals (hereditary effects). The present and foreseeable amounts of irradiation to which human populations are subjected are summarized in chapter V andthe doses of radiation from various sources are compared in chapter VI. Chapter VII summarizes theevaluations and conclusions of the Committee on the
problems discussed in earlier chapters.

Scientific staff

18. The Committee was greatly assisted in its workby a scientific staff provided by the Secretariat, which
was responsible for presenting to the Committee in a
useful form the data submitted by Governments andother bodies, and for seek-ing relevant information fromindividual laboratories and scientists. As requested by
the Committee at its first session, the scientific staff has
been recruited for short-term appointments which both
enabled highly qualified scientists actively engaged inresearch to assist it, and ensured, through rotation of
the assignments, a broad geographical distribution among
Member States.
19. A number of experts have acted as consultantsfor shorter periods of time and many scientists havecontributed to the work of the Committee on a voluntary basis.

23. As in the first report, the main text of the present
one is accompanied by a number of annexes in which
technical aspects of the problems with which the Committee is concerned are discussed in greater detailagainst the background of the current scientific information. The purpose of the annexes is to provide fulljustification for the statements made in the main text,
rather than to cover exhaustively the subjects relevantto the field of study of the Committee.

20. While the responsibility for the preparation of
the report rests entirely with members of the Committee, they wish to aclmowledge the help and advice received from other scientists whose names are listed inappendix II. The Committee's report owes much to theirco-operation and goodwill.

3

CHAPTER IIPHYSICAL AND BIOLOGICAL ASPECTS OF THE INTERACTION
OF IONIZING RADIATION WITH MATTER
1. Discussion oi the effects of radiation on humanpopulations requires an elementary knowledge of physics
and biology and of the relevant terminology. The present chapter is intended to meet this requirement as wellas to give such a description of the processes inducedby radiation in cells as is necessary to make the follow~
ing chapters understandable.
2. Formal definitions of physical quantities and units
are given in annex A and a detailed account of theinteractions between radiation and living matter at thecellular and molecular level in annex B.

Physical aspects
TYPES OF IONIZING RADIATIONS

3. Radiation is one way in which energy is emitted
and transferred. While the term radiation refers to awide range of modes of emission, propagation and absorption of energy, this report on the effects of ionizing
radiations will be concerned specifically with alpha rays,
beta rays, gamma rays, X-rays, neutrons, and all those
forms of radiation occurring.in cosmic rays.

4. These radiations may be considered jointly as they
all give rise, either directly or indirectly, to a common
phenomenon, ionization, when they interact with matter. Ionization is the removal of electric charges from,or their addition to, electrically neutral atoms and molecules, which then become either negatively or positively
charged. In this process molecules may split into separate fragments of either charge. Electrically charged
atoms, molecules or fragments of molecules are calledions.
5. Despite the common result of their interacting withmatter, the radiations considered in this report are sufficiently different in their origin and physical properties
to warrant separate description. X- and gamma rays areelectro-magnetic waves like light; other radiations consist of streams of individual particles. Alpha, beta andgamma rays and occasionally other radiations are
emitted during nuclear disintegration. Unstable nuclei** Atomic nuclei are complex structures forming the core of
atoms. They are made up of positively charged protons and electrically neutral neutrons which are both elementary particles ofapproximately the same mass as the hydrogen atom. A 1111clide
is a species of atom characterized by the number of protons andthe number of neutrons contained in its nucleus. The positively
charged nucleus is surrounded by a number of negatively
charged electrons which move in orbits around it. The chargeof the electron is the same as that of a proton but of opposite
sign so that the number of orbiting electrons in neutral atoms
is equal to the number of protons in the nucleus. These orbital
electrons participate in the formation of chemical bonds. The
number of protons defines the chemical element to which theatom belongs. For a given element, various nuclides with thesame chemical properties may be recognized which differ onlyin the number of neutrons and therefore in the mass of their
nucleus. These are called isotopes of the element.

are, in one or in a sequence of such disintegrations, converted to stable nuclei. Intermediate nuclides arising ina series of disintegrations are called radio-active daughters.
6. Nuclear disintegrations of an unstable isotope. do
not occur in all atoms at the same time. They are random
events occurring with a certain probability per unit time.
.The time ~equired for SO per cent of the atoms of a.n.uclide to disintegrate is a measure of the rate of disintegration and is called the half-life. It is constant andcharacteristic of the nuclide, and it may range fromover a thousand million years to a small fraction of asecond.

7. The activity of a radio-active sample is determinedby the number of distintegrations occurring per unit
time. The unit by which it is usually expressed is thecurie. One curie corresponds to 3.7 X 1010 distintegrations per second. A millicurie, a microcurie and a micromicrocurie (or picocurie) correspond to 3.7 X 107 , 3.7
x. 10' and 0.037 disintegrations per second. respectively.
It is convenient to remember that one micromicrocurie isapproximately two disintegrations per minute. It should
also be noted that radio-nuclides of very long half-lives
show only a slight radio-activity per unit mass (e.g. one
curie of uranium-238 with a half-life of 4.5 X 109 years,
has a weight of three tons, whilst one curie of radium-226
with a half-life of 1.63 X 103 years. has a weight of
one gram and one curie of iodine-131 with a half-lifeof 8 days has a weight of 8 micrograms).
·
8. Alpha ra'j•s are positively charged particles (helium
nuclei) emitted with definite and characteristic kinetic
energy by nuclei of some radio-nuclides during disintegration. Alpha rays produce dense ionization in matterbut their range, or penetration, is small, usually less than
0.1 mm in water and in living tissues.
9. Beta ra:ys are electrons emitted by nuclei of certain
radio-active nuclides.t They also produce ionization in
the matter through which they pass. The range of beta
rays, however, is much greater than that of alpha rays.
Few radio-active nuclides emit beta particles of range
greater than 2 cm in water and in living tissues, andnone of range greater than 8 cm.
I 0. Gamma rays are electro-magnetic radiation emitted
by nuclei of some radio-active nuclides; they have definite energies characteristic of the nuclide by which they
are emitted. Gamma rays ionize matter indirectly
through the ejection of high speed electrons from thematerial in which they are absorbed. These electrons
may be ejected at a considerable depth in matter; eachelectron then dissipates its energy within a short distance (from less than a millimetre to a few centimetres
depending on its energy). No definite range can be given
for gamma rays since they penetrate any thickness ofmatter but with progressively decreasing intensity. The
t In many cases beta rays consist of particles of the same massas the electrons, but of opposite charge.

•radiation reaches the body from sources outside it. In
the latter, radiation comes from radio-active materials
incorporated within the body after ingestion, inhalation,
injection, etc.

thickness of matter required to decrease the gamma-ray
intensity by one-half is known as the half-value thickness.
1 L X -w.ys are also electro-magnetic radiation andinteract with matter and produce biological effects inthe same way as gamma rays. They differ from gamma
rays only in that emission is extra-nuclear rather than
nuclear. In practice, X-rays are usually produced bytretardation of high speed electrons in the anode of an
X-ray tube. These electrons have been accelerated bythe' application to the tube of a difference of potential,
the magnitude of which determines the ma.~imumenergy of the X-rays produced and, therefore, theirpenetrating power. The X-rays used for diagnostic
medical procedures are less energetic and less penetrating than gamma rays from most radio-active nuclei. It
is possible, however, using special electron-acceleratingmachines, to generate X-rays that are more penetrating
than gamma rays from any radio-active nuclei.

18. In external exposure, highly penetrating radiations are generally the most significant although, in certain circumstances, hard beta radiation from outside thebody may reach important tissues such as the malegonads or the lenses of the eyes. Alpha and beta radiations are usually more significant in internal exposure,since radio-active substances may enter into the metabolism of the organism and become preferentially deposited in particular organs rather than being uniformly
distributed throughout the body. In these circumstances,even short range particles can damage these or adjacentorgans. Critical organs are those for which the effectsof radiation, under any given conditions of exposure,are most likely to cause impairment of essential bodyfunctions, because of the radio-sensitivity, the level ofradiation exposure, or the importance of such organs inbody function.:j:

12. Neutrons are constituents of atomic nuclei, fromwhich they are ejected during nuclear processes suchas fission (para. 20). Neutrons are uncharged and cannot produce ionization directly.

NUCLEAR REACTIONS

19. Radio-active materials occur naturally in the environment, but man has recently been adding to thisnatural radio-activity by artificially producing radioactive atoms on a considerable scale mainly through tworeactions, nuclear fission and nuclear fusion.

13. Fast neutrons (of energy greater than 10 keV)lose energy mainly by collision with nuclei of light atoms,
especially those of hydrogen. These nuclei recoil and,being charged, produce ions as they dissipate the energy
transferred from the neutron. The transmission ofenergy from fast neutrons to recoil nuclei can take place
at a considerable depth in tissue; like X-rays and gamma
rays, fast neutrons have no definite range.

20. Fission is the splitting of a heavy nucleus into two
fragments with release of energy. While with a few
nuclei fission may occur spontaneously, it may be induced artificially in a range of heavy nuclei by neutroninteraction. As a consequence of fission, two lighter
nuclei are produced, accompanied by one or more neutrons. Some of these neutrons may in turn be made tointeract with neighbouring nuclei to produce further
fissions and, under appropriate conditions, a chain reaction may be started. When the chain reaction occurs
quasi-instantaneously, a nuclear explosion is produced.
In nuclear reactors, however, the chain reaction is controlled, so that the energy released can be used industrially or for research purposes. The release of substantial amounts of energy by the fission process,whether controlled or explosive, is accompanied by the
production of large quantities of radio-active fission
products.

14. Slow neutrons have little energy to lose in collision with nuclei. They interact with matter mainly by
nuclear reactions that result in emission of charged particles or gamma rays while new nuclides (some of them
radio-active) are produced. Matter is ionized by theseparticles or gamma rays as well as by the radiation
emitted during the subsequent disintegration of the induced radio-isotopes.
15. Cosmic raysE•- 5 reach the earth from outerspace; they consist of a complex group of heavy particles with different energies, of galactic and solar origin(primary cosmic radiation). The highly energetic fraction of primary radiation interacts with atoms present
in the upper atmosphere giving rise to secondary cosmic
radiation which is composed of particles and.of electromagnetic radiation. Each component of secondary cosmic radiation produces ionization in its own characteristic manner. The low energy fraction of primary cosmic
radiation, trapped by the magnetic field of the earth,
becomes part of the inner and outer belts that girdle theglobe at two different altitudes.

21. In fiision processes two light nuclei are made toreact to produce one heavier nucleus. The total amountof energy that may be obtained is high; few radioactive nuclei are directly produced but their formation
is usually accompanied by the emission of neutrons.
22. Neutrons emitted in fusion or fission may reactwith nuclei in the environment, giving rise to the formation of radio-active nuclides (induced activity). In
particular, when neutrons are released into the atmosphere they are likely to react with nuclei of nitrogen,and give rise to the radio-active nuclide carbon-14.

ENERGY OF RADIATIOXS

16. The energy of radiation is normally measured inelectron-volts ( eV) and its multiples, kiloelectron-volts(keV = 103 eV), and million electron-volts (MeV =106 eV). It may be emphasized that the electron volt isa unit that may be used for any kind of energy, radiant,thermal, kinetic, etc., although it is primarily used forionizing radiation.

RADIATION DOSES AND UNITS§

23. Rad. When matter, including living matter, is exposed to any ionizing radiation, the resulting effects depend on the energy absorbed in the exposed object. The

t The definition of critical organ given here essentially corresponds with the fuller definitions given by ICRP (report of theCommission, 1958; report of Committee II, 1959).
§Formal definitions are given in annex A.

EXTERNAL AND INTERNAL IRRADIATION

17. Radiation sources .may give rise to external andinternal irradiation ·of living beings. In the former,5•a varying and sometimes extended period of time, either
the total dose over that period may be considered, or
the dose delivered per unit time, which is called thedose-rate. The importance of considering both doserates and total doses when dealing with pro~cted irradiations will become apparent later in this report.
Dose-rates are expressed in rad, rem or roentgen pert
unit time (e.g. per minute, per hour, etc.) depending on
the dose unit used.
t

amount of radiation received by a given tissue is therefore defined as the energy absorbed per unit mass ofthe tissue; this is called the absorbed dose and is measured in rad.
24. Roentgen. In some cases, for instance in medical
radiology, the quantity of X- or gamma rays is usually
measured in terms of the number of ionizations produced by those radiations in a given mass of air undercertain conditions. This quantity is called expositre doseand its unit is called roentgen. In this report, when theterm "dose" is used, it shall be understood to refer to"absorbed dose" except where the possibility of confusion makes it necessary to use the complete expression.
25. Relative biological effectiveness. Despite the basic
similarity of their interaction with living matter, ionizing radiations of different kinds and energies differ inthat the dose required to produce a given biologicaleffect (e.g. cell death or lens opacity) may vary. The
relative biological effectiveness (RBE) of one radiation with respect to another is defined as the inverse
ratio of the respective doses necessary to bring about agiven effect. If, for a certain biological system, the RBEof alpha rays is 10, this means that for such system, analpha-ray dose of 0.1 rad will produce the same biological effect as one rad of the reference radiation. Conventionally, X-rays within a certain energy range areused as the reference radiation. It must be understoodthat values of RBE strictly apply only to those conditions under which measurements are made, since theRBE for two given radiations can vary with a numberof factors. including the effect being observed, the doselevel and the dose rate.
26. Rem. For purposes of radiation protection, andthe calculation of maximum permissible levels, valuesof RBE have been adopted for various types of radiation to allow for the greater effectiveness of these radiations in causing harmful effects. The dose in rad multiplied by the relevant RBE factor is termed the RBE
dose and is expressed in rem.II
27. A similar method is useful when it is necessary
to compare the biological importance of doses of different types of radiation, or to give a biologically relevant dose for a total exposure to which different formsof radiation contribute. In neither case is it strictly appropriate to use the RBE values that are intended forprotection purposes and hence are designed to express
the maximum likely effectiveness of a radiation in causing any harmful effect under the conditions of exposure
relevant to protection work. Since the RBE of a given
radiation may vary according to the type of effect considered, as well as with the dose level, dose-rate, species
examined, and various other factors, a special value of
RBE should ideally be used for each situation. This
would be impossible in the present state of knowledge
as well as unmanageable in a general account of radiation effects. For purposes of either comparing or summating doses of different types of radiation, therefore,
the RBE factors adopted for protection purposes areused in this report. For all other purposes, e.g. when theeffect of any one particular form of radiation is reported(as in chapter III and in annex D), it is more appropriate to quote the absorbed dose directly (in rad) sincefurther assumptions as to the effectiveness of one, relative to other types of radiation, are here unnecessary
and irrelevant.
28. Dose-rate. Since radiation may be delivered over
11 The values of these RBE factors are given in annex A.

29. Distinction bef'"&een activity and dose. It is ess~­tial to bear in mind the distinction between "activity"
measured in curies (para. 7) and dose, measured in rador rem. Activity is defined in terms of the number ofdisintegrations occurring in the radio-active material ina given time; such disintegrations may be accompaniedby the emission of a variety of radiations of different
qualities and energies. Dose, however, is a measure ofenergy absorbed at some given point in tissue.

Biological aspects

30. Organisms are made of cells, the number ofwhich may range from one (unicellular organisms) tomany billions (multicellular organisms). This reportdeals mainly with multicellular organisms and, unlessotherwise stated, the word organism will indicate a multicellular one.
31. In multicellular organisms cells differentiate during embryonic development into tissues, each with a
specialized function; different tissues may be assembled
to form specific functional and morphological units,
systems and organs.
32. While the action of noxious agents affects individual cells, the over-all result of such action has muchwider repercussions in complex organisms. These mustin fact be viewed as integrated units where each change
in any constituent reflects to a lesser or greater extent
on the whole.
33. Most cells contain a recognizable nucleus andsurrounding cytoplasm. Both nucleus and cytoplasm arehighly complex; they contain about 70 per cent water
as well as other small molecules such as sodium chloride,and more complex molecules. Threadlike structuresthe chromosomes-become apparent in the nucleus during division ; their number is fi.'<ed for each species. The
hereditary factors, the genes, are located linearly along
these chromosomes. Chromosomes consist mainly of
deoxyribonucleic acid (DNA) and ribonucleic acid(RNA) associated with protein to form nucleoproteins.
DNA is believed to be the essential constituent of thegenes, whereas RNA carries the information from nuclear DNA to the cytoplasmic structures. Among these,
mitochondria and ribosomes, which consist mainly ofproteins and nucleoproteins, are the site of intense metabolic activity. Their integrated operation is a condition
for normal cell function.
34. Individual org-c:.nisms generally develop fromsingle cells through binary divisions (mitosis). In bisexual species the original cell, called a zygote, is the
product of a process of fusion (fertilization) between
two cells, called ganietes, contributed by male and female, respectively, and originating in the gonads (testes
and ovaries). After the first few divisions following
fertilization the cellular progeny of the zygote differentiates into different lines. One of these lines eventually

6•gives rise either to male (sperms) or female (eggs)
gametes and is called the germ line, all other lines being
called somatic. Since the zygote originates from theunion between gametes, it constitutes a material bridge
between successive generations, whereas the somatic
cells of an individual are destined to die when the individual has completed its life-course.
35. The inherited characteristics of cells and organisms are determined by genes. They are characterized by an inherent stability which ensures that at each
duplication two identical genes are produced. The
stability is not absolute, however, and changes of a gene,
resulting in an alteration in some hereditary characteristic, can occasionally occur. Such changes are called
gene mutations: their frequency is increased by a number of chemical and physical agents, ionizing radiations
being among the most studied mutagens.
36. Cellular division is accompanied by duplicationof the chromosomes and their separation into daughter
cells. Radiation damage to the chromosomes themselves
may also be observed. These are called chromosome
mutations or chromosome aberrations and consist of
breal{s of chromosomes and their consequences. Chromosome mutations may also result from unequal distribution o! chromosomes during cell division.
37. Somatic cells contain two sets of chromosomes,
one inherited through the sperm of the father, the otherthrough the egg of the mother. Since the zygote originates from the union of two gametes, the chromosomes,
and therefore the genes. would double at each generation if, during their development, cells of the germ line
did not undergo a process of reduction. Cells with two
sets of genes thus give rise tO gametes having only one
set through a sequence of two divisions called meiosis.
As a result of meiosis one chromosome from each pair,irrespective of its paternal or maternal origin, goes toform a gamete.
38. The gametes, which contain one set of chromosomes, are called haploid cells, whereas germ-cells prior
to meiosis ( oogonia and spermatogonia) and somatic
cells, contain two sets and are called diploid. The ploidyof a cell represents the number of haploid sets of chromosomes contained in its nucleus. Polyploids, cells withploidy higher than two ( triploids, tetraploids, etc.) are
known in some organisms and tissues. Malignant tissues, as a rule, have some cells with chromosome numbers different from those of normal cells.
39. The distinction between gen~ cells and somatic
cells is important, since injuries produced in somatic
cells will be confined to the individual, whereas thoseaffecting germ-cells can be transmitted to the next generations, and may therefore give rise to hereditaryeffects. Since somatic cells give rise to cellular progenies
which can be affected by damage to their genetic material (somatic mutation) and perpetuate such damage
within the individual, it is evident that "genetic" effects
can be produced in both somatic and germ cells. In thepresent report the expression "genetic effects" will referto genie or chromosomal alterations irrespective of theiroccurring in somatic or in germ cells. The term "hereditary effects" will be limited to those genetic effects thatcan be transmitted to the next generation.
40. Cells of different organs and tissues differ widelyin their morphology, metabolism, and proliferative activity. Cells of the nervous system, which divide during
the embryonic life, practically cease to do so after birth,whereas lhe cells lining the digestive tract are continually replaced.

41. Also rapid is the renewal of the circulating bloodcells, erythrocytes, leukocytes. and platelets, which arecontinuously supplied by the blood-forming tissue. Unlike the active blood-forming system which is localizedin specific organs, red bone-marrow and lymph nodes,
another system associated with it, the reticulo-endothelial
system, is present throughout most tissues. One of its
main functions is to scavenge the tissues of cellulardebris and of particulate foreign substances.
Effects of ionizing r~diation on cells

42. Comprehension of the action of radiation on living cells is still far from complete and is limited by lackof lmowledge of the normal cellular structures and functions likely to be injured. Celli;lar radio-biology cannot
be separated from cellular biology; any progress ineither discipline can be expected to be accompanied byadvances in the other.
43. The achievements of biochemistry and biophysics
in the past few years have meant a remarkable progressin cellular biology and have enabled us to obtain a better picture of the complex chain of events initiated whencells are irradiated. A detailed discussion of these eventsis given in annex B. Here only thos~ will be mentioned
which are necessary to follow the argument of the ne.xt
chapters of the report. The main end-effects of irradiation in cells will also be briefly described and an account will be given of the factors which may alter the
response to radiation.
44. Radiation-induced injuries are largely nonspecific; many other agents, both physical and chemical, are able to cause the same effects as those producedby radiation.
45. The first effects of radiation on living matter are
physical, in that they affect atoms and molecules irrespective of their arrangement in living structures.B~a
A result is the splitting of molecules into fragments
known as radicals and ions. These fragments are deprived o'f the chemical stability characteristic of theoriginal molecule.
46. Radicals may interact both between themselves
and with unaltered molecules. thus giving rise to new
chemical compounds and upsetting the chemical balanceof cells.B 3G-93 Since water constitutes about 70 per centof the cell, radicals arising from the splitting of watermolecules are important in the initial chemical changes
induced by radiation.
47. All the essential constitutents of cells and in particular comple.x molecules like proteinsBn-rs and nucleoproteins,nsa-ss may be affected through the action ofradicals. They may also be injured by radiation directly,
however. without the intervention of radicals. The respective role of the direct and indirect action of radiationin bringing about cellular lesions is not yet clear; it isprobable that in most effects both modes of action
operate. n 23-29
48. Radiation damage can also be caused by decay ofa radio-active nuclide incorporated into cellular constituents.n2i6-m The localization of such a nuclide in cellular
structures is therefore important. An example is carbon14, a nuclide with a very long half-life, which decays,
on emission of a beta particle, to the stable nitrogen-14.
The beta emission may obviously give rise to radiation
effects. However, since carbon is a basic constituent of
all essential living structures, it has also been suggested

7experim~i;it that would b~ necessary to reveal them. The

that the change of carbon-14 into nitrogen '~ill sometimes occur in a key molecular structure ; this change
may appreciably add to the effects of the radiation released by that nuclide in the form of beta particles.
Although direct eviden~e r~ga;di_ng the effects of transmutation of carbon-14 1s still lumted, the local effects ofdisintegrations have been convincingly demonstrated
with other isotopes such as phosphorus-32.
49. Depending on the dose of radiation, processes
leading to the synthesis of essential cellular constituentsare retarded to varying degrees and may even be completely inhibited; this is particularly true for the synthesis of nucleic acids.Bm--132 The integrity of thesesynthetic mechanisms is essential for the maintenance ofmorphological structures and for ensuring growth anddivision of cells. Inhibition of mitosis is, in fact, one of
the earliest effects of irradiation, but probably mostcellular functions and structures are to a greater or
lesser extent impaired by radiation.n 1ss-177 Cellular deathis an over-all and ultimate result of irradiation; it can bebrought about by different mechanisms, and has in somecases been ascribed to nuclear damage, in the form ofchromosome breaks.
50. Chromosome breaks sometimes repair through rejoining of the broken ends shortly after the breakage
event; however, a proportion fail to repair. Fragmentsof chromosomes may be lost if cellular division takes
place before healing; then the damage becomes permanent.n207-215 Certain rearrangements of chromosome
material through union of broken ends in new combinations may likewise cause death at cell division (para. 57).
51. The particular effectiveness of irradiation of thenucleus as compared to that of the cytoplasm might bedue to the fact that the nucleus contains the chromosomes, each of which usually occurs only once or twice
per nucleus. Cytoplasmic structures on the other handnormally occur in great numbers so that the eliminationof one or more of them may be of less consequence. The
role of cytoplasmic damage should however not be discounted, since such damage can be held responsible forsome cases of cellular death. It is, however, much moredifficult to prove, as only exceptionally do radiationinduced morphological changes in the cytoplasm become
apparent. Yet, the mere fact that metabolic processes arealways affected by radiation, and that most of theseprocesses take place in the cytoplasm, suggests that cytoplasm may have more critical importance than suS'pected.

detectability decreases with the dose, since at very low
doses the frequency or the degree of any effect becomesso small as to require unmanageably large numbers ofcells to become appar~t. ~diation-induced lysogenesis(the release of bactenal viruses from bacteria which do
not normally release them) is detectable at doses as low
as 0.3 rad.
S4. The dose of radiation necessary to produce agiven effect in a given fraction of different cellular populations is inversely related to their relative sensitivity.
When the effect investigated is cellular death, the natureof the cells (protozoa and bacteria are more resistant
than mammalian cells), the size of the nucleus (in anumber of plant cells sensitivity is related to the volumeof the nucleus) and ploidy (haploid cells'have a sensitivity different from diploid cells) are among the various
cellular factors which affect sensitivity.B 11s-1s5
SS. Sensitivity is also related to physiological conditions of the cells. Thus, bacteria grown in complex,
nutritionally rich media are often more sensitive thancells grown in simple media.
S6. Various factors influencing the development ofradiation effects are known. n 9 ' -11 ° Cell sensitivity varies
with the temperature and moisture content of the cells;
it is also modified by a number of chemical factors that
may raise or decrease sensitivity. Among those which
reduce sensitivity, lack of o:i..-ygen is the best known,
most radiation effects arising at higher doses or becoming less pronounced when cells are poorly oxygenated.
Certain chemical compounds, on the other hand, whenapplied before or during irradiation, are able to somee..xtent to protect cells from radiation damage. Thosechemicals may act by reducing the amount of oxygen
available to cells or by competing with radicals producedby the irradiation. Their study is important since it may
lead to methods of reducing radiation injury in man.
57. One of the major effects of radiation is the production of genetic damage.nm-m This can be caused by
two different mutational mechanisms, chromosome mutation and gene mutation. The former is the consequence of chromosome breaks. When two or more
breaks are produced in the same or in different chromosomes. the unions which may occur frequently involve
alterations of the original sequence of genes. Alterationof the gene sequence as well as loss of parts of chromosomes or even of avhole chromosomes often leads tocellular death. In some cases, however, the chromosomal
damage is transmitted to daughter cells.
58. The nature of gene mutations has been greatly
clarified by studies on bacteria and viruses. Nucleic
acids, along which genes are arranged within chromosomes, consist of a sequence of elementary units invarious specific permutations. Changes in the sequenceof these units result in mutation.
S9. The mechanism of mutation is, however, far frombeing understood. Studies in lower organisms haveshown that mutation is a complex process going througha first stage in which the damage may, at least to alimited extent, be reparable and only after a certain time
become irreversible.
60. Like all radio-biological effects, the induction of
mutations is dose dependent and is proportional to thedose down to the lowest levels investigated so far. The
proportionality factor, however, has been shown to varywith the dose-rate in a number of species, a!! will be
discussed in chapter IV.

52. Extensive quantitative work has been done on thedependence of the frequency of cellular death on
dose.Bia-so When a cell population is exposed to radiation, a fraction only of the cells becomes unable to reproduce, the size of the fraction depending on dose. It
is not predictable whether an individual cell will fail toreproduce, but the proportion of deaths reflects theprobability that individual cells may be killed. At low
doses proportionality between dose and fraction of cells
killed is frequently seen, but sometimes more complex
situations arise. In any case, however, the proportion ofaffected cells increases with increasing doses.
S3. The relationship between dose and effect is being
studied at lower and lower doses for a number of radiation effects. Since the frequency or the degree of any
effect is directly related to the dose, effects at very low
doses are very small and may be demonstrated only whenvery large numbers of cells are irradiated. The possibility of detecting effects at the lowest doses has therefore practical limitations determined by the size of the8CHAPTER III

SOMATIC EFFECTS
the best estimate of the median lethal dose (LD 50) for
man is 300 to 500 rad (short-term total body radiation;
the actual value depends on the type and distribution of
the radiation). This does not mean that man can tolerate
this amount of radiation, since all individuals exposedto this level would have serious symptoms and 50 per
cent would die. It must be stressed that the results of
exposure to 200 rad short-term total body radiation may
sometimes cause death.

1. This chapter discusses the effects of partial andwhole-body irradiation on man. Since observations in
man are few, they will be supported by, and interpreted
in the light of, information from animal experiments.

2. Owing to interrelationships between parts of theorganism, damage to an individual organ may induce
effects in other organs or even in the whole organism.
Repair mechanisms may play a major role, replacing
damaged cells or tissues through regeneration of surviving cells, but complete recovery may be only apparent
and residual injury may emerge long after irradiation.

9. When individuals are exposed for a short periodof time to high doses of penetrating radiation the injury
to the organism may take three different forms, depending on the dose received. With doses of several thousandrad, the outcome is fatal within hours and the clinicalpicture is predominantly neurologicaI.D 199

3. The somatic effects of ionizing radiations in man
and in animals are mainly determined by physical factors
such as the nature of the radiation, the absorbed dose,its distribution in time (instantaneous irradiation, fractionated, protracted for shorter or longer periods) andits spatial distribution, in particular the extent to which
the body is exposed.D 1 - 11

10. Between SOO and 2,000 rad of total body radiation, gastro-intestinal symptoms predominate.D 200 They
usually develop within a few hours, may then subside fora few days and then recur suddenly, leading to deathwithin about one week.

4. In assessing susceptibilities various end points canbe used; and the apparent radio-sensitivity of a tissueor organ depends on the method of observation. Sensitivity depends on age at the time of exposure, children
being more susceptible than adults.D 2 s-- 2s

11. With doses between 100 and 500 rad given withina short time, gastro-intestinal symptoms may develop
within a few hours, followed by apparent recovery. Conditions worsen, however, within a period of about three
weeks, when the first signs of injury to the blood-forming organs begin.D 20 ~ Damage to the blood-forming
organs may cause bleeding and increase susceptibility toinfection. When appropriately treated with general supportive therapy, patients may recover.

5. The initial effects produced by radiation may leadto clinical effects expressed promptly or months or years
after irradiation depending not only on the nature andextent of the initial radiation injury, but also on secondary factors, such as hormonal influences, exposure
to other carcinogens, nutritional and other host factors.
Animal experiments suggest that even viruses may besuch co-factors in carcinogenesis, but no human cancer
has thus far been linked to a virus.

12. Other organs and systems are always involved
concomitantly with those whose damage is or may be
conducive to death. Not all observed changes are morphological; functional effects also occur, e.g. modification of conditioned reflexes in animals given local doses
to the head as low as 5 rad.D 9 o

6. It is not possible to distinguish sharply between
early and late effects since effects observed soon afterradiation may persist. Nevertheless, it is convenient toconsider as early, such effects as are observable withina few weeks aiter exposure. Late effects are those thatappear many months or years later and are not always
obviously related to the early effects.D 12- 14

13. The radiation pathology of individual tissues andorgans was dealt with extensively in the 1958 report andis again reviewed in annex D of the present report. No
detailed account will therefore be given in this chapter.

Early effects

Late effects

7. All organs and systems in man and animals canbe temporarily or permanently affected by irradiation.
Injury to blood and blood-forming organs, to the alimentary tract and to the nervous system are the most criticalin determining the possibly fatal outcome of total body
irradiation.

14. The difficulties in the study of the late effects ofradiation are in part due to the long interval of time that
may elapse between irradiation and clinical manifestations, sometimes making it difficult to establish the connexion between the effect and its cause. They are also
due to the lack of specificity of the effects.

8. The clinical course of acute radiation injury in man
is well known from observations on individuals exposedto large doses of radiation. Evidence from the irradiatedpopulations in Hiroshima and Nagasaki and in the
Marshall Islands, from subjects irradiated therapeutically or in the course of laboratory accidents withcritical assemblies, as well as animal data indicate that

15. The late effects are, in fact, usually indistinguishable from diseases induced by other causes, and radiation
only increases their incidence in the population. The
causal relationship between irradiation and a possible
late effect in man can only be established in incfo,;dualcases from circumstantial evidence together with evidence derived from the observed induction by irradiation

9

populations. It now seems that the incidence, after
having remained fairly constant for a number of years,
is declining.

of similar effects in experimental animals. Large-scale
human surveys may confirm in man the association between given late effects and irradiation.
16. Such surveys must be carried out on sufficiently
large irradiated populations to ensure that the observed,
and always small, number of individuals showing theeffect under study is high in a control, untreated but
otherwise similar, population where the incidence ofthat effect may vary owing to chance alone. When theincrease in incidence of the effect in the irradiated population is higher than can be accounted for by chance fluctuations, the increase is said to be statistically significant.
17. In considering populations irradiated for medical
reasons, difficult problems may arise in excluding thepossibility that the disease which has prompted the irradiation is by itself responsible for an increased incidenceof the effect, in which case the association between theeffect and the irradiation could be misleading.
18. The main late effects comprise :(a) Many types of neoplasms, including leukaemia;( b) Local effects on tissues ;( c) Changes in the life-span;( d) Effects on growth and development.

25. Despite continued investigation, the doses received can only be inferred from the distance of thesurvivors from the hypocentre of the bombs. The doses,
therefore, are highly uncertain, and this uncertainty reflects on the dose-effect relationship. The data are notinconsistent with the hypothesis of simple proportionality (linearity) between dose and incidence. However,
because of the small number of cases occurring at doses
below 100 rad, various other hypotheses ean be envisaged.
26. The investigation of the incidence of leukaemia
among irradiated patients treated for ankylosing spondylitiSD2s+--262 also shows a clear dependence on dose, andthe data are not incompatible with a linear relationshipbetween dose and effect. The validity of these results islimited, however, both by the limited number of observed leukaemias and by the fact that the probabilityof developing leukaemia after irradiation among spondylitics may not be the same as for the general population. In any case, this study does not provide evidenceof an increase in the incidence of leukaemia following
doses below 500 rad.

INCIDENCE OF LEUKAEMIA AFTER RADIATIOND 241 - 286

27. Neither investigation, therefore, can definitely
answer the question as to the nature of the dose-effectrelationship; nor can they answer the further question
as to whether the association between radiation andleukaemia occurs below a certain dose. Whatever thedose-response curve at higher doses, it is impossible
either to establish or to exclude the possibility that a
critical dose might be required before irradiation brings
about the morphological and functional cell derangements responsible for inducing leukaemia.

19. In all countries for which mortality data are available, the recorded death-rates from the various forms ofleukaemia (malignant proliferation of some of theblood-forming cells) have been rising since the tum of
the century. Recent statistics, however, show a perceptible and consistent decline in the rate of increase of
these diseases in the United States since 1940. If thistrend were to persist, the incidence could eventuallystabilize or even decline. A similar trend has been noted
in Japan, but at later time periods. It will be necessary
to verify the uniformity of this phenomenon by datafrom other countries.
20. While the cause of the increased incidence ofleukaemias is unknown, the recent reduction in the rateof increase appears to discredit the hypothesis that thegrowing exposure of human populations to radiation is
the major factor responsible for the increase.
21. The relationship between external irradiation andthe occurrence of leukaemia in man, first suspected whenits increased incidence among radiologists was aoticed,
is now established by two continuing studies: the incidence of leukaemia among survivors of the atom bombs
in Hiroshima and Nagasaki and among ankylosing spondylitis patients given X-ray therapy. Very few data areyet available on the induction of leukaemia by internal
irradiation in man even at high doses, but this phenomenon has also been described in experimental
animals.

28. In the ankylosing spondylitis as well as in the
Hiroshima and Nagasaki surveys, no statistically significant difference can be shown between the observed incidence of leukaemia at the lowest doses investigated andwhat would be expected if the incidence was the same asin the general population. This cannot be construed as
evidence for the existence of a threshold. since the absence of difference may only reflect the fact that theincrease in the incidence of leukaemias at low doses is
too small to be detected.
29. Experiments to provide critical information concerning dose-response relationships, mechanisms of ra~
diation carcinogenesis and protection against radiationin whole organisms can only be done with animals, but
their usefulness is limited by the difficulty of making
valid extrapolations from one species to another, particularly to man from animals with a much shorter lifespan. Extrapolations should, in any case, be made only
from a species in which meaningful data can be obtained.
Each type of mouse leukaemia. for instance, should beconsidered as a specific disease, and inferences and data
drawn only from those truly analogous to diseases inman.

22. Two major and closely related questions are:what is the relationship between dose and iacidence? Is
there a dose of radiation (threshold dose) below which
leukaemia will not be induced?
23. The studies on the irradiated populations in
Hiroshima and NagasakiDm-~ 53 are particularly important because the populations involved are very large andare not selected on the basis of age, physiological conditions, incidence of previous diseases or occupational
habits.

30. Since so little is known about the effects of low
dose-rates, great care must be exercised in inferring,from the available experimental, or human data, theeffects to be expected from irradiation due to those artificial nuclides that are being released into the environment. \:Vhile the importance of the very low dose-rate towhich they give rise may be great, it is difficult to evaluate, since their effect cannot be studied experimentally

24. Since the first report of the Committee, a numberof new cases of leukaemia have occurred among these10diated radium dial painters, patients treated with radiumsalts for therapeutic purposes, and patients given X-ray
treatment of bones, particularly for benign or inflammatory lesions. Again, the latent periods for tumour induction are long and the dose, where known, is high, thelocal doses being of the order of hundreds of rad or
more.

owing to the unmanageably large numbers of animals
required.
31. An increase in leukaemia and other forms ofmalignant disease has been reported in children irradiated in utero, as a result of pelvic X-ray ex.amination
during the mother's pregnancy.Dm- 286 The dose of radiation may have been,..., 1-10 rad. These results and thoseof several other studies are equivocal. Results obtained
from a different type of study have shown that the incidence of leukaemia in children born of 40,000 mothers
irradiated during pregnancy was no greater than that
expected among children in the population in general.
Although the question remains open, it is a possibility
that embryonic and foetal tissue is more susceptible thanadult tissue to the induction of leukaemia following
irradiation.

38. Assessment of the risk of carcinogene.sis, including leukaemia, at low doses of radiation requires
a consideration of possible mechanisms of carcinogenesis.Dus-m In the present stage of our knowledge,
nothing can, however, be said about the mechanism ofradiation carcinogenesis without indulging in speculation. Various hypotheses may be formulated to accountfor the induction of tumours by radiation. Somatic (geneor chromosome) mutation, the action of latent viruses,
differentiation anomalies, are among the possible mechanisms through which radiation could give rise to malignancies. To show how different hypotheses might leadto different dose-effect relationships at low doses while
giving similar responses at higher doses, two hypothetical mechanisms of induction of tumours by radiation will be discussed. These have no particular merit inthemselves but are described for their simplicity andbecause they point out the possible fallacies involved inapplying to low doses dose-effect relationships observed·
at higher doses.

OTHER MALIGNANCIES

32. Data from irradiated animals and man indicatethat malignant tumours may be induced by radiation inmost tissues, provided the dose is sufficiently high.
33. Radiation-induced tumours often take long to develop, and need not be preceded by observable morphological changes in the cells at the site of origin of thecancer. Radiation can also induce malignant disease
through indirect mechanisms. Pituitary tumours, forinstance, can be observed in mice not as a result of irradiation of the hypophysis but as a consequence ofradiological destruction of the thyroid.nm The role ofindirect mechanisms has also been shown in the induction of ovarian and thymic tumours in mice.

39. If radiation induced tumours through somatic
mutation, it would be reasonable to expect proportionality between doses and corresponding incidence oftumours down to the lowest doses (no threshold). It isfurther conceivable that the number of tumours per unit
dose may be less than anticipated at low doses, if themutated cells are too few to develop into a tumour. But
it is also conceivable that with such a mechanism low
doses might give a higher incidence of tumours per unit
dose, since higher doses might kill the majority of mutated cells. Alternatively, it could be assumed that irradiation first involves general tissue damage and that thetumour only arises in the secondary stage of tissue repair. Again, there is the possibility that the productionof tumour cells is due to somatic gene mutation, arisingindirectly as a result of the increased proliferation that
accompanies the repair process. There might thus be a
critical level of radiation below which the damage would
be too limited to stimulate, during the repair stage, proliferation of such an extent as to give an opportunity forthe occurrence of a mutation.

34. Most animal e.'tperiments, usually performed withrelatively homogenous populations, have shown that
there are dose levels where no increase in incidence of
certain neoplasms can be detected. As in the case ofleukaemia, this cannot be interpreted as evidence forthe existence of a threshold. On the other hand, in the
induction of at least one type of tumour in rats, minimal
effective dose-levels are extremely low, so that there
may be practically no threshold for the induction oftumours. In some of these e.xperiments, the dose-effectrelationship seems to permit extrapolation to zero. A
difficulty with short-lived laboratory animals is that at
low doses the average period required for manifestationof the tumour may e.xceed the life-span and hence noeffect may be seen.
35. Most of the data on the induction of neoplasms
by radiation in man have involved e.'ttremely high doses.
Thus, skin cancers have appeared with low incidence in
man after local irradiation in the range of 1,000 rad peryear after prolonged latent periods of fifteen years or
more.

LENS OPACITYD: 9 ~ 301

40. Exposure of the optic lens to radiation may befollowed by lens opacities. Normally, doses greater than
500 rad of X-rays are required to produce clinicallysignificant cataract, but lens opacities have been reported
after as low as 200 rad of mixed gamma and neutron
irradiation. In most cases, lens opacities developed aftera latent period which shmved little relation to dose andduration of treatment. Radiation-induced lens opacities
are slowly progressive for a long time, but they may
remain stationary at any stage, or regress. For chronic
irradiation, neutrons seem to be much more cataractogenic than X- or gamma rays.

36. Since the first report, preliminary data on theJapanese survivors of the atom bomb have become available,° 281- 288 indicating an incidence of some forms ofcancer other than leukaemia higher than in the nonexposed population. The increase is highest among those
who were closest to the explosions. Because the latent
periods of induction of most tumours are long, data are
not yet available that would indicate whether this increase in the incidence of malignancies will persist, risefurther or decline.
37. Data on the induction by radiation of bonetumours in man-chiefly osteogenic sarcoma, probably
originating from those bone-forming cells that line bone
surfaces-have been obtained from occupationally irra-

INDUCTION OF STERILITYD 3 os-315

41. The effects of irradiation on gonadal tissue are
now fairly well known both in experimental animalsmice, dogs and monkeys-and in man. In all species, the11EFFECTS ON E.MBRYOS -~1''1) FOETUSESDi1o-m

eff~cts 'are ba~ically ·similai: but difference~ are observed,
due to the differences in the transformat10ns that germ
cells undergo during maturation in different species.
42. Gonadal doses causing sterility are similar forboth sexes. Single loca.l ~oses around 150 rad may ~nduce
brief lowering of fertility, doses around 250 rad mduce
temporary sterility for one or two years; at about 500
rad permanent sterility is obtained in many individuals
and prolonged temporary sterility in others. At 800 rad
recovery of fertility is e.xtremely unlikely.
43. The data on which these estimates were made arerather limited. They are confirmed by observations on
individuals exposed to radiation from atom bomb explosions in Japan and from certain radiat~on a~ci?en~s.
These observations show that whole-body irrad1at10n m
the range between 400 and 600 rad does not have apermanent effect on fertility.

. 49. The effects of radiation on embryonic tissues areespecially important because even a minor. irreversible
injury i11 an embryo may be amplified in the course ofdevelopinent and thus give rise to major anomalies. Susceptibility of embryonic tissue to radiation is hig~. but
probably not higher than that of actively dividing adulttissues. When mouse embryos are irradiated at a dose
as low as 25 rad, 40 per cent of the embryos are killed.
Irradiation of experimental animals may, at a later stage,
be followed by the development of malformations. Similar observations have been reported in man ; the mostfrequenfdefects involve the central nervous system, theeye and the skeleton.

50. The possibility of inducing somatic effects in
foetuses at doses within the ranges of X-ray pelvic examinations (several rad) is shown by the recent observation of an increased incidence of anomalous distribution of pigment in the iris of children which had been
irradiated in utero during such examinations of themothers. This harmless anomaly may perhaps be attributed to a: somatic mutation-either genie or_ chromosomal-occurring early in the embryonic development.

LoNGEVITYD llS-140, ~32-239

44. Animals having survived substantial or nearly
lethal doses of radiation have an average lifetime shorter
than controls, the life-shortening depending on the kindand amount of tissue irradiated (for partial body exposure) as well as on the dose. Under continuous ir.radiation at dose-rates as high as 0.5 rad per day, no ~ffer­ence in life-span between irradiated and control arumals
is, however, detectable with experiments of the size used
so far.
45. Irradiated animals develop some of the diseases
prevalent in their species earl!er than 1!on-i;radiated ?nes
and deteriorate sooner, showmg phys1olog1cal and h1stopathological changes sugg~stive o! early se~escen~e: Theradiation-induced shorterung of hfe-span is conditioned
by several factors. Some species are more likely to show
the effects than others; within a species, strains wifo
different genetic constitutions have their life-span decreased in various amounts.
46. It is not yet clear how much of the reduction inlongevity is due to an increased incidence of radiationinduced diseases and how much is accounted for bypremature aging. The difficulty arises both f_rom the lackof rigorous definitions of senescence and its progress,
and from the necessity of observing animals for theduration of their lives.
47. Information on life-shortening effects in man isstill inadequate. Mortality rates of United States radiologists are slightly higher than in the general male popi:lation, but the difference is not supported by the analysis
of mortality of British radiologists. These differences
may be due to different radiological practices. The survivors of Hiroshima and Nagasaki have so far shown no
detectable shortening of the life-span, but it may be that
not enough time has elapsed since the exposure as compared to the normal human lifetime.
48. Attempts to assess the risk of life-shortening by
low doses in man meet the same difficulties and necessitate· the same considerations as those entailed in theassessment of possible carcinogenic effects from low
doses. The problem of extrapolation of animal lifeshortening data to man is difficult because of the lack ofdata on life-shortening for large animals with life-spansintermediate between man and rodents:· Life-shortening in man as a consequence of short-term irradiation of
the whole body at doses higher than 200 rad would not
be surprising, but the effects of long-term, low-level
irradiation on the human life-span cannot be predicted.

Conclusions

51. Since 1958, no new data have emerged which
would warrant substantial modification of the views
expressed in the last report. The new data have notdisproved the .assumed proportionality between dose andeffect that was used for estimating risks at low doses,
but they have in fact made it apparent that such a relationship may not hold at doses lower than those whichhave been investigated. It is also now more fully realizedthat somatic effects are less likely to occur at low doserates than at the high dose-rates employed in many
experiments.
52. Short of obtaining adequate data on the frequency at low doses of such deleterious effects of radiation as leukaemia and other malignancies-and this will
involve extensive human surveys and animal experiments-the use of any relationship to predict effects at
low doses will. in fact, imply assumptions on the mechanisms through which specific radiation injuries arebrought about.
53. In the present state of our knowledge, any suchassumption would be largely speculative. The only justifications for applying to low doses relationships observed at higher doses, therefore assuming that there isno threshold for the induction of malignancies, are theexpediency of the procedure and the consistency of theassumptions regarding mechanisms in both dose ranges.
We do not know, however, whether in so doing the risk
is underrated or overrated.
54. Although more information is required before
firm conclusions can be drnwn, there is evidence indicating that embryos are more susceptible to radiation
injuries than adults and that even low doses may induce
both developmental disorders and malignant changes inembryos. Further studies on the effects of radiation on
foetuses exposed in utero are therefore crucial.
55. Search should be intensified for carcinogenic
agents in the environment besides radiation. To assess
the importance of radiation in carcinogenesis, radiation
hazard must be placed in the perspective of agents thatare understood at least as well as radiation.

12

56. Laborious though it may be to make observations
on the effects of low doses on large human populations,such observations will be invaluable in complementing
and confirming extensive animal e.xperiments. Anylarge-scale investigation, however, especially in man,requires accurate planning to ensure that there is areasonable likelihood of obtaining meaningful results.

Both clinical, and vital and health statistical studies ofsufficiently large populations living in areas of different
radiation background, of the survivors of Hiroshima
and Nagasaki, of persons receiving radiation for medical
purposes and of occupationally exp"osed persons requirecontinued support and prompt reporting.

13

CHAPTER IV

HEREDITARY EFFECTS

1. Genes are the determinants of the inheritable characteristics of organisms, and are characterized by aninherent stability which ensures that at each duplication
two identical copies are produced. This stability is not
absolute, however, and a sudden and fortuitous change
of a gene, and therefore of the character which it determines, can occasionally occur. Such changes are called
gene mutations and their frequency is increased by anumber of chemical and physical agents. Of these, radiation is one of the best known.
2. It will be recalled from chapter II, paragraph 37,
that cells of the germ line are diploid until they undergo
reduction during meiosis and thus become haploid
gametes. Depending on whether their diploid cells carry
identical or different genes at a given site (locus) on agiven chromosome pair, individuals are called homozygotes or heterozygotes for that locus. respectively-inother words, if A and A' are two different genes (i.e.,
alleles) which can occupy the same locus, then AA and
A'A' individuals are said to be homozygous, whereas
AA' individuals are said to be heterozygous. Heterozygous individuals may show the traits determined byeither gene, or an intermediate trait. The gene which
manifests itself more strongly in the heterozygote iscalled dominant, the other recessive.
3. The distinction between dominant and recessive
genes is essential for an understanding of the hereditaryeffects of radiation. Mutations which give rise to dominant genes (dominant mutations) are expressed in thefirst generation offspring of the subject in whose germ
cells the mutation has occurred. Recessive mutations, on
the other hand, can become apparent in the offspring
only if the offspring receives the same mutation fromboth parents, and this may take many generations tooccur, unless the parents have one or more common
ancestors, in which case it is likely to happen sooner.
4. Human diploid cells have forty-six chromosomes.
Of these, twenty-two pairs ( autosomes) are alike inboth sexes. Another pair consists of the sex chromosomes which are alike in females but different in males.
This is because all the eggs possess the same set of chromosomes, one of which is known as the X-chromosome.
Sperms on the contrary are divided into two classes
according to whether they possess an X-chromosome or,alternatively, a Y-chromosome, shorter than the X. Male
gametes are called X- or Y-sperms depending on the sex
chromosome which they carry, the two categories being
produced in approximately equal numbers. Fertilizationof an egg by an X-sperm will result in a zygote v.-ith two
X-chromosomes which will develop into a female organism. Zygotes resulting from the union of an egg witha Y-sperm will develop into males.
5. In man and mouse, and possibly in all mammals,
the Y-chromosome seems to have the principal role indetermining se..x, since it has recently been discoveredthat exceptional individuals carrying only one X-chromosome are predominantly female in their characteristics whereas other exceptional individuals who carry two

X-chromosomes and one Y-chromosome are phenotypicmales, contrary to what is observed in the fruit fly
Drosophila melanogaster. Sex chromosomes also carrygenes determining other traits, although at least in man
no such gene is known beyond question to be carried by
the Y-chromosome. On the other hand, some thirty locihave been identified in the X-chromosome, where specific mutations determine grossly harmful traits.
6. Characters controlled by genes located on a sexchromosome are said to be sex-linked. The fact thatfemales carry two X-chromosomes whereas males have
only one accounts for the special mode of inheritance of
sex-linked characters. Well-known examples are haemophilia and colour blindness.
Natural mutation frequencies

7. Mutations are said to occur naturally or spontaneously when their production results from conditions
usually not under the direct control of man. 0 42 The factthat mutations are rare events makes any estimation of
their frequency of occurrence difficult and uncertain.
Under ideal conditions dominant mutations would lendthemselves to reasonablv accurate estimations, since itwould be sufficient to count the affected individuals bornof unaffected parents. 058 In practice, however, diagnostic difficulties and those of ruling out morbid conditions
simulating a given hereditary trait may cast doubt on
the reliability of the estimates. The situation is evenmore difficult with recessive gene mutations when mostof the genes are hidden (carried by but not manifest)
in heterozygotes. Indirect methods when used rest on
assumptions which are often not easy to verify. 063 The
average frequency of occurrence of gene mutations per
locus per generation-the mutation rate-may differ
from one strain to another and within each species themutation rate at individual loci also varies. 093
8. Various methods are available and have been used
to estimate the frequency of occurrence of mutation!
affecting specific traits.oss-<1 4 The similarity of their results makes it reasonable to assume that the average
mutation rate in main is about 1/100,000 per locus per
generation. This frequency, however, may not be representative of all the mutations arising in man, but onlyof those which have been detected.
9. The causes of natural mutations are largely unknO\vn. Various environmental factors, both chemicaland physical, including natural radiation, might be responsible for their occurrence, but very little is k"Ilown
about their relative importance. It has been shown, however, that natural radiation cannot account for morethan a small fraction of natural mutations in man.
Radiation-induced gene mutations

10. When the germ cells of an organism are exposed
to radiation, mutations may arise which can be trans14

mitted to the offspring and their descendants. It is notpossible, however, to say whether a given mutation occurring in an irradiated individual has been inducedby radiation or has occurred spontaneously. The overall frequency of mutations is always increased by irradiation, and their relative frequency at different locimay not be the same for those of spontaneous and induced origin. 0120

16. The mechanisms responsible for the dependenceof the mutation rate on the dose-rate have not been
elucidated. It has been suggested, however, that at low
dose-rates part of the damage caused by radiation to
the genetic material can undergo a process of repair. 097
At higher dose-rates, the mechanisms leading to repair
could be impaired or inhibited, thus making the exposure more effective in inducing mutations.

11. Changes in frequency depend on such considerations as the stage of germ cells irradiated, the dose ofradiation absorbed by the germ cells and the rate ofdelivery of the dose of radiation. However, for any
single locus increases in frequencies are small, evenwith the highest doses possible in experimental animals.
The study of radiation-induced mutations therefore
necessitates the use of large numbers of animals observed over many generations. In man not only is experiment seldom possible but the intervals between
generations are long.

17. The evidence for the e..xistence of repair processes
has been considerably strengthened by recent investigations.osS-92 These have shown that in lower organisms
and in Drosophila a finite period of time elapses before
radiation damage to the genetic material becomes irreversible. Treatment with various agents interfering withthe metabolism of the irradiated cells during that period
can prevent the fixation of at least part of the premutfitional damage.
18. It should be stressed, however, that none of theexperiments carried out so far leaves any doubt as tothe effectiveness of radiation in producing hereditary
damage even at the lowest doses and dose-rates whichhave been investigated. At the time of the 1958 report,
few experiments had been performed in the low rangesof doses and dose-rates. Since then, geneticists haveconsistently found both in mammals and other animals
that the frequency of mutations is affected by radiation
throughout the range of doses and dose-rates investigated.

12. Knowledge of the nature of the relationship between dose and mutation frequency is of crucial importance to understand the effect of radiation onhereditary material. From experiments on mature germ
cells of animals, especially spermatozoa of Drosophilamelanogaster, it appears that when they are exposed toradiation the mutation frequency is directly proportional to, and depends alone on. the total dose absorbedby the gonads. 085 These results formed the basis of
the assumptions on which the conclusions of the firstcomprehensive report rested. The proportionality factor was expressed in terms of doubling dose-namely
the dose of radiation that is required to double thenatural mutation frequency in a species.

Chromosomal aberrations

19. Like gene mutations, chromosomal aberrations
may occur in cells either spontaneously or as a consequence of the action of the same agents which induce
mutations. Whereas gene mutations may be consideredas changes of the genes themselves, chromosomal aberrations may consist of duplications or deletions of partof, or of whole, chromosomes, transfer or exchange( translocations) of segments of chromosomes or even
inversions of the sequence of genes along one or morechromosomes. Addition or loss of a whole chromosome
usually arises through unequal distribution of the chromosomes during division.

13. Recent studies, while confirming that the assumptions were correct with regard to spermatozoa, haveshown that the dose-effect relationship is more complex
for other cellular stages in the germ-line. The new evidence comes mainly from observations on irradiatedmice, 085 but has also been confirmed in other animal
material. 080
14. It appears from these observations that whenimmature germ cells ( spermatogonia in males andoocytes in females) are irradiated, the results are notinconsistent with the hypothesis of proportionality between dose and mutation frequency observed with irradiated spermatozoa in Drosophila. The proportionality
factor, however-and therefore the doubling dosevaries both with the stage of the irradiated germ cells
and with the rate of delivery of radiation. The same
total dose induces fewer mutations when it is given at
low dose-rate than at high dose-rate.

20. Although chromosome aberrations have been
known for a long time to occur spontaneously both inplant and in animal cells, very little attention was paid
to them in the first report since no hereditary defects in
man had yet been traced to chromosome aberrations.
Progress in cytology and in the culture of human tissue
cells 06 T-T 0 has since made it possible to establish thenormal human karyotype (chromosome number andform) and to detect abnormalities.

15. The effects of irradiation on spermatogonia andoocytes are particularly important under conditions ofcontinuous exposure at low dose-rates such as those delivered by sources to which human populations are
exposed (e.g., natural sources and fall-out from nuclear
explosions). The spermatogonia continue to multiply
during the whole reproductive life, some of them giving
rise, through meiosis, to mature sperms. OOcytes, derived from oogonia in the course of embryonic life,
remain in a particular stage of the meiotic process until
just before ovulation. Sperms and ova survive only fora few weeks if they do not take part in fertilization. It
is therefore apparent that, under continuous exposure,the total dose accumulated in sperms and ova is much
lower than the total dose accumulated until the end of
the reproductive life by both spermatogonia and oocytes.

21. In 1959, some of the most important discoveries
were made in human cytogenetics, which showed that
Down's syndrome (mongolism), Turner's syndrome
and Klinefelter's syndrome (both of which involve alterations of the sex characters) are due to chromosome
aberrations. In Down's syndrome, one supernumeraryautosomal chromosome is observed. 021 In Turner's
syndrome. the individual is an abnormal female whocarries only a single sex chromosome, the X-chromosome ;0 ' 2 and in Klinefelter's syndrome the subject, anabnormal male, carries two X-chromosomes and one
Y-chrornosome. 0 22
22. The mode of inheritance of chromosomal aberrations in man is not essentially different from that of15

dominant gene mutations. 061 - 10 Many of the chromosomal aberrations so far observed in man have beenaccompanied by complete sterility, which precludes
transmission of the anomaly. However, individuals
with Down's syndrome can be fertile and some with
Turner's syndrome have had offspring. Furthermore,such aberrations as translocations are transmitted andcan lead to the occurrence of abnormalities in theprogeny of apparently normal and fertile individuals. 024

Effect of mutation in animal populations

28. When a new mutation is transmitted for a few
generations, according to the laws governing heredity
and in the absence of other factors which will be discussed later, there will be present in the population afraction A of individuals homozygous for the mutant
gene, a fraction B which is heterozygous for it and afraction C which does not carry the gene. Dependingon the dominance of the mutant gene, fractions A and
B, or only fraction A, will show the character for which
the gene is responsible.

Frequency of chromosomal aberrations

29. When the mutant gene is incompatible with thesurvival of the individual there are several possible outcomes. If the gene is completely lethal, even in theheterozygotes B, then the condition will not be transmitted, because all who receive it
die. If it is notcompletely lethal in heterozygotes, then occasionally it
will be transmitted through one or more generations.
A good example is retinoblastoma, a dominant genedetermined tumour of the eye, which is usually fatal
in childhood. Sometimes the tumour retrogresses, however, or may be removed by surgical treatment, thus
allowing the individual to grow up and transmit thegene. Dominant mutations less severe in their effects
may be transmitted through more generations, e.g. thosedetermining dystrophia myotonica or acholuric jaundice.

23. Since 1956 technical advances have been madewhich permit a much more accurate study of humanchromosomes. As yet, however, relatively few estimatesof the over-all frequency of anomalies are available.
Since, however, Down's and Klinefelter's syndromes
are each known to have a frequency of about 1/500
at birth, it is considered as not unreasonable to estimatethat 1/100 of all live-born children carry some chromosomal aberration. 0211- 29'"ill

Radiation-induced chromosomal aberrations

24. Aberrations involving deletions or duplicationsof whole chromosomes occur spontaneously and havealso been observed as a consequence of irradiation in
Drosophila and mice. In the mouse, it has been shownthat the frequency of chromosome loss, and the mechanism through which it occurs-namely, chromosome
breakage or unequal distribution of chromosomes during division-are markedly dependent on the irradiatedcell stage. o 108-111

30. \Vhen the mutant lethal gene is completely recessive, heterozygotes can live and reproduce, whereas
homozygotes only are eliminated. The gene will therefore not be eliminated at once but will be maintained fora period of time in the population and its eventual elimination will be completed after a very large number ofgenerations, unless the same mutation is continually produced, so that the frequency of the gene in the population will reach an equilibrium value determined by themutation frequency. Many severe traits in man arecaused by genes which fit the above description. Goode.xamples are phenylketonuria and galactosaemia; bothare disorders of metabolism which determine mental
deficiencies and are usually lethal in the above-mentioned
sense.

25. When the anomalies concern sections of chromosomes only, the prerequisite for their occurrence is one
or more breaks in one or more chromosomes. It has
been shown that the frequency of detectable single
breaks is proportional to the dose. As with gene mutations, their frequency is always rather low and here thepossibility of restitution through rejoining of the freeextremities of the broken chromosomes is well established. Furthermore, in order that complex chromosomal aberrations may be obtained-translocations, forinstance-two chromosome breaks are required simultaneously and the probability that this occurs is much
lower. In any case it leads us to expect a lack of simple
proportionality between frequency and dose. 0106

31. Recessive lethal mutations seem to be less frequent than mutations which only reduce the average
number of the progeny of homozygous individuals by
reducing their fertility or the probability of mating, orby making them more vulnerable to a given environment. In such cases the elimination of the mutants proceeds at an even slower pace. Various other situations
may also arise when mutant genes are not completely
recessive and heterozygotes show a certain degree of
disadvantage as compared to individuals who do notcarry the gene.

26. Some chromosome anomalies, unlike mutations,are often microscopically visible, and can be studied in
the laboratory even on human material. By irradiating
human and other cells grown in cell and tissue cultures,the effects of radiation on chromosomes as well as thedose-effect relationship can be studied. 0 m-m Doseeffect relationships for the occurrence of chromosomal
anomalies as derived from study of somatic cells in vitro
cannot at present be applied to germinal tissues in viva.

32. Some mutant genes cannot be appraised in absolute terms unless referred to a given environment. Inman, a mutant gene is known which in the homozygote gives rise to a serious blood disease, sickle-cellanaemia. 048 Most of the homozygotes die in the first
decade of their life and very few reach the third decade,whereas heterozygotes, although clinically recognizable,
live a normal life and show no impairment of fertility.
\Vith such a severe elimination of homozygotes it would,
at first thought, seem necessary to assume that the trait
is maintained in human populations by an unprecedentedly high frequency of mutation. It has, however, been
observed that the mutant gene is present mainly in areas
where the incidence of malaria is very high and there

27. Studies on in vitro production of chromosome
anomalies are of great value in showing differences insensitivity of different animal species to radiationinduced chromosomal damage. Preliminary results on
mammalian cells, including human cells, have been obtained, but these do not yet make it possible to decide
how human cells compare in this respect with cells fromother species.
16

is evidence that heterozygous individuals are more resistant to malaria than individuals which do not carry
the gene. The loss of homozygotes may thus be morethan compensated for by the increased survival, andtherefore the more numerous progeny, of heterozygotes
as compared to the normal population living in malarial
areas.

lity when homozygous, they would achieve the same
cumulative lethality as one single completely lethal gene.
37. The use of such an indirect method requires that
accurate records of consanguinity and detailed data regarding fertility, morbidity and mortality of both consanguineous and non-consanguineous marriages should
be available. The difficulty of securing that kind of information explains why the indirect method has not yet
been extensively used. From the results obtained so far,however, it appears that each individual carries on the
average from 2 to 4 lethal equivalents, 0 n the estimates
being based on mortality before thirty years, including
miscarriages and still births. The number of equivalents responsible for major malformations and hereditary diseases is not known with any certainty and those
responsible for sterility have not so far been studied.

Magnitude of the hereditary damage

33. Any estimate of the magnitude of the hereditary
damage, as measured by the total number of harmful
genes present in the germ cells of a population over one
generation, must necessarily rest on the observation of
the actual occurrence of hereditary defects and diseases.
The possibility of estimating this amount in quantitative
terms is hampered by our lack of precise knowledge
about many harmful traits. It is admitted that genetic
factors play an important role in the causation of these
traits, but the extent to which they do so is unknown.
The discovery of chromosomal aberrations in man enables us to give a more accurate picture of the total
hereditary damage than was possible in the last report,
since a whole new category of diseases can now be
ascribed to known hereditary mechanisms.

38. It should be pointed out that the visible damage,as estimated from its observable expression, and therecessive damage, as evaluated through the indirect
approach, do not lend themselves to straightfonvard
comparisons.0140 On the one hand their magnitude isassessed through radically different methods, eachaffected by different sources of error; on the other
hand they are expressed on different scales, the visible
damage in terms of actual hardship, the recessive one
in terms of potentially harmful factors.

34. It is convenient, if crude and oversimplified, todistinguish between visible damage and recessive(hidden) damage. The former is estimated to affectabout 6 per cent of all live-born infants. 01 S-37 One percent are afflicted by known chromosomal aberrations,
1 per cent by defects due to known dominant or sexlinked genes, 1.5 per cent are destined to suffer laterfrom serious mental or constitutional hereditary diseases
and the rest have malformations which, although due
to environmental factors, may also have some genetic
component in their causation. A certain but unknown
fraction of miscarriages and still births, 038 as well asof total or partial sterility in both sexes is also probably
due to dominant mutants or to chromosomal aberrations.

39. Furthermore, as most of the manifestations of
the visible damage are accompanied by either a total or
severe reduction of fertility, the largest part of thisdamage is confined to the generation being investigatedand only for minor detrimental characters can it be carried for a certain number of generations. The recessive
damage, on the contrary, is spread over an unpredictable
and always very large number of generations and thefrequency of its manifestations largely depends on thefrequency of consanguineous marriages.

Mutation and hereditary damage

35. The recessive damage cannot be estimated directly, although an indirect method is available which
has a very broad scope as it can be applied to very
diverse situations and estimate even the recessive damage
accounting for foetal deaths and sterility. 03941 Its potentialities have not yet been fully exploited owing mainly
to lack of adequate data. The method is based on theprinciple that spouses who are related are more likely
to be heterozygous for the same mutant gene than unrelated spouses. A greater fraction of recessive homozygous offspring, and thus of defects due .to homozyg~sity,
is therefore expected among consanguineous marriages
than among the others and the size of that fraction is
expected to be larger, the more closely related the spouses
are.

40. Gene and chromosomal mutations obviously contribute to the hereditary damage, and it is important toknow what fraction of these mutations occurred in immediately preceding generations. Dominant lethal traits
are certainly due to new mutations having arisen in thegerm cells of the parents of the affected individuals,
since these mutations cannot be transmitted for morethan one generation. The same is true for diseases suchas Down's and Klinefelter's syndromes where theaffected individuals are almost invariably infertile. 0 • 0
41. The role of mutation in maintaining the recessive
damage in human populations is difficult to evaluate because completely recessive genes are detectable in homozygous individuals only. Moreover, wh~i:t recessivenessis not complete, the heterozygous condition may result
in reduced fertility and this adds further complexities
to the problem of estimating mutation rates. 0046 The
same is true of those cases in which the heterozygous
condition for a lethal or quasi-lethal recessive gene results at least in some environments, in an increased
fertdity.C• 7 - 51 Data on the extent to which recessive
heterozygotes are selected for or against are generally
lacking.
42. If most recessive heterozygotes were favoured intheir present environment to such an extent a~ t<? ov.ercome the continual loss of genes due to the ehmmation

36. The relationship between the degree of consanguinity and the frequency of traits due to recessive genes
is, in fact, a very simple one. By comparing for instancethe differential mortality at a certain age between unrelated and variously related individuals of the same
population, it is possible to estimate the average number of variously harmful recessive genes per individual
which if present in homozygous conditions, would
each, ~n the average, cause one death at the age which
has been investigated. These indirectly observed genes(lethal equivalents) need not be 100 per cent lethal.
Indeed, if two such genes each caused SO per cent letha-

17

of homozygotes from the population, then the role ofmutation in the maintenance of the hereditary damage
would be much less important.

a lowering in the frequency of females born of irradiated fathers. Such an expectation, however, has not beenborne out by investigations on the offspring of irradiated mice, 0130 and a detailed analysis of the human observations has revealed inconsistencies in the sex-ratiochanges that cannot at present be explained.

43. The present consensus of opinion among geneticists is that most of the recessive damage is supported
by mutation . but it should be stressed that such a viewis still largely speculative.c 52

49. !~e addition to the re~essive damage occasionedby rad1at1on has not been studied because recessive genes
tend .to appear among the offspring of consanguineous
marnages. Since marriages between individuals moreclosely related than first cousins are not practised in mostsocieties, at least three generations must elapse before
any child is born to parents who have a common irradiated ancestor.

Effect of irradiation on quantitative characters

44. Many hereditary characters can only be e..xpressedin terms of measurements and are distributed more orless symmetrically around a mean.° 131- 135 Examples areheight, weight, birth weight and intelligence as measured by scores in intelligence tests. The effects of anincrease of mutation rates on this type of character wereconsidered rather fully in the 1958 report and there isno new information which would alter the conclusions.

OTHER CONSIDERATIONS

50. The scantiness of data on the hereditary effectsof radiation in man does not preclude the possibility ofassessing a part of the expected hereditary damage. For
that purpose, the results of experimental studies onother species need to be applied to man. This requires
careful biological judgement and is justified only forobservations obtained in species for which it is known
that the mechanisms of induction. transmission andmanifestation of the effects considered are similar to
those in man.

45. One of the quantitative characters-viability-is
known to be adversely affected by most mutations, sothat an increase of mutation rates can be expected togive rise to a substantial reduction of viability even if
the mutations produced are not responsible for visible
harmful traits. It has in fact been shown in mice thatthe offspring of irradiated parents have a higher mortality than control animals during the early part of life.
This effect on the viability of the offspring could be
attributed to the over-all effect of many mutations andperhaps also to chromosomal changes, each with a small
effect. It is difficult, however, to express this hereditary
damage in terms that can be compared with other typesof radiation-induced hereditary damage. It is hoped thatmuch more work will be done to investigate its natureand extent, as it might prove the most important damage
affecting the first generations of descendants of irradiated individuals.

51. The possibility of inducing mutations in all theorganisms that have been investigated, from bacteria
to mice, makes it beyond doubt that radiation can cause
the same types of damage in man. It is also reasonably
certain that in man, as in other species, the overwhelming majority of newly arising mutations have detrimental consequences and that, if beneficial mutations
arise at all, the frequency of their occurrence is so low
as to be unlikely to offset the burden occasioned by theharmful ones.
52. In all organisms investigated, the frequency of
induced hereditary changes has proved to be dosedependent even at the lowest doses investigated andthere is no reason to believe that this is not so in man. 083
Animal species differ from each other, however, in their
sensitivity to the mutagenic action of radiation.ca01 As
far as the induction of chromosome anomalies is concerned, some observations of wide variations in sensitivity even between closely related species of rodents
and between these and one species of monkey limit thepossibility of straightfonvard quantitative extrapolation to man.

Assessment of hereditary effects ofradiation on man
DIRECT EVIDENCE OF DAMAGE FROM RADIATION

46. Since 1958 very little new information has been
added to our knowledge regarding hereditary effects
induced by radiation in exposed human population.
47. The largest group now available is still represented by the descendants of tl10se e..xposed to radiationin Hiroshima and Nagasaki. The survey made in 1956
revealed no detectable effect on the frequency of prenatal or neonatal deaths nor on the frequency of malformations. 0121-122 It should be stressed again, however,that this does not mean that no visible hereditary effects
were produced by the irradiation. The number of exposed parents and the dosage received by them was suchthat we should not have expected a detectable increasein the offspring of the exposed population.

53. The effect of the dose-rate has so far been foundin the mouse, in Drosophila and in silkworm,cs4 -s 7 these
species being sufficiently different to allow us to assume
that other mammals, and in particular man, may show
an analogous pattern of response. The quantitative picture may, however, differ in different species to an unknown extent if, as has been assumed. the dose-rate
effect is accounted for by the intervention of metabolically conditioned recovery processes. 05 •48. A significant change in the ratio between males
and females (sex ratio) among children born of irradiated parents in Hiroshima and Nagasaki has been reported.cm Other more limited and not strictly comparable surveys on the offspring of parents exposed toradiation for medical reasons also show changes of thesex ratio. Shifts in the sex ratio are expected on the basisof simple genetic theory which predicts a lowering in
the frequency of males born of irradiated mothers and

54. An increased exposure to radiation therefore adds
to the hereditary damage affecting mankind. Of such
additional damage, a fraction will become manifest during, and will be confined to, the first few generations
following the exposure; another fraction, and perhaps
the main one, will become apparent at a later stage in aless conspicuous way but will be sustained by mankind
for an unpredictably large number of generations. Orn;
It should be noted that some of the harm to human popu18

lations both from spontaneous and induced mutations
may be spread over more generations because sociomedical care may relax selection against individuals
with certain traits.

harmful genes which are estimated to affect about 1 percent of those born alive.CH-17 Present knowledge of dosage effects on the induction of chromosome anomalies
is too scanty to predict a doubling dose.cus There areindications that monkey chromosomes and hence perhaps those of other primates are more radio-sensitive
than those of mice. The Committee is of the opinion
that ionizing radiation would increase the prevalence ofdevelopmental congenital malformationscao-32 and ofserious constitutional disorders, 033 - 35 but no quantitative estimates can now be made.
57. Accurate and reliable estimates can only be obtained through further progress in both experimental
and human genetics. Some fields of investigation will require particular encouragement and support, as thosethat are most likely to provide answers to the questions
arising from exposure to radiation. Studies of the roleof repair mechanisms in radiation-induced mutational
processes, and of factors which may influence mutation
frequencies, may help us understand better how radiation delivered at different rates induces mutations withvarying effectiveness. Rigorous in vitro and in viva
methods of comparing susceptibilities to radiation ofvarious species will provide a sounder basis for applying to man experimental results obtained in other species.
58. Careful, protracted study should' be continued on
those groups of individuals that are or have been exposed to higher doses of radiation, such as irradiatedpersons in Hiroshima and Nagasaki, populations livingin areas where natural irradiation is high and individuals
irradiated for medical reasons. Appropriate methods
should be devised to extract from these studies all the
relevant information on radiation-induced damage tothe hereditary material that they are likely to yield.
59. An understanding of the hereditary effects ofionizing radiation cannot be obtained without a thoroughknowledge of the factors which affect the maintenanceof hereditary traits in the population-principal among
them the pressures of mutation and selection and thegenetic structure of the population. To ascertain therespective role of these factors, accurately planned andcontinued large-scale investigation on human populations living in different environmental, social and cultural conditions should be undertaken or pursued.

Conclusions
55. Any increase in the amount of ionizing radiation
to which human populations are exposed is expected tobring about a proportional increase in the frequency ofmutation. This expectation is based on the fact that ionizing radiation is known to induce mutations in e.xperimental animals at all doses and dose-rates so far investigated. Experimental observations, however, are available
only at single doses not lower than 5 rad 083 and direct
information on the dose-mutation relationship in man
is presently lacking.
56. Much progress has been made in the field of radiation genetics during the last four years. Recent investigations have added to the information used in assessing
the genetic hazards of ionizing radiations to humanpopulations ; they have also focused attention on thespecific areas most in need of further research. It is
now known that the frequency of radiation-induced
mutation is not dependent solely on the accumulated
dose but is also dependent on rate of delivery. Furthermore, factors such as sex and germ-cell stage are important influencing factors. Nevertheless, under somedefined conditions it is possible to calculate a doublingdose for gene mutations in human populations. Calculations in the 1958 report, based on many considerations,
including a lower limit estimated from the data from
Hiroshima and Nagasaki, suggested that the representative doubling dose for man might well lie between 10
and 100 rad, with 30 rad as the most probable value.
Recent information from mouse experiments now suggests that for acute irradiation, the probable combined
value for both sexes is somewhat lower than 30 rad but
not less than 15 rad.cm For chronic irradiation the mostprobable value is 100 rad or possibly higher. No better
figures are available for estimates of doubling dose forgene mutation in man. A permanent doubling of themutation rate would ultimately double the prevalenceof those serious defects determined by unconditionally

19

CHAPTER V

SOURCES OF IRRADIATIO,N

1. Human populations are exposed to radiation originating from a variety of different sources. It is convenient to distinguish between exposure from natural
sources, from man-made sources excluding environmental contamination and from environmental contamination. Each may be further subdivided according to
the following scheme :A. Irradiation from natiwal sources:(1) Cosmic rays;(2) Radiation from naturally occurring radio-active
materials;
B. Irradiation from man-made sources excluding environmental contamination:( 1) Medical irradiation due to:(a) Diagnostic X-ray procedures;( b) Radio-therapy (external or from sealed sources);( c) Internally administered radio-isotopes ;( 2) Occupational irradiation;( 3) Irradiation from miscellaneous sources ;C. Irradiation from radio-active contamination of theenvironment due to:( 1) Explosions of nuclear weapons ;(2) Disposal of radio-active wastes;( 3) Accidental releases of radio-activity.

at the sea level in temperate latitudes is normally taken
as standard and amounts to about SO mrem/year.E6-8
The rate may, however, be much higher in areas ofhigh altitude.
6. This is higher than the figure given in the firstreport of the .Committee ( 30 mrem/year), the difference
being due to the fact that the contribution of neutrons,
which are among the components of secondary radiation,
was not taken into account. The tissue dose due to theneutron component is in fact very difficult to determine
since the broad energy spectrum of those neutrons has
to be taken into account-both to estimate the energy
absorbed and to determine the appropriate RBE values
required to express the absorbed dose in rem.
(2) RADIATION FROM NATURALLY OCCURRING
RADIO-ACTIVE MATERIALS

External. irradiation

7. The most commonly occurring radio-active nuclides in the earth's crust, and those which contributemost significantly to the external irradiation are uranium-238, thorium-232 and their daughters, such as
radium-226, as well as potassium-4Q.Eie-3i These nuclides are practically ubiquitous but their abundance
varies widely from area to area.
8. Soils and rocks containing these radio-active elements emit gamma rays which, owing to their power ofpenetration, contribute substantially to the irradiation oftissues. Dose-rates inside and outside buildings usuallydiffer, however, since walls may contain the nuclides
referred to above, and hence show a gamma activity of
their own, and also since walls provide a certain shielding effect against the activity of the ground.

A. Irradiation from natural sources

2. Irradiation from natural sources is essentially constant over a period of time in a given place. Geographical variation, however, occurs and populations living indifferent areas may be exposed to different dose-rates.

9. Despite wide geographical variations, it is estimated that the average external dose-rate from naturally
occurring nuclides to which the world population is
exposed is about SO mrem/year, allowing' for the fraction of time spent indoors and outdoors.Eai(1) COSMIC RAYS

3. Primary cosmic rays are of extraterrestrial origin
and are absorbed in the upper layers of the atmosphere
where, by interacting with nuclei, they produce secondary radiation . both electromagnetic and particulate,
to which living beings are exposed.E 1 - 5

10. In certain areas, where soil is particularly rich inradio-active ore, dose-rates are much higher.Ea8-vo Such
areas are found in Brazil, Niue Island, India and theUnited Arab Republic. In the areas located in the Statesof Kerala and Madras (India) where nearly 100,000
inhabitants live, ~verage values of 1,300 mrem/year
were observed. This appears to be the only densely populated area where the irradiation from naturally occurring radio-active nuclides is known to be so high.

4. Exposure to secondary radiation differs according
to geomagnetic latitude and longitudeE 0 - 12 and also according to altitude.Eu-u Exposure is lower at the geomagnetic equator than at the poles, the difference at sea
level amounting to about 10 per cent. Along the geomagnetic equator variations are observed amounting to about
5 per cent. The altitude effect is much more marked,
since the exposure nearly doubles for each I ,OOO metres
increase in altitude. Variations of the exposure with
timeE 15-is are also observed, but these are of a cyclicalnature so that if measurements are carried out for a
sufficient period of time the exposure proves to be fairly
constant. Such variations may be considerable at highaltitudes.

Internal exposure
11. Air, drinking water and food contain variable
amounts of radio-active material of natural origin which
may be deposited in the body after ingestion or inhalation. The main natural radio-activity of the body arises
from elements of the uranium and thorium series, frompotassium-40 and from carbon-14.

5. The dose-rate to all tissues due to cosmic radiation.2012. Elements of the uranium and thorium series aremainly deposited in bone tissue. E67 • 68 The amount contained in the skeleton depends on the presence of thoseelements in drinking water and food and therefore
varies widely between geographical areas. Our estimatesof the average dose-rates to tissues due to the presenceof !on&"-lived radium-226 and other bone-seeking radioactive isotopes are now more accurate than in 1958. The
cells lining bone surfaces receive about 10 mrem/year,
the bone-marrow cells contained in the bone cavities
receive about 2 mrem/year, and the gonads 1.6 mrem/
year from these sources.

14. Potassium-40 has a very long half-life (1.4 X 109
years). It is present in a constant proportion (0.012 percent) of total potassium in all natural materials.E•s-a'
The concentration of potassium in the human body
varies considerably with age. The dose-rate to the
gonads from potassium-40 is estimated to be around20 mrem/year, whereas the mean dose-rate to the bloodforming cells and to cells lining bone surfaces is about
15 mrem/year.
15. Carbon-14 is also a long-lived element (half-life
5,760 years) which originates in nature from the interaction between cosmic ray particles and nuclei of atmospheric nitrogen.Es 2- 93 Carbon-14 in the form of dioxide
is readily mixed in the atmosphere and later diffuses into
ocean waters, while plants also assimilate it in proportion to its concentration in the atmosphere. Carbon-14
thus enters into all living organisms, of which carbon is
one of the major components. Carbon-14 is fairly uniformly distributed in tissues and shows little geographical variation. The dose-rates to which body tissues are
exposed from this nuclide are 1 mrem/year for the
gonads and 2 mrem/year for the blood-forming cells
and for cells lining bone surfaces.

13. A further contribution to internal irradiation is
given by the inhalation of the gaseous decay products ofuranium and thorium which are present in the atmosphere above the ground wherever those nuclides are contained in the soil. E 37- 42 These gaseous radio-active elements (radon and thoron respectively), once inhaled,diffuse through the lungs into the bloodstream-thus
giving rise to dose-rates to body tissues of about 3
mrem/year. The daughter products of radon and thoron
become attached to dust particles which may be depositedin the lungs where they locally irradiate the surrounding
pulmonary tissues until they are removed by physiolo· .
gical processes.
T ADLE I.

DOSE-RATES FROM NATURAL RADIATION SOURCES (MREM/YEAR)
Cell1liningbo1teBlood-

Gonadssurfau•/ormi•tulh

External
Cosmic rays• ........................................ .
Terrestrial radiation ................................. .

50 (20)b50

50 (20)b50

50 (20)b50

Internal
Elements of Ra and Th series (ingestion and inhalation) . .
Potassium-40........................................
Carbon-14..........................................

5
20
1

13
15

2

5
15
2

TOTAL 126

130

122

a

The RBE values used in computing doses are ~ven in annex A.

b Approximate contribution of the neutron fraction.

exposed, medical irradiation is applied only when specifically indicated, so that a fraction only of the population is e.xposed to it in any one year and within thatfraction the amount of radiation received by the individuals varies according to the type of examination ortherapy carried out, as well as to the techniques
employed.

16. Dose-rates from natural radiation are summarized in table I. It must be pointed out that these doserates are to be considered as approximate only ; sincevariations are wide, the dose to the population will varywith locality. The variation of natural radiation is known
in sufficient detail to enable us to compute roughly accurate population-weighted world averages.

Genetically significant doses
B. Irradiation from man-made sources excluding
environmental contamination

19. The frequencies of the types of examinations ortreatments, and therefore the corresponding per capita
mean doses to the gonads. vary with the age of thepa:ients. Since there is a high inverse correlation between age and the probability of having further children(child expectancy) it is apparent that, for equal doses,
the amount of genetic damage transmitted to the following generations will depend to a large extent on the childe.xpectancy of the patients undergoing irradiation. It isclear, in fact, that even if mutations are produced in thegerm cells of old subjects, they will not be furthertransmitted.

(1) MEDICAL IRRADIATION

17. This category consists of those irradiations which
are administered to patients by radiologists, generalpractitioners, dentists, etc., for diagnostic or therapeutic
purposes. The value of radiological procedures in medicine is so well established that they have become indispensable. At the same time, however, these procedures
involve a certain amount of both somatic and hereditaryrisk which adds to the risk from other sources.
18. Unlike natural background and environmental
contamination to which whole populations are uniformly

20. Average gonad doses from medical irradiation, as
can be computed when populations are uniformly ex-Zlposed irrespective of age, do not therefore represent thedoses which are relevant in bringing about hereditaryeffects. Allowance must be made in their computation forthe child expectancy of the irradiated subjects. This isdone by computing for each type of irradiation aweighted dose to the population which is called thegenetically significant dose.G 9less than ten types of examinations representing only asmall fraction of the total number of examinations.G 32
The high contribution of those few examinations can be
accounted for by the fact that they give rise to highindividual gonad doses, by their high frequency or because they are carried out at ages when the child expectancy is high (paras. 19 and 20).

(a) Diagnostic X-ray procedures
21. X-ray examinations are at present the only diagnostic procedures which contribute to the external irradiation. Normally the whole body is not exposed toradiation, various devices and techniques being employed
to limit as far as possible the field of irradiation to therelevant part. The contribution to the genetically significant dose from different examinations therefore varies
so that a rather detailed analysis of the exposed groups,
as has been made in annex G, is necessary in order toobtain a comprehensive estimate of the dose to the population arising from diagnostic procedures. Furthermore,dose estimates have to be made on the basis of a limited
sample of the population; these estimates may be liableto bias since rigorous sampling methods have so far been
applied in only a few cases.
22. Table II shows the total annual genetically significant doses received from X-ray examinations by the
populations of those countries and areas from whichdata have been made available to the Committee. The
values of the genetically significant dose that have beenreported to the Committee appear to range from 6 mrem
to 60 mrem per year.Gtablexxni Such a variability may
be due to a number of reasons. Differences in radiological techniques are certainly responsible for part of it,
but so are both the over-all and the relative frequency ofthe various examinations, which may reflect either different epidemiological situations or different medical
methods prevalent in each country.
23. More than 80 per cent of the genetically significant dose from diagnostic procedures is contributed by

24. While these data refer only to countries with a
total population of about 200 million inhabitants, it is
to be expected that the populations of countries withcomparable hygienic and medical standards may receive
genetically significant doses of the same order of magnitude as those recorded in the table. These data may thus
be representative of a much larger fraction of the world
populations, including those in the USSR and the UnitedStates.

TABLE II.

GENETICALLY SIGNIFICANT DOSES (MREM/YEAR)
FROM MEDICAL PROCEDURES
A

B

c

3

J

Country-wide surveys
Austria ................................ . 16-25
Denmark .............................. . 29
France ................................ . 58
Japan ............................•..... 39
Norway ............................... . 10
Sweden ..............................••. 38
Switzerland ....................•........ 22
United Kingdom (except Northern Ireland). 14

Limited surveys•
Argentina (Buenos Aires). . • . . . . . . . . . . . . . .
Federal Republic of Germany (Hamburg). . .
Italy (Rome)............................
Netherlands (Leiden).. . . • . . . . . . . . . . . . . . . .
UAR:Cairo.................................

7

Alexandria . . . . . . . . . . . . . . . . . . . . . . . . . . . .
USA:Richland..............................
Oak Ridge. . . . . . . . . . . . . . . . . . . . . . . . . . . .

7

XXIX

2

45
50

A = Diagnostic X-ray procedures. G table XXIII
B = Radio-therapy in non-malignant conditions.

(b) Radio-therapy (external or from sealed sources)
26. In therapy not only X-rays but also beta andgamma rays are used; the latter provided either byapplication of sealed isotopes (for instance, radium) or
by exposure to cobalt and caesium teletherapy units.

27. The available estimates of genetically significant
doses due to external radio-therapy for non-malignant
conditions in three areas are also given in table II. These
are much lower than the corresponding doses due todiagnostic X-irradiations, although individual doses to
the gonads are generally higher. The frequency of therapeutic irradiations is, however, very much lower than
the frequency of diagnostic ones and the child expectancy of the patients is also often lower. Little contribution to the genetically significant dose is made by external
radio-therapy in malignant conditions ·where the childe.xpectancy is usually very small.
( c) Internally administered radio-isotopes
28. Internally administered radio-isotopes are usedboth for diagnostic and therapeutic purposes and areapplied on an increasing scale owing to their greater
availability in recent times.GeMa Iodine-131 is used toinvestigate the function of the thyroid gland where it isselectively concentrated, or to treat thyroid gland diseases, including thyroid cancer. Phosphorus-32 is chiefly
used in the treatment of polycythemia, a blood disease,gold-198 in the treatment of certain malignancies. Dataon the genetically significant doses due to both iodine131 and phosphorus-32 are available from four countries. Genetically significant doses from diagnostic applications range from 0.01 to 0.03 mrem per year, those dueto therapeutic applications from 0.15 to 0.40 mrem. The
largest part of the genetically significant dose is contributed by iodine-131.

4

37
18
43
6

25. A comparison between genetically significant
doses in countries for which both present and 1958 data
are available shows that there has been little change
during the last few years. In the United Kingdom, however, the genetically significant dose has apparently decreased from 23 mrem in 1958 to about 14 mrem in 1961.
The decrease, however, is probably only apparent andmay reflect the fact that the 1961 data, unlike the older
ones, are based on a properly devised sample of all the
hospitals of the country.G 2 s It may be pointed out thatthe British data show considerable variability within the
country and indicate that, if the best techniques andequipment were used throughout the country, substantial
reduction of the genetically significant dose would beachieved.

G tableC = Radio-therapy in malignant conditions. G table XXIX
• These may be representative only of the particular area surveyed and not necessarily of the practice in the whole country.

*
22

*

*

29. From this survey of the various components ofthe genetically significant dose due to medical irradiation, it appears that the diagnostic use of X-rays is by
far the major contributor. Radiological practices are atpresent the largest artificial source of radiation to whichhuman populations are exposed, at least in countries
with good medical standards. Any measure which would
reduce the genetically significant dose without decreasing the value of radiological facilities deserves serious
attention. Such measures might include the avoidance of
all unnecessary examination, especially in younger subjects, and the use of the best techniques and equipment
to reduce the individual doses to the gonads.
Marrow doses
30. The importance of marrow doses is due to the factthat the active, or red, bone marrow contains bloodforming cells which, under the effect of irradiation, may
give rise to leukaemias. The active bone marrow bas an
uneven distribution in the body, so that the extent towhich blood-forming cells are irradiated depends on thetype of examination performed. A lmowledge of themarrow distribution is therefore needed to compute
marrow doses.G 79 The active bone marrow is mainly
associated with spongious bone so that as much as 80
per cent of it is found in the bones of the bead, of thespine and of the lower limb girdle. Accurate quantitative
data are limited, however, especially as regards thechanges of distribution of marrow with age and withvarious diseases, and studies in that field should be
encouraged.
31. It has been assumed, as a basis for computing
bone-marrow doses, that the irradiation of, say, onetcnth of the bone marrow with a given dose has the same
effect as the irradiation of the whole bone marrow witha dose ten times lower. This leads to the use of per capita
mean doses to the bone marrow as estimates of the population doses from individual irradiations. Two factors,
therefore, enter into the computation of the per capita
mean dose from a given radiological procedure, the frequency with which that procedure is applied and themean dose to the bone marrow.
32. A limited number of estimates of the mean bonemarrow doses from diagnostic e..xaminations have beenmade.G 81 These indicate that the examinations involving
fluoroscopy, such as those of the upper and lower gastrointestinal tract, and examinations of the pelvic region
are those which give rise to the highest mean bone-marrow doses. The mean marrow doses received duringexternal radio-therapy treatments may be considerably
higher than those received during diagnostic examinations.Gas
33. The data submitted to the Committee are not sufficient to make possible an accurate estimate of the percapita mean marrow doses to the population. The data
are, however, consistent with the estimates made by theCommittee in its first report in which a value of 50-100
mrem was accepted as representative of the contribution
to the bone-marrow dose from diagnostic procedures,
including fluoroscopy. No reliable estimate of the contribution from therapeutic irradiation can be made at thepresent time. The Committee is aware that a number ofinvestigations are currently being carried out and expects that these will make possible, in the near future, amore detailed and accurate appraisal of the irradiationof the bone marrow due to medical procedures.
Irradiation of other organs and tissues
34. Although gonads and bone marrow are the organs
23of the greatest importance in view of the possible effectsof radiation on them, other organs and tissues may also
be irradiated in the course of radiological examinations
and treatments.G 9 i- 97 Some of them deserve particularattention during certain procedures, in particular theeye lens during examinations of the head, the thyroid
gland during administration of iodine-131, and foetal
tissue when radiological examinations are carried out
during pregnancy. Here also the reduction of the doseto these organs can be achieved by technical improvements and, in the case of foetal irradiation, by confining
radiological examinations during pregnancy to thosejustified by clear indications.

(2) OccuPATIONAL IRRADIATION
35. Individuals may be exposed to radiation as a consequence of their occupation, either because they are
directly engaged in radiation work (medical practices,
industry, research etc.) or because their occupational
activities take place where exposure to radio-activity issignificant. The exposures can be e..xternal or internal,
the latter arising through inhalation of radio-active gases
and dusts, and through ingestion of radio-active material.
36. Some data are now available from five industrialized countries on the number of subjects occupationally exposed.G 1 o11-io 7 These range from 0.3 to 0.8
individuals per thousand of total population, and figuresfrom countries with comparable medical and industrial
standards are probably not higher.
37. Data have also become available on the occupational genetically significant doses in three of the countries referred to above.G 115 These do not exceed 0.5
mrem per year as averaged over the whole population.
In one of these countries about 40 per cent is due to irradiation incurred in atomic plants.
38. Such low values were achieved through strict
adherence to protection practices based on recommendations of the ICRP.
39. A potentially significant source of occupational
irradiation is related to high-altitude flights (above
26,000 metres) during which persons on board aircraft
may receive high doses of cosmic radiation.Gm-m Such
irradiation is of little concern at present, since commercial aircraft seldom fly at altitudes higher than 12,000
metres and flights at higher altitudes are usually of very
short duration. A different situation may, however, arise
if high altitude flights are operated in the future.
( 3) !RR.ADIATION FROM MISCELLANEOUS SOURCES

40. Many objects in common use contain radio-active
material or emit radiation. Luminous watch dials are themost common, but a host of luminous devices are to befound on the market in increasing numbers. 0117 - 126 A
number of other objects also incorporate radio-activity:
these include static charge eliminators, smoke detectors,
electronic tubes, and ceramic glazes containing uranium.
X-rays are emitted from television sets and from certain
electronic devices. The contributions to the geneticallysignificant dose from each of these sources are small, but
their total annual dose may be a few mrem.
41. The contribution that X-ray shoe-fitting devices
make to the genetically significant dose is difficult toassess. However, when inappropriately used, they may
give rise to a substantial gonad dose, both to the customer
and to the sales staff, as well as a large dose to the customer's feet.Gm The use of such devices has been prohibited in some countries.

the troposphere, the cloud will be progressively depletedof its particles owing to washout by rain, gravitational
settling, and direct impaction on surfaces. About onehalf of the debris released in the troposphere is deposited
in some twenty to forty days.

C. Irradiation from radio-active contaminationof the envirollillent( 1) EXPLOSIONS OF NUCLEAR WEAPONS

42. Nuclear explosions, as mentioned in chapter II,
paragraphs 20 and 21, are sudden releases of energy
produced by fission or fusion reactions.* The release ofenergy is accompanied by the production of varying
amounts of fission products depending on the extent towhich the explosion involves fission processes. In addition, as was explained earlier, both fission and fusion
reactions also induce radio-activity in the environment
because of the neutrons they produce.

48. In the stratosphere latitudinal movements also
occur, but turbulent movements are much less marked
than in the troposphere, owing to the temperature stability of the stratosphere.Ftss47 From the stratosphere,
cloud particles are progressively transferred to the troposphere where they are eventually deposited on the
ground (stratospheric fall-out). The passage from thestratosphere to the troposphere is, however, normally aslow process, so that the debris injected into the stratosphere remains there for a time before being removed. Fhs-52 A stratospheric reservoir of radio-active
debris is thereby created.

43. Nuclear explosions can be carried out under avariety of conditions, in the atmosphere at various altitudes, underwater or underground. In each case theextent and type of the environmental contamination are
different. This report deals mainly with explosions in
the atmosphere since these have been, by far, the mostsignificant source of man-made radio-activity in theworld environment and because very few data have been
received regarding underground or underwater explosions.

49. The period during which radio-active debris remains in the stratosphere is of importance, owing toradio-active decay. Depending on the time spent in thestratosphere, a greater or smaller fraction of these radioactive nuclides will have decayed to stable ones by thetime they reach the ground, so that the shorter-lived ones
may have virtually disappeared. The time spent by thedebris in the stratosphere may be expressed as halfresidence time, the time required for half of it to be
removed.t

44. Underground explosionsFI 2 a should not give rise
to significant environmental contamination, but someleakage of radio-active vapours may occur. Since theradio-activity of some fission products persists for along time at the site of an underground explosion, somecontamination of the environment due to water infiltration, or to other factors, may occur.

SO. In the first report the half-residence time wastaken, for purposes of evaluation of future fall-out, tobe the conservative value of seven years, although thebest value was thought to be 3~ years. This estimate wasbased on simplified assumptions as to the mechanism of
removal and on the amount of debris present in thestratosphere, as well as on the observed rates of deposition. More accurate estimates are now available,FI' 5• 48
as a consequence of direct measurements of the amountof debris in the stratosphere and of improved methods ofdating fission products originating from individual explosions. Moreover, the discontinuance of significant
stratospheric injections from the end of 1958 to theautumn of 1961 made it possible to study the movementof radio-active debris in the stratosphere without thecomplicating factor of renewed injections.

45. Nuclear explosions result in the production ofradio-active nuclides of various half-lives, from a few
seconds to several thousand years.F111- 15 The composition of the radio-active debris will therefore be different
depending on the time which has elapsed since the explosion, as short-lived nuclides progressively disappear.
46. When an atomic device is exploded in the atmosphere, the extremely large amount of heat produced
makes the resulting fireball rise, while the coarser particles caught up in the explosion when this occurs close
to the surface, fall out onto the ground in the vicinity ofthe explosion site. These particles are heavily contaminated with fission products and constitute the so-called
local fall-out.F1° 2-ss Vapours of the substances involvedin the explosion which condense into smaller particles
continue their upward movement, the height eventuallyreached by the cloud so formed depending on the altitude
and power of the explosion. The debris from explosions
up to several tens of kilotons that are carried out at
ground level will mainly remain in the troposphere, i.e.,in the lower layer of the atmosphere (below approximately 10 km altitude), while that from more powerful
explosions will cross the boundary of the tropospherethe so-called tropopause-and reach the stratosphere,
and only a small portion will remain in the troposphere.

51. It has become apparent that the half-residence
time of the debris varies with the energy of the explosion since this affects the height to which the products
are carried. There is some evidence that half-residence
times are shorter for explosions in higher latitudes andalso for explosions at lower altitudes. Estimates haveranged from as short as a few months for low altitude
explosions in temperate and polar latitudes, to some five
years for explosions at altitudes above 45,000 metres inthe tropical belt.
Rate of deposition of radio-active debris on
the earth's surface

47. In the troposphere the cloud is carried by winds
and by the process of turbulent mixing.F!ss-6o It also
undergoes both horizontal and vertical movements owing
to various meteorological factors such as changes in temperature and pressure. In the course of its movements in

52. The rate and distribution of deposition of debris
from nuclear explosions depends on several factors,FI12-79 in particular on the amount of debris in theatmosphere, and on meteorological situations. The lattershow ·wide variations and account for the large differences in fall-out rates observed between different areasand in different periods of the year.

* In_ a nuclear e..'Cplosion the total energy release is comparedwith the energy release by TNT (trinitrotoluene) when it explodes. Thus a 1-kiloton nuclear explosion is one which produces
the same energy as the explosion of 1 kiloton (103 tons) of
TNT, namely of about 1012 calories. Similarly a I-megaton
explosion would correspond to the e..xplosion of 1 megaton(lQG tons) of TNT.

t The mean residence time of the debris in the stratosphere isalso frequently used and can be obtained by multiplying the halfresidence time by the factor 1.44.
24

53. The deposition is highest in the temperate latitudes and a peak in the rate of deposition is usuallyobserved in spring.Fiso-s 9 This may be attributable to therate of exchange of air between stratosphere and troposphere, to the positions where these exchanges take place
and to other meteorological conditions.n.a-G 2

through deposition on leaves, on inflorescences and on
the bases of perennial plants than on absorption from thesoil by the roots.FII 21 •103- 107 This was generally the caseup to the end of 1959. When fall-out rates decline however, absorption from the roots, and therefore the ~umu­
lative amount present in the soil, becomes the predominant factor. This occurred in 1960 and 1961.

54. Since the majority of tests were carried out in thenorthern hemisphere and since exchange between thestratospheric air of the northern and southern hemisphere is slow, the stratos~heric reservoir is larger northof the equator than south I 97 - 99 in the early period after
explosions and, accordingly, rates of deposition are
higher in the northern hemisphere.

61. The amount of strontium-90 taken up from thesoil depends on many factors, the most significant of
which are the available cakiumFII 15- 17 and the depth towhich the strontium-90 has penetrated.FII 19 Strontium90 and calcium enter plants from the soil approximately
in the same ratio in which they are available to plantroots; this may, however, be very different from theratio of the total quantities present in the soiJ.FIIir

55. The accumulation of the debris depends on theproperties of the ground on which it falls since the debris
can be washed off by rain from impermeable surfaces.
In soil, rain and agricultural practices affect the penetration. Part of the debris falling on plants may also be
washed off but some is retained on the surface orabsorbed.

62. The ratio of strontium-90 to calcium is lower infoods of animal origin such as milk, owing to discrimination against strontium-90 relative to calcium in passage
through the animal body. Thus the average ratio in milk,
both from animals and man, is about one-tenth of thatin the diet from which it was derived.FII 29

56. Many radio-active nuclides of various half-lives
are present in fall-out and those radiologically most important are zirconium-95 ( 9 weeks), niobium-95 ( 5weeks), caesium-137 (30 years), strontium-90 (28years), carbon-14 (5,760 years), iodine-131 (8 days).
Some of them contribute to both internal and external
exposure, others either to the external or to the internal
exposure only.

63. To evaluate the strontium-90 intake of humanpopulations, it is important to know the ratio of strontium-90 to calcium in the total diet.FIIn-~o All data available to the Committee are summarized in annex F, partII, table IV. While the information is still incomplete forlarge areas of the world, enough data have become·available since the last report to make indirect estimates possible for some areas where few measurements have beenmade.FIIe.- 99 The ratio in the diet depends on its composition and on the areas in which its components areproduced. Geographic, economic and cultural factors
therefore are important. It appears that differences indiet have usually not caused dietary levels to vary morethan about twofold in areas of similar fall-out.

External irradiation
57. The main contributions to the external irradiation
due to fall-out come from the first three above-mentioned nuclides which all emit gamma rays. In estimating
the tissue dose delivered from outside the body from
deposited fall-out, allowance must be made for theshielding effect of buildings and therefore for the fraction of time spent out of doors which in tum is subject
to geographical, age and social variations.

64. It has been found that the ratio of strontium-90 to
calcium in milk had hitherto borne a relatively constantrelationship to that in the total daily intakeFIIo.-9 e in diets·where milk is the main source of calcium. The ratio inthese diets has usually been about 1.4 times that in milk.
In countries where milk is important in the diet the magnitude of the ratio of strontium-90 to calcium in the
total can thus be inferred for measurements of milk.
When, however, milk is of lesser importance, otherdietary constituents must be examined to estimate theratio in the total diet.

58. On account of the great difference between theirhalf-lives, the respective contribution of zirconium-95+ niobium-95 and caesium-137 to the total tissue dosefrom stratospheric fall-out depends on the stratosphericresidence time. Because of the relatively short half-lifeof zirconium and niobium, much of their decay, when
the residence time is long, may occur before deposition,
whereas caesium-137, with a half-life of 30 years, decays
mainly after deposition on the ground and consequently
still contributes a substantial tissue dose.

65. Once strontium-90 has been absorbed from thegastro-intestinal tract, its distribution in the body follows closely that of calcium. It is therefore depositedin the skeleton and retained for a period of years.FII 31• 32
The concentration in new bone depends primarily on theratio of strontium-90 to calcium in the diet, but discrimination against strontium occurs during its absorption
through the gutFII 3 s-so and in other physiological processes, so that the average observed ratio of strontium-90
to calcium in bone is about one-quarter of that observedin the diet.FI133 •34 Values for the ratio of strontium-90 to
calcium measured in bone from many areas are given inannex F, part II, table XX, and a comparison of
dietary and bone values for broad geographical regionsin table XXIV. The highest ratios of strontium-90 to
calcium in both diet and bone have been found in northern temperate regions, where the deposition has been
highest.

Internal exposure
59. Strontium-90, caesium-137, iodine-131 and carbon-14 are the main contributors to internal exposure.
The chemical properties of strontium and, therefore, of
its isotope strontium-90 (half-life 28 years) are similar
to calcium, an essential clement for all organisms.Fn11-a
60. Diet, including both plant and animal foods, is theprincipal source of strontium-90 in man; inhalation anddrinking water usually make only a very small contribution. Since the last report, considerable progress has
been made in our understanding of the transfer of strontium from fall-out to the human body through the foodchain and of the importance of the various factors
involved. It has become apparent that, when the amounts
currently being deposited are relatively high, the quantity of strontium-90 which enters human diet may depend more on direct contamination of the vegetation

66. Considerable age-dependent variations have been
observed in the strontium-90 content of bone,rns 2-s~ the25highest value being for children between one and two
years of age. The average level is lower in children born
before the beginning of diet contamination and is lower
still in adults. The difference between age groups reflects
differences in the extent to which bone has been laid
down since fall-out commenced.
67. Strontium-90 and its daughter yttrium-90 giverise to beta radiation, which despite its limited range
irradiates not only the bone itself but also the bonefonning and blood-forming cells which line or are contained in the bone cavities.
68. With some exceptionsFIIm the absorption of
caesium-137 from soils by plant roots is relatively
poor :FIIm- 1 ~• thus its entry into man's diet depends
primarily on the rate of deposition. The cumulative deposit of caesium-137 is also important, however, because
it contributes to external irradiation and will enter thediet when the amount in the soil is high compared with therate of fall-out. Caesium-137 is distributed rather uniformly throughout the body and is retained for a much
shorter time than strontium-90, 50 per cent of it being
removed in about four months.Fniao-132 Fewer data are
available on its concentration in food than for strontium-90. but because it emits gamma radiation the bodycontent of living subjects can be measured directly withwhole body counters. The number of these is still limited,
but sufficient measurements are available to enable reasonable estimates to be made of the content of caesium137 in the body, at least in the regions of highest
deposition. Because of the relatively rapid turnover inthe body, large age-dependent variations do not occur.
69. The explosion of nuclear weapons has considerably added to the amount of carbon-14 in the atmosphere,
which rose by approximately 30 per cent between 1953
and 1959, althou~h this increase had a value of only 20
per cent in 1960. 161.-•115 This artificially produced carbon-14 follows the same mechanism of distribution asthat produced by cosmic radiation, from which it cannot
be distinguished. The dose-rate from the artificially produced carbon-14 is small compared with other nuclides
produced by nuclear explosions. Because of its very longresidence time in the biosphere, however, the carbon-14
produced by tests up to the present time will continue
to irradiate future generations for thousands of years,
although at a progressively decreasing rate.
70. Iodine-131 is readily absorbed through the alimentary tract and is selectively concentrated in the
thyroid gland. It is also secreted in mill(. Owing to its
short half-life, iodine-131 is important for only a few
weeks after an explosion. It reaches the body throughthe ingestion of fresh foods, milk being the principal
source in many areas.F1Ils2-15s
Future level-s of deposition

71. The global rate of fall-out depends, as was mentioned in paragraph 52, on the amount of debris present
in the stratosphere. It also depends on its half-residence
time as established on the basis of a simplified model ofdeposition.Fho 5- 108 In the absence of tests, depletion of
the stratosphere progressively takes place and the rateof fall-out decreases accordingly. Any injection ofdebris in the stratosphere is followed. after a period oftime, by a rise in fall-out rates of a magnitude roughly
proportional to the amount injected.

earth. The accumulated deposit will increase until itreaches a maximum when the rate of fall-out equals therate of decay and of removal of the accumulated radioactive material. The maximum will occur at different
times for different nuclides, depending on their individual half-lives. When rates of fall-out are lower than therate of decay and of removal, the amount of radio-active
material present on the surface of the earth will decrease
until a new equilibrium is set up. In the absence of deposition, the accumulated deposit of radio-active nuclides
will eventually be reduced to zero.
73. When the amount of debris present in the stratosphere and its half-residence time are known, it ispossible to predict the rates of deposition and the accumulated deposit in the near future for individual
nuclides.F1109 However, as accurate data regarding boththe amount of debris injected in the stratosphere and its
half-residence time are only available up to the end of1960, the estimates of future deposition are based onassumptions. According to these, one megacurie strontium-90 and 1ozs atoms of carbon-14 were injected during 1961 and the half-residence time of this debris is
2.5 years.FI110-1H
74. No realistic prediction regarding the fall-out frompossible future testing can obviously be made, since tests
might be carried out in a variety of conditions and atvery different rates. Theoretical calculations can, however, be useful insofar as they indicate the magnitudeof the contamination of the environment and of the radiation doses under hypothetical and arbitrary conditionsof testing. These are assumed for illustrative purposes
only, since different conditions of testing and different
rates of testing would result in correspondingly different
doses.FI110-1H,11s,120
75. Knowledge of the mechanism of transfer of nuclides from soil to man through the food chain enables
us to predict their expected concentration in the dietfrom estimates of future deposition on the basis of measured data up to 1960 and of the above-mentioned
assumptions regarding 1961.
76. Estimates of the future world average concentrations of strontium-90 in the diet can also be made on theassumption that test explosions will be continued at a
steady rate of one megacurie strontium-90 and 1028
atoms of carbon-14 injected annually into the atmosphere starting in 1961. Under conditions of testing at a
steady rate, an equilibrium between rates of deposition
and rates of decay and removal would eventually become
established so that the amount of radio-active nuclides
accumulated on the surface of the earth, and therefore
transferred into food. would become constant. The
equilibrium values for. long-lived nuclides depend primarily on the rate of testing. They depend to a lesser
e>.1:ent on the residence time of the debris, and therefore
on the latitude and altitude of the explosions. For shortlived nuclides, however, the residence time greatly influences the equilibrium values.
Doses of radiation from faU-out

77. The doses of radiation due to fall-out depend on
the type and amount of radio-active nuclides present in
the environment. Since both the amounts and the relative
proportion of different nuclides vary with time, andsince deposition shows geographical variations, the problem of estimating doses received by the world population
as a whole are particularly complex.Fm 1-5 ,zs-s 3 The doserate in a given year has little interest per se because all

72. The continuation of fall-out will add to the radioactive nuclides already present on the surface of the
26the separate and varying yearly rates must be added inorder to obtain an estimate of the total dose, and therefore to predict the effects from a given series of explosions. It is therefore more appropriate to compute thetotal dose contribution that is being, and will be, delivered by the material injected during past explosions.H1~21 This contribution is called the dose commitment of the population due to these explosions.
78. Table III gives the dose commitment from theTABLE Ill.

assumed testing practice, from 1954 to 1961, for exposure of the gonads, the bone cells and the bone marrow. It also shows the fraction of the dose commitmentthat will be reached by the year 2000. The dose commitment is the world average obtained by \veighting doseswith geographical and population factors allowing forthe non-uniform distribution on the globe of both fallout deposits and human population.FI1Iub1e:x:I

DOSE COMMITMENT FROM ASSUMED PRACTICE OF TESTING, 1954-1961(8 years)
DoJt

Gonadsreac~d by ZOOQ

30

0.97

................................. .

11
70

1.0
0.10

TOTAL

111

0.42

External. ..••.....•..• , .... , ..•.........
Internal
Sr 10 • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • •Cs111 •••••••••••••••••••••••••••••••••

30

0.97

79

D• ..............•....................

19
116

0.91
1.0
0.10

TOTAL

244

0.54

External ..........•...••... ,., ........••
Internal
Sr 10 ••••••••••••••••••• , ••• .'••••••••••
Cs117 •••••••••••••••••••••••••••••••••

30

0.97

c1• ................•........•.........

40
14
70

0.91
1.0
0.10

TOTAL

154

0.56

SOMru o/ radialion

External .. , ...........•. ,.,, •.... , ..... .
Internal
Cs117 • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • •()•,Cells liningbone surfaces

Bone marrow

79. It appears from the table that the dose commitment refers to an exposure which is almost entirelycompleted within fifty years, e-~cept for the further contribution of the very long-lived carbon-14. It can beshown that only after about 20,000 years will 90 per centof the total dose due to carbon-14 be delivered, whereas
the same fraction of the total dose due to strontium-90
and to caesium-137 is delivered in less than 100 years.
TABLE IV.

(2) DISPOSAL OF RADIO-ACTIVE WASTES
81. The controlled fission reaction which takes place
in a reactor produces, as was pointed out in chapter II,
paragraph 20, both energy and radio-active fission products. Some of these products have economic value orscientific interest but most have not, and therefore present a problem of long-term storage or disposal. Wastes
also inevitably result from chemical processing of radioactive materials and in the industrial and medical usesof radio-isotopes.

Dose eommilmenl

SOMrce of radiation

GonadsExternal .....•.........
Internal
Cs117 •••••••••••••••••

cu ................. .
TOTAL

Cells lining bone
surfaces

External •..............
Internal
Sr'° ................. .
csm ................ .

cu ................. .
ToT.U.

Bone marrow

External. ............. .
Internal
Sr•0 • • • • • • • • • • • • • • • • • •Cs117 •••••••••••••••••()•................. .
TOTAL

commjt,,..cJSt

80. Table IV gives the dose commitment per year of
future testing at the yearly rate of 1 megacurie of strontium-90 and 10~s atoms of carbon-14 injected into theatmosphere.

DosE COMMITMENT PER YEAR OF TEST IN
THE CASE OF FUTURE TESTING

Tissue or or1an

Frcution of dose

c.ommilmenJ(mrem)

Tissue or or:anper ~or of le1lin1(mrem)

3.8
3.1
22

82. In an ideal situation no wastes would be disposedof but would be stored in adequate containers so that noleakage would take place. As is well known from experience in the normal chemical industry this is practically impossible to achieve; airborne and aqueous
effluents will always contain some amounts, however
small, of waste material. It is practicable. however, tostore all highly radio-active wastes,FIVa-io if necessary
after concentration so as to reduce their volume, andpossibly after reduction to the solid state; in this way
the probability of their dispersion becomes very remote.

29

3.8
10.5
5.3
37
57

3.8

83. Wastes consisting of very dilute aqueous solutions
or suspensions of radio-active materials are customarily
released into rivers, lakes and seas, where further dilution is achieved.FIVu- 23 Such practices undoubtedly add
to the contamination of the environment which may

5.3
3.9
22
35

27

necessitate carefully planned monitoring m order toensure that no danger arises.

arid result in the exposure to radiation of persons who
are near the place where this happens. The amount andrange of contamination obviously depend on so manyfactors inherent in the accident itself, and in the sitewhere it occurs, as to preclude any simple discussion ofthis subject.

84. Once released into the environment, some radioactive materials may be taken up by plants and ~u~ betransferred into animals and man through the diet m asimilar manner to fission products from nuclear tests.
. 85. The still limited use of atomic energy for peacefuluses and the present waste disposal practices are believed to make a negligible contribution to the doses ofradiation received by the population of individual coi:ntries. It is to be expected, however, that the expandmg
applications of atomic energy will, in the foreseeable
future, make this aspect.of the control of environmental
contamination increasingly important.

87. Past accidents have sometimes entailed considerable irradiation of a few people only who were working
in the plant where the accident happen;d. Ii; one C<l;Se,
however, substantial amounts of rad10-acttve fission
products, particularly iodine-131, '''ere spread over anappreciable area. As a consequence of the measu.res
taken such as restrictions in the consumption of milk,
the d~ses received by individuals in the population in.volved were, however, quite low. . .
88. The possibility of serious acc!dents ea~ o:iJy ~eassessed on the basis of past expenence. This is still
limited but suggests that large accidental release~, ~fsuch a nature as to cause concern for the health of md1viduals in the population, are likely to be extremely rare.

(3) ACCIDENTAL RELEASES OF RADIO-ACTIVITYFIVs'- 39
86. Either during the operation of a reactor or during
the processing of radio-acti".e. ma~erial, accid~ts may
occur which may release activity mto the envtronment

28

CHAPTER VI

COMPARISON OF DOSES A_~ ESTIMATES OF IUSKS
1. The effects of radiation on human beings havebeen discussed in chapters III and IV. In the present
chapter the contributions of the main individual sources
to the total irradiation of the population 'vill be compared on the basis of the effects that they might produce.

latent period for the induction of gene mutations is extremely short. The latent period for leukaemia also may
well be short relative to the life-span since there is someevidence that the incidence of leukaemia is declining
among the irradiated population of Hiroshima andNagasaki (chapter III, para. 23). It will be assumed in
the present chapter that conditions (a) and ( b) are
fulfilled.

2. Among the effects of radiation which may be significant in those dose ranges to which large human populations are exposed, only the induction of mutations, of
leukaemia and of bone tumours will be dealt 'vith in thepresent chapter. Other effects, such as the induction ofother malignant tumours or life-shortening might beequally relevant, but our lmowledge is still too limited toenable us to assess the importance of radiation in theircausation.

7. If proportionality is assumed between dose andincidence of effect, only the ratio of the doses due todifferent sources needs to be calculated in order to obtainthe comparative risks from these sources.
8. In the first comprehensive report of the Committee risks were computed using tentative estimates of
the relevant proportionality factors between dose and thefrequency of effect. The theoretical character of theseestimates as well as the hypotheses on which they rested
were emphasized. The Committee is of the opinion thatless reliance can now be placed on such estimates, as has
been explained in chapters III and IV. Comparative
risks only will therefore be computed in the present report, by using the ratio of the doses delivered by thedifferent sources. It should be clearly borne in mind thatvarious assumptions are involved even in this approach.

Dose-rates and risks

3. The deficiencies in our knowledge of dose effectrelationships should be emphasized. In the induction ofgene mutations, the frequency of induced mutations isbelieved to be strictly proportional to the dose, for agiven dose-rate. 083 However, the proportionality factor
for man cannot be estimated adequately at the presenttime.
4. For the induction of malignant changes, the uncertainties are still greater, since it is not certain that theincidence of such effects is proportional to the dose, andthe only available information has been obtained at doses
and dose-rates much higher than those to which theworld population is exposed. No alternative hypothesis
regarding the relationship between dose and the frequency of induction of malignant changes is, however,indicated in the present state of our knowledge, and proportionality at low doses will therefore be assumed forthe purpose of calculation.m-13

Comparative risks due to irradiationfrom various sources

9. With regard to irradiation received in the course ofoccupational exposure, the definition of "maximum permissible doses" rests on the concept of a balance between
the practical requirement for the work concerned andthe limitation of the hazards involved. While appreciating the necessity in operational control of defining ma.ximum permissible doses for groups of individuals in
relation to particular circumstances, the Committee believes that the comparison of doses from various sources
with maximum permissible doses valid for different
circumstances is likely to be misleading here and would
introduce considerations e..'{traneous to the concept ofrisk, which is based on the appraisal of harmful effects
only.

5. For gene mutations and malignant changes, theeffects will be considered to be proportional to the percapita mean doses to the relevant tissues. This follows
from the assumption of proportionality between doseand effect, and it implies that the frequency of effects inthe whole population would be the same whether, forinstance, all individuals received the same dose of radiation, or half of them received twice as much. The basis
for this estimate of comparative risks applies particularly to the small doses and dose-rates with which weare concerned and is discussed in detail in annex H.

10. Comparative risks can be computed for any twosources of radiation. Since man has always been e..'{posed
to natural radiation at an approximately constant rate,natural sources will here be taken as the reference standard on which to base comparisons with other sources.
The annual doses arising from natural sources have been
given in chapter V, table I. As was mentioned earlier,these doses are subject to geographical variations which
are well enough !mown to make possible the computationof a rough population-weighted world average. Progressin the study of natural sources is, however, desirable
because they form a useful basis from which comparisons with other sources can be made.

6. The time in which radiation causes effects need not
influence this estimate of comparative risks and the
choice of the interval over which to define the expected
incidence is immaterial provided that: (a) the latent
periods elapsing between the irradiation and the onsetof the effect in various individuals are close to the average and ( b) the duration of the average latent period isconstant at all doses. If condition (a) is not met, allowance must be made for the expectation of life in the
population, and therefore for its age distribution. The

11. However, for each source of radiation, the corn-29rate. One way of computing a comparative risk is therefore to compare it with the total dose delivered by natural
sources over a finite period of time. The choice of theperiod of time may be arbitrary, and in this report theeight-year period of testing from 1954 to 1961 is used
(on the basis described in annex F).For conditions ofcontinued testing, the relative risk is estimated by acomparison of the dose commitment per year of testingwith the annual dose due to natural sources.

parison with natural sources presents some difficulties of
its own. Medical irradiation does not involve the whole
population of a given country, so that appropriately
weighted doses to the population, for example the genetically significant doses (chapter V, paras. 19-20),
must be computed. Moreover, medical irradiation involves short exposure times, and the dose-rates may be somuch higher than those arising from natural irradiationthat the factors of proportionality between dose andeffect may be different and therefore comparison withnatural irradiation may underestimate the risk arisingfrom medical sources. It must be also recognized thatdata regarding medical exposure are available only fromcertain countries and districts with high medical standards. Such areas are not likely to be representative of
the entire world situation.
12. Problems of a different nature arise when computing relative risks due to fall-out from any finite periodof testing. The whole population is continuously exposed to radiation from such a source, but at a varying
dose-rate. Since the rate in a given year is not representative of rates in preceding or following years, theconcept of dose commitment due to a certain period of
testing was introduced in chapter V (para. 77) to define
the total dose to be received by the population from theradio-active material initially injected into the atmosphere.
13. The dose commitment due to fall-out from a finite
period of testing is not an annual dose but a total dosedelivered over a very long period of time at a decreasing

14. Table I of this chapter shows the comparative
risks from the main sources of radiation in relation tonatural irradiation. Comparative risks were estimatedon the basis of the figures given in chapter V. The second column of table I is based on the ratio between doses
to the gonads (or the genetically significant dose in thecase of medical irradiation) from the various sources.
The values therefore compare the relative risks thatgene mutations will be induced by radiation from thevarious sources, taking a value of 1 for the risk fromnatural radiation. The third column gives the ratio between mean bone-marrow doses from various sources
and therefore estimates the comparative risks of theinduction of leukaemia. Comparative risks of the induction of bone tumours, as estimated from the doses tothe cells lining bone surfaces, are given in the fourthcolumn of the table. It must be emphasized that the comparison of risks can only be made separately for hereditary and somatic effects. No comparison can be madebetween somatic and hereditary risks, nor between risksof leukaemias and of bone tumours.

TABLE I. COMPARATIVE RISKS FROM MAIN SOURCES OF IRIU.IJIATION(RELATIVE TO THOSE FROM NATURAL R..uJIATION, TAKEN AS 1)

H eredilarya

Souru

Natural sources ...................................•
l\fedical irradiationb .•........••......•..••.•.......
Fall-out from tests up to December 1961 ...•.••..•....
Fall-out from continued testing ...............•.•. , .•Somatic e:ffeds&
Leukaemia

Bone /tlmour

1.00

1.00

0.30
0.11
0.23

0.4--0.8
0.15
0.28

1.00
?
0.23
0.43

effecl.3•No comparison can be made between hereditary and somatic effects (see para. 14).
b Calculated on the basis of all information received, largely from countries with advanced
medical facilities.

15. For illustrative purposes the table gives estimatesof risks due to fall-out if tests were to be continued at
an assumed yearly rate (of 1 megacurie strontium-90
and 1028 atoms of carbon-14) injected into the atmosphere.
16. The risk from testing is mainly due to carbon-14.
The doses from this nuclide are delivered at extremely
low rates over a very long period of time (chapter V,
para. 79 and table III).

17. The relative risks due to fall-out from tests during
the years 1954--1961 could alternatively be expressed interms of the number of years of natural irradiation thatwould be required to deliver a total dose equal to thisdose commitment. Thus, the dose commitment to the
gonads from these past tests is equivalent to 0.11 X 8 =0.9 years, and that to the bone marrow is equivalent to0.15 X 8 = 1.2 years of exposure to natural sources.

30

CHAPTER VII

EVALUATIONS AND CONCLUSIONS
upon the radiation dose received by human tissues fromeach source. A simple comparison of doses does not,however, indicate the likely frequencies of harmful
effects if these doses have been delivered at widely different dose-rates. The following paragraphs discuss thesources of radiation to which man is exposed and thedoses incurred.

1. In presenting its first comprehensive report to theGeneral Assembly in 1958 the Committee emphasizedthat the conclusions of that report, as with any scientificassessment, must be subject to revision in the light ofadvancing knowledge. Since then, considerable progresshas been made in the field of study of the Committee, sothat much more information is now available and ourunderstanding of the effects of radiation is much increased. Although this makes it possible in many
instances to give a clearer account of radiation exposureand effects, the complexities of the subject that havebeen revealed by recent investigations have necessitateda qualification of some previous statements.
2. Earlier chapters of the present report outline thepresent status of our knowledge of radiation exposuresand effects and provide the basis for an assessment of
the significance of these exposures. The annexes containdetailed information on which this outline is based. The
present chapter gives the conclusions arrived at in thereport. The Committee wishes, however, to emphasizethat the report should be regarded as a whole and that
individual sentences or assessments may be misleading
if taken out of their appropriate conte.xt.
3. The review and the evaluations made by the Committee are in no way final and will undoubtedly requirecontinuing revision as scientific knowledge advances andnew data become available, the present lack of which still
limits our understanding of some problems.
4. The Committee hopes that this report, by pointing
out subjects which require more investigation andsometimes a fresh approach, will stimulate research anddiscussion that will result in an improved understandingof the effects of ionizing radiation on man and his
environment.
5. The main questions which the Committee has again
attempted to answer are:(a) What are the levels of radiation to which man is
e.xposed from various e.xternal and internal sources(including those arising from radio-active contamination of the environment as a result of nuclear tests) and
how is this exposure distributed in time, in different
geographical areas and within different parts of his
body? It has been important to specify in particular what
doses and dose-rates of radiation from various sources
are received by the gonads (testes and ovaries), in viewof their genetic importance, and by those cells in whichmalignant change may be induced by radiation, such as
the blood-forming cells of the bone marrow and thoselining bone surfaces.
( b) What are the effects produced by radiation, bothon the irradiated individuals and on their offspring, particularly at those levels to which populations are currently exposed?

RADIATION FRO~! NATURAL SOURCES

7. The estimation of the radiation exposure fromnatural sources has considerable importance, particularly because part of the normal occurrence of hereditary,and perhaps some malignant, diseases may be due tonatural radiations. Moreover, as man has always been
exposed to such radiation. the dose received from natural sources forms a useful basis of reference with which
the doses received from other sources may be compared.
8. Natural sources of radiation include cosmic rays
and those radio-nuclides which occur naturally in theenvironment. The radiation that man receives from thesesources is described either as "external" when it reaches
the body from the exterior, as from cosmic rays or by
gamma radiation from radio-nuclides in the earth's crust
or atmosphere, or "internal" when it is derived fromnaturally occurring radio-nuclides which have become
incorporated into the human body.
9. Investigations carried out during recent years haveenabled us to achieve greater precision in estimating theradiation dose to which the world population is exposedfrom natural sources. In particular, the contribution tothis dose from the neutron component of cosmic rays,
which had been disregarded in the first comprehensive
report, can now be taken into account despite uncertainties inherent in its evaluation. The inclusion of this contribution explains why the present estimates of doses
from natural sources are higher than those given in theprevious report. Accurate estimates of the doses frompotassium-40 and carbon-14 have also become available.
Combining the estimated average contribution from cosmic rays, that from external radiation from radionuclides in the environment, and that from internalradiation from radio-nuclides within the human body,the average yearly dose from all natural sources is now
estimated for various tissue and is about 125 mrem tothe gonads, 120 mrem to the blood-forming cells and
130 mrem to the cells lining bone surfaces.
10. Wide geographical variation has been observed in
the dose from most natural sources of radiation, bothinternal and external. The e.xposure from cosmic raysvaries mainly with altitude, showing an approximately
twofold increase for each thousand metres rise in altitude. The e.xternal radiation from radio-active nuclides
occurring in the environment also shows geographicalvariation, depending largely on the composition of underlying soil and rocks. "While the average dose-ratefrom these sources is about SO mrem per year in mostinhabited regions of the world, areas are knO\vn, as inparts of the Kerala, and the adjoining, coast in India,

Levels of radiation

6. The frequency with which harmful effects arecaused by each form of exposure depends essentially31where the external dose-rates may be over twenty times
as high. The exposure from internal sources also varies
geographically owing to the variable intake of radiumand of some other naturally occurring radio-nuclides.
The contribution to internal radiation from carbon-14,
tritium and potassium-40 on the other hand is fairly
constant in different places.

Apart from those from shoe-fitting machines, the dosesdelivered are unlikely to present any significant hazard
to individuals. The average exposure from any one ofthem is likely to be very small, although taken together
they may make a small but significant contribution to thetotal genetically significant radiation dosage of populations in some countries. World average values of thetotal dose contribution to populations from these sources
are not available at the present time.

MEDICAL EXPOSURES

15. It is important that the exposure of populations
to radiation from such sources should be kept undercontinuing review, as regards both the exposure fromeach source and the aggregate exposure from them all.
The introduction of any new source involving substantial exposure of individuals or of populations should berecognized and evaluated at an early stage ..An example
in the future might be the exposure of individuals to
cosmic radiation in passenger aircraft flying at highaltitudes.

11. It is now possible to place greater reliance upon
the estimates of the dose received from medical procedures. Data from a number of countries with extensive
medical facilities and a total population of 200 million
are now available. They indicate that for diagnostic
radiology the annual genetically significant dose ranged
from 6 to 60 mrem in the particular years studied. These
countries may be considered as representative of otherareas with comparable medical practice on which adequate data are not available in sufficient detail. However, only a small fraction of the world's population iscovered and the estimates may not apply to larger areasof the world_ The upper limit of the range does not exceed
half of the dose received from natural sources, althoughno simple comparison is appropriate, owing to the muchhigher dose-rates at which the doses from medical procedures are delivered. A few types of examination,
which comprise a small fraction of the total examinations carried out in each country, contribute about threequarters of the genetically significant dose. One of themost important results of these investigations is theevidence that this dose can be very substantially reducedby the full use of appropriate techniques and equipment.
The genetically significant dose due to therapeutic irradiation ranges from 2 to 13 mrem and that from the
medical use of radio-isotopes is less than 1 mrem per
year.

ENVIRONMENTAL CONTAMINATION FROMNUCLEAR EXPLOSIONS

16. The contamination of the environment and theradiation exposure of human beings from any nuclear
explosion depends very much on the type and yield of
the explosion, on its altitude and geographical location,on the construction of the device as well as on whether
radio-active products are injected into the upper or lower
atmosphere, deposited locally on the earth's surface orinto water, or retained underground. The processes bywhich radio-active material from nuclear explosions
causes radiation to human tissues are described in detailin chapter V and in annex F.
17. Since the 1958 report of the Committee, ourunderstanding of the processes involved in fall-out fromthe stratosphere and the lower atmosphere has been
increased considerably by information and continued investigation on these subjects and in consequence of thethree-rear period during which no significant stratospheric injections of nuclear debris took place. The
resultant information has tended to confirm our views
as to the way in which fission products are removed
from the stratosphere and the mechanisms involved are
discussed in detail in annex F.

12. Limited data have been obtained for bone-marrowdoses and these are insufficient to furnish accurate estimates of mean doses. They seem to confirm, however,
the tentative estimates made by the Committee in its
first comprehensive report, in which a range from 50 to
100 mrem was accepted for the yearly contribution to thebone-marrow dose, as averaged throughout the population, from diagnostic procedures, including fluoroscopy. No reliable estimates of the contribution fromtherapeutic irradiation is possible at the present time.

18. However, it has become clear that owing tometeorological factors, the rate of fall-out tends to increase in the spring, and that the stratospheric halfresidence time (or period in which half of any injection
is removed from the stratosphere) is often considerably
shorter than was estimated in 1958. Geographical as wellas meteorological factors have resulted in higher deposition of fall-out in the northern temperate latitudes thanin the rest of the world.

0CCUPATIO~AL EXPOS'GRES

13. The available data obtained from five industrialized countries show that at the present time the numberof workers who are directly engaged in radiation work
does not exceed eight per ten thousand in the population.
It has been observed that when proper radiation protection methods are used, the great majority of theseworkers receive very low doses of radiation. From information collected in four countries, the geneticallysignificant dose to the general population resulting fromoccupational e.'posures is estimated to be less than 0.5
mrem per year.

19. In our previous report the amount of radio-active
debris present in the stratosphere (the so-called stratospheric reservoir) was estimated by calculation from theobserved fall-out rate and from a half-residence time
which was assumed to be as high as seven years. A highnlue was assumed as a precaution against underestimating the dose to which human tissues would be subjectedfrom long-lived radio-nuclides. It is now known that theamount of strontium-90 present in the stratosphere wasover-estimated in consequence. Direct measurements ofthe stratospheric reservoir have now been made bymeans of high-flying aircraft and balloons and the content of the reservoir in very recent years has been estimated by this means.

OTHER TYPES OF RADIATION EXPOSURES

14. In some countries, individual members of the
population mar be exposed to various other sources ofradiation such as X-ray shoe-fitting machines, luminous dials of clocks and watches, various devices incorporating radio-active materials, and television sets.

32

nificant variation in the levels of contamination and in
the quantity of strontium-90 received by man in food.
The estimates made suggest that, over large areas inwhich the rates of deposition are similar, differences in
the composition of the diet seldom result in more than
twofold, or in certain types of diet at most fourfold,differences in strontium-90 intakes.
26. Our prediction of possible future concentrationsof strontium-90 in dietary constituents continues to be
based on the use of two factors. one depending on therate of fall-out and the other on the accumulated deposition. Better values for such factors are now establishedfor various food materials from survey data and fromexperimental methods, so that the dependence of dietaryand hence of bone contamination on fall-out conditions
can be adequately estimated.
27. The highest contamination of human bone withstrontium-90 continues to be observed in the northerntemperate latitudes. The average human bone concentrations in various parts of the world appear to be simply
related to the observed or estimated amounts of strontium-90 present in the total diet, in the manner to be
expected from experimental studies. The concentrationof strontium-90 relative to calcium in new bone is about
one-quarter of that in the diet consumed while the bone
was being formed.
28. Caesium-137, unlike strontium-90, contributes toboth external and internal irradiation. Caesium-137 differs from strontium-90 also in so far as it is not fixedin the human body but is retained there for a period oftime, which is very short compared with that in which its
activity is significantly reduced by radio-active decay.
The rate of uptake of caesium-137, and therefore its
contribution to internal contamination, depends principally on the rate of its deposition on vegetation sincecaesium contained in most soils is usually very poorly
absorbed by plants, though there are some exceptions.ir11124 The contribution of caesium-137 to external
irradiation, however, depends on its accumulation on the
ground. There is some evidence that the contribution of
caesium-137 to external irradiation over undisturbed soil
is reduced by about 50 per cent in ten years.FI1115
29. Several years' data on mean concentration of
caesium-137 directly determined in the human body are
now available and apply to a large part of the world.
Geographical variation seems to be rather small. The
concentration of this nuclide, which showed a general
upward trend from 1956 to 1959, decreased in 1960 and1961.
30. The present report deals much more fully than
was possible at the time of the previous report with theformation of carbon-14 in nuclear tests and its contribution to human irradiation. As a result of these tests, theconcentration of carbon-14 in the atmosphere and in
biological material had risen at the end of 1960 by 25
per cent above the concentration of the carbon-14
formed by natural processes, but the concentration ofthis carbon-14 will decrease considerably in forthcoming
decades owing to the dilution of the nuclide in the oceans
if tests are discontinued. Although the irradiation of
future generations from this source will continue at adecreasing rate for thousands of years because of thelong half-life of this nuclide, the dose-rate to humanreproductive and other tissues will be small in any one
generation.

20. The half-residence time of strontium-90 in thestratosphere has proved to be critically dependent on anumber of factors, including the time of year at which
the explosion takes place, the latitude, and both theheight of the explosion above the earth's surface and thealtitude to which the fission products are carried into theatmosphere. Debris injected in polar latitudes appear tohave a stratospheric half-residence time of between 6
and 12 months, whereas this time may be as long as 2
years for injections in the equatorial belt. A shorter
half-residence time for injections is important because
the resultant fall-out will contain short-lived radionuclides which will somewhat increase the radiation received by man from fall-out by addinfi to the exposuredue to the longer-lived radio-nuclides. m 23 •60- 58
21. Much valuable information has become available
on the transfer of radio-active materials from fall-out
through the food chain, and our understanding of thisprocess is greatly improved. Estimates of the amount offall-out components, especially strontium-90, are now
available from many more areas and we also have more
information on the composition of the diet of many
populations.
22. There is now much more detailed evidence concerning the importance of direct contamination of theleaves, inflorescences and stem bases of plants in introducing fall-out material into the food chain, in addition
to that taken up by the plant from the soil. In some plants
such as cereals this effect is of particular importanceduring the season when the flowers and ears are being
formed. The new information has greatly helped ourunderstanding of the transfer of strontium-90 fromdiets of various types to human beings, in whom it isdeposited in bone.
23. Some data have become available on the rate at
which strontium-90 may be removed in harvested crops,
and also leached or washed down through the soil and soaway from the rooting zone of plants. These data indicate that the contribution to human irradiation of an
accumulated deposit of strontium-90 in soil is likely tobe halved in a shorter period than the 28 years that was
assumed for purposes of estimation in the previous
report.
24. It has been possible to obtain information on theamount of strontium-90 taken daily in the diet in a number of different regions of the world, and on the ratio ofstrontium-90 to calcium in the diets of these regions. The
ratio of strontium-90 to calcium in the whole diet usuallyis higher than that in the milk, the difference being lessfor diets containing a large component of milk and milk
products. When the ratio for the diet as a whole is compared with the ratio in milk from the same region, it isfound that the over-all value for this type of diet isusually about one and a half. But the value is higher ifplant products are important components of the diet.
25. Even for the many regions for which complete
dietary surveys are not available, therefore, it is possible
to make some estimate of the likely dietary intake ofstrontium-90, provided that its concentration in milk
samples from these regions is known. However, if milk
is a minor component of diet, information on the strontium-90 content of other foods also is required. The
levels of contamination of several components of dietshow wide geographical variations connected with thedifferent cumulative deposition of strontium-90 in thesoil and the rate of fall-out. These differences and thecharacteristics of the diet in different areas combinedwith the geographical variations of fall-out lead to sig-

DISPOSAL OF RADIO-ACTIVE WASTES

31. The operation of atomic plants for the production33

of energy and isotopes and the us~ of the latter formedical and research purposes may mvolve the release ofradio-active material into the air, ground or waters. At
the present time the contri~ution f_rom this s~urce tohuman radiation exposure 1s certamly small m comparison with natural radiation and is restricted to local
areas. Hmvever, with the increased utilization of atomic
energy and radio-active substances for peaceful uses,
releases into the environment are likely to become
greater than they are now, and consequently suitable
methods for safe disposal of radio-active wastes should
be maintained so as to minimize the dose of radiationfrom these sources.
Effects of radiation
Fu:ts"DAMENTAL RADIO-BIOLOGY

32. The study of the effects of radiation on cellularand subcellular structures is a necessary prerequisite to
the understanding of radiation effects on whole organisms_. in so far as the basic radiation injury occurs
at the lowest level of organization. Fundamental radiobiology has received new impetus froi;n the ~amaticadvances made in the past few years by b10chem1stry andbiophysics. Our knowledge of the structure and mode of
replication of macromolecules and in particular of
nucleic acids has greatly increased, so that new insighthas been gained into the fundamental problem of how
genes act in controlling cellular structures and functions
and in ensuring that they are maintained in the productsof cell division.
33. The nature of the initial disturbances caused byradiation at the molecular level has become better known,
as are the factors which may alter them. The changes
produced may be partly reversible, at least when studied
at the cellular or at higher levels. This may be the casewith gene mutation, which is believed to be due to a
specific change in chemically identifiable constituents ofnucleic acids.
34. The study of the relationship between dose andeffect at cellular and subcellular levels does not give any
indication of the existence of threshold doses and leads
to the conclusion that certain biological effects can follow
irradiation, however small the dose may be. When dose
effect relationships are studied at higher levels of organization. however, it is now being increasingly realizedthat the situation may be much more complex, since
many factors play a part between the occurrence of the
primary event and the final manifestation of radiation
damage.
SOMATIC EFFECTS

35. During the intenral since the last report, ourknowledge of the somatic effects of radiation on man(those effects which are produced on the individuals
exposed) has increased substantially with the demonstration of the induction of certain transient somaticeffects by low doses of a few rad of radiation, and withthe confirmation that embryonic tissues are more sensitive than many adult ones to injury by radiation. Even
low doses may induce developmental disorders or malignant changes in embryos. Recent work has emphasized
the complexity of radiation effects, and the importanceof the qualifications that we made in our earlier reportwith regard to the numerical estimates of the frequencyof the effects that would be caused by various doses ofradiation. The complexity of the dose effect relationships
is due largely to the fact that in different dose ranges,
different types of biological effect may be produced, anda simple mathematical relationship is unlikely to apply.

The data that have been accumulated since 1958 haveneither proved nor disproved the assumption made in
the first report that at low doses proportionality can beused to estimate risks.
36. The early effects of large doses of radiation in
man have become better known as a result of the dosestudy of people who have been accidentally or therapeutically irradiated. It seems likely that, for short-term
whole-body irradiation of man, the dose causing deathin 50 per cent of the exposed individuals may be about
400 rad, but possibly as high as 500 rad and as low as
300 rad. Persistent damage from radiation is apparent
after large doses approaching the lethal range. The predominant immediate changes after low doses are transitory ones, although persistent effects may be produced
after a long period of time.
37. Various chemical, physical and biological treatments have some value in decreasing the effects of radiation exposure in animals, but no specific treatment has
been established as having practical importance in man,except for the relief of symptoms that are induced bytherapeutic irradiation of parts of the body. Several
methods are, however, under investigation for the treatment of acute radiation injury, or to reduce the amountsof radio-nuclides which may have been taken into thebody.
38. Radiation exposure of animals, continued forshort or for long periods, causes a shortening of the lifespan by an amount depending upon the dose received andthe dose-rate. It is probable that a similar life-shortening
occurs in man but the evidence on this point is inconclusive and no estimate can be given of the amount of
any such effect.
39. Irradiation for short or long periods, either ofanimals or of man, may cause neoplastic changes, ofwhich leukaemia appears to be the earliest to develop inman. There is good evidence that in the range of doses
which it has been possible to explore (from 100 rad
upwards), the frequency with which leukaemia is induced increases with the dose of radiation received, but
no further evidence has been obtained as to the exact
relationship between the dose and the frequency of this
response. It does appear, however, that the annual incidence of leukaemia in the Japanese survivors of radiation at Hiroshima and Nagasaki, which had been rising
after the nuclear e:iq>losions in 1945, though still elevated, has been decreasing since 1958. There is evidence
to suggest that the incidence of some other forms ofmalignant disease may now have increased, but it is atpresent difficult to form a reliable estimate of the extent
of any such increase.
HEREDITARY EFFECTS

40. Progress in human genetics has been very significant since 1958. An entirely new field of study has been
opened owing to recent cytogenetic findings in man. The
normal diploid number of chromosomes for the humanspecies has been accepted as forty-six: and certain serious
diseases occurring in one per cent of all children born
have come to be recognized as due to chromosomalchanges. A new class of possible radiation-induced diseases, the importance of which was unrecognized at thetime of the first report, has thus been demonstrated. The
occurrence of chromosomal anomalies has been demonstrated in somatic cells of irradiated individuals.
41. The concept of mutation induction as an instantaneous process has been revised and evidence accumulates showing that for some mutations a finite period oftime elapses between the absorption of radiation energy
34

acute effects, may occasionally give rise to a wide varietyof harmful effects including cancer. leukaemia and inherited abnormalities which in some cases may not beeasily distinguishable from naturally occurring conditions or identifiable as due to radiation. Because of theavailable evidence that genetic damage occurs at thelowest levels as yet experimentally tested, it is prudent
to assume that some genetic damage may follow any
dose of radiation, however small.
49. It must be recognized that the human species has
in fact always been exposed to small amounts of radiation from a variety of natural sources and that thepresent additional average exposure of mankind fromall artificial sources is still smaller than that from natural sources.
50. At present even the wide use of radiation in medical diagnosis and treatment in countries with extensive
medical facilities does not usually involve more thanabout a 50 per cent increase in the genetically significant
exposure to radiation of their populations, and there isevidence that simple and inexpensive modifications oftechniques could reduce the figure considerably without
loss of medically important information. Advances innuclear science and industry are being achieved with
only slight resultant increases in the average radiationlevels to which populations are exposed, and with only
very occasional accidental over-exposure of individuals.
51. At the same time, the exposure of mankind toradiation from increasing numbers of artificial sources,
including the world-wide contamination of the environment with short- and long-lived radio-nuclides from
weapons tests, calls for the closest attention, particularly
because the effects of any increase in radiation exposure
may not be fully manifested for several decades in thecase of somatic disease, and for many generations in
the case of genetic damage.
52. The Committee therefore emphasizes the needthat all forms of unnecessary radiation e.xposure should
be minimized or avoided entirely, particularly when the
exposure of large populations is entailed; and that every
procedure involving tlle peaceful uses of ionizing radiation should be subject to appropriate immediate andcontinuing scrutiny in order to ensure that the resulting exposure is kept to the minimum practicable level
and that this level is consistent with the necessity or thevalue of the procedure. As there are no effective measures to prevent the occurrence of harmful effects ofglobal radio-active contamination from nuclear e..xplosions, the achievement of a final cessation of nuclear
tests would benefit present and future generations ofmankind.
53. The urgent need for research into many aspectsof radiation and its biological effects has been emphasized repeatedly in this report. Although we have extensive and increasing information about the levels ofradiation to which man is e.."<posed from various sources
and about the types of harmful effect which may result, we still know very little about the frequency withwhich such effects are likely to occur, particularly following small doses of radiation received at low doserates. It is of the utmost importance that investigationof this central problem should be actively pursued by
all relevant means, including not only studies of theways in which radiation may induce malignant and otherdelayed changes in tissues but also well planned surveysof the frequency with which such late effects occur inhuman populations following any accidental, medical
or other relevant type of exposure to radiation or inareas of high natural radiation.

and the completion of the mutation process, during
which depending on the physiological state of the cell,at least partial repair of the damage may be possible. The
effectiveness of the repair mechanisms may be altered bya variety of agents and conditions, and will also be dependent on the way in which the radiation is distributed
in time.
42. The frequency of gene mutations produced byirradiation has been shown to be proportional to thetotal dose received by the germ-cells. The proportionality, however, has been shown, in mice, fruit flies andsill.."Worms , to vary with certain factors including thedose-rate. The dose required to induce as many mutations as naturally occur, the so-called doubling dose,
therefore also changes with the dose-rate. Doublingdoses are higher for .low than for high dose-rates, theobserved difference in mice being fourfold for the maleand possibly larger for the female.
43. More data, however, are needed before the possible magnitude of this effect in man can be evaluated so
as to enable us to make better comparisons between different conditions of irradiation. In any event the recent
findings , while confirming the validity of the concept of
doubling dose in particular circumstances for a given
dose-rate, have shown that it is not possible to estimate
with confidence a representative doubling dose for man.
44. In spite of the preceding reservations there should
be no misunderstanding about the reality of genetic
damage from radiation. Although individual mutations
vary greatly in their effect, there is no doubt that any
increase in mutation is harmful. Further, we know that
mutations accumulate in germ-cells and we have no evidence from any experimental work for a threshold dose,or rate of delivery below which mutations are not induced. In fact, it has recently been shown that a single
dose as low as 5 r increases significantly the number ofmutations in the fruit fly. As regards man, the total dose
received by the average individual in the population isstill the most important indicator that we have of theamount of damage induced.
45. It is likely that the great majority of gene mutations induced by radiation are identical with those which
occur "spontaneously". There is some evidence, however, from lower organisms that radiation determines adifferent proportion of certain harmful mutations thanthat occurring naturally.
46. The most extensive study is still the investigation of the offspring of parents exposed to the atomic
explosions of Hiroshima and Nagasaki. The investigators detected no significant increase in the frequency
of malformations or early deaths in the children of irradiated parents. Both this survey and a number ofother more limited investigations have. however, consistently shown that in the progeny of irradiatedmothers there is a significant excess of females overmales. This has been attributed to the radiation-induced(sex-linked) mutations which would reduce the number of males born of those mothers. In the progeny ofirradiated fathers a more complex situation obtains
which has not yet been fully understood.
Conclusions
47. The review that we have made of the effects ofionizing radiation and of the present exposure of mankind to radiation affords a basis for general comments
concerning this source of hazard.
48. It is clearly established that exposure to radiation,even in doses substantially lower than those producing

35

ANNEX A

DEFINITIONS OF QUA.l'n'ITIES, U1'1TS AND S1"lIBOLS
1. The Committee has used in the present report theradiological quantities and units defined in the 1959
report of the International Commission on Radiological
Units and Measurements (ICRU), 1 the relevant part ofwhich is reproduced below.* It should however be notedthat ICRU has appointed an ad hoe committee to examine
the quantities and definitions of units and some modifications of existing definitions may shortly be recommended.
"1.1. Absorbed dose of any ionizing radiation is theenergy imparted to matter by ionizing particles perunit mass of irradiated material at the place of interest.
"1.2 The unit of absorbed dose is the rad. One radis 100 ergs/g.
"1.3. Integral absorbed dose in a certain region isthe energy imparted to matter by ionizing particles inthat region.
"1.4. The unit of integral absorbed dose is the gramrad. One gram rad is 100 ergs.
"1.5. Absorbed dose rate is the absorbed dose perunit time.
"1.6. The unit of absorbed dose rate is the rad perunit time.
"1.7. Exposure dose of X- or gamma radiation at a
certain place is a measure of the radiation that is based
upon its ability to produce ionization.
"1.8. The unit of exposure dose of X- or gamma
radiation is the roentgen (r). One roentgen is an exposure dose of X- or gamma radiation such that theassociated corpuscular emission per 0.001293 g of air
produces, in air, ions carrying 1 electrostatic unit ofquantity of electricity of either sign.
"1.9. Ex-pos1ire dose rate is the exposure dose perunit time.
"1.10. The unit of exposure dose rate is theroentgen per unit time.
"1.11. Intensity of radiatioti (radiant energy flux
density) at a given place is the energy per unit timeentering a small sphere centered at that place per unit
cross-sectional area of the sphere.

"l.12. The unit of intensity of radiation may be
erg per sqitare centimeter second, or watt per squarecentimeter.
"1.13. The unit of quantity of radio-active material,
evaluated according to its radio-activity, is the curie( c). One curie is a quantity of radio-active nuclide
in which the number of disintegrations per second
is 3.700 X 10 10•"1.14. Specific gamma-ray emission (specificgamma-ray output) of a radio-active nuclide is the
exposure dose rate produced by the unfiltered gamma
rays from a point source of a defined quantity of that
nuclide at a defined distance.
"1.15 The unit of specific gamma-ray emission is
the roentgen per millicurie hoitr (r/mch) at 1 cm.
"1.16. Linear energy transfer (LET) is the linearrate of loss of energy (locally absorbed) by an ionizing particle traversing a material medium.
"1.17. Linear energy transfer may be conveniently
expressed in kilo electron volts per micron (kev/14).
"1.18. Mass stopping power is the loss of energy
per unit mass per unit area by an ionizing particle
traversing a material medium.
''l.19. Mass stopping power may be conveniently
expressed in kilo electron volts per milligram per
square centimeter {kev cm 2/mg)."
2. According to ICRU :1"The absorbed dose, D (in rads), of any radiationmust be multiplied by an agreed £'actor, RBE (~elative
biological effectiveness), whose values for different
radiations are laid down by the International Commission on Radiological Protection (ICRP). This
product, called the RBE dose, is e.xpressed in rems
where
RBE dose (in rems) = (RBE) (D)"In the case of mixed radiations the total RBE
dose is assumed to be equal to the sum of the productsof the absorbed dose of each radiation and its RBE.

*The following is quoted from the above-mentioned ICRU •report:"Symbols and P10111enclature. There are numerous national
and international bodies that have reached varying degrees of
acceptance of the use of symbols and units for physical quantities. However, there is no universal acceptance of a11y one setof recommendations. It is suggested that each country modify
the symbols used herein, in accordance with its own practices.
Thus one may write: kev, keV, or Kev; HC or CH; rad per unit
time, rad per time, or rad divided by time; rad/sec, rad/s, orrad.s-1 ; etc. The most generally accepted system of symbols andunits may be that contained in document UIP 6 (1956) preparedby the International Union of Pure and Applied Physics. These
are in fairly dose agreement with the recommendations of theInternational Standardization Organization project ISO/TC 12,
the Conference Generale de Poids et Mesures, Union Intema·tionale de Chimie Pure et Appliquee, and the International
Electrotechnical Committee."

39"RBE dose (in rems)rads) (RBE) ]."~ [ (absorbed

dose in

For the sake of simplicity in the present report 1
roentgen of X-, beta or gamma radiation is assumed tocorrespond to a tissue dose of 1 rad and, since the RBEof these radiations is conventionally unity, the tissue
dose may also be expressed as 1 rem.
3. The RBE values that have been used in the present
report are those established by ICRP in establishingprotection standards. The table below gives the valuesof RBE for different types of radiation. 2 The ICRP
Committee on REE is currently examining the concept
and use of RBE in radiation protection calculations andnew recommendations may shortly be made.

TABLE I. RBE v.um:s

1. X-rays, elcctrOt1s and positrons of any specific io11i.1:atio11

RBE=l
2. H tavy ioni.r:ing particles
Arerage spaifie ionization(ion pairs Per

micro.s of wakr)

100 or less .•••.•..•.•.•.•....•.......•.• • .••••..••
100 to 200 ...••.•..•. ,, . • .....•..•...........•....
200 to 650 .••.....•...•....•.........•..•••••....•
650 to 1,500, • •.•...••...•..•...•..•. , . . .. . .. • ••. • .
1,500 to 5,000 ..••..•.•.••........... • •.•... . .....•.•

RBE

Aoerage litUar <>•erry
lranJf#T to water(kn ta micr°")

1
1 to 2
2 to 55 to 1010 to 20

3.5 or less
3.5 to 7.0
i.O to 23
23 to 53
53 to 175

For practical purposes, an RBE of 10 is applicable to fast neutrons and protons up to 10
MeV and an RBE of 20 to heavy recoil nuclei for whole-body irradiation and the most sensitive
critical organs.

REFERENCES
1. Report of the International Commission on Radiological Units and Measurements(ICRU) (1959). National Bureau of Standards, Handbook 78.
2. Recommendations of the International Commission on Radiological Protection.
Brit. J. Radial. Suppl. No. 6 (1955).

back

to
first page40

ANNEX B

FUNDAMENTAL RADIO-BIOLOGYCONTENTSParagraphs

I. INTRODUCTION •••••••••• • ••••••• • •••••••••••••
II. INTERACTION BETWEEN IONIZING RADL�TION A�"'ll
LMNG MATTER • ,,,,,, , ,,, ,, •,,,,, , •, ,, , , , , ,,,Energy dissipation by X - and gamma-rays andby corpuscular radiations....................
Ionization density-LET ... .. .. ..•. .. ... ..• ••Transport of energy..........................
Ill. QUANTITATIVE ASPECTS OF RADIATION EFFECTS,.,,
Hit principle (target theory) and dose-effect relationships ........••••.............•..••...
The threshold problem•..••...•..........•....
Direct and indirect effects of radiation ...•..••.
Influence of dose-rate and dose fractionation.•..
Relative biological effectiveness.••..•...•.•...•
IV. RADIATION CHEMISTRY ••••••••••••••••••••••••
Water and aqueous solutions of simple compounds .....••••••....•••..••••.•.••••••,.•
Nucleic acids ................................ .
Proteins ...•.•...•••.•..............., ,,, ••,,
Polysac:cbarides •.•...•.••....•........••••..•
Macromolecular complexes •....•..... , ., ,....
Detection of free radicals in whole cells by electron spin resonance (ESR) ................ ..

Paragraphs

1-3

General considerations of radiation effects in cellular metabolism ...•...................•... 161-167
Effects of radiation on integrated functions..••. 168-171
Growth rate ......•......••................ 169
1Iitotic delay ..............•...••.......... 170-171
Inhibition of mitosis and cellular death: reproductive and interphase death................. 172-177

4-9
6
7-8
9

VIL BIOLOGICAL VARIABLES INFLUENCING RADIATION RESPONSE ••, ,• ,••,,,,• , ,•,,,,•,• ,••,,•••••,,••• 178-185
Concept of radio-sensitivity............. ..... 178
V ariations in radio-sensitivity with stage of division .. ,. ,.•..•••,.•...••••....•.......... 179-181
V ariation of radio-sensitivity with ploidy....... 182-184
Genetic control of radio-sensitivity in bacteria.. 185

10-35
12-18
19-22
23-26
27-30
31-35

VII!. PRIMARY GENETIC EFFECTS OF RADIATION......... 186-225
The genetic material.......................... 187-189
Point mutation .............................. 190-192
Radiation-induced mutagenic effects•.....•.•... 193-194
Oxygen effect ..•.....•......••.•.••.••....... 195-196
Chemically-induced mutagenesis . .•. ••...... ... 197
Uptake of abnormal p_recursors................ 198-199
Comparison between various mutagenic agents.. 200
Biochemical aspects of mutation processes....•. 201-204
Mutation expression •...•..... ....••••....... 205-206
Chromosome breaks .......................... 207-210
Factors influencing the production of chromosome breaks •••••......•..................• 211-213
Genetic effects of incorporated radio-active substances ,........ ,..............•........... 214-215
Possibility of transmutation effect with cu..... 216-217
Local consequences of transmutation••......... 218-222
Ionization dose per transmutation under uniform
contamination •.••...............•........•• 223-225

36-93
38-49
50-61
62-78
79-82
83-88
89-93

V. CHE:\UCAL FACTORS MODIFYING RADIATION RE·
SPONSE L.._ CELLS,•••• ,,,,••••,,.,,,.,,••,,,•• , 94-110
Oxygen effect ••••...•••..••••.,..•.•.•.....•• 94-96
Effect of gases other than oxygen.....••..••••• 97
Effects of gases under pressure.•..........••.• 98
Hydration .....•.•••••......•..•....•......•• 99-100
Peroxide after-effects •.•..•............••.••• 101-102
Chemical protection .......................... 103-110
VJ. EFFECT OF R..\DIATION ON CELLULAR STRUCTURESAND THEIR FUNCTION ......................... 111-177
DNA synthesis •..•••.•...•.........••.•...••. 116-132
fu'l'A and protein synthesis.................... 133-157
Effects of radiation on antibody synthesis...•... 158-160

IX. RECOVERY AT THE CELLULAR LEVEL••,•••••••,,••• 226-243
X. GE�·ERAL COXCLUSIONS ................. ,.... • • 244-250
REFERENCES

the impact of molecular biophysics on fundamental radio­
biology is greater than in the past. The molecular ap­
proach will eventually enable us to understand the effectsof radiation on the impairment of fundamental processes
in the cell. The effects of radiation on macromolecules
or subcellular structures are thus of great importance infundamental radio-biology.
3. This annex deals essentially with ionizing radia­
tion ; investigations with non-ionizing radiations are re­f erred to only in so far as they bear on our understandingof the effects of ionizing radiations.

I. Introduction

1. The effects of radiation on living matter must be
envisaged at different levels of organization, those ofindividual molecules and macromolecules, subcellular
structures, whole cells, tissues and organs, whole organ­
isms, and populations of organisms. To understand theaction of radiation, each system must be studied inde­
pendently and in its natural context. The actions become
more complicated as the organization level rises. At
each level and for each effect studied, it is sometimes
helpful to think in terms of the sensitive molecule or
structure, the sensitive cell, tissue, or organ.

II. Interaction between ionizing radiation andliving matter

2. The present annex deals chiefly with macromole­cules, subcellular structures, or isolated cells and cell
populations. Our knowledge of the molecular organiza­tion of various cell organelles is increasing rapidly and4. The absorption of ionizing radiation by matter isfollowed by a comple..x of events the nature of which41depei:ds on abso~b.ed dose ~d th~ chemical a;id physicochenucal composition of the irradiated matenal. Various
stages can be recognized in the development of radiation
effects. These are not sharply demarcated but blend into
each other. Distinctions have some value, however, because they permit a partial analysis of the temporalsequence of events.
5. (a) Elementary reactions. These occur in a very
short period of time,,...., 10-11 -10-15 seconds. They are pnmarily physical and result from the interaction between
photons or ionizing particles and atoms and molecules.
These interactions give rise to excitations and ionizations. Excited and ionized atoms and molecules are highly
unstable and chemically active; rearrangements in theelectron configuration of the excited structures lead tothe primary products of radiation action which may bestable or unstable molecules, or free radicals.
(b) Primary reactions. Radicals and excited molecules formed as the result of elementary processes reactchemically with neighbouring molecules and between
themselves. This stage, the chemical stage, may last froma fraction of a second to hours.
( c) Secondary reactions. Elementary and primary
reactions give rise to secondary reactions in which macromolecules of essential biological significance and major
metabolic pathways are affected. Secondary reactions
result, therefore, in alterations and impairment of cellular structures and functions, and may lead to biologicallyobservable radiation injury. This, the biological stage,
may last from a few hours up to years in long-lived
multicellular organisms.

existence in condensed systems since they are inherently
unstable. Although excitation can lead to dissociation of
the molecule, it is less likely to do so in the case ofn;or~ complex molecules where excess energy can be
distributed over many bonds. Energy degradation within
the same molecule is known as internal conversion.
Through internal conversion, the excited molecule isdegraded in energy from a higher to a lower excitedstate, or returns to the ground state; the excess energy isconverted into vibrational and rotational energy and may
be transferred to other molecules. Energy can also betransferred from one molecule to another through processes known as exciton interaction and resonancetransfer.1 The increasing emphasis on the mechanisms
by which energy migrates and on their role in radiation
effects is reflected in recent symposia and reviews. 2- 'm. Quantitative aspects of radiation effects
10. Known dose-effect relationships may be describedunder a limited number of headings. Their graphic presentation is often simple, linear in a few instances, andin general exponential or sigmoid. Thus, oxidation offerrous ions and reduction of eerie ions in aqueous·solution is, in certain circumstances, directly proportional to dose. These effects may be interpreted as due
to radicals induced in the aqueous medium. However,in somewhat more complicated situations, e.g. the inactivation of enzymes in solution or in the solid state,
there- may be an exponential relationship between remaining activity and radiation dose. This relationshipexpresses, in part, the fact that inactivated molecules arestill able to capture radicals and thus to decrease thenumber of radicals for inactivation of still intact
molecules.

ENERGY DISSIPATION BY X- AND GAMMA-RAYS A:ND
BY CORPUSCULAR RADIATIONS

6. The elementary characteristics of ionizing radiationand the way energy is absorbed by ionization have been
described in chapter II. Only part of the energy absorbed by an irradiated tissue gives rise to ionizations;the remainder, in a process called excitation, raises electrons of atoms or molecules to a higher energy level
without expelling them. In its chemical or biologicalaction, the energy absorbed in the excitation process is
not considered to be as important as that absorbed in
the ionization process. However information is incomplete on this point.

11. Even for complex systems like living cells, theexperimental relationship between dose and effect is?f~en a sirr:ple one. In the study of these relationships
it 1s essential to define the effect clearly. For isolated
cells, reproductive ability has been used most frequently
as the criterion of damage. Cells which have lost reproductive integrity may still divide a few times. However,ceIIs affected in this way can sometimes maintain theability to accomplish for a certain time some metabolicor ~hys_iological fu~ctions at .near normal rates, e.g.,
respi_rahon, 5 • ~ pr~tem synthesis,7 motility. 8 The doses
required for impamnent of such metabolic functions areusually much greater than those necessary to impair
reproduction.

!oNIZATION DENSITY-LET

7. I;i any interaction of ionizing radiation with matter,the ultimate transfer of energy is carried out by a charged
particle. pie rate o! loss of energy by a particle along~ts path is prop~rttonal to the square of charge andi?versely proportional to velocity. Hence, for any parttcl~, the rate ~f loss of energy is greatest near the endof its track. Lmear energy transfer (LET) is definedas t~e linear rate of los~ of energy (locally absorbed)
and is usually measured m keV/ µ..

HIT PRINCIPLE (TARGET THEORY) AND DOSE-EFFECTRELATIONSHIPS

12. According to the hit theory,11-11 the biologicaleffects of ionizing radiation on cells are due to hits in asensitive component of the cell; hits produced outside
this "target" are. ineffective. Although, as originallyformulated, the hit was considered to be an ionization
or excitation produced directly in the target, the theory
has been enlarged to include hits produced by diffusible
products involved in indirect action. 12

8 .. At a given dose the biological effect may varycons1.derably with LET; it may increase or decrease depending on the object irradiated and the effect measured.
There is as yet no complete theory on the influence of
LET (paras. 31-35).

~3. If a cell is inactivated by a single hit in a target
or m any of a number of targets, it can easily be shownthat the survival curve is exponential. The number ofcelis escaping biological modification (N) is then related
to dose according to the formula N = N 0 e-aD where N
is the number of cells originally present, D i~ dose,

TRANSPORT OF ENERGY

9. Free radicals, whose intrinsic lifetime is indefinite
us:13:11y disappear quickly_ because of their reactivity'.
Excited molecules have, m general, only a transitory

and

42

a is a constant expressing the sensitivity of the cells.

From this formula it follows that the number of survivors will be N/N o = e-1 ,....., 0.37 for the dose 1/a whichis the dose that brings about one hit per target on the
average. This 37 per cent dose is important in calculations of the volume of the target.
14. When two or more hits are necessary to destroy
one target or when two or more targets in one cell haveto be hit before the damage shows, the survival curves
are no longer e..xponential but are sigmoid and havean initial shoulder when the logarithm of the survival isplotted against dose. In the latter case (two or moretargets), the number of targets can be estimated fromthe survival curve by e..xtrapolating the linear part of thesemi-log-plot to zero dose. The value (greater than one)thus obtained on the survival axis is equal to the numberof targets.
15. As a rule, with high LET radiations and neutrons,
and in certain cases with X- or gamma-rays, exponential
survival curves are observed for the inactivation ofviruses and micro-organisms. 9 When the fraction of cells
or subcellular structures affected is small, the numberof responses is approximately proportional to dose. Thishas been found for the induction of mutations in bacteria,
Drosophila, and other organisms; the mechanism seems
to be one hit.
16. X-irradiated polyploid yeast cells13• 14 and isolated
mammalian cells15 have sigmoid dose-effect curves. The
type of curve often depends on the LET of the radiation.
Higher LET values may result in exponential survival
for cells having sigmoid type curves for low LET
radiations.18
17. Sigmoid survival curves are also e.xpected whena population of individuals is irradiated, the susceptibility of which obeys certain distribution patterns.
18. Both exponential and sigmoid survival curves may
have breaks (resistant tails). The interpretation usuallyoffered is that the population studied contains a subgroup which is more resistant to radiation. In general
there are two ways in which this could occur:(a) The heterogeneity may be genetic; the more resistant individuals are mutants of the more sensitive.
This situation can be recognized by isolating a clone
from cells surviving higher doses and by establishing a new survival curve with the population from thisresistant clone. The slope found corresponds to the slopeof the resistant tail in the original curve. However, insome cases, attempts to do this have failed. With thewidely used strain E. coli B, the rate of mutation toresistance is only about 10-5 per bacterium per generation and therefore probably too low to account for theappearance of the tail. 17( b) The heterogeneity may be physiological; in thiscase, if cells surviving at the higher doses are isolated,
the survival curve of the new population shows the same
resistant tail as the original one. This holds in haploidyeasts where budding cells appear to be more resistant. 18
There is similar phenomenon with Pneumococcus transforming principle. 19 A resistant tail may also be seen
with a bacterial population containing cells in both thelogarithmic and stationary phase of growth; the logarithmic phase is more radio-sensitive. 20 • 21
THE THRESHOLD PROBLEM

19. The observation of an exponential survival curve
may be interpreted as a one-hit process. The same applies
43

to the linear relationship for mutation induction when
the number of mutations is small compared to the number of loci at risk; any dose, however small has aprobability of producing the effect.
'
20. Sigmoidal survival curves may be interpreted as
an indication that inactivation results from multiple hits
in a single target or inactivation of multiple targets by
one or more hits in each. There is also a finite probability that any dose may produce an effect. Thus theexistence of biological responses with sigmoidal doseeffect curves do not necessarily prove the existence ofa threshold dose.
21. Even if recovery processes occur at the cellularlevel, these conclusions remain valid; such recovery
merely changes the slope of the dose-effect curve.
22. Without e.xtensive empirical data and detailed
knowledge of the various steps between initial absorption of radiation and expression of biological effects,
discussion of the threshold question is largely limited totheoretical considerations. In the only instance in which
it has been possible to obtain unequivocal experimental
data, the induction of phage growth in lysogenic bacteria,
no threshold was found; one ion pair per cell was effective. 22 It is therefore prudent to assume, as in the lastreport of the Committee, that "biological effects will
follow irradiation, however small its amount". 23
DIRECT AND INDIRECT EFFECTS OF RADIATION

23. Of the models proposed to explain observed doseeffect relationships, the simplest is the target theory basedon the assumption that inactivation is caused only byionizations inside the target-"direct action".
24. Although the concept of a "target" has been maintained in most theories, it has become increasingly apparent that at least part of the biological effect is due
to chemical events outside the target. In this event damage to the target is secondary-"indirect action".16• 24
25. As yet there is no general agreement on the relative importance of direct and indirect action in living
cells. The modification of damage by oxygen or chemical
protective agents has sometimes been interpreted as evidence that indirect action is predominant. It has howeverbeen shown that the effect of oxygen and some protectants is also consistent with direct action, if it is assumed
that the effect of radiation on the target is a two-stage
one. 2 ~· 26 The primary event might then be partly or
totally reversible.
26. The problem of direct versus indirect effects ofradiation has been comprehensively reviewed by Timofeev Ressovski and Rompe 2 with an analysis of mechanisms of energy migration and transfer in the heterologous system. Their theory allows for chance fluctuations in the occurrence of both direct and indirect effects,
and for the mechanisms of propagation of radiation
injury in time and space. Depending on the structure orfunction damaged, either direct or indirect effects may
be considered predominant.
INFLUENCE OF DOSE-RATE AND DOSE FRACTIONATION

27. Variation of the irradiation rate (fractionation ofdose or variation of dose-rate) may influence the biological effect in some instances. When radiation damage isirreparable, no modification of the response is e."Cpected;
if a modification is seen, it is generally assumed to repre-

sent a repair mechanism. Mice, Drosophila, plants, andseveral other species (C, table VII) have been extensively studied. Other examples are Arbacia eggs 27 andmammalian tissue culture cells. In Arbacia sperm, however, no repair has been observed. 28 • 29

which RBE and LET are directly related, inYersely related, in which RBE shows a maximum for a certain
value of LET, and in which RBE is constant. Other
factors make the picture even more complex ; RBE values
may depend on dose, dose-rate, presence of O>..")'gen, andphysiological conditions.
34. The LET concept itself is complex. The kinetic
energy loss of a particle is discontinuous and subject tostatistical fluctuations. 42 Furthermore, it varies along the
track. For these reasons an average value must be calculated. In principle, however, RBE not only depends on
this average value of LET, but also on LET distribution.
The following figure 43 attempts to summarize experimental data on bacterial, plant and animal cells.

28. If the phenomenon under study is single hit, e.g.
induction of point mutations, repair processes would
reduce the magnitude of the slope of the dose-effectcurve. Russell 30 discovered that low dose-rates were lessefficient than high dose-rates in inducing mutations inmouse gonial cells. This dose-rate effect was maximal at
0.82 r/min; further reduction of the dose-rate had nofurther effect on mutation rates. 31 Russell's finding,which stimulated similar studies by others, has been confirmed in several species. Low dose-rates also greatly
diminish the sterilizing effects of radiation in female
mice and increase survival of spermatogonia. 39

10.0

s.o

29. The effectiveness of fractionated doses to themouse testes has been demonstrated with doses in therange of 1600 rad.' 0 In experiments with Drosophila at
low doses and different stages of spermatogenesis, noeffect of dose fractionation has been observed. 32

3.0

30. The effect of dose-rate on multi-hit processes is
not difficult to explain. If the rate of delivery is reduced
so as to increase the time between two successive events(hits) significantly, and if the individual lesions due tohits can be repaired within a certain time, lowering thedose rate or fractionation of the dose will result in adiminished frequency of effects for a given total dose.
The role of chromosome aberrations may be of particularimportance in monkey or human embryonic tissue cultures. Some reports indicate that these tissues are twoor three times more sensitive than those of mice. 83 • 84
Investigations of the repair of pre-mutational damage
have been carried out with many species, including mammals35• 36 insects 37• 38 and plants. 264 • 1516 This subject is
discussed more fully in annex C.

0,50.3 .......~~~~~--~~~~~_._~~~~~-1000
100lLET, keV/µFigure 1. Variation in RBE with LET. for biological materials
irradiated in aerobic conditions43

A: plant cellssrr-5s2
B : animal ce1Is203, 577, ss3-ss5

C: two strains of bacteria1s3, 5SG-5S7

35. To assess the RBE of a certain radiation, doseresponse curves of the particular biological effect are
determined for both test and standard radiations. If bothcurves coincide when all dose values of the test radiation
are multiplied by a constant factor, the RBE is equal tothis factor. Sometimes the curves do not have identicalshapes; the RBE value then depends on dose. This comparison pertains to absorbed dose. If this dose is not
uniform throughout, the average value is used. This may
not be strictly correct ii the biological effect depends on
dose. There are many other complications that make experimental RBE values difficult to interpret. The values
are, however, useful in the practice of health physics,
where upper limiting values of RBE are used to transform dosages measured in rad to rem.

RELATIVE BIOLOGICAL EFFECTIVENESS

31. \\Tith radiations of different quality, the absorbed
doses required for a given effect are usually not the samefor different types of radiation. The extent to whichradiations of different quality differ from each other inthis respect is a measure of their relative biological effectiveness (RBE). The RBE of two radiations is definedas the inverse ratio of the respective doses that are necessary to bring about a given effect. The radiation
standard chosen by the ICRU is an X- or gamma-radiation having a LET in water of 3 keV / µ. delivered at a
rate of about 10 rad/min.

IV. Radiation chemistry

32. In the simplest cases, the mechanism underlying
the difference in efficiencies of radiations can easily be
e:cplained. For an event which is inhibited by the absorption of a minimal amount of energy, such as the inactivati?n of an enzyme or virus, the low ion density radiation
will be more effective than high ion density, because someof the latter ionizations will be wasted. On the other hand,radiation with a high density of ionization will be more
e~ective when larger amounts of energy are needed( ~m~t.dtaneously or within a relatively short time or
w1th.n~ a certain volume) to produce the effect in thesensitive structure.

36. Since water constitutes 70 per cent or more of cellmass, water molecules take up most of the energy imparted to cells by ionizing radiation and may be importantin the damage to vital cell components. Knowledge collected during the last decade about the chemical changes
induced by irradiation of water and aqueous solutions ofsimple compounds is therefore of great importance toradio-biology. Work has been done on the radiation
chemistry of solutions of nucleic acids and other macromolecules to gain some insight into the mechanism bywhich reactive intermediates generated in water attack
these molecules. The main results from those fields ofresearch will therefore be summarized in this chapter.
37. In interpreting these results, it is generally assumed that free radicals are important in the chemical. 33. Thus, RBE depends not only on the LET of agiven radiation but also on the effect studied, and thisdepen~ence may assume various forms. Thus, Zirkle 41
has pomted out that there are e:iqierimental situations in44

reactions resulting from ionization and perhaps fromexcitation of water molecules. At present, there isabundant evidence to support such a view. Recently,
development of the electron spin resonance technique
has provided a method for direct study of free radical
formation in certain irradiated materials.

cals formed in close proximity, and the damage to certain
molecules will be much less in cells than in dilute solutions. Secondly, the presence of great numbers of simple
and complex molecules in cells may give rise to secondary
and tertiary reactions which differ from those in simple
solutions.
45. Knowledge of the primary reactions in irradiatedwater has been derived largely from the study of aqueous
inorganic solutions. Much e.'Cperimental work has also
been done on aqueous solutions of organic compounds.
However, for many changes in solutions of simple molecules, the reaction mechanism has not been unambiguously established.

\VATER AND AQUEOUS SOLUTIONS OF SIMPLE COMPOUNDS

38. Most reactions in irradiated water can be e.xplained satisfactorily by assuming the formation of H 0
and OH 0 radicals. Recent reviews 4'-i 6 of the chemical
effects of ionizing radiation have shown the usefulness of
the radical hypothesis in interpreting the rapidly growing
body of experimental data, although some uncertainty
still exists with regard to the H 0 radicals and their distribution around the track of an ionizing particle. It
might be that what has been called an "H 0 radical" is inreality a hydrated electron, H 20-.
39. For each 100 eV of dissipated energy some 4
H 20 molecules are split into OH 0 and H 0 • OH 0 radicals
can combine to H 20 2 and H 0 radicals to H 2. A considerable fraction of the radicals react in this way to give
"molecular products" before there is any significant
diffusion or reaction with solute molecules. In chemicallypure water, however, only very small amounts of molecular products can be detected, because they are reverted
to water molecules through back reactions with freeH 0 and OH 0 radicals.

46. There is evidence for the formation of hydroperoxides in the presence of oxygen :
RH
OH 0
R0
H20
0
R
02
RO~

+
+

reduction

ROf
R02
R02 + H+ --~ R02 H

47. In some instances hydroperoxides are believed tobe labile intermediates, but stable peroxides have also
been found, e.g. after irradiation of solutions of various
amino acids and of pyrimidine bases 48 and their nucleosides and nucleotides.' 9 • 50 The formation of hydroperoxides may enhance oxydation, e.g. increase oxydationof ferrous ions in acid solution where there are organic
impurities. This can be prevented by addition of Qions; these react with OH0 radicals ( OH 0
Cl- ---+
OHCl 0 ) and thus modify the sensitizing action oforganic molecules. 51

40. When solutes capable of reacting with H 0 or OH 0
radicals, thereby preventing the back reaction, are present, the products H 20 2 and H 2 are produced in measurable amounts. Their yields depend on LET, a greater
LET giving rise to a larger amount of molecular products
through combination of free radicals. The molecularyield also depends on the efficiency with which free radicals are scavenged by solute molecules. Some very efficient scavenging solutes can depress the formation ofH2 and H202 considerably.

++

48. Reactions between radicals and oxygen, andbetween radicals and hydrogen-atom-donating compounds, have been shown to be important biologically.
In the bacterial spore, radicals formed that are biologically effective if they react with oxygen may be removedby hydrogen donators such as H 2S prior to 0 2 reaction. sz, 53 Such mechanisms have been proposed forother systems.'9 • 5 '· 55

41. A very common solute is 0 2. It reacts with H 0
radicals to give the radical 0 2 H 0 • This e.'Cplains why theyield of various radiation-induced chemical reactions isdependent on the presence of 0 2 • The 0 2 H 0 radical ismore stable than H 0 and OH 0 • When no solutes otherthan 0 2 are present, most 0 2 H 0 radicals will combine
according to the reaction 2 02H 0 ~ H 2 0 2
02.

49. Further chemical reactions which may bear onradio-biology are the oxydative deamination of aminoacids, 66 the decarboxylation of organic acids, 45 the oxydation of SR-compounds to the -S-S- dimer, 57 and thedecomposition of glucose by ionizing radiation.u+

42. The primary products in irradiated water may
have oxydizing or reducing properties depending on theredox potential of the solute concerned, on the qualitiesof other solutes (e.g. 0 2 • which converts reducing H 0
radicals to 0 2 H 0 radicals which may have oxydizing
action), or on pH.

NUCLEIC ACIDS

50. Irradiation of nucleic acids in aqueous solutions
leads to several different chemical changes which affectboth the purine and pyrimidine moieties and the sugarphosphate backbone. As yet, it is impossible to give a
consistent and quantitative description of these chemical
effects of irradiation. Because of the diversity and complexity of the chemical changes, only the main pathways
are considered to be established.

43. The influence of pH is explained by the following
ionic equilibria: H 0
H+ ±::; H 2•; OH 0 ±:::; H+ 0- and0
0 2 H ±::; H• + 0 2-. It should be noted that, in neutral
solutions, 0 2 H 0 radicals have far less oxydizing power
than at low pH's. The oxygen effect in living systems
can therefore probably not be interpreted as an enhancement of oxydation through the reaction H 0
0 2 ---+
02H 0 •+++

51. The chemical changes produced by irradiation ofdilute solutions of nucleic acids are, for the most part,
initiated by radicals formed in the aqueous media. In
agreement with results of e.xperiments with simple
nucleic acid components, there are two main reaction
pathways by which radicals attack nucleic acids inaqueous solutions : (a) destruction of the bases, the predominant site of chemical attack, 'and ( b) oxidation of
the sugar moiety. 5 11-oi The products of irradiationof the bases in the presence of oxygen differ from+

44. Application of these data to radio-biologicalsystems is by no means straightforward. In the firstplace, the diffusion range of free radicals in living cells
is very limited,47 because many molecules can react withfree radicals, thereby protecting more vital components.
Cell structures can be attacked, therefore, only by radi45

hydrogen-bonded structure has been shown by the increase in ultra-violet absorption near 260 mµ. after small
doses of irradiation,61 • 70 • 12 and also by titrimetricstudies.10, •s
56. Degradation of DNA proceeds for some timeafter irradiation, as judged by viscosimetric measurements.76 This "after-effect" is more pronounced if DNA
is irradiated in air-saturated solution.79-8 1 There areseveral hypotheses to e..x:plain this kind of instability;
the decay of some unstable pyrimidine hydroxyperoxides, 60• 61• 82 and hydrolysis of labile acyl-phosphatesn, 64 are the most plausible of them.

those formed in its absence. In o>..-ygen-free solutions,
pyrimidines are converted into products of undetermined
structure, without any specific ultra-violet absorption. 61
Some guanine residues are converted to 2 :4-diamino-5-formamido-6-hydroxy-pyrimidine which is attachedto the sugar by a labellized glycosidic linkage; fromthis they are gradually released as free bases. It isbelieved that the attack on adenine forms the corresponding fonnamido-pyrimidines, although this has not been
directly demonstrated in irradiated DNA.59 The yieldof chemically altered bases is highest for pyrimidine residues and lowest for purine residues, 59 • 61- 63 a circumstance which reflects their comparative radio-sensitivity.
52. In aerated solutions of nucleic acids, the hydroperoxides of pyrimidine bases are formed with thesaturation of 5, 6 double bonds, and under oxygen thisreaction becomes the dominant one. 61 In DNA, onlyhydro>..-yperoxides of thymine are stable and only theseremain attached to the sugar-phosphate backbone.61 In
the presence of oJ'..-ygen the sensitivity of all bases in
DNA solution is increased two to three times; underthese conditions a presumed 80 per cent of radicals
attacking DNA combine with the base components.
53. The attack of radicals on the sugar moiety leads
to formation of labile phosphate esters. Evidence for thisis seen in the large quantities of inorganic phosphate thatcan be liberated by the acidic hydrolysis of irradiatedsolutions.12 It is believed that this results from oxidative
formation of carbonyl groups in sugar moieties. 61 In
addition to the formation of labile phosphate esters, theattack on the sugar component breaks phosphodiester
bonds and liberates small amounts of inorganic phosphate.60• 6~ From experiments with simple phosphate·esters,65 it appears that inorganic phosphate must comefrom end groups present in the intact molecule, having
been formed during earlier stages of irradiation by main
chain scissions.
54. The direct measurement, with prostate phosphomonoesterase, of the number of breaks induced in thesugar-phosphate backbone has revealed that the yieldfrom this process is 20-25 per cent of the yield in termsof base destruction.66 The same percentage is found if
the release of free bases from irradiated DNA isused to measure the attack on the sugar-phosphatemoiety. 59, 62, e1

57. In dilute solutions, the indirect action of radiation
prevails. With increasing concentration of DNA the
relative importance of this effect decreases in favour ofthe direct action. This has been shown in experiments inwhich damage to DNA, as a function of concentration,
was studied in the presence of iodine ions which almost
entirely prevent the indirect effects of radiation. 8 3-8~Thus, Mekshenkov ascertained that 0.1 per cent solutionsof DNA are almost entirely protected against X-radiation by iodine ions (predominance of indirect effect).
With increasing concentration of DNA, however, theprotective ability of iodine ions decreases so that in a 20
per cent solution, 80 per cent of DNA molecules present
are damaged 86•87 (predominance of direct effect).
58. DNA molecules irradiated in the dry state or ina slightly moist condition are damaged mainly by the
direct action of ionizing radiation. With radiation dosesof ,_, 106 rad, in addition to the main chain scission, anintermolecular cross-linking takes place which leads tothe appearance of branched molecules as judged by
viscosity, sedimentation and light-scattering studies.
With increasing doses up to 101 rad (the threshold dose
depends on water content), this process renders DNA
insoluble in water and gives rise to gel formation. Bothprocesses proceed simultaneously, but their relative rolein the damage depends on moisture content, presence ofoxygen, and nature of ionizing particles. 68 •11 • 8 8-9 0
59. The rates of main chain scission and branching
induced by electrons are about the same at moisture contents up to 25 per cent, and are largely unaffected byoxygen. With swollen DNA gels having a water content
of 2? to 70 per cent, intermolecular cross-linking predominates over the scission of the main chain in theabsenc~ of oxygen. However, in the presence of oxygen,the ratio between the effectiveness of the two processes
is reversed. Above 75 per cent water content, and evenin the absence of oxygen, no gel is formed. 88 • 89 Alphaparticles are much less effective in the branching process
than electrons. With alpha-particles only a limited
amount of cross-linkage is found in the absence ofoxygen, and this is independent of the moisture content.
In the presence of oxygen one main chain break is produced by nearly every alpha-particle traversing a DNA
molecule. 90
60. It is believed that clusters of ionization are responsible for the main chain breaks; cross-links result fromthe combination of active points formed by ionization89 • 110
for which carbon radicals are likely candidates. Some
direct support for the formation of metastable species
is provided by the obsen'ation of strong gamma-induced
phosphorescence in frozen solutions of DNA and~NA. 91 With direct irradiation of dxy DNA preparat10ns by gamma-rays, the ESR method reveals thepresence of one radical per 105 DNA molecules for adose of 2 X 103 rad. 9 2

55. Studies of physicochemical changes in nucleic
acids after irradiation are, so far, chiefly confined todeoxyribonucleic acids. In the double-stranded helical
DNA molecule, both types of chemical lesions introducedby ionizing radiation, destruction of bases and breakageof phosphodiester bonds, must lead to an altered configuration in solution and consequently to changes inphysicochemical properties. The destruction of the baseresults in local dissociation of the double-stranded structure, and the break in one of the chains results in increased flexibility; two independent breaks at approximately opposite positions in each of two intertwined
chains lead to a scission of the whole molecule. There ismuch evidence supporting this general picture. Thus,
the critical temperature for the thermal denaturation of
i:r;radiated DNA is reduced. 68 Like,vise, the intrinsic
viscosity of irradiated DNA solutions shows marked
decreases that reflect coiling of the partially denatured
molecule and a fall in molecular weight. 6 11-11 Further
evidence for degradation is provided by light-scattering,71• 72 flow birefringence,72 •73 sedimentation and diffusion studies, 04 • 78 and chromatography on ecteola cellulose
column. 17 The breakdown of some of the secondary46

61. It is worthwhile to mention that ultra-violet radiation also causes aggregation of DNA 94 and, to a lesser
degree, of RN A in the dry state. 95 • 96 In water solution,
irradiation of DNA with ultra-violet light induces covalent crosslinks.96• 91 The native secondary structure isalmost preserved as shown by ultra-centrifugation in
caesium chloride. These cross-link processes are probably
connected with dimerization of thymine or uracil
residues. 98 ' 99

unpaired electrons in the protein molecules disappear.
This confirms the previous assumption that prolonged
retention of unpaired electron-excited energy is a causeof radiation after-effects. 114

69. Model experiments with irradiated myosin haverevealed "oxygen effect" at the molecular level. Inactivation of myosin's ATP function by irradiation has
two stages: first (without the involvement of oxygen)is the long-lived "excited" state of the protein molecule
capable of interaction with molecular oxygen; its enzymatic activity is still preserved at this time. Inactivation occurs in the second stage as a result of interaction
with oxygen. In an aqueous solution of myosin, "oxygen
after-effects" constitute most of the total "O:h."}'geneffect" ,113 • 1111-111 These results from a molecular systemcorrespond well with those from studies on a biologicalsystem and thus demonstrate the biological importanceof these events. In dry spores of B. megaterittm, oxygen
interaction with radiation-induced states can be almost"immediate" as well as post-irradiation.118 The radiationinduced species have proved to be free radicals in experiments involving post-irradiation heat, nitric oxide,and H 2 S treatments . 119-m coupled with physical experiments (paramagnetic spin resonance studies) of a similar kind. s:, 124 In these experiments, as in those describedabove with myosin, most of the oxygen effect can occur
for an appreciably long time after irradiation. Furthermore, an intermediate state (the metionic state), theconsequence of the reaction of oxygen with radiationinduced active species, has been postulated from studiesof another biological system. 125

PROTEINS

62. Changes in the structure of proteins irradiated indilute aqueous solution are mainly attributable to attackby free radicals and other active species from water. In
cells, free radicals account for ,_, y.1-~ of the effect; invery dilute pure solutions they account for almost theentire effect.100
63. Thiol groups, when present, appear to be the mostsensitive parts of proteins. These -SH groups become
oxydized, as shown by titration,1°1 thus creating new
disulphide bonds with a G* value of about 3. The sameprocess has been observed with enzymes,1° 2 although thehigh G value for the oxydation of those enzymes which
depend on -SH groups for activity does not always
correspond to the G value for inactivation.103 Conversely,
by other mechanisms, disulphide bonds can be reducedby irradiation, a process which leads to the formation of
new thiol groups. 104 ·1°5

64. Proteins, amino acids, and peptides, in solution,
can liberate ammonia on irradiation with large doses,
and can at the same time form carbonyl and amide compounds.106· 101 These products are formed in part fromamino-groups and in part from peptide bonds. This
reaction involves the formation of imino-groups as intermediates. The imino-groups are hydrolized, leading
to the rupture of polypeptide chains. 102

70. The damaging effects of heat and oxygen in theafter-effect response of irradiated myosin solution have
proved to be independent of one another. There are thus
two distinct forms of latent damage in the same irradiated protein molecule; this agrees with the data of Gordy
and his colleagues, who established, by ESR studies, thepresence in irradiated protein molecules of two typesof spectra-some modified by the action of oxygen andothers insensitive to it. 126•127

65. The effect on aromatic rings of amino acids inproteins resembles closely the effect on aromatic
amino acids themselves. Changes in optical density in
the UV absorbing region of some proteins, when irradiated, are similar to those produced in a tyrosine solution.108 Similarly, a decrease in optical density at 280 mµ
has been found for tryptophan itsel£1° 9 as well as forproteins rich in this amino acid.110

71. As a consequence of the chemical changes ofproteins under irradiation, one can e.xpect changes inphysical-chemical properties. Changes in chromatographic,1:9 absorptive,1 29 and electrophoretic130 properties have been seen.

66. Protein peroxides have been detected after irradiation of proteins in oxygen-containing solutions.111

72. In contrast to irradiation in the dry state, themolecular weight of proteins increases after irradiation
in solution. 131-133 From chemical evidence there may be
several reasons for this. Attack of the tyrosine moieties
may induce polymerization as with tyrosine solutions13•(melanin formation). In addition, disulphide linkages
may be formed among protein molecules. Finally, a reaggregation of broken molecules may take place, themolecules being held together by freshly formed hydrogen bonds.m

67. Model experiments with protein solutions haverevealed that the latent damage, caused by radiation in
myosin molecules responsible for the radiation aftereffects, can be eliminated by formation of comple.x compounds with actin molecules if these are introduced into
the solution immediately after irradiation. 112
68. Long-lived activated states persist for a few daysin protein molecules irradiated in aqueous solution.
Activation is associated with disruption of the protein
electron structure; this has been confirmed by the ESR
method. 113 • 114 The ESR method has revealed prolonged
retention, by protein molecules ( myosin, pepsin), of
unpaired electrons appearing after irradiation of protein
solutions. A close relationship has been established between these electrons and radiation after-effects in thesame system. vVhen irradiated solutions are slightly
warmed there is an accompanying "thermal effect", and

73. Irradiation of certain protein solutions (withdoses up to 6 X 106 rad) does not lead to perceptible
effects on physical, chemical and biological properties immediately after irradiation. However, exposure to heat, 136urea, 137 or UV, 110 alters X-irradiated protein solutions'(coagulation, denaturation) more than non-irradiatedsolutions.
74. In the case of catalase and trypsin inactivation,
an after-effect has also been shmvn.138•1311 The extent of
this depends very much upon the post-irradiation temperature to which the irradiated enzyme was exposed.13 9* "G" represents the number of molecules changed or produced for each 100 eV of energy absorbed.
47

The presence of oxygen after irradiation appears t? be,in general, unimportant; the after-effect may be attributable to the formation of protein peroxides, of therrnolabile molecules, or to other causes.uo, 1u

POLYSACCHARIDES

79. The most noticeable effect of radiation on polysaccharides is chain degradation. This holds for all
conditions of radiation152 as shown by decrease in viscosity, changes in light-scattering, electrophoretic andultra-centrifuge patterns. The most probable mechanismof degradation is one involving free radicals formed
from water, because Fenton's reagent, used as a sourceof free radicals, induces the same damage.153

75. According to present knowledge, enzyme i:iactivation is attributable to the action of hydroxyl radicals. m,m This hypothesis is supported by the obs7rva~on 0at
iodine ions serve as protectors for catalase mactivat10n;
it is to be expected that these ions react more readily
with hydro:x7l than with hydrogen radicals.14•

80. New acid and aldehyde-reducing groups areformed in polysaccharides after irradiation.107•154 Smallfragments have been found, e.g. gluconic and glucoronic
acids in the case of dex'tran. Mass spectrometry data
demonstrate the formation of H 2 , CO and C02 when dry
cellulose is irradiated.

76. Very little is known of the chemical changes inproteins brought about by irradiation in the dry state.
The involvement of disulphide linkages has been demonstrated by the close resemblance between electron spinresonance spectra of a number of proteins and that ofirradiated cystine, 127 and by the fact that irradiated ribonuclease, like ribonuclease with its S-S bonds reduced,
can be digested by trypsin whereas the native protein isresistant.145 A general increase in ultra-violet absorption,135•146•147 accompanied sometimes by a shift in theposition of the absorption maximum, indicates an attack
on aromatic amino acids. Changes in content of otheramino acids have also been demonstratedw,us and differences in sensitivity between particular amino acids
have been noted. 147 The formation of ammonia andamines with the development of carbonyl and carboxylic
end groups in the hydrolysates of irradiated proteins is
attributable to an attack on amino acids side chains andon peptide bonds.60 Susceptibility of peptide bonds tomain chain scission is apparently rather low because nosuch breaks have been detected in serum albumin irradiated with doses up to 2.5 X 108 rad.m The oxygen effectobserved upon irradiation of dry proteins seems to beconnected not only with the excitation of protein molecules but also with the e.xcitation of oxygen molecules
which in turn act on hydrogen bonds within protein
molecules.117 The most typical changes in physical,
chemical property are those changes which occur invivo: isoelectric point, decrease in sedimentation coefficient, or aggregation as a result of hydrogen bond formation between molecules with disorganized secondary andtertiary structure.133 • 135 •14 7

81. While the effects of irradiation on polysaccharides
in solution and in dry state are much the same, cellulose
and pectin, when irradiated in a dry state show an aftereffect, but only if stored dry in the presence of oxygen. 155
This is probably due to long-lived radicals formed withoxygen. In addition to degradation, branching has been
obsen-ed in the dry state. 156 The branches are random
in length and spacing. All branch points are probably
tetra-functional. Branching of polysaccharides in aqueous solutions has not been reported.
82. High molecular weight polysaccharides such as
hyaluronic acid in solution (synovial fluid) are depolymerizedm when irradiated with relatively low doses of
X-rays (9,000 r), and the process continues about
twenty-four hours after irradiation. Viscosity and lightscattering measurements have proved that, during theafter-effect, depolymerization continues. The most probable sites of depolymerization are the -0-C-phosphoester bonds. The addition of cysteamine158 protects thesynovial fluid, although in the absence of oxygen (presence of nitrogen) synovial fluid is more radiationsensitive. A detailed study of ESR of irradiated polysaccharide has not thrown any light on the observed
chemical changes. Internal crosslinking has been suggested159 although direct proof, using hyaluronic acid,does not exist.

77. The important aim of studies of the action ofionizing radiation on proteins is to understand themechanism of radiation-induced enzyme inactivation.
The catalytic capability of an enzyme is determined,
most probably, by an active site composed of only a verysmall number of amino acid residues maintained at thesurface of the enzyme molecule by secondary and tertiary
bonds. Thus, enzyme inactivation can be accomplishedeither by chemical alterations in the amino acid residues
within an active site or by disruption of essential configuration.

MACROMOLECULAR COMPLEXES

83. There is growing interest in relating the results
obtained by irradiating isolated compounds of macromolecules in aqueous solution, and even in the pure solidstate, to those from integrated macromolecular complexes (section VI below). N ucleoproteins are probably
the closest models of nucleic acids as they exist in thecell, although the status of nucleoproteins in vitro may
be very different from that in viva.
84. Protein has a protective effect because it traps
radicals that would otherwise reach the deoxyribonucleic
acid (DNA), but the extent of this trapping is unknown.160 However, some protective action of nucleic
acids on the denaturation of ovalbumin as measured by
the number of titrable sulfhydryl groups has been reported.1e1

78. The efficiency of inactivation through ionizationis very high, with G,..., 1. This implies that one ionization or cluster of ionizations anywhere within or near amolecule inactivates that molecule. This makes the
hypothesis of inactivation via an attack on the site ofspecific activity improbable. Consequently, inactivationof enzymes by radiation is discussed here in terms of
disruption of the secondary and tertiary structure following the production of an electric charge inside themacro-moleculem and migration of the ionizing energy
along the covalently bonded structure. Energy then becomes localized on weaker bonds, 150•151 particularly on
S-S disulphide bridges responsible for maintaining thevarious chains of the enzyme in the native structure.

85. Nucleoproteins from the same source but withdifferent protein contents show different radio-sensitivities. Dilute solutions of DNA nucleoprotein with N/Pratio smaller than 2 are more radio-sensitive than DNA
with N/P greater than 2. Radiation damage is established from a decrease in viscosity. These differences
can be attributed to the influence of protein content on48

-the configurations of DNA in the compk""<es rather thanto some protective action of protein. 162 • lsa

simpler systems it is known that the presence of evenslight amounts of impurities can modify the spectrum
appreciably. It is not yet possible to identify those free
radicals that give rise to the particular pattern of electron spin resonance absorption in irradiated biologicalmaterial. Therefore, attempts have been undertaken toshow a parallelism between radiation-induced ESR
phenomena ar!d biological effects on the same material.

86. If there is a radio-lesion, several possible sitesof disintegration and disruption of a nucleoprotein canbe envisaged. These include bonds between nucleic acids
and protein. Their response may explain why irradiatednucleoproteins do not swell in water as readily as unirradiated material, and why trypsin yields free DNA
more quickly from irradiated nucleoproteins.164
4

92. In seeds of the grass Agrostis stolonifera, theeffect of irradiation on growth inhibition decreases whenwater content increases. This has been related to theobservation that the fraction of free radicals persisting
for longer times after irradiation also decreases withincreasing water content. 174 In seeds of Vicia faba, boththe sensitivity and free radical concentration after irradiation decrease with increasing water content.175 In barleyseeds, studies have been made of the influence of waterand LET on radicals detected by ESR techniques. 176
Attempts to relate biological and ESR results on dry
pollen grains have been reported. 177 A parallel between
biological end points and ESR data has been establishedin bacterial spores in studies of the effects of oxygen,heat, and NO treatments on the biological and physicalresponses. 5 "· ss, us, 124 The ESR method, applied to theinvestigation of lyophilized tissues of whole-body
irradiated rats, also demonstrates the presence of stableradicals i,vhich vary with the different tissues. After
irradiation with 1,000 rad the amplitude of the spectra
does not change in any of the tissues with the exceptionof spleen where there is a sharp decrease immediately
after irradiation. 178 The ESR method has also been used
to study the effects of different gases 179 (air, N 2 , NO)
and of protective substances like cysteamine and AET
on the production of free radicals.186• 1 s1

6

87. On irradiation with electrons (2 X 10 -2 X 10rad), part of the DNA of sperm heads is cross-linked toform a loose gel-like network ;165 this does not appear tobe due to seconda1y valence forces. Such cross-linkage
has been postulated to be the cause of inactivation of bacteriopbages by ionizing radiation. 165 This seems lessplausible than the hypothesis that inactivation is due to
production of carbon radicals in phage DNA. Such radicals may combine with oxygen, react with a hydrogenatom donor, or become inactive by an unknown process
if neither oxygen nor hydrogen is present. 166• 167
88. It is not yet clear which chemical changes aremost important in the loss of biological activity of nucleic
acids. No data clearly relate radio-sensitivity of biologically active nucleic acids to chemical changes producedby ionizing radiation. From studies on the inactivationof transforming DNA by ultra-violet radiation, by heat
denaturation, 165• 169 and by radio-mimetic substances, 170
damage to the bases seems important. On the other hand,a break in one of the chains of double-stranded DNA, oreven scission of the whole molecule, does not necessarily
lead to loss of activity. The molecular weight of thetransforming DNA can be lowered approximately one
order of magnitude by ultrasonic disruption withoutcompletely inactivating DNA.171 The inactivation yields,from decay of P 32 incorporated into single- and doublestranded DNA phages indicate that, whereas all breaks
in single-stranded DNA inactivate the phage, bothstrands must be broken in double-stranded DNA phages,
a fact which accounts for the lower efficiency ( ca.10 percent) .172

93. The results obtained so far through the ESR
technique are summarized in the following propositions :11" (a) Ionizing radiation produces free radicals in
living material;" ( b) The concentration of free radicals producedby radiation increases with increasing doses ;" ( c) The measurable concentration of free radicals
depends on the surrounding gas and on the water content of the specimen;" ( d) The concentration of free radicals decreases
relatively slowly after irradiation and is still wellmeasurable for minutes or up to many hours according
to the material and environmental conditions (watercontent and gas) ;" ( e) The opinion, widely held up to the present,that absorption of radiation in biological material generally leads within micro-seconds to states stable in
the physical sense, must be abandoned;"(f) It has been proved in some cases that a molecular interchange exists between protective substances and the protected material, and that it plays
a fundamental part in protective action."

DETECTION OF FREE RADICALS IN WHOLE CELLS BY
ELECTRON SPIN RESONANCE (ESR)
89. Although the radiation chemistry of water andof macromolecules in vitro can provide useful information on models of primary reactions in vivo, complete
information depends on studies on the chemistry of thebiological constituents after irradiation of living organisms. Progress in this field has been obtained recently
with development of the electron spin resonance technique (ESR); this allows study of free radical formation in biological systems. 173
90. Through this method, unpaired electrons havebeen detected in a variety of materials. When applied
to detection of free radicals, the material irradiated must
be stabilized to prevent diffusion of the radicals, e.g.
measurement has to be carried out in solids, in frozen
solutions and suspensions, or in dry biological material.
In principle, quantitative estimates of the number of
unpaired electrons in a sample are possible. In practice
it is difficult to attain reasonable accuracy.
'

V. Chemical factors modifying radiation
response in cells

91. Dat~ d~rived from irradiated biological materials
are not easily mterpreted. They do not necessarily relate
to t?ose ~r~e radicals responsible for the biological effects
o! irr~diation be~use many unpaired electrons arise inbiologically less important molecules. From studies of

OXYGEN EFFECT
94. The influence of oxygen tension on the responseof biological systems to radiation is one of the fundamental phenomena of radio-biology. This influence, ex49

erted during irradiation, is generally called "o_xyge_neffect". Gray's recent review integrates the data m ~hisarea.1s2 The effect has been observed _in a _great vanecyof biological systems and can be descnbed m the following way:(a) In the absence of ~A.~gen, or C1;t ~e~uced oxygen
tension the effects of radiat10n are dimtmshed but notelimin~ted; oxygen acts as a dose m~lti~lying ag:ent.
Considerable clarification of the quantttat1ve relations
between radio-sensitivicy and oxygen tension has resulted
from work with the bacteriwn Shigella flexneri. 183
Since, for this organism, survival is exponentially related
to dose at all oxygen tensions, th~ slope. ~f. the curve
may be used as a measure of rad10-sens1tiv1ty. It has
been found that when a sufficiently dilute suspensionof bacteria is vigorously bubbled throughout the periodof irradiation with gases containing ?iffer~t_p~rcentagesof oxygen, the relation between radio:sens1tiv1ty, _S, ~dthe concentration of oxygen ( 02) .m 0e medium mwhich the organisms are suspended is fairly accurately
represented by the simple relation:s - SN)[02]
SN= (m - 1 [02] K

95. The nature of radio-chemical reactions in theo:i..·ygen effect including the possible role of H,O~ radicals and of other reactive products whose yields are
influenced by oxygen tension, have been widely discussed
in recent years. 208 Proof has been cited52 •53 • 11 8 ~ato:A.-ygen-free radical inter~ctio~ takes place in bacterial
spores to bring about b10logical damage by X-rays.
However, the spores are semi-dry, and the role of Wf!-terin these interactions has been studied as yet only m apreliminary fashion. 209 • 210 Consequently, a generalization involving the metabolizing cell cannot be made now.
The belief that the oxygen effect depends on cellul~r
aerobic metabolism is challenged by experiments m
microorganisms with normal and defective cytochrome
systems in which 9xyge? effect is tJie sam~. ~owever,oxygen effect vanes with the cell s phys10log1cal state.
For instance, freshly harvested yeast cells, before starvation, have a considerably higher oxygen enhancement
ratio ( m = 3.6) than cells which have been starved. The
ratio m decreases as the starvation period is prolonged,
reaching a minimum value of m = 2 after two days'
stanration. 212 The observation that oxygen alone causes
chromosome aberrations when in high concentrations213
complicates interpretation at this time.

where SN is the sensitivity under anaerobic conditions,obtained by bubbling oxygen-free nitrogen throug~ thesolution, and m and K are constants. In general, m is theratio between the effectiveness of a given dose whenoxygen is freely available and the effectiven~ss whenoxygen is absent. Thus, ( m - 1) may be cons1der~d asthe ratio of the OA.'J-gen-dependent to the oxygen-mdependent components of radio-sensitivity. The cons~t. K
is the concentration of oxygen at which the sens1t1v1ty
is exactly midway between anaerobic and fully aerobic
values. The ratio m varies around 3 for a wide range
of cell types and effects: inactivation of bacteria, 181i-isa
and yeast,163 growtl;, 187 chro!11'osome aberrati~ns18 ~· 200
and mitotic delay201 m plant tissues, as well as mact1vation of isolated mammalian cells. 202•208 The similarity
between values of K (in the range of 4.5-5.0 µ.M/l) for
irradiation of bacteria, yeast, 20~ ascites tumour cells, " ~and plant root cells, 189 may be fortuitous, since a somewhat higher value of K (10 ± 2.8 µ.Mjl) has been reported205 for Tradescantia pollen tube chromosomes.
( b) In wet metabolizing systems, the presence ofoxygen during irradiation appears to be essential sinceno effect has been seen in bacteria irradiated underanoxic conditions when oxygen is introduced only 20
milliseconds later. 206 Even stronger evidence is suppliedby studies of the inactivation of Serratia marcescens byvery short pulses of high intensity electron beams. 201
Cell suspensions were irradiated with 1.5 MeV electrons
delivered either in a single pulse of two microseconds
duration ( 10-20 krad total dose) or for five minutes at
a dose-rate of 1000 rad/min; both treatments were applied either in hydrogen or in a 1 per cent oxygen and99 per cent nitrogen mixture. \i\Then irradiation was very
short, the radio-sensitivity of the bacteria was the sameas under anoxic conditions, whereas with the longer
irradiation, oxygen enhanced the sensitivity by a. factorof 2.5. However. in dry bacterial spores two act10ns ofoxygen, one realized only if oxygen is present during
irradiation, the other at appreciable times after irradiation, have been shown. 52•53 • 11 8
( c) Oxygen effect is usually less marked when cells
are exposed to high LET radiation. An important aspectof the oxygen effect is that the enhancement ratio, m,varies with type of radiation, being highest with radiation of lowest LET.

96. This oxygen effect must not be coniused with theeffect of oxygen given in the post-irradiation period.
Since the development of radiation injury depends on
metabolism, it is likely that there are systems in which
the magnitude of radiation lesions can be altered bychanges in oxygen tension after irradiation. 21"-211 Several
papers have also dealt with the effect of anoxia; thesehave shown that anoxic conditions in metabolizing cells
after irradiation reduce damage in some cases, 218 inothers enhance it. 219

211+

EFFECT OF GASES OTHER THAN OXYGEN

97. If oxygen exerts its radio-biological effects by reacting with radicals induced by radiation, other oxygenlike substances may react similarly. 125 In Shiqne_lla
flexneri Y6R bacteria, 220 nitric oxide enhances radiation
damage in the absence of oxygen. Nitric oxide has beenfound to enhance the effects of ionizing radiation onplant roots 221 and on ascites tumour cells. 222 In Drosophila, nitric oxide present during irradiation enhances
the production of dominant lethals and sex-linked recessive lethals. 223 The system seems to differ from that inbacteria and ascites cells in that the same concentrationof oxygen does not show an equivalent effect Althoughthese studies have shown that nitric oxide may freque~tly
simulate oA--ygen, differences in the effects of the twogases have been shown in dry biological materials. Dry
grass seeds irradiated and stored in nitric oxide are lessaffected by radiation titan those irradiated in anoxia.
However, when the water content of the seeds exceeds 12
per cent, nitric oxide is as effective as oxygen.179 In
spores of Bacillus megaterium, two actions of nitricoxide are known: a small sensitizing action during
irradiation and a large protective action after irradiation.m The latter action is a consequence of removal of
free radicals. 52 •rn The degree of hydration may influence the size of the two actions. 182

0

EFFECTS OF GASES UI\"'DER PRESSl.JRE

98. The Q}q·gen effect on V icia f aba roo~s an~ ascit~stumour cells is prevented when cells are irradiated mliquids in equilibrium witlt different gases underpressure. 224 •225 The following gases have this effect:50

helium, hydrogen, nitrogen, argon, krypton, xenon, andcyclopropane; the same applies to nitrous oxide intumour cells. The mode of action has not yet been established; the structures normally injured by radio-chemical
reactions involving oxygen may be protected by anabsorptive layer of the other gas. Proof that these substances interfere with injuries directly or indirectly dependent on oxygen is provided by the fact that they neverreduce the effects of the oxygen outside the limits ofanaerobic conditions. This research may provide a mostvaluable clue to the mechanism of oxygen effect.

102. A possible clue to the action of peroxides has
been found through studies of radiolysis of purines andpyrimidines. The addition of hydrogen peroxide andpersulfate to irradiated solutions increases the G valueof pyrimidines but leaves the G value of purines unaltered. 241, 242
CHEMICAL PROTECTION

103. Certain substances of different composition anddistinct physical and chemical properties, when added tocell suspensions, can reduce the effects of subsequentirradiation. Study of the chemical protection of the cell
is potentially helpful for understanding the primary
events of radio-biological processes. Among "protective
agents", the sulphur-containing compounds ( cysteamine,cystamine, aminoethyl-isothiouronium, glutathione, etc.)
are the more important. A few inhibitors of enzyme
activity (sodium cyanide, sodium azide, etc.), somemetabolites (gluconate, pyruvate, ATP)2 4 s- 246 and alcohols,247-m have the same action. Chemical protection
requires the presence of the protector before or during
irradiation, and is more effective against X-rays thanagainst other ionizing radiations. However, some metabolites can also have positive effects after irradiation,
possibly by influencing repair processes. 245• 246

HYDRATION

99. The precise significance of water radiolysis in thereactions induced in cells by radiation has still to be
determined. New facts on this subject have been given
by experiments of Hutchinson et al. 226 They measured
inactivation of two enzymes (invertase, alcohol dehydrogenase) and of coenzyme A in wet and in dry yeast cells.
They found that the sensitivity of these enzyme molecules were two times and twenty times greater respectively in the wet state, than in the dry state. Wet versus
dry sensitivity for coenzyme A was estimated as 100 to 1.
It has been assumed that the difference between the wet
and the dry sensitivities is caused by the migration ofchemically active intermediates formed by irradiation ofwater in the wet cells. Hutchinson 47 estimates that the
migration distances of the water radicals are about thesame ( 30 Angstroms) in all three cases.
100. Although increased water concentration enhances
radio-sensitivity in Aspergilfas, 227 several investigations 22 B- 231 comparing radio-sensitivity of dried and wet
plant seeds show that it is higher in the dried. Experimental results on Artemia eggs 232 • 233 parallel results onplant seeds. It is difficult to draw a general conclusionfrom the few investigations made on the comparative
radio-sensitivities of wet and dry cells. The possibility
must be considered that, in some experimental conditions, radio-sensitivity is modified by an inadvertentchange in oxygen tension within cells which is very likely
to be different for different moisture contents. Also, it
may well be that effects of moisture observed in plantseeds and Artemia eggs are due mainly to alterations inphysiological state rather than to participation of water
radicals in primary radio-chemical reactions.~ 31 • ~ 33

104. Protection has for long been associated w1th theindirect action of radiation. It has even been used as acriterion for distinguishing indirect from direct action.
This view can no longer be justified. Experimental
evidence has been presented wherein no indirect action
can be envisaged. 141 ' 250- 252
105. One action of protective agents may be e.."\:plainedby a decrease of oxygen tension. 253 • 255 • 256 The anoxic
hypothesis implies utilization of oxygen by the protector,
e.g. in transformation of cysteamine into cystamine.
Support for an anoxic effect of protective agents stems
from experiments in which the dose reduction factor
with cysteamine is similar to that of simple oxygen
removal. 254 However, several investigators consider thatsulphydryl compounds are protective by other means
than production of anoxia. The most recent observations
supporting this have been obtained in Escherichia
coli, 2 "&- 255 in isolated rat thymocytes, 259 and in HeLa cells
in tissue culture. 260
106. Alternatively, protection may be achieved by
combination of the chemical protector with free radicals
produced by irradiation. By comparison with chemical
data 182 a competitive type of reaction may be envisaged.
This reaction involves free radicals, oxygen, and protector. The protecting molecule may act either by combining \vith free radicals, thus avoiding formation of an
unstable active peroxy-radical. or by attacking theperoxy-radical and making it stable, i.e., non-active. 261
No clear-cut evidence has been presented in favour ofeither hypothesis.

PEROXIDE AFTER-EFFECTS

101. If phage particles are irradiated in buffer andallowed to remain in the suspending medium after
irradiation, the number of damaged particles increases
with time. 23 4-236 Similar phenomena have been reported 237- 2311 in bacteria, in lysogenic systems, and inphage bacterium comple..xes. This after-effect may be
attributed to the presence of H 2 0 2 or of organic peroxides formed in the broth. However, doses exerting
profound effects on whole cells are often not high enoughto produce damaging concentrations of peroxides in thesuspending media. This holds particularly if cells contain catalase, but hydrogen peroxide and organic
peroxides in dilute suspensions which contain little
protective organic matter may also exert a marked effect.
In synthetic media, the concentration of peroxides responsible for the after-effect decreases with time during
twenty days after irradiation. During this period therate of decrease depends on dose, at least in the 1-5
kilorad range. 236 Artificially added inorganic peroxides,
e.g. persulfate and urea peroxide, 240 can also increase
sensitivity of phages and bacteria.

107. Another e..xplanation is that protecting molecules
attach themselves primarily to cell structures, thus masking sensitive sites. The complex so formed would guard
these sites from the attack of free radicals (indirect
action). This complex may also dissipate absorbed
energy less harmfully (direct action). With SR-containing compounds, Eldjarn and Pihl m have proposed achemical model embodying this concept. The maskingeffect hypothesis is supported by experimental results
showing that decrease of protective ability of cysteine
injected into animals parallels recovery of the metabolic
activity which that substance had initially lowered. 262 • 263

51

108. Other substances with lmown pharmacologicalactivities (hormones, amines, neurodrugs), protectors
after injection in animals, seem to have no action in cellsuspensions. Thus, little information about the primary
events of radio-biological action can be obtained fromin vivo experiments in which they are used except forthat concerning their possible interference with metabolic
processes.
109. The chemical protective agents are also effective
against chromosome aberrations 264 and induction of
mutations by X- and gamma rays. 265 • 266 However, thissubject deserves much more attention, the data being
scanty.
110. Accumulated evidence on chemical protection 243 • 244 does not now permit an unequivocal recognition of mechanism. New data are needed to clarify this.
The ESR technique may become useful in this area.

"genetic" or "non-genetic" factors necessary for recovery of the damaged structure are functional. The contribution of the cytoplasm in radiation injury has been
partially clarified by recent investigations. In particular,
the presence of toxic products 289-290 and the existence ofchanges in IEP ( isoelectric point) perhaps associatedwith changes in RNP ( ribonucleoproteins) localized incytoplasmic microstructures may imply disturbances innuclear cytoplasmic interaction. 291-296
115. Particular emphasis has been placed on themetabolism of deoxyribonucleic acid (DNA) and on its
interaction with ribonucleic acid (RNA) and protein
metabolism. These metabolic functions are so intimatelyintertwined in the way they influence cell division andreplication that it seems logical to treat them integrally
to assess how radiation may affect this complex.
DNA SYNTHESIS
116. Recently Kornberg and associates 29 1-2 99 havesynthesized DNA in vitro from deoxyribonucleoside
triphosphates using purified extracts from E. coli. The
system requires "primer" DNA which, during thereaction, replicates. The product has a base composition
identical with that of the native primer. Single stranded(denatured) DNA preparations also provide excellent
primers. soo

VI. Effect of radiation on cellular structures
and their function
111. Some of the more spectacular and most extensively studied effects, such as inhibition of cell division,
mitotic delay and mutation, are most readily associatedwith nuclear damage and are apparent after exposure to
relatively small doses of radiation. However, inhibitionof cytoplasmic functions should be carefully consideredin assessment of total damage. Since nuclear and cytoplasmic functions are so clearly intertwined, it is imperative to consider their possible interactions in weighing
the relative importance of nuclear and cytoplasmic
damage.
112. These interrelationships vary with different
systems and different functions. The early works of\Vintemberger,2 67 Zirkle,2 68 Hensbaw, 269 Hercik 270 andPetrova 271 showed that mitotic delay and cell death are
principally manifestations of radiation damage sustainedby the nucleus. Recent experiments dealing with partial
cell irradiation have shown clearly that irradiation ofgenetic material is far more effective than cytoplasmic
irradiation in producing cell lethality. For example 50
per cent inhibition of hatching of Habrobracon ~ggs
requires 107 alpha particles to the cytoplasm; only 1alpha particle to the nucleus suffices to inactivate theegg. 272 Comparable results have been obtained in similare?Cper~ments with newt heart cultures. 273 Conversely,
situations may be expected where cytoplasmic damage isrelatively more effective in impairment of specific cellfunctions. For e..xample, changes in isoelectric point of
mitochondrial nucleoproteins of the adult nerve cell occur
during or immediately after irradiation with small
doses. 21 s-211 This indicates alteration of metabolic
functions and, in particular, of oxydative phosphorylation. 21s, 2;s117. This mechanism is compatible with present concepts on DNA replication in vivo. These postulate that
double-stranded DNA may split wholly or partially into
single strands that serve as templates and receptors forcomplementary strands. Moreover, Komberg et al., 301
identifying all the dinucleotides in synthetic DNA, haveshown that the in vitro system produces double-stranded
DNA molecules with each single spiral running in the
opposite direction as compared with its mate; this result
provides excellent support for the Watson Crick model.
118. The presence of polymerase, first found in E. coli
extracts, has also been demonstrated in e>.."tracts of mam~ian cells from ascites tumours, thymus, regenerating
liver, etc. 302- 3o5
119. In the nuclei of tissue cells, DNA synthesis islimited to a definite period during interphase. In the firsthours a~ter mitosis there is usually no DNA synthesis( G1-penod). In the next period ( S-period), lasting
several hours, the DNA content of the cell doubles. Theinterphase is concluded by the G:rperiod. This sequence~f events i~ the i_nterphase may be subject to modifications; thus, m ascites tumour cells the G1-phase is absent.
Precursors of DNA are probably produced in theG1 -phase and activated (to nucleosidetriphospbates) at
the ex~ense of energy-generating processes (e.g. nuclear
oxydative phosphorylation). Nuclear synthesis of RNA
also occurs in this phase, associated with the productionof new enzymic proteins. In the synthetic period theas_sembly of activated precursors most probably o~curswith t!1e. help of the ne:vly synthesized enzymes and withthe ongmal DNA servmg as template and primer. In theG2-p~riod J?N~ is further.p_r~pared for its subsequentrole m the immment cell div1s10n. In cells of lower organisms this stratification into well separated division
stages does not occur. Probably, however, the sequenceof metabolic events is similar.

113. Non-nucleated cells (Acetabularia, amoebae.~ 79
Paramecia,zso• 281 tissue culture cells) 282 ultimately die,but they may survive for a considerable time andeven cont!nue _to differentiate (Acetabularia). 250,283,mLethal!~ irra~ated E. coli cells retain the ability tos:rnthesize active bacteriophage. 236• 25 s- 25 s Owing to thishigh degree o~ cytoplasmic autonomy, nuclear radiationda~age aff~ctrng cytoplasmic functions may escape detection dunng the observation period.

120. Since the discovery by Hahn and Hevesy 306 thatp~osphor.us_incorporation into DNA is inhibited by ion-11~. Conversely, cytoplasmic damage affecting thephysiology of the cell may not become permanent if theizing radiat10n, a fact confirmed by similar evidence on
incorporation of various labelled precursors such as

52

cells in vitro using doses of 750-3000 r. They foundinhibition of the incorporation of (2-C 14 ) uracil in DNA
thymine, but the possibility that this effect was due toinhibition of mitosis has not been excluded. Further
results have been reported by Budilova 320 on the incorporation of several precursors into DNA molecules ofisolated thymus cells nuclei; incorporation was greatly
reduced in nuclei irradiated in viva, whereas there were
no changes when nuclei were irradiated in vitro.

adenine, erotic acid, formate, phosphate and thymidine,it has been generally accepted that DNA synthesis is aparticularly radio-sensitive metabolic process. Recent
investigations have cast serious doubt on the correctnessof this opinion. They lead, rather, to the conclusion that
relatively low radiation doses do not affect the rate of
DNA synthesis in various types of cells. It is now
realized that a diminished incorporation of precursors
into DNA after irradiation may not necessarily represent
primary inhibition of DNA synthesis. It may be the consequence of other differences between the irradiated andthe control cell populations, 301- 311 namely:(a) Accumulation of cells in the G2 -phase as a resultof mitotic inhibition;( b) Changes in the distribution of the various cell
types of a mixed cell population;( c) Increase of the fraction of dead cells in the irradiated population. The same argument obviously
applies to the synthesis of RNA and protein.

126. In bone marrow cells in vitro, high doses ofradiation (>SOO rad) directly inhibit DNA synthesis.
Lower doses ( < 300 rad) cannot inhibit DNA synthesis
in cells already in the synthetic period. However, cells in
the G1 -phase at the time of irradiation enter the S-phase
only after an appreciable delay. More recent observations
by Uyeki 321 are in accord; the number of cells entering
DNA synthesis after 800 r is strongly depressed.
127. Low doses of X-radiation (50-140 r) prevent
division of root tip meristem cells of Vicia faba but do
not interfere directly with DNA synthesis. 822 • 323 However, cells not yet in synthesis at the time of irradiation
pass on to the synthetic phase only after a delay of 10hours or more. In contrast, Das and Alfert 32• have reported an immediate effect of irradiation on DNA synthesis; even a dose as low as 200 r enhances DNA synthesis, whereas 800 r increases the uptake of tritiatedthymidine to approximately five times the control value.
128. From studies in regenerating liver 325 •826 it has
been concluded that DNA synthesis itself is not primarily
affected after partial hepatectomy by relatively feeble
radiation doses. 325 •326 In resting liver there is no appreciable DNA synthesis, but when regeneration is inducedby partial hepatectomy, synthesis begins 15-18 hours
after the operation and reaches a maximum at 24-29
hours. In this first stage of regeneration there is reasonable synchronization of DNA synthesis. High radiation
doses (up to 2,000-3,000 r) are needed to inhibit synthesis once it has begun; a dose of SOO r is ineffective.
However, the latter dose is quite effective in postponing
synthesis when given before the beginning of the synthetic period.
129. Few e..xperimental data are available on the sensitivity of DNA synthesis in micro-organisms to Xirradiation. Billen 321 studied mutants of E. coli and, inparticular, the influence of "unbalanced growth" andradio-sensitivity. He concluded that X-irradiation inhibits the synthesis of protein required for DNA replication.
130. In dividing H. inflitenzae, E coli B and B/r,
irradiation with doses between 19 and 100 k rad is followed by breakdO\vn of cellular DNA; after a certain
time this process stops and is followed by an increase in
DNA.32s,3w

121. Recent developments in the use of microspectrophotometry and autoradiography for the study of single
cells often make.it possible to account for these complications and thus to arrive at a more correct evaluation of
the biochemical effects of irradiation. Another method,
although at present often more difficult, uses more or lesssynchronously dividing cells. The following survey considers investigations using these techniques.
122. Irradiation of HeLa-cells with 5SO r leads to aconsiderable increase in the fraction of cells synthesizing
DNA as compared with control cultures. 312 This increase amounts to 100 per cent six hours after irradiation(this represents a larger fraction than can be accounted
for by inhibition of mitosis). Apparently, cells irradiatedduring active DNA synthesis continue to synthesize forlonger periods than normal; this may be related to giant
cell formation. Moreover, Painter 313 found that whenpost-irradiation mitosis resumes, added tritiated thymidine results in a lower fraction of labelled cells inmitosis of these cells than in mitosis of unirradiated controls. This could be due to sluggishness of irradiatedcells in the G2 -phase and/or in mitosis of the next division stage.
123. In contrast, Harrington m did not see any direct
effect of exposure to SOO r on the fraction of U-12
fibroblasts in DNA synthesis. The percentage of cells
synthesizing DNA began to drop after an interval corresponding to the duration of the G1 -phase; this decline
must be wholly attributed to inhibition of mitosis.
124. A similar conclusion has been drawn fromstudies of L cells (mouse fibroblasts) 315•316 in which
DNA synthesis continued in the absence of mitosis until
the double premitotic content per cell was reached. Veryhigh doses ( 4000-5000 r) retarded DNA synthesis
instantaneously. After e..xposure to 2000 r the cells still
completed an average of three divisions, whereas after
5000 r, only 20 per cent of the cells were still capable of a
final division. Such DNA synthesis as was observed
thereafter was in giant cells and occurred at a considerably lower rate than in normal unirradiated cells.

131. In H. influenzae, the biological activity of DNA,as characterized by its transforming activity, has been
determined after irradiation. All remaining DNA andDNA formed after irradiation is functionally normal.
No relation has been found between killing and severityof DNA breakdown. From this it has been concluded
that observed DNA breakdown is not the immediateradiation-induced process leading directly to cell death.a:i9

125. X-irradiation (800-1250 r) of Ehrlich ascites
tumours has not been found to inhibit DNA synthesis. 311• 818 Mitotic activity is arrested instantaneously
but volume, dry weight and total nucleic acid per cell
continue to rise considerably. The DNA content per cellrises to the pre-mitotic level. Harbers and Heidelberger319 cultured and irradiated Ehrlich ascites tumour

132. DNA is in a highly polymerized state in bacteriophages330•331 and certain tissues. 332•333 After irradiation,
depolymerization is seen, 33s-335 and shifts in the purine/
pyrimidine ratio in DNA synthesized after X-irradiationof spleen cells in viva have been observed. 336 • 831 Changes
53

selective irradiation of the nucleolus by UV microbeams,
Perry et al. 355 have concluded that RNA transport into
the cytoplasm originates from both nuclear locations ofRNA. From recent autoradiographic studies of the incorporation of tritiated precursors into RNA of Hel.acells, in which several correction factors were applied
for the conversion of grain counts into actual incorporation, the same authors state that their data do not show
a transport of RNA from chromatin to nucleolus. 356
Moreover, a few instances are known where labelling of
the nucleolus precedes that of the chromatin.357

in the thymine/adenine ratio in DNA synthesized after
irradiation of plants have been reported by Kusin andTokarskaya. 338 • 33~ These changes seem to be closely
related to disturbances in nucleotide metabolism. 34 o-m
RN A AND PROTEIN SYNTHESIS
133. In contrast to DNA, most RNA is in the cytoplasm; only a small fraction resides in the nucleus.
134. Little is known about the secondary structureof RNA. It is probably single-stranded. Physico-chemical data suggest that it may fold locally into incomplete
double spirals stabilized by H-bonds ; these orderly
structures would be held apart by unarrayed segmentsof the RNA chain. 343

140. Little is kno\vn about the mechanism of RNA
synthesis. An enzyme, polynucleotide phosphorylase,that catalyzes the synthesis of RNA from ribonucleoside
diphosphates has been found in micro-organisms by
Ochoa and associates. 358 The purified enzyme requires aprimer, but any tri- or tetranucleotide may serve in thiscapacity, and it is not the primer but the available nudeotide diphosphates that determine the base compositionof the product.359-361
141. On the other hand, extracts, not only from microorganisms but also from animal cells, polymerize ribonucleoside triphosphates to RNA. 362• 363 \/\Then DNA ispresent, treatment with DNA-ase destroys its activity.
Enzymatic activity depends also on the simultaneouspresence of the triphosphates of all four nucleosides.
Furth et al. 364 and Weiss and Nakamoto365 have shownthat newly synthesized RNA is a copy of the base composition of the added "primer'' DNA. The enzyme produces polyadenylic acid or poly-uridylic-adenylic acidwhen primed with polythymidylic- or poly-adenylicthymidylic acid respectively. With M. lysodeikticus or
TrDNA as a primer, the newly synthesized RNA has
the same nearest-neighbour base frequency as theprimer. 366 The resemblence of tliis enzyme to the polymerase of DNA synthesis is striking.

135. Nuclear RNA is not homogenous; an important
fraction is probably in ribosomes, as observed in thymus
nuclei. Cytologically, RNA may be divided into chromosomal and nucleolar RNA. Biochemically, two fractionsof nuclear RNA may be distinguished, one extractableby low concentrations of saline (n-RNA1 ), another remaining undissolved (n-RNA2 ). Generally, n-RNA1
incorporates labelled precursors less readily than doesn-RNA2 •84 ' -346 According to Zbarskii and Georgiev347 • 848
n-RNA1 represents the chromosomal RNAandn-RNA2
forms part of nucleolar RNA.
136. In the cytoplasm, RNA occurs in the cell sap(S-RNA) and in the microsome (liver, pancreas) andribosome fractions. The molecular weight of S-RNA isrelatively small (20,000-40,000) ; that of microsomal
RN A is considerably larger (approximately 1.7 X 106 ).
The possibility cannot be excluded that the latter molecular weight represents aggregates of molecules of lm·ver
molecular weight as it has been shown that ribosomes
may disintegrate into smaller particles depending on the
Mg++ concentration of the solvent. The RN A in thesmallest ribosomes, the so-called 30 S particles, has amolecular weight of only 5.6 X 105. Small amounts of
rapidly turning over "messenger'' RNA of an intermediate size, between the latter RNA and S-RNA, arepresent in uninfected and phage-infected bacteria. 849 • 850
This RNA attaches itself to existing ribosomes and confers on them the code for protein synthesis.

142. From e..xperiments with labelled RNA precursors, it has been shown that synthesis of RNA occurs
during the entire interphase, although in some cells theprocess is slower during S-phase. During mitosis, no
RN A seems to be synthesized.
143. Within the nucleus, DNA transfers its genetic
information to RNA. 367 • 368 The presence of an RNA
polymerase requiring DNA for action, and copying its
base composition, supports this concept. RNA formedin the nucleus then passes into the cytoplasm, carrying
its information to protein synthesizing sites. Rich369 has
demonstrated that, in principle, a single-stranded RNA
molecule can unite with a complementary single-stranded
DNA molecule. Moreover, Hall and Spiegelman370 haveshown specific hybrid formation between single-stranded
T2-DNA and the RNA synthesized subsequent to infection of E. coli. Geiduschek et al. do not favour singlestranded DNA as a necessary intermediate in RNA
synthesis in vitro. 311
144. Apparently, the base sequence of the DNA istranscrib_ed into newly formed messenger RNA, triplets(or multiples of 3) of nucleotides carrying the information for various amino acids (para. 151). The most
~rect proof of the ability of RNA to carry genetic
mformation is provided by the information that purified!obacco n;iosaic virus RNA is apparently infectious. How
mformat1on transfer between DNA and RNA is effected
is not known. Leslie372 recently postulated, from studies
on human liver cells and from the literature, that coding
for micro-organisms and for somatic cells of higherorganisms may differ.

137. Recent studies provide evidence that RNA is
synthesiz.ed exclusively in the cell nucleus, and is transported from nucleus to cytoplasm after synthesis. Thus,
Goldstein and Plaut351 transplanted P 32 RNA labelled
nuclei from intact amoebae into enucleated amoebae ;after a while the cytoplasm of the host contained labelledRNA. As these amoebae were viable, it seems unlikelythat leakage from damaged nuclei was responsible forthe effect.
. 138. So far, the type of the nuclear RNA transported

mto the cytoplasm has not been established. Woods andTay~or35 ~ have suggested that RNA is primarily syn-thesized m chromosomes and subsequently stored in the
nucleolus; from there it would be transferred to cytoplasm. This hypothesis is supported by other investigators353•354 who have found that, with a labelled RNA
precursor, radio-activity is first detected in chromatin
and only later in the nucleolus; continued incubation in
the absence of labelled precursor leads to an earlier andfaster fading away of the radio-activity of the chromosomal than of the nucleolar RNA.
139. Whether this hypothesis has general validity for
all types of cells is not known. From experiments on
54

actu~lly demons.trated that the new RNA(which, according to Volkm and Astrachan,3 ' 8 has a base composition corresponding to that of the phage DNA) is
associated with pre-existing ribosomes and provides
them with the necessary information for specific protein
synthesis. Gro:; et al., 3 ' 9 in "pulse e.xperiments" withtracers, have shown that e."'<:actly the same situation prevails in uninfected bacteria where an RNA component
with rapid turnover and which is physically distinct fromribosomal RNA or S-RNA can be demonstrated. The
fraction behaves in the ultracentrifuge and towards preexisting ribosomes in high Mg<+ concentrations exactly
as the phage specific RNA induced by T 2 infection; it
becomes associated with the active 70 S ribosomes, thesite of protein synthesis. According to this concept, thetypical ribosomal RN A carries no genetic information.
The concept of messenger-Ri'\TA has been greatly elucidated and amplified by experiments of Matthaei and Nirenberg380 who demonstrated that, in cell-free extracts ofE. coli containing ribosomes, poly-urydylic acid can induce the synthesis of poly-phenylalanine. At present,
triplet code letters have been assigned by Speyer et al.
to 14 amino acids. 381

145. About twenty years ago, a relationship between
RN A and protein synthesis was independently advanced
by Caspersson367 and Brachet368 as a hypothesis; thishypothesis has now become a finnly established biologicalconcept.
"146. Protein synthesis has been most studied in microorganisms and in the microsomal fraction of the cytoplasm of higher cells. The first step is activation ofamino acids in a reaction with ATP resulting in anamino acid adenylate. The latter compound does notappear freely in solution but remains attached to the enzyme ; amino acid activation is therefore usually studied
from the exchange between labelled pyrophosphate (oneof the reaction products) and the phosphate groups of
A TP or by the chemical transformation of the aminoacid adenylate by hydroxylamine into hydroxyamic acid.
147. The activated amino acid then becomes attachedto the transfer or soluble RNA (S-RNA). It is boundin the manner common to all amino acids, via the tenninal
nucleotide sequence cytidylic-cytidylic-adenosine; theamino acid residue is bound in ester linkage to the C3 'atom of adenosine. Although the method of binding is
identical, each amino acid has a high specificity for the
S-RNA to which it becomes attached. There are different
S-RNA molecules for each type of amino acid. The
specificity of S-RNA resides in its base sequence.
148. The function of S-RNA is that of acting as acarrier which brings the amino acid to the template.
Investigations of Bosch et al. 373 have shown that S-RNA
can be firmly bound to the ribosomes. On the other hand,
it is possible that this "transfer"-Ri'\TA resides permanently in the ribosomes. Thermodynamically, this latter~ypothesis is more attractive; it may be significant thatm one of the very scanty examples of net synthesis of
enzymatically active protein in vitro this could be accomplished by a cell-free system in which S-RNA
formed part of the ribosome particles.m·
149. The last phase in protein synthesis is the assembly <;>f ac.tivated amino acids into polypeptide chainsby peptide linkages, and release of these chains fromribosomal particles. For this step GTP is required. The
process is greatly stimulated by SH-compounds.374 • 375
150. Protein synthesis has been studied in microsomes of cells of higher organisms. It is, however, by
no means confined to this system. Net synthesis of~yto:hrome-c has been demonstrated by Bates et a1.a 1am mitochondria. Moreover, it has been shown by Allfrey
and Mirsky3 11 that protein synthesis in the nucleus isvery similar to that in the cytoplasm. These investigators
suggest _that t:J:ie energy for protein synthesis in the
nucleus is proVIded by phosphorylation in mitochondria.
. 151. 1:he part played by RNA in carrying genetic
mformauon fo_r the production of proteins is clearlyshown by the discovery of Astrachan and Volkin 378 that
infect!on of E. coli by v~rious bacteriophages immediately induces the production of a new RNA which resembles, in base composition, the DNA of the phage.
Nomura et al. 319 found that, after T 2 infection there isno synthesis of typical ribosomal RN A and that phage
specific RNA sediments at a slower rate (8 S) than;ibosom~ (16 S and 23 S). Apparently, the genetic
mf?fill!1tlon for the s~thesis of phage protein does notreside m the usual nbosomal RN A but is induced in
pre-existing ribosomes by a phage specific RNA which
m::;y b: considered a messenger RNA. Brenner et al.,3sousmg isotope labelling techniques followed by carefulseparation of the various RNA-containing fractions,152. The influence of ionizing radiation on RNA andprotein synthesis has not been studied to the same e.~tentas that on DNA synthesis, and available data do not
permit a satisfactory analysis of the effects.
153. Painter, 313 using 1,500 r, did not find a significant
disturbance of the uptake of tritiated cytidine into the
RNA of HeLa cells. Neither did Harrington 314 see any
effect on the incorporation of tritiated cytidine into
nuclear RNA of U 12 fibroblasts after SOO r. Shabadash,o~ the other hand, showed that cellular ribonucleoprot~ms .an~ ext~emely responsive to penetrating radiati?ns.·11•·91 This _was rece~tly c_onfinned biochemically.m
Ribonucleoprotems localized m structures of different
organelles do not have identical physico-chemical properties, as indicated by differences in their iso-electric
points,3112 which are more acid in mitochondria than in
microsomes. The former is more sensitive to penetratingradiation. 203 •296
154. Klein and Forssberg321 irradiated Ehrlich ascites~our cells in vivo with 1,250 rand found no changes
m RN A synthesis. However, in vitro irradiation of thesecells inhibits incorporation of labelled uracil into RNAof the nucleus but not into that of the cytoplasm. 819 This
result is difficult to understand in view of the probablenuclear origin of most RNA.
155. From the studies of Logan and collaborators 393 •354 it has been concluded that irradiation of isolated liverand cal~ thymus _nuclei in vitro distinctly reduces therate of mcorporatton of labelled precursors into nuclear
RNA. A similar effect on the incorporation of P 32 into
!1ucl~r _RN.('>. CCJ? be obtained with regenerating liver, if
i;rad1ation. 1s given ~t the earliest stage of regeneration: au This ~bservation agrees with data on the synthesis of certam enzymes necessary for the synthesis of
DNA in regenerating liver. Thus, Bollum et al. 3 1>$ havefound th~ ~ynth~sis of the .e~Y!11es DNA polymerase
and thym1dme kmase to be mh1b1ted by radiation dosesof 375-1,500 r if irradiation is given 6 hours after partial
hepatectomy. The same doses, given si.'<teen hours after
the operation, are ineffective. Other authors have also
r_oun? that polymerase synthesis is inhibited. by irradiation m the first phase of the regeneration process. a8 7, as5156. Relatively low doses of radiation can postpone
the onset of DNA synthesis in various types of cells.

55

pears to be more resistant to radi.a~on. ~pparently, an~­bodies formed when the system is 1rrad1ated dunng thisperiod do not differ fundamentally from normal antibodies. Studies of the degree of radiation sensitivity ofthe secondary response to antigen injection have yielded
conflicting results ; there have been several explanations,each of which might be acceptable for the particularantigen studied. 398 • 894

It seems reasonable to assume that inhibition of enzyme
synthesis is at least one cause of this delay.
157. Ionizing radiation also reduces the synthesis of
enzymes in micro-organisms. Pauly3 89 has reported a
37 per cent dose. of 7 X 104 r for t?e inhibit~on of theinduction of lysme decarboxylase m Bactermm cadaveris. Radio-sensitivity was the same for the rate ofsynthesis. and the maximum lev:el of enzyme formed.
This finding leads to the conclusion that every cell possesses one or more "centres of synthesis", each producing a definite number of enzyme mole~ules. ~hese
synthetic centres would be destroyed according to smglehit kinetics. The induction of catalase by 02 in a diploidmutant of S. cerevisiae, however, is stimulated by aradiation dose of 105 r. This stimulation may be due tothe production of peroxides in the cell, as suggested by
Chantrenne and Devreux. 890 Using serological techniques
and also various tagged amino-acids in newly synthetizedproteins of individual organelles of cells, Ilina andPetrov391 • 392 showed that qualitatively altered proteinsare formed after irradiation.

GENERAL CONSIDERATIONS OF RADIATION EFFECTS
IN CELLULAR METABOLISM

EFFECTS OF RADIATION ON ANTIBODY SYNTHESIS

158. Inhibition of antibody formation is a special
case in the formation of specific proteins, and appears
to be highly radio-sensitive. It involves the formation ofa specific protein complementary in structure to the
inductor antigen. The normal processes of antibody
formation are only just beginning to be understood, anda generalized theory has still to emerge from several
contradictory hypotheses. Antibodies are formed in theplasma cells of lymphoid tissues which themselves originate from undifferentiated cells of the reticular system.
The mechanism of radiation inhibition of antibody formation, recently reviewed, 398• 394 thus must account for :(a) The effect of radiation on the multiplication anddifferentiation of these reticular cells and their descendants;(b) The process of antibody synthesis, which probably occurs in the microsomes of plasma cells.
159. One of the characteristics of radiation is i"5greater efficiency in inhibiting antibody production whenadministered prior to the antigen. The final titer ofantibody is lowered only if irradiation occurs some hours
before antigen injection. In this case, and also whenirradiation takes place immediately before or after antigen injection, the latent period before the titer begins
to rise is increased and the rate of synthesis decreased.
Taliaferro 395 has distinguished a highly radio-sensitive ·(effects become detectable on the final titer for doses of
100 r) pre-induction period but this is not well definedin cytological or biochemical terms. The cause of thisinhibition could be twofold :(a) Decreased production of plasma cells from their"reticular ancestors", or from other types of cells also
involved in the process;(b) Delay and inhibition of the synthesis of new
protein when antigen is injected.
160. Stevens 396 has shown a correlation between de-press_io!! of the number of plasma cells formed after
irradiation and inhibition of antibody synthesis. Furthermore, i;xperiments by Taliaferro suggest that antibody£o:mation ~epends on cell multiplication in irradiatedammals; this does not exclude the possibility that specificeffects o~ the induction of synthesis of new proteinsare also mvoh-ed. The antibody-producing period ap-

56161. The importance of radiation effects that areclosely linked with cell division and replication, andwhich include mitotic inhibition, loss of reproductive
power and mutations. has been stressed. It would be
attractive to describe these changes within the frame ofa unitarian mechanism, although such a treatment would
be arbitrary. At least two key effects indicate a disturbance in the genetic properties of the cell. 897 One ofthese is the production of mutations. The other is thatdelayed effect on cell division in which cells multiply
immediately after irradiation but nevertheless fail toform macroscopic colonies.
162. The failure of cells to divide even once when
given higher radiation doses is also probably due todamage of genetic material. The inhibition of mitosismight be explained similarly, although here the implication that genetic material may be directly involved is lessobvious. Much may be said for the concept that the mainradiation effects are at some stage mediated throughDNA; this e.~plains why emphasis is laid upon themetabolism of DNA. DNA synthesis has been used in a
restricted sense throughout this report to indicate thestage where precursors are assembled into polynucleotides. Subsequent stages may include many more biochemical reactions before the full-fledged DNA-protein
molecule is formed and incorporated into daughter
chromosomes. These late stages of DNA metabolism
presumably take place in late interphase and in prophase.
163. There is some evidence. at least with radiationinduced mitotic delay, that the. G2 stage and early prophase may be the most radio-sensitive stages in the mitotic cycle of many cells. 398 Painter's work, 313 mentioned
earlier, may also be interpreted in this way. The dependence of radio-sensitivity on division stage may not always
prevail in somatic cells of higher organisms ;3911 survival
curves of somatic mammalian cells usually show no evidence of resistant fractions. 400 Because of considerable
radio-sensitivity during the G2 period, metabolic processes during this period are important. Unfortunately,
biochemical knowledge of G2 and subsequent mitotic
stages is still extremely scanty. Therefore it is not yet
possible to describe the effect of radiation at a molecularlevel on these phases.
164. In cells of higher oragnisms two patterns ofsynthesis of DNA probably occur. In tissue cultures
and ascites tumour cells, DNA synthesis continues moreor less unhampered if irradiation occurs during any
period of the division cycle, at least when doses are notexcessive; in cells of bone marrow. plant root tips andregenerating liver, DNA synthesis may be delayed whenlower doses of radiation are delivered before svnthesis
has begun. This latter effect is probably due to irihibitionof the formation of necessary enzymes as a result ofinterference with RNA synthesis. No inhibition. andsometimes even acceleration occurs in either patternwhen all ingredients are available for synthesis. Mitotic
inhibition interferes eventually because a feed-back}vfitotic delay

homeostatic mechanism precludes, or at least inhibits,
DNA synthesis beyond the premitotic level.
165. This concept has been confirmed by Lajtha etal. 310 and by Berry et al ;401 they found that dose-effectcurves for inhibition of DNA synthesis in bone marrowcells differ from those in ascites tumour cells. For bonemarrow cells the curve has two exponentials, a "sensitive" one and an "unsensitive" one, characterized by 37
per cent doses of 500 and 1,300 r respectively. The
curve for ascites cells lacks the sensitive component.
Ord and Stocken40z have, from similar curves for thymus
tissue, suggested that the sensitive component may represent the inhibition of nuclear phosphorylation describedby Creasey and Stocken.403 This inhibition would leadto a shortage of DNA precursors. However, there is noevidence for such a shortage; Ord and Stocken404 reported an accumulation of deoxyriboside mono- andtriphosphates after irradiation of the thymus. The significance and reproducibility of the inhibition of nuclear
phosphorylation seems doubtful.
166. Both cell types also differ in ploidy; tissue-culture
and ascites tumour cells are usually aneuploid. The problem of the relationship between ploidy and radio-sensitivity is complex (para. 182) but it is not impossible thatthe high resistance of these cells may be a consequenceof the aneuploidy. This suggests that DNA itself is theprimary target. The work of Opara-Kubinska et al. 405
and many studies on bacteriophages indicate that thisis probably so, at least for transforming activity andsurvival in micro-organisms.
167. The "primer" function of DNA in RNA syuthesis by the RN A polymerase enzyme means that the
explanation given for the delay of DNA synthesis,
namely interference with RNA metabolism, is at least
not incompatible with a primary radiation lesion in DNA
itself (in this case, the primer) (para. 155). This does
not e."'\:clude the possibility that effects on DNA-RNA
protein metabolism, even when mediated through DNA,may not result secondarily from quite another primaryradiation lesion, e.g. lesions on larger subcellular structures, proteins, membranes, lipoids.

170. When a cell has been irradiated before prophase,division is delayed. This delay can be modified by dose
ratem and by o:i..ygen concentration; this may mean thatmetabolic processes are involved:m The most informative experiments have been those of Carlson and
Gaulden 414 with neuroblasts of grasshoppers' embryos.
During mitosis there is a critical stage coinciding withthe condensation of chromosomes into visible filaments
and with the disappearance of the nuclear membrane andnucleolus. If a dose as low as 1 r is given to a cell before
that critical stage,- development of mitosis is delayed.
However.. this delay does not occur when the same oran even slightly higher dose is given later. In this lattercase subsequent mitoses are delayed. More recent experiments have shown that the critical stage may besomewhat earlier in the mitotic cycle, i.e., in midprophase. Gaulden irradiated one of the two nucleoliof neuroblasts with a UV-microbeam and concluded that
all cells treated at stages from late telophase to the middleof mid-prophase immediately show a permanent cessation of mitotic progress. This picture of mitotic delay
looks slightly different when other types of cells arestudied. In particular. the critical sensitive period andthe duration of the various phases of mitosis may differ
in different types of cells. In consequence, precise comparisons are difficult.
171. The main characteristic of mitotic delay is its
temporary nature. Although the mechanism of mitotic
delay is still far from being understood, some attempts
have been made to explain it. Since DNA metabolism
is known to be affected by radiation, it is tempting toattribute mitotic delay to inhibition of DNA synthesis.·115
This explanation is speculative, and it may well be that
reduction in DNA synthesis, when observed, is theconsequence rather than the cause of mitotic delay. In
particular, the radio-sensitive period for producing
mitotic delay usually occurs when DNA synthesis isalready complete. In some instances, DNA metabolism
is apparently normal despite inhibition of cellular division, e.g. in irradiated mammalian cells in tissue culture.
This suggests that delay in division may be a consequenceof injury to an unknown mechanism controlling theonset of division, 416 and that there is no direct involvement of DNA synthesis. Yamada and Puck showed thata reversible mitotic lag is produced by a block in the G2
period after X-ray doses of 34-135 r in hyperploid S 3
HeLa cells. m They proposed that this reversible mitotic
lag, like irreversible reproductive death, is due to chromosomal damage, and that the reversible lag may reflect
interference with chromosomal condensation just before,and perhaps in, the early stages of mitosis. Other
hypotheses have also been advanced: interference ofradiation with oxydo-reduction of sulphydryl compounds
produced during cellular division, 417 • 418 and inhibition of
the division mechanism of the cytoplasm419 or of theformation of the spindle. 420 Production of antimetabolites may be responsible, as suggested by
Kuzin, 296 • 421424 who used plant material from which he
was able to demonstrate antimitotic quinones.

EFFECTS OF RADIATION ON INTEGRATED FUNCTIONS

168. When irradiated in comparable conditions, different cellular populations react in similar patterns. With
increasing doses, effects often become e.xperimentallymeasurable in the following order : modifications ofgrowth rate, mitotic delay, inhibition of mitosis, delayedor reproductive death and interphase death.
Growth rate169. Under chronic irradiation, the total mass of cell

cultures first increases and then decreases. 4 06-ios The
initial increase of the total cell mass of the culture accompanies the emergence of giant cells, the volume andusually the ploidy of which increase without division.
This phenomenon has been observed among bacteria,
yeasts and mammalian cells, and seems therefore to be
fairly general. As dose accumulates, the total weight ofthe culture diminishes and becomes lower than that ofcontrols. In general, radiation reduces growth rate and· creases generation time; however, under certain meta~~~ olic conditions, the gen~ratic;in ?rn~ c~ be s)iorter than:;~~j l1n control cultures once irradiation 1s discontinued. 409 • 410:~',' !Interference with growth rate has also been detected in
Lf~ ~solated cells. In Phycomyces blakesleeamts, Forss:'.~-:. iberg411 has shown a lowering of the growth rate of
f:j;: \sporangiophores with extremely low doses of ,..., 0.001 r.
;;.; i:::-'C_j

iij

INHIBITION OF MITOSIS AND CELLULAR. DEATH:
REPRODUCTIVE AND INTERPHASE DEATH*

172. With increased doses, cellular death usually occurs. Cells can be killed either immediately (interphase*Under doses higher than 100,000 rad, instantaneous death isobserved, due mainly to protein coagulation.

57

structures produced immediately after irradiation. Nor
can other biochemical processes affecting permeability,m,
436 the maintenance of ionic balance 437 • 438 or the disruption of nuclear and cytoplasmic membranes ,439 be ignored
as factors in the mechanism of cellular death.

death) or after a few divisions (delayed or reproductive
death). In general, the doses required to achieve interphase death are higher, although there are cells which
undergo interphase death even if irradiated by relatively
small doses, e.g. small lymphocytes, primary oocytes in
insects and mammals, mammalian neuroblasts, insect
ganglia cells. Reproductive death occurs in bone-marrow,425
intestinal crypt cells, lymphomas and spermatogonia.
It should be noted that the latter group consists of cellswith a high mitotic index; with these, interphase deathwould probably require a higher dose.

VII. Biological variables influencing
radiation response
CONCEPT OF RADIO-SENSITIVITY

173. The processes leading to reproductive or to interphase death are still unknown ; it is likely that mo:-ethan one mechanism is involved. In delayed death, chromosome breaks and mutations have been invoked as
possible mechanisms. The mechanisms resulting in cellular death may be better understood when the role ofrepair processes in irradiated cells have been studied,since the ultimate expression of a radiation effect depends
not only on initial injury but also on the ability of thecell to repair the injury.425 Most chromosome breaks
rejo~n; metabolic and synthetic processes take part inhealing,4 26 energy from ATP being required. 427 • 4 ~ 8
Recent experiments by Elkind and Sutton429 have madeit clear that repair operates in mammalian cells and influences the ultimate expression of late effects.

178. Various criteria, e.g. death of cells, inhibition ofmitos~s. impairment of biochemical and physiological

funct10ns, are currently used to determine radio-sensitivity. However, when radio-sensitivities of different
types of living organisms are compared, survival after
irradiation is usually chosen as the parameter. The selective acti?n of radiation on different parts of the cell andthe relations between differentiation mitotic activity andradio-sensitivity were described within a decade of the
discovery of X-rays. In 1906, Bergonie and Tribondeau440 formulated the principle that cells in active
proliferation are more sensitive to irradiation than nonproliferat~ng cells, and that radio-sensitivity varies inversely with degree of differentiation. Radio-sensitivity
depei:ds on various factors, physical (e.g. temperature),chemical. (e.g. oxygen tension, hydration), biological(e.g. ploidy, phase in the division cycle in ·which the cellis irradiated). Radio-sensitivity further depends on themetabolic state of the cell.

174. A clear distinction should be made between biochei:iical p_rocesses leading to delayed death and thoseleading to mterphase death. In the former, synthesis of
nucleic acids and proteins continues. 315 Radiationinduced interphase death is sudden and marked by ana:rest of n:etabolic p:ocesses. in cells with very wide
differences m metabolic behaviour, e.g. cells which areno~. dividing (lymphocytes), cells dividing infrequently( oo9'tes ), and cells continually dividing (B spermatogoma).

VARIATIONS IN RADIO-SENSITIVITY \\'ITH STAGE
OF DIVISION. 179. The <?fferent phases of mitotic and meiotic divisions have different. sensitivities to radiation. Attempts
hav_e been mad~ to link these variations in sensitivity tovarious phases m the formation of new chromosomes andto the synthesis of nucleic acids during division.

175. The biochemical causes of interphase death are
not understood, but it is possible that Creasey andStocken's work403 on nuclear phosphorylation provides
a ~st ~lue. Their data indicate that nuclear phospho1ylat1?n 1~ a~ .extremely radio-sensitive process and is:ap1dly in111b1ted. As yet, this process has been detectedm nuclei of so-called radio-sensitive tissues only; it has,
therefore, been suggested that cells dependent upon thissource of energy are those which undergo interphase
death at smal~ doses. Creasey and Stacken remark, howeve:, tha~ failure to show nuclear phosphorylation inradio-resist':llt cells may be due to an increased activityof degradative enzymes rather than to absence of thismetabolic process.
176. Nuclear phosphorylation could also be involved
in reproductive death if the energy necessary to heal
chromoso~es was provided by this phosphorylation. A:ole of m1tochrondrial oxydative phosphorylations in
mterphase and reproductive death cannot be excluded.
~-irradiation in viva, in fact, damages mitochondria inliver cells43 0-432 even at doses as low as 25 r. Mitochondrial oxydative phosphorylation in plants is immediately and gr~atly reduced after a single dose of 3,000 r,
the effec~ bemg more pronounced when cells are irradi~ted :n vi-z:o than in vitro. 433 Similar effects are also seen
m microbial cells. 4 3-1. 177. ~t is ~cult to draw a coherent picture of thebioc~emical ba~is of cellular death at this time. The
possibl.e role ot nucleic acids and protein synthesis has
been discussed, but much more extensive information isneeded on the cytological alterations of sub-cellular180. Cell survival, gene mutation frequency, and frequency of 0romosomal aberrations all respond differently accordmg to when the cell is irradiated. It is difficult t? define the most critical moment as it may vary
for different cell types and for different lesions. 413 • 414
Mos_t experimental efforts to clarify this issue have been
carried out on germ cells, in particular on both fertilized
and unfertili:ed eggs of several organisms. The ende!fects mo~t trequently used as criteria of damage are~ther survrval, ?r f~equency of chromosomal alterations
m 0ese c_el~s: It i~ widely held that variation in sensitivity~urmg d1v1s1on is a gen~ral _phenomenon and is present!n all. c~lls. 'vhatever lesion 1s taken as the end-point of
irradiation.
1~1_. ~eYertheless. some recent results suggest thatsens1t1vity of mammalian tissue culture cells to the lethal
7ffe~t. of radiation is independent o_f the division stage
m which the cells are e.xposed. Survival curves291,400,H1443 obtained with mammalian somatic cells both in viva
and in vitro have failed to show the e.'Cistence of a resistant fraction in cell populations despite the existenceof heter?geneity in stage of division. However. experiments with synchronized cultures of HeLa cells have rev~aie.d s~ me fluctuations in sensitivity during mitotic
5 Cellular morphology does not affect radiodivi~1?n:s~nsitmty of these ce.lls app~eciably since the LD 37 ofdifferent cellular ... strams ( epitheliod, fibroblastic, etc.)
ranges between 7;,-166 r only.

58

recombination tests.' 59 Adler and Copeland~ 60 have produced evidence which indicates that radio-sensitivity inE. coli K 12 is influenced by at least 4 genes. The approximate locations of the four genes have been determined in genetic recombination tests. In E. coli B,
Rousch et al.' 61 have recently found mutations at two
different loci which have a cumulative effect in increasing radio-sensi~v1ty. They too ha~e determin~d the approximate location of these genes m the ge1!-etic .map byrecombination tests. Furthermore, comparative biochemical studies of these two independent mutations showthat one leads to loss of the tendency to form filaments,
the other to a strong inhibition of growth and of nucleic
acid and protein synthesis after radiation or other treatment. Such comparative studies of mutant strains which
differ genetically in response, seem especially promisingin elucidating the physiological basis of radiation sensitivity and resistance.

VARIATION OF RADIO-SENSITIVITY WITH PLOIDY

182. Ploidy is one of the biological factors aff~cting
cellular radio-sensitivity at the level o~ the pnmary
radiation injury. The shape of yeast s1;1rvival curves ~i;pends on the ploi~y of the str~in. L<i:tarJet and Ephruss1
showed that survival of hapl01d strains expose~ to.X-rays
follows a one-hit curve whereas that of dipl01d cells
follows a two-hit curve. These authors, and subsequently
Tobias,m propounded the hypot.hesis that in.activation. ofa haploid cell is caused by a single recessive muta~ion
whereas to inactivate diploid cells two homologous sites
must be injured.
183. Extending such studies to higher polyploids,
Mortimer found that radio-resistance reaches a ma.""{imum for diploid strains and then diminishes with increasing ploidy. 14 Mortimer's res~lts have been. confir~edby Magni,m but these authors. interpret ~etr fi.ndings
differently. According to Mortimer, haploid strain~ aremainly inactivated through lethal recessive mutahons,
whereas with strains of higher ploidy dominant lethal
mutations are chiefly responsible for the inactivation.
Both types of mutations would be produced in haploidand polyploid strains, the problem being to ev~luate
quantitative relationships of the two types. Magni suggests that, in a~di~i~n to recessive and ~ominant mi.:tations, non-genetic lllJUry accounts for a sizeable fractionof radiation lethality.
184. In some other systems a positive correlation between increasing ploidy and radio-resistance has been
seen. Sparrow et al:" 6 • 447 found that, on the average,
doubling of chromosome number in plants increased
radio-resistance by a factor of 1.67. Analogous results
were obtained with polyploid cereal seeds448 and withhyperploid tissue culture cells. 44- 51 In contrast, Till452
found identical dose-effect curves for cell lines withdifferent chromosome numbers and Rhynas and Newcombe453 have described radiation-resistant cell lines of
the L strain with a lower number of chromosomes than
the radio-sensitive line. Of interest in a considerationof the influence of polyploidy is the inverse relation
between nuclear volume and radio-sensitivity in 23
diploid species of plants. 447 The role of ploidy in cellularradio-sensitivity becomes more complex when stage ofdevelopment is considered. Clark454 showed that, in
Habrobacon. diploid female embryos are more sensitive
to irradiation than haploid males during the cleavage
stage, whereas during larval and pupae stages haploidmales are more radio-sensitive. Tul'tseva455 and Astaurov
have found that, during certain stages of development,
radio-resistance increases with increasing ploidy in
Bomby:r mori but that tetraploids are more sensitive than
diploids at the end of the larval stage.

VITI. Primary genetic effects of radiation

186. The tremendous headway in the last decade in
the analysis of genetic function and genetic material has
led to a clearer view of the need for a more full understanding of the mechanisms of radiation mutagenesis.
Some problems are related to the already-mentioned
macromolecular chromosome structure, others are related more particularly to the function and structure of
the genes. Since Muller's discovery in 1927 that radiations are mutagenic, much work has been accomplished,
but no complete answer to the mechanisms of radiogenetics has been given. It has been clear from the beginning that genetic effects include visible chromosomal
aberrations. On the other hand, many mutations do not
involve any abnormalities at the level of the light microscope, and it has become practical to divide radiation
genetics into the studies of point mutation and of chromosome damage.
THE GENETIC MATERIAL

187. \Vhile one of the most important advances ingenetics came from the studies of Morgan, who discovered the linear arrangement of genes along thechromosomes from investigations on Drosophila, themost important hypothesis advanced in recent years,
derived from work on micro-organisms and viruses, isthat of the linear arrangement of genes along the DNA
double helix.* Recombination studies in bacteriophages,
bacteria, and moulds, in combination with the demonstration that the genetic information is effectively carriedin the DNA (or in some cases in the RNA), give convincing evidence."° 3 Furthermore, the existence ofviruses containing single-stranded DNA+s4 or of viruses,
whose infon11ation is coded in single-stranded RNA
molecules, indicates that only one of the two strands ofa DNA or RN A molecule may carry genetic information.
On the other hand, it has also become clearer in recent
years that DNA replication probably concerns doublestranded DNA. Even in the one-stranded cp X-174 virus,
there seems to be a double-stranded stage during replication,m although priming of DNA synthesis in vitro
is much more efficient if the double-stranded molecule
has previously been "melted" to single-stranded units. 300
188. Hypotheses concerning the structural integrationof DNA chains into chromosomes must take into accountthe existing basic proteins and ribonucleic acids which

GENETIC CONTROL OF RADIO-SENSITIVITY IN BACTERIA

185. A number of mutations causing differences inradio-sensitivity in E. coli are known. The increased
resistance of strain B/r results from a single mutational
step in its parental strain B.11 Later, Hill discovered andinvestigated a more radio-sensitive strain, B/s. This
strain also differs from. strain B by only a single mutational step.456 • 457 A stable strain containing about threetimes as much protein, RNA, and DNA per cell, isolatedby Ogg and Zelle458 after camphor treatments of strain
B/r, was about 2.5 times more radio-resistant to ionizing
radiations and in addition had a sigmoidal survival curve
rather than the exponential survival curve typical ofstrain B/r. This radiation resistance segregated in a
fashion similar to any unselected marker in genetic*For a review of the subject, see references 462 and 463.

59

s.equence of s~ecific bacteria! or bacteriophage proteins
like ,8-galactosidase and alkalme phosphatase; it is hopedthat correlations between alterations of DNA obtainedby mu~genic agents and protein sequences will throw
some light on the problems of genetic coding. The error
in DNA, then, would be replicated in a minutely altered"messenger"-RNA carrying specific genetic information to ribosomes assembling activated amino acids in asJi>ecific sequence. 350•m This very much oversimplified
picture of the mechanism of phenotypic expression enables one, however, to understand present concepts ofmutagenesis and abnormal phenotypic expression.

are beginning to be thought of as factors stabilizing,
regulating or repressing the genetic units. 872 • 468 These
more refined concepts, fairly well established for microorganisms, will have to be extended to more complex
metazoan cells.
189. A big bar to understanding genetic processes inhigher organisms is ignorance of chromosome organization at the molecular level. Although the chromosomesfrom thymus are 90 per cent nucleohistone, plus nonhistone protein, RNA and phospholipids,467 it is notknown how these are made up into the chromosome
structure seen under the microscope. Electron microscope studies have repeatedly shown strands of 200 A
diameter,468 but nucleohistone strands are ten times narrower. Urea and versene can dissociate chromosome
fibrils or nucleohistones; this indicates the importance ofhydrogen bonds and of metal ions (Ca++ and Mg++) in
holding structures together.4119 The fact that the U V
action spectrum for chromosome aberration 470 is similar
to that of nucleic acid indicates that nucleic acid may
well play a major role in forming the backbone of thechromosome. That this might well be DNA is supportedby the fact that lampbrush chromosomes can be broken
in vitro by deoxyribonuclease but not by ribonucleases
or proteases.m On the other hand, Ca++ and Mg++ deficiency is known to induce chromosome breaks and rearrangements in plants 472 and other organisms, whichindicates that these metal ions may play a role in chromosome integrity.

RADIATION-I:!'<!)UCED MUTAGENIC EFFECTS

193. Damage to DNA of cells by radiation cannot be
so controlled that mutations can be obtained independen.tly of lethal events. Although all lethal effects of radiation should not be attributed exclusively to effects on
DNA, any alteration of DNA is liable to cause deathor mutation of the particular cell. So far, the damage
caused in vivo by ionizing radiation is not precisely
known ; the absence of damage to purines and pyrimidine
in nucleohistones irradiated in vitro475 proves clearly
that effects found in nucleotides or pure DNA cannot
be e..~tended to the same material in vivo. There areindications that DNA from irradiated bacteria has aslightly lower "melting point", suggesting that H-bonds
have b7en "'.eakened. Different elution patterns of DNA
from irradiated thymus cells have been obtained ,..76
these. indi~te some change in DNA structure or mole~u­lar size. Fmally the sequence of a certain number ofsh_ort nucleotid~ chains may be changed. 477 UV irradiation of bactena appears to lead to the dimerization ofsome of the pyrimidines, but other reactions such as~ydration of pyrimidines, are also probable. More work
is need~d to f o~low the new leads. given by recent advances m rad1at1on and photochemistry.99, 47s, 479

POINT MUTATION

190. The definition of the mutagenic event deserves
special attention because of the analysis of the genetics
of bacteriophage by Benzer:162 The size of the genetic
material (DNA) depends on the test used to study themutations. According to the genetic test used, Benzer
distinguishes three units:(a) The cistron or unit of gene function is what isbeing studied when phenotypic changes are observed.
. ( b) T~e muto? or unit of mutation is the sequencem nucleotides which has to be altered for a mutation to
occur. Benzer has calculated that a muton could consistof no more than a sequence of 4-5 nucleotide pairs in
the r II region of phage T4. As the same phenotypicchange (loss of an active enzyme, for instance) may betJ:ie res~lt o~ the alteration of many loci, the size of tl:e
c1stron 1s difficult to determine precisely but it is muchlarger, probably of the order of several hundred nucleotide pairs.
( c) The recon-or unit of recombination-is what is
assayed when recombination tests are made. One alteredmuton can be made to recover through recombination,
as the result of the replacement of one or two nucleotide
pairs which constitute the recon.

194. DNA could also be altered as result of uptake
through,normc;l ~etabolic processes, of an X-ray-alteretl
prec1:1rsor; this is to be expected from work demonstra.n~g. the mutagenic activity of certain purine or
pynm1dme analogues. On the other hand, Doudney andHac;s ~~ve postulated that UV alteration of purine andpynm1d111e precursors RNA might lead to mutations
after having been incorporated into an abnormal RN A.'80. OXYGEN EFFECT

195. Mutation to streptomycin independence, investigated by ~derson481 is not influenced by changes inoxygen tension, whereas other mutations in the sameb:l;cterial strain depend on oxygen tension during irradiation by ionizing radiation.m-.i5s
1?6: Ai:other important point needs clarification. Does
rad.1ation mduce mutation by affecting DNA directlyor is the J?N~ altered as a result of secondary action?
When DNA m the form of transforming principle 45 'or bacteriophage,4 85 is irradiated in vitro under con ditiC?n~ where indir7ct effects are presumably reduced to a
mimmum. there is no oxygen effect. In bacteriophage,
D N ·i\ ~ppears. to be m'?re. se~sitive to reducing than tooxy~mg. radicals._ This mdica~es that X-rays do not
act pnmanly on DNA, but that m certain circumstancest?is molecule is altere~ as the result of secondary reaction. However, Hutchmson showed that inactivation of
DNA in solution becomes oxygen dependent in thepresence of cystein.4 u

191. At present there is no reason to believe that
mutation processes in complex organisms are very different from those in micro-organisms; it is becoming increasin&"ly evident that similar concepts will eventually
be applied. It has been demonstrated that the mutation
leading to sickle cell anaemia in humans results fromthe su?stitution of only. one amino acid by another in
one pair of the four peptide chains of the normal haemoglobm molecule; the 2A chains each have one of theirglu~ami.c acid residues substituted by a valine residue.m
This mmute error in the protein is likely to be the resultof a corresponding error in the DNA code.

1

192. Studies are being conducted on the amino acid60

can result from replacement of one base pair (A-T) by
another (G-C) (or vice-versa), then a mistake would
appear in the DNA chain.

CHEMICALLY-INDUCED MUTAGENESIS

197. Important progress has come from the study ofthe effect of several chemical mutagens on DNA or RNA
and their correlation with lethal and mutagenic activities
in viruses and micro-organisms. Both purine or pyrimidine are known to be chemically changed by a variety
of mutagens. Nitrous acid is able to remove the aminogroup of adenine, guanine, and cytosine ;487 formaldehyde can hydroxymethylate amino groups, but its mutagenic activity in Drosophila depends on the presence ofadenylic acid in the medium which, after alteration,
could become incorporated into DNA.458 Alkylating
agents appear 489 to react in many cases with the N-7 ofguanine ; this could become unstable and be removed
from the DNA chain. Glyoxal derivatives appear toaffect guanine. Hydroxylaminem appears to react chiefly
with cytosine; hydrazine, to remove pyrimidine; a low
pH treatment,491 to remove purine. Acridines, like proflavines, are mutagenic; their action is believed to result
from fixation of this reagent between two adjacent basepairs, thus increasing their separation. A comparison of
the mutagenic effects of these chemicals with that ofradiation could be of great value. The linear dose response curves found in several cases of chemical mutagenesis indicate that, as for most radiation-induced
mutations, the process involves a single event. In thiscase the alteration involves a single nitrogen base in one
DNA molecule.

202. In the mutagenic actionofbromodeoxyuridineon
T 4 phage, the analogue might take the place of 5-hydroxymethylcytosine and pair with guanine (error in pairing) ;this would lead to the replacement of a guanine-5hydroxymethylcytosine ( G-H) pair by an adeninethymine pair after three DNA replications. Alternatively,
the bromouracil moiety of the analogue might replace
thymine during the first replication (error in replication) and pair with guanine at the next. This would leadto the replacement of A-T by G-H after the third replication.502 Effectively, mutants appear in a culture after
the third DNA replication. 2-amino purine could also
lead to the replacement of G-C by A-T, and would, likebromodeoxyuridine, on the basis of this hypothesis, be agood agent for back mutating a mutation due to bromouracil incorporation ; examples of chemically-induced
mutation and back mutation, interpretable in these terms,
are now becoming known.
203. However, it is not at all certain that the reversion
of a mutation to wild type is necessarily the e..'Cact reversalof the forward mutation, and different base pairs might
conceivably be involved in the forward and reverse
process as postulated by Brenner, Barnett, Crick andOrgel. 563 It is very possible that the hypothesis of Freeseis an oversimplification of the facts. A mutation andback mutation with proflavine might result from addition
or deletion of a base-pair; this might lead to a much
more substantial alteration of the protein, such as abreak or an alteration of sequence in the polypeptide
chain. With radiation, it is difficult at present to makeany hypothesis, but the concepts of chemical mutagenesis
will certainly have to be considered in radio-biology whenradiation-induced chemical changes in DNA are better
known.

UPTAKE OF ABNORMAL PRECURSORS

198. A number of base analogues have also beenfound to be either lethal or mutagenic. Bromouracil (orbromodeoxyuridine) once incorporated into bacteriophage, .. 92494 bacteria, and mammalian cells 495 • 496 canproduce mutations and lead to increased sensitivity to
X or UV radiation. 465 •493 • 491
199. 2-amino purine, another mutagen, is believed to
be incorporated or to permit the uptake of another base(perhaps adenine) instead of guanine.m-5oo

204. It had been knovm for a few yearsm that thefrequency of mutants in bacteria increases with cell
division. More recently, Witkin has shown that if protein synthesis is inhibited by amino acid starvation or bychloramphenicol, a lower frequency of bacterial mutants
is obtained. 505 · 506 This suggests that irradiation produces
pre-mutational damage which can eventually be lost, or
which can become fixed as a result of protein synthesis.
In a study of lethal mutations in Paramecium, Kimball 5° 7
has shown that loss of premutational damage is probably
due to metabolic repair of localized chromosomal lesions.
Lieb has recently shown508 that when DNA synthesis isretarded by treating the cells with chloramphenicol, theincrease in mutants, observed when growth is continued
after the chloramphenicol "challenge", parallels the increase in DNA; this strongly suggests that the terminal
event in this mutational process is DNA synthesis. Much
has still to be learned about induced mutagenesis. The
role of RNA suggested by Douclney and Haas480 is not
yet clear. However, one important fact emerges: it ispossible to inhibit to some extent mutation fi.'Cation in
micro-organisms by delaying protein or DNA synthesis.

COMPARISON BETWEEN VARIOUS MUTAGENIC AGENTS

200. When the frequencies of spontaneous and chemically-induced mutations in bacteriophage T 4 are studied,it appears that some regions of the genome mutate much
more frequently than others; the same region does notnecessarily mutate with comparable frequency after
treatment with various mutagens.162 -001 Proflavine seems
to induce a pattern of mutations which differs from that
produced by base analogues; the patterns produced bybase analogues show some differences when comparedwith the pattern of spontaneous mutations. One must,
therefore, suspect the existence of several classes ofmutagens; of these, the base analogue class induces amutation pattern similar to those produced by five bromodeoxyuridine and the proflavine class. Close study of
specific chemical mutagens. and their comparison withspontaneous and radiation-induced mutations, will no
doubt bring much light on the molecular basis of mutagenesis.

MUTATION EXPRESSION
BIOCHEMICAL ASPECTS OF MUTATION PROCESSES

205. The biochemical processes underlying the synthesis of cell constituents are becoming better known
each year. One of the major problems of present-day
biochemistry is the way specific enzymes necessary forthese synthetic processes become synthesized themselves.
Nisman 509 has succeeded in synthesizing in vitro an

201. From work on mutagenesis of various analogues
and UV radiation, it appears very probable that. mutation becomes fi.~ed during DNA replication. Examplesof bromouracil-induced mutations are pertinent to thishypothesis. 500 If, as postulated by Freese, 502 mutation

61

enzyme of E. coli, ,8-galactosidase, in the presence ofribosomes of these bacteria, a mixture of the four ribonucleoside triphosphates, and the DNA of a strain of
E. coli possessing the enzyme. The ~ynth~sis does notoccur with DNA extracted from an mduc1ble but noninduced strain of the same bacteria. Furthermore, Novelli
has shown 510 that this synthesis can be inhibited by X- or
UV-irradiation, and that restoration can be obtained byadding the genetically competent DNA to the system.
These experiments are pertinent to an understandingof radiation-induced mutagenesis and, together withthose on chemical mutagenesis, are the first leads to an
analysis of mutation processes at the molecular level.
Treatment of the genetic material (RNA) of Tobacco
mosaic virus with nitrous acid leads, after infection of
the plant, to the synthesis of viral protein with only threeabnormal amino acids. 511 • 512

FACTORS INFLUENCING THE PRODUCTION OF
CHROMOSOME BREAKS

211. The effect of oxygen on the occurrence of chromosome breaks produced by radiation is comple..x. On
the one hand, anoxia during irradiation reduces the production of breaks ;219 on the other hand, since the rejoining of chromosome fragments is a phenomenon which
requires energy, the absence of oxygen diminishes thefrequency of rejoining. 518 Probably connected with theoxygen effect is the effect of temperature. 203 The numberof breaks increases with a decrease of temperature;
this is consistent with the fact that the tension, and therefore the availability of oxygen, is reduced at lower temperatures.
212. Strictly mechanical agents such as centrifugation
and ultrasonics, when applied at the moment of irradiation, increase the amount of chromosome breakage.
When cells are irradiated with ultra-violet519 or infra-red
rays either prior to or after exposure to ionizing radiation, the frequency of chromosome breaks is reduced in
the former case but is raised in the latter. Infra-red
irradiation seems to act through changes in metabolicalprocesses. 5:0, 521

206. The problem of mutation expression is therefore
one of information transfer from the DNA to the cellularsites of specific synthesis, many of which are cytoplasmic.
One major problem concerns the formation of ribosomes; the way in which they receive their information
for specific protein synthesis is at present being extensively studied (para. 140).

213. Biological factors also influence sensitivity tochromosomal damage. 522 Cells from different tissues
show different sensitivities.m,m On the other hand, thefrequency of breaks per unit of radiation depends on
the stage of division during which cells are irradiated. 525
The highest frequencies are observed when cells areirradiated during metaphase and anaphase. 52 s-m In the
meiotic process, the diplotene stage is most sensitive inanimals.529

CHROMOSOME BREAKS

207. Point mutations in higher organisms probably
result from processes similar to those described for
micro-organisms, but the complexity of the chromosomes
may complicate the process. On the other hand, chromosome aberrations have been thoroughly analysed in various organisms and described at length in many valuablereference papers. Ionizing radiations can induce breakage of chromosomes or chromatids followed by restitution or illegitimate reunions. This may lead to a variety
of aberrations 513 which are visible at the first division
after irradiation, or in some instances, only after very
many cell generations. However, these aberrations often
lead to unequal distribution of chromosomes between
daughter cells ; these usually lead to cell death. Restitution may be at the morphological level only, and a point
mutation, probably due to DNA damage may eventuallyappear.

GENETIC EFFECTS OF INCORPORATED RADIO-ACTIVE
SUBSTANCES

214. Radio-isotopes introduced into organisms may
be incorporated into critical molecules. Although mosteffects are due to ionization by the charged particle
emitted from the isotope, some may result from disturbance of the molecule by transmutation of the incorporated atom. The new atom not only has different and,in most instances, incompatible bonding characteristics,
but also, in transmutation, gives off recoil and excitational energy.

208. Similar chromosome damage may also occur
after UV irradiation,513 but is less frequent than after
ionizing radiation. It may also occur as an effect ofalkylating agents 512 or aiter incorporation ofor H 3thymidine514• m or of bromodeoxyuridine•01 in cellularDNA.

215. Ionization and excitation from the ionizing particle are so large compared with the energy from transmutation that they usually outweigh the importance oftransmutation in radiation injury. However, certain
isotopes incorporated preferentially in vitally significant
molecules could, by transmutation, cause unique effects
not accomplished by ionization or excitation from acharged particle. Accumulating evidence, along withtheoretical considerations, indicates that transmutation
should be considered as a factor in the toxicity of internal emitters. The atomic number of the radio-isotope,
its type of decay, the particle emitted, and the energy
released, are obviously important in gauging the significance of transmutation.

cu_209. Studies of agents influencing chromosome damage have led WolfP 18 to postulate the existence of two
types of chromosome breaks : some which rejoin rapidly
and which presumably involve linkages through metal
ions, and some which are influenced by post-irradiation
protein-synthesis and which are believed to involve
covalent links.
210. The relative role of direct and indirect mechanisms in chromosome breakage has been partially clarified by comparing the modifying effects of various
chemicals with damage due to chemically induced radicals and radiation. 63 • 65 The effect of radiation in producing breaks is mainly direct; it certainly is so for dry
DNA. Evidence in favour of direct effect on DNA
in vivo is provided by experiments carried out with bonemarrow cells in vitro. m

POSSIBILITY OF TRANSMUTATION EFFECT WITH C 14

216. The disintegration by which CH exerts its biological effect is1
C e4 - N 11•
f3 0.155 MeV(1}
The mean energy of the ,8-particles is 50 + 5 ke V; thus
the reaction gives rise to fast charged particles for which

+ +

62

the RBE of the energy they release is probably 1. Mostof the energy of the reaction ( 1) passes via the kinetic
energy of the emitted /3-particle into ionization and e.'<citation of the surrounding material; a lesser part appears
at the site of the transmutation reaction itself. 530 Because
carbon is a part of every organic molecule in living systems, transmutation may significantly affect key molecules, especially those of the genetic apparatus. Indeed,
Totter et al. 531 have suggested that the mutational consequences of 0• transmutations might be comparable inmagnitude to those from the associated /3-particles. However, according to Pauling, 532 they are unlikely to amountto more than about 10 per cent of the total.
217. Although it is certainly established that P 32 ,when incorporated into the genetic material of a varietyof or~nisms, produces biological effects by transmutation (E. coli,5°1 • 533 • 53'• 538 bacteriophage, 538 • 637 Paramecium, 038 Drosophila 539- 541 ), the data concerning cutransmutation effects are less plentiful and less consistent. Apelgot and Latarjet, in tests with H 3 , P 32 and 0 4
labelled DNA in E. coli B/r found that, whereas thelethal effect with H 3 was due largely to the emitted
beta-particle, transmutation was mainly responsible forthe effect with P3 2and cu.m Kuzin et al.m have reported that the efficiency of incorporated cu in producing chromosome breakage in Vicia faba is 10-20 times
greater than that of external Co80 gamma radiation. By

contrast, Williams and Scully54' failed to observe an
increased rate of somatic mutations in Antirrhinimi
majus grown in a cuo2 atmosphere as compared toexternal gamma radiation. The work of McQuade andFriedkin 5 H is especially interesting, for despite the factthat no comparisons were attempted with external radiation controls, the frequency of chromosome breakage inAlliimi cepa root tips was about twice as great when thechromosomes were labelled with 0 4 thymidine bearing
the 0' in the methyl group as was the frequency observed when the 0·1 was in the 2' position.
LOCAL CONSEQUENCES OF TRANSMUTATION

218. Three processes may cause disturbances at orvery near the site of a nuclear transformation in whicha /3-particle is emitted:(a) Chemical changes ; C ~ N;( b) Mechanical recoil of the nucleus which emits the/3-particle;( c) The production of residual electronic excitationenergy due to the non-correspondence of orbital electrons and nucleus following the transmution. m
219. These and other features of transmutation reactions of especial biological interests are summarized
below.

PROPERTIES OF CERTAIN ISOTOPES RELEVANT TO TRANSMUTATION PROBLEMS

cu
Half-life .••..•............ 5,760 yrs.
Max. P-energy (MeV) ......
0.155
Mean P-energy (MeV) •..•..
0.050
Max. recoil energy (eV) .•.•
6.9
Mean residual excitationenergy (eV) .•..••.•••...
44.5
Chemicalchange ..•....... C...--.N

P'"

P1I

SU

H•

14.3 d
1.701
0.71
77.3

25.4 d
0.27
0.093
6.0

87.1 d
0.167
0.055
3.0

12.5 yrs.
0.0176
0.006
3.2

60.3
P--+S

60.3
P--+S

61.7
S--+CI

24.5
H--+Hetum to vibrational and other kinetric energy of surrounding atoms may suffice to break significant numbersof important hydrogen bonds in these molecules.

220. Except for P 32, by far the largest part of theenergy locally released is the residual electronic excitation of the transmuted atom. This energy and its magnitude closely resemble the corresponding release in a
primary or secondary ionizing event by a fast charged
particle. The effects of this electronic disequilibrium are
therefore qualitatively indistinguishable, except for site,from those of the emitted ionizing particles.
221. In P 32 decay, the large recoil energy is clearlysufficient to remove the disintegrating atom from themolecule in which it was previously bound, and to carryit into a neighbouring molecule, together with its associated electronic energy. m The recoil energies of all ofother transmutation reactions summarized above aremuch lower and are comparable to the relevant covalentbinding energies. Moreover, experimentally determinedchemical-binding energies are presumably lower than
the activation energies for reactions, even if reactions
take place by optimal paths in phase space; the isotropically distributed but directional nature of recoil momentum is likely to make a substantial part of it useless inrespect of the optimal reaction path. Hence, even though
its chemical binding is simultaneously weakened by thecllange in its chemical nature, it is doubtful whether,in substances of biological interest, atoms undergoingtransmutation other than P 32, effectively leave the molecule in which they were bound. An interesting possibility, with a transmuted atom that does not detach froma macromolecule, is that conversion of the recoil momen-

222. The most interesting possibilities of C1' transmutation lie in the chemical change, C ~ N; this may
leave a molecule altered rather than destroyed in function, giving rise to a special class of subtle and viablechanges in the genetic system different from those induced by the more destructive ionization or excitation.
The significance of the possibility of such changes underconditions of uniform contamination is discussed below.
loNIZATION DOSE PER TRANSMUTATION UNDERUNIFORM CONTAMINATION

223. As will be shown below with uniform incorporation, the practical limitation upon the effect of transmutation itself is likely to be dosimetric. Under suchconditions, for every transmutation of a C14 atom within
an important molecule, ,_, 5 X 104 eV of ionization andexcitation energy will also be liberated; this proportionality will only break down when the molecule underconsideration is part of a unit of dimension significantly
less than the mean range of the 0 4 ,8-particle ( ,_, 30 µ)and isolated from other carbon-containing units by distances significantly greater than the range. If the efficiency of transmutation in causing a certain effect is
1JT, and that of the ionization-excitation energy of conventional ionization ( 34 eV) is 711, then the fraction63added to the ionization-excitation effect by transmutation is only 6.8 X lD-4 TJT/TJi. This relation suggests at
once that, even for high T, C14 transmutation can besignificant only when TJL is very small; unfortunately,
it is not of much quantitative worth, since appropriate
values are not available. The only estimates available
for 'TJT are from P 32 incorporated into DNA, where'TJT is probably 0.01 or lower, 501 • 546 although the efficiency
with which the DNA molecule is broken may be in theregion of 0.1 for a double helix547 and reach a value close
to unity for single-stranded DNA.~ 4 • 548 For the destruction of infectivity of bacteriophage by P 32 incorporation
in DNA, 'TJT and 'TJ' values are available, and the ratio'TJT'/ 'TJ' is about 10. 536 • 549

IX. Recovery at the cellular level
226. The concept of "recovery" at the cellular level
covers various phenomena with different mechanisms.
At least three should be distinguished:(a) Spontaneous recovery of damaged molecules andstructures of the cell ; this constitutes genuine recovery;( b) Recovery through action of physical or chemical
agents immediately or soon after irradiation ; this constitutes a kind of "treatment" of the damaged cells;( c) Replacement of damaged molecules or structures by corresponding molecules or structures from undamaged cells. Here there is no recovery but there is a
restoration of cell function.

224. Mutation does not necessarily consist only ofdamage of this kind in the DNA molecule. Changes inat least three types of material might cause mutation:

227. The interval between irradiation and the biological expression of the primary damage indicates a complex process and suggests the possibility of interferingwith it to promote the repair of injury. Much work deals
with phenomena in bacteria and their related bacteriopbages using ultra-violet light. Some results have been
exi:ended by the use of ionizing radiation. The inclusionof ultra-violet data in this chapter is justified by thesimilarities and differences found between the action ofultra-violet light and ionizing radiation. These can enlighten several aspects of molecular biology, in particular those associated with the structure, replication, andbiological activity of nucleic acids.

(a) The gene code itself, i.e., in the double-helicalDNA (in most organisms);( b) Associated stabilizing material such as histone;( c) The machinery (other than the original gene) by\vhich a gene-replica is made, whether or not this machine!)' at any stage embodies the gene-code itself in a
non-DNA physical form.
The P 32 data presented relates almost solely to the firstof these, and even there is limited to events in the backbone of the DNA molecule rather than the nitrogenbases whose sequence presumably determines the information. Four of the carbon atoms of each averagenucleotide of DNA are likewise in the backbone, butchemical transmutation of carbon into nitrogen at mostof the otbers-4 or 5 in the nitrogen-base, 1 in deox7ribose linking nitrogen-base to backbone-could conceivably give rise to subtle viable changes unlikely to be duplicated by gross ionization damage or by P 32 disintegration in the backbone. In bacteriophage, some protein
synthesis necessarily precedes DNA synthesis and gene
replication after infection. 550• 551 Experiments on inactivation by P 32 decay suggest the possibility of a stage
at which the genetic information itself is carried in a
non-P 32 containing form. 547

228. Restoration is sometimes obtained by· destruction of some intermediate compound before the damage
is irreversibly established, e.g. photorestoration of ultraviolet damage, 552 • 558 restoration by catalase of lysogenic
systems treated with ultra-violet, 238 , 239 • 554 and restoration by ultra-violet light of X-irradiated yeast and bacteria. sss, ssa
229. Photorestoration (restoration by radiations of
the range 3,100-5,500 angstroms) is very general andhas been verified in a great variety of biological systems.
The study of photorestoration of a transforming factor
in vitro has led to the discovery of an enzyme in yeast
and bacteria which is necessary for restoration. 551 Work
with this system will soon give valuable information on
the mechanisms of ultra-violet inactivation and photorestoration. Recently, Marmur and Grossman97 haveshown that the PR (photorestoration) enzyme is able
to reverse induced linking of DNA strands by UV light.

225. In conclusion:(a) From theoretical considerations based on thelarge ionization-excitation dose per transmutation, thecontribution of transmutation to the biological effectwould not be expected to be significant under conditionsof uniform incorporation of 0 4 unless the efficiencyof transmutation in producing the effect is very muchgreater than that of ionization. Although experimental
data are as yet meagre and inconsistent, certain data indicate that 0 4 transmutation may contribute significantly to chromosome breakage;230. Several radio-biologists have attempted to achieve
photorestoration after exposure to X-rays. Dulbecco 558
has shown that coliphage T 2 , inactivated by X-rays insynthetic medium (predominant indirect effect), cannot be restored by visible light, but that the same phage
inactivated in organic medium (predominant direct
effect) shows a slight photorestoration. Similar results
have been obtained by Watson, 55 P• 560 with coliphages
T2, T 4 , and Ta. In general, however, there is no photorestoration after irradiation with ionizing particles.

( b) Because the C14 recoil energy is low and theenergy of electronic rearrangement strongly resembles
the usual ionization-excitation energy, such a contribution is most likely to be mediated through the c~ N
chemical change ;231. Some of the lethal damage provoked by UVlight in the coliphage T 4 can be repaired by some cellular
reactivation mechanism linked to the presence in thisphage of the gene µ.. This gene determines the difference in ultra-violet sensitivity between coliphages T 2
and T 4. The primary UV lesions are identical in bothphage types, but the presence of the µ. allele in T ~ (asopposed to theµ. allele in T 2 ) results in reactivation of
about 50 per cent of the otherwise lethal damage. Lethal
UV damage reactivable by the µ. allele action is almost
identical to photoreactivable damage. 561( c) The area in which to seek such a contribution
would seem to lie in phenomena brought about with very
low efficiency by ionization: probably not in simple dam'.lge to the genie material but perhaps in abnormalities
1~ the components of replicative apparatus where ionizatlon-excitation "'ould, in contrast, be more likely tocause total inactivation.
64

phage incorporated by P 3 ~ decay, 537 a more recent study
has detected this phenomenon. 573
237. The fact that some of the phenomena of recovery
of genetic structures are only seen after UV irradiationis, in general, interpreted as being due to the different
primary effects which follow UV and X-ray absorption
in nucleic acid molecules. It appears that UV radiation
primarily damages bases whereas X-rays primarily produce breaks in the DNA backbone.
238. The damage produced by UV light in temperatebacteriophages can be repaired to a certain extent by thehost cell. 5 ss, 574- 5 ' 6 It seems that the normal host cells
possess a genetic component which is capable of repairing the UV damaged virus. This is explained by Garenand Zinder in terms of genetic homology between the
genome of the phage and the genome of the bacteria inlysogenic systems. The homologous part of the bacteria
could replace the injured part of the virus genome
through a process of genetic recombination. Similar phenomena have been reported with Rous sarcoma virus190
and with the measles virus 191 in host animal cells.
239. Another phenomenon of host reactivation has
been described by Weigle ;192 it applies to temperate andvirulent phages. Among the progeny of irradiatedphages grown in irradiated bacteria, a, certain fraction ofplaque-mutants is observed. These mutants are not seenamong progeny of the same phage grow"Il in non-irradiated bacteria. This suggests that the phenomena ofreactivation and production of mutants are connected.
240. A restoration phenomenon linked to diploidy has
been observed by Latarjet and Ephrussi13 in Saccharomyces cerevisiae; after X-irradiation, haploid and diploid cells can undergo a few abortive divisions before
dying (delayed death). In diploid cells, however, a restored cell with normal morphologoy may sometimes
arise after a few abortive divisions. Repair of radiation
damage may occur in diploid yeast cells if they are
starved after irradiation.193
241. The replacement of damaged macromolecules byintact ones inside cellular structures also offers a possibility of repair. For instance, survival of E. coli B/r toirradiation is higher on a synthetic medium enrichedwith yeast extract than on synthetic medium only.194
Similar experiments are those of Daniels et al. 19 5-197 withthe large multinucleate amceba Pelomyxa illinoisensis inwhich individuals lethally irradiated with ionizing radiation may be restored to reproductive viability by meansof fusion with fragments of unirradiated individuals.
When the contents of this amceba are stratified by centrifugation, the heavy third containing nuclei are mostactive in restoring irradiated cells. Some desoxyribonucleotides were reported to have favourable effect on
restoration of hematopoietic cells from radiation injury
in vitro as well as in vivo. 198
242. Restoration of cells can also be obtained by treatments that modify the post-irradiation metabolism of thecells such as temperature, presence of certain nutrients,
metabolic inhibitors. This subject, which is related to thevariations in the conditions of the cell populations after
irradiation, has been extensively reviewed recently by
Alper. 199 Characteristically, the results reported indicatethat most treatments which reduce the response to irradiation provide an environment which is sub-optimal for
growth.
243. Some physiological functions of cells impairedby radiation may also be repaired. At present, knowledgeof recovery mechanisms after ionizing radiation is in its

232. The restoration effect of ultra-violet light subsequent to X-irradiation has been observed by Elkind
et al. in yeast cells. 555 Ultra-violet light increases thefraction of cells surviving the exposure to X-rays by afactor of 3 or 4. _i\nalogous effects with spores ofStreptomyces aureofaciens have been reported by Goldat
et a/,, 556 In the latter instance, the restoring action of theultra-violet was observed for both lethal effects andmutation induction.
233. Restoration by catalase of ultra-violet-induced
damage 238 • z39 • m is more restricted, as it applies only tolysogenic systems and is linked to the destruction oforganic peroxydes formed in these systems during irradiation.
234. The supply of metabolites to micro-organisms
which have lost the capacity to synthetize them can beconsidered as one possible mechanism of recovery; inthis case, however, restoration is apparent only, since
the intrinsic damage has not been repaired. Restitution
would be achieved if there was a possibility of replacing the damaged molecules or sub-cellular units by nonirradiated ones.
235. The phenomenon of cross - reactivation or"marker rescue" was discovered by Luria with theT-even phages (T 2, T 4 , T 6 ). When a bacterium is infected with active and inactivated phages differing fromeach other in a few of their genetic loci, some genetic
markers of the inactivated parents may appear among
the progeny resulting from such a mixed infection.
These studies were subsequently carried out in great
detail by Doennann et al. 56 ~• 563 and were extended tothe coliphage ,\, 564 and to the Salmonella phage P 22 • Thisphenomenon may be explained by assuming that the
UV lesion, while preventing or delaying the reproduction of the whole phage, destroys only a small piece ofits genome. The cross-reactivated loci would be thoseof the undamaged parts of the irradiated phage which
would reproduce only after their "rescue'' from theinjured genome through genetic recombination with theunirradiated parent. 56 ~· m After X-irradiation and after
decay of incorporated P~, marker rescue has also been
observed in the T-even phages 559 • 566• 567 and in the Salmo1iella phage P 22 , 565
236. A bacterium infected with a single inactivatedphage does not yield active virus ; but if two or moreinactivated virus particles infect a bacterium, active
phage may be released. 508 The phenomenon of multiplicity reactivation has been interpreted by Luria as
being due to genetic exchange of uninjured parts of the
genome of the parental phages. Further studies5GD havenot supported some aspects of Luria's original theory ofmultiplicity reactivation, but recently Hann570 and Barricelli571 have amended Luria's theory to reconcile itwith the experimental data. Multiplicity reactivation
seems to be restricted to certain strains of phages and tocertain types of radiation damage. It occurs with the
T -even phages and T 5 with high efficiency; it is lesseffective with T 1 , ,\and P 22 , and not at all effective withT 3 , T 7 and the Pyocyanea phage P 8 •547 Multiplicity reactivation occurs with high efficiency only when the phagebacterium comple.x is exposed to irradiation. To explain
the different response to X-rays of intracellular andextracellular phage, Weigle and Bertani 572 assumed theoccurrence of an "early step" damage connected with
DNA injection which prevents the uninjured parts of
the irradiated genome from participating in the sequenceof events conducive to reactivation. Although it has beenreported that no multiplicity reactivation occurs in T,.

65

infancy. This subject is of such importance to radiobiology that research on all aspects of the problem shouldbe emphasized.
X. General conclusions

244. The main conclusions of radio-biology in the1958 report remain valid and will not, in general, be
repeated here. However, because of the importance ofthe threshold problem, it seems prudent to restate theearlier conclusion that "biological effects will follow
irradiation, however small its amount". This conclusion,
based largely on theoretical considerations and on the
exponential character of many dose-effect curves, issupported by new data on the effects in macromolecularsolutions, intracellular structures, viruses, bacteria, andother cellular systems.
245. The main development since the last report has
been spectacular progress in the study of biologicaleffects at the molecular level. This applies in particular
to the genetic material, DNA, and the way in which thissubstance replicates itself (DNA synthesis) and controls the synthesis of specific proteins transcribing its
information to RNA by a triplet code. In the wake ofmolecular biology, a molecular radio-biology is now developing and, although still in its initial stages, hasalready provided some important results. Thus, evidence
is now coming forward that the most significant radiation effects (inhibition of mitosis, reproductive andinterphase death, mutation), at least in a number of
instances, are due to primary damage of the genetic
material, namely the chromosomes and, in particular,
DNA. How these lesions interfere with DNA, RNA,and protein synthesis has already been much clarified;
it is expected that studies on cell-free systems i1i vitro

66

now in progress ·will provide many answers to still open
questions.
246. Understanding of radiation damage in nuclear
material has been increased by studies of the effects on
the physical and chemical properties of macromolecules,
especially nucleic acids and nucleoproteins in vitro andin vivo. The ESR method seems promising for detection
and determination of the fate of free radicals producedby radiation in biological materials.
247. New knowledge of the effects on cytoplasmic
functions has contributed to an understanding of the
problem of radiation damage to cells. Only by taking
into account the mutual interaction of damaged structures in the nucleus and cytoplasm can this complex
problem be understood.
248. The important role of recovery at the cellularlevel in determining final radiation effects has been more
appreciated, especially the partial reversibility of initial
mutational damage in cells of various origins. However,knowledge in this field is fragmentary; further researchis needed.
249. Biological effects after incorporation of P 32 , 0 4 ,and H 3 have been studied. It seems that under most conditions, biological effects are due to radiation rather thanto transmutation. However, it has been shown that undercertain conditions, particularly after P 32 and 0 4 areincorporated into essential molecules like DNA, transmutation may lead to chromosome breakage.
250. Radio-sensitivity studies have received new
stimulus from recent analysis of genetic factors determining radio-sensitivity in bacteria and from investigations of how these genetic factors are metabolically
expressed.

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541. Oftedal, P., J. Mossige, Incorporation of P 32 andmutagenesis during spermatogenesis in Drosophila.
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ero BRJIID'lerrrrrr n if\IIBfile crpyli.Typfil. A1rnp;eMIIH na-

HOBCRHX !Iyqett na MyTaIQIOIIHfiltt npoqecc y
Streptomyces aureofaciences. ,Il;OK.lia,il;hI AEa;n;eMIIH
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558. Dulbecco, R., Experiments on photoreactivation ofbacteriophages inactivated with ultraviolet radiation. J. Bacteriol. 59: 329-347 ( 1950).

559. \Vatson, J. D., The properties of X-ray-inactivatedbacteriophage. I. Inactivation by direct effect. J.
Bacteriol. 60: 697-717 (1950).
560. Watson, J. D., The properties of X-ray-inactiYatedbacteriophage. II. Inactivation by indirect effects.
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82562. Doermann, A. H., M. Chase, F. W. Stahl, Genetic
recombination and replication in bacteriophage. ,J. Cell. Comp. Physiol. 45, Suppl. 2: 51-74 (1955).
563. Doennann, A. H., The analysis of ultraviolet lesions in bacteriophage T4 by cross reactivation.
J. Cell. Comp. Physiol., Suppl. 1 : 79-94 (1961).
564. Jacobs, F., E. L. Wollman, Etapes de la recombinaison genetique chez Escherichia coli K12. Comptes Rendus Acad. Sci., Paris 240: 2566-2568( 1955).
565. Garen, A., N. D. Zinder, Radiological evidence forpartial genetic homology between bacteriophageand host bacteria. Virology 1: 347-376 ( 1955).
566. Stahl, F. W., The effects of the decay of incorporated radioactive phosphorous on the genome ofbacteriophage T4. Virology 2: 206-234 ( 1955).
567. Stent, G. S., Cross reactivation of genetic loci of
T2 bacteriophage after decay of incorporated radioactive phosphorus. Proc. Nat. Acad. Sci. 39: 12341241 (1953).
568. Luria, S. E., Reactivation of irradiated bacteriophage by transfer of self-reproducing units. Proc.
Nat. Acad. Sci. 33: 253-264 (1947).
569. Dulbecco, R., A critical test of the recombination
theory of multiplicity reactivation. J. Bacterial. 63:
199-207 (1952).
570. Harm, vV., On the mechanism of multiplicity reactivation in bacteriophage. Virology 2: 559-564(1956).
571. Barricelli, N. A., A "chromosomic" recombination
theory for multiplicity reactivation in phages. Acta
Biotheoretica XI, Pars III/IV; 107-120 ( 1956).
572. Weigle, J. J., G. Bertani, Multiplicity reactivationof bacteriophage inactivated by ionizing radiations.
Virology 2: 344-355 (1956).
573. Symonds, N. D. A. Ritchie, Multiplicity reactivation after the decay of incorporated radioactive
phosphorus in phage T4. J. Molecular Biol. 3: 6171 ( 1961 ).
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radioactive phosphorus during development of atemperate bacteriophage. Virology 2: 737-752(1956).
575. Crawford, L. V., Deoxyribonucleic acid synthesis
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576. Kellenberger, G., J. J. Weigle, Etude au moyen desrayons ultraviolets de !'interaction entre bacteriophage tempere et bacterie hOte. Biochim. Biophys.
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577. Read, J., Radiation Biology of Vicia faba in Relation to the General Problem. Blackwell Scientific
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578. Conger, A. D., M. L. Randolph, C. W. Sheppard,et al., Quantitative relation of RBE in Tradescantia
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579. Neary, G. J., H.J. Evans, S. M. Tonkinson, et al.,The relative biological efficiency of single doses offast neutrons and gamma-rays on Vicia faba roots
and the effect of oxygen. Part III. Mitotic delay.
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580. Evans, H.]., G. J. Neary, F. S. Williamson, The
relative biological efficiency of single doses of fastneutrons and gamma-rays on Vicia faba roots andthe effect of oxygen. Part II. Chromosome damage:the production of micronuclei. Int. J. Rad. Biol. 1(3): 216-229 (1959).
581. Neary, G. J., S. M. Tonkinson, F. S. Williamson,
The relative biological efficiency of single doses offast neutrons and gamma-rays on Vicia faba roots
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ANNEX C

THE flEREDITARY EFFECTS OF RADIATIONCONTENTSParagraph.,
The dose-rate effect... ...• ........ .••... ..•.. 84-87"Repair" of pre-mutational damage. ••.. .•.• •• . 88-92
Locus specificity •..•••..•..•...., .•.•.••.•• , ,93
Sex and stage of gametogenesis•..•••.•••••••, 94-100
Species specificity •••.••••••••••.•.•••••••••,• 101
Induced chromosome aberrations................ 102-117
Observations on experimental organisms ....... 103-115
Observations on human cells.................. 116-117
Comparability of radiation-induced and naturallyoccurring mutations ..................,...... 118-120

ParagraJ,hs
1-10

J. b,"TRODUCIION

I!. THE PREVALENCE OF NATURALLY-OCCURRING HEREDITARY DEFECTS AND DISEASES......................
Survey of hereditary disabilities.................
Category la ,,••.,••,••.••••• •• ••••• .••.••.••
Category lb •.•• ••••...•••• •••• ••. . . ..•. .•.••
Category II • •• ••••••••.••• •••• ...•••••••••• •Category III •.•..•••...,•••.••• ••. •• .•• .•..•
Category IV ..• ...•.•...•.•..•. ... ••• •••••• .•Role of heredity in premature death..............
Lethal and detrimental equivalents...............
Ill. THE ROLE OF MUTATION IN SUPPORTING THE PREVA­LENCE OF HEREDITARY DIS."'1IILITIES,,, ••••••••••,•,
Relative genetic fitness••••...•••••••...•....••••Natural mutation rates at individual loci in man••
Autosomal dominant traits•••••.••.•.•..•.•.••
Sex-linked traits ....•...•.••..••.•..••..•,•.•
Autosomal recessive traits ••.•.....••.••..•,•..
Natural mutation rates at individual loci in experimental animals ..........., ..................
Naturally-occurring chromosome aberrations in
man .••.•..•...•••.•..••.•••.•••••.•.....•••Natural_Iy-occurring !=11romosome aberrations in
expenmental organisms .•••••••••••.••••••.••
Factors affecting the frequency of natural mutation

11-41
13-37
14-17
18-29
30-32
33-35
36-37
38
39-41

V. EFFECTS OBSERVED IY DESCEND-"..',TS OF IRRADIATED
POPULATIONS •••••••••••••,•,,•••••••••••,•, •, •• 121-135
Induced mutations in the immediate progeny ofirradiated humans ........................... 121-125
Induced mutations in the immediate progeny of irradiated mammals •.•••••••.•.•.••••.•..••••• 126-130
Polygenic traits ................................ 131-135

42-80
44-52
53-64
58-59
60-62
63-64

VI. INTERPRETATION ........,•••...... ••..•••••• •••• 136-157
Direct approach ... .•..••.• .•.. ..•••••. •. ...••• 137
Indirect approaches ............................ 138-157
The prevalence of hereditary diseases and defects 139-140
The role of spontaneous mutation in maintaining
the frequency of hereditary disabilities•••.••• 141-143
Dose-mutation relationship ..••....•.••••••..• 144-145
The doubling-dose concept in indirect assessments ................, .................... 146-152
Conclusions ................................. 153-157

65-66
67-70
71-72
73-80

IV. THE INDUCTION OF MUTATION BY RADIATION••• , ••• 81-120
Factors affecting the frequency of radiationinduced mutation ••••••••.•.••••..••.••••••.. 82-101
Linearity of the dose-effect relationship andabsence of a threshold...................... 83

TABLESREFERENCES

I. Introduction

4. Developments such as these have been of great
help in understanding the basic problems of radiation
genetics. At the same time they have re-emphasized its
complexities. The present annex gives particular atten­
tion to the effect which these recent advances have hadon our ability to estimate the extent of hereditary damage
which may be induced in populations by ionizing radia­
tion. In stressing current problems, the report does notenumerate but is nevertheless based on a vast amount of
information which has been accumulated over many
years in the field of radiation genetics. For an accountof earlier data and well-established genetic concepts,
reference should be made to the previous report. How­ever, to make this annex self-contained, this older
information is summarized at relevant places.
5. All organisms are subject to hereditary diseases
and defects. In man, estimates of the size of this burdenof undesirable traits are based on the frequencies of:(a) Abortions, still births and neonatal deaths;(b) Infertility;( c) Hereditary diseases and defects;(d) Detrimental deviations from normal in continu­
ously varying traits such as intelligence, life-span andresistance to disease.

1. In its consideration of the hereditary effects ofionizing radiation upon man this report, as did that of1958,1 centres its attention on the possible consequencesof the increases in the level of radiation to which humanpopulations are currently exposed.
2. The Committee's 1958 report presented a compre­
hensive outline of the genetic hazard of ionizing radia­
tion; the available evidence in man and other organisms
was reviewed thoroughly and a variety of approaches wasused to elucidate the problem. At the same time itwas emphasized that current knowledge was insufficient
to complete this task with more than partial success.
3. Since that time several significant developments
have been made in radiation genetics and in related
disciplines. In particular, progress has been very rapid
in the area of human cyto-genetics; considerable atten­
tion is now being focused on the induction of grosschromosome aberrations as a serious genetic hazard. In
addition, remarkable advances have been made throughinvestigations with mice. These have indicated theexistence of previously undetected intricacies in the dose­mutation relationship.
84

fects that are slight but nevertheless of importance tohumans are not easily recognized in other species. As aconsequence, generalizations based on the results ofinvestigations with experimental organisms entail many
uncertainties.

6. Deleterious genetic traits are a direct consequenceof the presence of specific basic faults in the genetic
constitution of affected individuals. These faults may beeither undesirable alleles or chromosome aberrations.
However, the prevalence of deleterious hereditary traits
in a population does not, in itself, provide a complete
picture of the amount of genetic damage present. In
some instances the fault is partially or completely
masked in the heterozygote. In other instances, its phenotypic e."--pression is so different in the homozygous andheterozygous states that it is impossible to express thetotal detriment to populations in simple terms. Furthermore, environment, in the form either of the remainderof the genotype or of external conditions, frequently
has a great influence on the manner in which the fault is
expressed.

II. The prevalence of naturally-occurring
hereditary clefeets and diseases

7. There is no doubt that any increase in the frequencyof radiation-induced mutation contributes to the burdenof undesirable traits. It is equally evident that the evaluation of this contribution must rely upon an understandingof the genetic structure of a population and the environmental forces to which it is exposed. Moreover, the effectof an increase in the amount of genetic damage, from
whatever source, must be considered in terms of a timeinterval; once inflicted on a population the damage may
persist through future generations and may be expressed
only intermittently and with varying degrees of severity.

11. It is generally accepted that there is a genetic component in much, if not all, illness. This component isfrequently too small to be detected ; in other instances theevidence for its presence is unequivocal. Nevertheless,the role of genetic factors in the health of human populations has not in the past been considered seriously invital and health statistics. As a consequence, data on theprevalence of hereditary diseases and defects are now
largely restricted to that collected by geneticists for special purposes in limited populations from a small numberof countries.
12. An assessment of the hereditary defects anddiseases with which a population is affiicted does notnecessarily provide a measure of the imposed burden of
suffering and hardship on the individual, the family,or society. Such evaluations require, among other things,
consideration of the development of medical services
and of the cultural values in communities. 2

8. There are a number of complementary approaches
to the problem of estimating the detrimental hereditaryeffects of an increase in rate of mutation in human populations. Estimates of genetic hazard can be obtained
empirically by the observation of irradiated populations.
However, information obtained in this way is meagre,
and estimates are more often calculated from what is
known about the induction of genetic damage by radiation and from a knowledge of the way in which thisdamage will be expressed. These more indirect ap•
proaches require information on:(a) The magnitude of natural genetic damage within
a population as ascertained from a knowledge of therole of heredity in morbidity, mortality, and infertility;( b) The role of recurrent natural mutation in maintaining the prevalence of this genetic damage;( c) The qualitative and quantitative relation between
a given dose of irradiation and the corresponding increase in mutation rate.

13. In the 1958 report, a detailed examination of data
accumulated in Northern Ireland over many years led
to a figure of about 4 per cent as the incidence of more
readily detected hereditary diseases and defects. That
survey has been the most comprehensive undertaken todate, and although limited to a single geographical region,it has provided a useful base on which to formulate overall estimates. New information now permits a ·revisionand reclassification of these. For instance, it is now possible to estimate the frequency of chromosome aberrations
and to transfer some conditions, such as Down's syndrome (mongolism), to a different category. The estimate of the incidence of congenital malformations has
also been increased. The revised values are summarized
below. Disabilities are placed in any of four categories.
They are classified according to the role which mutation
is believed to play in maintaining their frequency. Thissubject will be discussed in more detail in section III.

SURVEY OF HEREDITARY DISABILITIES

9. Every approach has its own difficulties and limitations. The direct approach is impeded not only by ameagreness of data but also by the absence of proper
controls. Furthermore, in man it is quite impractical,
through direct observation, to ascertain the spread ofdamage over what may be many generations. On theother hand, more indirect approaches require a knowledge of the genetic structures of populations and ofgenetic mechanisms which we do not fully possess at
this time.

Category la
14. This includes harmful traits whose mechanism ofinheritance is understood and whose prevalence is determined mainly by the frequency of individual gene, orpoint, mutations.
15. Several hundred traits determined by single genesubstitutions have been identified. A majority of thetraits, perhaps 70 per cent, are determined by autosomal
dominant genes. Approximately 5 per cent are SC.'C-linked
recessive traits, and the remaining 25 per cent are
determined by the homozygous e.'{pression of autosomal
recessive genes.
16. The majority of dominant traits are sufficiently
mild in their effects to be transmitted through several
generations. In contrast, the detrimental recessive
traits now recognized in man are very severe in theireffects and, with few exceptions, are lethal in the genetic
sense. As a result, although about 70 per cent of wellestablished specific traits are determined by dominant

10. All approaches often make use of investigations
with other organisms because the mechanism by which
hereditary information is transmitted is basically thesame in all forms of life. Experimental observations ina wide variety of organisms can thus provide a working
model of the effects of ionizing radiation on man. However, there may be radical differences in genetic structure
between populations because this structure is undoubtedly
affected by the environmental conditions under which
a population exists. Furthermore, many hereditary de-85

genes, in perhaps 90 per cent of persons who showmonomeric traits, these defects are determined by dominant genes. In terms of gene frequency, however, genes
for recessive harmful traits must far outnumber thosefor dominant harmful traits in a given population.
Furthermore, many hundreds of traits are encounteredin man for each of which a recessive mode of inheritanceis suggested, but each is so uncommon that adequate
evidence for this is lacking. It seems likely that many ofthese traits are in fact the homozygous expressions ofrecessive genes and that they contribute in total morethan any other class to the frequency of detrimental traits
in populations.

individuals with Down's syndrome are known to havea forty-six chromosome complement in which part of an
extra chromosome 21 is translocated to another autosome.16-18 Other disabilities that have been associatedwith translocations or other types of aberration are listed
in table II.
24. Defective traits caused by chromosome aberrations are sometimes, as might be expected, inherited
through successive generations. A chromosome rearrangement which permits Down's syndrome to betransmitted by phenotypically normal females with atranslocation in the balanced state has been demonstrated
repeatedly.11- 20 Cases have also been reported of translocation-carrying phenotypically normal males whosechildren exhibit Down's syndrome. 20021 Other balanced
and unbalanced karyotypes have been noted in parental
and child generations (table II). There are indicationsof differential transmission of aberrant chromosomal
types in the two sexes. 22
25. Mental retardation is one of the common consequences of gross chromosomal aberration. Relevant
data have been obtained through the procedure of nuclear
sexing of buccal mucosa to detect sex-chromosome anomalies. This procedure reveals deeply staining chromatinbodies within nuclei. The number of these Barr bodies
per cell is, in general, one fewer than the number of X
chromosomes present; the cells of a normal male arechromatin negative, whereas those of a normal female
contain one Barr body. In five sunreys, the combined
frequency of chromatin-positive individuals among
males attending special schools for the mentally backward was 8.77/1,QOO (29/3,306).2 s-: 7 Five surveys ofmale inmates of institutions for mental defectives indicated a frequency of 9.51/1,000 (70/7,358) chromatinpositive cases. 2 s-s 2 Two surveys of female inmates of
institutions for mental defectives showed a combined
frequency of 4.46/1,000 (12/2,689) females with double
sex-chromatin bodies and one chromatin-negative
female. 31 These figures may be compared with thosefound in the general population (para. 28 below).

17. Traits listed in this category are at present estimated to affect about 1 per cent of all live-born.

Category lb
18. Harmful traits which are determined by cytologically demonstrable chromosome aberrations are includedin this category. Their frequency is maintained mainly
by recurrent mutation.
19. There is direct evidence that congenital and otherphysical defects are sometimes due to chromosome aberrations. This important information has been acquired
as a consequence of improved techniques in human
cytogenetics. Because most research in this area is new,the subject will be considered here in some detail.
20. As with those traits caused by the action of specific alleles, there is often considerable variation in theclinical severity of defects caused by chromosome aberrations. For this reason, all the clinical aspects of somespecific defects remain to be described. Different degrees
of mosaicism may be partly responsible for this variationin expression. Many associations of physical impairmentwith chromosome aberrations are now being reported
and it must be suspected that some of these associations
are due to chance. Reasonably well-established associations are presented in table I, others, necessitating further
confirmation, in table II. All the disabilities noted intables I and II are congenital, but some diseases ofsomatic origin are known to be associated with chromosome aberration. Two of these are granulocytic chronic
leukaemia 3 and Waldenstrom's macroglobulinaemia.'
Such diseases are discussed in anne_ic D.

26. Sterility is a frequent consequence of chromosome
aberration. Males with sex-chromosome abnormalities
are almost always sterile. 38 A study of men attending
an infertility clinic showed that about 3 per cent of thepatients were chromatin-positive. 3 ' Among sixty-eight
women with a presumptive diagnosis of primary amenorrhoea, 28 per cent were found to have sex-chromosome
anomalies. 35
27. Some cases of still birth and abortion are attributable to chromosome aberration. In a survey for se..xchromosome anomalies in still-born children by nuclear
sexing, none of fifty-two females was found to be abnormal. but two of forty-nine males were chromatinpositive. 86 In two instances of miscarriage the embryos
have been shown to be triploid. 37 • 38 Here it was possible
to culture material from foetal remnants.

· 21. The fact that some well known defects occur as aconsequence of anomalies in the number of autosomes
was discovered in 1959, when it was demonstrated that
Down's syndrome is associated with trisomy of one of
the small acrocentric chromosomes (number 21 under
the Denver Convention). 5 • 6 There are two other wellestablished instances of trisomy syndromes. One involves a member of the 17-18 group, 7 the other a memberof the 13-15 group. 8 All three kinds of trisomy areassociated with mental retardation.

22. Some detrimental traits are attributable to anomalies in the number of sex chromosomes. This wasestablished when it was shown that a condition known as
Klinefelter's syndrome can be caused by an XXY constitution.9 Related clinical symptoms have now been
attributed to XXXY,1° XXXXY 11 and XXYY 12 karyotypes. Turner's syndrome has been associated with an
XO constitution. 13 Females with XXX and XXXX
karyotypes have also been described. 14• 15

28. A general picture of the prevalence of defective
traits caused by gross chromosome anomalies is beginning to emerge despite the newness of this field of research. Some specific traits are extremely rare. However, the frequency of Down's syndrome is about 1.5 per
1,000 total births in Europe, North America, andJapan. 3041 Comparative figures from other parts of theworld are rather scanty. Current data on the frequencyof sex-chromosome abnormalities have recently beensummarized.33 Cases of Klinefelter's syndrome (XXY),
or at least karyotypes containing a Y and more than one

23. Defects attributable to the presence of chromosome rearrangements have also been detected. Some86r
X, are relatively common, whereas cases of Turner's
syndrome (XO) are rare. Three surveys by nuclear
sexing of buccal mucosa, have been made among consecutive live-born. A frequency of 2.65 /1,000 ( 18/6,801)
chromatin-positive males was found in the combined
data. Chromosome studies of seven of the anomalous
cases showed that four were XYjXXY mosaics andthree had an XXY complement. The frequency of abnormal nuclear sex among females was 0.90/1,000 ( 6/6,642). 36, 42, 43

sion, a simple mode of inheritance has been postulated
for some of them. However, their frequency in the faceof strong selection and their distribution in families are
difficult to reconcile with a monomeric hypothesis. As aconsequence, simple modes of inheritance are not usuallyassumed. 49 Each of these traits is common and prevalent over most of the world. They were collectively estimated in the 1958 report to affect at least 1.5 of all
adults, but this estimate is very uncertain.

29. It is now estimated that about 1 per cent of all
live-born have some harmful trait determined by chromosome aberrations sufficiently gross to be detected bypresent techniques. Many of these individuals aremosaics. Rather more than half of the aberrations areanomalies in chromosome number. The rest are intrachromosome changes, translocations or combinations ofthese with numerical changes. Only a small fraction ofthese aberrations are transmitted to subsequent generations. It is likely, however, that estimates of the frequency of transmissible chromosome aberrations would
be greater with more refined techniques since theseaberrations, being less gross, are more difficult to detect.

Category IV

36. This category includes harmful traits which are
determined at single loci, but it is highly unlikely that thefrequency of the alleles is substantially influenced bymutation.
37. The frequency of these traits tends to be high inlocalized areas of the world. This high frequency is aconsequence of the fact that each of the traits e.xists as apart of a system of balanced polymorphism; selection
pressures maintain the related genotypes in a state ofbalance. Included in this category are sickle-cell anaemia
and thalassaemia. Many other traits, such as fibrocystic
disease of the pancreas, probably belong here. On theother hand, a change in environment at some time in
the future might remove some traits from the category.
Except in certain localized areas in the world, the prevalence of these traits as currently recognized is extremely
low. The subject of balanced polymorphism will be discussed in greater detail in a later section (paras. 47-52).

Category II

30. This category includes developmental malformations whose mechanism of inheritance is ill understood.
Environment is influential in the aetiology of these
traits. Drugs, certain infections, and radiation are known
to be teratogenic at critical stages of organogenesis, andmaternal (intra-uterine) environmental factors are also
known to have a great influence on prevalence. The roleof mutation in maintaining the frequency of these traits
has not yet been ascertained. They often show somefamilial concentration, but this fact does not necessarily
prove the existence of a genetic component.
31. Some of these malformations may be caused bychromosome aberrations. However, no cytological evidence of this has been found in many of the more commonly-occurring malformations. 4 4""' 6 It is of course possible that chromosome changes too small to be identified
by current techniques are responsible. Alternatively,
comple..x genotypes and unusual environments may becausal factors; it has been suggested that a fraction ofcongenital malformations are caused by an insufficientdegree of such heterozygosity as is necessary to ensure
normal development.40 • 47 However, it is difficult to distinguish between conditions due to individual recessive
genes of low penetrance and any that may arise becauseof a deficiency of heterozygosity at a multiplicity of loci.
32. Many of these traits are detectable at birth. The
frequency of live-born so affected is now estimated to beabout 1.5 per cent, but is higher if still births are included. At the age of five years, an additional 1 per centof affected children can be detected. 40· ' 8

ROLE OF HEREDITY IN PREMATURE DEATH

38. Abortions, still births and neonatal deaths present
special problems in a survey of hereditary defects; notonly is the frequency of these defects greatly affectedby environmental factors, but the role of heredity intheir cause is difficult to ascertain because they are nottransmitted to the ne..xt generation. In consequence, withthe exception of those cases known to be caused by grosschromosome aberration, these defects are not consideredin categories I-IV. Nevertheless, breeding experiments
in animals have shown that simple genetic mechanisms
contribute to their incidence. In other instances the additive effects of several genes with slight individual effects
may be responsible.
LETHAL AND DETRIMENTAL EQUIVALENTS

39. All the genetic damage within a population is not
expressed phenotypically in any one generation. To alarge extent, this is because many detrimental traits are
partially, if not completely, recessive; complete e.xpression occurs only in the homozygote. The amount of thisrecessive damage is an important measure of the genetic
health of a population. It can be estimated indirectlyfrom a knowled~e of the increase in mortality and morbidity observed m the progeny of consanguineous marriages; in these circumstances the hidden genetic damage
can be described in terms of lethal and detrimental
equivalents. A lethal equivalent has been defined as agroup of mutant genes of such number that, if dispersed
in different individuals, it will cause one death on the
average.~ 0 This death occurs with homozygosity. In thesame manner, genes leading to visible recessive defects
can be defined in terms of detrimental equivalents.51

Category III

33. In this category have been placed serious "constitutional" disorders in which the mechanism and contribution of inheritance are ill understood.
34. Included here are mental illnesses such as schizophrenia and manic depressive reactions as \vell as disorders such as diabetes mellitus, pernicious anaemia andsome affecting the thyroid gland.
35. There is general agreement about the e.xistcnce ofa major genetic component in these traits and, on occa-

40. The procedure outlined above is a powerful toolwith which to estimate the amount of recessive genetic
damage within a population. However, lethal and detri87

It is known that few dominant diseases and defects arecompletely dominant and it is becoming increasingly
clear that many recessive traits may not be, in fact,completely recessive. This. partial dominance can reflect
on the genetic fitness of heterozygotes. The effect thateven a minor change in heterozygotic fitness may haveon the estimated mutation rate required to maintain thefrequency of a defect at a constant level can be illustrated with a trait such as phenylketonuria. This trait
occurs with a frequency of 25 X 1~ in the populationof England and the genetic fitness of the homozygote isnearly zero.H Under the assumption that the heterozygote has the same fitness as the homozygous normal,
a mutation rate of 25 X 1~ per locus per generation isrequired to maintain the gene at its present level in the
population. If, however, the fitness of the heterozygote is
1 per cent, 2 per cent, or 5 per cent lower, as has beensuggested, then the corresponding mutation rates would
be three, five and eleven times the previously mentioned
rates. 50 • 51 • 58 In contrast, if a slight heterozygous advantage is assumed, a very different estimate is obtained;with only a 0.1 per cent or 0.2 per cent advantage infitness, the estimated mutation rate would be only 4/5 or
3/5 that of the original rate. 39 With an advantage of
0.5 per cent, mutation would not be required to compensate for the loss of genes due to deleterious homozygotes ; in fact, the gene frequency would increase to ahigher level.
46. Genetic fitness of heterozygotes cannot be treatedas an invariable property of the two alleles under consideration. Rather, fitness can be influenced not only by
the remainder of the genotype, as in the intricate situation involved in populations carrying genes for boththalassaemia and glucose-6-phosphate dehydrogenase deficiency, 55 but also by the external environment. For
such reasons an individual estimate of fitness may bevalid for the immediate future but less valid when applied
over several generations.
47. One of the advances in human population genetics
has been the discovery of several balanced polymorphic
systems (category IV). The term polymorphism, as
used here, describes "the occurrence in the same habitatof two or more discontinuous forms of a species maintained by a balance of selective forces, as opposed tomaintenance by recurrent mutation". 56 Such systems
arise when a gene confers reduced genetic fitness insome circumstances and increased fitness in others. The
increase in fitness may be a consequence of a shift in themacro- or micro-environment or it may be a consequenceof heterozygosity as contrasted with homozygosity. The
role of mutation in supporting the frequency of polymorphic traits is minor. To predict the over-all consequences of an increased mutation rate it is therefore
essential to know the extent to which balanced polymorphic systems contribute to the burden of detrimental
hereditary traits. It is also essential to know what fraction of new mutants are equivalent to alleles that are
already part of a polymorphic system.

mental equivalents do not represent genes determining
any special category of recessive detrimental traits;
when expressed phenotypically in the homozygote, thetraits may fall in any of the lists of defects in paragraphs 13 to 38. Furthermore, an estimate of thefrequency of equivalents does not provide any direct
measure of that fraction of genetic damage within a population which is expressed in the heterozygous condition.
Nor does a knowledge of the size of the pool of recessive
lethal and detrimental genes, by itself, indicate the mechanism by which these genes are maintained in a population.
41. Estimates of lethal equivalents obtained fromavailable surveys are presented in table III. The surveys
are of very unequal scope and reliability, the one carried out in Japan being by far the most extensive. In spiteof inconsistencies in the results, including some between
the two cities in Japan, it seems reasonable to conclude
that individuals in human populations carry from two
to four lethal equivalents which are expressed, in homozygotes, before the age of twenty to thirty. In addition,
each individual carries approximately the same numberof detrimental equivalents.
ID. The role of mutation in supporting theprevalence of hereditary disabilities
42. Mutation may be broadly defined as any change
imposed in the genetic constitution of a cell. In the present annex, mutation is considered in terms of the two
fundamental units of heredity, the gene and the chromosome. Natural mutations are generally referred to as
spontaneous though in fact it is understood that there
are causal factors over which we do not usually haveany direct control. One of these factors is undoubtedly
naturally-occurring ionizing radiation. Other physicaland chemical variations that occur in nature, and thegene complement itself, probably influence mutability.
43. Two mechanisms are involved in maintaining theprevalence of detrimental hereditary traits within a population. One of these is recurrent mutation. The other isdirect transmission of the basic genetic faults throughsuccessive generations. The role of transmission is generally e.."\:pressed in terms of genetic fitness of the relevant genotypes, i.e., the number of their progeny whichreach maturity. The importance of mutations in humanpopulations cannot be considered independently ofgenetic fitness because reliable estimates of specific natural mutation rates and of the over-all contribution of
mutation to ill health are frequently dependent on accurate information about this fitness.
RELATIVE GENETIC FITNESS

44. The relationship between mutation, genetic fitness,and the prevalence of hereditary disabilities is concisely
expressed by the principle which holds that each mutation, whether fully lethal or slightly detrimental, will on
the average, result in the death of a descendant or in a
failure to reproduce. 52 • 53 The more genetically unfit ofthese mutations, as for instance dominant lethals, will beeliminated quickly, and occasionally without provoking
any suffering or undue hardship on the population.
Mutations which have less drastic effects on fitness willusually be transmitted through many generations and~eir phenotypic effects will be expressed in correspondmgly more descendants.
45. Genetic damage can affect the phenotype of individuals in either the homozygous or heterozygous states.

48. The existence of balanced polymorphism is suspected when excessively high mutation rates must be
postulated to maintain the frequency of a detrimental
trait under the assumption that the heterozygote isneutral. An example of heterozygous advantage in genetic fitness is provided by sickle-cell anaemia, a trait
which is fatal in the homozygote. The distribution of thesickle-cell trait has been investigated over large areas of
the world and is very uneven: the trait is completely
absent in a number of populations, yet the homozygote
88alleles at loci involved in polymorphic systems are unconditionally harmful in contrast to those alleles which
support the polymorphic systems in nature. In thesecircumstances it is important to know the average reduction in fitness of the heterozygote, since this value determines the number of generations over which a temporary
increase in mutation rate would be felt by a population.
It also determines to some extent the magnitude of thetotal damage. There is no general information about thisvalue in man. In Drosophila, e."<tensive studies have indicated that the average reduction in fitness of heterozygous lethals and semi-lethals is about 2 per cent.50• 68
It would probably be larger in poor environmental conditions. 69 • 1°

bas a frequency of 3 to 4 per cent in some populationsof Asia and Africa.57 It has now been demonstrated thatheterozygous ii;dividuals .have an increased resistance. tomalignant tertian malana and a consequent selective
advantage in a malarial environment. 57 • 58 It is likely that
other serious haemoglobinopathies, including thalassaemia, are maintained by a similar mechanism. Current
world-wide measures to eradicate malaria will have theeffect of reducing the genetic fitness of heterozygotes.
As a consequence, a reduction in gene frequency is to
be expected. However, the rate of reduction will be slow
and the trait will continue to be carried for many generations. It has been suggested that the ine."<plicably highfrequencies of some detrimental traits are a consequenceof relatively greater genetic fitness of heterozygous carriers at some time or place in the past. 89
49. The frequency with which balanced polymorphic
systems occur in human populations has yet to be determined. Relevant to this problem are two contrasting
but not mutually e."<clusive hypotheses that have been
proposed for the construction of e.xtreme models of gene
behaviour. One has been termed the classical, the otherthe balance hypothesis. 59 Under the classical hypothesis,
it is assumed that genetic variability is maintained byrecurrent mutation. Furthermore, it is assumed that
almost all mutations are unconditionally deleterious andsubject to selective elimination; heterozygous advantage
is restricted to a small number of loci although it may
contribute greatly to existing genetic variability. Thebalance hypothesis, on the other hand, assumes thatgenetic variability is to a large e.""<tent maintained byheterozygous advantage; mutation may not be unconditionally deleterious and a certain level of heterozygosity
is essential to high fitness.
SO. Using the concepts of lethal and detrimental
equivalents, it is possible to deduce the relative importance of these two models. It has been calculated that an
inbreeding depression of such a high degree as has been
detected experimentally cannot be expected from systemsof balanced polymorphism ; this has led to the conclusionthat most hereditary defects revealed by inbreeding are
maintained by recurrent mutation.60 A similar conclusion
has also been reached from different evidence ; an analysis of the frequencies and modes·of inheritance of deafmutism, limb-girdle muscular dystrophy and low grade
mental defects has suggested that the mean genetic fitnessof a population would be impossibly low if the prevalence of these and other traits were not maintained bymutation. 51 On the other hand, in a recent study of two
Japanese populations, the detected inbreeding depression
was so slight as to indicate that the role of balanced polymorphic systems in maintaining the prevalence of hereditary effects is greater in those populations than in others
previously studied.61
51. Investigations \vith irradiated experimental organisms have also produced conflicting evidence, 0 2-6 1 a factwhich may well reflect the importance of strain differences and environment in the phenotypic expression of
genotypes. It is also possible that a variation in frequency of gross chromosomal aberrations with different
doses of radiation contributes to differences between
results.
52. In the absence of complete information about therole of balanced polymorphic systems it is usually assumed that most of the genetic damage within populations is mutation-maintained ; this avoids the risk ofunderestimating radiation damage. Even if this assumption is incorrect, it is possible that most new mutant

NATURAL MUTATION RATES AT INDIVIDUALLOCI IN MAN

53. The frequency of mutation at a locus can only be
studied when the mutation determines a specific detectable trait. Mutation is always an uncommon event; afreshly-arisen specific mutation seldom occurs with afrequency of more than one in fifty thousand gametes.
It follows that very large populations must be studied
to obtain a reliable estimate of this rate.
54. In many respects man is a very ·suitable organism
for the observation of mutation rates because large freeliving populations can be defined and close relatives areeasily identified. Furthermore, the high efficiency of
medical diagnostic procedures renders relatively easy
the identification of many traits in man that might bemissed in e.xperimental animals. For these reasons, moreestimates of natural mutation rates are available for man
than for most species other than micro-organisms. There
are, however, difficulties in relating traits to specificmutant alleles in man. These difficulties do not arise as
frequently in animals, because planned breeding andgenetic analysis can be employed.
55. Some of these problems are specific to dominant,some to sex-linked, some to recessive gene mutations,and some are common to all three. Those common to all
three derive from the following circumstances :(a) Certain mutant gene traits are mimicked byphenocopies. These are identical or nearly identical traits
determined not by the genotype but by abnormal development in the embryo of foetus in utero. However, careful clinical study often serves to distinguish such phenocopies, as for example in the case of certain cataracts,
and in cases of congenital deafness;( b) Certain traits which are difficult if not impossible
to distinguish clinically, are sometimes determined bymutations on different chromosomes. For example,
ichthyosis vulgaris is determined by an autosomal dominant gene and also by a recessive gene on the X-chromosome;( c) Some clinically identical traits seem to be inherited as if they were autosomal dominant at sometimes and recessive at other times. Examples are achondroplasia and a number of degenerations of the choroid
in the eye. This variation may be a consequence of mutations to different alleles at the same locus, of mutations at
different loci on the same chromosome, or of mutations atloci on different autosomes;( d) Some traits, though apparently inherited in thesame manner, show differences between families whichsuggest that the causal mutations are different in kind.
Although different loci may be involved in these cases,
it is conventional to e.xpress mutation rate in terms of a89

single locus. Such difficulties lead to over-estimates ofmutation rates.
56. Precision in the estimation of the mutation rates
of genes determining harmful traits in man depends
upon the completeness of ascertainment of the characterin a large defined population. High precision can only beachieved where the medical and social services for the
population are well organized. Even so, complete ascertainment is virtually impossible and can never be assumed as certain. Incompleteness of ascertainment tends
to result in under-estimation of mutation frequency.
57. In generalizations of the mutation rates per locus
in man one further factor must be considered. If themutation rate of a gene is very low the trait may arise
too infrequently to be recognized as of genetic origin,or even if so recognized, it may not attract study becauseof the great difficulty of collecting a sufficient numberof cases. In consequence, only those traits occurring witha sufficiently high frequency to give a reliable estimateof mutation rate are selected for investigation.

Autosomal dominant traits
58. A direct method is applicable for estimating rates
of mutation to dominant traits. This method attempts to
identify all cases of a certain trait in the offspring ofparents not affected by the trait. If it is assumed thatthe gene is fully manifested, then each case must represent a mutation in the germ cells of one parent. As
each birth results from two gametes, the mutation rate
per gamete is one-half the frequency per birth. Thismethod can seldom be employed and can be fallacious if
unrecognized phenocopies occur.
59. An indirect method can also be used. This metl1od
assumes that an equilibrium has been reached in which
the frequency of the trait is more or less constant. At
this equilibrium, the number of fresh mutations arisingin the population in each generation is approximatelybalanced by the number of mutations eliminated by
selection. The equilibrium equation is µ. = ~ (1-f) %,where µ. is the mutation rate per gamete per generation, xis the trait frequency in the population, and f is therelative fertility of ilie individuals bearing the trait. In
such an equilibrium the value off is of great importance.
It is, however, difficult to estimate with accuracy. If f iszero then the condition is not recognized as genetic in
origin. On the other hand, relative fertility of the affectedindividuals can be estimated only if it is as low as 85 percent. As a result, estimates of mutation rate tend to bemade for traits with a value of f between 0.0 and 0.8. A
number of estimates are listed in table IV.
Sex-linked traits
60. Estimates of the recessive mutation rate at locion the X-chromosome must be made by an indirect
method. The equilibrium equation is µ. = 73 (1-f) %. In
tllis case, it is assumed that the fertility of heterozygous
females is the same as that of homozygous normal females in the population.
61. The most reliable estimates of mutation rates fora sex-linked recessive gene are those for Duchenne-typemuscular dystrophy. However, there is some evidence
that even this trait is clinically heterogeneous. In consequ~nce, current estimates may represent the sum of mutations at more than one locus.
62. No reliable estimates of the mutation rate forhaem?philia ~ have beer; ma.de since haemophilia B(Christmas disease) was identified as a separate entity.

The proportion of haemophilia types A and B varies indifferent countries. Possibly the older estimates of themutation rate for haemophilia, if reduced by about onetenth, serve as reasonable estimates for ilie locus determining haemophilia A. However, ilie trait can be so mildthat ascertainment is almost certainly incomplete. This
tends to produce under-estimates of the true mutation
rate. Some estimates are presented in table V.

Autosomal recessive traits
63. Only indirect estimates of autosomal recessive mutation rates can be made and these are of very uncertain
reliability. The equilibrium equation is µ. = (1-f) x.
In man, the value off is zero or extremely low for thegre~t.majority of recessive homozygotes. Exceptions arealbm1sm and some forms of recessive deaf-mutism. Even
with these conditions, however, the value of f is not over
0.5. If f has a value of zero then ilie estimate of mutation
rate corresponds to the trait frequency. Here, however,there are many difficulties. It is assumed, as for sexlinked genes, that the fertility of the heterozygote is thesame as. the average in ilie population. However, a highproportion of all mutant genes in the population are inheterozygotes. For this reason any selection in favour ofor against the heterozygote has a much greater effect on
the prevalence of a trait at equilibrium than has the loss
due to homozygosis. Furthermore, a shift in the environment can upset the population equilibrium by affecting
the genetic fitness of the different genotypes. When thishappens, many generations may pass before equilibrium
is restored. Again, changes in marriage customs canaffect the frequency of different genotypes. A decline in~e amount of inbreeding has been noted in Europe durmg the last century or two; such a circumstance is likely
to lead to estimates that are too low.11 Some estimates ofautosomal recessive mutation rates are presented intable VI.
64. In spite of all the reservations, there is a large
group of grossly harmful mutations, autosomal dominant, recessive, and sex-linked recessive, whose estimatedmutation rates cluster around 10 X 10-S per generation.
However, this clustering may be conditioned largely byilie selection of traits for study.
NATURAL MUTATION RATES AT INDIVIDUAL LOCIIN EXPERIMENTAL ANIMALS

65. With experimental animals it is possible to estimate natural mutation rates with methods that involve
test matings. In the mouse, the rates of natural visible
mutation have been estimated at seven loci. These loci are
identified by recessive visible alleles namely: a (nonagouti), b (brown), c (chinchilla), d (dilution), p (pinkeye), s (piebald spotting), and se (short ear). The lociare distributed on five of the twenty chromosomes. Thereis linkage between d and se and between c and p. These
alleles were selected for various radiation studies andshould not be considered a random sample. The over-all
mean mutation rate is estimated to be about 7.3 X 1()-6
per locus per gamete (table X).
66. Estimated values of natural mutation rates at specific loci in Drosophila were discussed in ilie previous
report and in a recent review .'2
NATURALLY-OCCURRING CHROMOSOME ABERR.~TIONS
IN l'l!A.."'i'67. Man has a relatively stable karyotype; the diploid
chromosome number is forty-six. 73 • H Nevertheless,90with the development of improved techniques in mammalian cytology, examples of aberrations already wellknown in plants and insects are bein~ accumulated. The
detection of chromosome anomalies m man is aided by
the relative ease with which associated abnormal phenotypes can be recognized. On the other hand, cytogenetic
techniques are not yet far enough advanced to permit thedetection of less obvious aberrations. Those which are
not now detectable include reciprocal translocations ofnearly equal size, inversions and either small duplications
or small deletions having a length less than 10 per centthat of the affected chromosome. Other aberrations may
be undetected because they are lethal at a very early stage
in embryo development. 33

nate maternal and paternal derivations of the X chromosome) the relative frequencies are 0.7 per cent and 0.02
per cent, and on the fact that primary XO's are notrandomly distributed. 86 • 87 Deficiencies and monosomies
that would have been detected in e..xtensive e..'Cperimentson certain genetically marked autosomes in the mouse
have so far not been found. 85 • 88 Spontaneous translocation has been observed in the rat. 89
72. In Drosophila, maternal non-disjunction andmeiotic loss of whole chromosomes from dividing cells
both operate to produce abnormal eggs. This information
has been deduced from the fact that the frequency ofeggs with two X chromosomes is less than that of eggs
with no X chromosomes. The frequency of abnormal
eggs that arise as a result of non-disjunction has been
estimated at 0.08 per cent and the frequency of thosearising as a result of meiotic loss of the X chromosome
at about 0.12 per cent. This produces an XO :XXY ratio
of about 4 :l.90 There is also a considerable rate of nondisjunction of se..'C chromosomes in males; the ratio ofscored XHO to XUXPyP individuals is 2.8 :l.91 Monosomy and trisomy of the small fourth chromosome occurs
spontaneously but non-disjunction or loss of the second
and third chromosomes has not been detected by genetic
or cytological methods of analysis. It is probable thatthese events occur but that monosomy or trisomy of longautosomes leads to elimination in embryonic stages. 00 An
early study showed that aging of females by itself has noeffect on the natural rate of non-disjunction, although thefrequency of non-disjunction following irradiation ofvirgin females increases through the first ten days. 02
More recent studies have confirmed that maternal age
per se has no appreciable effect on the frequency of spontaneous non-disjunction. 93 In view of the recognized increase in frequency of Down's syndrome with advancing
maternal age 39 and similar observations on the two otherautosomal trisomies, 9 ' this observation shows the difficulty of comparing natural chromosomal mutation rates
of flies and man.

68. The most common of detected aberrations are
trisomies of the smaller autosomes and either monosomy
or polysomy of the sex chromosomes. It seems likely thatmonosomy and trisomy of autosomes other than that
producing Down's syndrome, are rare or usually lethal. 75
Triploidy has been detected, 37• 38• 76 and translocations andother aberrations are frequently reported (tables I andII).
69. Whole-chromosome anomalies may be a consequence of either chromosome loss or "non-disjunction".
Monosomy can result from either process, but polysomy
is attributable only to non-disjunction. It seems likelythat the majority of whole-chromosome aberrations occur
in meiotic divisions of a parent or in early cleavage divisions of the zygote. Little is yet known about the relative
importance of non-disjunction and chromosome loss
during meiosis. However, there is considerable evidence
that one or both of these processes frequently occurs inmitotic divisions following fertilization. This evidence is
supplied by the existence of mosaics16-a: and of exceptional nvins. 83 The occurrence of whole-chromosome
anomalies during mitosis may be more frequent thanpresent data suggest ; mosaicism is not likely to be detected when it does not originate in early cleavage divisions. Moreover, selection pressures may eliminate oneof the stem lines. The possibility that the processes leading to mosaicism tend to recur in a cell line is suggestedby the fact that two or three types of cells are sometimes
present in the growth from a single biopsy of bone marrow or even of skin.84
70. For one reason or another, most individuals withdetrimental traits caused by gross chromosome aberrations fail to produce progeny. Exceptions so far recognized are those phenotypically normal persons withbalanced translocations. The general incidence of suchtranslocations is, however, low. As a consequence, theincidence of gross chromosome aberrations in a population tends to correspond with their mutation rate. For
estimates of frequency, see paragraphs 28 and 29 above.

FACTORS AFFECTING THE FREQUENCY OF
NATURAL MUTATION

73. It has long been observed that the frequencies withwhich natural mutations are found may vary in different
circumstances. This variation provides an opportunity
to identify and study individual causal or influencing
factors. In man, some of these factors can be detected
because a relatively long childhood and reproductive span
permit the factors to work over a prolonged period oftime.
74. With some hereditary diseases and defects it has
been observed that mutant frequency among offspring
increases with parental age. Such conditions are epiloia,
neurofibromatosis and retinoblastoma. This effect of timesuggests a simple dependency of mutation frequency on
the accumulated dose of the causal factor. Here, by implication, some cumulative influence is involved. 39 In
other conditions, such as Down's syndrome, an increasein mutant frequency accompanies rising maternal age but
not rising paternal age. Again, a contrasting situation
holds with achondroplasia, where the increase in theoccurrence of the anomaly is associated only with risingpaternal age. Each of these latter examples suggests thepresence of influencing factors which are not common
to both sexes. Thus, when paternal but not maternal age
affects mutant frequency, a dependence of mutation on
frequency of cell division in gametogenesis may be
involved.

NATURALLY-OCCUIDUNG CHRO:MOSOME ABERRATIONSIN EXPERIMENTAL ORGANISMS

71. In the mouse, non-disjunction of se..x chromosomes
has been shown to occur in meiotic divisions. However,non-disjunction in the first meiotic division is rare in themale and possibly non-existent in the female. In contrast
to man, XO karyotypes occur much more frequently thando XXY karyotypes. 85 There is evidence that XO individuals most often result from the loss of the paternal sex
chromosome some time between sperm entry into thevitellus and the first cleavage. This evidence is based on
the observation that when XMO and XMXPy mice arescored simultaneously (the superscripts M and P desig-

9175. A number of factors are known to affect natural
mutation frequency in experimental organisms. One of
the most studied of these is se.x; the spontaneous mutation .rate to sex-linked recessive lethals is apparently
lower in females than in males of Drosophila. 95 • 96 An
effect of sex on mutation frequency in the silkworm has
been noted. Here locus specificity is a factor; at one locus
the frequency of mutation is higher in the male, at another it is lower. 97 In the mouse, the data on seven lociunder detailed study provide some indication that mutation frequency is lower in females than in males (table
X). Females have yielded one mutant among 98,828 offspring. In contrast, males have yielded thirty-two
mutants among 544,897 young. However, in man, a studyof mutation to the sex-linked trait, Duchenne-type muscular dystrophy, has provided no evidence of a sex difference.98

environmental changes. This concept has been formulated as a mathematical model by introducing what iscalled the principle of minimum genetic load. 115 A species
must adapt itself to progressive changes in the environment and the ability to do so comes from genetic variation, the ultimate source of which is mutation. The importance of new mutation for the future adaptation of thehuman species is problematical.
IV, The induction of mutation by radiation

81. For obvious reasons, most of our information on
the induction of mutation by radiation comes from experimental organisms. However, there is ample evidence
that the mutation process is fundamentally similar in all
forms of life and there is no reason to suppose that man
is exceptional in this respect.

76. Genetic constitution can also affect the frequency
with which naturally-occurring mutations are found. A
number of specific genes in Drosophila have long been
known to modify the natural mutation rate by a factorof ten or more over at least a segment of the entire
genome. 99 A difference between two geographical races in
the frequency with which sex-linked lethals are produced
has been demonstrated.100 In addition, there is no doubtthat the mutation rate varies with different loci. The
mutability of a gene is also affected by its position in thechromosome. 827 • 828

FACTORS AFFECTING THE FREQUENCY OF
RADIATION-INDUCED MUTATION

82. The genetic hazards to populations cannot be determined in the absence of a knowledge of the relationship between frequency of mutation and dose of radiation. It is now well recognized that many factors caninfluence this relationship. The foundation for our
knowledge in this field was laid through investigations
with Drosophila. More recently, studies with mammals
have yielded significant information.

77. In man, tendencies towards diverse chromosome
aberrations in the same individual and towards familial
occurrence of diverse chromosome aberrations have been
noted. For example, cases of Down's syndrome ( trisomy21) and Klinefelter's syndrome (XXY) in the same individual have been described. 101-1° 5 Associations of XXY
with a translocation between chromosomes 14 and 1510•
and of XXX with trisomy 18107 have been reported.
Trisomy for the 13-15 group and an XO constitution has
been noted in two sisters.108 Trisomy 21 has been reported in the progeny of a female carrying an autosomaltranslocation.109 Such clustering of gross chromosome
aberrations has led to the suggestion that the cells of someindividuals may be labile in this respect, 21 or that theoccurrence of a first aberration predisposes the chromosomes of a cell towards a second. 84

Li11earity of the dose-effect relationship and absence ofa threshold

83. The assumption of a linear dose-effect relationshipdown to zero dose, and thus of an absence of thresholdfor mutagenic effects has been considerably strengthenedby the results of investigations with Drosophila. Studies
of mutations at more than fifty loci which affect minutebristles have indicated that acute doses as low as 5 r havea significant mutagenic effect and that the dose-effectcurve is linear from lower to higher doses.117 A linear
relationship in the low dose range down to 5 r has also
been found for radiation-induced recessive lethals.118
However, in germ cell stages such as spermatogonia andoocytes, where the repair of some of the pre-mutational
damage is possible, the effect at low doses may tum out
to be somewhat less than expected on a linear basis fromthe mutation frequency at high doses.119 A departurefrom linearity has been found for mutations induced withhigh doses of acute radiation in mouse spermatogonia. A
dose of 1,000 r produced significantly fewer mutations
than expected on the basis of linearity with results atlower doses. 120 The view that this effect might be due tocell selection gains some support from the finding thatfractionation of the dose gave a higher mutation rate
which was consistent with linearity.121 In E.coli, evidenceof a linear relationship down to doses as low as 8.5 r
has been presented. 122

78. There is evidence that natural mutations occur atdifferent rates in cells in different stages of gametogenesis. Relevant investigations in Drosophila have recently
been reviewed. 72 Some loci are more mutable in the germline than in the soma, while for others the reverse
applies.110
79. No doubt other as yet unrecognized influencing
factors exist. For instance, a significant increase in thefrequency of sex-linked recessive lethal mutations has
been reported in each of two strains of Drosophila as aconsequence of space flight. 111 Similar circumstances arealso reported to result in an increased frequency of chromosome anomalies (non-disjunction) in germ cells of
Drosophila. 112 The intensity of cosmic radiation during
flight was insufficient to account for these phenomena,
and an influence of some other factors must be suspected.

The dose-rate effect

84. The rate of delivery of ionizing radiation has now
been demonstrated to affect the frequency of mutations
induced by a given dose. This has been shown for bot11
mice and insects.
85. In mice, the effect of differences in dose-rate on
the frequencies of mutations induced at seven specific locihas been studied.119• 1 21 • 1~ 3-127 It has been observed that(tableX):

80. It has been hypothesized that the genetic responseof a species to the factors influencing mutation rate isitself modified through selection. This concept presupposes the existence of an optimum mutation rate for survival of a species ;11s-115 if the mutation rate is too highthe species may be crushed under a heavy mutational load
and if it is too low the species may not be able to adapt to92

(a) When spermatogonia are exposed to doses of300-600 rat a rate of 8.5 X 10-3 r/min (90 r/week), thefrequency of induced mutations is less by a factor of
about four than is the frequency following the same dosedelivered at a rate of 90 r/min;( b) There is an even more pronounced .dose-rate
effect in parallel studies of irradiated oocytes ;( c) The dose-rate effect for spermatogonia is notdemonstrably greater when the lower rate of delivery is
reduced from 8.5 X 10-3 r/min to 1 X 10-3 r/min;( d) Most of the dose-rate effect in spermatogonia isdisplayed within the range of 24 r/min and 0.8 r/min,whereas in females the range of effectiveness appears to
be greater;(e) As in Drosophila, no dose-rate effect is evident inspermatozoa.

However, there are several lines of evidence including
the shape of. 0e dose-effect curve, that sugg~st that, alt~ou~h multi-hit aberrations are easily induced by radia~on m ~ouse spermatozoa, the specific-locus mutations
11?-duced 1;I1 mouse spermatogonia are almost never associated with such multi-hit effects. .Most mutations in
Droso P!iil~ sperma~ogonia c:Iso appear not to be a resultof mulh-hit a?errations. Th1s.evid~nce supports the viewthat. the specific-locus mut<3:t10ns mduced in spermatogoma of the mouse are pomt mutations or extremely
small deficiencies, ss, 136• 1 37 and that it is repair of the
pre-mutational damage associated with this type of mutation that is involved in the dose-rate effect. 1 ~ 1 Current
investigations in other organisms confirm the e..x.istenceof processes of natural repair or elimination of premutational (primary) damage at low dose rates. The
subject of repair will be discussed in detail in the next
section.

86. In Drosophila a significant dose-rate effect on
lethal mutations in chromosome II has been reportedwith irradiation of oogonia 128 and spermatogonia. 129 In
spermatogonia, a lowering of the intensity from 0.10
r/min to 0.01 r/min at a total dose of 200 r results in asignificant reduction in mutation frequency. However, adose-rate effect for contrasting doses of 2 r/min and2000 r/min at a total dose of 3,000 r gamma radiation has
not been observed. In the silkworm there have beenfound two different types of dose-rate dependence ofmutations affecting egg colour and induced during earlylarval development. 97 In one type the mutagenic effectiveness of chronic irradiation at 0.15 r/min is lower thanthat of acute irradiation at 320 r/min, and in the otherthe mutagenic effectiveness is higher with chronic irradiation than with acute irradiation. The former is observed
only in the very young larval stage_ when primordial cells
are prevalent in the gonads, whereas the latter is foundwhen germ cells are irradiated in later stages of development. This latter result, which is opposite to the expected
effect of dose rate, may not be a dose-rate effect on themutation process, for it is suspected that cell selection is
reducing the yield of mutants at the high dose rate. In any
case, it resembles an effect observed at a high dose ratein the mouse, where a dose of 1,000 r gave fewer mutations than a dose of 600 r. 12° Cell selection was invokedto account for this odd result also. In the chalcid wasp
Dahlbominus no significant dose-rate effect on mutations
affecting eye colour has been found when female larvae
receive a total dose of 1,000 rat 1,000 r/min and at 0.17
r/min.130''Repair'' of pre-mutational damage

88. Studies of a variety of organisms have indicatedthat the process of induction of mutation is not irreversibly fixed at the time of irradiation, but that there isa limited interval between the absorption of radiationenergy and the completion of the mutation process during
which, depending on the physiological state of the cells,
modification of pre-mutational damage is possible. Repairof broken chromosomes by restitutional unions of the
breakage ends has been known for a long time and has
been studied in some detail. The subject has recently
been reviewed. 138 Though there are some reasons to thinkthat restitution and recovery from pre-mutational damage are separate though analogous phenomena, this distinction has not been established by e.."'\:perimental means.
89. In Paramecium, post-irradiation treatments are
known to alter the e..'<:tent of recessive damage from agiven radiation exposure, provided they are applied before a certain critical stage has been reached in thesubsequent division cycle. Moreover, in cells not receiving post-irradiation treatment, the effect of irradiation isincreased the later it is administered prior to that criticalstage.139- 141 It was shown earlier that a large fraction of
the mutational effect of exposure of bacterial cells toionizing radiation can be reduced by post-irradiation
treatment with chemical reagents in certain circumstances.14~ A similar pattern of results has been observed
when investigators have worked with UV instead ofionizing radiation.14 3-150 It now appears that all theseresults are consistent with the hypothesis that the terminal event for fixation of some major part of the potential mutation corresponds to the first post-irradiation
replication of DNA.1 H,H 7 • 148 • 151
90. Recent data obtained with Drosophila show thatmodification of pre-mutational damage is possible inspermatids, meiotic stages, and late spermatogonia. 152- 157
In cells with peak sensitivity, spermatids and spermatocytes, post-treatment with cyanide following exposure to
X-rays at a high dose rate may lead to either an increaseor a decrease in radiation-induced mutation frequency.
Inhibition of oxidative respiration by means of posttreatment with nitrogen causes an increase in mutation
frequency in spermatids, meiotic stages, and spermatogonia. On the other hand, fractionation of a dose given
at an intensity of 55 r/sec results in a decrease of themutation frequency in exactly those stages where cyanide
is effective. Inhibition of protein synthesis by means of
pre-treatment with either chloramphenicol or ribonuclease leads to a significant reduction in the frequency ofmutation in spermatids, and in the case of chlorampheni-

87. Although some of the factors that affect the doserate phenomenon have been uncovered, investigation has
not yet proceeded far enough to elucidate the mechanism
involved. Nevertheless, there is strong evidence that it is
the mutation process itself which is affected. Thus, cellselection, which may at times play a role, can, in somespecific instances, be eliminated as the causal factor. For
example, the effect is observed in those mouse oocyte
follicle stages in which cell-killing by the doses of radiation used is negligible.11 9 • m Furthermore, the amount ofspermatogonial killing induced by radiation is approximately constant over a range of dose rates in which thedose-rate effect on mutation is evident.125 • 1 31 •m If themechanism for the dose-rate effect does indeed involvethe mutation process itself, then it seems likely that somekind of "repair" of pre-mutational damage must be taking place at the lower dose rates.119 It has been suggested133 that many of the mutations observed at theseven loci under study may be a consequence of multi-hit
chromosomal aberrations which would be e.."'\:pected tooccur with reduced frequency at low dose rates. 134• 135
93

col, in the earlier stages as well. Since a ring-shaped X
chromosome has been used in such experiments, thereported changes refer to lethal gene mutations and pos~sibly to small deletions. These results have been explainedby assuming that, in analogy to the findings in Paramecium, two contrasting processes are involved, one
associated with the rate of disappearance of pre-mutational damage, the other with the time or rate requiredfor its fixation. 141 Thus, the enhancement of mutation
frequency after post-treatment with nitrogen is thought
to result from an inhibition of the metabolic repair
process. On the other hand, the reduced mutation frequency observed after pre-treatment with both chloramphenicol and ribonuclease suggests that inhibition ofprotein synthesis prolongs the time-span available forrepair of pre-mutational damage. Although it is notknown at present what process is involved in fixation ofpre-mutational damage in spermatids, the reported findings suggest a correspondence of repair mechanisms insuch. widely difierent organisms as Drosophila and Para-

all thirty-ei~ht at the locus s were lethal. In contrast, of
t:I;ose at loci b, c and p, twenty out of thirty-eight wereviable.

S ez and stage of gametogenesis
94. The frequency of radiation-induced mutations canbe influenced both by sex and by stage of gametogenesis.
Th~ c.ell stages of greatest importance in determining
ra~at10n hazards to man are the oocyte and spermatogomal, and the genetic effect of ionizing radiation onthese stages of the germ cells of mammals has received
considerable attention. 166-168 The most extensive investigations have been concerned with the mouse.
~5. ¥ale i;nice i~r_adiat~d with doses as high as 1,000 r
mamtam their fertility briefly, and then undergo a periodof sterility. Near-normal fertility is then resumed. The
temp?rary sterility is a consequence of the fact thatcertam spermatogonial stages are eA-tremely sensitive toirradiation. 169 • 17° Cells in these stages have an LD 50 of
20 to 40 r. However, a few of the early type A spermatogonial cells survive high radiation doses ; these cells
repopulate the germinal epithelium and are responsible
for the resumption of fertility of the irradiated animal.
The existence of the sterile period aids in distinguishing
between genetic effects induced in spermatogonial andpost-spermatogonial stages.

mecmm.
91. The interaction of oxygen and X-rays in the production of genetic damage, as detected in the progeny oi
irradiated males of Drosophila, has been studied extensively.158-165 Dose-fractionation experiments, in whichpart of the dose is delivered in nitrogen and part in airor oxygen, indicate that X-irradiation destroys a protective oxygen-sensitive system. It has been variously postulated that this system acts to reduce the initial amow1tof damage and that it acts to increase the amount of
repair. The system affects both recessive lethals andchromosome aberrations.
92. Table VII summarizes some of the phenomena andmaterial studied both before and since the drafting of
the Committee's 1958 report. The similarity of the effects
observed is striking, considering the wide range of organisms observed. From these data it can be concluded
that a proportion of radiation-induced mutational or premutational changes are subject to natural repair for a
finite but relatively brief period after they occur, and thatthe natural repair process itself is subject to interference
by radiation and by metabolic inhibitors. It is important
to determine whether this effect is applicable to man, andif so, the single dose-levels or continuous dose-rates atwhich the natural repair processes are effective, and thecritical period of tin1e and the circumstances under which
they act. It is emphasized that probably not all premutational damage is reparable and that a linear dosemutation relationship independent of dose-rate is to be
expected at low doses which do not appreciably affect the
repair process.

96. Irradiation of female mice with doses as low as
50 r can result in permanent sterility after an initialperiod of post-irradiation fertility. A dose-rate effect on
this induced sterility has been detected.171 The permanency of induced sterility is attributable to the fact thatthe majority of oocytes are in early stages of folliculardevelopment, and are extremely sensitive to radiation ..
Since there is no new formation of oocytes in the adultmouse ovary, sterility sets in when the supply of radioresistant oocytes in older follicles is exhausted.
97. It has been possible to distinguish two kinds ofradiation-induced cell death in different types of germ
cells in mouse gonads. Most spermatogonia die immediately after irradiation, while spermatocytes show no
response until they reach the meiotic divisions. In bothcell types, chromosome damage in the classical sense of
aneuploidy can, at most. account for only a small part ofthe cell loss.172 A similar situation has been found in the
rat-kangaroo. 173 These studies suggest that chromosomal
damage is a minor cause of cell death in spermatogonia
irradiated with moderate doses. The subject of the radiosensitivity of the gonads is treated more fully in annex D.
98. Peak sensitivity to the induction of dominantlethals and recessive visibles in the mouse has been foundin spermatids and spennatocytes11'°"178 for the male, andmetaphase primary oocytes for the female. 179 With anacute dose of 300 r of X-rays, the mean frequency formutations at specific loci following irradiation of postspennatogonial stages is twice that induced in spermatogonia.178 It has also been shown that exposure of adultfemales to an acute dose of 200 r of X-rays results inmore mutations than a similar e..xposure of 17~ day old
foetuses. In males the induced-mutation frequency has
also been observed to be higher in adults than in foetuses,
but the difference is not statistically significant. 175

Lorns specificity
93. Both the natural and induced rates of mutation
have long been known to vary markedly at different lociin various organisms. This observation has now been
firmly established in the mouse. 85•136 Among the sevenloci under study, the lowest and highest rates for mutations induced in spermatogonia differ by a factor of
thirty. This information is based on 174 mutations induced with doses of 300-1,000 rand high-dose rates. Of
these, seventy-one mutations were induced at locus s,ninety-nine were induced among the four loci, b, c, d andp, and only four were induced at the two loci, a and se.
Ninety-two of the mutations were analysed for viabilityof the homozygotes. Seventy-one (i7 per cent) were
lethal prior to maturity and twenty-one were viable.
There was some variability among the seven loci in thisrespect also. All the t\velve mutations at the locus d and

99. The ratios of induced mutation frequencies at theseven loci under study in mice differs with irradiationof spermatogonial and post-spermatogonial stages. 88 •13"
Deficiencies large enough to involve both the d and seloci (with cross-over value of 0.16 per cent) are common
among the mutations induced in post-spermatogonial94

cells, but irradiation of spermatogonia yields such deletions only with extremely low frequency, if at all. Such
deficiencies are, however, induced in oocytes. It thus
seems that mutations contributed to progeny as a resultof spermatogonial irradiation differ systematically fromthose due to post-spermatogonial and oocyte irradiation.
100. In Drosophila, the influence of se.x and stage of
gametogenesis in radiation-induced mutations is well
documented. 12 •1 50 • 1 81 •329 The lowest and highest freguencies of induced mutation for a given radiation dose varyby a factor of fifteen. Spermatogonia and oogonia are theleast sensitive; oocytes are somewhat more sensitive thanoogonia. In contrast, spermatocytes and spermatids areseveral times more sensitive than spermatogonia. Spermatozoa -vary in sensitivity depending on their stage ofmaturity. The difference in radio-sensitivity between
Drosophila sperm and spermatids is attributable both todifferences in 02-tension 164 • 182-186 and to changes associated with protein synthesis.m-155

guide to those effects which might be e.xpected. They arebriefly summarized here.
.104. Most of the Drosophila information has been obtamed through irradiation of spermatozoa. Aberrations
are de~ect~d in ~i~er the first or subsequent generationsf<;>llowmg 1rrad1ation. Cytological as well as genetic techniques can be used for this purpose.
105. V~ble aberrations resulting from chromosome?reakage mclude duplications, deficiencies, and intra- or
1i:ter-chro?1osome rearrangements. The ability of individuals :v1th deficiencies or duplications to survive thisaneuplo1dy d~pends upon the length and genie content of
the segments mvolved. Both duplications and deficiencies
upset genie balance, and tend to lower viability and to betransmitted as recessive lethals. Viable intra- and interchromosome rearrangements include inversions andtranspositions of segments within chromosomes as wellas translocations between chromosomes. These' aberrations do not involve aneuploidy, and affected individuals
are phenotypically normal if "position effect" is not involved. However, their progeny may be geneticallynormal, or again contain the balanced rearrangement, orbe aneuploid.

Species specificity
101. Species differ widely in their genetic sensitivity
to radiation. The induced rate of mutation at the sevenloci studied in mice is about fifteen times that for a comparable group of loci in Drosophila. 181 Comparisons ofdominant lethals in mammals and Drosophila188 and ofchromosome mutation in plants189 have likewise indicatedthe existence of species specificity. Radio-sensitivity indifferent species of rodents has been determined in termsof the number of chromosome rearrangements in the
nuclei of spermatogonia exposed to a low acute dose of
4 r.uo, i 9 i Such measurements are difficult to make because the frequency of chromosome breakage varies
greatly in different cell stages, a fact which can lead tothe confounding of species and cell-stage differences.
Nevertheless, the percentage of cells with rearrangements
has been reported to vary from 2.6 in guinea pigs to 0.6
in rats, 0.2 in mice, and 0.1 in rabbits. A comparison of
the cytogenetic radio-sensitivity of germ cells of themonkey and mouse at doses from 50 to 400 r has suggested that sensitivity of monkeys is twice that ofmice.1ss, 1s2106. At low doses, the frequency of individuals withaberrations caused by single breaks tends to increaselinearly with dose. In some instances it has been notedthat small intercalary deficiencies also increase linearlywith dose. The frequency of individuals with aberrations
caused by two breaks, such as inversions and translocations, increases more rapidly than the first power of thedose, approaching the second power of the dose at lower
levels of treatment.
107. Whole-chromosome aneuploidy in Drosophila isalso caused by ionizing radiation. The induction of primary non-disjunction was first reported in 1921.19'• 195
Using irradiated females of Drosophila virilis it has been
demonstrated that there is a linear increase in the occurrence of primaryXO males in the dose-range400-l,200 r,
and that the induced rate of occurrence of XO males isapproximately 1 X 10-5/r/egg.196•197 The rate of occurrence of XO males is approximately fifteen times that of
XXY females. The ratio of XO :XXY flies is thus
greater than the naturally-occurring ratio which is about
4:1. l\fore recently a similar investigation has been carried out with Drosophila melanogaster.93 With exposure
to doses of 600 r, 2,400 r, and 3,600 r, the frequency of
non-disjunctional males increased at a rate of approximately 2.5 - 3.0 X 10-5/r. Non-disjunctional males
were more frequent than non-disjunctional females by
about one order of magnitude.

INDUCED CHROMOSOME ABERRATIONS

102. Because some serious hereditary defects in man
have recently been found to be associated with chromosome aberrations, the role of ionizing radiation in producing these anomalies will be considered in detail. The
fact that radiation can cause extensive chromosomechanges has been known for many years; investigations
in plants193 and in animals 90 have been reviewed in detail.
Actually, it is not always possible to make a sharp distinction between gene mutation and chromosome aberration.
Minute chromosome aberrations often cannot be distinguished from gene mutations. Furthermore, rearrangements of chromosome segments sometimes involve"position effects" in which the phenotypic e.xpression ofgenes is altered. 85

108. In mice, gross chromosomal anomalies are rarely
found as a consequence of irradiation of parental premeiotic germ cells. This rarity has sometimes been attributed to failure of transmission rather than to lack ofoccurrence. However, for at least two types of chromosomal aberrations, reciprocal translocations and deletions, this e.-..;:planation does not seem to be correct.
Translocations induced in post-meiotic stages can betransmitted through subsequent meioses to become heritable traits.166 Thus, a more likely explanation for therarity of these aberrations following pre-meiotic irradiation is either that the necessary chromosome breaks do
not occur or that the broken parts do not e.xchange. The
same situation exists for deletions. An exhaustive studyof what appear to be deletions in the d-se region of linkage group II in the mouse has shown that these are produced as a consequence of post-spermatogonial andObservations on experimental organisms
103. One of the most suitable organisms for studies of
induced chromosomal changes is Drosophila,· in thisorganism small chromosome changes can be detected
cytologically by e.-..;:amination of salivary gland chromosomes. Furthermore, detailed information on the linear
sequence of specific loci is available. Although observations made with this organism cannot be used for direct
extrapolation to man, they nevertheless serve as a useful95

oocyte irradiation, but not of spermatogonial irradiation.88 Transmission of the induced deletions ranges
from poor to normal or near normal. Since transmission
is possible, it is apparent that either lack of breakage orrejoining is responsible for the non-appearance of thedeletions following· spermatogonial irradiation.
109. Some types of chromosomal damage are, however, produced with high frequency by irradiation of
spermatogonia. Many abnormal anaphases have beenfound in spermatogonial cells of monkeys two years after
exposure. 198 More recently, cytological evidence of chromosome damage in irradiated spermatocytes has been
noted at the first post-irradiation cell division in mice.172
Those particular types of aberration probably cause cell
death before maturation of the gametes. However, a
recent report suggests that structural changes induced in
pre-meiotic germ cells can occasionally be transmitted toprogeny.100
110. Data on the induction of whole-chromosomechanges in the mouse are at present largely restricted to
sex-chromosome changes. Experimental work in thisfield has developed rapidly in recent years. 85 The availability of useful sex-linked marker genes and improvement in cytological techniques have contributed to thisprogress. The sex-determining mechanism of man has
recently been shown to be much more similar to that of
the mouse than it is to that of Drosophila.
111. In mice, irradiation of sperm increases the frequency with which paternal sex-chromosomes are lost:
1.3 per cent of progeny suffered such a loss after a doseof 600 r as compared with 0.1 per cent in the control.200·201 HoweYer, the bulk of spontaneously occurring
XO individuals are believed to arise from events following sperm entry into the vitellus. 85• 202•203 Irradiation of
the zygote in the interval between sperm penetration andthe first cleavage is particularly effective in inducing lossof a sex chromosome. Thus, 100 r yielded S per cent XO
individuals as compared with 1 per cent for controls. Bothmaternal and paternal losses can be induced by radiation,
whereas only paternal losses have occurred in the controls. No autosome loss has been detected in these experiments in which four and in some cases five autosomes
carried genetic markers. This suggests that such losses,
if they occur with an appreciable frequency, are lethal.
112. Extensive investigations of the in vitro cytogenetic effects of radiation on mammalian somatic cells
have been undertaken. Although from the point of viewof heredity the important chromosomes are those of thegerm cells, these studies of the radio-sensitivity ofsomatic cells provide a direct method for determining theeffect of radiation on chromosomes. It is to be expectedthat they will play an important role in the future. Measurements are usually based on the frequencies of aberrations detected at the first post-irradiation cell divisionbecause many types of aberration are lost in subsequentdivisions. Commonly-used mammals include the Chinese
hamster, 20 4-we the mouse 201- 209 and the monkey.wa
113. Most of the previously known types of aberrations have been detected in these investigations. Breaks
are of the chromatid or chromosome type depending upon
whether the chromosomes are effectively double at thetime of irradiation. Data on the frequency of breaks are
not always in good agreement and it is apparent that oneof the influencing factors is the method by which cells
are cultured. Nevertheless reproducibility of results isgood under standard conditions.
114. As is to be expected, terminal deletions increaselinearly with the dose but total breakage occurs more fre-quently than the first power of the dose. 206 At low dosesa measure based on linearity is of practical use but a moreaccurate measure of damage is the "coefficient of aberration production". 210 Values for chromatid aberrations invitro cultures of epithelioid-type cells of monkeys andChinese hamsters have been found to be in general agreement with those for Tradescantia microspores. 211
115. With experimental mammals it is possible tocompare the in vitro and in vivo rate of induction ofvisible chromosome aberrations. Somatic cells cultured
in vitro frequently have a much higher spontaneous mutation rate than do in vivo cells. 211 However, investigations with Chinese hamsters and with monkeys indicatethat the radiation-induced aberration rate of epithelioidtype cells cultured in vitro is not greatly different fromthat of rapidly dividing cells in vivo. 205• 200

Observations on human cells
116. No measure of the radiation sensitivity of humangerm cells has yet been made. Nor have extensive quantitative measurements been made of chromosomal damage induced in somatic cells of individuals. However, it
has been clearly shown that chromosomal aberrations areproduced.' 6 • 212- 210 This subject is dealt with in annex D,paragraphs 155 to 158.
117. The effect of ionizing radiation on chromosomesof human cells cultured in vitro has received considerable
attention in recent years. 2060211-223 As with e.-x:perimental
mammals, data on the frequency with which breaks occur
are not in good agreement. For epithelioid-type cells theobserved rate at metaphase is about 0.3/cell/100 r2 00 • 217
but for "fibroblasts" the rate is about 2/cell/100 r. 218 • 220
The frequency of chromosome breaks has been reported
to be 0.9/cell/100 r for fibroblast-type cells 220 and 2/cell/
100 r for leucocytes in freshly-drawn human blood. 222
The coefficients of aberration production for chromatid
breaks in epithelioid-type cells in vitro and for chromosome breaks in leucocytes are in remarkably good agreement with those for Tradescantia miscrospores and forchromatid breakage in epithelioid-type cells of themonkey and Chinese hamster. 222
COMPARABILITY OF RADIATION-INDUCED AND
NATURALLY-OCCURRING MUTATIONS

118. Mankind has long been exposed to natural radiation and it is to be e.-x:pected that an increase in the levelof exposure would not result in any mutations whichhave not occurred in the past. Nevertheless, naturalradiation is only one of the causes of "spontaneous"mutation and it is therefore possible that there may bedifferences between the spectra of radiation-induced andnaturally-occurring mutations.
119. Evidence concerning the comparability of thetwo sorts of mutations was presented in the Committee's
last report. 22 • Most of this information came from studies
with lower organisms and suggested that, in general,mutations induced by ionizing radiation are similar inkind to those of natural origin.
120. There is evidence that in Drosophila the radiation-induced and natural rates of se..x-linked recessive
lethal mutations are similarly affected by sex and stage of
gametogenesis.~ 2 Close correspondence between induced
and spontaneous mutations is not found, however, inmice.137 Furthermore. in mice loss of the maternal X
chromosome can easily be induced by irradiation but
spontaneous maternal loss is very rare. 85 There is also
96

'.Lvailable methods for. det~ctir:g induced ~enetic damage
m humans and for estrmatmg its extent. Six such studies
have been reported. 225 • 221• 235 - 235 In interpreting the results, the effect of maternal irradiation is more appropriately considered independently of the effect of paternal irradiation. The effect of maternal irradiation on the
proportion of male offspring is summarized in table VIII.
A consistent reduction in proportion of male offspring
has occurred following maternal irradiation. In terms of
the simplest genetic interpretation, this can be attributed
to the induction, in irradiated women, of se.'<-linked recessive mutations having a lethal effect on the foetus. The
effect of paternal irradiation is summarized in table IX.
These latter data are not amenable to a single interpretation; the proportion of male offspring is apparently increased with higher doses, but, in at least some instances,
reduced with low doses. The former effect is interpretable in terms of the induction of dominant se.x-linked
lethals. However, the validity of such a simple genetic
interpretation has been questioned on the grounds that the
Y chromosome cannot be considered genetically inert. 239
In addition, the induction of XO and XXY karyotypes
may also affect the relative frequency of male and female
offspring. Furthermore, e.xplanations based on the assumption that the effect on sex ratio is due to damage tosex chromosomes cannot be accepted without reservation.
For instance, the drop in proportion of males which has
sometimes been noted could be attributed to autosomal
mutations which further increase the e.icisting higher
mortality of males. The occasionally erratic control
Yalues must also be considered in any interpretation.

very good evidence from E. coli that the natural mutabilities of loci are sometimes not correlated with theirradiation-induced mutabilities.m
V. Effects obsenred in descendants of irradiatedpopulations
INDUCED MUTATIONS IN THE IMMEDIATE PROGENY OF
IRRADIATED HUMANS

121. Direct observations of the genetic consequences
to man of exposure to ionizing radiation are now limited
to observations of first-generation offspring. Such surveys can be expected to detect only autosomal dominantor se.x-linked gene mutations and chromosome aberrations. Among the difficulties of such inquiries are thoseof estimating the gonad doses actually received by parents, and the small absolute and relative increases to be
expected in the frequency of traits determined by suchmutations.
122. In these surveys, the data are usually concernedwith such matters as abortion, still birth, neonatal death,congenital malformation, and shifts in the sex-ratio ofprogeny. Results frequently indicate a detrimental effectof radiation but this is seldom statistically significant.
One study detected a significant effect of radiation on tlle
frequency of congenital malformations in the progeny ofirradiated individuals but interpretation is hampered by
the incomplete response to the questionnaires used.m
Another similar study failed to show this effect. 226 The
most e.xtensive survey was carried out in the Japanesecities of Hiroshima and Nagasaki following the atomic
bombings ; data were collected on more than 30.000 offspring of irradiated parents and on a comparable control
group. 227 Observations were made of still births, neonatal
deaths, birth weight and congenital malformations. Analysis of these data failed to detect a significant effect ofradiation on either the frequency of early death or congenital malformations. It did, however, detect a significant shift in the sex-ratio of immediate progeny. Morerecently, an analysis of the sa.m~ dat~ b~ an independ~t
investigator has produced statistical significance of radiation effects for some other categories of defects and also
for over-all early death of progeny. 228 • 229
123. The comparatively high frequencies of Down's
and Klinefelter's syndromes permit the effect of parental
irradiation on the incidence of these defects in offspring
to be studied with relatively little effort. Three such investigations have already been reported. In one of these
the radiation history was obtained of the mothers ofeighty-one children with Down's syndrome, ninety-one
children with cleft lip and seventy-one children with nodefect. A possible association between maternal irradiation and Down's syndrome was indicated. 230 However,results of the other two investigations, one of which involved fifty-one patients with Down's syndrome andfifty-one controls, 231 the other 197 patients and 197 controls,232 were completely negative.
124. A survey of the incidence of congenital malformations in different regions has indicated that higher incidences are associated with geographical areas with highbackground radiation. 233 Another survey has reported
that the frequency of malformation varies with the geomagnetic latitude to which is related the cosmic-ray
energy flux. 23• However, it is difficult to prove that natural radiation is the direct influencing factor.
125. A shift in the proportion of male offspring of
irradiated individuals has been considered one of the best

INDUCED :MUTATIONS IN THE IYYEDIATE PROGENY OF
IRRADIATED MAMMALS

126. By means of properly controlled e.xperiments it
is possible to detect induced dominant mutations in ~e

immediate progeny of ir!adiate~ m_ammals. Curr~nt mformation has been obtamed pnnopally from mice. In
mammals it is particularly difficult to distinguish between
gene mutations and minor chromosomal changes.
Reduction in litter size, following irradiation of spermatozoa or oocytes, is most plausibly e.xplain~d in terms of
the induction of chromosome aberration, althoughgene mutations may also be involved.
127. Spermatogonial cells and oocytes are of greatest
concern in a consideration of radiation hazards. Oocytes
are not replenished, and it has been shown that there isno significant change in mutation rate with time after
irradiation of spermatogonia.m Irradiation of spermatogonia has much less effect on litte~ size than does irradiation of later germ-cell stages. This no doubt reflects adrastic reduction in frequency of gross chromosome
aberrations. For instance, individuals with deficiencies
involving more than one gene locus ai:e commonlr fou~dafter irradiation of post-spermatogornal cells but irradiation of spermatogonia yields such deletions only withe..'<tremely low frequency, if at all. These aberrations do
occur, however, among progeny produced after irradiation of oocytes. 88 • 137
128. The fact that dominant detrimental mutations are
induced and transmitted after irradiation of post-spermatogonial stages has been demonstrated by a shorteningof the life span in the offspring of male mice exposed toneutrons. 241 In another study, a significant increase incertain types of skeletal abnormalities was found in thefirst-generation descendants of irradiated male mice.m
Evidence that some dominant lethality is transmitted
after irradiation of spermatogonia has been provided by97

analysis of the cause of litter-size reduction following
exposure to 1,200 r. 199 The same data indicate that translocations are occasionally found in progeny following
irradiation of spermatogonial cells.

gators. hai.:-e adopted the procedure of expressing induced
mutation m terms of the resulting increase in the genetic
component of the variance, with or without reference toth~ genetic component ob_se:"ed in natural outbred populat10ns. The. extent of this mcrease has, in general, beenmeasured either directly by variance analysis or indirectly ~y calculation of the capacity of an irradiatedpopulabon to respond to selection. Pertinent informationfrom e..xperiments concerned with natural and radiationinduced mutation rates is summarized in table XL

129. The specific-locus method of detecting mutations
in mice has yielded further information on the dominanceof mutations induced in spermatogonia. About threequarters of all the induced mutations have been recessive
lethals. However, some of these have a visible effect on
the beterozygote. 1ss In a freely-breeding population thesemutations might well produce greater total damage asheterozygotes than as homozygotes.

133. Such experiments are of special value in indicating whether the genes determining polygenic traits differ
in thei; pattern of mu!ability from those individually
recognized through discrete changes. Estimates ofdoubling dose for abdominal and sternopleural bristles in
Drosophila agree well with those for major genes. 252 On
the other hand, the estimated induced rates for polygenes
controlling viability are high. 253

130. In mice, several studies of the effect of paternal
irradiation have not revealed any consistent effect on thesex ratio of offspring.166 • 239• 248 Another comprehensive
investigation has shown that although the presence of
sex-linked recessive lethals in the second generation
progeny of irradiated males can be detected, neverthelesssex-ratio changes do not now provide a reliable methodof estimating the genetic hazards of radiation because of
the comple."\:ity of factors governing this ratio. 244 This
comple.x.ity has been emphasized by the fact that strain
differences in the ratio can be obtained through differential selection for low and high blood pH.m In fowl, asignificant decrease in the frequency of female progeny
resulting after exposure of male birds to 600 r has been
noted. m In Drosophila, most investigations have demonstrated some tendency toward an excess of males among
the progeny of irradiated males. 241 • 2 ' 11 A significant shift
in this direction has been reported recently. 2' 9 Researchon sex-ratio shifts needs to be continued m the hope oflaying a firm foundation for the application of thismethod in analyses of radiation-induced mutation in man.

134. Loss of genetic variance per generation in an
unselected, random-mating Drosophila population oflin;U.ted size is ont;v a small p~rtion. of the natural variability of the species. Polygemc traits are evidently wellbuffered against the effects of mutation. Thus the radiation damage from an increased rate of polygene mutation,although possibly considerable when summed over many
generations, is probably small in its impact on the firstfew generations. Variability in these traits may be maintained in part by a balance of selective forces, a possibility which further complicates the estimation of radiation-induced mutational damage to polygenic systems inan organism such as man, that cannot be directly e..'Cperimented on.
135. The learning ability, as measured by a maze test,of a population of rats which were irradiated in eachgeneration has decreased in preliminary experiments. 264
If further experiments exclude other interpretations,these results will support the view that radiation resultsin the induction of many small but deleterious mutations.
Again, a significant accumulation of recessive or sublethal mutations affecting ability to survive irradiation
has been reported in mice after ten generations ofchronic gamma irradiation.m

POLYG£NIC TRAITS

131. The subject of polygenic traits was treated atsome length in the 1958 report \vith special reference tointelligence, life span and birth weight.250 Attention was
drawn to the paucity of information regarding the inheritance of continuously varying, or quantitative, traits.
These traits, which are influenced to varying degrees bymany genes, present a special problem in the estimationof genetic hazards of ionizing radiation to populations.
For example, intelligence is influenced by certain raregenes having major effects and by a multiplicity of genes,
each with a small effect. In those instances where a mutation has a drastic effect on the trait, or concomitanteffects on some other trait, it is individually identifiable
and classed as a qualitative mutation. Mutations resulting
in such conditions as phenylketonuria and mongolism
belong to this category. Where the effect is less drastic
no such identification is possible. Furthermore, the frequency of mutations having minor effects is many times
greater than is the frequency of mutations having major
effects. Finally, a great deal of genetic variability withinthese traits is common in a normal population, and phenotype is, in addition, often strongly influenced by theenvironment. In such circumstances the relative contributions of heredity and environment to the over-alJ phenotypic \·ariability are difficult to determine. A few traits,
such as dermal-ridge count, are relatively unaffected byenvironment after birth; here a more accurate genetic
analysis can be made.251 However, the role of mutation in
supporting the genetic variability of polygenic traits has
defied any simple analysis.

VI. Interpretation
136. The preceding sections of this anne."\'. were concerned with the genetic concepts and information now
available for estimating the hereditary effects of anincrease in the level of ionizing radiation. The present
section considers the practical problems involved in formulating reliable estimates from this knowledge.
DIRECT APPROACH

137. An estimate of the genetic hazards of radiation
to man can, in principle, be obtained by a direct comparison of the descendants of irradiated with those ofcontrol populations. To be reliable, such surveys must be
e..xtensive, since most severe genetic defects tend to be
rare. Furthermore, many aspects of genetic well-being
must be considered and it is desirable to continue theobservations over many generations. These conditions
have not been fulfilled in any study to date. All surveys
made so far have, in addition, been hampered by problems of dosimetry and the difficulty of obtaining proper
controls. In the most extensive of these, that dealing withthe populations of Hiroshima and Nagasaki, the investi-132. Because rates of mutation of the individual genes
in a polygenic system cannot be studied, most investi-

98

gators were unable to detect a significant effect of radiation on either the frequency of early death or the occurrence of malformations. At least, this negative finding
suggests that the human genetic mechanism is not substantially more sensitive to radiation than are those ofother organisms that have been investigated. It has beensuggested that the acute dose required to double thefrequency of mutations causing the defects under study
is probably more than 10 r. 227 The Japanese survey
detected, as did others of lesser scope, a shift in the proportion of first generation male offspring suggestive of
the induction of se..x-linked lethal damage in irradiatedparents. The precise nature of this damage is not knownat present.

gene sometimes conferring reduced fitness, but neverconferring increased fitness, must be maintained entirely
by recurrent mutation. On the other hand, if a gene confers increased selective advantage in some circumstances,mutation may have only a minor influence on its frequency:
142. The extent to which such balanced selective
forces are responsible for maintaining hereditary disabilities in human populations is unknown at present. Of
the defects listed in section II, only among the specificdisabilities now recognized to have a high genetic component is it possible to discriminate between those thatare mutation-maintained (categories la and lb) andthose that are maintained by a balance of selective forces(category IV). At present, traits of category IV provide
but a small fraction of the total amount of serious illhealth of known or suspected genetic origin. Suitably
designed studies will undoubtedly produce more examples in the future. In the meantime, estimates of theimportance of balanced selective forces are dependent on
the use of indirect procedures or are based on conceptsof the genetic structure of human populations which have
yet to be confirmed.
143. 'When the prevalence of defective traits is maintained by recurrent mutation, the genetic hazards ofradiation can be estimated if the factor by which mutation rate will be increased by a given radiation dose is
known. However, when the frequency of induced mutations has been determined at only one dose it is necessary
to know the spontaneous rates to estimate the hazard.
Reliable estimates of spontaneous rates can be made only
when the genetic fitness of both homozygote and heterozygote is known. It is possible to measure fitness where
dominant traits are concerned. However, with recessive
traits it is difficult to determine genetic fitness of heterozygotes; as a consequence, reliable estimates of natural
mutation rates are rare. Point mutation rates so far
estimated cluster around the value 10 X 1~ per locus
per generation. The total mutation rate for grosschromosomal aberrations is now estimated at about 1
per cent per generation.

INDIRECT APPROACHES

138. Indirect approaches attempt to predict the genetic
consequences of e.."posure to ionizing radiations throughan understanding of basic genetic mechanisms and theirreaction to radiation. More specifically, estimates arederived through a knowledge of the prevalence of naturally-occurring hereditary ill health within a population,
the role of mutation in supporting this burden, and therelation between the dose of radiation and the mutation
rate in man.
The prevalence of hereditary diseases and de/ ects

139. There is probably a genetic component in the
aetiology of most diseases. It is now estimated that about
6 per cent of all live-born suffer at some time during theirlives from serious disabilities in which this component iseither known or suspected to be of major importance.
Without doubt the estimate of natural genetic burden will
increase with future research. In about one third of thesedisabilities, those of categories la, lb, and IV, the genetic
component is high and the underlying genetic mechanism
is understood. Of these defects, about half are associatedwith what appear to be specific alleles, and about half
are associated with gross chromosome anomalies. For theremainder of the defects, the developmental malformations and serious constitutional disorders of categories
II and III, neither the size of the genetic component nor
its underlying genetic mechanism is known with any
assurance. These disabilities are almost certainly heterogeneous in aetiology ; some are probably almost completely environmental in origin, but in others genotype
may be an important factor. However, even where theimportance of genetic constitution is suspected, the basic
nature of the fault is not clear; complex constellations ofgenes, specific alleles of low penetrance, or cytologically
undetected chromosome aberrations may be responsible.
140. The amount of recessive damage, that hidden inheterozygotes. has been estimated at 2-4 lethal equivalents and an equal number of detrimental equivalents.per
individual. When e..xposed by homozygosis, the lethal
equivalents are expressed as an increase in miscarriages,
still births and in neonatal, infant. and juvenile deaths.
The detrimental equivalents are associated with viablemalformations and overlap the previous listing to someextent. A comparable measure of genes producing recessive infertility has not been made. No similar method is
yet available for estimating the· amount of dominant
genetic damage within populations.

Dose-mutation relationship144. The genetic effects of ionizing radiations cannot
be understood without establishing a firm relationshipbetween frequency of induced mutation and the dose ofirradiation delivered. Most of the earlier information
about this relationship was accumulated from the resultsof experiments with Drosophila sperm. Past research led
to the working assumptions that: (a) the dose-mutation
curve is linear in the low-dose range, ( b) there is nothreshold dose, and ( c) mutation frequency is not dependent on dose rate over the range under consideration.
Much effort has been put into the task of either confirming or disproving these three assumptions. Recent investigations have strengthened the first two, but havedisproved the last. It has now been conclusively demonstrated that rate of delivery of radiation can have aneffect on the frequency with which mutations are found.
In male mice, low dose-rates of ionizing radiation produce one fourth as many mutations as do high dose-rates.
In females. this phenomenon is even more pronounced.
145. Recent research has increasingly emphasized thefact that radiation-induced mutation frequency can be
drastically affected by circumstances other than dose anddose rates:(a) Radiation-induced mutation rates may vary forgenes in the same species and this variation need not

The role of spontaneous mutation in maintaining thefrequency of hereditary disabilities

141. Various mechanisms by which detrimental traits
can be maintained in a population are well recognized. A
99

correspond to the variation in natural rates. In mice theinduced rates per unit dose in spermatogonia at sevenspecified loci may vary by a factor of thirty.
( b) Rate of radiation-induced mutation per unit dose
varies in different species. Furthermore. it has been reported that the frequency of cytologically observed induced chromosome abnormalities in spermatogonia of theguinea pig is nearly thirty times that of the rabbit, aclosely related species.
( c) It is clearly established that sex and stage of
gametogenesis can have a profound influence on bothspontaneous and radiation-induced mutation frequencies.
The existence of such interactions between radiation
effect and the circumstances of its delivery add to thecomplications of estimating radiation effects in humans.
For example, it increases the possibility that errors may
be involved in extrapolating from one species to another,from non-gonadal tissues to germ cells, and from one
germ-cell stage to another.

mates of doubling dose were consequently based on several other considerations. These included a simple genetic
interpretation of sex-ratio changes in man based on theassumed induction of sex-linked dominant and recessive
mutations having a lethal effect in tttero. Account was also
taken of the investigation of seven specific loci in miceand of extensive observations on sex-linked lethal mutation in Drosophila. As expected, advances in our knowledge have indicated that this estimate is in need ofrevision.
148. The usefulness of se..x-ratio changes in estimatinga doubling dose must be considered doubtful because ofinconsistencies in the sex-ratio change in the progeny ofirradiated fathers (table IX). Furthermore, there is no
significant effect on the sex-ratio in the progeny of irradiated male mice.
149. Recently acquired information has also stressed
the fact that, apart from the radiation dose alone, there
are a number of specific factors which should be taken
into account in calculating the doubling dose. Dose rate,sex, and stage of gametogenesis are all factors which
affect the frequency and quality of mutation in both miceand Drosophila and it must be suspected that they are
effective in man. An example of the influence of rate ofdose on the calculated doubling dose can be obtained fromtable X where the main results of irradiation of spermatogonia and oocytes of the mouse have been summarized.
The most important single comparison is that for males
between the dose rates of 80-90 r/min and 8.5 X l(rll r/
min. The former rate provides a doubling dose of 30-40
rad, the latter 100-200 rad. A significant dose-rate effectis also evident for oOcytes, and the doubling doses for
acute and chronic irradiation show an even greater
spread than in males.

The doubling-dose concept in indirect assessments

146. The indirect methods for assessing the hereditaryeffects of an increase in level of ionizing radiation towhich a population is exposed involve the estimation of"doubling dose" and the assumption of linearity of thedose-effect relationship. The doubling dose for a particular mutation is that dose which will increase the mutation rate to double the spontaneous rate. A prediction of
the phenotypic effect of an increase in mutation rate canbe calculated from the fact that the number of affected
persons arising as a consequence of a doubling dosedelivered in one generation, is equal to the number ofaffected persons normally present in any one generation
as a result of recurrent mutations of natural origin. This
increase in affected individuals will be spread over one ormore generations depending on the genetic fitness which
specific mutations confer on their carriers. The genetic
fitness of the heterozygote is of more importance than thatof the homozygote in most cases, because rare mutant
genes occur much more frequently in the heterozygous
state in a random-breeding population. When genetic
fitness of the heterozygote is very low, most of the impactof the new mutations will be felt in the subsequent generation; if fitness is reduced by one-fifth, most of the effectwill appear within the first five generations; if reduction
in fitness is slight the effect will spread over very many
generations. A permanent doubling of the mutation rate
eventually results in a permanent doubling of the incidence of those traits normally maintained by recurrent
spontaneous mutation. On the assumption of an average
reduction of 2 per cent in genetic fitness of heterozygotes,
most of the impact of a permanent doubling of mutation
rate would be felt in about fifty generations. Where systems of balanced polymorphism are in force, natural
mutation is a relatively minor factor in the maintenanceof genetic variability and a doubling of the mutation ratewould have little effect on the prevalence of the associatedtraits.

150. It is becoming increasingly evident that the spectrum of mutations in man is too wide to be included in asingle category for the purpose of estimating a meaningful representative doubling dose. For instance, thedoubling dose for gross chromosome mutations may welldiffer drastically from that for point mutations. If so, thefrequency-distribution of hereditary defects resulting
from a specific increase in the level of exposure to radiation would not be parallel to the natural spectrum.
151. In view of the undoubted complexities of thedose-mutation relationship, it is evident that this methodof assessing hereditary effects of ionizing radiation caneasily yield imprecise estimates. At the same time it isequally evident that none of these recently discovered
complexities invalidates the doubling-dose concept itself;they merely emphasize that the method must be applied
under carefully defined conditions if accurate estimates
are to be obtained. In particular, it is important to discriminate between the genetic hazards of chronic lowlevel exposures and more acute medical and accidental
exposures.
152. The difficulties of obtaining information on thehazards of ionizing radiation would be reduced if thelarge amount of data collected in other organisms could
be applied directly to humans. Differences in species
introduce into this procedure uncertainties the extent of
which is difficult to estimate. A second approach isthrough the observation of human cells grown in tissue
culture; reproducible results relating to radio-sensitivityof cells can be obtained in this wav. However. here also
extrapolation of information is at present associated withuncertainties. Nevertheless it is clear that in. viva andin vitro research in different organisms will ultimately

147. The usefulness of the doubling-dose procedure
was considered in detail in the 1958 report of the Committee. To a large extent this usefulness stems from thefact that whole classes of mutation can be handled as aunit in the absence of any information about the numberof loci invoked or their individual mutation rates. Tentative numerical estimates of the doubling dose for man
were presented in the 1958 report. It was pointed out
at that time that little direct information was available
on the sensitivity of human genetic loci to radiation. Esti100

provide a valuable source of information. Such investigations must be accompanied by an tmderstanding of thegenetic stmcture of human populations and the respectiveroles of mutation and selection in moulding that structure.

doubling dose is about four times the 1958 value of 30
rad. For chronic low intensity irradiation of females
mutation rates seem to be lower than in males. The corn~bined doubling dose for both se..""Ces cannot exceed twice
the value for males and is not likely to be much lower
than. that value. ~or these est~m'.'ltes, uncertainty due tospecies extrapolation and the hm1ted number of loci usedin experimental studies probably does not exceed threefold in either direction. A permanent doubling of themutation rate would ultimately double the prevalence ofthe serious defects under consideration. These are now
estimated to have a prevalence at about 1 per cent.

Conclusions

153. Sufficient information is not now available tocalculate with a useful degree of accuracy a representative dose which would double the mutation rate (doublingdose). Nor is it yet possible to predict directly the quantitative or qualitative effects of such a dose on populations. Nevertheless, information regarding some aspectsof the genetic hazards of ionizing radiation can beobtained by the doubling-dose method. This involves thecalculation of separate doubling doses for different dose
rates, and, in addition, for different specific categories of defects. The complexity of the calculations is
reduced by the fact that differential sensitivity of germcell stages within each sex can be largely ignored; as far
as the genetic hazards of radiation to man are concerned,
the significant germ-cell stages are the spermatogonia
and the oocyte. This is true whether irradiation is chronic
or acute.

155. The doubling dose for the defects of category lb,
those due to gross chromosome aberration, cannot now
be estimated for lack of data. However. the effect ofradiation on the frequency of gross chromosome mutation is amenable to study, and it can be expected that
continued research in this field will enable estimates tobe made in the near future. A doubling of the mutation
rate in one generation would almost certainly double theprevalence of these defects in the next generation. Thisprevalence is now estimated to be about 1 per cent.
156. It is not possible to estimate the doubling dose forthe genetic changes contributing to developmental malformations and serious constitutional disorders of categories II and III. The prevalence of these defects might
be doubled by a doubling dose but the increase would
probably be much less; environment is suspected to havea strong influence on their aetiology, and unrecognizedbalancing selective mechanisms may also be effective inmaintaining their frequency.

154. The group of disabilities to which the doublingdose can, at present, be most usefully applied are those
severe defects maintained by recurrent point mutation(category la). Calculations of the 1958 report suggested
that the over-all representative doubling dose for man
might well lie between 10 and 100 rad, with 30 rad as themost probable value. This estimate was based on studies
which involved acute irradiation and the production ofpoint mutations. In the absence of better evidence, thedoubling dose for acute irradiation of males does not
require revision. However, there is evidence that thisvalue is lower in females; experiments with mice haveshown that oCicytes are somewhat more sensitive to acute(but not to chronic) irradiation than spermatogonia. The
doubling dose for the two sexes combined must therefore
be lower than that for males and may well be about half
this value. For chronic irradiation of males, new information from mouse e..xperiments suggests that theTABLE l.

157. Significant progress towards an understandingof the genetic effects of ionizing radiation has been madein the last four years. The Committee emphasizes that:(a) all research has confirmed the fact that ionizing
radiation produces genetic damage at all doses and dose
rates so far tested, and ( b) further progress in understanding the genetic hazards of radiation will come not
only from ad hoe research in radiation genetics but froman increase in all types of genetic research in man and inexperimental organisms.

CHROMOSOME ABERRATIONS ESTABLISHED IN MAN

Associated clinical condition

Chromosome complmwo1

Chromosome
numberFirsl
re/tTe>IU

47
47
47
47

6

I. Anomalies related to chromosome mm1ber
Down's syndrome (mongolism) .....•• Autosomes: Trisomy-21
Trisomy-(17-18)
Complex congenital malformations....
Trisomy-(13-15)
Complex congenital malformations....
Klinefelter' s syndrome ............... Sex-chromosomes: XXY
Klinefelter's syndrome...............
XXXY
Klinefelter's syndrome.,.............
XXXXY
Turner's syndrome..................
XO
Mild mental defect.... . .. .. .. .. .. .. .
XXX
Mental defect .....................•
xxxx
II.

48
49

7
8
9
10
11

48

13
14
15

46

16

45

47

Struct11ral anomalies
Down's syndrome with trisomy-21 .... 21 ,...., (13-15)

101

TABLE II. DISABILITIES WHICH HAVE BEEN ASSOCIATED WITHABNORMAL KARYOI'YPES, EXCLUDING KNOWN MOSAICS
Clinieal anulition

I.

II.

Anomalies related lo chromosome number
Klinefelter's syndrome ......••..•.••..•••.••••. XXYY
Klinefelter's-Down's syndrome ...•.....•...•...• XX:Y, trisomy 21
Prenatal death ................................ Triploidy
Mental retardation •••.•••.••.••••...•..••••••• Trisomy 6(?)
Facial anomalies .............................. Trisomy 22(?)
Structural anomalies
Polydysspondyly .............................. 22,..., (13-15)
Familial mental and speech defect ...•......•.... 22,..., (13-15)
Primary amenorrhoea ......................... X
partlydeleted X
Down's syndrome ...••.............•....••...• 21 ,..., 22
Down's syndrome •.•••..•..•••.•...••••.•.•.•. 21 ,..,,, 21, or
trisomy 19 andmonosomy 21
Convulsive disorder ........................... (1-2),..,,, (6-12)
Klinefelter's syndrome .....•....•...•....•..... XXY and 14-15
Congenital abnormality .•... , ••..•..••• , ••••••. 16,..,,, 21, or
trisomy 21 andmonosomy 16
Pseudo-hermaphroditism ............... , •••.••. 21 ,..,,, Y
Turner's syndrome ..••••••..•••••..••...••.... Enlarged X
Familial Marfan's syndrome .................... Enlarged satellite
Transmissible hypospadias •.•.............••••. Y deletion
Gonadal dysgenesis .• " ..•...••..•......•••..•• X or Y deletion
Auricular septa! defect ......................... 2 ,..., (6-12)
Familial malformation of central nervous system .. Enlarged satellite+

TABLE III.

48
48
69
47
47

12
102
37
256
257

45
45
46

258
109
259

46
46

18
21

46
46
46

260
106
261

46
46
46
46
46
46
46

262
263
264
265
266
267
268

LETHAL AND DETRJME!ITAL EQUIV.AI.a.IS DERIVED FROM STUDIES OF OFFSPRING FROM FIRST-COUSIN MARRIAGES(Modified after Newcombe 2 G9)Consanguineous(first eousin 011ly)(3)

equi!NllenJR.efeUf'.U

16.01
11.62
12.89
2.98
0.61
9.82

6.92 ± 1.50
5.20 ± 1.55
1.63 ± 3.29
0.35 ± 1.73
5.73 ± 1.81
6.33 ± 2.91

2.21 ± 0.48
1.66 ± 0.50
0.52 ± 1.05
0.11 ± 0.55
1.83 ± 0.58
2.03 ± 0.93

270
271 '

16

837
3,184
194
196
164
163

84
182
227
176

4,094
4,010
3,822
4,094

2.05
4.54
5.94
4.30

2.07 ± 0.65
4.32 ± 0.96
5.80 ± 1.12
11.90 ± 1.18

0.66 ± 0.21
1.38 ± 0.31
1.86 ± 0.36
3.81 ± 0.38

273
274

2,091 63,145
808 17,33131
567
651 63,796

3.31
4.66
5.47
1.02

1.16 ± 0.40
1.91 ± 0.88
6.18 ± 1.96
0.40 ± 0.17

0.37 ± 0.13
0.61 ± 0.28
1.98 ± 0.63
0.14 ± 0.05

40
275

2,778
672
248
212
205
192

22.93
16.82
14.52
3.33
6.34
6.15

134
370
25
5

43
87
104
169

1,043
982
886
1,043

4.12
8.86
11.74
16.20

125

2,798
822
352
4,845

4.47
6.57
11.65
1.42

637
113
36
7
14
31

FranceStill birth ..................
Infant death •••...•....•...
Death from 1 to 30 years ....
Abnormality• ...•..........
Japan
Still birth; neonatal death ....
Infant death ...............
Juvenile death ..............
Abnormality* ..•............

DiffutnU

Total

U.S.A.
Infant death; juvenile death .•Death under 20 years •...••.
Miscarriage ••..•.•.•.•. , .•.
Still birth; neonatal death ....
Infant death; juvenile death .•Abnormality .......•.•..•.•

54
41
69

LttMI ordetrimental

FrtfJ!:iney

AJ!eckd

Total

Condition

Fre{%)"'

3)

Affected

Plau

Co111rol•Indicates some overlap with the preceding classes.
•• Controls drawn from offspring of sibs of the consanguineouspair.
See also Book:r.1 who found no significant difference in themortality in small samples of offspring of first-cousin and control
marriages, but a considerably greater proportion of the cousin

3)

212••

offsering having hereditary diseases (16 versus 4 per cent), andhaving lower than average intelligence (26 versus 15 per cent).
Since the individual offspring were observed for varying periodsof time the mortality data are not readily presented in the above
form. An average of three recessive deleterious genes per person
is estimated from these data.

102

TABLE !V.

ESTIMATED MUTATION RATES AT LOCI DETERMI?-t"ING AUTOSOMAL
DOMIN ANT DISEASES IN MAN(Modified from Stevmsoii 277 and Penrose39)
Trail

Estima~d ra!e/lccus/ten.

Region(X 10-<)

Epiloia

England..........................

8

Achondroplasia

Denmark.. . • . . . • . • . . • • . . • . . . • . • . •Sweden..........................
Northern Ireland..................
Denmark.........................
Michigan ...•...••.•• ,............

43*
68*
13

Aniridia
Microphthalmos

278
279
280
281
282
283

5
4

Neurofibromatosis
Huntington's chorea

Sweden..........................
5
England •.•......•.•• ,............ 15
l'vlichigan......................... 23
Northern Ireland........ . . • • • . . . . • 29
Germany, Fed. Rep. of.... . . . • • • • • • 4••
Michigan ...•.••••.•.•••.•••••••.. 100+

285
286
287
288
289

~lichigan.........................

5

290

Arachnodactyly
Acrocephalosyndactyly

Northern Ireland •••.• ,............

6

291

England..........................

3292

Retinoblastoma

0284• This estimate probably includes phenocopies.
This figure is adjusted for presumptive phenocopies.

TABLE V.

EsnMATED MUTATION RATES AT LOCI DETERYnfING
SEX-UNKED DISEASES IN MA."i(Modified from StevensonZ11)
Basis of estimation Estimakd rak/loeKS/ten.

Trail" - 1/J (J - 0 x*

(X 10 ...)

&ference

Englandf = 0.25
Est:: = 0.8 X 10-•

20

293

Haemophilia... . • • . . . . . . • • Denmarkf = 0.286
Est x = 1.33 X 10-•32

294, 295

j = 0.333
x == 489/4,092,025

27

296

f=O

95

297

f""' 0

59

298

f=O

39

299

f=O

47

300

Limb girdle muscular
dystrophy ...........•... Northern Ireland

••

34

51

Recessive deaf-mutism ...... Northern Ireland

••

13

51

Denmark andSwitzerland

Utah, USAx = 18/63,000

Northern Irelandx = 48/271,896

Duchenne typemuscular dystrophy ...•.
Englandx = 16/138,403

Englandx = 15/105,310* µ. = Mutation rate/locus/generation.
f = Relative genetic fitness.
0x = Frequency of trait in population.

Estimates made by special methods. 11

103

TABLE VI.

ESTIMATED ~!UTATION RATES AT LOCI DETERMINING
AUTOSOMAL RECESSIVE DISEASES IN MAN(Modified from Pe11rose3 9 )TrailBasis of estimation(µ - (1 - f) x*

RegionEstimated rate/l«us/len.
(X JO-<)

Rtfertnu

38

301

28

302

f=O

Juvenile amaurotic idiocy ...... Sweden

Est x = 3.8 X 10-1
f = 0.5
Est x = 5.5 X 10-t

Albinism ..................... Japanlchthyosis congenita ........... Japan

f=O
f = 0.5

11

302

28

302

f=O

11

302

23

280

45

280

49

303

25

54

Est x = 1.1 X 10-t

Total colour blindness ......... JapanEst x = 5.5 X 10--1
Infantile amaurotic idiocy ...... JapanEst x = 1.1 X 10--1
f =0:c = 1/44109

Amyotonia congenita .......... Sweden

f=O

Epidermolysis bullosa .......... Sweden

x = 2/44109
f = 0.02
Est x = 5 X 10-1

Microcephaly .•............... Ja pan

f=O

Phenylketonuria .............. EnglandEst x = 2.5 X 10--1* p. = Mutation rate/locus/generation.

f = Relative genetic fitness.
x = Frequency of trait in population.

TABLE VII.

STUDIES OF TIME-DISTRIBUTION OF DOSE-MODJPICATION OP PRE-MUTATIONALDAMAGE AND ASSOCIATED PHENOMENA

Radiation

Mouse spermatogonia ...•.............. X, 'Y.l\fouse oOcytes .•••••••••••••••••••••••• X, 'Y

Drosophila oogonia .....•............... 'Y

Silkworm, early stages of spermatogonia
and oogonia ...................•..... x. 'Y
Dahlbominus, wasp <>Ogonia ............. 'Y

Plaenmmnon

Remarks

RLferenee

Recessive visibles
and letbals atseven selected lociRecessive visibles
and letbals atseven selected loci

Fourfold reductionin effect at low
dose-rate
1\fore than fourfold
reduction at low
dose-rate

Differential viabilityof cells, radiation
quality eliminatedInter-cell selection
differential
viability, radiation
quality eliminated119,124,
127,132

Sex-linked
recessive lethals

Reduced effect at
low dose-rate

Egg-colour mutants
at two specificloci
Eye-colour
mutants infemale larvae

Reduced effect at
low dose·rate

Mutations

Drosophila spermatogonia •...........••. 'Y

2nd chromosome
recessive letbals

Drosophila spermatogonia ............... 'Y

2nd chromosome
recessive letbals

Drosophila spermatogonia ..•.•••.•. , .... X

Sex-linked
recessive lethals

Drosophila spermatogonia .......... , .... X

Sex-linked
recessive lethals
in ring-X
chromosome

Drosophila spermatogonia (?) ............ X

Sex-linked
lethals104

No effect at
intensity
differences of
1,000 r/min and
0.17r/min
No intensity
effect at
2,000 r/min and
2.0 r/min
Reduction at
intensity
differences from0.01 r /min to
0.10 r/min
Reduced (?) effectof fractionateddose

121,123304
128
97

After elimination ofcell selection andlater stages
Probably oc)gonia

130

Total dose 3,000 r

129

Total dose 200 r

129

Shifts in brood305
pattern of mutation
rates cannot be
excluded
Intensity of
153,154,
radiation for
155, 156
fractionation and
N: post-treatment
55 r/sec

No effect of dose
fractionation;enhancement by
post-treatment
with N~; reduction
by pre-treatment
with chloramphenicol
Decrease by
Stage not defined,feeding of larvae
probablywith actinomycin D
sperma togonia
and penicillin

306,307

TABLE VII.

MakrialSTUDIES OF TIME-DISTRDIUTION OF DOSE-MODIFICATION OF PRE-MUTATIOXALDAMAGE AND ASSOCIATED PHENOMENA (continued)

Radiation

MutationsPhenomenon

Remarks&Jere nu

Drosophila spermatids and spermatocytes .. X

Sex-linked
recessive lethals
in ring-X
chromosome

Reduced effect ofGene mutations anddose fractionation
possibly small
and of predeletions;
treatment withradiation given at
chloramphenicolhigh dose-rates;
and ribonuclease;inhibition ofenhancement by
metabolic repair
post-treatment
and delay ofwith N,; both
mutation fi....ation
increase anddecrease by posttreatment with HCN

152,153,
154,155,
156,157

Drosophila sperm ............•......... X

Sex-linked
recessive lethals
in ring-X
chromosome

Increase by pretreatment withribonuclease andchloramphenicol153, 154

Drosophila sperm ...................... X

Reduced (?) effectSex-linkedof doserecessive lethals;
fractionation inchromosome breaks
absence of 02

Drosophila sperm ...................... X

Chromosome breaks

Drosophila oc5cytes ..................... X

Critical period~ 40 min; criticaldose for breaks

158, 161

01 affects bothbreakage andrejoining ofchromosome
fragments; nosaturation of Os
sensitivity systems

Radiation given in
N~. air, or at
1 At of 02

163

Half-translocations,detachment of
attached
X-chromosomes

02 alTects bothbreakage andrestitution of
breaks

N: between X-ray
fractions, or as a
post-treatment
increase halftranslocation
frequency

308, 309

Habrobracon oocytes .................... X

Hatchability ofeggs treated infirst meiotic
meta phase

Drosophila spermatids .................. X

Translocation

310
Realization of
Post-treatments
potential radiation
with N. and CO
damageincrease radiation
damage152, 311
After both low andCyanide posthigh dose-rates;
treatment increases
CN delaysfrequency
restitution of breaks,
more translocations
139,140
Effect of various
Effect of timepost-treatments
between irradiation(nutrition,and chromosome
metabolic inhibitors)
duplication
143,144,
Pre- and postObserve mutation
145,146,
treatment withfrequency
147,148,
various temperadecline, mutation
149
tures, nutritional
stabilization,
factors, andmutation fixation,
metabolic inhibitors,
and mutation
relations to protein,
expression
RNAand DNA
synthesis

Paramecium . .......................... X, UV,aRecessive lethals
expressed after
autogamy

E. coli; Streptomyces spores; SerraJia ...... UV, X

Biochemical
reversions,"EMB colour"

Neurospora ..•.. ....................... UVBiochemical
mutation

Trijolium . .•..........................

Somatic mutationsat leaf marking
locus

Chromosome breaks
Vida ............................... .. X,
Neutron105

Protein synthesis
decreases mutation
at low UV doses,
but increases
mutation at highdoses
Reducing effect ofdose fractionation
Process ofrejoininginhibited byradiation

RNA derivatives
increase mutation
frequency at low
doses only

150

312
Protection by doseof 12.5 r, dependent
on 0.-tension andtemperature
313,314
Repair requires
cellular metabolism
and protein
synthesis

TABLE VITI.

EFFECT OF IRRADIATION OF MOTHERS ON THE PROPORTION OF
MALE OFFSPRING
CMltrol

Irradi4Ud

No.
birthsIi••

Per cenlJapan • .........•... {43,544

52.085Countr;ymak

U.S.A . .............. Control not available
355
54.6
674
50.1
225
53.3

Franee.· · · · · · · · · · · · · {Netherlands.... . . . . . . .

TABLE IX.

Dose ra,.ge
rads

No.Ii'<
birthsPer Unlmak&fcre"ceea. 8
ea. 75ea. 200
50-200
20Q-400
2-10
JOQ-600

19,610
3,958
2,268
407
161
797
221

51.97951.44051.190
49.1
44.7
52.2
48.0

227,315

Japan •••••.,. ••••...

Irradi4Ud

No. livebirthsPer cullmale

43,54452.085

609

51.72

51.24
Averagefor Japan
52.42
U.S.A.. • • . . . . . . .. .. • 3,491p"~··············i

Netherlands •••••••.••

238

EFFECT OF IRRADIATION OF FATHERS ON THE PROPORTION OF
MALE OFFSPRING
CMllrol

Cout1lr;y

235
236

1,185
1,926
828
657

51.5
52.7
46.6
52.3

Dose ranie
rads

No. li•ebirthsPer unimale&ferenceea. 8
ea. 60ea.200Many dosesof unknown
amount

5,168
1,226
753
4,201

51.58753.26352.722
53.64

227,315

Many small
doses
20Q-400
2-20
JOQ-608
1-10

4,277

51.39

225

656
1,394
635
668

56.1
46.0
52.3
53.4

236

237

238

TABLE X. NATURAL AND INDUCED MUTATION RATES AT SEVEN SPECIFICLOCI IN ADULT MOUSE SPERMATOGO!'o'lA AND 00CYTES

De/ails of i"adialion

Source

Total
Dose
(r)

X-ray.................
300
X-ray.................
600
X-ray................. 1000
X-ray ..•.••.•••••..•.• 600 400h
X-ray.................
600
Co'°...................
600
X-ray.................
600
csm..... .............. 600
Cs137 • • • • • • • • • • • • • • • • • • •300
Cs111 •••••••••••••••••••
516
esw................... 861
Co'°...................
603•
Co 1111 and radium. . . . . . . .
37.5d
Cs137 • • • • • • • • • • • • • • • • • • •86+

Alton'""

of rnutalions
per locus
per garr.,,te(X 10-')

Dose Rat<:(r/min)No. ofojfspri11i

No.of
mutalions

80-90
80-90
80-90
80-90
60-70
24
9
0.8
0.009
0.009
0.009
0.007-0.009
0.0011-0.0078
0.001

40,408
119,326
31,815
4,904
10,76144,35228,33927,84058,45726,32524,281
10,76363,322
56,993

25
111
23
10
11
33
14
10
10

8.84
13.29
10.33•
29.13
14.60
10.63

5
12
2
6
6

2.71
7.06
2.65
1.35
1.50

119
119
119
121
126
121,316317
125
121,316
121
121
126
318
121

544,89732

0.84

119, 121,316,318

12,85336,083
10,117
27,174

16
13

Control. .............. .

7.06
5.13
2.44

Mula.lions in o6cytes

X-ray.................

esm ..... ·····. ... . . . ..

Co1111 • • • • • • • • • • • • • • • • • • •csw...................

400
400
600•
258

92-96
0.8
0.05
0.009

Control. .....•.........

98,828•For a possible explanation of the low mutation frequency, seeparagraph 83 above.
b The two fractions were delivered 15 weeks or more apart.

17.78
5.15

1

1.41

2

1.05

319
121,123

0.14

121, 123,316• Delivered in 90 12-hr. or 16-hr. days.
d Delivered in 5, 25, or 35 16-hr. nights.
• Delivered in 12 16-hr. nights.

106

121, 123
304

TABLE XI.

Trealmo11l

Material and charatlers

Drosophila mela11ogas/er
Abdominal bristle number .....••.

Drosopltila melanogasler
Abdominal bristle number ...••...

.......

0

POLYGENIC TRAITS: MUTATIONAL DATA

llfelllod

Response to selection for highand low lines

Nil

Analysis of increased varianceassociated with second
chromosome
Ditto

0.0014/generation

0.006/generation

8.7 X 10-1 /radSternopleural bristle number •.....
Drosophila nu:lanogaster
Abdominal bristle number •.......

Nil

Analysis of variance associatedwith second chromosome
Ditto

Sternopleural bristle number ......

?

Regression of variance on dose forlarge chromosomes
Ditto

Rice
Heading date ......•.......•....

Nil

3.3 X 10-1 rad
Not significant hut:I> 0.006/generation

Cmmuents

Refere11te

Natural genetic variance cited as 5 units
for abdominals ancl 1. 7 units forslernopleural320(10/25)Nil'lin gt11eli' variauc'(a) 1,800 r per
generation as
adults(b) NilSternopleural bristle number •••...
Drosophilti mela11ogl1sler
Abdominal bristle number ..•...•.

Drosophila nu:lanogaster
Sternopleural bristle number .••...

ReJults: i11creaJe(a) 3,000 r X-rays
Selection for high no.
every generation (a) Top 15% every generation(b) 3,000 r X-rays(b) Top 15% every otherevery othergeneration
generation

321

0.0004/generation
322

0.002/generation

3.5 X 10-1/rad

Details of X-ray treatment and dose
not given:I> 4.7 X 10-1/rad•323> 2.5 X 10-1/rad*rr suppose inbreeding system leaves

6 or 12,000 r
X-rays to seeds

Variance analysis 5 generations
after irradiation of highly
inbred line

1.5 X 1Q-1(day)2/rad

Plant height. .•.................

Ditto

Ditto

8.4 X JO-l(cm)2/radMaize
9 attributes .•..•...•.......•....

Nil

Analysis of shifts in plot meansover 6 generations of selling
doubled monoploids

Average of 4.5 X 10-1
mutations per attribute per
gameteVariance analysis fnilecl to give significant
results because of high environmental
component

325

2 X 10-1/rad

Variance of flowering data in natural
populations not known. Controls
probably not significantly different from,..., 0.00043: good linearity with dose
obtained

326

Arabidopsis lhaliana
Logarithm of flowering data .....••Secretariat calculation.

0-150 kr X-rays to
dry seeds

324

variance equiv. of 3-5 generationsof spontaneous mutation, can calculatespont. rates of 8-10 X 10-1 (day) 1 /generation for heading date and6-7.5 X 10-t(cm)2/generation forplant heightREFERENCES
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1'L PoHIPieBcKaa, IO. l\L Py&a-r.

BIImmmon II ,lijl., remffiftI8CKaJI pa~IIOtI}'BCTBIITemi­
HOCTb I\.'leTOK paaHii!X: BH,ll;OB M11e&OIIIITaIOm;nx. ,TI;oRyi.teHT OOH A/AC.82/G/L.416.

168. Apcell.bena, l\L A., r. r. Tnnmrnn, II;nToreHeTif!IeCKa.lI

paJJ;II01JY1lCTBIITelbHOCTb

IIOJIOB:bIX:&.JeTO&o6e3l>Jm II Ml>llIIeii Ha ypOBHe Ma..m:x II p;pyrux ,ll;03.
AKa,ll;e:~m.lI nay& CGGP, Mocli.Ba (1960); v.e. p;o-:&YlleHT OOH A/AC.82/G/L.424.

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Teill>HOCTI> pa3HhlX ~Tap;nit crrepMaTorene3a y Drosophila melanogaster. ,TI;oKyMeHT OOH A/AC.82/G/L.409.
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188. illamrpo, H. H., E. ,n:. II.;roTIIIIItoBa, c. H. C'I'pamilleHIW II ):qi., 0THOCIIT8ill>HaJI reHeTIPiecxasr paAHOTIJBCTBIITB:ThHOCTb pa3llillllli:JIX BH)J;OB ;mreKomrrarom;nx n ,11;posoqrnm. ,Il;on.yareIIT OOH A/AC.82/G/L.415.
189. XBocToBa, B. B., .iI. B. HeB3ro.n;1ma, IlpIPirnm pap;rroycroi:l:lJIIBocrn pacTemtii. ,Il;OEJMeHT O;QH A/AC.82/G/L.4L4.
190. Eep1rnc, IO. R., r. :M. P-0HlI'!e1rnr..a.ir, IO. H. HayMeHEo, B.rnmme rerroTIIIIa opra.Hn3~Ia '.Ha 1IJBcTJnrrenbHOc.TI> .ll,U;epHoro aIIIIapam & :r.ra.lThIM ,rr;o3a:1r
nonn3npyrom;ett pa,wr~. )l;oR,y:MeHT OOH A/AC.82/G/L.418.
191. )l;y6IIIDIH, H. II., l\I. A. ApceHoeBa, IO. H. Eep1mc,
renern11ecxaJI onacnocn, MaJiblx µ;03 pa.n;naTI;llll ,n;nH-cie.lIOBem II lIX acpcpeKT na nac:ie.n;cTBeEHOCTI> o6eabmr 11 rpbI3YHOB. ,1!;0Ky.11reHT OOH A/ AC.82/GjL.406.
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117

124, M 4:922-924 (1959).

SOMATIC EFFECTS OF RADIATIONCONTENTS
ParlS{JraN.s

ParlS{JrapJu!. PHYSICAL FACTORS INFLUENCING SOMATIC EFFECTS 1-18
1-2
Introduction ........•.....•••.......••.••..••
Definitions ...•....••••..•....•......••••.••.• 3-9
4
Short-term exposure ..........•.....••...•.
5Long-term exposure •.••..•...•......•..••.•
Cumulative dose ......••••..•.......•.•..•• 6-7
Consequences of exposure •....•.....•.....••• 8-9
10Type of radiation ....•...•.......•.......•..••
11
Time distribution of dose ..................... .
12
Early effects •...••••..•..••.....•••..••.•....
Late effects .•...•......•.•.•..•••••...•...••. 13-14
15
Anoxia ..................................... .
16
Temperature .•.•..•••••••.••.•••••.•••••.••.•Nature of radiation injury ................... .. 17-18
18
Chromosome damage •.••.....•.•.••.•.....•

Partial-body exposures .. . . . . .. . . . . . . . . • . . 130
Role of genetic constitution and physicalstatus •...•...••..•.....•............•• 131-138
Life-lengthening •••.•....................
139
Nature of the lesion in life-shortening ..... . 140
Radiation carcinogenesis .••.•.....•.••.••... 141-165
Relation to rate of mitosis ............... .
145
Relation to age .....•....•...•..•.•.•.•.• 146
Relation, to radiation dose ............... . 147
Mechanisms of carcinogenesis .•.•......... 148-150
Somatic mutation theory ................. . 151-153
Chromosomal changes and carcinogenesis •. 154-158
Radiation leukaemogenesis •.•...•..•••••.. 159-163
Vrrus theory •....•..............•.•..•..• 164
Risk of carcinogenesis from low doses ..•••• 165
Recovery and the concept of irreparable injury .. 166-169
Early and late effects on embryos and foetuses •. 170-192
The mammalian embryo ................•... 170-180
The human embryo ...•...•.....•.........• 181-185
Recovery and protection in irradiated germ
cells and embryos ........................ 186-192

I!. LETHAL AND LESSER DAMAGE IN CELLS, TISSUES,ORGANS, NEOPLASMS, AND ORGANISMS ••••••••••••

Introduction ..•••...••.•...•.......•.....•...
End-points .•...•..•....••..•....•.••.•..••...
Death of cells as end-point. ................. .
(a) Law of Bergonie and Tribondeau •.•...
( b) Radio-sensitivity of cells in the adultmammal .........................•••(c) Radio-sensitivity of tissue in the adultmammal ..••••......•.•..••.....•...
Age and radio-sensitivity ..................... .
Mammalian cell survival curves ..•...........
Radio-sensitivity of malignant tumours ...•...•.
Factors influencing radio-sensitivity •..•........
LD.. values for mammals ................... .
LD,.and age .•..•••••••....••.•..••......••.
LD,. in man .....••...•..•••.....•••.•...•••LD.. and dose-rate ...••••.....•.•...•••.....
Radio-sensitivity •••.•.••.••.•...••••..•.••••.

19-47
19
20-24
22-24
22

IV. ACUTE RADIATION INJU11.Y IN MAN •••••••••••••• 193-231
Acute radiation syndrome ..............•..... 193-206
Sources of information .................... . 194
Total body response ....................... . 195
Radiation sickness •...•..•...••.•...•.•••.•• 196-197
General clinical picture .................... . 198
CNS form ••..••••.••.••....•••.•.••••..•• 199
Gastro-intestinal form •....•..•..••.•.••..•. 200-201
Haematopoietic form ..................... .. 202
Prognosis •..•....•.••..••..••..••••••...••• 203-204
Prognostic value of the leukocyte count ....•• 205-206
Analysis of past accidents ................... . 207-229
First and second Los Alamos accidents ••.•.. 208-213
Argonne accident ........•.........•..•.... 214
USSR accident ........................... . 215
Oak Ridge accident ................•.•..... 216
Yugoslavian accident ...................... . 217-220
Third Los Alamos accident .......•.....•... 221-223
Lockport accident ............•..•....•..... 224-229
Assessment of injury ........................ . 230-231

23
24
25-28
26-28
29-34
35-46
36-40
41-42
43-45
46
47

Ill. SoMATIC RADIATION INJU11.Y AND ITS REPAIR, PAR·
48-191
Modes of death with TBR ......•....•..•...... 48-54
Partial body irradiation .................... . 51-54
Early and late organ effects ................... . 55-112, B~ood .and blood-forming organs •.........•. 55-60
D1gesbve tract ........•..•......••...••.•.. 61-64
Reproductive organs ....................... . 65-87
Male animals ..........•.......•....•.•... 66-75:r.,,fan ................................... .
76
Female animals •••••........••.•••......•. 77-81
Sexually immature animals •.....•......... 82-87
Nervous system ..........•...••....•.....•• 88-90
Eye ..............•............•........... 91-93
Liver ..................................... . 94-95
Kidney ................................... . 96-97
Circulatory system ........................ . 98-99
Endocrines ................•.......•....... 100-101
Skin ..........•............................ 102-108
Bone ........•............................. 109-112
Late effects ................................. . 113-164
Life-shortening .••.•........................ 113-140
Introduction .....•....................... 113-121
Liie-shortening by single doses in animals .. 122-126
Life-shortening by multiple doses or protracted irradiation in animals ...•........ 127-128
Age effects •..........••...••.......•.... 129
TICULARLY IN MAMl!Al.S . . . . . . . . . . . . . . . . . . . . . . .

V. LATE EFFECTS OF IRRADIATIOS IN MAN, INCLUDINGCARCINOGENESIS • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • 232-327
Life-shortening . . • . . . . . . . . . . . . . . . . . . . • . • . . . . . • 232-239
Effect of long-term radiation on life-span inman •...................................• 232-239
Carcinogenesis in man . . . . . . • . . . . . . . . . . . . . . . . . 240-286
Leukaemogcncsis •...•............••...••... 241-286
Situations in which a relationship between
radiation and leukaemia has been established ......................••..•...... 241-244
Situations in which a relationship between
radiation and leukaemia has been suspected but not established .............. 245-247
Leukaemia in the Japanese survivors of theatom bomb ............................. 248-253
Leukaemia in ankylosing spondylitis . . . . . . . . 254-262
Leukaemia in children . . . . . . . . . . . . . . . . . . . . 263-273
Leukaemia in radiologists . • . • . . . . . . . . . . . . . 274-276
Pelvic irradiation and leukaemia in children .....••...•..............•••.•..•.. 277-286

118

CONTENTS (continued)
Paragraphs

Parograp/ss

V. LATE EFFECTS OF IRRADIATION IN MAN, INCLUDINGCARCINOGENESIS ( contiimcd)
Malignant neoplasms in the Japanese survivorsof the atomic bomb ........................ 287-288
Local effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . • • 289-327
Radiation cataract . . • . . . . . . . • . . . . . • . . . . . . . . . 289-307
Radiation effects on fertility . . . . . . • . . . . . . . . . 308-310
Sterility doses for men and women .......•.. 311-315
Degenerative diseases and histopathologicalchanges ..•.............................•. 316-323
Effects on growth and development . • . . . . . . . . 324-327

Lanthanide and actinide rare earths (including
yttrium) ................................. 392-396
Caesium-137 .•.............•.......•....... 397-401
Iodine-131 .........................•....... 402-404
VII. DOSE-EFFECT RELATIONSHIPS ..............••... 405-491
Early effects ......••..........•....•......... 405-442
Immediate.. • . . . . . . . . .• . . . • . • • . . . . . • . . . . . . . 405
Early death ...•.•.•..•.•.•...............•• 406-407
Body weight loss and organ atrophy .•.•...... 408-412
External irradiation • . . . . . . . . . .. .. . . . . • . . • 411
Internally-deposited radio-isotopes ...... : . 412
Intestinal atrophy ....•..................... 413-416
The atrophy of spleen and thymus .......... 417-421
External irradiation . . . . .. . . . . . . . . . . . . . . • • 418
Internally-deposited radio-isotopes ..••..•. 419-421
Testicular atrophy ....... ."................. 422-425
Lymphatic tissue • . . . . • • • .. • . • • • • . • . . . . . . . • . 426
Depression of mitotic activity .•.•....•..... 427-433
Depression of iron uptake by erythrocytes anderythrocyte-forming tissues . . • • . . • . • . • . . • • 434
Quantitative studies ..•...•.•••••..•...... 435-439
Suppression of immunological mechanism • . . . 440
Leukaemia transplantation ••.•••.....•...... 441-442
Late effects • . • . . . • . . . • . . . . . . • • . . . • . . . . • . . • . . . 443-490
Induction of lens opacity • . . . . . . . . . . • . • . . . . . . 443-455:Methods ..••.......•............•........ 445-446· Human studies .......................... 447-451
Experimental studies . . . . . . • . . . • . . . . • . • . . • 452
RBE • . . . . . . . • . . . . . . . . . . . . . . . • . . . • • . . . . . . 453-454
Dose-effect correlation . .. • . .. . . .. . . . .. . .. . 455
Shortening of life-span .••••.•..••.....•••• 456-470
Induction of tumours •.•..•................. 471-490
Quantitative studies •......•..•...••.....• 477-4i9Radiation-induced leukaemia in man ..••..• 480-482
The Hiroshima and Nagasaki surveys ...... 483-484
Children irradiated for thymus enlargement................................... 485
X-ray treated ankylosing spondylitis ......•. 486-489
Concept of threshold . . . . . . . . . . • • . . • . . . • . . . 490
VIII. PROI'ECTION AND MODIFICATION OF RADIATION
INJURY .....•..•. , ....•....•.••.••.•••••....• 491-527
Introduction . • . . • . . . • • . . . . . • • • • • . • • . • • . . • • . • • 491
Protective agents ............................ 492-524
Anoxia . • . . . . . . . . . . . . . . . . . . . . . . . . • . • . . . . . . . 492-493
Protective chemicals . • . . . . . . . . . . . . . . . . . . . . . 494-503
Modifying treatments • • . . . . . . . • . . . . . . . . . . . . 504-524
Internal decontamination . • • • . • . . • • • • . . • . . . • • . 525
Treatment of acute radiation syndrome • . . . . . • • 526-527
SUMMARY . . • . • . . . . . . . . . • . • . . • • • • • • . . • . . . . . • . . . 528-539
TABLES

Vl. SPECIAL FEATURES OF INTERNAL AND EX~"IAL
CONTAMINATION •.....•.•..•...•....••...•• , .. 328-402
Physical consideration . . • . . . . . . . • . . • . . • . . . . . . • 328-333
Special problems associated with internal emitters 334-347
Localization of radiation • . . . . . • . . . . . . . . • • • • • 334-335
Concept of RBE .. . • . . . . . . . . . . . . . . . . . • • • . • 336-337
Modes of entry of radio-isotopes into animals
and man . . • . . . . . . • • . . . . . . . • . . • . . . . . . . . . . . 338-347
Ingestion . • . . • • • • • • . • • . . . . . . . • . . . . . • . . . . • 339-342
Inhalation . . . • . . . • . . . . . . . . . . . • . . . . . . . • . • . 343-346(a) Size of inhaled particles............ 344( b) Radio-activity of inhaled particles. . .
345( c) Solubility of inhaled particles. . . • . • . 346
Skin absorption . . • • • . . . . • .. . . .. . . . . • . • .. . 347
Effects of radio-isotopes after absorption ......• 348-382
Early effects •........•...........•.....•.. 349-350
Late effects ........•...•................... 351-382
Effects of internal emitters on the lung,including cancer of the lung . . . • . . . . • • . . 352-365
Long-term effects of internal emitters inanimals . . . . • . . . . . . • . . . . . . • • • • . . . • . . . . 354-355
Effects of internal emitters on the lung inanimals . . . . . . • . . . . . . . . . . • . . . . . . • • . . • . 356-364
Effects of internal emitters on bone ..••.•.• 365-380(a) Histological damage in bone ........ 365-367(b) Histogenesis of bone tumours ...... 368-370(c) Relationship between the pattern ofradiation dose in space and time, histological bone damage, and bonetumour induction .................. 371-372(d) Accumulated radiation dose to the site 373-377(e) Radiation dose-rate to the site •.•..• 378-380
Dose and dose-rate in carcinogenesis byinternal emitters ........................ 381-382
Internal emitters and leukaemia . . . . . . . . • . 383
Internal emitters and life-shortening . . • . . . 384
Metabolic characteristics of particular isotopes . • 385-404
Alkaline earths (calcium, strontium, barium,
radium) •.•.•••.••...........•.......•..• 385-391
Radiurn-226 . . . • . . . . • • • . . . . . . . . . . . . . . . . . . . 386-387
Strontium-90 ................•........... 388-391

REFERENCES

The inhomogeneity of dose in man, particularly after
accidental exposure, raises an important practical difficulty in assessing e.'Cposure in man : one can ascribe nosingle meaningful value for the dose delivered.

I. Physical factors influencing somatic effects
INTRODUCTION

1. The present anne.x summarizes lmowledge of thebiological effects of ionizing radiations on animals andman; the object is to assess the effect of radiation on theindividual.

DEFINITIONS

3. To facilitate prospective and retrospective classification and study, definitions used by the United States
National Academy of Sciences-National ResearchCouncil Sub-committee on Hematologic Effects ( 1961) 1
are recommended. Some terms cannot be defined precisely. Others, because of ambiguity, e.g. "acute" and"chronic", are best avoided in describing e.'Cposure andeffects and reserved for use in their usual medical sense.

2. The principal physical factors determining thebiological effects of ionizing radiation are the absorbed
dose (rad), its distribution in time (instantaneous doserate, fractionation, short-term or long-term e."<posure),
its spatial distribution (anatomical region, fraction of
total body, organ depth, distribution, etc.) and the qualityof radiation (energy: a-,{3-,y-, X-rays, neutrons, etc.)119Short-term exposure
4. Short-term exposure includes: (a) total or substantial body exposure to radiation over a short time(e.g. in nuclear warfare from direct exposure to initialradiation from the detonation of nuclear weapons andnuclear reactor or accelerator accidents), and ( b) exposure of limited yet substantial body areas in which theradiation is given either as a single dose or fractionatedover a few days or weeks (e.g., in therapeutic radiation,
diagnostic radiology, or tracer or therapeutic use ofradio-active isotopes). A dose > 50 rad is defined, forthe purposes of the present report, as a high dose, < 50
rad as a low dose.

there are possible differences at the microscopic level;
but superimposed on this uniformity they may have a
different relative biological effectiveness ( RBE), e.g.
densely ionizing particles (a rays, neutrons) are more
efficient in producing most forms of cellular damage
than y- and X-rays giving lower ion densities. The RBE
quoted for a particular kind of radiation depends on thespecific biological effect observed, the tissue irradiated,dose, and rate at which it is given. Annex B details theconcept of RBE; difficulties in its application to internal
emitters are described in section VI of the present annex.
TIME DISTRIBUTION OF DOSE

11. A dose which is lethal if given in a short time
may, if spread over a long time, produce effects difficult
to relate to the exposure or. especially when recovery
intenrenes, to detect at all. This poses the key questionin assessing somatic effects in man : what are the effectsof low doses, single or long-term?

Long-term exposure
5. Long-term e..xposure refers to continued or repeated exposure to radiation over months or years. Such
exposure is greatest in certain occupations and in persons
containing radio-active isotopes with relatively longeffective half-lives. X-ray examinations repeated frequently over a long time also constitute long-term exposure, as do exposures to cosmic radiation, naturallyoccurring radio-active isotopes, and fall-out.

EARLY EFFECTS

12. The early effects in man of large doses are fairly
clearly known from the therapeutic use of X-rays andof radio-nuclides such as Ra226 (used in teletherapy)
and I1 31, from atomic energy workers in nuclear accidents and from clinical studies on atom-bomb survivors.
The acute radiation syndrome is detailed in section IV
below.

Cumulative dose
6. Although the total dose of radiation is important inlong-term exposure, it is sometimes useful and convenient to indicate degree of exposure as dose per unit
time, usually cumulative dose per week:(a) Very low weekly dose< 100 mrad.
( b) Low weekly dose : 100-1,000 mrad.
( c) High weekly dose > 1, OOO mrad.
7. The very low weekly dose is less than that impliedby the 1960 maximum permissible dose (MPD) recommended for occupational exposure by the International
Commission on Radiological Protection (ICRP) 2 andthe United States National Committee on Radiation
Protection and Measurements ( 1958). 3 The dividing
line between low and high dose corresponds to the first
MPD recommendations of these groups in effect between
1936 and 1948.

LATE EFFECTS

13. Late effects in man are inferred from knowledgeof specific effects produced in animal e..xperiments, fromlarge-scale observations on population, and from occupational and medical exposures in man. Late effects
comprise:(a) Many, if not all types of neoplasm, including leukaemia;( b) Local effects on tissues, e.g. skin changes, precancerous lesions, cataract and sterility;( c) Changes in life-span;(d) Effects on growth and development, e.g. irradiation of the foetus can produce abortion, still birth anddevelopmental abnormalities;( e) Effects on subsequent generations, covered inannex C.

Consequences of exposure
8. The initial effects produced by radiation may leadto observable alterations expressed promptly or months
or years after irradiation. The development of clinicalfindings depends not only on the nature and extent of theinitial radiation injury, but also on the operation of
secondary factors, e.g. the influence of hormonal secretions on the development of radiation-induced mammary
tumours. A distinction should also be made between
those effects that produce only a cytologic abnormality,e.g. binucleate lymphocytes, and those that produce a
serious disease, e.g. leukaemia.
9. It is not possible to distinguish sharply between
early and late effects since effects observed soon afterradiation may persist. Nevertheless, it is convenient toconsider as early, effects observable \Vithin a few weeks
after exposure. Late effects are those that appear later
not obviously re1ated to the early effects. Late effects
include cataracts and tumours; they may not appear until
many years after exposure.

In general, the late effects are not unique to radiation;
for the most part they are indistinguishable from diseasestates induced by other causes commonly present in the
population.
14. Although the main late effects are known-indeed
familiar-the possibility of other effects being produced
cannot be excluded, notably in the foetus. Not enoughis known about the relationship between dose and incidence of late effects. Accurate measurement of dose andincidence may be very difficult.
AKO XIA

15. Reducing the oxygen concentration inside cells
during irradiation with X- or y-rays diminishes cell sensitivity by a factor of 2-5, as measured in several ways.
This effect of anoxia in the active bacterial cell is independent of eYents later than 0.02 seconds after irradiation." Analysing such phenomena within such time limits
is not easy. 5 The effect of oxygen is re\·iewed in an-

TYPE OF RADIATION

10. Different kinds of radiation produce essentiallysimilar biological effects at the macroscopic level, though120nex B and anoxia is discussed further in section VIII
belmv (Protection and modification of radiation
injury) because of circumstantial evidence suggestingthat many protective agents act by interfering with oxygenation of the cell.
TE~1PERATURE

16. Lowering temperature soon after irradiation, thus
temporarily slowing metabolism, promotes recovery inmicroorgMisms. In amphibia and mammals, loweringbody temperature after irradiation may delay the onsetof symptoms, but there is so far no evidence of an increased degree of recovery.
NATURE OF RADIATION INJURY

17. A big bar to understanding the nature of radiation
injury arises from the difficulties in discerning the immediate processes in the interaction between radiations
and living cells: (a) the low concentration of the reaction products between initial interaction and final expression of damage after biologically effective doses ofradiation, makes characterization of these reactions difficult by present physico-chemical techniques ; ( b) thevery rapid completion of these interactions allows little
time for detection of the intervening events. 5 • 6 • 7
CHR0:).!0SOME DAMAGE

18. Much evidence points to chromosome damage as
the central mechanism of radiation-induced cell injury
and death. This and the considerable effort to explain
effects biochemically are reviewed in annex B.

ral blood . by F e59 incorporation in bone marrow and byblood cells, by degree of aplasia, or by the likelihood ofleukaemia being induced years after radiation.
Death of cells as end-point(a) Lcrw of Bergonie and Tribondeau
22. In 1906, Bergonie and Tribondeau 9 proposed a"law" of cellular radio-sensitivity which on the ·whole isvalid in radio-therapy: the most radio-sensitive cells arethose which ( i) have the highest mitotic rate, (ii) retain
the capacity of division the longest, (iii) are the leastdifferentiated.
(b) Radio-sensitivity of cells in the adult mammal
23. Cells in the adult mammal can be arranged approximately in the order of decreasing sensitivity on thebasis of clinical and experimental data with death ofcells as end-point: lymphocytes, erythroblasts. myeloblasts, megakaryocytes, spermatogonia, egg cells, cells of
jejunal and ileal crypts, epithelial cells of cutaneous appendages, cells of eye lens, cartilage cells, osteoblasts,
endothelial cells of blood vessels, glandular epithelium,
liver cells, epithelial cells of renal tubuli, glia cells, nerve
cells, alveolar lining cells of lungs, muscle cells, connective tissue cells, and osteocytes.10( c) Radio-sensitivity of tissue in the adult nz.ammal
24. The body's organs reflect differences in the radiosensitivities of their cells, usually of those in the generative compartment. The radio-sensitivities of different
cells, tissues, and organs of mammals are detailed in
section III and quantitative relationships between effectand dosage in section VII of the present annex.

II. Lethal and lesser damage in cells, tissues,organs, neoplasms, and organisms
I~TRODUCTION

19. Knowledge of the comparative radio-sensitivity ofdifferent cells and organisms is significant in studying
somatic effects. A theory e..'<:plaining the large differencesin radio-sensitivity among different cells and organisms
would be decidedly valuable in understanding radiobiology. Differences in the radio-sensitivity of organs are
the principal factors defining the organ whose damage
by a gi~en radiation dose impairs the body most.

AGE AND RADIO-SENSITIVITY

25. Man's sensitivity depends on age at the time of
exposure. Embryonic neuroblasts are killed by a muchsmaller dose of radiation than that which kills adult nerve
cells. Children are more susceptible than adults in a
number of respects. For example, the child's growingbone is more sensitive than the adult bone. These are but
a few examples of the relation between age and susceptibility to radiation. The radio-sensitivity of embryos andfoetuses is discussed more extensively in section III, andof children in subsequent sections covering effects onman.
klammalian cell survival curves

END-POINTS

20. Various end-points are used to determine comparative radio-sensitivities: (a) death of cells ; ( b) doseto inhibit mitosis; ( c) alteration or loss of functions ;( d) time taken to regenerate; ( e) time taken to atrophy;(f) LDso· In general the morphological end-points
hitherto used cannot be regarded as satisfactory anddetermination of radio-sensitivitv is better based onfunctional criteria, e.g. the concept of radio-resistanceof nerve tissue based on morphology has proved incorrect, since functional transient changes in synaptic transmission result from doses of ,...., 0.025 r. 8

26. Puck et az.n- 1 ~ plotted the first survival curves for
mammalian cells cultivated in vitro ; they measured the
reproductive potential of each individual cell after radiation. They found that human squamous carcinoma(HeLa) cells responded with a two-hit type inactivationcun•e, and that the logarithmic fraction of surviving
cells was linear with increasing dose beyond the initialshoulder of the curve. The D 37 was only ,...., 100 rad incontrast to ,_, IOS rad for virus inactivation. They suggested that the more sensitive mammalian cells may havemore unit targets vulnerable to inactivation.
27. Estimates of D 37 by Puck for various normal andneoplastic cells in vitro have been very close to one another. This may reflect the high rate of growth of normal
cells in tissue culture ; indeed there is strong evidence ofmalignant transformation in many types of cells in vitro.

21. The apparent radio-sensitivity of a cell or tissue
thus depends on the method of observations. e.g. lymphocyte damage may be measured by structural changes in
the cell nucleus, by change in DNA content, or by degreeof lymphopenia; bone marrow damage may be measured
by examination of bone marrow smears, blood counts.
haemoglobin and haematocrit estimations in the periphe-

28. Hewitt and Wilson 13- 14 and Till and McCullough 1 5-16, in ingenious extensions of the Puck tec~que121to in vivo conditions estimated the sensitivity of mouse
leukaemia cells and haematopoietic stem cells irradiatedin vivo in mice. In both experiments survival curves werevery similar to those obtained with human tumour(HeLa) cells irradiated in vitro. These observations areimportant for radio-biological theory, but much work
remains to be done to determine how far the results
apply to cells in their normal in vivo environment. The
sigmficance of the shapes of the survival curves for thebasic mechanisms involved is still obscure. Elkind's
work11 underscores the considerable significance of repair mechanisms in the response to fractionated or protracted exposure.
RADIO-SENSITIVITY OF MALIGNANT TUMOURS18

29. Radio-sensitivity of a tumour depends primarilyon the radio-sensitivity of the cell of origin. Gross reduction in tumour size depends on the proportion of cells
immediately affected by radiation. A lack of immediatevisible response does not necessarily indicate radioresistance. Radio-sensitivity is not synonymous withradio-curability.
30. Therapeutic irradiation of malignant neoplastic
tissue may induce almost immediate inhibition of mitosis
followed soon after by increased abnormal mitoses andcell death. 19 If new radiation reinduces this effect, complete tumour destruction may be expected; but in many
tumours intensive radiation may not induce this response
and the tumours keep growing.
31. Cells within a tumour may differ widely in susceptibility to radiation. In tumours of predominantly
radio-sensitive cells (lymphosarcoma, myeloma) a small
dose of radiation destroys immediately most cells withevident reduction in tumour size, although the growth
may recur rapidly. In tumours havings cells in different
stages of differentiation ( epidermoid carcinoma), evena large dose of radiation may not visibly affect the mostdifferentiated cells : no gross effect may be seen for days
or weeks, yet destruction of basal cells eventually causes
complete disappearance of the tumour. In tumours ofradio-resistant cells (malignant melanoma, rhabdomyosarcoma), a most intense radiation may not cause any
immediate or late effect.
32. Misunderstanding of response of tumours to radiation has resulted in semantic confusion about radiosensitivity (see discussion of this situation by Stewart
and Warren 2 0-21 ). The number of mitoses or the proportion of undifferentiated cells may indicate the immediate
response of radio-sensitive malignant tumour, but anaplasia and reproductive activity are not per se signs ofradio-sensitivity in any or all malignant tumours.
Marked differentiation in an epidermoid carcinoma may
imply a lesser degree of radio-sensitivity, but no epidermoid carcinoma merits the description radio-resistant;nor does a basal-cell carcinoma simply because it fails todisappear as rapidly as others.
33. Clinical observation has established a scale ofradio-sensitivities of malignant tumours, in order of decreasing radio-sensitivity: malignant tumours arisingfrom haemopoietic organs ( lymphosarcoma, myeloma) ;Hodgkin's disease; epidermoid tumours of the upper air
passages; seminomas and dysgerminomas; Ewing's sarcoma of the bone; basal-cell carcinomas of the skin; epidermoid carcinomas arising by metaplasia from columnar epithelium; epidermoid carcinomas of the mucous
membran~s, mucocutaneous junctions, and the skin;adeno_carcrnomas of the endometrium, breast, gastroin122

testinal system, and endocrine glands; soft tissue sarcomas ; chondro sarcomas ; neurogenic sarcomas ; osteosarcomas; and finally, malignant melanomas. Evenamong the latter radio-resistant tumours there may berare instances which show unpredictably a higher degreeof radio-sensitivity (fibrosarcoma and melanoma). Onevariety of liposarcoma is definitely radio-sensitive and iseven radio-curable; this is an exception to the experiencethat radio-sensitivity of malignant tumours depends
upon radio-sensitivity of their cell of origin. This list
represents only average radio-sensitivity in each group ;individual tumours may show more or less radio-sensitivity than their place. Rare tumours of uncertain radiosensitivity are omitted.18
34. Oinically it has been known for a long time thatinterference with blood supply of a radio-sensitive tissue
diminishes its radio-sensitivity22 and the important effectof anoxia on radio-sensitivity has already been discussed.
FACTORS INFLUENCING RADIO-SENSITIVITY

35. Factors influencing radio-sensitivity are reviewed
in annex B as are the radio-sensitivities of viruses,bacteria, protozoa, and other unicellular organisms.

LD so values for mammals
36. The data on LD 50 values (table I) 23 permit tentative generalizations. Other references to LD 50 values
are: mouse and rat, ~ hamster, 29 monkey, 3 0-32 dog, 3 a- 35
burro, swine, sheep and cattle. 36 Additional LD 50 values
for guinea pig will be discussed below.
228

37. There is a clear demarcation of LD 50 values (expressed as midline absorbed dose) between small andlarge animals. Air doses do not reveal this relationship.
The LDr;o for large species is ,...., 250 rad or less for
X-rays with uniform dose distribution in tissues, that forsmall species is approximately double this value orgreater.
38. The tissue-dose LD 50 values for small animals
presently available are all ,...., 400-800 rad for X-radiation, and between ,...., 550-800 rad if the guinea pig is
excluded. The differences might be smaller if different
species were irradiated with identical relative dose distributions. The monkey (Macaca mulatta) cannot be
considered, radio-biologically or haematological!y 37 any"closer" to man than any other small species. Man isdifficult to simulate quantitatively in total body radiation
TBR studies with smaller animals (table I). 38 The dog
is not large enough for direct comparison.
39. The data on guinea pigs given by several previous
investigators 24• 3 - 1 are often difficult to evaluate owing
to dosimetric and statistical difficulties; possible effects
of animal strain; possible disease in some animals. 24• 42 • 43
40. Large animals exposed under similar geometricalconditions have rather uniform LD 50 's (again, the higher
LD:;o values for animals given y-radiations should becorrected for RBE, and dose rate factors before strict
comparison 'vith X-rf.y data), perhaps partly because
large animals, unlike small, provide their own constant,maximum scatter.

LDso and age
41. The average or median acute lethal dose (LD 50 =30 days) for young adult mammals is within ,..., 300-900
rad. ·while it is customary to give the LD 50 for a given
strain independently of age, age causes variations.

42. In the mouse susceptibility is maximal at 30 days,
decreases rapidly to that in young adults, remains constant until advanced age and then increases rapidly. In
the rat the LD50 at age 3 months is ,_, double that at 3
weeks; beyond 3 months it diminishes approximately
linearly with age. More study of this relationship isneeded, but it is now evident that susceptibility of awhole population cannot be adequately denoted by asingle LD 50 • Published values are usually obtained fromyoung adults and are therefore maximal or nearly so forthe strain. This age-dependence must be taken into account in estimating the LD 50 for man.
LD 60 in man

43. Several sources of data are relevant to the LD 50
in man, but each has serious limitations. There are dataon large animals, and also on Japanese at Hiroshima andNagasaki, on Marshallese, and on patients given therapeutic TBR.

44. If the data for large animals apply also to man,the acute LD 5o for man should be ,_, 250 rad for uniform total body radiation, dose expressed as absorbed
dose at the midline. This accords with the low value estimated from the Marshallese exposed to fall-out y-radiation 88 • ... and indicates that the true value probably lies
well below the 450 rad air dose commonly quoted. From
the Marshallese data, the near sub-lethal dose for man
could be estimated; this fixes the lower part of the survival curve at ,_, 200 rad. In dogs and swine an increaseof 100 rad over that received by the Marshallese would
be well within the lethal range. If one uses the same slope
for man as for dogs, the 90 per cent mortality dose isabout 500 rad. By splitting the difference, the LD 50 forman, in the absence of complicating thermal injury,
trauma or therapy, is ,_, 360 rad. 45 Recent data on patients treated with TBR also indicate this low value.'-'• 46 •4 1
200 r TBR depresses haematopoiesis severely but one
must recall that these subjects are already infirm. Blair 48
extrapolating from the same Marshallese data, concludes
that the LD 1;o (air dose) for man probably is not below

400 r. Both authors, using the Marshallese findings,

extrapolate from data in animals, and emphasize thelarge uncertainty in the quantities deduced. Conflicting
facts of trauma, thermal injury, poor nutrition, high andlow neutron component in the Hiroshima and Nagasaki
bombs, and incomplete knowledge of the position ofindividuals and surroundings, complicate calculation of
the LDM for man from the Hiroshima and Nagasaki
data.
45. Recent data on large doses of radiation on
man 49 • 54 do not suffice for accurate estimation of the
LD 50 •53• 55 Difficulties in evaluating complicated dosage
situation in reactor accidents have been reviewed elsewhere, 54 and are discussed later in sections IV and VIII
on effects in man and on treatment.
LD so and dose-rate

46. Figure l 5 6 summarizes data on the relation between LD 50 and dose-rate. For all species the LD 50 increases with decreasing dose-rate.
RADIO-SENSITIVITY

47. This discussion has dealt with only certain aspectsof radio-sensitivity. A survey of the different radiosensitivities of cells, tissues, organs, neoplasms, and organisms indicates that radio-sensitivity is a complicatedconcept: theory is incomplete (para. 20) and radiosensitivities of isolated cells may apparently differ fromthose of the same cells fo viva. Investigators should beaware of these differences and not use radio-resistantorganisms in their study of radiation effects from fallout or for those circumstances in outer space where low
dosages are to be expected. Different radio-sensitivities
of cells, tissues and organs underlie the hierarchy ofdeaths in the different lethal dose ranges and also thedifferent patterns of recovery after radiation below thisrange. This is discussed in section III.

ID. Somatic radiation injury and its repair,particularly in mammals
MODES OF DEATH WITH TBR

48. Acute total-body and regional exposure may cause
various syndromes or modes of death depending on doselevel time after e.'\:posure, type of radiation, and species.51-59 Very high doses (tens of thousands of rad)cause death in mammals in minutes or hours ; this syndrome61l-61 depends on irradiation of the brain. The
marked symptoms of brain dysfunction suggest thatdeath may be from neurological damage. This type of
death can also be produced by radiation of the head
only.6~a

0.1

0.5

I

5

10

DOSE RATE r /MIN

50 10049. The order of events preceding death are dosedependent. As dose is reduced.. survival time increases
until the 3-4 day "gastrointestinal" type of death isseen. This familiar dose-survival time-curve 58 has been
examined for X-rays, thermal neutrons, and fission
neutrons. 64
50. In the "bone-marrO\v" syndrome, in the low-lethal
dose ranges, no doubt the sequelae of pancytopenia(infection and haemorrhage) cause death; the precise
mechanism of death remains open. 6 s-a 6 Sporadic deaths
occur in the few weeks after the bone-marrow death
period, when the marrow has essentially recovered. The
cause of these deaths remains obscure.

500

Figitre 1. Dependence of LDso/30 on dose-rate•s
X Rats (SPRAG-DAW) Logie, Harris et azm
o Chicks (LDso/21) Vogel and Stearner771
0 Mice (CF-1) Vogel, Clark and Jordan 775
Co&O'Y• Mice (CF-1) Thomson and Tourtellotte 7Sl
250 kvp{l:;. Mice (WR-BAGG) Dacquisto and Blackburnm
X-ray O Rats (WR-CF) Dacquisto and Blackburn1110Mice (CBA) Neal'97l12356. Levels of cells in the peripheral blood reflectchanges in number and maturation time of precursors
a.'ld their own life span and changes in their distribution
throughout the body. With some species variation,
lymphocytes decrease most rapidly, granulocytes a little
more slowly; later, platelets decrease and much later,
erythrocytes. Usually an overwhelming bacteremia accompanies profound granulocytopenia; germ-free animals die of anaemia. 92
57. Leukopenia appears faster and is more severe in
irradiated weanling rats and hamsters than in adults, but
recovery is more rapid, indicating a more labile homeostasis.s3-94

Partial body irradiation
51. Quastler et al. 61 have reported deaths two weeks
after irradiation of the head, jaw or tongue of the mousewith 1,500 r or more. The mechanism remains obscure.
Similar deaths have been reported after 1,500 r to thehead of rats. 68 Dogs given 1,750 r to the head only survived five months or longer. 69 In the "total head" (brain)studies of Mason et al judging from survival time, theeffect described by Quastler 67 probably caused death.
52. The gut syndrome is identical if caused by
TBR or by local irradiation of a large segment ofbowel. 5 1-S"ll, n-12 Re-section of irradiated intestine increases survival beyond the time when death from thegut syndrome would otherwise be lethal. 73 Depletion of
fluids and electrolytes contributes greatly to the immediate cause of death since massive fluid repla~ement
prolongs survival. 74 Death from this syndrome can beprevented in some animals by shielding only a small
portion of the duodenum or ileum, but not by shielding
the caecum or stomach ;75 the authors feel that protection
operates through protection of some bowel function
rather than by repopulation as in spleen or bone-marrowprotection. 76
53. The bone-marrow syndrome and shielding havealso been studied by Lamerton et al. 7 7-7 9 They showed
clearly by weight changes two phases of radiation injury,
and confirmed that shielding of even a small portionof bone-marrow minimized haematopoietic depression.
They also emphasized the importance of anaemia in theacute bone-marrow syndrome in the rat. The remarkableprotection given by marrow shielding and the degree towhich this may be masked by bowel damage have beenshown by Swift et az.sa
54. Maisin et al. in Belgium have studied shielding indetail 81 -s 3 and concluded that :(a) There are at least two syndromes after TBR;
( b) Shielding of bone-marrow or bowel prolongs survival; and( c) Protection of bowel and bone-marrow by shielding acts synergistically.
These conclusions agree with those of many workers. s•. 5B, 1s, s4, ss

58. Extracellular fluid and plasma volume increase
after irradiation in dogs, 95 rats. 96 mice, 97 and rabbits 98 at
the e..xpense of intracellular fluid. An initial decreased
plasma volume of rats accompanies radiation diarrhoea. 99
59. In rodent spleen, as in marrow, LD 50 irradiation
inhibits mitosis and damage to lymphocytes is evident
within an hour. In survivors regeneration begins on days
9-10 but in lymph nodes, destroyed follicles may not be
restored for three weeks. As in bone-marrow, injury
increases with dose within certain ranges. In different
species, a particular dose-level damages lymphatic tissue
similarly, regardless of lethality. 99
60. Cell destruction shrinks lymphoid tissues. The
dose-dependency of the weight response of spleen andthymus is discussed in section VII (dose-effect relationships). Weight loss is in part directly due to radiation
damage and in part indirectly mediated through theadrenal has a stress effect.iao
Digestive tract
61. Sensivity of the epithelium of the small intestine
is second only to bone-marrow in deciding survival after
TBR with X- and gamma rays. After irradiation at highLET, the intestine may be the critical organ determining
survival at the LD 50 in mice.101 In mice, doses below
1,000 r damage the intestinal mucosa but animals do not
generally die from this cause but rather between days
10-14 from bone-marrow damage. From 1,000-10,000 r,
mice die 3-4 days after irradiation with complete denudation of intestinal epithelium :71 death is due to failure offood absorption, dehydration from diarrhoea, and bacterial invasion, and toxaemia.1020 103
62. The radio-sensitivity of the various parts of thealimentary system varies greatly: stratified squamous
epithelia are of the same sensitivity as the epithelium inthe skin ;1a. intestinal mucosa is much more sensitive
than gastric mucosa; small bowel more than large. 105 • 100"Oral" radiation death has been described in mice. 67
Death does not resemble that from intestinal or bonemarrow damage.
63. The stomach and esophagus are more radio-resistant than the intestine.1 n7 • 1 ns Two effects may be seen in
the stomach : (a) functional and degenerative morphological changes with subsequent repair: ( b) developmentof gastric ulcers in man several weeks after 1,600 r tissue
doses given to the gastric fundus over ten days in divided
doses via anterior and posterior fields. 109 Destructive
changes seen as early as thirty minutes after moderate
doses in rabbits exposed to LD 50/30 days of X-rays,_, 800 r are most pronounced after eight hours andrepaired within four weeks.110 Similar effects are seen inmice after 350 r, in rats after 400 r, and in chickens after
800 r total body radiation. There is hyperplastic regen-

EARLY AND LATE ORGAN EFFECTS

Blood a11d blood-forming organs

55. Haematopoietic tissue is one of the most radiosensitive tissues with cell death as end-point. In general,
the sensitivity of bone-marrow of different species increases from rat, rabbit. mouse, chick, man, goat, guinea
pig to dog. 86 After an LD 50 dose the mitotic index falls
and erythroblasts decrease within an hour. \Vithin a few
hours there are many dead cells and cellular debris.
Myeloid elements regress increasingly with cytoplasmic
and nuclear disintegration. After 9-10 days, the marrow,filled with a gelatinous, relatively acellular mass containing degenerating cells, has only the relatively radioresistant fibroblasts, blood vessels. and primitive reticularelements. Animals which will survive. regenerate normoblasts and myeloblasts from spared haematopoietic
precursors, and eventually the marrow may be completely
regenerated. In rats and rabbits, after doses in the lethalr~nge, e91:hr?poiesis regenerates earlier than myelopoies1s ;61- 88 m mice both types regenerate at the same time,or myelocytes first. 81 - 99 The effect of radiation on bonemarrow has been reviewed extensively. 8 s- 91
124erative activity with continued degeneration of manycells for the first few days. At twenty-one days all
mucosae, possibly with the exception of duodenal crypts,
are normal. Damage is greatest in duodenum, least incolon and rectum.
64. Doses of 1,000-1,200 rad given locally 111 • 112
diminish gastric acidity and gastric ulcers may develop
after several weeks.11 a-i 16 Although radiation increases
intestine tone and contractions, gastric emptying isdelayed.117- 119 In dogs, gastric emptying time is prolonged only after three or four times the LD M,120 but
after as little as 25 r in rats.
Reproductive organs
65. Acute doses of radiation causing only marginalchanges in the gut or blood-forming tissues may induce
permanent sterility and endocrine dysfunction in thefemale. Males may become temporarily sterile, but theacute doses required to produce permanent sterility in themale are above LD100 in all species that have been studied. Understanding the effects of radiation on the reproductive organs is important because those germ cells
which survive to form gametes can transmit the genetic
changes induced by radiation. Since genetic damage isqualitatively as well as quantitatively dependent on the
germ-cell stage in which radiation was received 89• 121 - 124
it is obviously important to know the relative radio-sensitivities of various germ-cell stages over a wide rangeof doses and dose-rates.

Male animals
66. In the male, the various stages in the developmentof spermatozoa, from the earliest spermatogonia to themature spermatozoa, have very different sensitivities toradiation. An understanding of normal sperrnatogenesis
is, therefore a prerequisite in understanding radiation
effects on the testis.
67. The spennatogonia of monkeys can be divided
into type A 1 , A 2 , B1, B2 , B3.123 In rodents spermatogonia
can be divided into type A (dusty) and type B (crusty)
by cell morphology and developmental potentiality; atransitional type between A and B, designated as intermediate spermatogonia, can also be identified in rodents.
In mammals, type A spermatogonia are the true stem
cells and through stem cell renewal form an unlimited
number of spermatocytes while maintaining a constantcell population. This wave of activity leading to newspermatocytes is cyclic. In the monkey, type A spermatogonia undergo mitosis and transform into type A2
spermatogonia and so on until type B3 spermatogonia
divide to form resting primary spermatocytes. In themouse and rat type A spermatogonia undergo a series ofmitoses, and most of the products of the final divisiontransform into intermediate spermatogonia. The intermediate spermatogonia divide to form type B cells, which
in tum divide to form resting primary spermatocytes.
Determination of the developmental potentiality of individual spermatogonia takes place before the last divisionof type A cells, in which certain spermatogonia form thestem cells for the next multiplication cycle.127 • 128 This
basic process is essentially the same in all mammals
studied including the monkey and man, 125• 1~ 6 variation
is associated with differences in the number of identifiable spermatogonial types and duration of spermatogenesis.
68. Because of the similarity in normal gametogenesis,
the radiation response of the testis is basically the samefor all mammals, but modifications are required in extrapolating from the response of laboratory animals to thatof domestic animals and man. Thus species may differin: (a) duration of spermatogenesis (i.e., the time fortype A spermatogonia to develop into mature spermatozoa), e.g. spermatogenesis takes 35 days in mice, andaccording to Arsenyeva and Dubinin ,..., 70 days inmonkeys. 1 ~ 9 It is probable that duration of spermatogenesis in man is nearer that of the monkey than that of
the mouse; ( b) time for spermatozoa to travel from thetestis to the ejaculate; ( c) regeneration rates, which area function of (a) above; and ( d) possibly, intrinsic
sensitivity.
69. Adult male mice given acute doses of 200 to 1,000
r either to the testes only or to the whole body (highdoses, of course, are limited to partial-body exposure),
are initially fertile, owing to continued development andutilization of gametes irradiated as mature spermatozoa,
spermatids, and possibly spermatocytes. An infertile
period follows owing to destruction of spermatogonia.
A few type A spermatogonia, however, survive and repopulate the seminiferous epithelium, and almost normal
fertility eventually is regained. Doses of 100 r cause
temporary sterility in the monkey for,..., 2 to 3 months.129

70. Sensitivity of the different stages in spermatogenesis has been most thoroughly investigated in themouse. Intermediate spermatogonia and early type B
spermatogonia have LD 50 's in the range of 20-24 r.128
Type A spermatogonia show a wide range of sensitivities. At doses below 25 r, survival is comparable tothat of intermediate spermatogonia; but, at higher doses,
survival is relatively much greater. 128 A few type A
cells survive doses as high as 1,500 r. Thus the paradoxof high sensitivity of spermatogonia, which results inthe temporary sterile period coupled with high resistance,
which leads to return of fertility, is readily e.'Cplained.128
The primary effect leading to depletion of spermatogonia
is cell death, mostly in interphase or early prophase,before cell division. 130 With doses of 100 r or more, somecells die after cell division, probably because of chromosome imbalance ; a few cells appear to divide several
times before degenerating, but these effects involve only
a very few cells. As a result of extensive necrosis, particularly in interphase and early prophase, it is difficult toestimate the amount of spermatogonial depletion arisingfrom mitotic inhibition; this inhibition is probably comparable with that seen in other germinative tissues. 131
Doses of 100 r caused the death of all Bi, B2, and Ba
spermatogonia in the monkey.1 :?S
71. In mice, spermatocytes show no immediate damage even after radiation doses of 1,000 r, but degenerate
during meiotic division. From the number of spermatids
formed, LD~ 0 's ranging from 205 r for preleptotene to837 r for diakinesismetapbase I have been obtained.132
In the monkey, resting spermatocytes are damaged after
100 r.m Spermatids formed by irradiated spermatocytes
show anisocytosis, indicative of aneuploidy and heteroploidy; this later results in many abnormal spermatozoa
in the ejaculate.
72. Spermatids and spermatozoa show no morphological changes after irradiation nor is the rate of spermiogenesis altered. Mature sperms may be motile after
50,COO r. 133 Such sperms, however. have such severe
genetic damage that normal development of a resulting
zygote is precluded.
73. The efficiency of fractionated vs. single doses isinfluenced by size of the fractions, intervals between
12579. In the adult mouse, all oocytes, except those about
to be ovulated, are in dictyate stage. Dictyate oocytes inearly follicles are the most radio-sensitive cells in theadult ovary, and are completely destroyed by SO r. 1 • 3
As the follicles mature, resistance of the contained oocyte
increases, and at least one litter usually is obtained fromfemales given 400 r.1 u A similar increased resistancewith development of the follicle has been observed in
the rat,1"" but the dose required to sterilize the female
rat is higher. Resistance of mature follicles also is shownin women, since there are a few ovulations after 300 r;
early follicle stages must be resistant, however, because,
after a period of amenorrhea, ovulation begins again. 145

doses and total dose. In the mouse, fractions given
withi~ a 4-day period act as a single dose.m Maximum
effectiveness of fractionated doses in different species
depends on duration of normal spermiogenesis and reproductive potential. Because information is scarce on
the dynamics of spenniogenesis in species other thanmouse and rat, contradictory assumptions have been
made, in planning experiments and in interpreting data.
In dogs, a single total body dose of 300-375 r results inonly a partial and temporary reduction in spermiogenesis, with return to normal within a year. This contrasts with complete aspermia after 375 r given overtwenty-five weeks at 15 r/wk, there being no sign ofrecovery within a year after irradiation. 45 In the dog,
long-term radiation gradually reduces the number, motility and viability of sperm. Such damage is one of themost sensitive indicators of chronic damage seen so far
in dogs given 3.0 r/wk, i.e. 30 times the average ma.ximum permissible dose-rate (occupational).
74. With prolonged exposure at low dose rates, anequilibrium is established between the cell death, mitotic
inhibition, and regenerative activity of the seminiferous
epitheliurn,135 this equilibrium being dependent on dose
rate rather than total dose. If dose rates are low enough,e.g. 10 r/wk in the mouse or 0.1 r per day 136 in the
dog and some other species, fertility remains unaffectedeven after thirty weeks' exposure. Histologically, however, a decrease in cell populations can be demonstrated
after 100 rat this dose rate. 187 At 90 r/wk, cell populations are severely depleted, and if doses of 300 r or moreare given, temporary sterility is comparable to that following the same dose of acute irradiation.188

80. Species comparisons are very difficult in thefemale, since meiotic prophase stage, relative frequenciesof resistant and sensitive oocytes, rate of follicle growthand number of oocytes required for normal fertility undoubtedly vary widely. Valid comparisons of intrinsic
sensitivities require more information on the cytology
and dynamics of normal oogenesis.
81. In mice lowering the dose rate decreases thesterilizing action of a given dose of radiation. The shortening of the breeding period-the characteristic effect ofradiation on female fertility-is dependent on dose rate.
Fractionation and even more directly, long-term administration of a given total dose postpones the onset ofsterility. The greater the fractionation and the more protracted the long-term dose, the longer is the onset ofsterility postponed. These results indicate that some radiation damage to oocytes can be repaired, and that repair
is greater at lower dose rates.141 Conflicting conclusions
in the literatureHs-Hs are due to the use of the first postirradiation litter, not length of breeding period, as theindex of effect.

75. Testis weight as a biological indicator of radiation
damage is discussed later under "Dose-effect relationships" (section VII).

Sexually immature at1imals
82. Studies in laboratory mammals show that germ
cells may change sharply in radiation-sensitivity as theanimal develops. In the female mouse, for example, thelate foetus 141H 51 and the newbom152 are relatively moreresistant than the adult; but, only two days after birth,a two-week period of extreme sensitivity sets in, during
which sterility is much more readily induced than in theadult. 152

Man

76. A single dose of 400-600 r to the testes may cause
permanent sterility.139 Temporary sterility of twelvemonths' duration usually follows 250 r; even 30 r to thehuman testis may be injurious. 140 In relating studies onlaboratory animals to the response in man, it is of primary importance that corrections be made for differences in time-sequence arising from differences in therates of normal gametogenesis. Such a correction factor
would for example explain the slower recovery in man.

83. The fertility of animals irradiated in utero or inearly post-natal life can be understood only in terms ofthe normal development of germ cells and the sexual
dimorphism which exists in this respect. During mitotic
divisions of the primordial germ cells or their precursors,
males and females are about equally sensitive to radiation-induced depression in fertility. In the mouse, both
sexes, when irradiated with 200 r as 70 or 90 day
embryos, show somewhat depressed fertility throughout
their lives.153 In the female, the fertility depression becomes greater following irradiation at a later stage, day
110 postfertilization, and even greater for day 130.163
Similarly, the developmentally corresponding stage inthe rat. day 15 is, by histological criteria, the most sensitive of the foetal stages.154 It should be noted thatmitosis of the primordial germ cells in the female is at a
ma.ximum at this stage. In the male rat, on the other
hand, sensitivity continues to increase and is highest on
day 19.m

Female animals

77. Since there are no cells comparable to type A
spermatogonia (stem cells) in the adult mammalianovary, females of some species are more easily permanently sterilized than are males. The supply of oocytes
if once destroyed is not replaced.
78. The adult female mouse given 300 r acute TBR
produces, on the average, 1.4 litters as compared with
14.9 in controls. A dose of 100 r TBR produces complete
sterility in twelve weeks, 50 r in twenty-two weeks. 141
Even 30 r, given in three divided doses at weekly intervals, produces sterility in some animals. 142 The mouse
ovary tends to develop invaginated tubular downgrowths of germinal epithelium and ovarian tumours.
These changes, which are readily increased by relatively
low doses of radiation, are, however, not the cause ofsterility: sterility results from the killing of oocytes indeveloping follicles. Since oogonia are no longer present
in the adult, there can be no repopulation of germ cells.

84. With the onset of meiotic prophase, sensitivity isfound to decrease, well in accord with the relative radiation-resistance of this stage demonstrated in a wide variety of organisms. In the female mouse and rat, meiotic
126prophase begins about four days before birth. In malefoetuses of the same age, however, the germ cells present
are still in a primordial stage and undergoing mitosis.
This sexual dimorphism in development explains theapparent reversal from the adult situation of differential
sensitivity of the sexes that has been observed for latefoetal stagesull-151 when males are more sensitive thanfemales.
85. Shortly after birth, when the progress of meiotic
prophase ceases in the female, and the oocytes assume theearly dictyate phase, a period of extreme sensitivity
sets in. This has been demonstrated by fertility studies 152
and histologically156 in the mouse, and histologically inthe rat. 1« In the mouse, an LDM of 8.4 r (95 per centconfidence limits: 7.2 and 9.7 r) has been observed for
oocytes in the smallest follicles of ten-day old females 161
and even long-term irradiation has severe effects on
fertility. 152
86. It may provisionally be assumed that the mouseand rat results here summarized can be e.xtrapolated toequivalent germ-cell stages (rather than equivalent ages
in other species. In particular, the existence of periodsof extreme sensitivity at certain stages in the development of the human ovary is a possibility of the utmost
importance.

Eye
91. The lens of the eye is highly susceptible to irreversible damage by radiation. Sensitivity varies withsubjects and with type of radiation. Doses of 15-30 r,
X-rays and possibly 1 rad of fast neutrons11• induce
minimal lens opacities in the mouse; the threshold sensitivities of rats, rabbits, dogs and man decrease progressively for X-rays, {3-rays and neutrons.
92. The retina is more resistant than the lens. In themonkey, 2,000 r destroys the rods; 30,000 r inducesmorphological change in all retinal elements. 11 s-170
Retinal haemorrhages, retinitis, choroiditis, and iridocyclitis developing days to weeks after TBR are due tosystemic alterations. 177

87. The effect on foetal cells is discussed further
under the section on embryos in this chapter.

93. Some very low doses-0.5 to 1.0 mr-give thesensation of light in man. 178 In frogs, electroretinograms(ERG) and the discharge of nerve impulses by retinal
ganglion cells in response to retinal irradiation have beenmeasured.17° Less than 11 r caused an immediate temporary rise in the light threshold, and 0.7 r caused an
immediate temporary rise in the X-ray threshold 5 X
greater than the rise in light threshold caused by athreshold light stimulus. Doses of 5-100 r, after temporary intensification of the electrical response of theretina to light depress it down to complete loss evenafter the lowest dose. 180 The conclusion that high-energy
irradiation of the eye produces effects with doses as low
as 0.5 mr needs further study. 179

Nervous system
88. The brain is more radio-sensitive than generally
supposed. Although no morphological change has been
seen at LD 50 doses, transient functional changes havebeen reported at low doses. Doses of 100,000-200,000 r
kill almost instantly, probably by destruction of medullary centres. 1 G7 With lower doses that kill hours after
exposure, there is a question how much brain damage iscaused directly by radiation and how much is secondary
to vascular destruction. The effects of 2,500-10,000 r
have been described in rabbits 15s-i 59 and monkeys. 1 eo-u 2
Doses in the LD 50 range163 cause no EEG changes inmonkeys but these are induced within 1-2 minutes after
rradiation at 1,000 r/min. 1 0. Single exposures of 1,0001,500 r of X-rays may quickly kill a few oligondendroglia and some neurons. 165 The developing nervous
system is much more susceptible to radiation injury.
Single doses of a few 100 r kill the most primitive embryonal neural cells, and as little as 20-30 rare damaging
in animals.166 This is discussed later in this section(paras. 170-192).

•

radiation to the abdomen of 54-108 r induced avoidance ·similar do~e~ to other areas of the body failed to do so'.
but such hm1ted exposure was not as effective as TBR.
Changes in the conditioned refie.xes of dogs have beenreported after single TBR and local head irradiation at
5, 10 and 20 r. 171 vVork in the USSR on effects of radiation in the central nervous system11z and on its sensitivity to low-level radiation was recently reviewed. 1 n
Some effects of low doses, interpreted as effects on the
nervous system, are based on the concept that the CNS
controls all reactions in the organism. Thus, postirradiation pancytopenia is considered an effect mediated
via the CNS. 112

Liver
94. Judging by morphology, the liver is radio-resistant as compared with other organs although minor
cytological changes have been seen.181- 185 A low (6 percent) casein diet tends to result in cirrhosis several
months after rats are given 500 r.1 ss-u 7 Liver regeneration, as measured by weight recovery, is not impairedby 20,000 r. 188 On the other hand, sublethal TBR greatly
increases the frequency of abnormal mitoses in regenerating liver of the rat for at least 250 days.189 Decreased
incorporation of P 32 into DNA of irradiated regenerating liver190 may, in part, be due to decreased uptake byreticulo-endothelial cells.

89. In contrast to the brain, the spinal cord and peripheral nerves are highly resistant. No alteration in
structure or function of monkey spinal cord was foundafter twenty-four hours y-radiation at 135 r/hour. 167
Damage of the spinal cord blood vessels by doses of
3,000 rand more can induce occlusive disease leading toischemia of the cord, i.e., radiation myelopathy as a lateeffect.

95. Changes in liver mitochondria were found in mice
6-8 hours after 500-1,200 r; their structural stability decreased; they became vesiculated, globulated, and fragmented; and were also decreased in number. 191 These
alterations are not specific for radiation.

90. Radiation can condition the behaviour of rats,
mice and cats so that they avoid identifiable stimuli previously associated with radiation exposure. 16s-11° Fastneutrons as well as y- or X-rays can condition such
behaviour. A TBR dose of 7.5 rad given animals was
sufficient to alter preference for saccharin. Animals
learn to avoid a compartment in which they had been
irradiated, and this avoidance is more pronounced whentaste cues are coupled 'vith radiation exposure. Localized

Kidney96. Because impairment of renal function does notcontribute to mortality after TBR, the kidney is considered radio-resistant; this is supported by clinical127

zation of the collagen. The skin reactions generally are
more severe after exposure to less penetrating radiation.
104. From extensive studies on the effects of locallyapplied radio-isotopes on the skin, it has been found that
exposure of the skin to external /3-irradiation may induce
severe skin lesions.
105. According to Moritz and Henriques~ 18 /3-irradiation of pig skin produced epidermal atrophy, appearing
one to two weeks after exposure and lasting for two to
three weeks, often with ulcerations and transepidermal
necrosis. Healing was slow, and often a chronic radio
dermatitis persisted.
106. Presumably the late deleterious changes in irradiated skin are the direct result of radiation damage toepithelial cells and indirectly the result of starvation andanoxia of these cells due to ·vascular radiation trauma.
Radio-sodium clearance measurements have, however,led to the startling observations that the effective bloodflow in these densely fibrotic, scarred, and atrophiedtissues is functionally unimpaired at any time up to years
after irradiation.m This indicates that vascular damage
plays little role in the deleterious changes after skinirradiation. Some of the changes in the skin after irradiation may be secondary to infection in radiation-induced
ulcerations.
107. The skin is more resistant to tumour induction
by irradiation than most internal organs. Cutaneous
tumours, however, were the first noted in man, owing to
the relatively soft X-radiation used earlier and lack ofadequate filtration.
108. In animals. tumours of the sJ...-in have been induced mainly by /3-radiation, and co-carcinogenic or promoting effects have been observed from application ofchemical carcinogens 215 or croton oil216 respectively.

radio-therapeutic experience. Only if several tlmes 0elethal dose is given the kidney are marginal changes mrenal function seen in dogs 192 and rats. 198
97. Nephrosclerosis developing several months after
exposure has been described in mice given 50~ r ;194 mi~esurviving doses of 800 r after treatrn~nt wit!; spl~ruc
homogenates died probably of renal failure. 19 a Similar
lesions (radiation nephritis) have been seen in dogs andman after local irradiation of the kidney region ·withlarger doses. Avian kidneys are much more sensitive
than mammalian kidneys.196
Circulato1·y system
98. "Within a few hours after exposure to single dosesof X- or y-radiation in the LD 50 range, arterial bloodpressure drops. It usually soon returns to normal an.cl
remains so until a few hours before death. Although thts
initial decrease has been reported in every species examined, death from circulatory collapse may be inducedby LD 50 doses in the rabbit, chick, duck and burro.
99. Although only massive doses of radiation induce
histological change in the heart, ECG changes have beenfound in dogs,197 hamsters, 1118 and rats199 after LD50
doses. ECG changes are at least in part due to change inpotassium concentration in serum ;200 radiation causes
release of potassium from the isolated rabbit heart andfrom the heart irradiated in situ.199 Doses of 1,0002,000 r produce slight vasodilation in the per!us~d isolated rabbit ear; doses of 2.500 r and above brmg immediate vasoconstriction ;201 - 202 after 8,000 r flow is completelv inhibited for fifteen to twenty minutes ; the bloodvessels are damaged at all those doses as indicated by theappearance of increased amounts of protein in perfusion
fluid.
Endocrines
100. In general, doses in the LD:;o range induce few
signs of damage in endocrine tissue. The normal a.dult
thyroid gland is fairly radio-resistant: 17,200 r given
locally causes negligible changes in rats ;203 10,000 r _may
cause histological change in dog thyroid. 2 G4 Local tr~a­diation of the thyroid of young or mature rats with
5 OOO r X-rays does not cause morphological change,~edified basal oxygen consumption, or loss in bodyweight. 205 In tadpoles more than 20,000 rare needed toalter the thyrotropic function of the pituitary. 206
101. Doses of 5.000 r alter the alpha cells of the islets
of Langerhans in the pancreas ; beta cells show littlechange below 20,000 r. 207 Adrenals show degenerativechanges after heavy local irradiation ( > 5,000 r) but
after 1,000 r only minimal morphological change in cortex and medulla. 208 ; 209

Bone109. Bone tissue is generally believed to be relatively
radio-resistant. Some observations, however, indicatethat bone tissue damage may follow even a rather low
dose. This is especially so in young individuals. The
foetal skeleton is highly radio-sensitive; the system responsible for bone growth may be especially severely
damaged by irradiation. The growth of long bones may
be inhibited. This is seen in rats after a dose of 600 r.m
A single dose of 400 r TBR of rats reduced the numberof osteoclasts.
110. The retardation in osteogenesis is permanent andirreversible after 2,000 r local irradiation in rats, and
5. 000 r to the femurs of guinea pigs caused a complete
osteonecrosis.
111. A characteristic feature after irradiation of bone
tissue is the absence of any demarcation between normal
and irradiated parts. Irradiated bone is more easily infected than normal bone, especially if necrotic spots arepresent but healing of fractures is not significantly
altered after moderate doses.
112. The effects of internal irradiation on bone aredescribed in section VI below.

Skin102. Degree of skin damage after irradiation depends
on the dose received and also on the species of animal.
Individual differences in sensitivity are fairly large.
Furthermore. the various structures of the sJ...-in havelarge differences in sensitiv-ity.
103. Epithelial changes in the skin of the mouse ear
have been described after a dose as low as 35 r. 210
Epidermal mitoses are much reduced. After 600-800 r
TBR some inflammatory reactions with slight hyperemia
and some oedema are seen. 89 • 10•· 211 • 212 After higher
doses the epithelial cells become swollen and vacuolated.
Vascular changes presumably play a great role. Aftersevere irradiation the inflammatory changes may be followed by sclerosis \Vith loss of elastic fibres and hyalini-

LATE EFFECTS

Life-shortening 218
lntrodttction
113. In mammals radiation in substantial doses towhole- or part-body shortens life-span. In part-body128•

exposure, the life-shortening effect is variable dependingon the kind and amount of tissue irradiated as well as
dose. Radiation may shorten life-span by: (a) damaging
a specific tissue (e.g., dermatitis followed by skin cancer) ; ( b) inducing a specific disease (e.g. leukaemia) ;( c) producing more generalized changes (e.g. lowered
immunity, damage of vasculo-connective tissue and premature aging).
114. Data for man are yet inadequate to assess theeffect of radiation on life-span. From animal data andthe increased incidence of leukaemia in man after totalbody or marrow irradiation, some life-shortening is to
be expected.
115. Comparisons of mortality rates of United Statesradiologists with other physicians and the general malepopulation indicate that occupational exposure may haveslightly increased mortality rates of radiologists in past
decades. The cumulative doses are not known for individuals; the dose-life-shortening relationship cannot
therefore be measured. British radiologists showed noclear increase in mortality rates. This subject requires
further study.
116. In animals, the survival time for given dose rates
is generally shorter the more energy absorbed. Lifeshortening is less for a given dose absorbed over a longtime than over a short one. Some evidence suggests thatradiation-induced life-shortening depends on genetic
constitution, age, and clinical status at exposure.
117. Animals irradiated with substantial but sublethal
TBR, after recovery from the acute early illness, dieprematurely. They develop the diseases of their species
earlier than usual and deteriorate sooner than nonirradiated controls, with various physiological and histopathological changes suggestive of senescence. At a first
approximation, comparison of mortality curves of survivors of acute radiation mortality and controls suggeststhat radiation causes premature aging in an actuarial
sense.
118. Some premature deaths after radiation are due tothe increased incidence of such diseases as malignant
neoplasms. This is especially tme after localized irradiation from external sources or from locally depositedradio-active materials. After TBR the number and variety of diseases induced are greater than after localized
irradiation. At their respective median death times, animals whose lives are shortened by single TBR and controls usually have approximately the same diseases,
although not necessarily the same proportions. Irradiation may separately induce each of the diseases of advanced age or cause a general deterioration of bodytissues that advances the onset of most diseases toroughly the same extent. Some animal species or strains
are unusually susceptible to certain diseases, e.g. ovarian
tumours and lymphatic leukaemia in mice, and mammary
tumours in rats.
119. In general, irradiation increases the incidence
and severity of recognizable diseases at given chronological ages. When these cjiseases appear rarely or not at
all in controls, or are thought to have different pathogeneses from similar diseases in controls, they are regarded as having been induced by radiation. Diseases
common to the population which appear earlier in irradiated animals than in controls are regarded as having been
advanced by radiation. In many experiments both effects
may be combined, with induction relatively greater after
local radiation and advancement relatively greater after
TBR.

120. The life-span of animals often falls short of thepotential because infectious diseases kill many well before senescence. In man, the counterparts of these lifelimiting diseases have been largely eliminated in countries with adequate medical services; non-infectious
diseases associated with senescence are prominent. In
animals, diseases of long latency may rarely or neverdevelop spontaneously within the life-span observed.
Consequently, it is possible that some, if not all, diseases
considered induced by irradiation may be diseases oflong latency whose onset has been advanced. When intensive, localized irradiation causes a high incidence of
certain diseases, induced or advanced, to the irradiatedpart, the incidence depends on the latent period of thedisease relative to the development of other terminal
diseases to which the animals are susceptible. This, inturn, depends on the age of the animals.
121. These considerations on the effects of irradiation
on life-span, mortality curves, cause of death, and timeof onset of disease. together with available information
on clinical, physiological and histopathological effects ofirradiation. indicate a resemblance between the pathological events underlying radiological life-shortening andpremature aging processes. Whether the two processes
are similar is not clear, and whether they are identicalcannot be decided until the causes of radiological lifeshortening and physiological aging are better understood.
Life-shortening by single doses in animals21 8122. Recent data demonstrating life-shortening ofmice and rats by single TBR with X- or y-rays have been
given.21 0- 231 Data on rodents indicate that the lifeshortening effectiveness of single TBR \vith X- or y-rays
increases as dose increases. The life-shortening can be
expressed either as an absolute time interval or as apercentage reduction of life span. The use of the latter
definition in the following paragraphs does not imply thata value obtained for one strain or species will necessarily
hold for another of different life-span. For doses up to
300 rad, the reduction per 100 rad is constant or slowly
increases with dose, but increases rapidly for doses approaching the LD 50 • Other data are not inconsistent witha linear relationship. 232 At doses from 200-500 rad ( i'),the reduction is 2-4 per cent per 100 rad depending on
dose. As one approaches the LD 60 (600-800 rad) etc.,
reduction of life-span is accelerated about 25-50 per cent(5-10 per cent per 100 rad).

123. Doses < 200 rad do not usually significantly
shorten life in the numbers of rodents tested to date.
On the assumption that effect remains proportional todose down to the smallest doses, extrapolation from present data gives an upper limit of ,_, 1-5 per cent per 100
rad to the life-shortening effect of single doses below
200 rad. It is possible that effectiveness falls below thisvalue for 10 rad or less.
124. Female mice show more life-shortening thanmales at all dose levels, presumably due to endocrine disturbance after radiation damage to the ovary. The extraordinary radiation sensitivity of mouse ovary has no
known parallel in other species, nor is there evidence ofdisproportionate life-shortening in female rats or guinea
pigs. There is no basis for expecting a large sex differential in life-shortening in man.
125. The RBE of fast neutrons for shortening life iscompared to X- or gamma-radiation ,...., 2-3 at the LD 60
level. The RBE for life-shortening is thus about thesame as that for acute lethality. Although survival data129

after a wide range of neutron doses are !lot yet ava~labl~,
accumulating evidence suggests that hfe-shortemng isnearly proportional to dose, rather than an acceleratedfunction as after X- and gamma-rays. Consequently, theneutron RBE for life-shortening increases as dose decreases. If the X- and gamma-ray effectiveness becomes
proportional to dose, at sufficiently small doses the RBE
for life-shortening by fast neutrons may approach alimiting value. The highest value so far experimentallyseen is,...., 10.

found that exposure of mice 730 days old did not reduce
life-span. An explanation for this decrease in effect withage is perhaps found in experiments 240 in which mice
435 days old exposed to 500 r of TBR had an increased
death rate over controls twenty-four weeks later in malemice and sixteen weeks later in females. Thus the damage which induces premature death evolves slowly andsince twenty-four weeks are an appreciable fraction of
normal life-span, irradiation of animals late in life does
not allow sufficient time for damage to express itself.

126. Several studies are in progress 220 • ~ss, 234 on lifeshortening after a wide range of dosages; data fromOperation Greenhouse194 remain the most extensive. The
conclusion235 that life-shortening is a non-linear functionof dose, with an accelerating rate of loss of life withincreasing dose, has been challenged. 236 The data ofGowen and Stadler2 31 covering a wide dose range indicate a curvilinear relationship ; and the data of Storer
and Sanders226 compatible with a linear relationship, do
not permit a choice between the alternatives. No studies
to date provide direct evidence for or against a thresholddose below which radiation is ineffective.

Partial-body exposures130. Partial-body exposure of mice and rats is far lesseffective in shortening life-span than TBR. 2281230•:2 4 0- 243
The extent of life-shortening depends on area irradiated,size of field, and total dose. Maisin et al. m found that inrats survival curves had different shapes depending on
body part exposed. They concluded that the TBR survival curve is a composite of partial-body curves andthat injury to various body regions summates to produce
the total-body effects. Lamson et al. 240 reported that lifeshortening was roughly proportional to the percentage
of body radiated. But no clear-cut relationship allows
direct extrapolation of TBR information to partial-body
exposure.

Life-shortening by multiple doses or protracted irradiation in animals 218

127. Small animals given comparatively small daily
doses of X- or y-radiation for several months or more
have about 11 per cent life-shortening per 1,000 rad.
The effect is proportional to dose, or nearly so, for accumulated doses of 500-2,000 rad or more. This factor isconsistent with the rough estimate given for life-shortening by small single doses.
128. The dose-effect curve for exposures over days
and weeks falls between those for single doses and thosefor highly fractionated exposure ; the slope of the curve
diminishes as exposure time lengthens. But, there is no
sharply defined point on one side of which response issimilar to that with a single dose and on the other response is similar to that for continuous exposure. Effects
intermediate between single and continuous exposure
have been shown. 235 At present, data are insufficient forformulation of empirical relations to predict responses
for all conceivable fractionation schedules. One difficultyis the variable response of different strains of mice.
Appropriately timed fractionated exposures are clearly
more leukaemogenic than single exposures 231• 2 ss for certain strains with a high susceptibility to radiationinduced lymphatic leukaemia. In such mice if leukaemia
is a major cause of death, fractionated exposures may be
more potent in life-shortening than single exposures 238
even though the incidence of degenerative diseases, suchas nephrosclerosis, decreases with increasing fractionation. Such data can be corrected for the high incidenceof leukaemia, or other strain or sex specific tumours toevaluate life-shortening from other causes. 224 Corrected
data, unfortunately, are not usually reported. Data onlife-shortening effect of a long-term protracted radiation
with fast neutron compared to X- or gamma-radiationsuggest an RBE of around 10.

Role of genetic constitiition and physical sfatus218
131. Information on the influence of genetic constitution on long-term survival after radiation is meagre but
permits preliminary discussion. Most work on genetic
constitution in radiation-sensitivity of mammals examines differences in response of genetically homogeneous(inbred) mouse strains and their hybrids. Susceptibility
to early, acute death differs by somewhat less than afactor of 2 between the most sensitive and the mostresistant strains. Resistance to acute death is apparently
correlated with general vigour; most radiation-resistantstrains are longer-lived and less susceptible to spontaneous infectious disease. A short life-span, if due to highsusceptibility to leukaemia does not appear to influence
susceptibility to acute death.

132. Lifetime follow-up of several inbred strains andtheir hybrids after radiation indicates that the number ofdays lost varies less between strains than does acutesensitivity. Most strain differences in life-shortening isdue to strain difference in susceptibility to radiationinduced leukaemia; when leukaemia mortality is excluded, life-shortening due to all other causes varies
comparatively little between strains and is independentof normal life expectancy. Thus, in the mouse, a major
component of life-shortening is independent of genetic
make-up, aside from the variable susceptibility to leukaemia and ovarian tumour. The contribution of thesestrain-specific diseases to total mortality is greater inthe mouse than in other species for which data are available; nevertheless, the range of variation in over-all lifeshortening between strains is less than a factor of 2.
133. These results only partially answer the role ofgenetic constitution on life-shortening even in the mouse.
Inbred mouse strains are highly selected genetic material
from which many genes that could alter viability may
have been eliminated. These genes are maintained in wild
populations by various mechanisms, some of which could
make an additional contribution to life-shortening byradiations. Furthermore, several of the most widely usedmouse strains are genetically related, and are therefore
unrepresentative of the genetic potentialities of thespecies.

Age effects218

129. Kohn and Guttman 229 studied the important
problem of the effect of age at time of radiation on lifeshortening in mice. Mice given single X-ray exposuresat ages 160, 435 or 535 days had less life-shortening thanmice irradiated at later ages. Total gross tumour incidence was also decreased. In another study, Kohn 239
130134. Human populations are genetically heterogeneous. There is as yet no way to determine the influence of
this heterogeneity on radio-sensitivity from individual toindividual. Ethnic differences in spontaneous leukaemia
incidence suggest that, in man, as in the mouse, genetic
constitution plays a role in susceptibility to radiationinduced leukaemia.

presently recognized genetic apparatus. Statisticaltheories based on fluctuations in mean physiologic
state 234 • 256 point to whatever the investigator is familiar
with as potential areas for study. Theories based on
irreparable levels of injury 257 • 258 point out methods formeasuring the level wiiliout achieving its identificationand similarly the hypoiliesis of progressive loss of ability
to repair damage 259 does not tell anything about the
repair function itself. Life-shortening probably summates so many insults that one must be careful not tosingle out any particular lesion as of primary importance-at least not without ovenvhelming new evidence. The
only clear candidate as an especially vulnerable site ofradiation damage is the replication of DNA as noted
earlier.

135. A fraction of the human population may have
hereditary traits giving e.x.traordinary susceptibility toradiation-induced malignancies. E..x.istence of such a trait
can only be established from data on familial tendency
towards such susceptibility or from a demonstrated correlation between such malignancy and some other genetically determined trait. Large numbers of presumptive
radiation-induced cases would be required; may they
never become available.

Radiation carcinogenesis

136. Vigour or fitness probably correlate with acuteradiation-sensitivity in man-as in e.x.perimental animals. Study of the influence of nutrition, e.'Cercise, disease, and other environmental and physiological variables
on radiation effects has only begun; present judgements
must therefore be based on incidental clinical and e-'\.perimental observations.

141. Data from irradiated animals and man indicatethat enough radiation to almost any part of the body increases the incidence of malignant neoplasia. 89
142. Radiation-induced tumours often take long todevelop, not beginning necessarily· immediately after
obvious changes in ilie cells. Obvious tissue disorder need
not e.'Cist at the site of origin of the cancer: radiation can
induce malignant disease ilirough physiological mechanisms as with e.g., ovarian, thymic and pituitary tumours
in mice which are clearly indirect (i.e., where irradiationof ilie cells of origin of the neoplasm is not the criticalfactor).
143. Most animal experiments, usually with relatively
homogeneous populations, have shown that there aredose levels iliat induce no detectable increase in incidenceof certain neoplasms. Some investigators construe suchdata to mean that there is a ilireshold dose of radiation
below which certain neoplasms cannot be induced or theirage-specific incidence increased. It must be recognizedthat no dose-incidence experiment can prove the existence of a true threshold dose since, however large thenumber of animals used, ilie tumour incidence at a givendose may be too small to be demonstrated. On the other
hand, a linear dose-effect relationship e.'Ctrapolating backto zero dose would strongly suggest the absence of athreshold dose. This has been demonstrated in a few
experiments for certain types of tumour.
144. A major difficulty in short-lived laboratory
animals is iliat at low doses the latent period for tumour
induction may exceed the life-span and hence no effectmay be seen.

137. Stresses may activate chronic or latent diseases.
Radiation may so act in certain disease; e.g. inactive
tuberculosis in monkeys and man and diseases caused by
Bartone/la or Salmonella in rats. The nature of activation is unknown, but is probably due to impairment of
immunological response.
138. In contrast, a therapeutic or prophylactic effectof irradiation on certain infectious diseases can mask
the life-shortening effect in e.'Cperimental animals. The
observed life-span of animals is sometimes greater withdaily doses of 1 rad or so throughout adult life than thatof their controls.

Life-lengthening
139. Data on rodents exposed to small accumulated
doses (about 100 to 400 rad per lifetime) at low dose
rates were puzzling because such animals frequently
survived longer than controls. 2 H,m Although sampling
errors and bias in experimental conditions may have contributed, some recent findings suggest this effect may bereal. us In many experiments showing increased survival,
there was considerable intercurrent mortality early inlife in control animals, presumably from infectious
disease, whereas irradiated animals had less mortality inthe same period. There is no evidence the maximal Ii fespan is extended in t11is situation, or that the incidenceof cancer or degenerative disease is decreased. Since thecause of ilie prolonged survival is unknmvn, the significance for man is unknown.

Relation to rate of mitosis260
145. Aliliough neoplasia arises most commonly in proliferating tissues, in ilie long-term effects of Operation
Greenhouse (mice exposed to atomic bomb radiationtable II) tumours of lung, liver, mammary gland stroma,and anterior hypophysis-sites of relatively slow cell
turnover-were more frequent than iliose of skin, bonemarrow, and intestinal mucosa-sites of more rapid cell
turnover.

Nature of the lesion in life-shortening
140. The primary lesions responsible for non-specificlife-shortening in irradiated animals have not been
identified. Casarett and co-workers 2 n,us view arteriolocapillary fibrosis as ilie major radiation effect. If iliey
are correct, it should be possible to show deficits in circulation in various organs and decide whether these
deficits go with normal aging. Such findings would notprove a cause-and-effect relationship, but would at least
show an association. Various hypoilieses and models to
explain aging and life-shortening by radiation have nothelped as guides for histological or physiological studies.
Information theory and somatic mutation 249- 255 do notindicate experimental approaches going beyond theRelation to age
146. In the same study 260 ilie incidence of all tumours
increased wiili time after irradiation, wiili one exception.
This was lymphoma of thymus, which reached a ma..x.imum early in life in heavily irradiated populations.
Tumours arose earlier in irradiated mice and ilien advancement in onset corresponded to reduction in mean
age at death of the entire population. As regards theinfluence of age at the time of irradiation, diverse effects
131

have been seen. Osteogenic sarcomas and tumours of thegastro intestinal tract have shown a higher incidence inanimals irradiated when young, whereas the reverse
occurs with leukaemias and tumours of the mammary
gland.261
Relation to radiation dose
147. The relation between tumour incidence and dose

varied from one neoplasm to another. The incidence ofsome increased with increasing amounts of irradiation(e.g., thymic lymphoma), the incidence of others was
maximal at intermediate dose-levels (e.g., hepatoma,
ovarian tumour, pituitary adenoma), and some usuallycommon, decreased in frequency with increasing dose(e.g., non-thymic lymphoma, sarcoma of breast, adenoma of lung) .260 In no instance did tumour incidence
vary as a simple linear function of dose, and extrapolation, therefore from the high doses in this experiment
to doses near those from natural environmental radiation
is not possible, and the question of whether or not very
low doses of radiation cause some slight increase in theover-all risk of malignancy (so-called threshold) remains unsettled. As a general rule, single-dose irradiation is more effective in producing cancer than greatly
protracted e..xposure with the same dose.
Mechanisms of carcinogenesis
148. Of the various neoplasms induced by radiationsome may be caused indirectly without irradiation of tl1e
tumour-forming cells themselves. Thus in certain strainsof mice, presence of the thymus is necessary for induction of lymphomas 262 although the thymus itself neednot be irradiated. Strong evidence that induction isindirei:t is given by the neoplasm arising in a normal
thymus transplanted to an irradiated host. 263 In otherstrains, thymectomy shifts the site of origin of thetumour to other lymphoid tissue. 264 Repeated radiationin proper sequence causes a higher incidence of lymphoma in mice than do single exposures to the same total
dose. 237• 264 •265 Inoculations of normal bone marrow or
spleen,1 95 partial shielding 265 • 267 • 268 and certain radiation-protective agents,7° decrease incidence. There isdose-rate dependence in response 269 • 271 that, together
with the incidence after various radiation dosages 255
suggests a curvilinear relationship between dose andresponse.
149. Indirect carcinogenesis also appears responsible
for the development of thyrotrophic pituitary tumours
in mice thyroidectomized by I1 31 • 272 Such tumours may
possibly be more readily induced if the pituitary is also
irradiated. 273 .m Other pituitary tumours are as readily
induced by local radiation of the pituitary as by TBR,
suggesting that their pathogenesis is direct. 214 For theseas for many other types of radiation-induced tumours,
the relative importance of direct and indirect causes is
not yet understood. In certain instances, both causes
seem to operate; e.g., the induction of ovarian tumours
depends on destruction of ovogonia and ovocytes bydirect irradiation and on gonadotrophic stimulation ofremaining ovarian stroma by pituitary hormones. 275

the greatly increased incidence at 400 r depends on intact
ovarian function and direct radiation injury to the breastis necessary for an increased incidence of radiationinduced neoplasia. These results indicate that primaryradiation damage to the breast tissue is necessary, but
this primary damage can be dormant and not result in
neoplasia unless an additional mechanism is operative.
Somatic mutation theory
151. Under a broad definition of mutation, generally
used by geneticists, as including all sudden heritablechanges in a cell line, the somatic mutation theory ofcarcinogenesis can embrace almost all currently proposedmechanisms (e.g., gene mutation, chromosome breakage
or loss, mutation or loss of cytoplasmic particles, or evenvirns infection). Under such circumstances the theory
is reduced to a truism and merely serves to describe
well-known characteristics of malignant disease. As a
special case of this, simple gene mutations or othersingle-hit changes have often been invoked as a single
basis for radiation-induced neoplasia, and incidentally asa basis for predicting effects under conditions that preclude direct observation. The simple point mutation
hypothesis remains to be substantiated, as does thetheory that naturally occurring point mutations cause"spontaneous" cancer.281•m A widely held view has
been that, if a single hit on a gene or other cellular structure were the basis for radiation-induced neoplasia, thenthe dose-effect relationship might well be linear withno-threshold. The rat mammary tumour data and others
indicate both a primary and secondary mechanism inthis type of radiation-induced neoplasia. The neoplasms
themselves were seen only when both mechanisms wereoperative. The secondary mechanism in the present situation (normal ovarian function) could not reflect asomatic mutation. Even if the primary event were asomatic gene mutation (or a single-hit chromosome
break), the dose-effect curve 278 would not have been
linear with no-threshold unless the secondary mechanism
were operative. It follows therefore that lack of linearityand of an apparent threshold does not rule out somatic
mutation as the primary event. Lack of such a response
might simply indicate a non-operative necessary secondary mechanism.
152. Furth 3311 concludes from the findings of several
authors that radiation-induced rat mammary gland neoplasia ''are best interpreted by supposing that radiation
causes a subtle, irreversible change in the mammary
gland which remains latent until the organ is subjected
to proliferative stimuli".
153. The demonstration of a two-stage mechanism in
the induction of some neoplasms throws doubt on theuse of dose-response curves as arguments for or against
the point mutation theory (or any simple one-hit theory).
No "one" experiment even if the animals are numerous
can settle this question for all types of malignancy andall circumstances. If the dose-effect cunre is not linear,nothing would have been necessarily proved about the
primary mechanism. If a linear no-threshold response
obtained down to the lowest doses, the somatic mutationinterpretation, if it could be made under these circumstances, would apply only for the particular neoplasm inthe particular strain and species. Extrapolation would
not be valid.

150. _Studies on radiation-induced mammary glandneoplasia in the rat 276•::so have shown that a single sublethal dose of X- or y-irradiation in young male or female
rats res?lts in an increased incidence of mammary glandneoplasm. The dose-effect relationship appears linear
over 25-400 r, and the curve within limits oi error, e.xtrapolates to zero. No data are obtained below 25 r; above
400 r, etc., the curve was either flattened or declined, since

Chromosomal clza11ges a11d carcinogenesis
154. The role of chromosomal changes as an inter-mediate cause in carcinogenesis has been widely de132

irradiated. Here radiation probably merely favours selection of spontaneous carcinogenic mutants, possibly byexcessive growth stimulation during recovery.

bated.m,m Malignant tumours often have aberrant(usually aneuploid) chromosome numbers and a highdegree of instability in chromosomal constitution.~ 56 It
by no means follows that the chromosomal changes are
the cause of the malignancy; inaccuracy in the transmission of genetic information may be merely the priceof proliferation at unrestricted speed. Association ofchromosomal variation with tumours therefore does notof necessity imply any cause-effect relationship.
155. Chromosomal aberrations can be induced in
norlllal human and monkey cells cultured in vitro by
X-ray in doses as low as 25 r~ 81 • 288 and such aberrations(presumably of mixed 1-hit and 2-hit origins) in in vivo
monkey bone marrow cells show a rough proportionality
with doses from 50-100 r. Blood cells cultured from twopatients given radiation for ankylosing spondylitis
showed numerous chromosome structural abnormalities
but these rapidly declined in number. 289 Similar changes
have been seen in patients with chronic myeloid leukaemia after X-ray treatment.
156. The persistence of chromosome aberrations inperipheral blood leukocytes,....., 2.Vz years after accidental
whole-body irradiation of eight men by mixed gamma
and fission neutrons has recently been reported. 781 Fivemen received doses > 230 rad; three others, < 70 rad.
The frequency of cells with chromosome counts differingfrom 46 ranged from 4-23 per cent in the irradiatedcompared to 2 per cent in controls. In the five cases withhigh doses, there were grossly altered chromosomes suchas rings, dicentrics, and minutes; these were often in cellswith abnormal count with a frequency of 2-20 per cent.
No polyploidy was seen. A detailed karyotype analysis
of some normal-looking cells from irradiated individuals
revealed the presence of pericentric inversions, translocations, and deletions. A comparison of the frequency of
induced chromosome breaks in tissue culture preparations suggests that the frequency of aberrations diminishes with time, and that polyploid cells are eliminatedmore quickly.
157. There is increasing evidence of an association of
specific types of leukaemia with chromosomal anomalies.
In many cases of chronic myeloid leukaemia there is a
specific abnormality (possibly a deletion) in one of thechromosomes of pair-21 or pair-22 (the Philadelphia
chromosome). Variations in the proportion of cells withthis Philadelphia chromosome in blood-cell cultures fromdifferent patients with myeloid leukaemia and its absencein skin cultures from the same patients strongly suggest
the presence of a somatic chromosomal anomaly in thesepatients' leukaemic cells. Moreover, the incidence ofacute leukaemia is greatly increased in mongolism, adisease 2111 now known to be associated with trisomy-21.
These observations suggest that either a deficiency orexcess of genetic material of chromosome pair-21 may
result in different types of leukaemia. For other types ofleukaemia, no such consistent associations have been
established as yet. 290• 782• 783 • 7 8-1
158. These chromosomal aberrations and especiallythe possibility of a specific chromosome abnormality inmyeloid leukaemia and the hereditary nature of theneoplastic change in subsequent cell generations suggestthat cancer reflects a genetic change in the cell. But thecourse of evolution of malignancy in certain tumours
argues against a one-stage cause, such as single point
mutation or chromosomal aberration.~ 85 • 292 • 293 Moreover,induction of neoplasia by indirect effects on the hostcannot be due to the mutagenic action of radiation on thecancer-forming cells, since the cells themselves are not

Radiation leukaemogenesis

159. Studies of radiation leukaemogenesis use themouse because of ease of leukaemia induction and theavailability of different leukaemias associated with various inbred strains. Mouse leukaemia is not a single
disease; much confusion arises because precise classification is often lacking.za..,m The most studied mouse
leukaemia is lymphatic arising in the thymus, classified
variously as thymic leukaemia, thymic lymphosarcoma,
malignant lymphoma, and "mouse leukaemia''. In themouse, the thymus normally atrophies in early adult life
instead of in early childhood as in man. Extensive studies
by Upton et al.2 84 show that factors inducing this neoplasm differ from those inducing myeloid or granulocytic
leukaemia. Since most radiation-induced leukaemias in
man are granulocytic, thymic leukaemia of mice havelittle relevance to man. 294 Myeloid leukaemia in mice,possibly more analogous to human radiation-induced
leukaemia, has been shtdied less.
160. In spite of these reservations about the comparability of human and murine leukaemias, the leukaemia
responses of the two species share certain features. 296
Both species show an increased incidence of leukaemia
after TBR. In mice, the leukaemia incidence in irradiatedgroups returns to or near control levels 18-20 months
after exposure. 223 • 291 The Hiroshima and Nagasaki
survivors 298 had still some excess leukaemia mortality
over their unirradiated controls by 1959. By adjustingtime scales. human and murine experiences can be superimposed ; for comparable radiation exposures, thefactor of in~rease in age-specific leukaemia mortality
over control is nearly identical for the two species. 296
161. Data of Kaplan et al. 263 indicate that lymphoma ta
in thymectomized irradiated mice can appear at the siteof transplantation when the thymus from non-exposed
mice is transplanted into the irradiated animal. The
origin of the neoplastic tissue has been studied ':!ea, 299 • 301
and although in some instances the cells may be derived
from the donor cells, in others they are derived definitely from recipient cells.
162. Radiation-induced myeloid leukaemias of themouse are uninfluenced by the thymus but are reducedby splenectomy.264 They are more effectively induced byrelatively lower radiation dosages than is the thymic
form and their induction is apparently not similarly enhanced by fractionation of the exposure. 264 Partial
shielding reduces incidence 264 as does prophylactic administration of mercaptoethyl guanidine, 302 a radioprotective agent. The incidence reaches plateau at radiation doses above 150 r. 264 The shape of the dose-response
curve is not definitely known, but data after doses of 16
and 32 r 1 ~ and after 128 or more254 • 303 suggest curvilinearity in the low-dose range. In rats and mice injectedwith strontium-90, more differentiated forms of leucosis
predominate when the accumulated dose to the bonemarrow is small and less-differentiated forms when thedose is large, i.e., of the order of 6,000 rep or above. 304
163. Variables besides radiation dose affect the probability of an animal developing leukaemia, e.g., strain,
age at time of irradiation, sex, and endocrine status.
Leukaemia incidence can be modified by endocrine status
and genetic inheritance (by selection, hybridization, etc.),
or by removal or implantation of tissues. 2 1H, 3os- 311
133

Virns theory
164. Evidence that viral agents cause vari~us types ofcancer in mices12- 315 stimulated the search ror filtrable
leukaemogenic agents in mice with radiation-~nduced
leukaemias. 31G-318 Results as yet are not conclusive, ~ut
they suggest viruses a.s J?Ossible eti~logic agents. in rad~a­tion-induced leukaemia.- 93 Depression of host immumty
by radiation may promote infection by a!l ~"\".ogeneous
carcinogenic virus or radiation may activate. a lat;nt
carcinogenic virus infection analogous to the. mduct10nof lysogenicity in bacteria. To ~h~~e hypoi;hetical mechanisms must be added the poss1bil1ty of viral transduction of carcinogenic substances from one cell toanother. 312 ' 3u

no higher than that of certain a.ctiyely :fividing and ~f­ferentiating adult tissues. Irradiation ot an embryo with
5-25 r causes evident changes; similar exposure of adulthaemopoietic or epithelia~ tissue~ is likewise follow~d bymorphological and functional disturbances. The difference between embryonic and adult response to lo~ dosesof radiation is that an over-all effect in embryos is evenmore extensive than in the adult probably because aminor irreversible injury in embryo, particularly after
the blastomeres have lost totipotency, is amplified indevelopment: morphogenetic relations are upset t;hroughdeath of cells in various precursor fields, and this leads
to faults-in the formation of adult structures.
171. Radiation effects in embryos may reflect two
mechanisms: developmental alterations through cell
destruction in the embryo and physiological disturbancesin the mother.

Risk of carcinogenesis from low doses
165. Carcinogenesis is the most imp~rtant late .e~ectof radiation. Knowledge of the mechanism of radiation
carcinocrenesis is a prerequisite for the accurate assessment of risk at low doses. Since the mechanisms of carcinogenesis are unk11own, any such assessment of risk
must be purely speculative, although possibly of somevalue in estimating upper limits.
RECOVERY AND THE CONCEPT OF IRREPARABLE INJURY

The mammalian embryo
172. l\fammalian pre-natal development can bedivided into three periods with respect to radiation
effects : (a) pre-implantation when early deaths are
induced but survivors are mostly normal; (b) majororganogenesis. yielding neonatal deaths and abnormalities; ( c) the foetal period when sensitivity to death ar:dgross malformations decreases. The general pattern mmice is given in figure 2.

320166. Radiation injury, like other injury, immediat~ly
sets off the classical reactions of homeostasis and repair;
to some extent, radiation affects the repair processes
themselves.
167. In the weeks after a single sub-lethal dose,
damage gradually is repaired. Many, if not all, cells
destroyed by radiation are replaced by regeneration fromsurviving cells. Irradiated organisms may resume anormal or near-normal appearance. With time there isrecovery of resistance to lethality from furth~r radiat~on.
:Most radiation injury from X- and y-rays is thus irequently reparable. Animals, therefore, survive a prolonged dose several-fold larger than a single dose.
168. Despite apparent recovery residual damage (e.g.,incomplete regeneration or residual defects in cells andtissues) and late effects seen after maximal recovery
show that some injury is irreparable. Certain specifici11juries associated with the formation of bone tumours
caused by radiation are reparable. Recovery is more
likely with injuries which are caused by {3- than bya-radiation. 2G1, 3o4, 321

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individuals at term after irradiation at various intervals(separated by 24 hours) pre- and post-fertilization. Abnormal
individuals may have more than one abnormality 3 2 4169. Life-shortening by radiation implies that an
irreparable component of injury is detectable. This component is detectable as premature aging in an actuarial
sense. But how closely this process parallels and contributes to that cumulative injury called natural aging is
unclear in the quantitative sense. Likewise, it is notknown whether the irreparable component represents
abrupt aging at the time of injury or initiation of gradualaging. Limited observations in rodents, dogs. and swine
indicate that irreparable injury is measurable, after aninterval of presumed complete repair, as a reduction inacute lethal dose. This suggests that irreparable injury is
at least partially sustained at the time of radiation and ispotentially observable as a persisting tissue change; thedistinction between reparable and irreparable injury has
not yet been related to morphology.

173. When females are irradiated after fertilization
but before implantation, high and rapid mortality of thefertilized ovttm is the main effect. Studies by the
Russells m, 323 indicate that deaths are maximal for radiation given during the first two post-copulation days, andthat one-third of total deaths are in the pre-implantation
period. Most deaths, especially among embryos irradiated later after fertilization and closer to the expected
implantation time, ensue shortly after implantation. No
deaths in excess of controls occurred after day IO}'S.
174. Survivors of irradiation in the pre-implantation
period were free of obvious defects 322 had normal birthand post-weaning heights, exhibited normal fertility andshowed no evidence of decreased survival throughout
life. 153 The all-or-none response to irradiation during
cleavage stages which has also been observed in rats andguinea pigs 323 has led Russell to suggest that mammalian
blastomeres are totipotent. 3 : 3 , 3 :~ On the other hand, Rughand Grupp 325 showed that a dose as low as 50 r to a pre-EARLY AND LATE EFFECTS ON EMBRYOS A:\D FOETUSES

170. Ionizing radiations profoundly disturb developing embryos. Their susceptibility while very high may be

134

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implantation embryo might induce cerebral abn~malie~.
This result has not yet been confirmed by other mvestlgators.
175. The pre-implantation mouse embryo is highly
radio-sensitive. Earlier studies indicated that 200 r prevented about 80 per cent of all embryos from reaching
the tenth day of gestation. It was recently shown that25 r killed 38 per cent of embryos exposed before firstcleavage. A dose of 5 r increased resorption. 325 However,the degree of radio-susceptibility of an. embryo ~y bespecies specific: the rat embryo before 1mplantat10n can
withstand a dose of 300 r. ~1

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176. Mouse embryos given 200 r or more between
gestation days 6.5-13.5 developed but had a high incidence of abnormalities. A certain proportion of theabnormal foetuses died at birth. The proportion of prenatal deaths was much lower than in animals exposedin the pre-implantation period. The LD 5o for neo-natal
death was > 200 r for irradiation in the pre-implantation
period and through day 8.5; decreased to between 100200 r for days 9.5 and 10.5 and then increased to 200-300
r for day 11.5 and finally to > 300 r for later periods indevelopment. 323 • 324 'With 200 r the incidence of grossly
abnormal new-horns is 100 per cent for irradiation ofmost stages during major organogenesis. Doses as low
as 25 r have been shown to be effective in causing morphological changes. 326
177. Neo-natal mortality is greatest in embryos irradiated between gestation day 83/i to day 12. Exposure in
the same period decreased the weight of new-born
mice124 • 323 • 324 comparable quantitative studies have notbeen made in other mammals but there are frequent
reports of marked decrease of size among rats andrabbits irradiated during development.
178. Several investigators have tried to decide
whether specific developmental abnormalities depend on
the stage of development at which radiation is given.
Early work by Kosaka 327 indicated that the brain andspinal cord are the most sensitive tissues at the beginning of major organogenesis, while at later stages thymus
and, to a lesser degree, liver and spleen, become the mostsensitive. A more detailed description of "critical
periods" has been given by Job et al. 328 The peak incidence of abnormalities was reached with embryos irradiated between gestation days 8-11. Hydrocephalus
was easily induced in embryos irradiated at day 9, eyedefects at day 10, jaw defects at day 11. According toKaven s29 the structure of the tail was most affected inembryos e.."<posed on day 11, brain hernias on day 8, andskin defects on days 13-14. The results of Russenm.sso
and others on critical periods are given in figure 3. Ma.ximum susceptibility to defects was between days 7-13
the beginning coinciding with the appearance of manydifferentiating centres. Irradiation at day 9 caused anencephal~, at day 10 ~ye defects, at day 11 hydrocephalus
and spmal anomalies, and at day 12 anomalies in thefore-brain.
179. Embryonic neuro-blasts are particularly susceptible to radiation. Within two hours after 100 r, there arescattered areas of necrosis. and necrotization of individual neuro-blasts after doses as low as 40 r. With increasing exposures, more areas of developing neuraltissues are affected. Intermitotic neuro-blasts are more
susceptible to radiation than those in mitosis. 331 Cells
during active differentiation may well be more sensitive
than completely differentiated cells. Further studies areneeded, and the radio-sensitivity of erythro-blasts, myelo-

blasts, and spongio-blasts should be compared withcorresponding mature cells.
180. The existence of "critical periods'' in development has thus been demonstrated, but the use of the term
must be properly qualified. 3 ~ 4 For some anomalies, thecritical period is greatly e.xtended, e.g. e.."<encephaly canbe induced by radiation at any time before neural differentiation. 332 Sometimes induction of a specific anomaly
does not coincide with an apparent period of increased
developmental activity, e.g. induction of polydactyly.l 24
Also, the limits of periods of sensitivity seem to dependon the dose 323 • 3 ~ 4 and how it is fractionated ;153 however,stage of maximum sensitivity is usually revealed by theuse of low-dose single exposure.
The human embryo
181. The first harmful effects of ionizing radiation onhuman embryos were recorded in 1901-1904. Soon afterwards, reports drew attention to serious hazards in irradiating pregnant women. Earlier clinical literature has
been reviewed extensively. 33 ~ 36 Table III summarizes
observed malformations. Malformations specifically reported for human embryos are marked with an asterisk.
The most frequent abnormalities are in the central
nervous system, then eye defects and skeletal malformations.
182. Malformations among children irradiated in
1ttero have been reported. In a 1929 survey of 75 children
born of 106 irradiated women, 38 were abnormal, andin 28 of those the likeliest cause of malformation wasradiation. 337 The dose was estimated to be 30-250 r.
183. The frequency of malformations in man, as inother animals, depends upon developmental stage.
184. The marked qualitative similarities between radiation-induced abnormalities in man and other mammals make extrapolation of e.xperimental studies to man
apropos. For that purpose, a graph correlating development of mouse and human embryos constructed by Otis
and Brent is useful3 38 (figure 4). The correlation between the appearance of some morphological featuresin the mouse and in the human embryo is given intable IV. Since mouse experiments have shown that

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137

irradiation dunng the period of ~ajor organogenesi~ ispotentially most hazardous and smce part of that penod
occurs at a time when pregnancy may still be unsuspected
Russell and Russell have suggested that whenever possible pelvic irradiation of women of child-bearing age
be restricted to the two weeks following the menses. 339 • 340
185. Besides abnormalities in embryos, foetuses, andin early childhood, several effects of irradiation durU;ggestation have been reported, appearing at a later age 111
children. Stewart and collaborators341 concluded that
there was an increased incidence of leukaemia and cancer
among children irradiated in ·utero, and also an increased
incidence of mongolism. 342 Children of Japanese mothers
exposed, during gestation, to atom bomb radiation tended
to show stunting343 and some mental retardation, especially among boys, 344 but neither observation has been
supported by other studies. m, 346 Among children who,
while in utero, had received an average of 3-5 rad during
maternal diagnostic X-ray, 15 of 1,101 had phenotypicchanges involving colour sectors in the iris of the eye.
The incidence was only 11 in approximately 7,092 nonirradiated control siblings and parents. The differenceis highly significant. This somatic effect is only seen in
the children of women irradiated at 6 to 6~ months ofpregnancy. It is not yet known whether the effect is due
to genie chromosomal or other changes. These studies
are discussed further in section V under the heading"Late effects".
Recovery and protection in irradiated germ
cells and embryos
186. In the sea-urchin egg, as time elapses between
irradiation and fertilization, there is the increased proportion of cleavages pointing the possibility of recovery. m The effect was described by Miwa348 for
Pseudocentrolus depressus irradiated with a:- or y-rays.
This does not imply recovery to pre-irradiation stage. 349
The delay between irradiation and fertilization counteracts the delaying effect of irradiation upon cleavage, butdoes not increase the number of embryos capable ofnormal development. In frogs Rollason 350 found no evidence for this kind of recovery.
187. Recovery was seen when an organ from an irradiated embryo was transferred to a normal one. The
irradiated organ, e.g. of a frog 851 or chick embryo 352 developed further and survived longer than it would havein its original environment. This does not necessarily
denote recovery; it is perhaps better explained by assuming that the transfer of the organ removes it fromthe noxious environment of a dying embryo.
188. Recovery in embryonic tissues has been postulated by several authors from the observation that irradiation of embryos at an early stage brings early death,but survivors develop normally. Recent experiments 825
have shown that exposure to radiation, even almost immediately after fertilization, caused marked abnormalities (brain hernia) ; survivors that developed without
big abnormalities nevertheless showed stunting and some
impairment of the ability to learn. 353
189. After radiation-injury the embryo as a whole
rr:a~ show a _certain recovery in that survivors of rad1at10n continue to develop despite morphologicaldamage. 354 This does not imply that the injured tissues
have ~ecovered; the survivors are usually stunted andthere is some topographical reorganization of undamaged tissues, which might indicate that the maintenanceof viability and shape is due to some of the cells fromsurrounding areas invading the lesion. 332 Recovery ofan embryo is more the outcome of a regenerative process,aided by the remarkable powers of reorganization ofembryonic tissues and scavenging actiYities of macrophages, than recovery of the cells actually damaged.
190. Expected radiation injury may be prevented tosome extent by several factors; hypoxia, lowered temperature, and various thio compounds. Lowering theambient temperature protects against immediate radiation effect in frogs, an effect lasting only as long as a
low temperature is maintained ;855 in salamander larvae,
protection appears to persist. 356 Also in chick embryos
Goffinet357 protected against radiation by lowering temperature.
191. The effects of hypoxia were studied by Russelland collaborators :m, 35s mouse embryos e..xposed todoses 100-400 r had a lower percentage of abnormalities
if irradiated in 5 per cent o:x-ygen in helium. Allen,
Schjeide and Piccirillo359 showed that the proportion ofcells injured by radiation was reduced if irradiated cells
were maintained afterwards in mildly anoxic conditions ;anoxia reduces cell division.
192. Cysteamine as well as several other compounds
protects to some extent against radiation if given before
irradiation. The survival of chick embryo was llnt:>roved
after giving cysteamine, cystamine, and methylamine ;the efficacy of these compounds was highest when thecirculatory system began to function. 357• 360 It has been
observed that mercaptoethylamine can protect the rat
foetus if irradiated on days 15-18, 301 and that cysteamineand similar compounds permit mouse foetuses to maintain a higher growth rate and lower mortality than irradiated untreated controls. 362 • 863
IV. Acute radiation injury in man
ACUTE RADIATION SYNDROME

193. The acute radiation syndrome differs from ordinary injuries since there are integrating patterns ofsymptoms after higher doses, or a latent period at lower
doses during which hidden histological changes are taking place from the time of exposure until the recrudescence of symptoms and frank danger of death.
Recovery from the initial symptoms does not signify real
recovery. Review of reactor accidents (see below) emphasizes the problem of inhomogeneous irradiation of
the body in man and the inHuence of the part irradiatedupon the symptoms that follow. Effects of localized irradiation on individual organs are discussed in earlier
sections of the present annex.

Sources of information
194. There are four sources of information on acuteradiation effects in man: (a) the largest, but studied
under obvious difficulties, is the experience of theJapanese at Hiroshima and Nagasaki: ( b) the less serious and smaller experience of the Marshallese, American
servicemen, and Japanese fishermen to fall-out radiation
during atomic tests in 1954; ( c) exposure of a few people to reactor and radiation accidents in the UnitedStates, the USSR and Yugoslavia; (d) exposure of patients to therapeutic radiation. Some shortcomings ofsuch information have been discussed earlier in paragraphs 43-45 above. Information on atomic bomb, fallout, reactor accident, and \Vhole-body radiation injuries
has been summarized. so, 364, 312, s;3, 3ss, 393, ;02138

Total body response 365

Gastro-intestinal form 53 • 69

195. The total body response in man to radiation in
sufficient doses includes: (a) radiation sickness beginning during or very soon after acute e..xposur~, and overlapping with other responses; ( b) degeneration and. repair of proliferative ti~sues; ( c) l<?cal and gen~rah~ed
toxaemia; ( d) changes m homeostas1s ; ( e) deteriorationin physical and mental fitness.

above given to whole-body, symptoms have appeared in
1-2 hours. The onset, duration and severity of all symptoms varies depending largely on dose and partly on
susceptibility. 366 Symptoms may include :367 (a) general:
headaches, vertigo, debility and abnormal sensations oftaste or smell; ( b) gastro-intestinal : anorexia, nausea,
vomiting, diarrhoea; ( c) cardiovascular: tachycardia,
arrhythmia, fall of blood pressure and shortness ofbreath ; ( d) haematological: leukopenia, thrombopenia,
and increased sedimentation rate; and ( e) psychological :increased irritability, insomnia, and fear.

200. The gastro-intestinal form predominates withlower doses (500-2,000 r). The prodromal nausea andvomiting begin promptly and do not subside. For somepeople these symptoms develop within 0.5 hours after
e..'Cposure ; in others not for several hours. Gastro-intestinal symptoms may continue (anorexia, nausea, vomiting, and diarrhoea). Sometimes these symptoms disappear after 2-3 days and recur ,__, day 5 just when thepatient's condition seemed to have improved, owing toinjury of intestinal epithelium, leaving bare villi. Rather
abruptly, malaise, anorexia, nausea and vomiting prevent
normal food and fluid intake, leading to serious electrolyte imbalance. Simultaneously high fever and persistentdiarrhoea-rapidly progressing from loose to watery tobloody stools-appear. The abdomen is distended andperistalsis is absent. Rapid deterioration leads to severe
paralytic ileus. Exhaustion, fever and perhaps delirium
follow ; dehydration and haemoconcentration develop ;the circulation fails, and the patient becomes comatoseand dies a week or so after e..'Cposure from circulatory
collapse.

197. The incidence of radiation sickness is affectedby the part of body irradiated. 368 • 369 Exposure over thewhole trunk and partly over the upper abdomen causes
more radition sickness than does exposure of comparable tissue volumes in the extremities. Explanations forradiation sickness include : (a) release of toxic substances from disintegrating cells ;370 ( b) disturbance of
pituitary-adrenal cortical function ;311 ( c) tissue destruction giving rise to histamine and mildly toxic histaminelike products.

201. After doses where regeneration is possible, fluid
replacement during days 4-6 keeps dogs alive. 74 The
epitheliµm regenerates and vomiting and diarrhoea subside. This is only a temporary respite as evidence ofmarrow aplasia and panctyopenia begin within 2-3
weeks. After doses that cause this severe intestinal damage, marrow regeneration is unlikely, so that even if
there is spontanous recovery or successful treatment,
individuals have yet to experience the effects on haematopoiesis.

General clinical picture

Haematopoietic form

198. Although the different organs have widely different radio-sensitivities for the acute radiation syndrome in man, three are important :n• 372 • 373 the central
nervous system (CNS), small intestine, and bone marrow, together with lymphoid tissue (table V). The acuteradiation syndrome may therefore take three primaryforms---cerebral, gastro-intestinal, and haematopoietic,
depending on the dose. To induce acute effects in thecentral nervous system requires several thousand r; damage is seen within minutes to hours. The dose for theacute small intestine form is 300-500 r, with a latent
period of ,__, 5 days. For severe haematopoietic changes,
the dose is > 200 r and the effect takes ,__, 3 weeks todevelop.

202. In the haematopoietic form, after lower doses ofradiation, e.g., < 500 r, the haematopoietic symptoms
are due to different origins and appear in two successive
phases. Leucopenia, thrombocytopenia and haemostatic
abnormalities are a direct consequence of lesions of thehaematopoietic organs. Symptoms such as haemorrhage
and anaemia may be secondary to the visceral lesions andassociated with ulceration of mucous membranes. Anorexia, apathy, nausea, and vomiting, and some diarrhoea
are maximum 6-12 hours after exposure. The symptoms
may subside so that by 24-36 hours individuals feel well,
but their bone marrow, spleen, and lymph nodes areatrophying. The patient enjoys apparently normal health
until,..., days 19-20 (many Japanese soldiers returned towork only to die later in the pancytopenic phase), when
the patient has chills, malaise, and fever, headache,fatigue, anorexia and dyspnoea on e..xertion. and at thistime partial or complete loss of hair is likely. Within a
few days the general condition worsens, hospitalizationis needed. The patient then develops sore throat andpharyngitis, accompanied by swelling of gingiva andtonsils and petechiae in the skin with a tendency to bruise
easily, followed by bleeding from gums and ulcerations
on gingiva and tonsils. Similar ulceration in the intestines causes a renewal of diarrhoea. The patient has highfever with complete anore..xia. Weeks 5-6. with agranulocytosis, anaemia, and infection, are critical. The increased susceptibility to infection is caused by the dose
dependent decrease in circulating granulocytes and lymphocytes, impairment of antibody production, impairment of granulocyte and RES function, lessened resistance to diffusion in subcutaneous tissues, andhaemorrhagic ulceration permitting entrance of bacteria.
Thereafter, if the patient recovers, fever, petechiae andRadiation sickness

196. After a single dose of radiation of SO rad and

CNSform

199. The clinical picture of the CNS form must be
extrapolated from animals and a few accidents in man.
The onset is prompt and death may occur in minutes tohours. After the initial phase of radiation sickness, thereis swift progression from listlessness, drowsiness, andlanguor to severe apathy, prostration, and lethargy probably caused by small non-bacterial inflammatory fociappearing throughout the brain in 1-2 hours; this development of vasculitis or encephalitis gives rise to cerebral
oedema. After > 5,000 r, one deals with seizures ranging
from generalized muscle tremor to epileptoid convulsions similar to grand mal. This convulsive phase lasts a
few hours and is followed by ata.'Cia from vestibulocerebellar disturbance. Convulsions and ataxia probably result from the degenerative pyknosis in the granule layerof the cerebellum within two hours after exposure,concomitant with brain oedema. TBR causing the CNS
syndrome is fatal.

139

exposure; a fall in white count beginning within the firstweek denotes a rather high exposure whereas late falls,
such as observed in Marshallese, indicate a less serious
e.xposure;(iv) The platelet count, while being of some prognostic value, is of more importance in the general management of the patient. In general, the fall in platelet
count would parallel the change in neutrophils, althoughoccurring somewhat later, and the neutrophil count ismore readily available, particularly in accidents awayfrom hospital centres;(v) The reticulocyte count would sen•e as a guide as
to the extent of erythropoietic damage. Fe59 turn-overstudies would be of little value; to be meaningful, theywould have to be done serially and even then would add
little information beyond that derived from the reticulocytes.
( d) Recovery potential
The type and extent of injury following radiation represents a spectntm and it is not possible to divide injury
into clear-cut syndromes. In general, however, at higher
doses, the predominant injury would be cerebral and theoutcome uniformly fatal. With doses lower than this, themajor injury would be to the gastro-intestinal andhaematopoietic systems. Judicious use of fluid. electrolytes, and treatment of the haematopoietic injury as
outlined below provide hope for recovery. In the socalled lethal dose ranges with X- and y-radiation, theinjury is primarily to the haematopoietic system. At
doses of approximately S0-100 rad, symptomatology ismild, and below SO rad, symptoms are virtually absent
even though there is some injury, particularly to haematopoietic tissues.

ecchymoses subside; ulcerations heal and convalescence
begins about the end of the second month after exposure.
These symptoms tend to merge into one another.
Prognosis
203. Early symptomatology in the diagnosis of radiation injury is a useful guide to management.H, 375 • 316
Subjects with intractable nausea, vomiting, and diarrhoea
will generally die-the survival-improbable group. Thosein whom nausea and vomiting is brief, 1-2 days, followed
by well-being. have a good chance to survive.
204. After initial symptoms, the effects of haematopoietic damage predominate. The survival-possible groupare in the lethal dose range. The survival-probable group
includes those with no initial symptoms or only mild andfleeting ones disappearing within a few hours. Practicalexperience on the Marshallese, Los Alamos, Argonne,
Y-12, Vinca and Lod"Port accidents demonstrate thatphysical measurements to compute probable doses takemore time than do several haematological procedures.
The dose must be judged on the basis of symptoms. Thisis especially important in determining management andprognosis when physical measurements are not available,or when radiation exposure has been non-uniform.

(a) Na us ea and vomiting
In general, if nausea and vomiting are absent, it may
be assumed that the dose was relatively low. Nausea andvomiting warrant hospital admission for observation.
The rapidity of onset of nausea and vomiting provides
some notion as to the severity of the exposure: usually,
the earlier the onset and more protracted the vomiting,the higher the dose.
(b) Erythema
Much depends on the type of radiation as to whether
erythema will result. It is difficult to make judgementsof the dose on the basis of erythema but its presence isevidence of a serious exposure.

Prognostic value of the leukocyte count
20S. At Operation Crossroads depression in leukocyte count correlated with distance from the bomb. 377
At Operation Greenhouse 378 there were four groups ofdogs with mortalities of 100 per cent, 100 per cent, 80
per cent, and 10 per cent. In the group given 800 rad,the total leukocyte count fell to zero; all the animals
were dead by day 10. Group 2, given about SOO rad,had a smaller fall in leukocycte count. Group 3, with
80 per cent mortality, received ,...., 400 rad, and group 4,
given 200 rad with 10 per cent mortality, had a smaller
decrease in leukocyte count.
206. Extrapolation to man directly is difficult, because
the rate of change in leukocytes in man as shown in the
Marshallese and various clinical experiences is muchslower.H• 372• 373 Jacobs, et al., 379 re-analysed the leukocyte counts done in Hiroshima and Nagasaki after the
explosion ; despite the limitations of the data depression
in total leukocyte count at different times correlates
well with survival. The treatment of the acute radiation
syndrome in man is discussed in section VIII.

( c) H aematopoietic and bone-marrow picture
Where casualties are few it is simple to carry out all
haematological procedures and other studies that might
be of value. In a radiation disaster, extensive studies
would be impossible, although many leukocyte counts
would be practical with modern electronic counting
devices:(i) Lymphocytes are valuable as an early criterion for
judging radiation injury. In normal individuals, a fall in
lymphocytes is seen within the first 24-48 hours. If at
48 hours the lymphocyte count is 1,200 or above, it isunlikely that the individual has received a fatal exposure ;if the lymphocyte count is in the 300-1,200 range, a dosein the lethal range may be suspected ; counts below 300
indicate an extremely serious exposure;(ii) Early bone marrow examination is advisable fordetermining whether the patient was haematologicallynormal at the time of exposure and might give someinsight to the extent of damage. Some workers consider
that multiple bone marrow examinations would be no
more helpful than peripheral blood examinations andhave the disadvantage of being potential sources ofinfection. Cronkite and Bond have proposed a determination of the mitotic index in bone marrows on day 4
as a measure of dose exposure--a mitotic index of zero
indicates an exposure of 200 rad or more.
(iii) The total white-cell count is of particular value
for following the patient throughout the course. In general, the drop in neutrophils will reflect the degree of

ANALYSIS OF PAST ACCIDE!\TS

207. There have been at least eight major radiation
accidents:
Los Alamos I ......... 21Aug.1945 Criticality (experimental
assembly)
Los Alamos II ........ 21 May 1946 Criticality (experimental
assembly)
Argoooe ............. 2 June 1952 Criticality (reactor)
USSR ............... ?
Criticality (reactor)
OakRidge ........... 16June1958 Criticality (processing)Yugoslavia ........... 15 Oct.1958 Criticality (reactor)
Los Alamos III ....... 30 Dec.1958 Criticality (processing)
Lockport, New York .. 8 Mar.1960 Radar X-radiation

140

Several isolated cases of pericardia! effusion and constrictive pericarditis have been reported in patients given
radiation therapy to the chest. aso-as~

The Idaho SL-1 reactor accident on 3 January 1961 is
not discussed because the three fatalities were caused byblast from the nuclear excursion. The immediate dose
calculations in the above accidents were of necessity very
uncertain and probably not too meaningful. In the studyof reconstituted accidents more accurate dosimetry has
been obtained particularly from the point of view of nonuniformity of the exposure. Even here, there are important practical difficulties in assessing e."Xposure when with
the neutron component significant dosimetry is further
complicated by considerations of distribution and RBE.
In the present state of knowledge the doses presented
should be considered as approximate orders of magnitude rather than exact measurements.

211. The second fatality received an estimated average dose to his torso of about 2,000 r of soft and 150 rof penetrating radiation, with considerably greater exposure of his hands. The patient vomited on his way tothe hospital. Both hands were swollen within an hour<:fter the accident. His temperature, pulse. and respiration rose abruptly on day 6 and increased until death on~ay 9_. His hospital course was characterized by severe
mtestmal symptoms, with almost complete paralytic ileus
and extreme abdominal distention. Continuous 0CTastricsuction was required. He had no diarrhoea. Both arms
packed in ice, were in effect amputated. The most strik~
ing features of the patient's blood count were the initialhigh white count, the complete disappearance of all
lymphocytes from the peripheral blood by day 2, and theabrupt fall of the total white count on day 6. Thesefindings are similc:r to those in the first case. At autopsy,
am<?ng other findmgs, there was severe damage to intestmes.
212. Case 4, a 34-year-old man, received an average
estimated dose to the entire body of 400 r of soft and
40 r of penetrating radiation. His head and upper chest
are believed to have received a larger dose than the restof his body. On day 5 he developed fever, along withlethargy and somnolence for no clear cause at the time.
The fever may possibly have been associated with damage to the CNS like that in the Lockport accident. His
lymphocyte count fell to below 1,000 cells/mm 3 by thesixth hour after exposure.
· 213. This patient had severe fatigue 15 days after exposure on discharge from hospital, and at first had 16
hours bed rest per day, improved gradually and wasback to normal in 10 weeks. Although completely aspermic for several years after e."Xposure, he recovered completely, lived an active normal life, and became the fatherof an additional t\vo normal children. The patient had
mild hypertension at the time of e."posure. In the ne."tseveral years his blood pressure rose but ''tas treated successfully with reserpine. In 1955, aged 43, the patient had
a severe posterio-lateral cardiac infarction. (It is difficult
to relate this to his radiation exposure. The patient's
coronary vessel probably received a relatively small dose.
Patient's father died of a heart attack in his early 40's.)
Within a year after the heart attack a diagnosis of acute
myxedema was made. From clinical findings and laboratory tests this condition had undoubtedly been present
for several years, and contributed to the coronary thrombosis. Whether radiation exposure to the neck was responsible for the thyroid damage is uncertain.

First and Second Los Alamos accidents
208. The first nuclear accident occurred at Los
Alamos on 21 August 1945 and the second on 21 May
1946. 380 • 381 The accidents occurred during experimentswith critical assemblies of a fissile core surrounded byneutron reflector material. In the first accident the reflector was tungsten carbide; in the second beryllium.
In both accidents the man doing the experiment wastouching the reflector at the time of the reaction. Exposure of these two fatally injured operators was nonuniform; hands and arms received the largest dose,abdomen and chest somewhat less, and head and legs thesmallest. All others were presumed uniformly exposed,e."'Ccept for case 4, whose body from mid-chest down waspartly shielded at the time of the second accident. The
head, upper chest, and left arm of this patient received
the highest dose.
209. Dose calculations are uncertain and probably notparticularly meaningful; e.g., if 5 per cent of neutrons
had an energy exceeding 5 mev the dose ·would havebeen increased by 45 per cent; the choice of RBE wascritical. 'With these reservations, five cases received an
estimated dose of less than 100 rem of soft radiation andless than 10 r of penetrating radiation. Case 6 (dose unavailable) had no symptoms of any kind after exposure.
:r~~ on~y l~boratory findings of significance were an
1mtial nse m granulocyte count and a lymphopenia ofless than 1,'?00 cells/mm 3 from day 40. The lymphocyte
count remained low for two years. In 1959 the patient
retired, aged 68, with no signs of injury and a normal
blood count.
210. Case 1, received an estimated average body doseof 840 rem of soft radiation and almost 500 r of y-rays.
His hands and arms, especially the right, received many
thousand r. His hands and arms were tensely swollen
30 minutes after the accident, and soon thereafter hebegan to vomit and retch almost continuously for - 24hours. His temperature rose gradually reaching 41.7° C
re~tally on. the day of death 24 days after e.xposure.
His pulse increased abruptly on day 6 and remained
high with an episode of acute paroxysmal tachycardia
on day 15 following a blood transfusion. Cardiac symptoms, abnormal electro-cardiograms, low blood pressure,enlargement of heart with friction rub were related at
the time to his known congenital defect (WolfeParkinson-White syndrome). The patient had e.xtreme
necrosis of the tissues of hands and arms, and extensive
third-degree bums of the body extending to the precardial region. The underlying heart undoubtedly received a high dose. At autopsy, the heart showed extreme
fibrinous pericarditis with no microscopic evidence ofdamage to cardiac muscle. At the time this response wasrelated to his known cardiac defect but in retrospect thisprobably represented radiation injury to the heart.

Argonne accident
214. A reactor criticality accident occurred at Argonne Laboratory on 2 June 1952. Four persons were
exposed to a mixed field of radiation, y-neutron dose
ratio - 10 : 1. Clinical and dosage details were reported. m, ass There were no deaths. The calculated doses
range from 10.8-159 rad.
USSR accident
215. One reactor accident has been reported in the
USSR causing "short general external e.."posure" of two
people to neutrons and y-rays. 386 Doses of 300 r and
450 r were assigned but no y-neutron ratio was given.
Since fuller data are not available these dosages are
uncertain.
141

slavs showing generally more severe injury; (c) haematological recovery occurred at about the same time after
exposure in the two groups of patients ; this and the factthat the bone-marrow was given just at this time to the
Yugoslavs, makes enluation of its therapeutic effectdifficult.
219. An international group under the auspices of theInternational Atomic Energy Agency studied the dosimetry of the Vinca accident in a reconstitution of theaccident. 396 The recalculated doses, still under discussion,
were between ,_. 320 to 440 rad in the five treated.

Oak Ridge accident

216. A criticality accident occurred on 16 June 1958
in the Y-12 plant at Oak Ridge. Enriched uranium component was drained ~nadve.rtently into a w'3:ste d~u~387
causing a chain reaction. Eight persons recetYed s1gmficant TBR; five were exposed to 236-365 rad including aneutron component of slightly more than one quarter.
There was no associated trauma, the whole body was
fairly uniformly exposed, and the radiation dose wasrather accuratelv determined. Three persons received
between 20-70 r'ad. In the five higher-dose patients thehaematological values emphasized that TBR in man
causes clearly defined symptoms. Blood and bonemarrow changes appeared over several weeks in welldefined stages : early and persistent lymphopenia andvariable transient leukocytosis ; mild leukopenia during
the first ten days; abortive rise in white cells, and someincreased erythropoeisis at about two weeks ; severe depression of neutrophiles and platelets greatest at weeks
4-6; rapid recovery of platelets and neutrophiles; andanaemia maximal at week 7, with recovery accompanied
by reticulocytosis. This sequence is uniform in different
persons and similar after radiation over a wide rangeof dose. The patients showed the greatest depression ofleukocytes and platelets between days 24-37. All fivepatients recovered from the early post-radiation effects
and have now no visible damage. 888- 890

220. In the follow-up 397 on the Yugoslavs the patients
continued to have slight reticulocytosis, 0.5-1.7 per cent,for several months. Electro-encephalograms showedslight abnormalities characterized by low voltage andinstability ; the tracings lacked the usual individuality ofpatterns expected in five patients and all looked remarkably alike. At 2 years, basal metabolic rates are normal.
Lens opacities developed, decreased, and are no longer
present. The female patient has had persistent menstrual
difficulties with excessive bleeding. In the male patientssperm counts are still very much depressed 2 years later.
The peripheral blood shows light lymphopenia. The patients complain of fatigue and neuro-circulatory instability-evaluation of both symptoms is difficult.
Third Los Alamos accident

Yugoslavian accident

221. A third radiation accident at Los Alamos on
30 December 1958 of a critical e..xcursion, during a routine plutonium salvage operation caused massive overexposure of one man. 398 • 399 The average TBR exceeded
3,000 rad; the dose to the anterior chest was ,_. 12,000
rad, that to the front of the h@ad ,_. 10,000 rad. The victim went into a state of profound shock within minutes.
The outstanding finding was right-sided heart failure
with resulting renal ischemia and nitrogen retention. The
patient died 35 hours after injury.
222. Less than 30 seconds after the accident the patient was ataxic and disoriented, needing support toremain erect. He complained of "burning up" and appeared flushed at this early time. Within 5 minutes hewas virtually unconscious and was admitted to hospital
25 minutes after the accident. At this time, he was semiconscious but disoriented and clearly in general shockwith depression of blood pressure. Vigorous efforts toreturn the patient's blood pressure to a satisfactory level
and to maintain it were made by giving pressor aminesin heroic doses. Five hours after the accident the patient
appeared to be in a satisfactory condition, he was relatively comfortable and mainly at ease. By this time it
was obvious from dosimetric studies that his radiation
exposure had been supra-lethal. His leukocyte count rosesteadily to a peak of 28,000/mm3 but lymphocytes had
virtually disappeared from the circulating blood in < 6hours. He had marked oliguria, voiding a total of < 600
ml of urine onr 22 hours with a total fluid intake of
14 litres in the same period. More than 30 hours after
the accident the patient abruptly became worse. developed increasing abdominal cramps, became more cyanotic, and despite oxygen. lapsed into coma. His heart,that had received nearly 12,000 rad, stopped 34-M hours
after the accident.
223. At autopsy. the picture was that of acute rightheart failure caused by right-side myocarditis complicated by e..xcessive fluid intake. The most striking histological findings were in heart muscle : severe oedema
and beginning degeneration of muscle fibre with cellular217. On 15 October 1958, the zero-energy reactor at
the Boris Kidrich Nuclear Science Institute, Vinca,
Yugoslavia, became super-critical, injuring eight people,
The reactor 'vas constructed with natural uranium rods
suspended in a large tank that could be filled to various
depths with heavy water. Six received significant dosesof neutrons and y-rays. 391- 393 Following a brief hospitalization in Belgrade, the six patients were transferred to
the Fondation Curie in Paris under the care of Dr. H.
Jammet. The early dose estimates described by Jammet,
et al., 391 on the basis of local information from Vinca
were 1,000-1,200 rem for the highest exposure and 300500 rem for the lowest, placing five of the six in a range
considered to be above the LD 50 • All six had the acute
TBR syndrome: nausea, vomiting, anorexia, asthenia
beginning after the first hour and lasting 2-3 days ;thereafter their general condition was relatively good,in contrast with the progressive evolution of haematological and cutaneous changes: fall in lymphocytes, thengranulocytes, thrombocytes, and erythrocytes. Towards
the end of the fourth week and during the following
weeks there was a worsening in general condition withfever and clinical evidence of haemorrhagic disease. The
individual originally believed to have received the highest dose was given foetal bone-marrow on 11 November,and the four patients having the next highest exposure
were given homologous bone-marrow from adult donors
at various times between 11 and 20 November. The man
who received the foetal bone-marrow died as a result ofradiation with no immunological reaction. Extensive
clinical studies have been detailed. 391 • 394
218. Comparison of the haematological and otherclinical effects of the four YugoslaYian accident victims
who survived after bone-marrow infusion with the fiye
men exposed to 236-365 rad at the Y-12 plant, leads tothe following conclusions :395 (a.) the effects of injury
suggest a somewhat higher dose in the Yugoslavian thanin the Y-12 accident; ( b) haematological patterns in thetw"o groups of patients are remarkably similar, the Yugo142

exudate between fibres showing the presence of true
interstitial myocarditis. In short, this could be termed a
cardiac death. It should not be regarded as representativeof all kinds of radiation injury to the heart, as in aslightly different position he could have received mostof his e.xposure to the left side of the heart. In otheraccidents, other parts of the body might receive thegreatest dose and other mechanisms of quick radiation
death are possible.

Lock port accident
224. On 8 March 1960 nine technicians were exposed
to pulsed X-radiation from an unshielded klystron tube
at Lockport, New York.~ 00 Two of the exposed wereseriously injured, five others less seriously damaged,
while two remained asymptomatic during observation.
Shielding of greater or lesser areas of the body in men
working closest to the tube was critically important indetermining the outcome. To date, satisfactory integrated dose estimates of the entire body in any of themen are not available. Clinical e.xposure appeared tohave been greatest over the right side of the head, rightarm, and axilla of A, the man most seriously injured.
Exposures of the nine varied with their individual activities. The best present estimates are that doses to A
could have been as high as 1,200-1,500 r over certain
parts of the body. Since even a few inches back andforth would result in major changes in e.xposure there
is considerable uncertainty. B's e.xposure is slightly lessthan A's due to his smaller stature and slightly different
position. C's position on the floor limited his e.xposure
largely to head and upper chest. The ne.xt four, D, E,
F, and G, were exposed over greater portions of theirbodies for 60-120 minutes at 6 inches at 4-6 feet, and
H and J were minimally e.xposed for ,...., 120 minutes
at 8 feet. Nevertheless, because of the pulsed nature of
PLATE.
10-3

x

WBC

x 10-3 ·400-10350

9B

INITIALERYTH.
2nd WAVEERYTH.

l

3rd WAVEERYTH.

K.S. HEMATOLOGICAL CHANGES300(MODIFIED CURVES, REPRESENTATIVE POINTS)

7250

the radiation, the actual e.xposure time was only 7.2
secondsjhr.
225. A was exposed from head down to mid-thigh,B from head to pubic symphysis. C was e.xposed largely
above the shoulder level. Throughout e.xposure the men
were unaware that they were being irradiated. Nevert11eless, symptoms appeared during e.icposure, severe
enough to make B and C seek medical aid on their way
home. Headache was the first complaint, beginning during exposure and described as severe, deep within thecentre of the head, and unlike any headache ever experienced before ; even walking around caused intolerable pain. The headache persisted for several hours after
exposure. Nausea and vomiting began in the most seriously injured shortly after the beginning of the headaches. Vomiting persisted throughout the first day;nausea subsided very slowly. The most seriously injured
man continued to have morning nausea for a week after
exposure and sporadically for several weeks. Of all thesymptoms, nausea and fatigue were the most persistent.
With the exception of F all the e.xposed developed conjunctiva! reddening. In A conjunctivitis and acute eyepain was followed by the development of haemorrhage
and exudates in botl1 eyes, with severe interference ofvision in the right eye due to macular involvement. His
eye difficulty has continued to be present and has changed
only in that the acute symptoms have subsided. Visionin the right eye did not improve and that in the left
eye remained stationary. Parotid swelling was the most
severe in A. Both A and B had temporomandibttlar
tenseness and pain on moving the jaw. Treatment wasconservative throughout the patients' hospital course.
In A an initial wave of erythema was present during thefirst 7 days after exposure, a second wave between days
13-19, and a third wave, also seen in B, D and C, between
days 24-29. These waves are shown in figure S that also

6

200-5

•

• (

TOTAL WBC/mm3

•
0

150

3
100
2
3
/YMPHS./mm

50""-MoNOS./mm3

30

40
50
60
DAYS POST EXPOSURE

70

80

90

100

Figure 5. Graph showing the periods of erythema and levels of leucocytes, platelets, lymphocytes,
and monocytes in K. S. (A) injured in the Lockport accident•o 0143

shows changes in the total white count, platelets, lympho·cytes, and monocytes.
226. A's total leukocyte count fell from the time ofadmission until approximately the sixth post-exposure
week. At that time minimal counts of,.., 1.400/mm3 wereseen. Monocytosis was a prominent feature of the peripheral blood during acute stomatitis present days 7-15.
Lymphopenia was severe in this patient and was an important indication that A had sustained major radiation
injury. Platelets reached minimal level of 35,00040,000/mm3 cluing the fifth post-exposur<: week. There
was no evidence of abnormal bleeding, with the exception of a few petechiae on the palate and one foot during
the fourth post-exposure week.
227. At day 38, A became febrile, somnolent andmentally depressed ; these symptoms increased, so thatat day 44 he was moderately ataxic with transient paresthesias of the right arm and left hand, and mild transientreflex changes. These neurological symptoms varied over
12 days. Electro-encephalograms showed multiple, large
and small focal abnormalities. The records improved
gradually, until a normal record was first obtained on
12 September 1960. Mild fatigue with improvement inover-all symptoms continued at day 210.
228. In A there was complete aspermia by the sixth
month, with complete return to better than normal values
at the end of one year. Sperm samples of the others
showed at most only the minimal depression during theacute phase.
229. Follow-up examinations on A, B and D at one
year showed all observations on B were normal, progressive deafness in D-apparently traumatic-but no othersignificant findings, continuation of the eye symptoms
in A, complete correction of aspennia, secondary loss ofhair over the right temple and eyebrow, and mild
asthenia.
AssESS:MENT OF INJURY
230. At present, the severity of illness following radiation damage can only be assessed by comparing the
response of the patient with that of others previously
exposed under similar conditions, who have survived orhave been fatally injured. For this reason, detailed information concerning radiation dose, exposure conditions, and the clinical course of each patient injured byradiation should be available to all likely to be concernedwith these conditions. There is need for further biological indicators of radiation damage, other than theexisting methods, of which the early rate of fall andultimate depression of lymphocytes appears the mostsensitive. A number of patients from reactor accidents
showed a high urine level of amino acids 380 •" 01 and it was
hoped that this might serve as an inde.x of tissue breakdown.381 The metabolism and re-utilization of aminoacids by the body is so rapid that their release fromproteins being quickly broken down after irradiation canbe shown only by the use of special research techniques402"403 not yet applicable to clinical diagnosis.
231. Creatine excretion in the urine is a good indicator of muscle break-down. Patients with muscular
dystrophy excrete large amounts of creatine. It is possible that the weakness of irradiated patients might also
be reflected in e.xcretion of excess creatine. Radiationinduced creatinuria has been studied. •04-ti0s There is acorrelation between large integral doses of radiation tomuscle and creatinuria. Since creatine estimations are
simple and accurate this would appear to be a promisingline for further study. Similarly the excretion of betaamino isobutyric acid is an index of the break-down ofcell nuclei but the analytical method is less simple.
V. Late effects of irradiation in man,
including carcinogenesis

LIFE-SHORTENING
Effect of long-term radiation on life-span in man
232. The problem of extrapolation of animal lifeshortening data to man is difficult because of the lack ofdata on life-shortening for large animals with life-spansintermediate between man and rodents. TBR of rodents
shortens life-span; this effect has not been shown unequivocally in man. Three studies have compared mortality of radiologists with other physicians or with thegeneral male population.
233. Dublin and Spiegelman409 investigated 2,046
deaths of United States medical specialists age 35-74,
1938-1942. Mortality in all specialist groups was lessthan that for all physicians, but mortality of radiologists
and dermatologists was l 6 per cent and 25 per cent respectively above that of all specialists combined. Fromtheir data, the mortality of radiologists and dermatologists, combined or separated, differs from that of specialists not using radiation routinely by an amount bordering on statistical significance. Dublin and Spiegelman
did not calculate occupational risk in differences in life
expectation, but estimated from their data and life
tables for physicians that the difference between radiologists and dermatologists and other specialists is 1-3
years.
234. 'Warren 410 used 82,441 obituaries of physicians
reported 1930-1954 in Journal of the American Medical
Association to compare the mean age at death of UnitedStates radiologists (60.5 years) to that of other physicians not exposed occupationally to radiations ( 65.7
years) ; he concluded that radiologists died 5.2 years
earlier.
235. Court Brown and Doll 411 • 41 " compared the mortality of British radiologists 1897-1957 ·with those of all
physicians and of men of equivalent social class (definedby the Registrar-General). Correcting for age distribution and various biases in vital statistics, they concluded
that British radiologists show no eYidence of lifeshortening. They attribute this to early adoption ofeffective safety measures.
236. These studies suffer from uncertainties and limitations that bedevil evaluations in man. Dublin and Spiegelman did not intend an analysis to apply to mortality
in radiologists specifically. For this purpose their work
suffers from small sample size. Warren's data were notcorrected for age distribution of groups at risk. Seltzer
and Sartwell 413 found "the difference between radiologists and other physicians as to average age at deathcan be accounted for simply by differences in age composition between the two groups". The differences foundby Dublin and Spiegelman included consideration of age
distributions. These data were analysed in annex G of
the 1958 report. 414
237. Vvarren has compared the survival of radiologists averaged over five-year periods ·with survival of
the general population. 415 The latest report giving survival of the general population and radiologists (Warren,
personal communication) suggests that the slope of the144radiologists group is approaching that of the general
population, i.e., the survival of radiologists has increased
from 1930 to 1957 at a more rapid rate than that of thegeneral population. This suggests in retrospect that theevidence of life-shortening in American radiologists
should not be dismissed out of hand. The fact that nolife-shortening was found among radiologists in the
United Kingdom probably reflects not only differences insafety procedures, but also in practice. In the United
Kingdom, most radiology is done in hospitals, and therefore many examinations are made by radiographersrather than radiologists themselves. In the United States
the private practice of radiology is much more extensive,
and the radiologist tends to do this himself. Fluoroscopy
is much more extensively practised in the United States
than in the United Kingdom and probably the numberof X-ray films used in radiographic examinations islikewise greater.
238. A lower limit can be set for life-shortening of
United States radiologists by considering leukaemia incidence only. A statistically significant excess of leukaemia among those radiologists has persisted for years,
decreasing recently;ns-m This is equivalent to a lifeshortening of 3-12 months, depending on assumptions.
239. In conclusion, occupational exposure of UnitedStates radiologists increased mortality in past decades,
but the radiation doses and distribution are unknown.
The exposures must have been heterogeneous withhands, arms, and upper body receiving the most. A lifeshortening effect in man after substantial TBR is to
be expected from animal data. Despite uncertainties,
data on radiologists and other medical specialists represent one of the best available means for studying lateeffects of radiation in man.
CARCINOGENESIS IN MAN

240. It was early known that skin cancers were common in radiologists and dermatology patients. Later,
radiation-induced tumours were seen in haematopoietic
tissue, bone and thyroid. Increased leukaemia has beenreported in United States radiologists, in Japaneseatomic bomb survivors, in children irradiated in infancy
for benign conditions (usually thymic enlargement) andin ankylosing spondylitis patients. Some retrospective
studies have reported that a greater proportion of children with leukaemia and other malignancies were e.'Cposed to X-ray in utero than selected controls \vithout
malignant disease.

fifteen-year period, is about 100 cases per 105 persons
per 100 rad for each year at risk. This estimate is probably too low in children and too high in adults. Additional data are needed for selected age groups.
242. Large amounts of e.xternal radiation, protracted
over a long time given to the entire body or a large segment of bone marrow, are leukaemogenic in man. Nevertheless, present uncertainties about the influence of doserate, fractionation and total dose make it impossible toestimate the probability of leukaemia other than undershort-te~ exposures to high doses. l\foreover, long-term
exposure 1s probably less leukaemogenic than short-term
e.xposure for the same total dose.
243. !1 31 given in high doses, e.g., therapy of carcinoma of the thyroid has in some cases caused leukaemia. •55
244. Cases of leukaemia in which a relationship toradiation exposure was shown' 27 • 428 indicate that withfew e.xceptions the leukaemia was either acute or chronic
granulocytic. In the United States and United Kingdom,
the commonest chronic leukaemia is lymphocytic; its
increasing incidence has not been correlated with irradiation.
Situations in which a relationship betwee!I- radiation andleukaemia has been suspected but not established245. It is not known whether short-term e.""<posure todoses of less than,...., 100 rad given to the entire body or a
portion is leukaemogenic. In particular there is a question about an increased incidence of leukaemia amongchildren exposed in utero, during diagnostic pelvimetryof the mother.' 28431
246. There are no documented cases of leukaemia as alate effect of radio-isotopes such as Sr89• 90 and radium
at any body burden. With thorium while there are ninerecorded cases, the relationship between thorium andleukaemia is hard to gauge because of scarce clinical anddosimetric information.
247. Since leukaemia has been seen after irradiationin Japanese, British and sporadically in other nationalities, there is no reason to believe there is any outstanding
racial sensitivity to radiogenic leukaemia.
Leukaemia in the Japanese survivors of the atom bomb
248. The increased leukaemia incidence in Japanese,e.""<posed to nuclear explosions in Hiroshima and Nagasaki, is inversely related to the distance from the hypocentre. Dose-estimates are uncertain even after the results of recent tests which simulated an actual nuclear
explosion with extensive shielding. Heyssel et a/., 425
summarizes studies by the Atomic Bomb Casualty Commission since 1951 on the increased leukaemia in the
Hiroshima survivors and relate incidence to calculated
dose from y-rays and neutrons combined in the open air
at various distances from the hypocentre. In these calculations, they used an RBE of 1 for neutrons. They
estimated that 60 per cent were indoors at the time ofthe explosion, reducing the air dose by 30-70 per cent.
With leukaemia cases diagnosed up to 1957 they postulated a linear relationship between incidence and calculated open-air dose of 177 rad or more. The point, representing the leukaemia incidence of 3,605 persons receiving a mean estimated air dose of 77 rad, falls almoston the line drawn through points at higher doses. No
cases of leukaemia were seen in 3,512 and 1,305 persons
receiving an average estimated air dose of 34 and 19
rad respectively.

Leiekacmogenesis
Sitt1atio11s in which a relationship between radiation andleukaemia has been established
241. Single doses of external radiation to whole bodyat
100 rad or more and irradiation of an appreciable
portion of the bone marrow with ,.._, 500 rad or more.
slightly increase the incidence of leukaemia in man.
There is no evidence of an increase in the first fifteen
months after exposure. In the Hiroshima data, limited
to 2 km from hypocentre, the incidence increased to a
maximum between years 4-7, declined thereafter but was
still above the e.xpected incidence in 1959. The Japanese
data00428 shows that with short-term exposures to doses
greater than ,...., 100 rad, the incidence of leukaemia integrated over fifteen years increases with dose. The exact
quantitative relationship between dose and incidence ofleukaemia is unknown. Assuming proportionality, theincrease over the natural incidence. averaged over the
,-J

145

249. These authors also show that the latent period
between exposure and development of leukaemia depends on dose. They report that nearly all cases in the
exposed and non-exposed persons were acute leukaemi2.
or chronic granulocytic leukaemia. Among the Japanese,chronic lymphocytic leukaemia is very rare ; a very few
cases were found in exposed and unexposed groups andtheir significance, if any, is hard to evaluate. Heyssel
et al., estimate that radiation increased the incidence ofleukaemia rather than accelerated the appearance of
spontaneous cases.
250. For several reasons, individual dose values canbe appreciably in error. At least 200 survived where themean open-air dose was calculated to be 2,620 rad. 488
Allowing for shielding and assuming that they were at
the edge of zone, the doses received, by these calculations, must have been > 100 per cent lethal. In the lowdose region, the accuracy of the calculated doses may beseriously questioned since many victims in the 2,0002,499 metre zone, where the calculated average dose wasless than 10 rad, had symptoms ( epilation, oropharyngeal lesions, and purpura) 427 suggestive of severe radiation dosage. The calculated dose is far below that producing radiation sickness after TBR and it may be thatthe quoted doses are a serious underestimate because of
the contribution of induced radio-activity. On the other
hand, since victims even farther away were also said tohave similar symptoms it is the consensus of opinion of
the observers 438 who interviewed these patients that their
symptoms were complicated by malnutrition and factors
other than radiation exposure.
251. These studies by Heyssel et aJ,.;m suggest astraight-line relationship between doses above __, 100 rad
and the incidence of leukaemia among bombed Japanese.
Considering the large variation inherent in incidence anddose estimations, the data could also have been represented by a straight line with a different slepe, or by acurved line.428 Although the data are not enough to say
whether the relationship is linear over the entire dose
range, they do allow a conservative estimate of theprobable incidence of leukaemia in a population of allages over the first 10-15 years after a single exposure tohigh doses. A reasonable estimate might be an averageof 100 additional cases per 106 persons per 100 rad foreach year at risk during that period.
252. It is not possible to demonstrate an age-incidence
relationship because of the small number of cases ofleukaemia in Japan although there is some indication ofa higher rate among bombed children than bombed
adults. Hence, prediction of incidence in selected age
groups or calculation of the probability of leukaemia
among the individuals exposed may be speculative.

data of all suspected of dying of leukaemia or aplastic
anaemia ; they calculated from dose records mean doseto spinal marrow and whole-body integral dose of a large
sample. There were thirty-two proved and five probablecases of leukaemia and four cases of aplastic anaemia ;the number e..xpected from national vital statistics was
2.9 for leukaemia and 0.3 for aplastic anaemia, a significant increase in mortality from these causes.
255. They estimated the annual incidence of leukaemia for the general male population not therapeutically
irradiated to be 50/106. The annual incidence in man
given a mean dose of over 1,750 rad to only spinal marrow was 1,600-1,700/106 • For all patients regardless ofsite of exposure, the. annual incidence was 7,200/106,
with a mean spinal marrow dose of over 2,250 rad.
256. Classifying cases by mean spinal marrow andintegral dose shows a correlation between dose and leukaemia incidence. The shape of the incidence-vs-dose
curve depends upon whether mean spinal marrow or
integral dose is used, and whether the cases given e..rjraspinal radiation are excluded. However, whatever the
method of analysis, the relatively small number of casesof leukaemia and the dose parameter used make it impossible to decide whether the dose response relationship is or is not linear (figure 6).
25.0

i!!"'

fj

r:..

.

•

l!ll,0i5§

a 1.5.oe;"":s~ 10.0l!s~eu s.o:;;2.0

MEAN DOS£ lO SPllW.. IMRRO\V, Crl

Figure 6. Incidence of leukaemia in relation to mean spinal
marrow dose of therapeutic irradiation. The regression line
was obtained after weighting the rates according to theirreliability and is given by Y 0.00586X 0.380; the 95 percent probability limits of the value of Y for each value of X
are shown by the curved lines. Redrawn from Court Brown
and Do111ss=+

257. The single point below 500 rad is based on twocases of lymphatic leukaemia, one chronic that developed
after a mean marrow dose of 471 rad, and the other inwhich the spine received 113 rad but extra spinal regions
received additional larger doses.

253. There are some data which suggest an increasein leukaemia incidence in Hiroshima among persons who
were not directly exposed to the atomic explosion but
who entered the area very soon aftenvards. These data
should not be overlooked, although there is great difficu~ty, at the present time, in making any accurate calculation of the dose received from the induced radioactivity.439

258. There were ten cases of leukaemia within five
years after a single course of therapy. 0£ the thirtyseven leukaemias, including those with multiple courses
over years and those with a single course in a month,
the diagnosis was made in thirty-five within five yearsof the last treatment. Of the fifty leukaemias in spondylitic patients after X-rays, including those reported by
Court Brown and Doll, thirty-eight were acute and only
eight were chronic-with only one of the latter being
chronic lymphatic leukaemia. Data in the remainder wereinsufficient to establish clinical type.

Letlkaemia in ankylosing spondylitis
254. Court Brown and Doll 412 • 440 in the United Kingdom reviewed 13,352 patients, presumed to have anh.7Josing spondylitis give;i X-ray treatment to theirspmes, from 1January19;,3 to 13 December 1954. They
reviewed death certificates and clinical and pathological146

259. Some leukaemia patients showed a sequence of
pathological changes : a persistent damaged or aplastic
marrow was a precursor rather than a consequence ofleukaemia; other cases of aplastic anaemia were seen
after the same dose range.

mus glands of normal size at birth. The radiation factors
were uniform; 88 pe~ cent were giv~ 75-300 r (usually
150 r) to the manubnum ; the remarnder were restudied
11-18 years after therapy. Four cases of malignant disease, including one of leukaemia, were expected in thisgroup; none was found. There was no significant difference between the number of expected and observed casesof cancer and leukaemia in untreated siblings.

260. In attempting to e."'{trapolate the incidence data
to low doses, use of the incidence of spontaneous leukaemia in the general population as a control is questionable since there appears to be a strong hereditary
factor in ankylosing spondylitis.441 This is underscoredby the report of Abbott and Lea4 ·12 showing an association between untreated rheumatism and leukaemia. The
only available control group of 399 untreated spondylitic
patients is too small to be useful.

267. The failure to find the four expected cases ofneoplasia is not significant, since one-tenth of the group
was not located. One can conclude, nevertheless, that
there was no evidence of an increased cancer rate intreated children or of a greatly increased leukaemia
frequency.
268. To avoid variables due to considering children
given X-ray therapy to the mediastimal region only, a
study was made of 6,473 children in Rochester, New
York, treated with X-rays for various benign conditionsin the past twenty-five years. 434 The difference between
the eight leulrnemia cases observed and the two e.xpected
is significant. There were five leukaemia deaths in 2,750
children treated for thymic enlargement; two were inseventy-five children treated for pertussis and one in
1,073 children given X-rays to the head and neck region,
mainly for lymphoid hyperplasia of the nasopharynx.
There were no leukaemia deaths in 2,460 children treatedwith superficial X-rays for benign skin lesions.

261. Because of limited data in the lower dosi;! range
and lack of an adequate control group, this study does
not provide evidence on leukaemia incidence after doses
below 500 rad.
262. Leukaemia is a rare disease; cases after radiation represent only a small portion of its incidence.
Nevertheless, in a single case where the onset of leukaemia associated with radiation exposure occurs within
an appropriate interval after a known single exposure
to over 100 rad, the probability that the disease is due toradiation is high. It is possible to estimate this probability by considering the normal incidence in the population and the probable increase in the incidence of leukaemia after a single high dose.Ha, H 4 This probability
will increase to a ma..ximum around the fourth-seventh
year after e."'{posure and thereafter decrease perhaps ultimately diminishing to the level of the incidence expectedin the general population.

269. Similar surveys of children treated for thymic
enlargement and other benign lesions are now being
made in the United States. Latourette and Hodges 450
reported the incidence of neoplasia in 861 children
treated for thymic enlargement, 1932 to 1951. Most children were treated with 200 r or less, through a large
10 x 10 cm port. The two cases of lymphoma (one being
leukaemia) were more than expected, but not significantly so. One child had a carcinoma of the thyroid andothers had various benign tumours. Snegireft4 51 found
two thyroid tumours in 148 children followed out of
1,131 children treated for thymic enlargement; Moloney,
in a discussion of Simpson's work4 47 mentions sevencases of thyroid neoplasias including two malignancies
in 125 of 700 children so treated.

Leukaemia in children (table VI)
263. Some investigators found an increased incidenceof leukaemia in children given radiation to the thymus;
others have not. There is no satisfactory control groupfor a conclusive statistical evaluation. Simpson, Hempelmann, and Fuller,4'15 Simpson and Hempelmann 446 andSimpson 4 H found in 2,393 such cases in upstate New
Y ork-87 per cent traced ·138-twenty-one cases of malignancy instead of 3.6 e.xpected, and nine confirmed and
one unconfirmed leukaemia deaths instead of one exexpected. Most other malignancies were thyroid carcinomas. There was no significant difference between
expected and observed incidence of cancer or leukaemia
in 2,722 untreated siblings of children in this study.

270. Saenger et al452 reported on 1,644 out of 2,230
children treated for various benign conditions. Of 675
given treatments e.xclusively to the chest, mainly forthymic enlargement, only 124 received more than 200 r.
Eighteen cases of thyroid neoplasia (eleven diagnosed
as malignant) and one case of leukaemia were found in
the entire group. They also report a striking incidence ofmorbidity of all types of non-fatal illnesses in thesechildren, indicative of the selected nature of the group.

264. Exposures measured in air were known or calculated from radiation factors for all but 299 children.
Four of the IH1own leukaemias were in 1,050 children
with a cumulative exposure of less than 200 r, 5 were in
1,025 children given 200-600 r. All other malignant neoplasias were among children given 200 r or more. Average survival between irradiation and death from leukaemia was 5.3 years.

271. From these studies it is clear that an association
between radiation e.xposure and subsequent leukaemia
has been established only in one group of children treatedwith X-rays for thymic enlargement. Further epidemiological studies are needed to establish the true incidenceof leukaemia in children given thymic irradiation, andespecially the relation of incidence to dose, port size, andpart of body treated.
272. Numerous studies of children given radiation to
the thymic region showed an increased incidence of thyroid neoplasia; in contrast, an increased leukaemia incidence was found only in one study.
273. Long-term exposure to radiation will increaseslightly the incidence of leukaemia in man. This opinion
is based mainly on the reported increased incidence of

265. Since the state of the thymus gland in the siblinggroup is unknow-n and is, in general, normal in childrenof the general population, this study does not differentiate between the association of leukaemia and (a) X-ray
e.xposure, or ( b) thymic enlargement. Because it is impractical if not impossible to get an accurate control
group, (i.e., children with thymic enlargement at birth
not treated with X-rays), children irradiated for otherreasons must be studied.
266. Conti et al:m,m studied in 1948 1,564 children
treated with X-rays in Pittsburgh-96 per cent had thy147

leukaemia in United States radiologists and the appearance of sporadic cases f?llow.ing long:term exposure
from diverse sources. 428 Smee mformabon on dose andother data are poorly documented, this evidence is not as
good as that for short-term radiation. Data are inadequate to allow even a guess as to relationship between
dose and induction of leukaemia after long-term exposure. Experiments in animals indicate that the leukaernogenic effects of cumulative doses are less in longterm than in short-term exposure. 269 Whatever the dose
rate in long-term radiation, it is likely that the cumulative
dose exceeds ,...,, 100 rad in those cases where leukaemia
is believed to have been induced by radiation.
Leukaemia in radiologists
274. Among United States physicians the ratio of leukaemia deaths to total deaths between radiologists andnon~radiologists was 10.3 :1, 1929-1943,416 6.7 :1, 1944 to1948 417 and 3.6:1, 1952-1955.418 The downward trend
probably reflects better precautions by radiologists andpossibly an increase of leukaemia among non-radiologists. From 1938 to 1952, there were seventeen leukaemic
deaths in United States radiologists ( 35-74 years of age)-an average annual rate, after correction for age distribution, of 610/10 5 compared with the population average, 121/106 •410 The ratios vary, depending upon timeand corrections for age distribution.
275. Braestrup' 53 estimates that radiologists working
with old-type X-ray equipment and few protective measures received as much as 100 rad per year ; that exposure
before 1930 was considerably higher; and that at present
it averages considerably less than 5 rad per ye'!-r. ~isestimates of accumulated total exposure of a rad1olog1st
using old-type X-ray machines was about 2,000 rad during forty years of practice. Lewis09 assumes the average
exposure of all radiologists to be 30 rad per year or
1,200 rad in forty years. However, these estimates andassumptions of dose must be treated with great reservein view of the uncertainty involved in their derivation,and it also has to be recognized that the distribution ofradiation dose throughout the body was far from
uniform.
276. In contrast, British radiologists who began practice after 1921 have had no increase in leukaemia; theonly two known cases were among those in practice
before this time,m probably for reasons previously discussed in the differences in life-shortening.
Pelvic irradiation and leukaemia in children (table VII)
277. In an extensive retrospective survey, Stewart.
Webb and Hewitt430 interviewed mothers of : (a) 677 of
792 children under ten certified as having died of leukaemia in England and Wales, 1953 to 1955; and (b)739 of 902 children under ten certified as dying in thesame period from other cancer. They also interviewed acontrol group of mothers whose children were still alive
and who were matched with the study children for age,
se.x, and locality. They found a higher frequency ( 13.7
per cent) of diagnostic X-ray pelvimetry in mothers ofchildren dying from cancer than in mothers of control
children (7.2 per cent). There was some correlation
between size of the ratio between numbers exposed toabdominal irradiation and number of X-ray films reported to have been taken. The ratio was highest formothers exposed during the first few months of pregnancy.
278. Four similar retrospective studies were made indifferent parts of the United States. Ford et al.' 31 corn-pared seventy-eight leukaemic children and seventy-fourchildren having other malignancies with 306 dead controls matched for colour, age and place of death in New
Orleans. Their findings are in line with observations of
Stewart et al. 430 26.9 and 28.4 per cent of the children
with leukaemia and other forms of malignancy were
irradiated in utero, compared with only 18.3 per cent ofcontrol children.
279. The three other studies, using other methods forselecting controls, do not show the same excess of foetal
irradiation in leukaemic children. Polhemus and Koch' 33
found no significant difference in the history of pre-natal
irradiation in 251 diagnosed leukaemic cases in theChildren's Hospital of Los Angeles, compared with thesame number of matched control children with nonorthopaedic diseases on the surgical service of the same
hospital. In a current study of childhood leukaemia in
California, Kaplan and Moses 432 found that the numberof children with leukaemia having a history of pre-natal
irradiation exceeded that of the group of siblings used
as controls; such an excess was not seen, however, when
the leukaemic children were compared with healthy playmates. Murray et al. 434 found no significant differencein the history of pre-natal exposure of sixty-five children
with leukaemia, sb::ty-five matched dead controls, andthe 175 living siblings of both groups.
280. In these retrospective studies, the choice of thecontrol group is crucial. The studies as presented do notdifferentiate clearly behveen the association of leukaemia
and (a) the effect of the medical condition which
prompted the diagnostic e...xarnination, or ( b) the effectof X-rays.
281. In an extensive prospective study on the incidence of leukaemia after exposure to diagnostic radiation in utero, Court Brown, Doll and Bradford Hill " 8 ·" 36
followed up 39,166 live-born children whose mothers had
been subjected to abdominal or pelvic radiation during
pregnancy, 1945to1956. Among their children nine were
found to have died of leukaemia before the end of 1958,
instead of the normally e...xpected number, 10.5.
282. It is clear, therefore, that existing data on sequels
to irradiation in utero have led to conflicting conclusions.
Stewart's data are very important for evaluating somaticeffects in man as they are the only data pointing to low
doses of radiation being carcinogenic. Because of theirserious implications, the circumstances surrounding
these data must be understood. If these data are not misleading for reasons yet unknown, one would have expected double the incidence of leukaemia in the Court
Brown, Doll, Bradford Hill study just cited. i.e., twenty
cases instead of the nine actually found. The data of
Court Brown et al. thus put into doubt the conclusions of
Stewart et al. On the other hand, if the ratio from
Stewart et al.'s 429 earlier report is used, 1.7 :1 instead of
2 :1, the difference between the expected figure of 17-+- 4
and 9 -+- 3 is not such that a definite conclusion can be
drawn.
283. The conclusion of Stewart et al.4 30 also implies
that foetal haematopoietic tissue is much more susceptible to the leukaemogenic effect of irradiation than adulttissue. As previously stated. it is not known whether
short-term exposure to doses less than ,_, 100 rad to theentire body or a portion is leukaemogenic. Neverthelessto answer the question raised by the data about the incidence of leukaemia among children exposed to diagnostic
pelvimetry in utero certain theoretical estimates can be
made. Such estimates for the adult suggest that 1 rad tobone-marrow produces one case of leukaemia per million
148

closed sample, are subject to the factors of selection thatmight enter into the admission of cases to this series.
With this important reservation the incidence increased
in inverse proportion to hypocentre distance. If the background incidence of all malignant neoplasms. i.e., 280
per 100,000 among the non-irradiated population is subtracted from the incidence of malignant neoplasms thecurve is linear and parallels the incidence of leukaemia(figure 7). The incidence correlated to site was higher
in all age groups (figure 8). Table VIII shows a significant difference between observed and expected cases ofcancer of stomach and lung at the 1 per cent confidence
level, while differences in cancer of the cervix and ovary
are significant at the 5 per cent level. though the numbers
are still small. These preliminary observations need extension in numbers and time so that the increased incidence of carcinoma developing only after many years oflatency after irradiation can be correlated with dose andtemporal occurrence.
288. Despite the numerical weakness of the data, 455 thedegree of initial leucocyte count depression in the first
fourteen weeks after e..xposure correlated with the occurrence of late effects. The data indicate that the more
severe the initial exposure as indicated by clinical signs
and early laboratory work, the oftener late effects appear(figure 9).

persons per year for perhaps ten years of risk. Since thenormal annual incidence of leukaemia in England and\:Vales under age ten is ,...., 37 per million and the amountof radiation received by the foetus from irradiation of
the mother's abdomen is estimated to be ,...., 1 rad, it follows that if this dose were to double the incidence of leukaemia in children it would have to be ,...., 40 times moreleukaemogenic than the same dose in the adult.
284. Although foetal tissue appears more radiosensitive than adult tissue, e.g., foetal nervous and thyroid tissues are more radio-sensitive than their corresponding adult tissues, there is no evidence that thisholds for haematopoietic tissue. In fact, adult haematopoietic tissue appears to be the one adult tissue that is as
radio-sensitive as embryonic tissue. From their study ofpatients irradiated for ankylosing spondylitis, Court
Brown and Doll412 estimated the dose to marrow that
doubles the expected incidence of leukaemia to be
30-50 r. Assuming that the leukaemogenic effect of radiation is the same in foetus and adult and that 40 r is the
doubling dose, and that radiation to the foetus in utero
is as high as 4 r, one would not expect to find more than a
10 per cent increase in leukaemia in children irradiatedin utero, i.e., in the Court Brown, Doll and Bradford
Hill study the increase to be expected over the estimated
10.5 would be one case.
285. Doubts about the controls in Stewart et al.'s
study have been discussed.rn A probable bias is underreporting of radiation exposures by the control mothers
since it is reasonable to suppose that mothers of deadchildren would recall the events of pregnancy more completely than mothers of children who are alive and well.
In the light of the study of Court Brown et al. 435 thequestion of the effect on the foetus remains open. Clearlya further study of this problem is needed.
286. It has not been established whether internal emitters selectively deposited in bone (bone-seekers) but notdelivering a uniform dose to the marrow are leukaemogenic in man. The apparent increase in leukaemia among
patients with polycythemia vera treated with P 32 is suggestive but not conclusive in the absence of an adequate
control population. Leukaemia has followed giving !1 31
in high and repeated doses in patients treated for carcinoma of the thyroid. Leukaemia has also been reported
after treatment of hyperthyroidism with relatively small
doses of !131 • In the latter instance, since the number ofcases is small and there are metabolic and other complicating factors in these patients, it is not possible to decide
whether or x;ot. radiation alone at this ~osage level isleuka_emog~mc m ~1.1· ~ recent ~xtens1ve survey byPochm• 55 gives no mdicat1on that this treatment induces
leukaemia. Mouse leukaemia has been induced with boneseekers ;456 however, it is questionable whether this disease, or the conditions or irradiation and tissues irradiated, are comparable to those for man. An estimate of
the probable incidence of leukaemia from deposition of?r90 has be~n computed. 419 No confidence can be placedm such estimates because of lack of meaningful estimates of dosage to the marrow. Data obtained from e..--.;ternal exposure studies• 2 ~ 2 e,._.o, 4H are not directly applicable in the case of non-uniformly deposited isotopes.

LoC.\L EFFECTS

Radiation cataract
289. Exposure of the optic lens to X-rays, y-rays,,8-particles and neutrons causes cataracts in man.

2000

1000

roo
400
0
0
0

200

CJ~

... 1000......

"'c.

u
"'
c:

u"'

60
40

~~\

',

~,

',

'O

= 20
10

\.

~Total Ieukaemias

6
4

\.

2

Distance from hypocentre in metresI I
I I I IMALIGNANT NEOPLASMS IN THE JAPANESE SURVIVORS OFATOMIC BOMB

1000

100 50 10 5

Air close {rad), without consideration for individual shielding

287. Harada and Ishida•~r have recently reported on
the incidence of neoplasms among survivors at Hiroshima during May 1957-December 1958. These aretumour registry figures and the data, not based on a

Figure 7. All malignant neoplasms (including leukaemia) among
atom bomb survivors, May 1957-December 1958, and total
leukaemias, 1950-1957, by distance from hypocentre per 100,000
population per year. Modified from Harada and Ishida •57

149

small granules and vacuoles develop as it enlarges. The
central opacity develops a relatively clear centre, giving
it a doughnut appearance by the time the opacity is
3-4 mm in diameter. At this time, granular opacities andvacuoles may develop in the anterior sub-capsular regionof the lens, usually in the pupillary area. The opacity
may remain stationary at any stage. Often it shows aslow progression for a long time to the point described
before it remains stationary. If the opacity progresses,
it takes on a non-specific appearance and cannot be differentiated from cataracts from other causes.

J.coo

:.ou

C>
C>
C>

g

.

c.

i.:c
-3

]

291. X- or y-radiation have caused,_, 200 cases of radiation cataracts in man. 459 • 467 :Most had latent periods
but in many these were not related to radiation variables
such as quality, dose, or duration of treatment. The doseand factors that might permit its calculation were notreported in many cases.
292. The problems of minimal cataractogenic doseeffect of dose and mode of exposure on incidence of stationary or progressive cataracts, influence of dose fractionation and dose or duration of exposure on the latent
period, effect of radiation quality, and age on lens sensitivity-are still unsolved for man.
293. From animal studies, radiation cataract resultsfrom radiation destruction of the anterior epithelium,
which supplies cells that differentiate into fibres of thelens. Young animals exposed pre- or early post-natally
have greater lenticular radiation-sensitivity than older
animals.

...•••...
d"--J;l Exposed between S00· 1499 m

••
"
"

Ii.~

Excluding l11<1koemios
ond lymphonua0-·~ Nan-posed (beyon.! 10,000 m)

••

••

:o

.

"

AG• In y..;,.s"Figure 8. Malignant neoplasms (excluding lymphoma and leukaemia) per 100,000 per year by age and exposure status, May
1957-December 1958. Modified from Harada and Ishida 4 57

294. Merriam and Focht464 studied in man 100 casesof radiation cataract and seventy-three cases of irradiation to the head without subsequent cataract. Duplicating
the radiation factors, they measured X- or y-ray dose to
the lens in a phantom. Any clinically recognizable characteristic opacity was regarded as a radiation cataract
regardless of whether vision was affected. Numerous
uncontrollable variables in this study made it impossible
to determine the threshold dose.
295. The minimal effective doses were the least radiation producing some lenticular opacity. It was impossible
to classify cases by dose and degree of lens opacity ;they were classified by whether opacities were stationaryor progressive and this was then related to dose.

2400

woo
0

1600
0

1200

0

800
0

296. Ninety-seven of the radiation cataract cases andseventy without radiation cataract were classified bytiming of treatment: single, fractionation over three
weeks, to three months, and fractionation > 3 months.
The minimal doses for production of lenticular opacity
in cases for each group were 200 r, 400 r, and 500 r
respectively. These figures suggest that the thresholddose increases with duration of treatment.

0

400

0
0

0

0....._-<>---'-~-f-~,._-.-t----'~-+~-'-~+---'>1000080006000400020000·
8999
6999
4999
2999
999
9000·
70005000300010009999
7999
5999
3999
1999
LOWEST WBC IN
14 WK POST- BOMB PERIOD

297. Of thirty-seven cases irradiated in a single treatment (with radium plaques), all twenty with doses from
200-L150 r developed lenticular opacities. The otherseventeen received doses from 40-175 r to the lens without developing lens changes. There were only two casesof stationary lens opacities of minimal degree at an
estimated dose of 200 r, first seen nineteen and twentytwo years after treatment. Because of the small numberof cases (four) with doses from 200-350 r, the fact that
there were none without cataracts does not prove thatthe lens cannot tolerate higher single doses. Further information on the effects at these dose levels is necessary
to determine the upper limits of tolerance. The maximal
non-cataractogenic dose in this treatment group was
175 r in a patient followed for 8}'2 years.

Figure 9. Incidence of late effects among Hiroshima atom bomb
survivors, plotted against the lowest leukocyte count in thefirst 14 weeks after exposure•ss

Although changes in the optic lens have been detectedaiter doses as low as 200 r, the minimal effective X-ray
dose (200 kv) for the production of clinically significant
cataract is 600-1,000 rad; this dose may be lower for
infants or children and is highly dose-rate dependent.
Neutrons are 5-10 X more effective in causing cataracts
than X-rays.
290. The characteristics of radiation cataract in earlystates of development are: an initial dot-like opacity,usually at the posterior pole of the lens, around which150298. Of eighty-seven cases given multiple treatments
for three weeks to three months, forty-nine developed
lenticular opacities with X- or y-ray doses of 400-6,100 r
to the lens. Lens opacity after 400 r (one case) was firstseen 20 years after treatment and was stationary. The
maximal non-cataractogenic dose in this group was

1,000 r with a treatment time of 20 months and a followup period of 13 0 years. The following table gives theincidences and types of lenticular opacities in patients
after irradiation in various dose ranges for a three-week-three-month over-all time.
Cataract lype

Dose range (r)CaJartut incicknce

40-350 ............................ 0 of 18 patients
351-550 ............................ 4 of 9 patients
551-750 .•..•....................... 6 of 10 patients
751-950 ......................••.... 16 of 26 patients
951-1,150 .......................... 2 of 3 patients
1,151-1,399 .......................... No cases
1,40D-6,100 ...............•...•.•.... 21 of 21 patients299. Of forty-three cases irradiated over a period
longer than three months. twenty-eight developed lenticular opacities after X- or y-ray doses of 550-6,900 r
to the lens. There were two cases of cataract after 550 r,
one progressive and one stationary, first seen forty-fourmonths and four years after treatment respectively. The
maximal non-cataractogenic dose in this group was
1,100 r, with a treatment time of 10 years and a followup period of twenty-two years.
300. The 100 per cent incidence level of lenticularopacities occurred at the lowest-dose level for the single
treatment group (200 r) and at any greater dose. In themultiple treatment cases, the longer the duration of treatment, the lower the incidence at a given dose range below
1,150 r; the higher the dose for a given treatment, theshorter the time of appearance of the lens changes andthe higher the incidence of progressive opacities withresulting decrease of vision. In general, fractionation ofdose delays the time of onset of cataracts and decreases
the incidence of severe opacities.
301. The lenses of children under one year of age
seem to be more sensitive to radiation than those of older
children and adults.
302. Cataract production by fast neutrons comparedwith X-rays increases significantly with protracted e.xposure; i.e., the RBE is about 2-4 for high-intensity and
9 or greater for low-intensity radiation, only because thedose of the "standard" radiation changes, not that forneutrons.
303. By December 1948, at least ten nuclear physicistsof mean age thirty-one had incipient cataracts after
cyclotron exposure. 468 Three cases were severe with definitely impaired vision. Four were moderately severe, andthree were minimal. It was estimated that over periodsof 10 to 250 weeks, these men had received total doses offast neutrons to the lens of 10 n-135 n with a mediandose of 50.* At the time the cataractogenic exposures
were received, periodic blood counts done on mostshowed no change in blood picture warning of overexposure to radiation.

Stationary

Progressite

Intkterminale

3
5
7
1

0
1
6
1

1
0

2

18

3
0

not reported, but it is inferred that they were generally
mild.
305. In 1955, Sinskey 41 z reported an intensi:re in':'estigation of 3,700 exposed and non-e.xpo~ed Hiroshima
Japanese from May 1951-December 19::>3: there. were154 survivors with posterior sub-capsular plaques m thelens large enough to be visible with the opthalmoscope.
Opacities not so visible in the greater percentage of survivors were not considered because they did not decrease
visual acuity in standard tests. Because '?f the relatively
negligible effect of the atom bomb on visual loss sevenyears after the bom~ing, the t~rm cataract, ass?ciat~dwith severe loss of vision or blmdness, was avoided mthis survey.
306. Sinskey found that of 425 survivors in Nagasaki
between 400-1,800 metres from ground, 47 per cent hadlens changes detected by slit-lamp examination, with orwithout history of epilation and shielding. Although most
opacities were so insignificant as to be invisible with theopthalmoscope, statistically significant lens changes were
present in survivors with no other known early or lateevidences of radiation damage.
307. Among,....., 8,000 e.xposed survivors of Hiroshima
and Nakasald e.xamined by 1956 (eleven years after theatomic bomb explosions), ten cases of severe cataract
were found. The relationship between these cases andradiation alone is not clear.
Radiation effects on fertility

308. The late pathological effects in gonads are chiefly
a hastening in involutional changes associated with advancing age. In animals, there is little evidence of radiation-induced testicular tumours, but ovarian tumours are
increased by radiation.
309. Histological sterility is complete absence ofgametes and even gametogenic elements. It is difficult topredict its permanency by biopsy ?r froi;n necro:p~y sections. Permanent and complete histological stenlity requires large doses to the gonads; such doses would be
lethal given in a short time to the whole body or a substantial part.

304. After the finding of radiation cataracts in thephysicists, Cogan et al. 469 • 410 found 10 heavily irradiatedJapanese atom bomb survivors with radiation cataracts.
In studies by Kimura in 1949, described by Fillmore.471
98 cases of lenticular opacity were reported, 85 among
the 922 survivors in the high-dose region 1,000 metres orless from the hypocentre. The severity of the lesions was

310. Functional sterility can be induced by sma~lerdoses; this may be temporary or permanent depending
upon size and intensity of dose. In the male, the rate ofsperm production need. only be reduced to \yhere th~reare insufficient sperm m semen to be effective. An mcrease in abnormal sperm after irradiation also reduces
the number of effective sperm. Since the number of nor-

* 1 n is equal to ,....., 2 rad.
151

mal sperms per ejaculate necessary for reproduction islarge sub-fertility may be associated with considerable
but s~bnormal spermatogenesis. These conditions can be
induced by doses to the gonads sub-lethal if given as TBR.
Sterility doses for men and women

311. The long-term pathological effects of radiation
on gonads have had little study with accurate dose estimates. From fragmentary data certain estimates areattempted.
312. Gonadal doses affecting fertility are probably
similar for men and women: a single dose of ,._, 150 rad
to gonads may induce brief, temporary sub-fertility inmany men and wome_n; a single dose of ,._, 250 rad may
induce temporary sterility for 1-2 years, and 500-600
rad permanent sterility in many, especially in people
with borderline fertility, with temporary sterility inothers for several years ; single doses of 800 rad or more
would probably cause permanent sterility in all but a
few most resistant men and women.
313. Gonadal doses causing only temporary alterations in fertility in fertile people are sub-lethal if given
as TBR. Gonadal doses that permanently sterilize mostfertile people are likely to equal the TBR lethal dose.
314. Limited experience with the Marshallese, exposed Japanese, and certain accident cases suggest that
substantial fractions of the mid-lethal dose for man( 400-600 rad) do not have a serious, permanent effect on
fertility, but gonadal doses are not known with certainty;
few people have been studied for this purpose for a longtime after exposure.
315. Men may be sterilized permanently withoutprominent changes in interstitial sex cells, hormone balance or libido. Women sterilized by radiation undergo
greater physiological changes since ovarian production ofsex hormones is intimately related to development anddischarge of ova. Radiation termination of productionof ovarian follicles induces an artificial menopause in
women similar to natural menopause, with amenorrhea,"hot flushes", diminished libido, and occasionally psychic
depression. From experimental data, long-term radiation
may seriously impair fertility in animals such as man
with relatively poor gonadal regenerative ability.
Degenerative diseases and histopathological changes

316. Injuries of the skin, atrophy, dermatitis, epilation, and epidermal neoplasia were among the first recognized late radiation effects. In human skin, 500-700 rad
may induce permanent epilation. Smaller doses cause
temporary epilation, may decrease pigmentation or graythe new growth of hair in irradiated areas. This effect has
not been reported in Japanese. Doses in the erythemarange or higher may also increase pigmentation of skin,epidermal atrophy, and decrease sebaceous and sweat
glands in irradiated regions. Hyperkeratotic areas inskin, and vascular sclerosis are also late effects of skinradiation. Surface doses of ,._, 1,600 rad may cause considerable permanent dilation of capillaries (telangiectasia) in irradiated areas. In the past late changes wereseen more commonly than today in the skin of hands
and faces of persons occupationally exposed to radiation ;radiation dermatitis and ulcers were often followed by
epidermoid carcinomas.

hypertension may be induced in man within months or a
few years by single localized X-ray doses of ,..., 3,0005,000 rad or by fractionated doses of lesser size (e.g.,a total dose of 2,300 rad to both kidneys in 35 daily
doses).4 73 These conditions have been induced in experimental animals in a short time by local radition of thekidneys with large doses. More recently, nephrosclerosis
with renal hypertension and associated generalized arteriosclerosis were induced in rats and mice as late effects
of TBR with much lower doses (sub~lethal or LD 5orange). Although the pathogenesis·of nephrosclerosis asa late effect is not clear, histopathological data indicatethat changes in fine vasculature are important in earlyand late initiation and development.
318. Nephrosclerosis and related hypertension may
appear as a late radiation effect in animals in which it
has rarely or never been seen within the average lifespan(later periods are not well studied) or its onset may be
advanced in animals in which the disease has appeared
spontaneously. Renal hypertension, once established andprogressive, increases vascular sclerosis throughout thebody; progressive arteriosclerotic changes often induce
progressive atrophy of parenchymatous organs. Consequently, when irradiation has induced or advanced
nephrosclerosis with related hypertension in animals orman, the incidence of death from related causes (e.g.,
renal and cardiac failure, and cerebral haemorrhage):increases with corresponding reduction in death fromother unrelated causes or from diseases having longer
induction times. Irradiation of human brain or spinal
cord with several thousand rad, given singly or in large
fractions over a few weeks, may injure blood vessels,cause ischemic damage of tissues, and progressive sclerosis of blood vessels, with subsequent secondary degeneration of brain or spinal cord. Blood vessels may rupture one to several years after exposure.
319. Atrophic and fibrotic changes, often with arteriosclerosis, have been seen in human haemopoietic organs
long after local radiation. Secondary anaemia has been
associated with myelofibrosis after long-term radiationof bone marrow and also as a late complication of radiation therapy. Radiation osteitis is a late degenerative
effect of intensive irradiation (a few thousand rad) of
bone. The degenerative and destructive processes develop
slowly, and after many years lead to necrosis, pathologic
fracture, and osteogenic sarcoma.
320. The gastro-intestinal tract has shown some permanent and late effects after fractionated doses of several
thousand rad; atrophic and fibrotic changes and sometimes late ulceration in mucosa, and permanently reduced
secretion of acid and pepsin by the stomach.
321. Intensive irradiation of the lungs in radiation
therapy causes slowly developing progressive fibrosis,
with vascular damage and arteriosclerotic changes. Radiation fibrosis 474 usually develops slowly, but there havebeen fatalities eight weeks after therapy. Lungs show
fibrosis with thickening of alveolar walls and vascularsystem. The alveolar walls may be lined by cuboidal
epithelium and the remaining alveolar sacs may be filledwith cells. Cough and dyspnea are the principal symptoms. Roentgenographs are similar to those of pulmonary fibrosis from other causes. There is considerable
unexplained individual variation in post-irradiation
fibrosis but in general the incidence depends on dose.
The degree of disability depends also on the amount oflung tissue irradiated; thus. treatment of intrathoracic
neoplasms where a large part of pulmonary tissue is317. Nephrosclerosis is long knO\vn as a complicationof over-exposure of the kidneys in radio-therapy. Renal152

exposed is apt to be more serious than treatment ofcarcinoma of the breast, where usually only part of one
lung is ex:posed. 415 Malignant neoplasms of the lung havebeen seen in miners who inhaled radio-active substances,and have been induced in animals by intra-tracheal injection and implantation of radio-active substances.
322. Substantial doses of radiation to actively proliferating mammalian tissues reduce their regenerative
capacity. Failure of such tissues to regenerate parenchymal cells to normal numbers is often associated withincreased connective tissue and vascular changes. In general, incomplete regeneration varies directly with size ofthe single dose or with dose rate in long-term radiation;
in some tissues such as testis, fractionation may increase
dose efficiency in damaging regenerative capacity. It is
not clear to what e..xtent the permanence of this effect isdue to the direct effect of radiation on stem cells, or todamage of supporting tissue. Nor is it clear to what e..xtent in each tissue incomplete regeneration is due to: (a)decreased reproductive capacity of existing stem cells,( b) decreased stem cells surviving, ( c) asynchrony inregeneration of histological elements with increase inconnective tissue, or ( d) damage of fine vasculature,
although any or all factors may be implicated depending
upon dose. Little is known quantitatively about the reproductive capacity of individual stem cells or the numbers of primitive stem cells surviving in the post-recovery
period after irradiation. Fibrosis of small blood vessels
with general reduction in vascularity is often associatedwith subsequent reduction in number of parenchymatous
cells and increase in connective tissue.
323. Changes in vascular and lymphatic systems, withdestruction of radiation-sensitive parenchymatous cells,
are important in the pathogenesis of many late radiation
effects. :Many late effects may come from metabolic andnutritional disturbances due to impaired blood supply
that reduce function and reparative capacity, and increase susceptibility to traumatic damage, infection anddisease in general.
Effects on growth and development

324. The regenerative processes of the body are fairly
sensitive to radiation; their inhibition may be prolonged
especially if vascular integrity .is impaired. More quantitative study is needed after local and TBR.
325. Some quantitative studies in rats indicate that
repeated TBR at 24 rad/wk inhibits growth. A significant decrease in growth can be caused by repeated TBR
without decrease in haemoglobin or absolute neutrophils
levels.
326. Localized· irradiation of the epiphysis inhibitsbone growth and shortens bones in man and animals, theeffects being greatest in youngest animals. Localized
irradiation of the jaws decreases tooth growth.
327. Studies in Japanese children after the atomic
bomb indicate a statistically significant if slight retardation of growth and maturation. However, the effect of
non-radiation factors has not yet been adequately evaluated. Extensive measurements on 4,800 children at 6, 7
and 8 years after e.xposure in Hiroshima showed generally that growth was retarded and maturation delayed.476• 411 In another study of several hundred children
in Hiroshima and Nagasaki. in years 2, 4 and 5 after
irradiation, physical growth and development wereaffected adversely, and retardation of height, weight,
and skeletal development was still evident at the end of1950. 478 The investigators believed that factors otherthan radiation-e.g. malnutrition-may have contributed
to these effects.

VI. Special features of internal andexternal contamination
PHYSICAL CONSIDERATION 479

328. The hazards of exposure to radio-nuclides depend greatly on their physical and chemical properties ;these determine their entry into the body and retention
in various organs. The duration of radiation depends also
on physical half-Ii fe and in some instances on complicateddecay chains causing a shift of the emitter from one place
to another as the isotope undergoes transmutation.
329. The nature of the emitted radiations may determine the range of exposure and hence the pattern of
injury e.g., an energetic a-ray will penetrate no further
than 0.07 mm. in tissue; /3-rays deposit their energy
largely locally; y-ray energy will be absorbed in larger
volumes or an appreciable portion of the energy will
escape the body altogether.
330. The degree of damage depends to some e..~tenton the concentration of ions along the path of ionization.
For an equal energy, this is greatest with the shortest
range emissions i.e., a-rays. For most types of response
the effects are greater where ionization is dense.
331. In recent years, attention has centred on thelong-term hazards of radio-nuclides of long half-life,e.g., Sr 90 and Csm. But, intermediate and short-lived
isotopes may be important, depending on circumstances.
Possible accidental discharge of radio-active materiaJ
from reactors, as nuclear detonations, may contaminate
local areas with various fission and activation products.
Even in global fall-out from the thermo-nuclear tests,
fission products of intermediate half-life are a source ofy-radiation which, for a few months after detonation athigh altitudes, has exceeded that from Cs 137 • 480 Amongthe short-lived isotopes the most interesting, especiallyin nuclear accidents is !1 31 •332. The important isotopes of intermediate halflife include Ba 140 , Ru 103, Ru 106 , Co 60 , Ce 1 n, Ce 144,
Y 91 , Zr 95 , and Sr 89• Some are so poorly absorbed that forpractical purposes they may be considered as external
y-ray sources; Ba 140 and Sr 89 are absorbed and must be
considered with Sr 90 as contributing dose to the skeleton.4B1
333. In past weapon tests, studies of fall-out patterns
have shown that the geographical distribution of isotopes
depends on many factors, including the altitude of e..xplosion and the nature and amount of surrounding material. Particle size and their solubility vary with distanceas with other factors. 482 Any nuclear accident is likely to
produce a unique pattern of variables, e.g., due to thefeatures of the accidental discharge from the Windscale
reactor in Great Britain the contaminating fission mixture had a lower content of radio-strontium relative toradio-iodine than might have been anticipated.
SPECIAL PROBLEMS ASSOCIATED
WITH INTERNAL EMITTERS

Localization of radiation
334. Theoretical and experimental considerati<:>nssuggest that the effects in tissues from uniformly appl~ed
radiation may differ from the effects of radio-active

153

particles aggregated into a "point source". 483 In the latter,dose-rates close to the point source differ from those near
the end of the range of the particles. Dose-rate near theorigin is extremely high; these high rates may be important, if the relationship between injury and dose-rate
is non-linear. Dose-rates are unimportant if the effectsof radiation are related to dose in a linear non-thresholdway. Then, the effect may reflect a single-event so that
only total dose is important; dose-rate and spatial distribution are inconsequential. When the radio-element
is diffusely deposited, the probability of the distributionof injury is the same for all cells in the tissue, whereas
in discrete deposition, the probability of injury of cells
close to the aggregate is increased but that of injury to
the cells far away is reduced.
335. If the relation between dose and degree or probability of injury is not linear then spatial distribution
is important. Also, different biological effects may show
different relationships with dose. Present data are notadequate to define differences in hazard between focal
and diffuse radiation.
Concept of REE

336. Even with uniform irradiation the concept of
RBE is by no means simple, as is discussed in otherparts of the report, since the relative effectiveness ofradiations of different quality may depened on manyfactors other than LET, including dose, dose-rate, biological end-point, and other factors. With many internal
emitters and particularly with the bone-seeking isotopes,
there is the additional problem of a very non-uniform
distribution of radiation dose, which introduces further
severe problems into the use of RBE factors, which have
not yet been solved.
337. Because of the many difficulties, the concept of
RBE can be applied only in a very general way, especially to internal emitters, and care must be taken whenusing it to establish standards of radiation safety forvarious types of ionizing radiations. In particular, it
must be emphasized that an RBE established for one
biological effect is not necessarily valid for another.
Modes of entry of radio-isotopes into animals and man

338. Among the :fission products only few are of significance with regard to internal contamination. The uptake and metabolism in the organism depends on thenature of the materials and their chemical and physicalproperties. The routes of environmental contamination
into the body are ingestion, inhalation, and skin absorption.
Ingestion

339. Gastro-intestinal absorption is the most important route of uptake of Sr90 and Cs137 from nuclear
weapons tests. The levels of these isotopes in animals andman correlate with their levels in the diet; they arereadily absorbed.

to fall-out levels except where rainwater is used for
drinking and cooking because of the relatively long times
in the ecological pathway.
341. Another factor is whether the isotope is a radionuclide of an element required by the body or of one
chemically similar to a required element. The actinide
and lanthanide rare earth series of elements have no
chemically similar counterparts among required body
constituents and are usually poorly absorbed by plants
and animals. For these radio-nuclides, inhalation may
be relatively more important than ingestion.
,
342. Although some generalizations are possible fromthe similarities of elements with families of the periodic table and from similarities to required body constituents, each radio-nuclide has its own metabolic properties. There is a continuing need, therefore, for data on
gastro-intestinal absorption of all radio-nuclides that arepotential contaminants of the environment.
Inhalation
343. In industry, inhalation has been found to be themost important route of entry of potentially hazardous
materials. Inhalation of radio-active isotopes creates
three potential hazards: absorption into the systemic
circulation and subsequent deposition in a critical tissueor organ; irradiation of the lungs themselves from materials deposited on respiratory surfaces and picked up by
bronchial lymph nodes ; ingestion. Inhalation is generally
the most important route of entry of short-lived radionuclides and of insoluble radio-active materials.

(a) Size of inhaled particles484344. The relationship between size of radio-active
particles and their deposition in the respiratory tract iscomplex, since retention and movement vary with particle size. In general, very small particles may be deposited throughout, freely entering the lower portionsof the lung. As particle size increases, deposition
throughout the respiratory tract decreases, and reaches aminimum at a particle size of ...... 0.4 µ.. With further increasing particle size, up to ,_, 10 µ., the fraction deposited in the total respiratory tract increases. Particles> 10 µ.will not penetrate the passages to the alveoli, andare deposited mainly in the upper respiratory tract,
where there is rapid clearance. As particle size increases
further, the point of deposition is further up the respiratory tract, until the probability of inhalation of large
particles becomes low because of the filtering action in
the nostrils.
(b) Radio-activity of inhaled particles
345. Suspended radio-active materials may be very
heterogeneous in particle size and in other physical andchemical properties. Compounds of several radioelements can be attached to a particle of inert material,or a single radio-active compound can be the entire
particle. Usually radio-nuclides become associated withinert materials during information or after subsequent
agglomeration.
( c) S olttbility of inhaled particles
346. Once a radio-active substance is deposited in thebody, its fate-translocation and excretion-is partly determined by its solubility in body fluids. Solubility depends principally on chemical composition, but physicalproperties such as size, shape, and surface area are also
important, especially of heterogenous particles in whichradio-active substances are adsorbed on the surfaces ofinert nuclei.

340. Ingestion is an important mode of entry only forsoluble isotopes. The solubility of interest is solubility
in body fluids rather than solubility in water. Many soluble compounds may be converted to relatively insolublehydroxides at the pH of body fluids. Also, relatively
insoluble compounds may be converted to soluble compounds in body fluids. Only those having intermediateor long half-lives can be absorbed by man in proportion154

Effects of internal emitters on the lung, including cancerof the lung352. In 1939, Rajewsky reported a technician in aradium plant who died with pulmonary fibrosis similar
clinically and anatomically to that after e..""ttemal irradiation.500 The technician was twenty-four years old andhad worked three years in the plant. At death, his lungs
contained ,..., 6.2 X 10-2 µ.c of radium which would
give a mean dose rate of ,..., 0.2 rad per week. Most radium previously deposited had almost certainly beencleared from the lung at the time of death; therefore
earlier dose rates must have been much higher. The lungcancers in the miners of Joachimsthal and Schneeberg,in Czechoslovakia. are familiar. The mines were first
opened in 1410 for copper and iron; in 1470 silver andarsenic were discovered and mined, and later bismuth,
nickel and uranium. Other metals found were tin, zinc,cobalt, manganese, magnesium and lead. At the beginning of the twentieth century, uranium was the principal
element mined for the dye industry. Three surveys weremade to establish the incidence and determine the causeof cancer of the lung among the miners. 50 1-5°3 The concentration of radon in the air of the mines 50'· m varied
considerably in different shafts (0.36 X 1()-6 -47 X
lQ-6) and averaged 2.9 X 1()-6 µ.c/cc.
353. Although the exact role of radium in the etiologyof the lung cancers is unknown, there seems little doubtthat their incidence among the Schneeberg and Joachimsthal miners is at least 50 per cent higher than that in thegeneral population. The cancers of the lung are morphologically similar to those in other groups of the population, with the possible exception of the absence ofadenocarcinoma. The average latent period for the induction of lung cancer in these miners was ,..., 17 years,
and calculations have suggested that assuming uniform
distribution the dose to the lung would have been,..., 1,000 r during this time. 606

Skin absorption
347. Absorption of radio-isotopes through the skinhas not been sufficiently studied. The skin is not usuallyconsidered an actively absorbing organ, especially for
inorganic substances. Animal experiments have been
limited because anatomical and physiological dissimilarities between human skin and that of the more common
laboratory animals lead to problems of interpretation.
The skin does not appear to be an important route ofentry of nuclides contaminating the general environment. However, skin absorption of radio-active materials
should not be ignored, especially when large quantities
may come in contact with the skin surface in industrial accidents. A specific example is tritium as tritium
water ( H 3 20). The amount of atmospheric tritium waterthat exchanges with moisture on the skin surface andenters the circulation is about equal to that entering via
inhalation of the same tritum-containing atmosphere.485• m Absorption of a few other radio-nuclides
through human skin has been studied. 487 When the skinis broken, e.g. in wounds, absorption of radio-nuclides
is greatly accelerated and increased.
EFFECTS OF RADIO-ISOTOPES AFTER ABSORPTION

348. The effects of radiation from materials within
the body are similar to those of external radiation.
Important differences arise because (a) radio-isotopes
are not distributed uniformly within the body; and(b) they serve as more or less continuous sources ofradiation.
EARLY EFFECTS

349. In animal experiments, haematopoietic symptomsof acute radiation disease appear 7-10 days after lethal
amounts of radio-isotopes given intravenously or parenterally488• 496 Sub-acute effects, frequently seen 1-5
months later, may include haematopoietic symptoms aswell as malfunction of those organs within which theradio-isotope is deposited most heavily, e.g., polonium
leads to kidney damage, plutonium and the rare earths
to liver damage, radio-iodine to thyroid damage, andradio-strontium to bone damage. 489 • 492 A recent paper on
the accidental e..xposure of 103 luminous-dial painters
to Sr00 gives data on its urinary excretion in man andgives some information on possible early haematologicaleffects. m A more complete account on urinary excretionof Sr90 in man is given in a report on a case of accidental
inhalation. •94

Long-term effects of internal emitters in animals
354. In animals, effects are generally measured interms of tumour induction and life shortening. Tumours
may appear in those tissues in which the isotope islocated and also in adjacent tissues within the range ofthe radiation. Thus radio-strontium, which localizes inbone, induces in mice osteosarcomas and rarely epidermoid carcinomas of the oral and nasal mucosa. 491 In man
radium has caused, in addition to the usual sequela ofbone malignancy, epithelial tumours arising in the mastoid cavity and the accessory nasal sinuses!99 Other instances in which tumourgenesis is associated with thedirect action of ionizing radiation on tissues include tumours of the liver, gastro-intestinal tract, lungs and skin.
In the case of thorium, for example, hepatic carcinomas
and hemangio-endotheliosarcomas have been noted abnormally often in patients given thorotrast intravenously
for angiography. 507 The incidence of these tumours increases with the quantity of incorporated radio-isotope,
the dose up to a given point and may also depend on thedose-rate within the critical organ. 3 ~350. It is unlikely that many human cases of acute or
sub-acute poisoning due to internal emitters will everoccur. In nuclear war or a reactor accident, the chance ofserious damage from e..xternal radiation greatly overshadows that from radio-nuclides which might enter the
body. On the other hand, the long-term effects of small
amounts might become a serious problem.

Late effects
351. Experience with the long-term effects of internal
emitters in man is essentially limited to radium, usedtherapeutically and in the dial-painting industry, tothorium used as a contrast medium for roentgenographic
diagnosis, and to elements in the decay chains of radium
and uranium to which miners have been exposed. Cancer
has appeared in these groups.• 9 ~ 99 More recently, radiophosphorus, radio-iodine, and other new nuclides havebeen used in treatment and diagnosis; scanty reports oftumour induction require verification.

355. In other instances, however, irradiation by radioisotopes may lead to abscopal (other than local) effects.
Neoplasia of endocrine glands and of sex organs (typified by the hypophysis and ovaries) are induced by various radio-isotopes irrespective of their organ distribution. Their incidence is not clearly related to dose or
dose-rate, and may depend strongly upon such factors as strain and se.x. Hormonal dysfunction inducedby radiation plays an important role in their etiology. 304
155

bronchial epithelium, or 12,000 rad to epithelium one cm.
from the source. They were unable to produce carcinoma
in mice at doses > 70.000 rad to bronchial epithelium.
For Sr 90 the dose given bronchial epithelium to withinfiye mm from the source was 13,000 rad after 200 days.
Not all mice developed epidermoid carcinoma.
362. Other e..xperiments with relatively insoluble particles retained in the lung for long times have shown an
increase in malignant tumour incidence. Intratracheal
Pu 239 0 2 , 0.06 to 0.16 microcurie, caused fibrosis, sterile
pneumonitis, and benign papillary cystadenomas in 60-80
per cent of mice within 100 days. 519 Similar results wereseen after intra-tracheal Ru 106 0 2 • Malignant lung tumours were seen in these mice. For various tumours adose has been calculated assuming uniform distributionof radio-isotope in lung tissue and exponential loss fromlung. 520 The authors original estimate of dose to lungwas used where reported (table IX).m The smallest
lung doses mean values associated with malignant tumours were 115 rad after 0.003 µ.c Pu 239 0 2 and 300
rad after 0.15 µ.c Ru 106 0 2 •521 However, the etiology ofthese tumours is uncertain because autoradiograms failed
to show radio-activity in the area of the tumour.
363. In other studies, at least 2,000 rad was the estimated dose to lungs that developed tumours. The estimated dose is questionable in many cases because of the
non-uniformity of the distributed radio-active materials.
Autoradiograms showed that inhaled particulates werelocalized in discrete areas of the lung. 519 In these cases,
dose to microvolumes of tissue could be considerably
greater than that estimated by assuming uniform distribution. Therefore, from the dose estimates given intable IX one should not conclude that the dose required
to induce lung cancer is necessarily as low as 2,000 rad ;it may, indeed, be much greater. Lung carcinogenesis
after inhalation of radio-active particles has not beenvery common; only a few studies have been completed.
Lisco 522 has described epidermoid carcinoma, adenocarcinoma, and hemangio-endothelioma in 50-100 per centof rats inhaling about 0.2 to 1 µ.c Pu02 smoke. Recently,
Temple et al., 523 in preliminary work, found a bronchiolar carcinoma in a mouse killed SOO days after depositionof 0.01 /LC of Pu 239 0 2 by inhalation. In most reportssummarized in table IX, the authors also found significant metaplastic changes, some at doses lower than thosegiven in the table. Other effects causing death of mice
were seen after inhalation of Pu2390 2 •524 Ninety per centmortality occurred within ten months after depositionof 0.34µ.c. No increased mortality occurred after deposition of smaller quantities, although some lung pathology was present. Cember reported no increase in nonspecific mortality after implantation of sufficient Sr9°in glass beads to produce bronchogenic carcinoma. 514
364. Although radio-isotopes accumulate in pulmonary or tracheobronchial lymph nodes, little is known of
their effects. A tracheobronchial lymph node from a dog
two years after 20 µ.c of intratracheal Pu 239 0 2 showedcharacteristic radiation damage . The architecture of thenode was destroyed and there was only limited regeneration of lymphatic tissue. In other dogs, possible histologic changes were seen within a year after inhalationof 2 µ.c Pu23902.s2s

An intermediate position is occupied by mammary tumours and lymphomas, where the incidence is dependenton dose, but which are unaffected by the pattern of isotope distribution ..In mice, lJII?phocytic neoplasms n:ay
arise where the pnmary target is bone, perhaps resultmg
from the TBR occurring while the isotope is circulating.491
Effects of internal emitters on the lung in animals
356. More striking effects were seen after depositionof radio-active gases and particles in the lungs. e.g. highincidence of pulmonary tumours in mice inhaling radon. 508 They were exposed continuously to air containing
radon at 1.2 X lQ-11 µ.c/cc, and lived 161-453 days. Tenor twelve animals had lung adenomas, and one an adenocarcinoma arising in a small bronchus. There was one
adenoma in the controls. Tracheal administration of 50
mg of quartz and three-hour e...xposure to air containing
8 X 10--G curies radon per litre retarded weight increase
and changed the peripheral blood composition . 509 Radon
affected the silicotic process significantly inducing metaplasia of bronchial and alveolar epithelia, and in somecases, malignant tumours and bone tissue in the lungparenchyma and in blood vessel walls. Proliferation of
bronchial epithelial cells along with atrophy and proliferation of the tubular epithelium of the kidney were seenin mice five months after an eighteen-hour e..xposure to
2.4 X 1Q-1 curie of radon per litre of air. ~ 10 The carcinogenic action of radon is due to its distintegration products. 511• 512 Pneumoconiosis does not play a decisive partin the pathogenesis of lung tumours due to the effect ofradon. 513
357. Changes in pulmonary histology have been seen
after various a- and ft-emitting elements, Ru106 , Rh106,
Sr90 , Ce1+1, Pu 239 , Po 210 and Co60 , were given to rodents,
mostly by intratracheal injection.
358. Strontium-90 was given by transthoracic injection of glass beads 514 and in one study Ru'1° 6 was plated
on a platinum cylinder introduced into a bronchus. 515
In most studies, squamous metaplasia of the bronchial
epithelium was seen in many of the animals; fibrosis andpneumonitis were common. Because of the high frequency of lung pathology in rodents, it is unsafe toascribe all changes to the radio-active elements. The
tumours thought to be bronchogenic were unencapsulated and invasive. In studies with implants many of thetumours surrounded the implants.
359. Cember intra-tracheally injected up to 4 . 5 millicuries of S 35 as BaS0 4 , in rats, and found no effects definitely attributable to the radio-active particles. m In another study after 375 microcuries of BaS 35 04 given
intra-tracheally to twenty-four rats once a week for ten
weeks, two of sixteen rats surviving showed severe squamous metaplasia in the lung. and two had bronchogenic
squamous cell carcinomas. The estimated average doseto the lung during ten weeks was 12,000-20,000 rad. 517
360. Cember also reported bronchogenic squamouscell carcinoma after pulmonary implantation of Sr90
glass beads. 514 Four squamous cell carcinomas, twolymphosarcomas, and one lymphoma were seen in rats
carrying the Sr90 beads. Six tumours were intimately
associated with the beads. The total dose given the lungranged from 5 X 1()4 rad to > 2 X 105 rad.
361. vVarren and Gates 518 induced epidermoid carcinoma of the bronchus in mice with Sr90 glass beads andwith Co 60 implants. For Co 60 the radiation doses werehigh, up to 400,000 rad in 200 days, to the nearest viable

Effects of internal emitters on bone 526(a) Histological damage in bone365. Whatever the source of radiation, external orfrom internally deposited isotopes. the general patternsof histological change are remarkably similar in different

156species. Histological damage includes: (i) empty lacunae (ii) vessel injury, (iii) irregular abnormal new
bon'e, and (iv) varying degrees of fibrosis_; in '!-ddition,
in rats and mice where endochondral ossification continues in adult animals and in young rabbits there maybe (v). unresor?ed cartilage, (vi) ab!:ormaliti.es of cartilage m the ep1physeal plate, and ( vn) severmg of old
and abnormal resorption of new spongiosa.
366. Bone damage takes two forms. First, bone may
be injured probably by indirect destruction through vascular injury and by direct action on the osteocytes. The
presence of osteotropic isotopes especially Sr90 during achronic phase of injury (after 180-200 days and later)induces a sharp deterioration in the blood supply, as aresult of the emptying of considerable sections of thevascular bed of blood forming and bone tissues with thedisruption of vascular innervation.m,m The damage toosteocytes and vessels can be seen within a few days inanimals given a large short-term radiation; but it is best
seen as a late change in bones of patients with radium
poisoning, as well as in experimental animals. Secondly,
radiation having damaged osteoblasts and osteoclasts,
can initiate abnormal activity in osteogenic connective
tissue. Short-range a-emitters, radium, mesothorium,
radio-thorium and plutonium affect the osteogenic connective tissue lining endosteal surfaces and resorption
cavities of bone trabeculae, inducing marked terminal
fibrosis, especially when the dose injected is high. The
longer-range ,8-emitters, Sr9° and P 32 , and external irradiation affect loose connective tissue in the bone marrow
spaces between bony trabeculae as well as on the surfaceof the trabeculae. They induce variable degrees of active
cellular fibrosis often characterized by proliferation ofpleomorphic spindle cells with conspicuous numbers ofmitotic figures and abnormal giant cells.
367. At higher dose levels most changes are seen indifferent species. Their severity decreases considerablywith time, especially with an isotope of relatively shorthalf-life, e.g., P 32, where irradiation is short comparedwith that of longer-lived isotopes. With decrease in doseor end of radiation, these changes become less severe,and at sufficiently low doses, the initial damage is repaired so that no histological evidence of damage remains ; bone has a considerable capacity for repair.

(b) Histogenesis of bone tum,mrs
368. Gross damage causing dead bone and repair may
occur without malignant change. Tumours do not necessarily arise at the site of maximum damage. In fact, it ispossible that, in very heavily irradiated bone, the tumour
incidence decreases, since the capacity of the tissue toproliferate will be greatly influenced. There is no obvious
correlation between incidence of sarcoma and degree ofradiation damage. Thus external irradiation of the knee
joint and adjacent ends of the femur and tibia of rats
damages and induces tumours in the epiphysis and metaphysis of both long bones; but not in the patella, whereenergy absorption is lower. In the long bones of rats
given P 32 and of rabbits given Sr00 , the earliest microscopic tumours appear as small foci of proliferating cells
amongst spindle cells of osteogenic connective tissue
that show fibrosis in rats. In rabbits fibrosis is Jess evident. This does not mean that the tumour arises from
cells responsible for fibrosis-only that it arises in thesame region of bone. To have a reasonable chance ofseeing microscopic tumours when animals are killed, onemust use a radiation dose large enough to give hightumour incidence. The types of cells giving rise to tu-

mours cannot be defined morphologically because of theextremely abnormal environment in damaged tissue. The
histological characteristics of tumours seen in various
species show that the cells at risk are the "osteogenic"
connective tissue cells. There is no precise evidence as towhether all these cells are equally susceptible to irradiation, though it appears unlikely that the osteocyte is.
The cell may be an undifferentiated "reticulum cell";
if so, it is surprising that there is no evidence of myeloid
leukaemia unless there are at least two different types ofundifferentiated "reticulum cell". The increased leukaemia in mice after Sr90 was always lymphatic.
369. The sequence of bone tissue changes in rats fromthe moment of introduction of the radio-isotope ( Sr90 ,Sr89 , Cew) to the appearance of the primary tumour
nodule, postulated by Kraevsky and Litvinov3 21 is:( i) lst to 20th day: initial unspecific response of thebone in the form of development of endosteal tissue andintensified remodelling of bone ;(ii) 20th to 80th day: inhibition of bone modelling.
Slowing down of osteogenesis. Abrupt dystrophic
changes in the osteogenic tissue. Reduction in the number of osteoblasts and vessels. Coarsening of the basic
material. Onset of atypical bone formation-the background for subsequent tissue malignancy;(iii) 80th to 120th day (first pre-tumour phase): onset of redundant and degenerate bone formation.
Intensified formation of pathological bone structure ina radically changed environment;(iv) 120th to 150th day (second pre-tumour phase):
growth of polymorphous osteogenic tissue among pathological bone structures. Appearance of accumulation of
atypical, free, intensively-dividing, osteogenic cells;(v) 150th to 180th day (third pre-tumour phase):proliferation of atypical osteogenic and immature bone
tissue;( vi) 180th day and later: tumour-appearance of primary tumour nodules and their subsequent growth.
370. Whether antecedent histological bone damage isalways found in a bone having a radiation-induced
tumour must be left undecided at present.

( c) Relationship betwem the pattern of radiationdose in space and time, histological bone damage,and bone tumour induction
371. The radiation dose, i.e., the absorbed energy e.xpressed in rad, is important in relation to histologicaldamage. Some investigators have considered only thedose given or retained in µ.c without attempting to calculate rad, since there are many difficulties in calculatinga meaningful dose in rad. Calculations in rad should be
encouraged since it is only in this way that a quantitative
relationship between radiation and biological effect canbe obtained. The relationship between dose, dose-rate
and the formation of bone tumours has been studied ine."rperiments with Sr 9o, Ce•u, Pu22a, PmH1 yin, ao•,629, Gao
Within certain limits the incidence of osteosarcomas increases with dose and dose-rate.
372. l\fost difficulty in interpreting the response ofbone to bone-seeking isotope arises from the considerable
spatial and temporal non-uniformity of dose, and fromthe changing spatial relationship between cells and radiation source, especially in young growing animals. The
difficulty is knowing which of the many variables predominates in inducing histological changes. Two variables are: (i) accumulated dose and (ii) dose-rate to thesite. The incidence of osteosarcomas increases with dose
1157

nificant incidence of tumours, a more detailed histological search or a new indicator might reveal persistingdamage. Pre-tumour proliferations of immature osteogenic tissue can be resorbed if the dose-rate (Sr89 , Y 90 ),is reduced, thus demonstrating that repair of "carcinogenic" injuries is possible.mand dose-rate. Accumulated dose and dose-rate are interrelated: a great problem with accumulated dose is thetime over which it should be integrated. The dose accumulated up to the time of tumour induction is useful,
but a proportion of radiation given in the later stages
may be "wasted" for tumour induction. Attempts havebeen made to relate accumulated dose and dose-rate todamage and tumour production in studies in space andtime with Sr90 and P32 in rats and rabbits. Information
on dose and bone damage with other isotopes is far lessdetailed.
( d) Accumulated radiation dose to the site373. With isotopes that emit long-range /3-rays, e.g.,
Srv 0 , Y90 and P 32 , maximum dose-rates in different partsof the skeleton of rats and rabbits varies considerablyfrom one bone to another, mainly because of variation inbone size. In a small bone, contribution to dose-rate fromcross-fire in neighbouring deposits is less than in a larger
bone. This causes variation in the maximum accumulated
dose in different bones. When maximum accumulated
dose is compared with distribution of osteogenic sarcomas in the skeleton with Sti 0, sites of maximum accumulated dose correlate with sites of osteogenic sarcomas.
However, other factors must also be important: sites ofmaximum accumulated dose (usually the ends of thelong bones in young animals) are also the areas of maximum growth and therefore of actively proliferating
tissues ; they are also the largest volume of irradiatedbone.
374. Where damage was compared with dose-rate intime and accumulated dose in the upper half of the tibiaof young rabbits, given Sr90 (i) as a single intravenous
injection or (ii) as daily pellets by mouth, the bone volume given maximum dose-rate and accumulated dosecorrelated with the sites of tumour origin. In animals
given a single injection, maximum dose-rate and accumulated dose and site of tumour origin were confined toa small length, - 5 or 6 mm., of bone. In fed animals,
maximum dose-rate and accumulated dose were along a
3-cm length of bone along which abnormal bone tissue
appearing to be the tumour origin was wide-spread.
375. The injection of P 32 at different time intervals(fractionated doses) shows that the rate at which tumours appear can be altered for a given total injected
dose. The maximum accumulated dose was approximately the same in groups of rats injected at different
intervals; this indicates that factors other than maximum
accumulated dose also influence the induction of bonetumours.
376. From a comparison of the dosages in mice given
Ca°' 5 and Sr1'0 causing the same incidence Of bone tumours, the conclusion was that cells on the surface ofthe bone and bone trabecules ( osteoblasts and connective
tissue cells) were the cells at risk and not osteocytes,
This conclusion is not necessarily unique. In this comparison, two difficulties are: (i) at the dose levels compared there were fewer tumours in long bones with Ca• 6
than with Sr90 ; and (ii) dosimetry of Ca45 is subject toerror. These data suggest that after Ca' 5 and Ra 226 "hotspots" might soon become buried in bone and hence
unimportant in giving significant radiation to bone surfaces. The "diffuse component" with these isotopes, may
be the more important in giving the effective dose.
377. Several workers have reported complete histological recovery in bones of young animals of all species
with maximum accumulated dose (to time of sacrifice)2,000 rad. However, since this dose still induces a sig·( e) Radiation dose-rate to the site378. A range of dose-rates from 50 rad/min. for
X-rays, 0.2 rad/min. for P 32 and 0.05 rad/min. for Sr00
induced similar tumour incidence, i.e., 30-60 per cent for
maximum accumulated doses of 3,000-8,000 rad. In asmall group of rabbits a maximum dose of - 20,000
rad over 6-8 months gave 100 per cent tumour incidence.
Over this relatively high range, the dose-rate may not be
important in carcinogenesis.
379. At the relatively high radiation dose levels maximum accumulated radiation dose correlates with bonedamage and tumour incidence with Sr00 in rabbits; thisrelationship is less clear with P32 in rats. Data are not
yet available from which to plot the relationship of radiation dose to damage with short-range ,B-emitters or
a-emitters.
380. Many other variables, such as volume and oxygen
supply of tissue, proliferative activity, and irradiatedmovement of cells at risk must be important in determining the effect of dose-rate and accumulated dose; theirrelative importance is unknown.
Dose and dose-rate in carcinogenesis by internal emittl!1's

381. The relationship between tumour induction andabsorbed dose of radiation is obscured by a series ofproblems. The basic difficulty is that internal irradiation,
unlike external irradiation, continues indefinitely, but at
an ever-changing intensity. Consequently, questions suchas the relative importance of dose-rate and total dose intime and space are difficult to attack experimentally.
382. Several lines of evidence indicate that dose-rate
is a major factor in the induction of osteosarcomas bybone-localizing isotopes. In mice, tumour incidence has
increased as the second or third power of the dose expressed in terms of amount of radio-activity given, andtumour incidence has varied with the time pattern ofadministration.
Internal emitters and leukaemia
383. An increased incidence of leukaemia after in-

ternal emitters have been seen in mice but it is overshadowed by far greater induction of bone tumours. 581
An increased incidence of leukaemia induced by incorporated isotopes was obtained in rats with Sr90 , Cerium144, Niobium-95, Caesium-137 and other isotopes andin dogs with Sr90 .582• 538 The disease has been reported
in radium patients, but only in those exposed occupationally also to much external y-irradiation. 5 a. In studiesof tumour induction by radium in dogs, no leukaemiasor allied conditions have been seen under conditions thatinduce a high incidence of bone sarcoma. 585
Internal emitters and life-shortening

384. Reduction in life expectancy is an important consequence of radiation from internal emitters: this response has been seen in mice irradiated at low levels thatfailed to show an increased incidence of neoplasms.
At such levels of radiation it has not been possible toattribute reduction in life span to any specific degenerative or infectious disease. The animals die with the same
pathological conditions seen in control populations.
158

METABOLIC CHARACTERISTICS OF PARTICULAR
ISOTOPES' 79

Alkaline earlh.s (calcium, strontiiem, barium, radium)385. These nuclides are metabolized qualitatively like
calcium: they are rapidly and almost exclusively deposited in the skeleton, where they are retained verytenaciously. Unless the physical half-life of the isotope
is short, the significant residence time of these boneseeking radio-elements may cover the life span of man.
Like calcium, they are readily absorbed from the intestine, provided they are in soluble form.
Radium-226
386. Radium-226 is of special significance since its
toxicity in man is well established. It has, therefore,
been used for estimating the potential toxicity of otherbone-seeking radio-elements. The value for maximum
permissible burden was established without reference tothe time of exposure. The symptoms of radium poisoning and body burdens alluded to earlier were found inpeople ,.., 20-30 years after their exposure to radium.
During the early part of the post-exposure period, theamount of radium in the body was certainly considerably
higher than that finally measured. The best estimates arethat an individual retaining 0.1 µ.g Ra 226 30 years after asingle exposure must have initially absorbed about

391. Recent work with Sr8 5 retention in normal adults
shows results similar to those in animals. 538 The retention of the alkaline earths, including Sr9°, can be described by a power function of the form
Rt= At-b
where Rt is retention at time t, in days after injection,
A is equal to Rt at one day, and b is the slope of the loglog line. The slope, b, for strontium in man is about halfthat estimated for Ra 226 in man, i.e., the rate of excretion of Sr110 at time t is considerably less than that rateof excretion of Ra 226 at the same time after e.."'Cposure.
However, experiments with rats and dogs indicatedqualitatively the opposite; this further complicates directcomparisons between Ram and Sr9°.
Lanthanide and actinide rare earlhs (including yttrium)
392. The lanthanide rare earths are produced in highyields in fission reactions : the parent materials in suchreactions are members of the actinide rare earth series.
These elements behave similarly in their chemical andbiochemical reactions. However, differences in chemical
behaviour within these groups (particularly the lanthanides) are reflected in changes in their biologicalbehaviour.m
393. Members of both classes are distributed over theearth from nuclear devices; they have not as yet been
identified in appreciable quantity in mammals and man.
This is undoubtedly because of their e..xtremely low solubility and correspondingly low absorption from the intestine. In animals, less than 0.01 per cent of an ingested
dose is absorbed. Very young animals may be exceptional
since suckling mice absorbed 2-3 per cent of plutonium
given orally in milk or as citrate. m Distribution studies
suggest concentration of plutonium in bone, liver andovary. In the latter organ, auto-radiography has shown aselective uptake in certain follicles. 541

lQ µg.53S

387. Many dial painters, who provided much of theinformation on Ra 226 toxicity, were also exposed to otheremitting elements, specifically Ra228 and Th 228 • Thus
they received a much greater radiation dose than is estimated from Ra 220 burdens alone. Such a single exposure,or exposures of reasonably short duration, produce heterogeneous deposition patterns in bone. Continued exposure, as shown for Sr9°, causes a much more uniform
pattern. This further complicates definition of the effective dose. There has been no work showing how theeffects of Ra 226 in the adult may differ in children.

394. These materials, put directly into the bloodstream, behave like colloids and are rapidly taken up in
the reticulo-endothelial system and in the more superficial parts of the skeleton. In the skeleton retention isvery tenacious, but movement from the reticulo-endothelial system is appreciable over a few months."2

Strontium-90
388. The general qualitative similarities in the distribution and metabolism of the alkaline earths have beenshown from single-dose studies after strontium, radiumand calcium in several species, although their rates oftransfer are not identical. Thus knowledge of the metabolism of the other alkaline earths assists in understanding
the fate of Sr90 in the human body. This information,
combined with tracer experiments with strontium andstudies of stable strontium, enables reliable estimates tobe made of the body burden after a given intake of Sr'°,but some uncertainties remain in estimates made on newborn and young children.

395. Locally injected solutions of the uncomple..xed
ions tend to remain at the site of injection. The complexed ions are removed from the site fairly rapidly andfollow the pattern of the intravenously injected material.
396. Attempts to damage the intestinal mucosa by repeated high doses of the rare earths Cr.ttrium and plutonium) have shown that the susceptibility of rats tosuch an exposure is low. Considerable energy is absorbed
within the contents of the large intestine, while passage
through the small intestine is quite rapid.

389. Sr 90 is found universally in the biosphere, and its
primary source in man is from calcium-rich foods, especially milk. It follows calcium qualitatively in the biosphere and its absorption into plants varies somewhat
with availability of calcium. This may be partly true also
in animal uptake of Sr9°; however, there is evidence thatthe absorption of Sr9° from the intestine proceeds independently of calcium to some extent. Growing animals
retain Sr90 more efficiently than adults, reflecting themore active calcium deposition in young animals. 537

397. Caesium-137 is present in the biosphere. Early
spectrographic studies failed to detect radio-caesium inany animal. More recently, it has been found in mammalian and other vertebrate species. In man, the concentration of stable caesium is about 1 X 10-10 g/g wet tissue.
Cs 137 from nuclear debris has now been measured infood and man. 6 • 3390. The metabolic patterns of the alkaline earths differ quantitatively, e.g., preferential absorption of calcium over strontium from the gastro-intestinal tract andgreater renal excretion of strontium.

398. The amount of Cs131 in the bodv reflects thequantity of isotope in the diet in turn affected by the degree of radio-active contamination. As a result of therelatively short residence time of Cs131 in man (the bio-

Caesium-137

159

logical half-time is about 140 days)5H attention is being
focused on this isotope as a means of studying fall-out
rates and mechanisms.
399. The major portion of the Cs137 burden of theUnited States population is probably derived from milk,
and meat products are the second most importantsource.m The 1959 mean Cs13 ' burden of a United States
resident is estimated at 0.01 µ.c. 546 This burden contributes a dose of ,....., 1 mr/yr., i.e., ,....., 2 per cent of naturalradiation background.

to the carcinogenic effect of large doses of !1 31 • In thechild's thyroid weighing ,....., 5 gm, 1 µ.c of I 131 per grammeof thyroid was estimated to yield an integrated dose ofabout 130 rad. After the Windscale incident, milk samples from nearby farms contained more than 1 µ.c/litre.
To limit radiation to the thyroids of children to 20 rad,it was necessary to prohibit consumption of milk containing more than 0.1 µ.c of !131/l of milk. This meantdiscarding much milk for six weeks.

400. Because of the chemical similarity of caesium,
potassium and rubidium, their metabolism is similar.
Caesium, like potassium, occurs chiefly intracellularly,
with low concentrations in body fluids and bone. Tissue
distribution studies have shown that muscle mass contains the largest part (perhaps 60 per cent) of body
caesium, with visceral organs, brain, blood, bones andteeth following in that order. 547 Radio-autographic
studies in mice have confirmed the high accumulation inmuscles and also indicated a rapid and high uptake of
Cs 137 in cartilage. 5 • 5401. Caesium salts are quite soluble, and are quickly
and completely absorbed, more or less independently ofroute of administration. The ion is excreted through thekidney, except in ruminants where a considerable portion is excreted by way of the gut. Tracer studies in the
cow show that about 13 per cent of a single dose willfind its way into the milk within 30 days.kll
Jodine-131

402. !1 31 is produced abundantly in fission and being
volatile is readily liberated. Therefore, under special
conditions, !1 31 may constitute a problem. Wheneversuch a situation arises, the concentration of iodine in thesmall volume of the thyroid gland is the primary hazard.
403. The Windscale reactor incident in England in1957 550 is an example of this. An accident during reactor
operation released fission products from the reactor
stack. The fission products escaping through the filters
were predominantly !131 • Significant downwind contamination covered an area of 518 square kilometres. The
only major vector for human intake of !131 was milk.
The adult thyroid tolerates at least 4,000 rad with nodemonstrable ill effects. However, evidence from young
children given 200 r of X-rays to the neck suggests that
this dose may produce carcinoma of the thyroid in ,....., 3
per cent.H9 This comparison of the carcinogenic effects
at high levels (thousands of rad) of irradiation with !1 31
in the adult thyroid and effects of lower levels (hundredsof rad) of external' radiation with X-rays should not betaken to mean that the child thyroid is more susceptible
than the adult to the carcinogenic effect of radiation.
Evidence of a carcinogenic effect of external X-irradiation on the adult thyroid is still most scanty, but very
limited data suggest that irradiation of the neck of young
adults treated for tuberculous adenitis has induced thyroid cancer, 551 Moreover, the very low incidence of
thyroid carcinoma in patients with hyperthyroidism mand the well-documented experimental evidence thatcarcinogenic dose response curves eventually reach amaximum and decline at high levels with many types ofneoplasm, and particularly in the induction of thyroid
tumours by P 31 in rats, (figure 10), 553 presumably due tocomplete thyroid destruction at higher dose levels, casts
considerable doubt on the significance of the apparent
resistance of the adult, and usually hyperthyroid thyroid,

1131 Doss !µcl

Figure 10. Incidence of thyroid tumours in male Long-Evans rats
given injections of various doses of pa1 ns, 1so
o Follicular adenoma
D Alveolar carcinomab,. Papillary and follicular carcinoma

404. Two problems in radio-isotope metabolism are of
special concern: (a.) estimation of body content fromexcretion data ; ( b) acceleration of e.""<:cretion of a deposited radio-isotope by therapeutic measures. Where
total body counting methods are inapplicable, due to theradiation characteristics of the isotope, measurement ofradio-isotope levels in excreta offers the only method for
estimating body content. The relationship between bodycontent and excreta levels as a function of time after
exposure and route of exposure is therefore an important
study in large animals and in man after exposures giving
rise to detectable radio-isotope excretion. Efforts to promote the excretion of deposited radio-isotopes are discussed in paragraph 525 below.

VII. Dose.effect relationships
EARLY EFFECTS

Immediate405. At very high doses, usually > 10,000 r, mammals
die in minutes or hours probably due to brain injury.
Typical central nervous symptoms develop soon after
irradiation (acute ataxic phase), similar to irradiationof the head only. 62 An experimental exponential relationship has been established for mice6 • between dose andsurvival time: log (median survival time, hrs) =a - bdose (figure 11).
Early death406. Between 1,200-10,000 r, the survival time ofanimals is ,_, 2-6 days. Death is caused by "intestinal
syndrome". No dependence of survival time on dose
within this range was found (according to Cronkite375
the range is even broader. up to 30,000 r), but this may
be fortuitous: injury to intestines might be decreasing
160

100

tissues. Damaged metabolism and lowered food intake
contribute to weight loss.

e 250 1cvp X-rays
0 F1ss!on neutro!lll

80· 409. Voluntary food and water intake by an irradiatedanimal can be used for plotting dose-effect curves · no
doubt other indices would serve also.
'

X Thermal column radlatlon

§

g 60

410. Unfortunately assessment of atrophy has usually
been limited to weighing the organ. Some componentsof tissues decline rapidly after radiation; biochemical
descriptions are lacking. In mouse spleen after TBR
concomitant atrophy of some elements and hyperplasi~of others result in a comple..'{ dose relationship. 55•

•

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t::
.:l

~

§

C1l

~
E

?<
40

External irradiation~

411. Smith and Tyree 555 irradiated rats with 250 kvp
X-rays and showed that three responses to radiation
increase with dose-weight loss, time required to regain
pre-irradiation weight and limitation of food and water
intake. The linear relationship was obtained (24 hours
after radiation) for percentage of weight lost or percentage of food intake against log of dose over 25-1,000 r.m(figure 12). Weight loss of rats increased linearly withdose over 100-1,200 rad. 556 When weight loss of irradiated rats was compared with that of starved and dehydrated rats, no linear relationship was found within
50-1,400 rad for X-rays and thermal column radiation. 111

30

0

5

10

15

20

:15

30

Dose, 103 r or rep

Figure 11. Relationship between high dose and survival time inirradiated mices•with decreasing dose, and the effects of the "bonemarrow" or other injury might become more pronounced.
Autopsies of animals always show changes in manyorgans.

Internally-deposited radio-isotopes

407. From 1,000 r down to SO per cent of the LDGodose survival time is increased. Death after weeks is due
to bone marrow injury accompanied by secondary infection. Survival vs. dose follows the familiar sigmoid
curve, often seen with delayed toxicity. From such
curves, conveniently after probit transformation, themean lethal dose can be calculated. The mean lethal dose,
LD 50 for mammals, is,....., 200-900 rad (table I).

412. Pregnant rats were injected with P 32 and embryos weighed days 6-10 after fertilization to measureweight loss due to internally-deposited radio-isotopes.
Weight loss of 6-day-old embryos correlated linearlywith dose but was curvilinear for older embryos. 557

Intestinal atrophy

Body weight loss and organ atrophy413. The weight of intestines decreases sharply after
irradiation; correlation between dose and effect is linear.

408. Irradiated animals lose body weight ; this loss
is dose dependent, and represents atrophy of different
organs and a general deterioration of nutrition of many

414. The weight of intestines ( e..'{pressed as percentage of control) of rats given 250 kvp X-rays andthermal column irradiation depended linearly on dose
100

10
9

I

I

90

decrease in food uptake

80

8

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70

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25

50

100

250

500

800

Dose,rFigure 12. Relationship between body weight lost or decrease in food intake in rats plotted against dose 117161gover 100-400 rad. 556 The equation of the regression line
was: intestinal weight (per cent of control) = 102.1 0.075 dose (rad).
415. The method, although simple and rapid, is notconvenient for studying dose-effect relationships because
the change is small: even at high dose (about 400 rad)no more than 30 per cent weight reduction of intestines
was found. This is because the radio-sensitive componentof intestines, the epithelium, forms only a part of thetotal weight, the rest being radio-resistant muscle.
416. DNA content as an index for measuring radiation atrophy of intestines was recently suggested by Mole
and Temple 558 but detailed studies have not yet been
published.
The atrophy of spleen and thymus

differences. 5j) 2 The dose-effect curve in mice indicated atleast two components ; in hamsters and rats only one.
The first component was highly radio-sensitive: after
75 r, testes weight was ,...,, 75 per cent of control. The
over-all equation of the dose-effect curve, over 0-1,500 r,
was:
W = Ae-kaD
Be-kbDin which W = weight, D = dose.

+

423. In mice irradiated with 250-kvp X-rays, Co 80
y-rays, thermal-column neutron, and a-particles together
with Li 7 recoil nuclei dose dependence was entirely different. The relationship was exponential, over 50-300
rad with 20 per cent weight loss at the lowest dose and55 per cent at the highest. The computed equation was:W = a-b log D. This discrepancy cannot be resolved atpresent.

417. Thymus and spleen weight decrease in irradiatedanimals. This effect has been used to correlate dose andeffect, and to estimate the RBE of various radiations.

424. The exponential equation of Kohn and Kallman562 suggests that a single event inactivates one biological unit in testes; the effect appears independent of
dose-rate.

External irradiation
418. 'Weight loss of spleen and thymus in mice exposed to various radiations was related linearly to thelog of dose. With 250 h."Vp X-rays, organ weight decreased 10 per cent after 50 rad; no experiments withother radiations have been done at doses < 100-150
rad, at which a 20-30 per cent weight loss was foundwith ColHl ,.-radiation, 4MeV ,.-radiation, thermal, 14
Me V, and fission neutrons. 558

425. However, this interpretation is questionable in
the testis containing various cells, ranging from diploidto haploid, with numerous intermediates. One type of
spermatogonia is extremely radio-sensitive; their number is significantly reduced after 20 r. Testes atrophy is
due to loss of mature cellular components, along with
inhibition of differentiation of earlier stages.

Internally deposited radio-isotopes
419. The dependence of organ atrophy on dose frominternal sources of radiation suffers from uncertainties
in dose estimation and chemical toxicity. In mice given
tritium-water the rapid equilibration of water enables
dose to be calculated on the assumption of an even distribution of tritium. The percentage reduction in spleen
and thymus weight was linear with log of dose over
150-600 rad; the corresponding weight loss was 30-70
per cent.

426. Recently in rabbits given 35 r-1,000 r with 220
kvp X-rays sensitivity of lymphatic tissue was measured
by the volume of the appendix in vivo and in vitro. 583
The appendix volume decreased 55-75 per cent. The
percentage decrease of appendix vs. dose has two components; from 35-100 r linear and > 100 r exponential(figure 13) .

Lymphatic tissue

80420. Correlation between organ atrophy and radiationfrom internally deposited fission products (plutonium
plus products of neutron irradiation of plutonium deposited in tissues) showed a linear relationship between
reduction of spleen weight and log of the concentrationof radio-active isotopes in tissue. The dose-range was,...,, 400-1,600 rad. The thymus did not incorporate any
isotope and could not be used as an index.
421. Thymus is useful for correlating dose andatrophy because of its relatively simple cellular composition. However, there are two competing processes inthymus atrophy: (a) decrease of mass, predominatingin the lower-dose range, and (b) weight gain predominating at higher doses especially > 1,000 r. 559 Perhaps .
measurement of ribonucleic acid (RNA) would be amore useful index of radiation injury to thymus. ConcenFig1tre 13. Decrease in volume of appendix irradiated in vivo intration of RNA 560 (per wet weight of tissue) correlated
rabbits plotted against dose ss3
linearly with dose; RNA decreased 10-80 per cent within
lQ0-.600 r. Activity of nucleodepolimerases in thymus
was also dose-dependent, varying from 40-60 per centDepression of mitotic activity·
with 40-160 r.m
427. Suppression of mitotic activity is a prominent
effect of ionizing radiation.
Testicular atrophy422. Testes weight (expressed as log of percentage
control) of mice, rats and hamsters irradiated with 250kvp X-rays varied with dose, but with important species

428. With isolated single cells, e.g. grasshopper
neuroblast, mitosis and the influence of radiation may befollowed directly. Radiation given in late prophase162

shortly before dissolution of the nuclear membrane ismore efficient in inhibiting mitosis (in grasshopper
neuroblast) than if given later.Wf
429. The numerous mitoses in irradiated animal
tissues make quantitative evaluation more difficult;results depend not only upon irradiation but also upon
the stage of mitosis at the time of irradiation. The
general picture from many studies is that irradiation
decreases the number of prometaphases, metaphases,
anaphases and telophases. This is probably because
cells irradiated in one of these phases complete
mitosis regularly while cells in interphase are prevented from entering mitosis. The decrease in prometaphase-through-telophase cells correlates with dose.
If the dose is sufficient to reduce mitotic cells to zero,
the time of their reappearance also directly relates todose. 565 (figure 14).

fibroblasts: ,...., 30 r reduced the mitotic index ,...., 70 per
cent, and doses of 180 r decreased the mitotic index tozero. Grasshopper neuroblast was still more sensitive ·the dose-effect curve was similar (figure 1S).
'
432. Doses as low as S r of X-rays depressed by SO
per cent the mitotic activity of the adrenal glands.
jejunum, lymph node and epidermis of mice (figure16). 568 Log of dose vs. percentage reduction of mitosis
was approximately linear. Some curves showed athreshold effect ; others did not.

.,..

•

90 .mu. all8r osposme

H

120 m1ll. after exposure

TS

I

180

•

)(

j

GO

il

1
l

25

Dose, rFigure 16. Relationship between dose and mitotic activity of theadrenal glands, jejunum, lymph node and epidermis ofmice 5"I

1•433. Probably a more useful method of following
dose-effect relations is by measuring the time for the
mitotic inde."< to return to normal. This method used to
study the mitotic inde.."< of mouse ear epidermis cells
irradiated with thermal neutron or X-rays over 5-55 radshowed a linear relationship between log of duration ofdepression of mitotic activity and dose. 585•.

.Tlmll allR lmldllllal

Figure 14. Relationship of dose to time of reappearance of
mitosis &65

430. The effect of radiation upon mitotic activity ofanimal somatic cells has been studied quantitatively onchick fibroblasts, rat retina cells, grasshopper neuroblastand epidermal and lymphatic cells of mice.

Depression of iron uptake by erythrocytes anderythocyte-forming tissues
434. The functional state of erythrocyte-forming
tissue is usually gauged from incorporation of Fe59 • Moreextensive studies usually measure Fe 59 in erythrocytes
simultaneously with isotope content in isolated bonemarrow cells and various other tissue compartments,
e.g., spleen, liver and plasma. Irradiation depresses ironincorporation. 569

431. The doses of X-rays in chicken fibroblasts were80-450 r; the smallest depression of mitotic inde.."< was,_, 60 per cent.588 The relationship between dose andpercentage of normal mitotic index was curvilinear, butlack of data at lower doses precludes extrapolation of
the curve. A similar curve was obtained with rat retina
cells ;561 their radio-sensitivity was higher than chicken100...._.....

Qimntitative studies
435. Iron incorporation by bone-marrow of animals(mice) irradiated with X-rays (250 kvp), y-rays(4 MeV Co60 ), neutrons (14 MeV fission and thermalcolumn), and tritium f3 particles over 40-300 rad m wasdepressed 10-80 per cent. Correlation between dose andeffect followed the exponential equation; effect = a - b
log dose.

,Clllckmircbluta>c >e cenao1c!OTo1Dp1agrcN111&-e--e- ~·~blut

I

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200

soO

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100

400

·-

436. A different dose-effect was found in rats irradiated with Co 60 gamma-rays and with thermal neutron(with REE equal about 1) over 40-500 rad (figure17) :610 iron-uptake decreased steeply with increasing
dosage ; it was significantly lowered at 60 rad and reachedabout 30 per cent of control value at 150 rad; further
increase in dose had less effect on iron uptake. The two-

IOO

Figure 15. Relationship between dose and percentage of normal
mitosis in chicken fibroblasts,568 cells of developing rat
retina,567 and grasshopper's neuroblast

163

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20
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eo60

ra19

x Flaalml nouh'on wUh gamma-ray oOl1tamllWfOD
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30

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O

100

200

300

400

500

600

Dose, rads

Figure 17. Depression of Fes9-uptake in bone-marrow of rats
irradiated with eoso Y-rays and thermal neutrons5rocomponent character of the curve corresponds probably
to two main systems of iron incorporation in blood
marrow (a) in dividing and differentiating cells of
normoblast series, ( b) in surviving, less sensitive cells(e.g. reticulocytes), and perhaps the iron-protein storage
complexes in bone-marrow.
437. A plot of log percentage iron uptake vs. dose over
40-150 rad gave a straight line. The graph shows that
doses below about 40 rad have very little if any influenceon iron uptake by bone-marrow. The equation derived islog-effect = a - b dose (figure 18).
438. Results obtained by various authors disagree,
possibly due to differences in experimental methods.
Storer's and Rambach's studies show a threshold dose
for iron incorporation at 30-40 rad while others found
an impairment of bone-marrow erythropoietic function
at 5 rad. A still more pronounced difference is apparent
between dose-effect function of the two groups of investigators: in Storer's results effect varies proportionately to log-dose; in Rambach's data, log of effect variedwith dose. Experimental differences were considerable; the incorporation time for iron in one groupwas 6 hours, in the other, 72 hours; the amount of radioactive iron given controls was five times larger in
Rambach's work than in Starer's.

·50

100

200

SOO

Total dose, radFigure 18. Effect of dose on Fe59-uptake in bone-marrow of rats
after 40-150 rad s10

useful in evaluating the effects of radiation on erythrocyte-formfug cells. Unfortunately no satisfactory experiments have been done. In some reported so far, long-term
irradiation has been given as repeated single irradiationand this, obviously, might permit recovery between
irradiations; also, the time between the last irradiationand the assay of the iron uptake was in some experiments
10-11 days-ample to make injury negligible by repair.
Some injury persists as shown by experiments of Baumand Alpen m who computed the exponential correlation
between number of exposures and decrease of Fe incorporation into erythrocytes. In long-term exposure,
this irreversible or very slowly reversible injury might
accumulate and become a noticeable injury.
Sitppressi01i of immunological mechanism
440. TBR damages the immune response of the body:
production of antibodies is suppressed, susceptibility toinfection increased and transplanted heterologous tissues
survive in the host for a long time. Neither antibody
production nor susceptibility to infection is a convenientindex of the effect of radiation. However, the incidenceof successful tissue transplants has been used to study
the dose-effect relationships.
Leukaemia transplantation

439. The high sensitivity of erythropoietic tissue andthe ease and precision with which its functional status
can be followed make it one of the most suitable for workon the sensitivity of mammalian cells. It is doubtful
whether single dose experiments will solve the problem,
as fast division leading to numerous cell types at each
moment in bone marrow implies a mixed population ofpresumably different radio-sensitivities. Long-term irradiation, preferably at very low levels, might be more

441. The incidence of successful transplants of mouse
leukaemia into another strain increases with dose over
100-500 r. A straight line can be plotted of probit of percentage of leukaemia vs. log of dose.
442. In mice irradiated with X-rays or neutrons 100600 r or rep-log of dose was linearly related to percentage
of successful leukaemia transplants (after probit transformation) .m Different strains of mice showed marked

164differences. The mean dose producing 50 per cent leukaemia deaths ranged from 327-+- 20 r-470-+- 41 r for
X-rays, and from 258-363 rep for thermal column
irradiation. The slope of the probit percentage incidence
vs. log dose line varied 5-10 for various strains.

one out of three patients given 600 r of 200-kvp X-rays
developed a cataract; with increased exposures the time
for appearance of opacity was shortened. A survey of
100 cases of radiation cataract and 73 cases of patients
given radiation to the head was made by Merriam a;id
Focht:164

LATE EFFECTS

451. The patients were grouped according to thetime-schedule of irradiation. For the cases given a single
dose, the minimum cataractogenic dose was 200 r, forthe cases given doses spread over 3-12 weeks the cataractogenic dose was 400 r, while for those whose treatment spread over more than three months the dose was
550 r. The greater the dose the less the time for the appearance of cataract. In figure 19, incidence of cataract
is shown as a function of dose among patients irradiatedwith doses given over more than three weeks.

Induction of lms opacity

443. Cataract formation is not understood; but
opacity of the lens is due to radiation damage of lensepithelium that has a relatively high mitotic activity. The
mitotic index decreases to ,..., 0 after ,..., 1,500 r, followed
after a time (dose-dependent) by recovery with atypical overshoot in mitotic index. Abnormal cells areformed: some showing increased size, decreased transparency and multiple nuclei. Similar abnormal cells canalso be seen in many other tissues of high mitotic activity,
but they cannot be shed from the lens as they can frombone-marrow. They remain inside the lens structure(probably because of the restricting tough capsule surrounding the lens) and form centres of opacity. Recent
data indicate that slight recovery of the lens is possible. 573

----

100

so f.

444. Cellular homogeneity along with inability toslough the injured cells make the lens useful for studies
on dose-effect correlation, only limited by the methods
for assaying the injury and by difficulties in estimating
the dose.

0'"

Methods
445. The degree of injury (i.e. the degree of opacity)
is estimated by an ophthalmoscope or slit lamp; thisnecessarily subjective method has a rather high thresholdof resolution. Comparison of the effect of radiation invarious animals is more difficult because of variation insusceptibility among species and dependence on age.
Lastly, estimation of the dose to the lens has a large
margin of uncertainty; especially with neutron-irradiation.

zo

'"
100

300

500

700

~00

1100

1300

Dose at lens, 1'

Figure 19. Relationship of cataract incidence to dose given overmore than three weeks• 0 •Experimental studies

446. Reduced glutathione decreases in an irradiatedlens, as does the activity of the enzymes of glutathione
metabolism. m Irradiation also decreases the weight andRNA content of the lens, even when no opacity is seen. 575

452. A number of experimental studies permit roughestimation of the lowest dose for cataract formation.
Storer 576 found that any doses of 250-kvp X-rays, 12.5 r
and up increased the incidence of cataract in mice (lower
doses were not tested); this agrees well with the increased incidence of lens opacities after 15 r of
X-rays.174 •m The lowest dose for rabbits for hard
X-rays ( 1,200 kvp) was ,..., 250 r.

Human studies
447. The lowest dose for lens opacities formation has
been estimated from experimental as well as humanaccident studies. The slow formation of cataract makes
the outcome difficult to interpret.

REE

448. Notwithstanding these reservations, a number of
estimations of the critical dose for cataract formation
have been made. Among Japanese survivors up to 1950,
100 people with radiation cataract have been found~mong those who received an estimated dose of 5-15 rep
m neutrons and about 600 r of y-rays.

453. Neutrons have a higher efficiency in inducing
cataract: their RBE for purposes of human protection
has generally been taken as 10 by ICRP (A). Someearlier studies on neutron-induced cataracts employed
cyclotron-produced beams, i.e. neutrons together withhardy-rays: Evans 578 found that 80 rep of fast neutrons
produced lens opacity in 100 per cent of mice. Storer576
found the REE of neutrons was 15 relative to 250 kvp
X-rays; 2.9 rep of fast neutrons produced lens opacities
in 50 per cent of exposed mice.

449. In 10 cases of nuclear accidents, August 1945September 1946, cataract formation was seen in only
one person who received whole body dose of 15 rep
neutrons and 26 r of y-rays ; the calculated dose to theeye was 45 rep. The critical dose for cataract formation
apears to be ,..., 20-45 rep.

454. During Operation Greenhouse, mice receiving
1-10 rep of fast neutrons (together with about 1 r of
hard gamma-rays) all showed cataracts. In rabbits,
Cogan et al.1'119 estimated the threshold dose of 14 MeV
neutron for cataract induction to be ,..., 10 rep (RBE ofneutrons ,..., 220).

450. The data on radiation-induced cataract in man
are hard to analyse quantitatively. Dosage is often very
uncertain and the follow-up time of patients not longenough. A report of Cogan and Dreisler"60 shows that165

~erefore, to short-lived animals. Exclusion of multiple
mterc!'lrrent fa~tors, e.g. infections which in long-term
expenments might affect any group is essential. Moreover, for adequate study of the cause of death, large~umbers .of ~mmals are needed, especially when the maininterest lies ma rare effect, e.g., as in studying the incidence of tumours. Strains with higher incidence of thiseffect may be selected but this may restrict the validityof the results. Usable results are therefore still rather
meagre.
. 4?7. .The life of animals exposed to continuous irrad~atton.is us~lly shortened. Survival plotted against time
gives s1gmo1d curves ; the median survival time is shortened with exposure. Different strains of mice differ ins:nsitivity. to radiation as i;neasured by LD~ 0 's 28 and in~ifferent hfe-span shortemngs linearly related to theirlife expectancy. m .
458. If shortening of life-span is plotted against doserates, the relationship is linear for y-rays and fast neu-

Dose-effect correlation
455. Cataract formation is dose and dose-rate dependent: the RBE of different radiations is perhaps morediverse than with other radiation injuries and does not
permit setting up an equation for dose vs. effect. The
dose dependence of cataract formation for neutronsM 0
and for y-rays114 shows a clear correlation between dose,energy of neutrons, and degree of opacity (figures
20-21). Constants cannot be derived.
Shortening of life-span

456. Continuous exposure to low doses of radiation
does not cause the dramatic effects seen at high doses.
The symptoms are not specific to radiation. The effects oflong-term exposure necessitate study of life-span andcomparison of ~uses of death between exposed and nonexposed populations. Observations have to continue until
the death of irradiated subjects. Experiments are limited,+
01-.----------~20~0-----------4~0~0-----------.J60~0-----------J80~0--Dose (rep)Figure 20. Relationship between dose and degree of opacitym

"100

81!0

~00

fOO

l)ose (rep)Figure 21. Relationship between dose and degree of opacltysso

166

llOO

trons within the range of dose rates shown in figure22.681459. When irradiated animals are given a second
course of irradiation, the LD 1m depends on the time between the first and seconQ. e.xposure, and increases
asymptotically with time. 582

.•

100
80

••

•
•• •
•
•
•

60
40

i=

0

., Lorenzc.
"'"' 100~'O• Upton fil.fil.

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80

i=

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i:;
·:::>

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• Henshaw~ Henshaw et al.

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•

20
#

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o Upton .fil.il.
A Henshawu

""0

c

40

0

20

0

D

0.1

a

0

~

1.0

10

100

Dtlse rat~ <rad/day!
Figure 22. Reduction of mean or median survival time in mice
exposed daily for the duration of life (solid symbols, X- and'Y-rays; open symbols, fast neutrons). Redrawn from Upton663

460. From these data, Blair formulated a theory on
the shortening of life-span by irradiation :257(a) The total injury caused by radiation is proportional to the dose;( b) The injury is partly reparable;(c) Recovery from reparable injury is exponential;( d) Irreparable injury accumulates in proportion tototal dose;( e) Reparable and irreparable injury are additive anddeath occurs when their sum reaches a level inversely
related to the age of exposed animals.
461. Blair's theory has stimulated design of e.xperiments and many results fit its predictions.48 Blair's postulates have been challenged. Radiation damage is made upof many individual injuries,683 mostly unidentified, andthe pattern varies from strain to strain. 224 Accordingly
any simple recovery mechanism is over-simplification.
Recovery also differs according to kind and manner ofirradiation.66 That the lethal threshold is inversely related to life expectancy is doubtful, since the LD 50 varies
with age but less simply than as proposed by Blair.m-m

observed statistically is not aging but mortality-something related to it and which measures it. The analogy is
supported by the pathology of irradiated animals showing histological damage resembling lesions of sen~scence.
464. Sacher2 31 • 256 has stated that the physiologicalstate of an individual fluctuates around some central
value and any individual leaves the population when his
state reaches a limit called the lethal boundary. It is
assumed that such a limit is a fixed one, common to allindividuals of the population. The physiological state of
the individual decays with time, approaching asymptotically the lethal boundary. From mathematical argument
Sacher asserted that log rate of mortality follows linearly the mean physiological state of a homogeneous
population. If it is assumed that the physiological state
decays linearly with age, as seems the case for many
physiological characters, the force of mortality will also
be linearly related to age. This is indeed observed formost animal populations. A corollary of Sacher's theoryis that impairment of the physiological state brings it
closer to the lethal boundary, so that the probability oftransgressing it through random fluctuations increases.
Irradiation would shift the physiological state so that theforce-of-mortality curve of the e.xposed population
would coincide with the curve for some later age.
465. Sacher's brinkmanship theory is closely related
to the information approach to lethality and radiation
damage. Although cloaked in different language andusing different mathematical conventions, this theory as
expounded by Quastler2 52 and by Y ockey687 leads to aparallel with Gompertz' law.
466. In their present state these theories are so allinclusive that they are not concerned with the natureof the radiation injuries or with the recovery processes;
physiological state (or degree of orderliness according toYockey) is largely undefined, as is the death to which
the theories refer. Accidental deaths are not consideredby them; it is less clear whether the only relevant deaths
are not those ascribable to senility-the observed causesof death are dependent on diagnostic accuracy. Radiation
studies have been confined mostly to recording the overall mortality, thus lumping specific and "senile" causesof death; but as the experiments are expanding, consideration of the causes of death becomes unavoidable.
467. Differences among strains disappear for males
when deaths from leukaemia are e.xcluded. On the other
hand, when animals dying from leukaemia or females
carrying ovarian tumours are e.-.ccluded, even differences
between sexes disappear. 224 Larger numbers of animals
might well have brought out further differences ascribable to the differential incidence of other conditions.
Something of the kind is seen in human populations
where Gompertz' law holds, but only approximately andover a limited age range. However, on plotting the forceof mortality for individual causes against age, linearityof most of the resulting graphs is striklingly improvedand can be carried down to a much earlier age.

462. Demographers have long known that the log ofage-specific death rate of a population ("the force ofmortality") plotted against age at death, is roughly
linear beyond early childhood. This relationship, Gompertz' law, applies to irradiated populations. Force-ofmortality curves for exposed animals parallel control
curves at a distance directly related to dose for single
exposure, whereas for constant long-term irradiation,
the slope of the curve increases by a factor depending on
dose rate. 235

468. Although nothing is known about the lesions
shortening life-span in multi-cellular organisms, knowledge that irradiation is powerfully mutagenic has incited
speculation about the role of somatic mutation.
469. Somatic mutation has been invoked by Szilard588
as the cause of aging. He thinks a cell dies when both
homologous genes of a pair responsible for an essential
cell function are impaired by mutation. Mutation can be
inherited, when it is called a fault, or be spontaneous, and463. These observations have encouraged analogies
between chronic irradiation injury and aging. Aging,while familiar to everyone, is difficult to define. What is167called an aging hit. The number of faults carried by anindividual is fixed at birth, whereas the aging hits accumulate randomly with time, so that at any moment the
number of surviving cells carried by an individual depends on his hereditary load and on his age. Death occurs
when the number of sun-iving cells carried by the individual approaches a critical limit. Szilard calculated theaverage number of faults carried by the individual in
human populations, and predicted the shortening of lifespan by radiation in man. His results cannot be checkedin our present state of ignorance about the life-shortening effect of radiation in our species. The theory in its
present state does not predict the expected parentoffspring correlation in life-span; if it did it would
prompt a not too difficult test on human populations.
470. Besides Szilard, Faillam also interpreted aging
as a mutational effect, and showed that Gompertz' law
can be derived by assuming that the change in mortality
rates with time is a one-hit process. It is none the lesspremature to attribute such a comple..-x: phenomenon as
aging to somatic mutation which in vertebrates has beenstudied mainly in cell cultures. There is littleimowledge
about possible repair and recovery mechanisms of mutational effects. Even in unicellular organisms, radiation
damage is not confined to the genome and it would be
surprising if this were not true for the cells of higherorganisms. Attempts to shorten life-span by giving
chemical mutagens were unsuccessful, 5 S11 but more recent
work in two laboratories has confirmed the radiomimetic
effects of chemical mutagens for life-shortening. 219 • 500
Induction of timiours

476. Change in susceptibility with age of animals is
still another complication in studies on tumour-induction. 696 This and the long latent period for tumourinduction make correlation of injury with accumulated
dose difficult in animals exposed to long-term low-level
irradiation.
Quantitative studies
477. The rate of tumour development and amount ofstrontium-89 injected into mice were related linearly,
after a latent period which increased with diminishingdose. 597 However, the plot of the number of tumours at
any time after treatment becomes curvilinear and appears as a higher power of the dose. 286
478. Dose-response curves for mouse lymphomas,2 97
ovarian tumours and myeloid leukaemia were nonlinear.303 Bone tumour induction in mice by strontium-90
is not proportional to incorporated radio-isotope and may
be described as proportional to the square or cube of thedose. 698

479. Data on the influence of dose-rate in the induction of neoplasm by ionizing radiations are as yet fragmentary. In most instances a given dose is substantiallyless carcinogenic absorbed over a long period at low doserates than it is absorbed in a single short exposure. 559 • 599
Blum, 600 from skin-cancer induction in mice by ultraviolet light, suggests that the time for the appearance oftumours is inversely proportional to the square root of
the dose-rate; the dose-effect curve would have a rising
inflection with increasing dose-rate, and a threshold, if
any below limits of observability.

471. In man the induction of leukaemia at present provides a basis for inferences about the dependence ofincidence on dose, and data being accumulated as to the
induction of bone tumours by radium is adding valuable
information to this. 691 Animal data prove that ionizing
radiation induce benign and malignant tumours. If tumour incidence increases with dose, taking into accountthe statements made later on threshold, studies on doseeffect relationships are by their nature inconclusive
about ·what the mechanism is.

Radiation-induced leukaemia in man
480. Radiation-leukaemia surveys may examine a
population of exposed and non-exposed people and observe directly the incidence of leukaemia in the twogroups. In retrospective studies, groups of leukaemic
and non-leukaemic populations are selected, the frequency of irradiated and non-irradiated individuals calculated, and the risk of leukaemia estimated.

481. Retrospective studies, beginning with people selected without prior knowledge of their radiation history,
are likely, in the present state of radiation records, tomisestimate exposure ; the reliability of information
about past radiations depends largely on memory.

472. Knowledge on tumour growth is limited and experimental difficulties abound. The long latent period in
the appearance of tumours impedes work at higher doses,
since other radiation-induced pathological disturbances
may cause death before tumours appear. At low level ofirradiation animals have to be kept a very long time;intervening infections often vitiate experiments. Moreover, the incidence of tumours is low; low-level irradition studies require unwieldy numbers of animals.

482. Three major prospective studies are the Hiroshima and Nagasaki atom bomb survivors, 420426 children treated with X-rays for thymus enlargement,438 · 40
and adults treated with X-rays for anl-ylosing spondylitis:m, oo

473. _/\s a further complication, radiation is not necessarily the direct cause of tumours: lymphoma in miceand mouse ovarian and pituitary tumours are an indirect effect of irradiation.

The Hiroshima and Nagasaki .rurveysuo-m

483. The Hiroshima and Nagasaki explosions offer aunique and most important opportunity to study theradiation-leukaemia problem. They should answer thequestion about the long-term effects in child and adult.
The irradiation dose was large and the population exposed substantial : ,_, 1,000 survivors received an LD:;odose, and 10,000 a dose over the greater part of the bodyof ,_, 100 rad or more. Important effects could hardly be
missed. Overlooked effects could only be those produced
from prolonged exposure to smaller doses or those requiring intense radiation to a restricted part of the body.
Such effects would be observed most readily amongpeople occupationally exposed and among patients given
large doses of therapeutic radiation.

474. The role of co-carcinogens is almost completely
unknown in radiation carcinogenesis. In chemical carcinogenesis, \•.;ith a co-carcinogen. the amount of carcinogenic agent was related linearly to tumour incidence ;carcinogen alone has a threshold. 592 Croton oil after radiation increased the incidence of benign tumours inskin. 593
475. Combined radiation and methylcholanthrene
were synergistic in inducing leukaemia, P 32 and methylcholanthrene5~ in inducing skin tumours, and mechanical irritation and X-rays in inducing sarcomas. 395
168

484. Data from the Hiroshima and Nagasaki populations will be less clear about dose-effect relationships.
The irradiation was instantaneous ; the results cannot
tell what is likely to happen where the dose is spread out
in time or intermittent. Great efforts are being expended
to make exposure history as accurate as possible; nevertheless, how people were shielded is, in many instances,
uncertain and hence there will always be some uncertainty about the exact irradiation received. Therefore,
information about dose-effect relationships must also be
sought elsewhere. Here data from hospital patients or
persons occupationally exposed should prove useful. The
dose-effect relationship is discussed in paragraphs248-253.

Children irradiated for thymus mlargementi 38 • 438 · " 5
485. The data are too scanty to warrant conclusions
about the relationship between dose and incidence of leukaemia or thyroid cancer among children given radiation
to the thymus (see paras. 263-272).
X-ray treated ankylosing spondylitism, « 0486. An extensive survey on irradiated ankylosing
spondylitis in England by Court Brown and Doll gave
special attention to dosage e.'Cpressed as maximal bonemarrow dose, mean bone-marrow dose, and whole-body
integral dose for every leukaemic, and for every patient
belonging to a random sample of the whole exposed population. The results are familiar. As there were only two
leukaemic female patients, the quantitative study was
limited to males. Age distribution ranged from fourteen
years onwards.
487. The clinical treatment of ankylosing spondylitis
consists usually in irradiating the affected bones with adose of ,_, 1,000 r. If the symptoms recur, re-treatment
is often given. This is the e.'Cplanation in this study ofthe positive correlation between cumulative mean bonemarrow dose, and the time between the first treatment
and death of the patient. One possible explanation of thefindings not excluded by the data could be that patientswith ankylosing spondylitis, irrespective of the methodof irradiation, are more likely to develop leukaemia thanhealthy people.
488. "With these limitations in mind, the incidence ofleukaemias was plotted against maximal bone-marrow
dose, mean bone-marrow dose, mean bone-marrow doseamong patients whose spine and sacroiliac regions only
were e.'Cposed, and whole body integral dose. The incidence in all depends on dose and the dose-response curve
bends upward. This suggests a non-linear relationshipbetween exposure and incidence.
489. Owing to the fewness of cases on which it isbased, the ankylosing spondylitis survey only proves that
there is a dependency of incidence on dose but gives little
information as to quantitative relationship. Further
details on the dose-effect relationship are given in paragraphs 254-262.

Concept of threshold
490. Thresholds have been observed for many somaticeffects, but it is a question whether radiation and leukaemia incidence are related below a certain dose. \Vbatever the dose-response curve, a critical e.xposure level
might be required before irradiation brings about thecellular derangements responsible for inducing leukaemia and other tumours. Experimental and clinical dataon tumours and leukaemia considered as demonstrating
the linear character of the dose-effect curve are all oh-tained in the higher dose-range, 100 rad and above. The
nature of this relationship has not been studied for lower
d?se levels. Kan;b and Pauling 801 have e.xpressed theview that the existence of a very low threshold or its
absence cannot be feasibly determined by studies inanimals. A. V. Le~edinsh."Y's 802 conception may prove to
be correct : he believe~ that for initial changes in any
structures of an orgamsm at the molecular leyel there isno threshold dose at which the various types of ionizing
radiation begin to have an effect, whereas a thresholddoes e.'Cist at the level of the cell, the tissue, the organs
and the organism due to compensatory responses andregenerative processes. The ankylosing spondylitis andthe Hiroshima surveys hint that at the lowest doses nodifference can be shown between the observed incidenceof leukaemia and the incidence e.xpected in the general
population. In such circumstances a search for a threshold is futile. It cannot be taken as a...xiomatic that if atmoderate or large doses an effect is proportional to dose
it is justifiable to extrapolate the same relationship tolower doses. Recent evidence neither proves nor disproves the existence of a threshold for radiation effects
in inducing tumours in man. To avoid the danger ofunder-estimating the probability of radiation-induced
leukaemia and other malignancies, it seems reasonable
to assume that the observed cases of malignancy will not
exceed the number predicted, if the relationship between
incidence of malignancy and dose were considered linear(no threshold) for all doses.

VIII. Protection and modification ofradiation injury
INTRODUCTION

491. This chapter discusses the physiological, biochemical and biological methods that have been developed
to protect against and modify the injury of living organisms by radiation. Although to date work on radiation
protection and recovery has found few practical applications to the survival of higher organisms, this is a rapidly
developing field and more recent ways of promoting
recovery by transplanting blood-forming cells may develop practical significance.
PROTECTIVE AGENTS

Anoxia492. That anoxia reduces radiation mortality was firstshown by Lacassagne603 in newborn mice. Also, rats
e.'Cposed to 800 r in S per cent 0 2 + 95 per cent N 2 werealive 30 days after exposure; all controls died. 6 G4 At
1,200-1,400 r, 50 per cent of treated animals survived 30
days. Results with mice in 7 per cent 0 2 + 93 per centN 2 were less impressive; ,...., 80 per cent of the treatedanimals survived 800 r, lethal to all controls. Similar
results were obtained in chicks, 605 rats, 60 6-60 7 andmice. 608 • 609 Some symptoms, e.g., desquamation, can bealleviated by hypoxia.610 Lamson et a/.m.s 12 studied
long-term effects, such as life-shortening, tumour incidence, hypertension, and nephrosclerosis, in rats surviving 1,000 r of hypoxic TBR. Carbon monoxide also
reduced the radio-sensitivity of mice. 613 • 814 guinea pigs,
rabbits, and rats.615 C02 was ineffective.616 Correlationof anoxia with various responses has been reviewed 617
and the mechanism discussed. 618- 62° Cyanide-induced
anoxia was particularly effective in mice ;821 otherworkers have had difficulty in getting similar re-169

suits. 95 • 96 • 622 • m Nitrate also reduced radiation mortality
somewhat. 624 • 625 P-aminopropiophenene, a methaemoglobinaemia-producer, gave 72 per cent survival in mice
given an LD 10o radiation exposure. 6260627 Another wayof lowering 02 tension, hypothermia, increases survival
rate in newborn mice 628 as confirmed in mice andrats. 629 • 530 On the whole, this approach, while illuminating the mechanism of protection, offers few practicalpossibilities.
493. Radiation response may be modified in two ways:(a) preventing injury to vital parts of the organisms;( b) aiding recovery of the affected system. Injury can beprevented by supplying cells with chemicals interferingwith or limi~ing formation of free radicalS or making
the cell constituent less susceptible to interaction with theradical; the protective chemical might even reverse
actual damage, e.g., oxidized thiol groups. A pharmacological drawback of preventive chemicals is that theymust be given immediately before irradiation so as to
be at the target site during irradiation. Biological entities-cells or tissues-introduced after radiation canreplace affected cells and tissues and thus permit recovery. Modifying factors in irradiated organisms may betransient or permanent.

501. Differences in activity of closely related compounds might reflect inability of some to enter the cell.
Protection against the direct action of radiation might
be explained by assuming that thiol compounds restore
enzymes to the -SH condition needed for their function-an hypothesis suggested by Pihl and Eldjarn. 634 Proteins form mixed disulfides ea!ily, e.g., insulin fragments.
502. Compounds containing the labile - SH groupprotect molecular structures against direct and free
radical-mediated-action of radiation. Undoubtedly, an
additional action is lowering intraceIIular 0 2 tension andreducing number of free radicals ;m thiols share thelatter property with several other chemicals e.g. choline
derivatives.u 2 Several thiols protect animals against 0 2
poisoning; this supports the belief that lowering of 0 2
tension is important in the action of protective chemicals.643
503. These theories of the action of protective chemicals cannot account for the protection given by certain
pharmacologicaJiy active substances, e.g., reserpine6 "which can protect rats if given as early as 24 hours before
irradiation; its action correlates with obvious changes intissue metabolism. Similarly, the effects of parathyroid
hormone and EDTA could be related to the effects ofcalcium on cell permeability that prevent the loss of intracellular constituents due to the radiation-induced increasein permeability.6'~• 646

Protective chemicals
494. Serious study of protective chemicals began
after Barron's demonstration that sulfhydryl compounds
protect many enzyme systems in vitro. 681 Patt 632 firstused a sulfhydryl compound for protection of animals,
and was soon followed by others. oss

Modifying treatments

504. Death of an animal exposed to the lower rangeof lethal doses is mainly due to bone-marrow injury.
This suggested treatment with viable bone-marrow cells
that might permanently or temporarily take on the function of the destroyed cells. The feasibilty of repairingradiation-induced damage by biological means was suggested from the prevention of thrombopenia in X-irradiated guinea pigs by shielding of bones in the early experiments of Fabricius-Moller 647 and by the shielding
experiments of Jacobson et al.us The success of bonemarrow therapy depended on genetic similarity between
irradiated host and donor animals. Isologous marrowgave many more survivors than homologous marrow,and heterologous grafts were even less effective.M9 - 651
Proof of cellular colonization was given by Lindsley,
Odell and Tausch in 19SS,m using as index antigenic
differences between ceIIs of host and donor. Ford et al.,1°
distinguished host and donor cells by means of marker
chromosomes.

495. Table X m lists many varied compounds tested
for protective effects.
496. The way in which protective compounds work is
controversial. Table X shows how widely different chemical entities offer varying degrees of protection. Presumably, no single theory encompasses all substances.
497. Protective chemicals may act in the following
ways:(a) Inactivation of radiation-induced free radicals;( b) Minimizing free radicals formed by inductionof hypoxia;( c) Induction of metabolic changes;( d) Reversion of injury in the primary target.
498. Inactivation of free radicals formed in water byradiation is the most widely accepted theory of chemical
protection.

SOS. The survival of transplanted bone-marrow isdetermined by the compatibility of its antigenic patternwith that of the recipient. As a rule, only bone-marrowfrom a uni ovular twin or from another individual of thesame highly inbred strain (isograft), persists; transplants from another individual from the same outbred
species (homograft) or from another species (heterograft) are rejected. If the immunological mechanism of
the host is suppressed, the graft may take. One way of
suppressing the immunological mechanism is irradiation ;this is why animals exposed to much radiation accept
marrow transplants. However, if the suppression of immunological mechanisms in the recipient is transient. as
may happen if the dose of radiation is not high enough,the graft will eventually be rejected. If the dose is highenough, the graft will take, but owing to the immunological competence of the transplanted marrow, a reverse
immunological reaction will take place, i.e. reaction of499. Thiol compounds are known to react rapidly withfree radicals 6 3.5 thereby scavenging intra-cellular free
radicals. Some sulfur-containing compounds are protective in vivo through the formation of a thiol, e.g.,alkyliso-thioureas rearrange into mercaptoalkylguanidines. u6, 63<

SOO. The radical-scavenging hypothesis does not account for several facts in radiation protection. Marked
differences in protection are given by structurally closely
related compounds (e.g., N -diethylcysteamine andN-methylphenylcysteamine) ;638 reaction products ofthiols with free radicals in irradiated serum are a minutefraction of the total free radicals formed ;639 also, it does
not explain protection against the direct action of ionizing radiation which is probably responsible for mostdamage. iHo170the grafted tissue against the host. This reaction, called"secondary disease", is a wasting syndrome characterized by atrophy of the host's lymphatic tissues, which
frequently results in death.
506. The antigenic pattern of tissues is determinedby isoantigens. Two broad groups of isoantigens are
distinguished: (a) the so-called H-antigens evoke production of humoral antibodies ; ( b) the other type,T-antigens, produces tissue immunity by accelerated rejection of grafts, but does not elicit the appearance ofantibodies in blood plasma and body fluids.
507. The chemistry of H-antigens is understood,
mainly from studies by Morgan and Kabat. 653 H-antigens are polysaccharides in which an amino-acid or
lipide moiety is firmly bound but does not contribute to
immunological specificity. Immunological specificity isdetermined by a small segment of the polysaccharide
molecule. Several more-or-less distinct molecules of thesame immunological specificity may be found in the same
individual: blood-group substances in erythrocytes arelipopolysaccharides, while blood-group substances intissue fluids are polysaccharide-amino-acid complexes;
the latter show broad polydispersity.

specific agglutination. 563-665 Identification of donor's
granulocytes was carried out by demonstrating alkaline
phosphatase in the circulating cells, alkaline phosphatasebeing present only in the rat's (donor) granulocytes andnot in the mouse's (recipient) granulocytes. aeH1a1 The
repopulation by rat's lymphoid cells in irradiated micehas been shown by finding rat's chromosome number
and structure in dividing lymph node cells of the recipient 78 and by employing cytotoxic sera with cell-culture
technique. 688
511. When animals, irradiated with doses sufficient tocause acute death due to bone-marrow syndrome, areinjected with living erythropoietic cells, they survive.
The 30 days' median lethal dose is roughly doubled ifbone-marrow transplantation is used to protect mice ;with other types of irradiation the results are less consistent, but at certain dose levels of y-rays and 14-MeV
neutrons marked protection has been shown." 9512. Many authors confirmed the protective action ofbone-marrow transplantation in acute radiation syndrome in various species. Homologous bone-marrowprotected rats, 670 hamsters, 8 n rabbits, 812 dogs, 813 andguinea pigs.en
513. The feasibility of bone-marrow transplantationin man has been studied to a limited extent. An exchangeof bone-marrow cells can occur between non-identicaltwins before birth.m-e 75 The phenomenon can be explained as acquired immunological tolerance, due totransplantation of immunologically immature cells, asseen by Owen. 671
514. In studies on man, suppression of immunologicaldefence of the host has been achieved by "acquired
tolerance". Attempts at homo-transplantation of bonemarrow into donors whose immunological mechanism
has been suppressed by radiation or by radiomimetic
drugs have met with little success, and indeed contraindications seem clearer. The studies may be divided into
two groups : (a) patients accidentally exposed to highdoses of radiation ; ( b) patients deliberately irradiatedto replace diseased with normal marrow. Thomas
et al. 618 have shown that transplanted marrow functioned
temporarily in leukaemic patients given TBR: the donor
cells in some cases persisted for two months in the recipient though they disappeared completely after ,_, 3months. In another study,879 9 patients with acute leukaemia irradiated with 300-500 r were given marrow(obtained from excised human bones) containing about
5 X 109 viable cells without evidence of a successfultransplant. Bone-marrow given to patients with bonemarrow aplasia, without irradiation, gave similar results.
There is evidence of a temporary acceptance of bonemarrow in irradiated leukaemic patients.080- 682 In moststudies, the percentage of donor's type blood cells in therecipient's circulation was low at the beginning andsteadily decreased; a notable exception is a patient withbone-marrow failure due to chemotherapy of Hodgkin's
disease 882 given bone-marrow taken from her sister. The
difference in blood groups between donor and recipient
was marked, and skin grafts were rejected. Nevertheless, bone-marrow transplantation was successful, thedonor's blood cells, low at first, began to increase in therecipient's circulation at about the sixth month after
transplantation and were still present after nine months.
The success in this case is probably due not only to pretreatment with radio-mimetic drugs but also to Hodgkin's disease: a patient with Hodgkin's disease 683 may
tolerate a skin graft for a prolonged period. Hodgkin's
disease is accompanied by a production of abnormal

508. The chemistry of T-antigens is largely unknown.
The relatively insensitive and imprecise tests available
for assessing their activity, along with the inherent difficulty in isolating them from living mammalian cells,
made it appear that "T-antigenicity" is the property ofliving cells only. However, R. B. Billingham, L. Brent
and P. B. Medawarm isolated an antigenically active
substance in a DNA-containing fraction of disintegrated
lymphoid cells. Activity was destroyed by DNA-ase
treatment, by periodate oxidation, and by digestion with
crude enzyme preparation known to be mucolytic andcapable of destroying the activity of blood-group substances. Current information shows that T-antigen may
again be mucopolysaccharide,865 and therefore not unlike
H-antigens.
509. Even though repeated skin-grafts do not cause
the appearance of precipitating or cytotoxic antibodies
in the blood of recipient animals,6 511 several studies indicate an association between tissue transplantation and theappearance of cytotoxic, haemaglutinating or otherantibodies ;851-m H-antigens and T-antigens may bedifferent complex molecules but with the same haptenicgroups in their structure.680 The antigenic potency as well
as chemical stability depend on molecular components
not directly determining immunological specificity.
Morgan 661 has shown that purified somatic hapten of
Sh. shigae may acquire full antigenic potency if coupledwith protein derived from the same or other bacterial
species ; human blood-group substance A from erythrocytes (lipopolysaccharide) is resistant to hot alkali,
while blood-group A substance from body fluids (anamino-acid-polysaccharide) is easily hydrolyzed by thesame treatment. 662 If the T-antigens were lipopolysaccharide, ·then their lesser potency compared with Hantigens in eliciting the production of humoral antibodies,and their liability to lyophilization and other procedures,
would be explicable. The T-antigens and the H-antigens
might well be a diverse group of substances upon which
the histo-incompatibility genes have imprinted specificantigenic configuration, probably in their polysaccharide
components.
510. The ability of transplanted bone-marrow cells
to persist in irradiated animals has been variously demonstrated. Erythrocytes and platelets were identified by171

y-globulins and a marked decrease of immunologicalreactivity; proliferation of abnormal and immunologically incompetent cells may be taking place at the expenseof normal lymphoid cells.
515. Bone-marrow was given five men accidently irradiated in Yugoslavia on 15 October 1958. Of six
exposed, the five who received the higher doses were
given marrow. The man in most serious condition was
injected at first with foetal bone-marrow ( 4 X 109 cells),
and then with adult bone-marrow. There was no evidence of improvement after foetal marrow; after adultmarrow the number of blood cells, mainly platelets andgranulocytes, increased sharply. Neverthless, the patient
eventually died with symptoms of delayed intestinal
damage and haemorrhages from the respiratory tract.
The remaining four patients were given bone-marrow amonth after the accident from donors of a similar bloodgroup pattern; about 1010 marrow cells were injected.
Soon after transplantation of marrow, the number ofcirculating blood cells increased. However the initial
number of donor's cells, ,..., 20 per cent of the total,
dropped to negligible values in 3-4 months. 394 It appears
that for a short time the transplanted bone-marrow assumed normal haemopoietic activity, although the evidence supporting this has been challenged by Fliedner 785
and it was certainly ultimately rejected. The relatively
low percentage of the donor's type blood cells, and theirrapid disappearance demonstrates that the recipient's
bone-marrow maintained its activity although diminishedthroughout the period of acute radiation sickness.
Furthermore, as discussed earlier in paragraphs 217-220,
the haematological recovery patterns were similar to
those of patients recovering spontaneously from lesser
amounts of radiation.
516. The transplantation of foreign bone-marrow inexperimental animals prevents acute death; the same ispresumably true for man. Survivors usually die later,
the mortality beginning usually in the fifth week postirradiation, but sometimes earlier. Death of animals is
preceded by diarrhoea, loss of weight and dermatitis;
at autopsy a generalized atrophy of lymphoid tissue isvisible. The syndrome is usually called secondary
disease, but sometimes also homologous disease or foreign bone-marrow disease. The main cause of secondary
disease is reaction of grafted tissue against the host, thelatter having been rendered immunologically incompetent by irradiation. Minor factors influencing both timeof onset of secondary disease and its final outcome include late radiation effects in the host and decreased
resistance to infection.-0 84
517. Evidence for the immunological pathogenesis ofsecondary disease is based mainly on genetical studies,F 1 -hybrids do not usually react against grafted tissues of
either parental strain but may in certain circumstances
react immunologically against inbred parental strain
tissue. However, when irradiated hybrids received parental tissue, fatal secondary disease ensued. In thereverse case, i.e. irradiated parental strain grafted withhybrid tissues, the survival was almost complete. In thefirst case, parental tissue encounters foreign antigens in
the host, derived from the other parent and produces
antibodies to histo-incompatibility antigens ; in the othercase, the specificity of transplanted tissue is broader thanthat of the host and no antibody production is possible.6es,ess

519. These two lines of evidence indicate that theimmunological reaction of grafted tissues against thehost form the basic pathogenetical factor in secondary
disease; several other factors enter. Delayed radiation
effects in the host is one881 • 658 and the delayed reactionof the hosts' recovering immunological system against
grafted tissue is another. 684 Transient decrease in resistance to infection, at a time when the host lymphoidsystem has not yet recovered and the grafted bonernarrow is not potent enough, contributes considerably tothe mortality due to secondary disease.
520. The indications for transplantation of bonemarrow in cases of radiation damage are limited. It may
be useful when the patient's bone-marrow remains viable
even though seriously affected : the implanted tissue
may in this case help the organism through the mostdangerous period of haemopoietic failure; eventually theforeign tissue will be rejected and the danger of fatal
secondary disease will disappear. In serious cases, grafting bone-marrow, substituting for the patient's haemopoietic cells, may eventually cause death by secondary
disease. 689 The dangers in bone-marrow treatment of
acute radiation disease influenced the decision not to use
it in the Y-12 accident in June 1958.588
521. There are at least three possibilities of increasing
the usefulness of bone-marrow treatment: (a) pretreatment of the recipient with "enhancing antibody";( b) use of foetal marrow; and ( c) antigenic adaptationof transplanted marrow to the hosts' antigenic pattern.
522. Enhancement might be useful when the host's
immunological reaction is not completely abolished andis sufficient to cause speedy rejection of the graft before
it might exert supportive action. Enhancement supports
the growth of transplanted tissues by inducing the immunity status in the host, before transplantation. It canbe effected by injection of the lyophilized tissue to be
implanted~ 90 or by passive immunization with a serum
containing anti-implant tissue antibodies. 688 The latterbut not the former method might be useful clinically.
523. The persistence of grafted bone-marrow could
be improved if its antigenic pattern was made compatible
with the antigenic pattern of the host. Very little work
has been done in this direction. From the studies on thetransplantation of neoplastic tissues, it is known thattumours after passage through F 1 -hybrids (strains oftumour origin and some others) have more takes whentested in backcrosses with the same two strains. 691 Thisfinding is open to more than one interpretation: Klein 59 z
showed that the increased frequency of takes in backcrosses is due to antigenic adaptation of tumour tissues
and not to selection of more resistant cellular clones
during the passage. The phenomenon resembles thechanges by pararnecia of their antigenic pattern to suitunfavourable environments containing specific antibodies, in which the newly-acquired character is inherited
cytoplasmically.698 • 494 In tissue transplantation, somepreliminary experiments aimed at inducing antigenic
compatibility have been carried out :695 parathyroid
embryonic tissue was cultured in media containing increasing concentration of recipient sera before implantation. The evidence for the successful grafting was clinicalimprovement. No analogous experiments have been doneon marrow cells, but with modern techniques of marrowcultivation, it should be possible to assess the probabilityof increasing takes and survival time in donors.

518. Secondary disease can be potentiated if transplantation of bone marrow is accompanied by even asmall amount of the donor's lymph-node cells. 654

524. On the basis of the immune tolerance theory,
foetal marrow, theoretically, might lead to the creation
172

of a permanent chimera where there has been total destruction of lymphoid tissues. The grafted marrow cells
would not be rejected and in time should acquire tolerance to the host's antigens. If foetal cells are used, as has
been shown, immunological interaction between donor
and recipient is reduced. 696 - 698 Similar e..xperiments in
man are limited and very preliminary. Mathe et al. injected foetal marrow in one of the victims of the Yugoslav reactor accident but found no evidence of haemopoietic activity of implanted tissue: the patient, however,
was apparently in the preterminal stage with intestinal
symptoms. 394 In toxic bone-marrow failure, injection of
foetal liver cell suspensions produced circulating blood
cells characteristic of the donor's for about three
weeks. 6119

logical effects of small dose irradiation should now bebased primarily on an analysis of functional changes andnot only on morphological changes as in the past.
529. ·while the mechanisms of radio-sensitivity have
not yet been clarified, the radio-sensitivities of cells
tissues, and organs can be arranged in order, and show ~remarkable similarity in all mammalian species.
530. The clinical course of the acute radiation syndrome in man is well known through observation on
Japanese and Marshallese e..xposures, criticality accidents, and radio-therapeutic experience. Howeverlargely because of uncertainties as to the physical factors'
the e.xact relation between dose and effect is not wellunderstood. The best estimate of the median lethal dose
for man is 300-500 rad, short-time TBR.

INTERNAL DECONTAMINATION

531. At low doses, functional changes appreciably outweigh permanent somatic damage. Among the more sensitive of these are transient changes in gametogenesis,
neural function, and haematological responses, especially in the lymphocytes. However, evidence of permanent damage becomes apparent only with larger doses
approaching the lethal range.

525. Recent efforts to promote the excretion of deposited radio-isotopes, such as plutonium, thorium,
yttrium and the rare earths, have been encouraging. For
these elements, the chelating agent, diethylenetriaminepentaacetate (DTPA) has proved much superior to theearlier studied ethylenediaminetetraacetate (EDT A)
and should be a practically useful agent for the prompt
treatment of accidental e..xposure to these radioisotopes.100 Prolonged treatment with DTPA is effective
in removing substantial fractions of firmly deposited plutonium from bone. 701 The removal of strontium or radium appears less hopeful; no practically useful treatment can be recommended for radio-isotopes of theseelements. Increasing the level of dietary calcium deserves to be studied further as a possible means of delaying the uptake of strontium-90. However, the benefits tobe obtained therefrom must be large enough to justify
any risks entailed in greatly increasing the intake ofcalcium,

532. Life-shortening in animals has been well established as a consequence of long-term and of short-term
irradiation. Life-shortening in man is probable, however,results are still inconclusive.
533. The development of neoplasia may follow shortterm or long-term exposures of both animals and man.
Apparently, leukaemia is the earliest neoplastic changethat has been observed in man. Leukaemia induced in theJapanese and in other groups of e.xposed human beings
has usually been of the chronic myeloid type or of theacute type, and the incidence has increased roughly with
dose.

TREATMENT OF ACUTE RADIATION SYNDROME1o 2 , ;03534. There is some evidence of an increased incidenceof some malignant tumours other than leukaemia inJapanese survivors, but the evidence so far is inadequate
to permit reasonable inferences as to dose-effect relationships.

526. The management of radiation injury is governedby the same considerations that influence the management of any other clinical problems, namely the history,
clinical picture, laboratory data, and estimated magnitude of exposure to the injurious agent. In most instances, it is not possible to estimate dose accurately.
Even if it were possible, knowledge of the dose would
be of limited value in governing the management of thepatient since there is individual variation in the response
to a given dose as well as great uncertainty about thedose-effect relationship in man. Experience with theJapanese atom bomb casualties, the Marshallese exposed
to fall-out radiation, reactor and critical assembly accidents, and other accidental e..xposures to radiation, haveshown that some estimate of biological effects can bemade from careful clinical and haematological data. Suchcontinuing scrutiny should determine therapy.
527. The conservative medical management of theacute radiation syndrome is recommended,«, 399 , 7 o4 reserving for desperate situations those therapeutic measures that carry a high intrinsic risk to the patient.

535. There is no satisfactory evidence as to the concentration-effect relationships in man as regards carcinogenesis from internal emitters. No tumours have thus far
appeared with residual radium of less than 0.7 µ.g.
536. Consideration of possible mechanisms of radiation carcinogenesis, including a number involving thegenetic apparatus of somatic cells, indicates a wide divergence in possible dose-effect relationships as a consequence, and indicates further that the question of thesemechanisms may be amenable to experimental testing.
Further analysis of carcinogenic action of radiation will
require careful study of the dependence of such action
on the type of radiation {alpha, beta, etc.) and its
physical properties (quantities of energy, ionization
density, etc.) and, in particular, a study of the role ofdose-rate. These data will provide the key to an understanding of the relevant mechanisms. However, elucidation of this problem will require an equally careful studyof the processes of regeneration, particularly in relation
to dose rate and the temporary characteristics of irradiation. An analysis must be made of the types of mutation
which result in the formation of tumours, and theirprobable character. Lastly, there must be a stage-bystage analysis of data to establish a scale of effects related
to the conditions of irradiation.

Summary528. Biological effects depend not only on total dose(energy absorbed) but also on type of radiation; distribution of dose in time and space and on the physicalstate of the organism and species. Determination of bio173

537. The embryo, at least in certain stages, is more
susceptible to radiation than the adult.

except possibly in instances of localized therapeutic
irradiation.
539. Many investigations are under way to determine
the value of general supportive and specialized therapy
for the treatment of acute radiation injury in man andfor decontamination.

538. Radiation protection can be achieved in animals
by a variety oi chemical and physical procedures, noneof which has yet been established as of value in man

TABLE l.85 LD,. VALUES FOR MAMMALS•
LD..•ol:us~Rodiolion used

Riulioli<ni faaon

Air
d4u

Ab1orbtd(r)(r<Jd)

IU/. Ne.

521+ to
638+
55s+
666+

(70S)

"'u

rOkvpX-ray

O.S mm. Cu, 1 mm. Al HVL 1.6 mm. Cu

Mouse.. . . . • . . • • • • . 200 kvp X-ray
Bomb gamma

0.2S mm. Cu, 1 mm. Al HVL 0.8 mm. Cu
High energy and dose rate362+ to
443+
405
759

{200 kvp X-rayat· • · • • · · · · · • • · · · 200 kvp X-ray

0.4S mm. Cu, 1 mm. Al HVL 1 mm. Cu
0.5 mm. Cu, 1 mm. Al HVL 1.05 mm. Cu

665
640

sis+
796+

(708)
(709)

Ground squirrel. ••••. 2SO kvp X-ray

0.25 mm. Cu, 1 mm. Al HVL 0.9 mm. Cu

700

>700+

(710)

r,000 kvp X-ray
Hamster. . . . . . • • • . . 2SO kvp X-ray
200 kvp X-ray

HVL 5 mm. Pb
0.5 mm. Cu, 1 mm. Al HVL 1.6 mm. Cu
0.2S mm. Cu, O.S mm. Al HVL 1.5 mm. Cu

800
460+
700

>BOO+
586+
>700+

(711)
(712)
(671)

0.2S mm. Cu, 1.0 mm. Al HVL 0.8 mm. Cu
0.2S mm. Cu, 1.0 mm. Al HVL 0.8 mm. Cu(crossfire exposure)
Multiple sources
Dose rate 70 r/min (w exposure)

337
400

400+
380+

(42)
(649)

SOO

490+

(43)

0.5 mm. Cu, 1.0 mm. Al HVL 0.98 mm. Cu(bilateral exposure)
3.2S mm. Cu HVL 3.4 mm. Cu(multiport exposure)
Parabolic filter HVL 2.0 mm. Cu(crossfire exposure)

800

73s+

(24)

805

1s1+

(713)

100+

680+

(714)

1,094

911+

(715)

760+

S46+

(65)

550

s22+

(716)

R

roo

kvp X-ray
186 kvp
X-ray

Guineafpig. . • . . . • . . C "o gamma
1.10 Mev (S03)
1.33 Mev (S03)
200 kvp X-ray

2SO kvp X-ray
Rabbit ..•.•....... 2SO kvp X-ray
Co•o gamma
1.10 Mev (S03)
1.33 Mev (SO%)

Monkey ...........

r·

kvp X-ray
250 kvp X-ray

(706)
(707)

HVL 5.1 cm. Al
Dose rate 50 r/hr (multiple sources)
HVL 1.6 mm. Cu Dose rate 3 r/min.
(bilateral exposure)
O.S mm. Cu, 1.0 mm. Al HVL 1.0 mm. Cu(animals rotated}

174

TABLE I. 85

LD.. VALUES FOR Mli.MMANs* (continusd)
LD .. •ah«

Radialion wud

250 kvp X-ray
1,000 kvp X-ray
2,000 kvp X-ray
Dog ............••. Co" gamma
1.17 Mev (503)l.33 Mev (503)
250 kvp X-ray
Bomb gamma
1.000 kvp X-ray
2,000 kvp X-ray
2,000 kvp X-ray
Swine •....•....... Bomb gamma
Co" gamma

Air
doJe
(r)

Absorbed{rat!)

IU/.No.

281

244+

(717)

304
312
465+

250+
260+
303+

(38}
(37)
(718)

14.2 mm. Al Parabolic filter, 0.5 mm. Cu
HVL 2.15 mm. Cu (unilateral exposure)High energy and dose rate

450

322+

(38}

271

250+

(378)

HVL 2.0 mm. Pb (bilateral exposure)
HVL 4.3 mm. Pb (bilateral exposure)
HVL 4.3 mm. Pb (unilateral exposure)High energy and dose rate
HVL 5.1 cm. Al Dose rate 50 r/hr
(multiple sources)

510
388
500
225
618

247+
237+
305+
187+
242+

(38}
(719}
(719}
(720)
(721)

HVL 3.9 cm. Al Dose rate 20 r/hr
(multiple sources)

524

205+

(722)

0.5 mm. Cu, HVL 0.98 mm. Cu(bilateral exposure)

350

237+

(723)

HVL 5.1 cm. Al Dose rate 50 r/hr
(multiple sources)784

HVL 4.3 cm. Al Dose rate 20 r/hr
(multiple sources)651

HVL 3.9 cm. Al Dose rate 20 r /hr(multiple sources)

585

Dose rate variable (plane field)

350 (?)

Radiolio~ '""'""

0.5 mm. Cu, 1.0 mm. Al HVL 1.5 mm. Cu(bilateral exposure)
HVL 2.0 mm. Pb (bilateral exposure)
HVL 4.3 mm. Pb (bilateral exposure). HVL 5.1 cm. Al (bilateral exposure)dose

1.17 Mev (503)
1.33 Mev (503)!

Nb" and Zr"

Sheep ..••.•....... o./:~~~s(933)0.23 Mev (73)Goat ............... 200 kvp X-ray
Co'° gamma
1.17 Mev (503)
1.33 Mev (503)
Tam gamma
Burro ••••••..•.•.• 1.22 Mev (573)
1.13 Mev (373)
0.2 Mev (63}Nb•-Zr 115 gamma

(721)

256+

(724)

(722)

0.73 Mev (933)0.23 Mev (73}!

Fall-out gamma
1.5 Mev (19%)
Man.············· 0.75 Mev (573)
0.1 .Mev (24%)

300 (?)(53)

with Co60 gammas to approximately 45 per cent with 250 kvp~orlower energy X-rays.n• 121, TH Ellinger quotes the LD 60 /14-day
value for guinea pigs, which is not significantly different from his
LD10/30-day value. Depth-dose measurements under the unusual
geometrical conditions of the Oak Ridge multicurie .,..ray exposure
field were made by the present authors in collaboration with
Col. Bernard Trum. The large ratios, air dose-midline absorbed
dose, obtained for burros, sheep, and swine result principallyfrom geometrical factors. 31 In most positions, occupied by the
exposed large animals, over 50 per cent of the dose is received
from a target to skin distance of less than 1.5 m.; thus inverse
square fall off is appreciable. Large animals standing in the fieldreceive much of the dose at the midpoint in the animal from theanterior or posterior directions, as opposed to the transverse(shorter) a.'tis with bilateral irradiation in the laboratory (thiswould not apply to an upright man). All midline doses probably
are maximal for an acute LDu value, since if the data for theeffect of dose rate on LD 5o in the rat131 apply to the larger
species, the values should be further reduced by a factor of
approximately 0.8 to allow comparison with radiation deliveredin the course of minutes. The values should be also reduced further
for comparison with X-ray LDu values because of the apparently
reduced effectiveness of 'Y·radiation relative to X-radiation.i7
The LDn value for man can be considered only a rough approximation, since the dose is poorly known and there was no mortality
in the exposed group (see below).

•See text for additional explanatory material relating to thetable.
+Value not given in work cited. Calculated or estimated fromdata given.
All dose-rates used were of the order of 5 to 60 r/min., and all
exposures were unilateral unless otherwise noted. The LD1avalues in rad represent the absorbed dose in soft tissue at thecentre (midline) of the animal. The dose in rad was estimated asfollows: the tissue dose in r was first estimated, if not given, fromthe air dose by estimating all scattered radiations and taking into
account the geometry of the exposure conditibns used." Scattercan be approximated from standard depth-dose data.u• 101, 1:is, m
The present authors duplicated as nearly as possible many of theexperimental conditions and used the air/tissue dose ratio thus
obtained. The tissue dose obtained represents the dose a dosimeter would indicate if it were embedded in tissue (or phantom
material). The tissue dose in r was converted to absorb dose inrad, using the appropriate soft-tissue conversion factor.m. nt
The conversion from air to tissue dose is an approximation madein many cases from incomplete physical data, and the conversion
factors from tissue dose to rad are still open to question (seeabove). Additional details of the conversion used for any of thesituations will be furnished on request. Total scatter varied withessentially full scatter, from less than 5 per cent of the air dose

175

TABLE II.

DISEASES OF MAJOR FREQUENCY IN Y-IRRADIATE.D MICE (OPERATION GREENHOUSE)2so

Perunlate obsnwd i...:Uknu in mice reuil'i11t indualed .,..,.oy dcse
Co,.ITol

DiseaseZZJ rod

368 rad578 rod697 rod

Malu

FemausMaks Ftmolu

Maks

FemaksMaks

FemaksMaks

Females

None ....................................•
Pneumonia .............••.................
Nephrosclerosis, mild .......................
Nephrosclerosis, moderately severe .••........
Nephrosclerosis, severe .••..•........•.......

4.25
9.48
1.31
0.33
0

0.97
12.01
2.60
0.33
0.65

1.90
6.19
2.38
0
0.48

0.94

0
6.21

1.68
4.36
6.71
3.02
18.79

4.07
5.56
3.70

1.38
3.45

1.96
5.23
3.59
1.63
10.13

3.76

2.36
0.47
0.47

3.16
7.91
2.85
0.63
1.58

21.48

4.51
7.14
37.22

Nephrosclerosis, severity unspecified ..........
Enteritis and colitis .........•.......•.......
Dermatitis ••.•....•....•...........•..•....
Emaciation ..........•...................•.
Cyst, liver ........•..•..•..•...........•...

0.33
4.58
10.78
0.65
2.61

1.95
2.27
1.95
1.62
1.30

3.81
3.33
10.48
0
1.90

2.36
2.36
2.36
0
2.83

7..59
1.90
8.86
1.27
0.95

4.48
2.41
0.69
1.03
2.07

24.51 17.79
4.90 3.36
4.90
0.67
0.65
1.68
1.96 4.36

28.52
1.85
3.70
5.56
1.11

15.79
1.88
0.38
3.38
1.88

Cyst, kidney .....•..••.......•.............
Cyst, ovary ..............••................
Cyst, all sites ...............•. , ......•.....
Atrophy, bone marrow .•....................
Atrophy, testis ...•.............••..........

0.65

0
1.30
3.25
0.32

1.43

0
1.42
4.25
0.47

0.95

0
1.72
4.83
0.69

2.94

1.48

0.75
1.50
4.89
0.75

Atrophy, adrenal cortex .....................
Dental defects •............•.•.......•...•.
Volvulus ................................•.
Abscess, all sites .. , .........................
Hyperplasia, endometrium .......•...........

0.33
8.83
0.98
7.52

8.12
1.63
0.65
2.92
1.95

3.33

Hyperplasia, adrenal cortex ....•..........•..
Hyperplasia, Harderian gland ................
Hyperplasia (myeloid), bone marrow •........•
Hyperplasia (myeloid), spleen .•..............
Hyperplasia (lymphoid), spleen, lymph nodes ...

0
0.98
0.33
0.33
0

0.97
0
0
1.30
0.32

2.86
0.95
0
1.43
0

Haemorrhage, testis ...........•..•......•••
Haemorrhage, brain ..•.....................
Haematoma, testis ..........................
Haematoma, ovary ...........................
Haematoma, adrenal. ....•......•......•....

0
0
0.65

0

0
0
0.95

Thrombosis, auricle ....•..••..•.............
Infarct, all sites ........................•...
Angiitis, all sites .•.•.........••...........•
Hepatoma .........•.......................
Luteoma .....••.........•........•.........

0.65
0.65
0.65
7.84

3.6-0
0
0.65

0

13.31
0
1.62
0
0
3.25
1.30

3.33
0.48
1.90
1.43
7.15
8.10

0
1.90
1.43
0.95
7.62

0.32
0.32
0.32
19.16
0

Granulosa-cell tumour, ovary .......••.......
Tubular adenoma, ovary ••..................
Mixed tumour, ovary ••..•....•........•....
Supcapsular cyst, ovary ...•.•............•••
Cystadenoma, ovary ........•...............

3.77

2.53
0.32
0.95

3.79

4.90
0
0.95

1.01
1.34
9.06
1.68

3.33

2.96
1.48
1.11

2.63

8.96
1.42
0.47
1.42
1.89

1.27
8.86
0.63
3.48

7.93
2.07
1.03
1.72
1.38

1.63
6.86
0.65
1.31

8.72
1.68
0.34
1.34
0.67

2.96
1.48
1.11
1.11

10.53
1.13
1.50
0.75
0.38

3.77

2.12
2.85
1.27
1.90
1.27

3.45
2.07
0.34
4.48
1.03

3.92
1.31
4.58
6.21
1.63

3.36
1.01
2.35
6.38
1.01

5.18
0.74
4.44
7.41
2.59

6.01
0.75
3.01
15.41
2.26

0.63
0.63
0.95

0.34

2.29
0.33
1.31

1.68

1.11
1.85
1.85

1.13

13.42
2.01

0.37

0
0.94
3.37

0.47
0
10.38
0
0.47
0.47
0.47
10.38
16.51

0
2.85
1.58
1.03
11.71

3.30
5.19
10.85
2.36
2.83

12.76
0
2.41
0.69
2.98
14.83
19.66

0
1.96
2.94
6.71
8.82

2.35
2.01
5.04
8.05
17.11

0.37
1.48
7.04
4.44

Adenoma, pituitary ...•..•..................
Adenoma, lung ......•....•..•..............
Adenoma, kidney ........•.....•...••....••.
Adenoma, adrenal .•...•...........•........
Cytadenoma, lung .......•........•.........

0.98
9.48
1.96
0
2.29

3.57
9.42
0
0.97
3.25

1.43
9.05
1.43
2.86
3.33

4.25
8.49
0
0
1.89

0.95
11.08
1.90
2.22
4.75

7.59
7.59
1.72
3.10
4.48

1.96
7.19
1.63
3.27

Cystadenoma, Harderian gland ...............
Squamous-cell carcinoma, stomach ..•......•..
Squamous-cell carcinoma, skin •..............
Adenocarcinoma, lung ..•.........•..........
Adenocarcinoma, breast .....................

0
0.98
0.33
2.94
0

0.32
0.65
0
0.97
0.97

0.95
2.38
0
0.48
0

1.42
1.42
0.94
2.36

1.27
1.58
0.32
1.27
0.32

Adenocarcinoma, Harderian gland ............
Sarcoma, voluntary muscle .........•........
Sarcoma, breast ...........•................
Sarcoma, bone •.................•..........
Lymphoma, thymus ........................

0
0
0
0
1.64

0
0
6.82
0.65
3.24

0
0.48
0
0
2.86

Lymphoma, abdomen .......................
Lymphoma, other ......•...................
Myeloid leukemia, all sites ................••.

7.52
10.14
0.33

NumlJer of neoplasms per mouse
Neoplasms, all sites ••..........•..........

1.08

1.13
2.63
13.91
1.79
15.41
2.26
1.50
5.64
0.38
2.26

4.36
2.68
7.05
1.68
0.67

4.14
4.48
10.69
2.41
2.76

7.52
2.63

0.74
2.96
1.11
1.48
1.48

3.38
2.26

3.59

12.42
6.04
1.01
3.69
2.01

1.38
1.38
0
1.38
3.79

0.33
0.65
0.98
0
0

2.01
0.34
0.67
1.01
3.02

0.37
0
0
0.74
0

0
0
0.38
0
1.88

1.38
0.69
4.14
0
4.13

0.33

0.33
0.65
0.33
6.86

0.34
0.67
2.01
2.01
11.08

0.74
0.37
0
0
13.07

0
0

0
5.66

1.58
0.63
0
0
2.85

0.75
10.15

20.22
18.52
0.65

12.38 14.62
7.21 10.85
0.48
1.42

13.30
12.34
0.95

8.64
16.21
1.03

3.92
9.14
1.31

6.72
9.06
0.34

2.60
4.81
1.11

3.63
4.89
0.38

1.15

1.37

1.46

2.26

1.11

1.73

0.66

1.07

176

3.77

1.42
0.47
3.77

2.21

0.38

1.88
1.13

0.38

TABLE Jil. 732

MAJOR ABNORMALITIES INDUCED IN M.·UI~ALS BY FOET.-U. IRRADIATION

Brain

Exostosis on proximal tibia
Metaphysis
Amelogenesis•
Scleratomal necrosis

Anencephaly
Porencephalyl\Ucrocephaly*
Encephalocoele (brain hernia)
Mongolism•
Reduced medulla
Cerebral atrophy
Mental retardation•
Idiocy•Neuroblastoma
Deformities
Narrow aqueduct
Hydrocephalus"
Rosettes in neural tissue
Dilation of 3rd and lst ventricles
Spinal cord anomalies•
Reduction or absence of some cranial nerves

Eyes
Anophthalmial\Iicrophthalmia •Microcornia*
Coloboma•
Deformed iris
Absence of lens and/or retina
Open eyelids
Strabismus*
Nystagmus•
Retinoblastoma
Hypermetropia
Congenital glaucoma
Partial albinism
Cataract*
Blindness
Chorioretinitis*
Ankyloblepharon

Skeleton
General stunting
Reduced skull dimensions
Skull deformities•
Head ossification defects•
Vaulted cranium
Narrow head
Cranial blisters
Oeft palate•
Funnel chest
Congenital dislocation of hips
Spina bifida
Reduced and deformed tailOvergrown and deformed feet
Oub feet•
Digital reductions
Calcaneo valgus
Abnormal limbs"
Syndactyly*
Brachydactyly 0
Odontogenesis imperfecta•

Miscellaneous
Situs inversus
H ydronephrosis
Hydroureter
Hydrocoele
Absence of kidney
Degenerate gonad*
Abnormalities in skin pigmentation
Motorial disturbance of extremities
Increased probability of leukaemia
Congenital heart disease
Deformed ear*
Facial deformities
Pituitary disturbances
Dermatomal and myotomal necrosis• These anomalies have been found in humans exposed in ulero to radiation and are attributed to the action of radiation.

TABLE 1v.1s2

CORRELATIONS IN DEVELOPMENT: MOUSE A,.~D MAN DEVELOP:MENTAL
STAGE IN HUMAN: ORGAN PRIMORDL.\

Age in days
Embryo

mm

Mouse

Man

5

9

6
14
16
20.5
25.5

0.15
0.40
1.5
2.4

10.5

28.5

4.2

11.5

33.5

7.0

12.5

36.5

9.0

13.5

38.0

12.0

14.5

47.0

17.0

15.5

65.0

40.0

8

Implantation
Germ layers, extra emb. membranes
Primitive streak
Neural groove, blood islands, notochord
Cephalization, extensivevascularization, neural folds meet, primordia
of sense organs, th}Toid, limbs, muscles, pronephros, branch,arches, somites
Prim. brain w. vesicles, complete circulation, GI tract and derivatives,
mesometanephros, vertebrae, 31 somites, yolk haemopoiesis
Genital ridge, heart, liver, mesonephros protuberant, limb and lungbuds, 5 brain vesicles, all sense organs, cardiac septs and 38
somitesHeart chambered, nerves and ganglia differentiating thyroid anlageo.
bilobedSexless gonad primordia, liver haemopoiesis, brain flexures, limbs,
thymus, GI tract actively differentiating
Cerebral hemispheres, corpora striatum, thalamus, blood vessels all
actively differentiating, endocrine glands, peripheral and sympa·
thetic nerves, eyes well formed
Cerebral cortex, intest, villi, thyroid follicles, first ossifications, se.~differentiation with sex cords and germinal epithelium

177

TABLE V.T83

fun:crs OF IONIZING llADIATION ON MAN-SCHEMATIC SURVEY
A""4 radiation IYftbome, form

Cerebral

Gastro-i..u.rtinal

Determining organ...........

Central nervous system

Small intestine

Bone-marrow

Threshold dose, r. • • • . • • • • • . •

2,000

SOO

100

Latent period.. . • . • . • • . . • . . • .

31-3 hr.

3-S days

3 weeks

Characteristic signs andsymptoms

Lethargy, convulsions, ataxia

Diarrhoea, fever, disturbanceof electrolyte balance

Leukopenia, purpura, infection

Underlying pathology. • • • . . . •Inflammatory reactions in
Denudation of gastro-intestinal
central nervous system, brain
mucosaoedemaAtrophy of bone-marrow

Time of death (if occurring)...

Within 2 days·

Within 2 weeks

Within 2 months

Cause of death. . • • • • • • • . . • • •Respiratory arrest

Circulatory collapse

Haemorrhage, genera!U.ed
infection

Prognosis. • . . . . . . . • • . • • . . . • • Hopeless

Poor

Good

Source of information........

Animal experiments, bomb
casualties, nuclear accidents

Bomb casualties, nuclear
accidents, radio-therapy

Animal experiments

TABLE VI. EPIDEMIOLOGICAL STUDIES OF THYROID NEOPLASIA AND LEUKAEHIA IN CHil.DREN
TREATED m INFANCY ON THYMIC REGION: SUMMARY OF PUBLISHED DATA

Refernsu

Reason for
inadiatioa

Dose1'}1tl~'","f

Numberi"adiatechilbt11

Control''" ci rwma.

UuAIUfflia~iJ11uMh<:rThyroid

Conti et al. "'Pittsburgh

Prophylactic thymus
irradiation

7S-300

1,S64

2,923

0

0

3 cases of malignancy! leukaemia

Simpson-HempelmannFuller 4'li

Thymic enlargement(1) 200

2,393(80%
traced)

2,722

21

9

3.6 cases of malignancy(2) 20(}600

Simpson-Hempelmann m

1 leukaemia

Simpson " 7
Latourette and Hodges m

Thymic enlargement

Average200

861

Murray et al. "'Various benign
Averagediseases (45% chest)
400

6,473

Snegireff 451

Thymic enlargement

Cronkite-Moloney·
Bond •21

Thymic enlargement

Saenger <.1•

Chest-mainly forthymic enlargement

Stasek et al. m

Average400

148

1 lymphoma 0.1 carcinoma! leukaemia 1 lymphoma andleukaemia
8
162

12S

SC>1,200 r

1,644

Cervical lymphadenitis 10(}300 r

S2

178

3,777

0

0

2 (out of
7 neoplasias)

0

11

2 leukaemia

0.12 carcinoma

TABLE Vll.435 FREQUE.~CY OF ABDOMINAL IRRADIATION DUIUNG PREGNANCY OF J.!al'HERS OF
CANCEll. CHll.DREN AND MOTHERS OF CONTROL CHILDREN: SUMMAll.Y OF PUBLISHED DATA

Can&6 ehildn:11

CorrJrol diildre11

Praj>artw11 of rr.olhers"'/w reeei'Ped abdominal
irradwtion dsui111

Description of poup

P,tinancy

Propcrtkm of""'thers

ir/so rati'Ped obdomi"alirradialkm d11rin1

Descriptkm of poup#•g><ancy

Kjeldsberg no ••.•...•••••.•.••.•••.••

Children withleukaemia seen at
Riks-hospitalet,
Oslo, 1946-56

5/55 (9.13)

Healthy children

8/55 (14.5%)

Kaplan"' 3 ••••••••••••••••••••••••••••

Children dying ofacute leukaemia
in California,
1955-56

31 /150 (24.7%)
34/125 (27.2%)(a) Oosest Sib

24/150 (16.03)
21 /125 (21.6%)

Children withleukaemia seen at
the Children's
Hospital, Los
Angeles, 1950-57

72/251 (28.7%)

Children attending
the Children's
Hospital, Los
Angeles, 1950-57
with otherselected
conditions

Polhemus and Koch~ •..•••.•.•••••.•.

Ford el al."'' ........................ . Children dying ofleukaemia under
10 years of age
in Louisiana,
1951-55:(a) White(b) Coloured
MacMahon na ••••••••••••••••••••••••

20/70 (28.6%)
1/8
8/114 (7.33)

Children dying ofcancer under 10
years of age in
New York City,and born in a
specified maternity hospital,
1947-57(b) Moi;t habitual
playmate

58/251 (23.13)

Children dying ofcauses other thancancer under 10
years of age inLouisiana, 1951-55:(a) White(b) Coloured

1% sample ofchildren born in
one of 11 specified
maternity
hospitals,
1947-57, residents
of New York
City only

48/247 (19.43)
8/59
173/2,520 (7.33)

TABLE VIII.OT CoMPAJUSON OF OBSERVED AND EXPECTED INCIDENCE OF MALIGNANT NEOPLASMSIN SELECTED SITES AMONG SURVIVORS IN Hll!.OSHIMA EXPOSED WITHIN 1,5()() METRESFROM THE HYPOCENTRE, APRIL 1957-DF.CEMBEll 1958

Obs..wd

24
10

Cancer of stomach, sexes combined ....•...
Cancer of lung, sexes combined .......... .
Cancer of breast. .•.....................
Cancer of cervi:< uteri ...................•
Cancer of ovary •••....•................•

5
8
4

N.S. Not significant.
•Significant at the confidence level of 13.
••Significant at the confidence level of 53.

179

12.41
2.32
2.49
3.67
1.01

Rolw

T1ll rttall

1.93
4.31
2.00
2.18
3.96

•
N.S.
••
••

•

TABLE !X,H9

OBSERVED TUMOURS AND CALCULATED DOSE FROM RADIO-ACTIVE MATERIALS DEPOSITED IN THE LUNG

J{attri4J

end

}to.

redial ion•

Potto (alpha)

Rat

PutnO, (alpha)

Mice
:Mice
(inhalation)Rats(inhalation)

BaS"O, (beta)

Mice
Rat

Ru 1oeo, (beta)

Mice

Ru1oe
(metal cylinder)(beta)Sr" (glass beads)(beta)
Ce1UF I (gamma)

Rat

Co'° (gamma)

Mice

Rat
Rat

(wire)Squamous cell carcinoma
Fibrosarcoma•
Squamous cell carcinoma
Bronchiolar carcinoma

2/15
1/21
2/17
1

Calculattd
dose

Remuks(rod)b2,500

Refertncu

115
2,300
600

5 and 15 months after S µe/Kg
SOO days after 0.003 µe
400 days after 0.06 µc
SOO days after 0.1 µc

S10
521

522

517

Epidermoid carcinoma

Bronchiolar carcinoma

1/41

4,000

Between 50 and 100 per cent surviving 2SO days after depositionof 0.2 to 1 µc developed malignant tumours
100 days after 0.16 µC

Squamous cell carcinoma

2/16

12,000 to
20,000
300
4,000
9,000

300 days after 37S µc/week for 10
weeks
340 days after 0.15 µc
422 days after 2 µc
3SO days after 4.S µc

Lymphosarcoma•
1/23
Alveolar cell carcinoma
1/10
Non-differentiated tumo:ir 1/11
Bronchogenic carcinoma
5/26

Lymphosarcoma
Carcinoma
Carcinoma

4/23

2-9 x 101
S0,00070,000

1/27
1/23
7/28
4/15

2,200
5,500
8,900
15,000

Epidermoid carcinoma of
bronchus

12,000 to
400,000•All materials administered iritratracheally or otherwise as
indicated.
b Assuming uniform distribution and exponential loss unlessotherwise indicated.

TABLE X.7 3 7224 to 337 days after implantation of
2.1 to 14 µc (dose calculated at 100
microns from source)
131 to 375 days afterimplantation of
1.1 to 59 µc
127 days after 5 µe
48 days after 15 µc
93 days after 2S µc
83 days after 50 µc
200 days after implantation

523

523

521

515

514
736

518

• Classed as incidental by author because autoradiograms
showed no radio-activity in area of tumour.

CHEMICALS USED FOR PROTECTIVE EFFECTS

Thiols related to cysteine a11d C)'Steamine
CompoundAnimalDase mi/kt

Proltcli•eefft~

Refermcts

N-Alkyl and N-aryl derivatives of cysteine and cysteamine

Cysteine ........................................ .
Cysteine ....................•...................•
Cysteamine ......•...............................
Cystine ..........................•...............
Cystamine ...•...•.•...•.........................
Cystamine ...................................... .
N-Monomethylcysteamine ........................ .
N-Dimethylcysteamine ........................... .
N, N'-Tetramethylcystamine ...................... .
N-Diethylcysteamine ............................. .
N-Piperidylcysteamine ............................ .
N-Methylphenylcysteamine ...................... .
N-Phenylcysteamine ............................. .
S,2-Aminoethylisothiruonium bromide HBr (AET) ... .
S,2·Aminoethylisothiuronium bromide HBr .......... .
S,2-Aminoethylisothiuronium bromide HBr .......... .
S,2-Aminoethyl-N-methylisothiuronium chloride HCI..

Mice, rats
Rats
Mice, rats
Mice, rats
Mice
Mice, rats
Mice
Mice, rats
Rats
Mice
Mice
Mice
Rats
Mice
Mongrel dogs
Macaca mulatta
monkeysMice

950-1,200 i.p.
1,900 per OS
75-2SO i.p.
240-280 i.p.
150-300 i.p.
4~00 peros
60-120 i.p.
40-70 i.p.
60 i.p.
50-60 i.p.
2S i.p.
2SO i.p.
150 i.p.
240480 i.p.
100 i.p.
200-2SO i.p.

3
2
3
0
3
2
2
2
2
2
0
0
0
3
0
3

738, 739, 632
740
741, 738, 742, 363, 743
744, 74S
744, 746, 747, 363
748, 749, 750, 751
638
752, 638
638
752, 638
638
638
638
753, 636
754
755

150 i.p.

2637

Mice, rats
Rats
Mice, rats
Mice
1\Hce
Mice

800-1,000 i.p.
2,000 per OS
120-250 i.p.
240 i.p.
250-300 i.p.
350-550 i.p.
150 i.p.

3
0
2
0
1
0
0

744, 756, 7S7, 745
745
752, 638, 747
637
752, 738
746, 752, 738
638

N-Acyl derivatives of cysteine and cysteamine

Glutathione ..................................... .
Glutathione .................... , ................ .
N-Acetylcysteamine .............................. .
N-Acetoacetylcysteamine ..........•..........••...
Aletheine ....................................... .
Pantetheine ..................................... .
N-Acetylmethylcysteamine ........................ .

Mice

180

TABLE X. 737

CHEMICALS USED FOR PROTECTIVE EFFECTS

CompoundAnimal(co1itinued)

Dose mg/kg

Protectire

effect•&feren=Compounds with covered sulfur function

a-Homocysteine thiolactone........................
N ,S-Diacetylcysteamine. . . . . . . . . . . . . . . . . . . . . . . . . . .
S-Methylcystearnine................... . . . . . . . . . . . .
S-Benzylcysteamine. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Methionine. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
S,2-Dimethylaminoethylisothiuroniumchloride HCI. . . .
S,2-(1-Morpholyl) ethylisothiuronium bromide HBr...
Di(ethylaminoethyl)sulfide. . . . . . . . . . . . . . . . . . . . . . . . .

+Mice1\'lice
Mice
Mice
Mice
Mice
Mice
Mice

280-320 i.p.
850 i.p.
160 i.p.
500-1,500 i.p.
350 i.p.
150 i.p.
140 i.p.

0-1
0
0
0
0
0
0

Mice
Mice
l\tiice
Mice
Mice
Rats

90 i.p.
125-250 i.p.
450 i.p.
35 i.p.
40 i.p.
100 i.p.

3
3
2
0
0
0

752
637
738
638
638
638

Thioglycolic a;i? ... : ............................. .
Mercaptosuccrn1c acid ............................ .
2,3-Dithiopropanol (BAL) ......................... .

Mice
Mice
Mice, rats

0
0
0-1

744, 738
744
82, 752, 737

Dithiopentaerythrit .............................. .

Mice

180 i.p.
350 i.p.
150-200 i.p. ands.c.
75 i.p.

0759.r..Iice
.Mice
Mice
Mice
Mice

100 i.p.
420 i.p.
500 i.p.
270 i.p.
50 i.p.

0
0
0
0
0

637
759
744
759
759

Mice
Mice
!Vlice
Mice
Mice
Mice
Rats

500 i.p.
600 i.p.
2,500 i.p.
200 i.p.
150 i.p.
150 i.p.
5 i.v.

3
3
2
0
0
0
0

760
760, 761
762, 763, 738, 760, 764
744744, 759
750
745

220-350 i.p.
500 i.p.
75-95 i.p.
95 i.p.
25 i.v.
95 i.p.
80-275 i.p.
80 i.p.
50 i.p.
75-300 i.p.
3-5.5 i.p.
2.75 i.p.
0.7-1.4 i.p.
5 i.m.
1 i.p.
78 i.p.
6 i.p.
23-40 units/kp
i.p.
4 s.c.
5 i.p.
6.5 i.p.
15-30 i.p.
10 i.p.
10 s.c.
250 or.

2
0
3
3
3
2

744, 746
765
744, 746, 765
746
766
746
744, 746

758
339, 636, 752, 738
744
738
738
637

637
752

Compounds with branched or prolonged carbon chain

3-Mercaptopropylamine...........................
3-Mercaptopropylguanidine. . . . . . . . . . . . . . . . . . . . . . . .
Homocysteine . . . . . . . . . . . . . • . . . . . . . . . . . . . . . . . . . . . .
1-Mercapto-5-diethylamino pentane.................
1-Ivlercapto-7-arninoheptane. . . . . . . . . . . . . . . . . . . . . . . .
a-l\Iethylcysteine. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Thiols with alcoholic or carboxylic acid groups

Thiophenols

2-Mercaptothiazoline..... . . . . . . . . . . . . . . . . . . . . . . . . .
1 (-)-2-Thiolhistidine.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Ergothioneine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4,6-Dirnethyl-2-mercapto pyrimidine. . . . . . . . . . . . . . . .
o-Aminothiophenol. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . • .
Miscellaneous sulfur-containing substances

Ammoniumdithiocarbonate.... . . . . . . . . . . . . . . . . . . . . .
Diethyldithiocarbamate.... . . . . . . . . . . . . . . . . . . . . . . . .
Thiourea. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Thiocyanide......................................
Thicacetamide.... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Sodium tetrathionate..... . . . . . . . . . . . . . . . . . . . . . . . . .
Sodium sulfide....................................

Compounds with pronounced pharmacological and toxicological activity

Histamine........................................

!VliceTryptamine ..................................... .
Serotonin ....................................... .

Mice
Mice

DOPA ......................................... .
TyTamine ....................................... .

Mice
Mice

Hydroxytyramine ................................ .

Mice

Arterenol ....................................... .

Mice

Epinephrine ..................................... .
Amphetan1ine ................................... .
Ephedrine .......................•................

Mice{Chickens
Mice
Mice

Oxytocine ....................................... .

Rats, mice

Reserpine ....................................... .
Sodium cyanide .................................. .
!Vlalononitrile .................................... .
p-Aminopropiophenone ........................... .
Apresoline ...................................... .

Mice
Mice
Mice
Rats
Mice

Amine oxides .................................... .

Mice

181

3

0
0

765

2
0
1
1
1
0
0
3

765
744, 746
746
765
767, 768
605
766
746
766
767, 769

3
2
3
3
2
2
2

644
744
744
7i0
771
771
772

3

TABLE X.737

CHEMICALS USED FOR PRorECrIVE EFFECTS (continued)

AnimalVarious metalJol~s and "inert" compounds
Fructose..................... . • . • • • . . . • • . • . . . . . • .

Mice

Glucose................. . . • • . . . • . . . . . . . . . . . . . . . • .

MicePropylene glycol. • . . . • . • • . • • • • . . . . . . . . • . . . . . . • . . . .
Glycerol. • . . . . . . . . • . . . . . . • . • • . . . . . • . . . . . . . . . . . . . .
Formic acid....... • • . • • • • . . . . . . . . . • . . . • . • • . . . . . . .
Pyruvic add. . • • • . • . . • • • • • . . . . . . . . . . . • • . . . • . . . . . .

Mice
Mice
Mice
Mice

Lactic add. . • . • • . • • • • • . . . . . • . . . . . . . . . . . . . . . . . . . . •MicetJ-Ketobutyric acid................................
Caprylic acid. . . . • . • • • • • • . . . . . . . . • . . . . • . . . • . . . • . . •Saliqil!c ac:!d. , • . • . . • . . . • . . • . . . • . • . • • . • . . • • . . . . . . .
Sucawc acid .•..• , . • . • . • . . . . . • . . • • • • . . • • . • . . . . • . .
a-Ketoglutaric acid................................
Ethylenediaminetetraacetic add. • • • • . . . . • • . . . . . . . . •

Mice
Mice
Mice
Mice
Mice
Mice

• Protective effect. The grading of the optimal protective effecthas been carried out according to the following arbitrary scale:
0 - no protective effect; 1 = slight or dubious protective effect(e.g., a-ketoglutaric acid); 2 - moderate protective effect (e.g.,

182

Dost rnr/'ft.i

13,500 i.p.
5,000 i.v.
13,500 i.p.
5,000 i.v.
3,000 i.p.
185 i.p.
92 i.p.
700 i.p.
250 i.v.
180 i.p.
250 i.v.
250 i.v.
290 i.p.
275 i.p.
950 i.p.
250 i.v.
580 i.p.

Prol«:liu
tfd

2
0
1
0
3

0
2
1
2
0
0
1
2
2

Re/ertneeS

744608, 773
744
773
744
744
744
744
608, 773
744
608, 773
773
744
744
744

1
1

773

2

744

formic acid); 3 = strong protective effect (e.g., cysteamine, AET).
i.p = intraperitoneally; i.v. = intravenously; i.m. = intramuscularly; s.c. "' sub-cutaneously; or. - orally.

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760. Van Bekkum, D. vV., The protective action ofdithiocarbamates against the lethal effects of X-irradiation in mice. Acta Physiol. Pharm. Neerl. 4:508-523 (1956).
761. Bacq, Z. M., A. Herve, P. Fischer, Rayons X etagents de chelation. Bull. Acad. Merl. Belg. 18:
226-235 (1953).
762. Betz, E. H., Sur le mecanisme de protection par lethiouree chez la souris irradiee a dose lethale derayons-X. Comptes rendus Soc., Biol., Paris 148:
1915-1918 (1954).
763. Langendorff, H., R. Koch, p. Hagen, Zu~ Wii:kungsmechanismus des Th1ohamstoff belID b10logischen Strahlenschutz. Arch. Int. Pharmacodyn.
100: 1-16 (1954).
764. Mole. R. H., J. S. L. Philpot, C. R. V. Hodges,
Reduction in lethal effect of X-radiation by pretreatment with thiourea or sodium ethane dithiophosphonate. Nature 166: 515 only ( 1950).
765. Langendorff, H., R. Koch, Untersuchungen iiber
einen biologischen Strahlenschutz. XL Haben
Amine eine · Strahlenschutzwirkung? Strahlentherapie 98: 245-254 ( 1955).
766. Langendorff, H., R. Koch, Untersuchungen iib~reinen biologischen Strahlenschutz. XVIII. Die
Wirkung zentralerrengender Pharmaka auf das
bestrahlte Tier. Strahlentherapie 102: 58-64( 1957).
767. Gray, J. L., E. J: Mol;llden, J. T .. Tew ~t al., ~ro­tective effect of p1tressm and of epmephnne agamst
205

total body X-irradiation. Proc. Soc. Exp. Biol.
Med. 79: 384-387 (1952).
768. Van Bekkum, D. W., J. de Groot, "Observations
on chemical protection in vivo and in vitro'', pp.
243-248 in Progress in Radiobiology. J. S. Mitchell,
B. E. Holmes and C. L. Smith, eds., Oliver andBoyd, Edinburgh (1956).
769. Herve, A., Action radioprotectrice de l'ocytocine
chez la souris. Arch. Int. Physiol. 63: 136-137(1955).
770. Gray,]. L., J. T. Tew, H. Jensen, Protective effectof serotonin and of paraminopropiophenone
against lethal doses of X-radiation. Proc. Soc. Exp.
Biol. Med. 80: 604-607 (1952).
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75-76 ( 1960).
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in mice. Nature 184: 198 only (1959).
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and guinea pigs. Amer. J. Roentgenol. 84: 699-704(1960).
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780. Potter, G. D., S. Lindsay, I. L. Chaikoff, Inductionof neoplasms in rat thyroid glands by low doses ofradio iodine. Arch. Pathol. 69: 257-269 (1960).
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backtofirst page

! .

206

ANNEXERADIATION FROM NATURAL SOURCESCONTENTSParagraphs

lNT.RODUCTION ••.• , , ... , , . , ... , .• , .• , , , .....•. , . , • , . . .

1-3

I. CosMic RAYS • • . . . . . . . . . . . • • . . . . . . . . . . . . . • . . . • . 4-18
Nature of radiation ............. , . .. • • .. .. .. . .. • 4-5
Radiation dose-rates • . • . . . . . . . . . . • • . . • . . • . • . . . • . 6-8
Variations with latitude and longitude............ 9-12
Var!a~ons w~th a~titude ......................... 13-14
Vanattons with time ............................ 15-18

II. NATURAL RADIO-ACTIVITY IN THE EARTH'S CRUST.,., 19-31

Paragrop/u

V. NATURAL RADIO-ACTIVITY IN FOODSTUFFS .••......•. 58-66
Total alpha-activity •.....•..••.••.•...••....... 59-60
Radium-226 ..•...••....•.•.••..•........•..•.•• 61-63
Thorium •••.... .. . .•. ..•••. .•. .•. . . .. .. .• . . .•. 64
Pb210, Bi21om and Po210. . • • • • . • • • • • . . • • . • • • . • • • • 65
Potassium-40 • . . . • . • . . . . . . • • . • • • • . • . . . . . . . • • . . . 66

VI. NATURAL RADIO-ACTIVITY IN THE HU!.!AN BODY •• , •. 67-84

Naturally ~ccu_rring radio-active nuclides......... 19
Concentration m common rocks.................. 20
Uranium and thorium ............ ,.............. 21
Radium-226 •.•..•.•..•.•..•..•......•..•..• , . . . 22
Potassium . • . • • . • . . • . . • • • . . • . . . . . . . . • . . • . . • . . . . 23
Rn 222 and Rn 220 in the earth's crust. ...... , •• , . . . . 24
Dose-rates from the earth's crust ..........•. , ..•. 25-31

Total alpha-activity •..•....•. , •••....•..•.•.... 68-69
Radium-226 ••......••....•.....••....••.....•.. 70-74
Thorium . . .•. . . .•. ••..•..••. ..••... .. .. ... .•. • 75
Pb210, Bjnom and Pono......................... 76
Dose-rates for naturally occurring U and Th series 77-78
Potassium-40 . . . . . . . . ... . • . • • • . • . . • . . . • . . . . . . • . . 79-81
Carbon-14 ...................••........••....•. 82-83
Tritium • . .• • • . • • . . ••• . . . . . . . • •• . • . . .. . . .• . . . . . . 84

III. NATURAL RADIO-ACTIVITY IN WATER ............... 32-36

VII. HIGH NATURAL RADIATION :\REAS ..... , .. ,, .. , .•.• 85-93

Public water supplies. • . . . • • . • . . . • • . • . . . • . . . • . . • 33-34
Ocean water, rivers and natural springs... . • . . • . . . 35
Skeletal Ra 228 content due to drinking water...... 36

IV. NATURAL RADIO-ACTIVITY IN THE LOWER ATMOSPHERE 37-57
Rn 2 22 and Rn 22 0 and their decay products ••..•.•.. 37-42
Pb21 0, Bi21om and Pono......................... 43
Carbon-14 •••..•••..•..•.......•.........•..•.. 44-54
Tritium • • • . • . . . • . . . . • . . • . . . . . . . . . . • . . • . • . • • • • . 55-56
Beryllium- and other cosmic ray-produced nuclides • • . . . . . . . . . . . • . . • . . . . . . • . . . . • . • • • • • • • . • • 57

High natural radio-activity in the earth's crust ..•. 86-90
High natural radio-activity in the air • • • • • • . . . . • • • 91
High natural radio-activity in buildings........... 92
High altitude areas .. . • . . • • • .. . . • • • . . . . .. . • • .. . . 93

Vlll. SUMMARY OF EXPOSURE DATA ....•.... ,., ....••... 94-95
TABLESREFERENCES

posed for radiation protection purposes1 • 2 and are generally thought to be rather conservative, particularly inthe case of a-particles and neutrons. For the estimationof biological damage it is quite probable that lower values
are more applicable. For instance, the 1959 ICRP Committee II report3 states the following with regard to the
RBE for a-particles :Introduction

1. The radiation from natural sources at any specificlocation remains relatively constant with time; it does,
however, vary from place to place. Natural radiationarises from two sources-cosmic rays and naturally occurring radio-active materials. While cosmic rays are
predominantly an external source of irradiation, naturally occurring radio-active materials give rise to both
external and internal irradiation of the human body.
A distin~ishing char~cteristic of irradiation by natural
sources is that the entire world population has been e.....:posed to it since the beginning of time and will continue
to be exposed to it in the future.

"Many experiments4 indicate that (REE) a ismuch smaller than 10 for biological damage resulting
from acute exposure-perhaps as small as 1.4--but
for chronic exposures, much higher applicable values
have been reported. 5 Therefore, until more data forchronic exposures are available, it would be unwise touse a value of (REE) a < 10."

.2. The biological. e~ect of ionizing radiation varies
with the type of radiation, and, in order to take this into
account, a weighting factor is used to obtain the tissue
dose in. rem fro?l the corresponding absorbed dose in
r31d. This factor 1s known as the relative biological effectiveness (REE) and the usual definition is given inannex .A .. Ho.wever, the RBE factor for a particular typeof radiation is not a constant, and varies with a numberof other l?arar:ieters such as dose-rate, dose fractionation,
type of biological effect, oxygen tension and temperature.

For low energy electrons of$; 0.03 MeV, Shtukkenberg4
suggests that the REE is 2.8-3.0 (i.e., greater than theusual value of 1.7). when one takes into account thesmaller biological effect produced by chronic irradiation
when compared to a single exposure. In the light of all
the uncertainties, it is thought prudent to use the RBE
values given in annex A in order to estimate the exposure
pattern in man, but to keep in mind that in general thesevalues will be too high (see also annex H). Where possible in the present annex, tissue doses will be given in
rem as well as in rad.

3. The RBE values given in annex A are those pro-207

I. Cosmic rays

made with the Pioneer V space probe have been somewhat enlightening on the behavior of solar protons infree space. The probe encountered outbursts of solar
protons at a distance of about 5 million km from theearth during the period from 27 March to 6 April 1960.
Unlike the radiation belts, the solar particles are not
restricted to a small region of space that could be avoided
or traversed rapidly, but would apparently be encountered throughout the solar system. Consequently, steps
will have to be taken to shield directly against theseparticles in order to achieve manned missions of any
appreciable time duration.
5. The primary particles interact with nuclei of theupper atmosphere, producing secondary radiation, which
consists of mesons, electrons, photons. protons and neutrons-all with a very wide range of energies. Electronsand photons constitute the soft component of the secondary radiation, protons and neutrons the nucleoniccomponent. The primary radiation intensity gradually decreases with decrease in altitude and at about 20 km it
has practically disappeared, so that below this altitude
cosmic radiation is almost entirely secondary in nature.
In the altitude region above 20 km, the proportion of
secondary radiation rapidly decreases until, at about 50
km, the radiation dose-rate is due predominantly to theprimary component, except in the case of the auroral
regions and the inner and outer radiation belts (para. 4).
The increase in cosmic radiation dose-rate with altitude
is such that above about 2 km, cosmic radiation becomesthe major dose-rate contributor in man.

NATURE OF RADIATION

4. Primary cosmic radiation may be divided into
three categories: galactic cosmic radiation, geomagnetically trapped radiation, and solar cosmic radiation.
(a) Galactic cosmic radiation presents a more or lessconstant space environmental factor, and its particle
composition has been quite well determined. Outside theatmosphere at latitudes above 55°, primary cosmic raysof galactic origin consist of 87 per cent protons, 12 percent alpha particles, and 1 per cent heavier nuclei (C, N,
0. Mg, Ca, Fe).1 - 10( b) Geomagnetically trapped radiation is the sec?nd
category. At higher altitu~es, in regions sym~etncal
with regard to the magnetic equator, there exist tyvo
radiation belts containing electrons and protons whichhave been captured by the magnetic field of the earth. 11 - 14
The inner belt begins at about 1,000 km altitude, reaches
a maximum intensity at about 3,000 km and extends
from 30° N to 30° S. The outer belt begins at an altitude
of about 12,000 km, passes through a maximum in~en­sity at about 15,000 km and extends from 60° N to 60 S.
The energy spectrum of the particles in each belt differs
considerably but has not been investigated fully enoughto give an accurate estimate of the radiation dose-rate inthese regions. The dose-rates will be dependent on theamount of shielding assumed and, for the inner radiation
belt, values of 10 and 120 rad per hour have been suggested15• 16 for 1 and 2 g per cm 2 shielding respectively.
Dose rates in the outer belt may be of the order of 10'
rad per hour 17 owing to soft electron bremsstrahlung,but this can be reduced considerably by shielding. A further high intensity field of low energy electrons18•1 9 is tobe found at high latitudes ( > 60°) and altitudes ( > 25km) and is associated with auroral processes.
( c) Solar cosmic radiation is the third major radiation
phenomenon. Large fluxes of protons are observed toreach the vicinity of the earth following severe solar
flares which occur on the surface of the sun. Because of
the potential danger of space travel and because of therelationships to solar physics, magnetic fields, and manygeophysical events, this radiation is under intense study.
Solar cosmic ray events may be divided into two classes:"high energy" and "low energy". During high energy
events a significant number of particles have energies
high enough to produce effects observable by groundlevel neutron monitors, whereas high altitude measurements or riometer measurements are necessary to detect
the low energy events. The high energy events appear to
be much less frequent than those of low energy. Only
five such events were detected during the twenty years
preceding 1959; however, an additional five events havebeen detected during 1959 and 1960, three of which
occurred in one month, November 1960. The low energy events, on the other hand, have been observed tooccur at the rate of ten per year since 1957. The mostintense high-energy outburst of solar protons recorded
to date was observed following the great solar flare of
23 February 1956. Shortly after the beginning of theflare, solar particles with energies of several Bev began
striking the ionosphere. Data available from a numberof flare events seem to indicate that the initial flux
reaching the vicinity of the earth may be monodirectional with the flux, then becoming isotropic after about
the first hour. There is also some evidence that the
spectrum of the initial particles may be considerably
harder than that of those arriving later. Measurements

RADIATION DOSE-RATES

6. The radiation dose-rate due to the ionizing component of cosmic rays is generally estimated by measuring the number of ion pairs per on3 /sec, using an energy
independent ionization chamber, and then converting
this value to the rate of absorption of energy assuming that 34 eV are required to form 1 ion pair. Manymeasurements of this type have been made. These measurements, however, do not take into account the radiation dose-rate due to the neutron component of cosmic
rays, and this must be measured separately. Many measurements of cosmic ray neutron flux have been made but
there are relatively few estimates of the resulting tissue
dose-rate. This is due to the fact that the tissue dose-rate
is very dependent on the neutron energy spectrum20
which is extremely difficult to determine. The cosmic
radiation dose-rate often used as a "base level" is thatat sea level for high altitudes (,...., 70°). There are indications21· 22 that the most reliable figure for the ionizing
component in this region is 1.90-1.96 ion-pairs per
cm 3/sec. which gives a soft tissue and gonad dose-rateof about 28 mrad/y.
7. The cosmic ray neutron component results in atissue dose-rate which. at sea level for middle latitudes,
has been estimated by Patterson et al. 23 using three different type neutron detectors, which could respond todifferent ranges of neutron energy. Patterson's calculations show that the dose-rate from the neutron component of cosmic rays at sea levels is 25 mrem/y. This estimate is the dose-rate at the skin using the values of RBE
established by the United States National Committee on
Radiation Protection and Measures and ignores the absorption of neutrons in building structures and the bodyitself. It has been assumed that there is an average of 10
cm of building materials in roofing materials, timbers
and ceilings, and that the average depth of the gonads andbone-marrow is 4 cm. By applying corrections for the208absorption of the various energies of neutrons, assumingthese materials to be tissue equivalent, and assumingthat the average time spent out of doors is seven hours
a day, the resultant tissue dose-rate is 13 mrem/y. (These
data are based on the depth dose curves for neutrons
given in reference 24.) This is probably more reliable
than the value of 18 mrem/y for sea level at 51° N given
by Tobias19 whose estimate was based on measurements
using a single type neutron detector which did not givea direct measurement of fast neutron flux, the most critical portion of the neutron energy spectrum with regard
to dose-rate considerations. According to Shtukkenberg's25 calculations, the cosmic radiation fast neutron(> 10 MeV) tissue dose-rate at sea level is approximately 10 per cent of the total dose-rate. He suggeststhat the total dose-rate resulting from cosmic radiationis 88 mrem/y, if an RBE value of 10 is assumed for
densely ionizing particles with energies up to 15 MeV,
and 57 mrem/y, if a value of 6.5 is used.

paragraph 4. Figure 1 gives the measured variation ofcosmic radiation dose-rates in mrem per year with altitude for the ionizing component32 at 3° N and 55° N andfor ~e neut\on. component23 in the latitud~ rang~ 28490 N. The significance of curves A and B 1s explainedin paragraph 15.
,. Neutron component (28-490 N)/

A (low solar activity)//

B (blgh solar activity)//~ 1,000j

8. It is therefore suggested that 50 mrem per year
be taken as a typical value for the total cosmic radiation
tissue dose-rate for sea level at middle latitudes. The
value is subject to variations with a number of parameters, as discussed in paragraphs 9-18 below.
VARIATIONS WITH LATITUDE AND LONGITUDE

9. Cosmic ray intensity exhibits a latitude effect whichis due to the earth's magnetic field preventing the incoming primary particles below a certain critical minimum
energy from reaching the earth's atmosphere. This critical cut-off energy decreases with increasing latitude,
the net result being that the cosmic ray intensity at thegeomagnetic equator is lower than at other latitudes.
The intensity remains relatively constant between 15° N
and 15° S, then shows a rapid increase until about 500
latitude, after which it remains practically constant again.
The latitude effect is generally expressed as the percentage increase at 50° over the intensity at the equator.
10. The average value26 for the latitude effect of theionizing component of cosmic radiation at sea level is
10 per cent. The percentage increases slowly to a value ofabout 30 per cent at an altitude of 5 km and then much
more quickly to a value of about 350 per cent at thetransition region (about 20 km) of the atmosphere(para. 15).
11. Since the neutron component of cosmic radiation
includes neutrons produced by interaction with the atmosphere, it also exhibits a large latitude effect. 27 At altitudes from sea level up to about 3 km, the latitude effectis about 150 per cent and at 9 km, is about 250 per cent.
12. Changes in cosmic ray intensity with longitude
are expected to occur2 8 since the magnetic centre of theearth and the geometrical centre do not coincide, themagnetic centre of the earth being approximately 300 km
from the centre of the earth along a line passing approximately through 100 N geomagnetic latitude and 160° E
longitude. The intensity of the ionizing component at
sea level has been found to vary about 5 per cent along
the geomagnetic equator, 29 the effect diminishing at
higher latitudes. 30 The nucleon intensity shows similar
but larger intensity variations with change in longitude.21,a1

lOOL-~~--"10~~~--"20~~~--'30~~---,•0~~~-'50

AlUtude (km)• Sec annex A for comment on RBE values used.

Figure 1. Variation of cosmic radiation level with altitude

14. Typical values for the total cosmic radiation tissue
dose-rates for various altitudes at the equator, 300 and
50° latitude, have been estimated, assuming that Pa~ter­son' s23 results for the neutron component at vanous
altitudes apply to a latitude of 50° and that the latitude
variations are as suggested in paragraphs 10-11 (table I).
VARIATIONS WITH TIME

15. Time variations of cosmic ray intensity result
from a number of causes including solar flares, the 11year solar cycle. the 27-day lunar period, temperaturechanges in the upper layers of the atmosphere, barometric pressure changes and air fronts. The modificationin cosmic ray intensity which is associated with the
11-year cycle33 of solar activity is most pronounced forthe lower part of the energy spectrum of the primarycosmic radiation and is therefore only evident at highaltitudes where it results in a minimum intensity at theper'.od of maximum solar activity. This is illustrated bycurves A and B in figure 1 which show~ 2 the total ionization as a function of altitude in 1954 (curve A) when
the sun was at its lowest ebb in twenty-two years, andin 1937 (curve B), a year of high solar activity.
16. Further variations associated with the sun are
the so-called cosmic ray storms which are of short duration, one day up to a couple of weeks. They start with asudden decrease, or series of decreases, in cosmic rayintensity and are followed by a slow recovery. Thesestorms and decreases in intensity are correlated with the

VARIATIONS WITH ALTITUDE

13. The variation in composition of the cosmic radiation with altitudes up to 50 km has been described in
209number and size of sun spot groups as well as the appearance of solar particles. 3 ~ Therefore they also follow
the 11-year solar cycle.
17. The sun also acts as a powerful source of cosmic
radiation during prominent flares. The spectrum of protons produced by these flares is much more enhanced in
the low energy portion than that for the primary cosmic
radiation 32 and in most cases moderate amounts ofshielding will be effective. The largest flares, for example
the giant flares of 4 May 1960 and of 23 February 1956,
may, however, produce dose-rates which are quite highat altitudes of the order of 10-20 Ian and their effect isconsiderable even at sea level. Calculations for the February 1956 increase show 35 that the integrated exposure
over the duration of the increase was 5 to 10 rad at analtitude of 15 Ian. Sola; particles produce a strong influx
at high latitudes of protons having energies from a few
tens to many hundreds of MeV. As these protons continue to bombard the earth's atmosphere for days they
may represent a major radiation problem in the stratosphere especially as they may produce dose-rates of theorder of 10 remjhr at 20-25 km altitude. 36 During yearsof high solar activity a dozen or more such events may
occur per year.

18. The neutron intensity would also be expected to
exhibit a dependence on solar activity corresponding to
the solar modification of primary cosmic radiation.
Short-term variations at high altitudes and latitudes andassociated with periods of high sunspot activity havealso been observed. For instance, Simpson27 reports increases in intensity of at least 30 per cent at 9 km altitude which persist for the order of days. Further variation in the neutron component will also occur near theearth's surface due to alterations in the moisture conterltof the soil, and it is also affected by the moisture content
of dense cloud formations. 57

II. Natural radio-activity in the earth's crust
NATURALLY OCCURRING RADIO-ACTIVE NUCLIDES

19. Naturally occurring radio-active materials arewidely distributed throughout the earth's crust and theresulting gamma ray dose to mankind varies from avalue somewhat less than that due to cosmic rays tovalues many times higher. Some of the more importantof these nuclides are the long-lived U 238 , Th 232 andRa 226 (and their shorter-lived daughter products). K~ 0
and the cosmic ray produced isotopes cu and H 3. Other
isotopes such as Rb 87 , La138 , Sm1 H and Lu176 also exist
in nature but their abundance is so low as to make anegligible contribution to the dose received by mankind.
The physical characteristics of some of these isotopes are
given in table II.
CONCENTRATION IN COMMOK ROCKS

20. In general, natural radio-nuclides are found to be
more concentrated in granitic rocks than in basaltic
rocks. 38 • 39 Limestones and sandstones are low in radioactivity, but certain shales are more radio-active, especially those containing organic matter. 40 Marine sediments appear to be more radio-active than either nonmarine or estuarian deposits. 38
URANIUM AND THORIUM. 21. Ura~ium ore has been found in large quantities
m Australia, Canada, Czechoslovakia, Republic of theCongo (Leopoldville), South Africa, the United States,

210

the Soviet Union and other areas. Large deposits ofmonazite, the principal thorium-bearing mineral, arefound in Brazil, the United Arab Republic, China, India
and the United States. Although thorium is more abundant than uranium, uranium is found in a much greater
variety of chemical combinations. Table III shows theirconcentration in various rocks, as determined by a number of workers, expressed as µ.µ.c/g.
R.AnruM-226

22. Ra is one of the daughter products of U 238 but,because of leaching and weathering, it is not necessarily
in equilibrium in soil with its long-lived parent. Thereis a considerable range of concentration in various rocks,
as indicated by table III. Particularly high concentrations
are found in alum shales in Sweden.n• 42 The Ra226 concentration in the soil in various parts of the United Stateshas been found by measurement to vary between 0.09
and 0.8 µ.µ.c/g soil. 26
226

POTASSIUM

23. Potassium is relatively abundant in nature. Its
radio-active isotope K 40 constitutes 0.0118 per cen~ 3 ofthe total amount of potassium and contributesH 28 ,8-dps
per g Kand 3.45 y-dps per g K. The K• 0 content of various rocks is given in table III. It has been estimated thatthe potassium content of soil is about 10-3 to 3 X 10-2 g
K/g soil 45 (1 to 30 µ.µ.cK. 40/g soil.)
RN 222 AND RN 220 IN THE EARTH'S CRUST

24. Since uranium and thorium are almost universally distributed, their respective short-lived gaseous
daughter products, Rn 222 and Rn220 , accumulate in soil
and rocks. The daughter products of this trapped Rn222
and Rn 220 contribute over half the observed gamma
activity of uranium minerals. 41 The Rn2 ~ 2 and Rn 220 in
the soil diffuse into the air at a quite variable rate, depending on a number of factors including moisture content of the ground, 46 presence of snow/ 7 amount of rainfall,48•49 conditions in soil and atmosphere, particularly
atmospheric turbulence and pressure.
DosE-RATES FROM THE EARTH'S CRUST

25. The gamma dose-rates in air over radio-active
rocks and soils can be calculated from the energies,
absorption factors and relative abundances of the various component gamma rays, allowance being made forscattered radiation. The expressions obtained by Hultqvist'2 and O'Brien et al. 50 for the gamma dose-rates in
air above ground containing uniform concentrations of
U 258 , Th 232 and K• 0 agree to within 10 per cent. The
average of their expressions gives the following relations
bet\veen the dose-rate in air (D, mrad/y) at a height ofone metre above ground containing uniform concentrations (S, µ.µ.c/g) of U 238 , Th232 (both in equilibrium with
their daughters) and K• 0 :
Du = 17.8 X Su }(1)
DTh = 25.5 x Srh
DK = 1.56 x SK
26. The ,B-particle emission of these naturally-occurring radio-nuclides can contribute an external dose to
the human skin. These skin dose-rates have been calculated by O'Brien et al.~ 0 for ,8-emission from U 238 , Th 232
and K• 0 in soil assuming homogenous distribution andcomplete equilibrium between the U 238 and Th232 andtheir decay products. The external contribution to thedose-rate deliYered to susceptible organs (such asgonads, bone, etc.) resulting from ,B-emission, must be
regarded as negligible.
27. Typical estimates of the average dose-rates in air
at a height of one metre above limestone may be of theorder of 20 mrad/y and that for granite areas may beof the order of 150 mrad/y. It is obvious, however, that
there will be quite large variations in these values, andthis is borne out by the measured terrestrial dose-rates
in air reported for areas in various countries as given
in table IV. Further, much higher values are reported
for some areas, e.g., monazite sands, where the uranium
and thorium contents are very high (see section VII
below).
28. The terrestrial gamma dose-rate inside buildings
will, generally, be different from the value out of doors
owing to the different radio-active content of the building materials and also the attenuation effect of the walls
for the radiation from sources outside the building.
A further small increase in dose-rate may be producedby the accumulation of Rnm and Rn 220 as a result ofpoor ventilation in the buildings (see section IV below).
Reported terrestrial dose-rates in air inside buildings invarious countries are given in table V.
29. In order to obtain tissue dose-rates to specificorgans due to e..xtemal gamma sources, allowance must
be made for attenuation by intervening portions of the
body. O'Brien et az.~ 0 have calculated the dose-rates in
man at various depths as fractions of the free-air gamma
dose-rates. Assuming that the testicles, ovaries andbone-marrow are at depthsn of 1, 7 and 4 cm, the resulting screening factors are 0.68, 0.58 and 0.62, respectively. These are in very good agreement with theaverage experimentally determined screening factors obtained by Spiers52 using a water-filled model-0.70, 0.56
and 0.64 respectively. It is, therefore, suggested that avalue of 0.6 be used as the screening factor for gonads
and bone-marrow in the case of terrestrial radiation.
(F III, 18)
30. The estimation of mean dose-rate to a population
should be made by a carefully planned series of measurements of dose-rates both indoors and out of doors andthen weighting the measurements according to time spentin each place. A very good example of such a survey is
one which was recently made in four areas in the Umted
Kingdom. ~ 3 The mean values of local gamma-radiation
dose-rates obtained are given in table VI. In computing
the mean dose-rates to the gonads and bone marrow,screening factors of 0.63 and 0.64 respectively were used
and it was assumed than an average of six hours per
day per person was spent out of doors.
31. Insufficient measurements have been made to enable a reliable estimate of the mean dose-rate to the world
population to be made. It should be pointed out that the
major part of most people's lives in most areas of theworld is spent inside buildings. With this in mind, consideration of tables IV and V seems to indicate that,except for certain regions of high activity, the averageterrestrial gamma dose-rate in air is of the order of
80 mrad/y, i.e., a mean gonad and bone dose-rate to theworld population from terrestrial gamma radiation is
only about 50 mrad/y (para. 29).

36. The skeletal content of Ra228 is determined by its
introduction into the body through food, water and, toa lesser extent, air. Muth et al. 62 have shown that undernormal environmental conditions only about 10 per centof the Ra 226 enters the human body through water andabout 90 per cent from food. \Vhen the Ra 220 concentration in water is relatively high and the intake fromwater exceeds the intake from food, some correlationi; found to exist between the skeletal concentration andt.l1e concentration in water. 54 With relatively low (normal) Ra 226 concentrations in water, no such correlation
is observed as the skeletal Ra226 content is then basicallydetermined by its intake from food.

Ill. Natural radio-activity in water

IV. Natural radio-activity in the lower atmosphere

32. An e..xtremely wide range of natural radio-activities exists in various types of water, depending largely
upon their origin. The levels of natural activity originat-

RN 222 AND RN 220 AND THEIR DECAY PRODUCTS

ing from uranium and thorium series are found to behigh in certain natural springs which are found in areas
where there are high concentrations of uranium andthorium in the soil. Similarly. drinking water e.xhibits
wide variations of activity depending upon its origin
and on the treatment it receives before it becomes available for consumption. High levels of natural potassium40 activities are found in sea-water.
PUBLIC WATER SUPPLIES

33. Public water supplies are of interest since drinking water is one of the modes of entrance of naturalradio-activity into the body. Table VII gives concentrations of Ra 226 and Rnm present in various public watersupplies. It should be pointed out that the radium content of water is reduced by the introduction of filtration
and/or softener systems, so that the intake of radiumfrom a particular supply may be modified in the caseof some individuals by the use of domestic water softeners. Lucas 54 quotes a case where one of these units(ion-e.xchange type) removed 98 per cent of the Ra226
present in the normal water supply.
34. :Many drinking water supplies will also containnaturally occurring Th 232 and/or its decay products.
Krause 55 has investigated the Ra228 content of twentysix samples of well-water from the Illinois (UnitedStates) sandstone area and has compared them with the
Ra 226 contents of the same samples which had been previously measured by Lucas. 56 The Ra 228/Ra2 ~ 5 ratio covered an e.xtremely wide range of values, 0.04 to 2.43,
with an average of 0.60. The Ra228 concentrations ranged
from 0.9 to 7.9 µ.µ.cjl, whilst Ra 226 went from 3 to36 µ.µ.cjl.
OCEAN WATER, RIVERS AND NATURAL SPRINGS

35. Typical concentration of U 238 , Th 232 , Ra220 and40
K. in sea-water are respectively 0.2-9 µ.µ.c/l, 57 0.11.10-3 µ.µ.cjl,~ 8 0.02--0.3 µ.µ.c/1 59 and 300 µ.iicjl. 60 Table
VIII gives the concentrations of U 238 , Ra226 and Rn:!!! 2present in various natural waters and springs. Springwaters may exhibit extremely high radio-active concentrations, particularly of Rn 222 , but as they are consumed
regularly only by a very small percentage of populations,and since Rn 222 ingested from drinking water probably
has a mean life of about one hour in the body, 01 the remlting mean dose to the world population from springwater is negligible.
SKELETAL RA226 CONTENT DUE TO DRINKING WATER

37. Wherever there are uranium or thorium bearing
minerals present in the soil, the gaseous decay products211

Rn 222 and Rn220 are injected into the atmosphere by diffusion (para. 24). The rate of injection varies considerably with seasonal and meteorological conditions. Measurements of Rn 222 and Rn 220 and/or their daughter
product activities is often carried out by a combinationof filtration and ionization chamber or scintillation methods.63 The daughter products, in the form of ionizedatoms, attach themselves to the aerosols and dust particles which are always present in the air. The collection
efficiency of filter papers for these particles is often very
uncertain and depends on the linear air velocity throughthe paper and the size range of the dust particles in the
air. 6 ~• 65 Thus, in low dust atmospheres such as those of
air-conditioned rooms, the retention of the daughter
products by filter papers may be very low. Ion collection efficiency may, however, approach 100 per cent by
the application of a suitable electric field. 60 In addition,
the Rn222 and Rn 220 present in the atmosphere are notnecessarily in equilibrium with their daughter products
and will also contain varying fractions of uncombined
atoms of daughter products, both of which affect thedose-rate to the lungs upon inhalation (para. 42). The
concentration of Rn 222 and Rn 220 will also vary withheight, for instance the average value at a height of
10 m for Rn 222 is 90 per cent of that at groundlevel. 25 • 67 • 88 Rn220 , by virtue of its very short half-life,
will virtually have disappeared at heights of 10-20 m.
The average concentrations of Rn 222 and Rn 2 " 0 present
in free air at ground level in various regions are given
in table IX. Values are particularly dependent upon thelength of time the air mass spends over continental landmasses. 67 • 69 • '° Also, in areas of high radio-activity andunder special meteorological conditions, e.g. smog andtemperature inversion, values may be higher by several
factors of ten.
38. As the majority of the people spend a large partof their time in buildings, the average natural radioactivity concentration in air which refers to the world
population is more dependent upon the level in buildings
than in free air. In general, the level indoors is higher
than that out of doors and it is dependent upon thebuilding construction materials and the ventilation conditions. The level out of doors will determine the concentration that will be reached by very efficient ventilation of the building. The results of measurement by
Hultqvist' 2 in three types of buildings in Sweden for
conditions with and without ventilation are given intable X. A ventilation rate of 1()-8/sec was used, i.e., theair in the building was renewed every seventeen minutes.
39. Reported Rn 222 content of the air indoors at various localities is given in table XL Consideration of thesedata indicates that the best estimate of a "world average"
concentration of Rn 222 in air may be of the order of 0.5µ.µ.c/l. The corresponding figure for Rn 220 may be of theorder of 0.02 µ.µ.cjl.
40. The external gamma dose-rate in air (D) produced by a concentration of C µ.µ.c/1 of Rn 222 or Rn 220 inequilibrium with their decay products per litre of air canbe calculated by Hultqvist's relation :42
D = 14C mrad/y
In obtaining the dose to various body organs allowance
must be made for body shielding. The screening factorof 0.6 used previously for terrestrial radiation (para. 29)
will again be used here. Hence, for "average" air concentrations of Rn 222 and Rn 220 (para. 39), the total bodytissue dose-rate will be of the order of _1.5 !11rem/y.
It should be pointed out, however. that this contribution
to the tissue dose-rates will have been included in any

measurement of local gamma-radiation dose-rates thathave been made and so is allowed for in the average local
gamma dose-rate given in paragraph 31.
41. There will also be a further total body tissue dose
produced by the Rn 222 and Rn 220 in the air resulting
from that portion which is transferred via the bloodfrom contact with the alveolar air. Using Spiers53 results,
the total dose-rate to soft tissues due to the inhalation of
air containing 0.5 µ.p.c/I of Rn 222 in equilibrium with its
daughter products, is of the order of 3 mrem per year.
Ruzer's results 71 indicate that the whole body dose-rate
due to the inhalation of 0.5 µ.p.cjl of Rn 222 is of the orderof 0.01 mrem per year.
42. The dose-rate to the lungs from Rn 222 and Rn220
and their decay products occurs as a result of deposition
and/or passage back and forth through the tracheobronchial tree of these decay products72 and depends
largely on their size, specific activity and percentage of
uncombined atoms, 73 since these determine the amount ofradio-activity retained in the lungs. Rn222 and Rn220 ,being gases, are retained only to a very small extent.
and so do not make a very large contributon to the doserate. Stannardu gives the mass deposition of small particles in the respiratory tract (figure 2), derived fromthe results given by Hultqvist.'2 Values for dose-rates
to the lung for e.xposure to Rn 222 or Rn 220 in equilibrium
have been calculated by various workers. For instance,
using the expressions of Hultqvist,42 Morgan,' 2 Ruzer, 71
Shapiro,75 and Schraub,76 values are obtained of 20 mrad(200 mrem), 90 mrad (900 mrem), 10 mrad (100mrem), 10 mrad (100 mrem), 250 mrem. respectively,
for the annual dose to the lungs from a continuous concentration of 0.5 µ.µ.cjl Rn222 in equilibrium. The variations in these estimates are chiefly due to the differencesin the assumption regarding time spent in the relevant
locale. respiration velocity and the weight of the irradiated lung tissue. Hultqvist4 2 has estimated the dose-rate
100

90

80

70

-:

"
~60

\

.,,
~

/'

§_so
.,,
"
~"' 40D

Lower
respiratory
tract only

.."

0

u

0..

30

zo
10

0
0.05

.0.1

0.2

o.s
1.0
Particle •lze - microns

2.0

Figure 2. Percentage mass deposition of small particles in the
respiratory tract212

to the lungs from Rn 222 and its decay products and from
Rnm and its decay products in the case of radio-active
equilibrium and also where this equilibrium has been
greatly disturbed by a high ventilation rate ( lQ-3/sec.).
The dose-rates to the lungs along with the average concentrations of Rn 222 and Rn 220 in air for three types ofbuildings in Sweden are given in table X. It is apparent
that the lungs receive a higher irradiation from natural
sources than any other body tissue.
PB" 10, B1 21 o•n AND Po 210
43. The daughter products, Po 218 , Pbm, Bi214 andPom, because of their short half-lives, are normally notvery far from secular equilibrium with the parent Rn222 ,but the concentrations of Pb 210 , Bi 210 m and Po 210 will be
relatively much lower at ground level than their equilibrium values, as they will be washed out of the atmosphere long before equilibrium has been reached. Measured levels of Pb2 1.0, Bi210 m and Po210 in the air at groundlevel are given in table XII. These concentrations are
insignificant with respect to dose considerations.

in nat~re .. Thus, for example, the C13/C12 ratio in plant
matenal is 1.7 per cent less than that in the atmosphere78' 79 and the change for the C14/C12 ratio is twice
this amount. 80 • 81
·Production of natural C1 4

47 .. The_C 14 p~oduccd in the atmosphere owing to absorption ot cosmic ray neutrons may be estimated fromflux-energy data and the neutron cross-sections of thevarious constituents of the atmosphere. These cosmic
ray neutrons are entirely secondary in nature.

18·

The neutrons are slowed down by collision and all
ultimately undergo neutron capture by nuclei present in
the atmosphere. It is generally assumed that virtually allof the cosmic ray neutrons result in C14 production,8 2i.e., the NH (n,p) C14 is the only reaction of importance.
However, Hess et al. 83 conclude that only 67 per cent ofcosmic ray neutrons are captured by this process, 16 percent are captured by other processes, 17 per cent leakout of the atmosphere, and 0.2 per cent are captured by·
the earth.
49. The short-term variation of cosmic ray neutron
flux with time. altitude and latitude is considerable(paras. 7,_11,_J~,_ 14, 18), making it quite difficult toobtain an average value for neutron production to be
used for the estimation of C14 production. The computation of the cosmic ray C1' production rate has been
carried out by several workers 82 - 88 who have obtained
values ranging from 1.3 to 3.1 atoms/cm2 /sec. (i.e., average 2.2 atoms/cm 2/sec which is equivalent to 3.4 X 1026
atoms cu/y/earth's surface).

CARBON-14*

44. Carbon is one of the elements that are essential to
all forms of life and thus is involved in most biologicaland geochemical processes on the earth. Associated withthe stable isotopes of carbon ( C12 and about 1.1 per centCP), there is always a very small but variable amount of
C14 , a pure ,8-emitting (E max = 0.165 MeV) radioactive isotope of carbon with a half-life of 5760 ~ SO
years. 71
45. C14 is formed upon absorption of neutrons in thenitrogen nuclei of the atmosphere. When the neutrons
involved are of cosmic ray origin, the CH formed isreferred to as ''natural", and when the neutrons originate from nuclear testing, the resulting C14 is "artificial".

50. If the average value of the cosmic ray flux. has
been constant over the last tens of thousands of years(several C14 half-lives), the c1-1 activities in the carbon
cycle would be in a "steady state" situation, for production of cu would be balanced by decay of ci~. The specific activity of CH would then be given by the following
relation:

46. Due to isotopic fractionation in most processes inwhich carbon is involved, small variations occur in therelative amounts of the three isotopes of carbon foundSpecific activity of CH(disintegrations/min/g carbon)_Production rate of CH (atoms/cm 2/min)-Carbon in exchangeable carbon cycle (g/cm 2 )2.2 x 60=
_ dpm/g,..., 16 dpm/g
81

51. Experimental determinations of the specific activity of natural C14 in the biosphere have ranged from
12.9 to 15.3 dpm/g carbon, 81)-93 the most recent measurement being 14.46 dpm/g. 89 The absolute disintegration
rate for C1 4 in pre-1900 biospheric carbon . tnay thus betaken to be 14-+- /dpm/g, which corresponds to a C14/C12
ratio of 1.20 X 10-12 •53. All these data support the basic premise that the
average cosmic ray flux has been essentially constant for
hundreds of millions of years, and that any variation over
the time period of interest for natural C14 ( 100-50,000
years) is less than a few per cent. It has been pointed out
by Stuiveru 9 that available evidence on sunspot activity(which is known to affect the cosmic ray level in theupper atmosphere) suggests some correspondence between sunspot activity and the CH concentration in theatmosphere, as indicated by tree ring measurements.95 •1®
Recent measurements of C14 variations in an 800 year
old Kauri tree show 101 a gradual increase in the C14 content of the atmosphere over the last 850 years which
could be attributed to an increase in the cosmic ray flux.
54. This natural CH in the biosphere results in a negligible e.xtemal dose-rate to man, and a larger, but stillquite small, dose-rate due to its presence in the bodytissues (para. 82).

52. The constancy of the cosmic ray flux with tim~ isof considerable interest, and three independent types ofexperiments have been carried out to give further information on this question. These three methods, which
cover different time periods, are:(a) Measurement of the C14 activity in biosphericsamples of known age (time range of several thousandsof years).s2,9f-96( b) Comparison of radio-carbon and ionium ages ofocean sediments (time range of a few thousands to tensof thousands of years). 9 '( c) Comparison of observed activities of various cosmic ray induced radio-isotopes in meteorites (time rangeof hundreds to millions of years) .98

TRITIU:II

55. Tritium, H • a radio-active isotope of hydrogenwith a half-life of 12.26 years, is, like C1 4, _continuously
beingyroduced in the atmosphere by cosmic rays, thus
3*For discussion on 0 4 see also annex F, part I.

213

giving rise to concentrations of tritium in nature. Thesenatural tritium levels have, since 1952, been modified by
the addition of tritium to the atmosphere by nuclear
weapons tests, especially by high yield fusion devices.
56. The tritium content of molecular hydrogen in the
troposphere of the middle latitude regions of the northern hemisphere in 1949-1951,1°2 1954-195610 ! and mid1959103 respectively was about 30, 300 and 1500 µµc/g H.
The resulting tissue dose-rate due to the incorporationof tritium in the body is considered in paragraph 84.
BERYLLIUM-7 AND OTHER COSMIC RAY-PRODUCEDNUCLIDES

57. Other radio-active nuclides known to exist naturally owing to the interaction of cosmic ray neutrons·with the atmosphere include Be7 , Na22 , P 32 and sis.
Of these, Be 7 , with a concentration of the order of2 X 10- 5 µ,uc/litre, 104 •105 has the highest concentration.
The tissue dose contribution from each of these nuclides
is negligible.
V. Natural radio-activity in foodstuffs

58. The natural radio-activity in soil and water becomes transferred to man via the food-chain cycle. Studyof this aspect requires measurement of activity levels inplants, some of which are used directly as human foods,
while others, such as grasses, form the principal foodof animals which in turn themselves become humanfood (F II). There is a wide range of activities in vegetation and there appears to be no simple correlation withthe corresponding activities in soil for which the range issmaller. As there is not much information regarding thediscrimination factors for the soil-food and food-man
processes, the dose-rates to particular body organs are
best related to measured concentrations in the particularorgans.
TOTAL ALPHA ACTIVITY

59. A number of measurements have been reportedof total a-activity in various dietary materials, but as thevarious daughter products in both the U 288 and Th 282
radio-active series may exist in different degrees of nonequilibrium, the individual isotopes should be identified
in order to obtain the maximum information.
60. An extensive set of data on the total a-activity offoods has been published by Turner et al.,1 00 and values
vary from less than 1 up to 1.7 X 10' ,uµc/kg of food.
In general, their measurements show low activities inmilk products, fruit and vegetables, but higher values incereals and nuts. They estimate that an adequate dietwill not contain less than 2 µµ.c total a-activity per day,but it is obvious from the large range of values ofactivity in the different ioods that small changes in eating
habits can result in a large change in the intake of radioactivity. Mayneord107 estimates that an adequate Western
diet is not likely to contain less than S JLJLC of a-activity
per day.
RADIUM-226
61. Regular three-monthly measurements108 of theRa226 content of the various foods in the average diet ofthree areas in the United States are being carried out
by the Atomic Ener~ Commission's Health and Safety
Laboratory and their results are given in table XIII.
By using the Department of Agriculture's food con-sumption figures for the United States, Hallden and
Fisenne 108 conclude that the average daily intake of Ra 226
for the two surveys in New York City, Chicago and
San Francisco is 2.4, 1.9 and 1.7 µµc respectively. Measurements of the Ra 226 in the diet of infants in New York
City109 indicate that if the August 1960 samples are
typical, then the intake of infants during the first yearof their life is 212 µ.µ.c (0.6 µµc/d) of which about onethird comes from milk and one-half from cer~s.
62. Muth et al. 62 have reported the Ra 226 content of awide variety of foods in Germany which give a rangeof activities 0.1 to 6 µµcjkg. Their values, some of which
are given in table XIV, agree very well with the UnitedStates figures in table XIII. Muth et al. estimate that thedaily intake of Ram is about 3 µµc, of which about 10
per cent is contributed through intake of Ra226 in water.
63. In addition to total a-activities for different foods,
Turner et al. 106 reported the Ram activities for a few ofthe same samples. Some of these values are given intable XV for purposes of comparison with the UnitedStates and German results. It is thought110 that the highvalues for cereals might be due to a contribution from
Australian wheat for which total a-activity content has
been reported for some samples to be higher than thatfor wheat from the United Kingdom and Canada.m
THORIUM

64. No evidence has yet been found of the presenceof Th232 in dietary materials. Mayneord and Hillm havepublished the a-spectrum of a sample of breakfast cereal
made from whole wheat. This shows the two long-lived
a-emitters, Ra 226 and Th 228 and their daughters. U 238
and Th 232 are absent and the Th 228 may therefore be
presumed to originate from Ra228 (a ,8-emitter which
therefore does not appear in the spectrum) rather thanby metabolic uptake of the element thorium. Later evidence113 on the a-activities of leaf ash indicates uptake ofRa 228 in preference to thorium. Turner et al. 106 reported
both Ra226 and Th 228 contents for twenty-three different
food samples, and the average Th 228jRa226 activity ratio
for these was 0.9.
PB210, BI21om AND Po210
65. It has been observed112 • 113 that the a-activity observed in certain samples of grass is mainly due to thepresence of Po 210 , accompanied by its parent Pb 210 (,8-yemitter). Hill114 suggests that this largely originatesfrom a process in which Pb 210 , resulting from the decayof atmospheric Rn 222 , together with a fraction of theequilibrium amount of its descendant Po 210 are depositedby rainfall directly on to the foliage. This fractionation isprobably explained by the fact that both nuclides arise
from the decay of a gaseous precursor. It is evident that
Po210 or one of its precursors, such as Rn 222 or Pb 210 . may
also be taken up directly from the soil. Since snow andeven moderate rainfall can restrict the rate of escape ofRn 222 from the surface of the soil (para. 24 above), it isclear that these factors could result in concentration of
Pb 210 , and in tum Po 210 , being produced in the top layer.
The relative uptal<:e by vegetation from the soil and fromdirect deposition on the foliage probably varies from site
to site, depending on parameters such as species of plant,
soil drainage characteristics, depth of water table below
the surface, etc.
POTASSIUM-40

66. K 40 is present in a fixed proportion (0.0118 percent) of total potassium in all natural materials. The
214

potassium content of food varies considerably-for example in the United Kingdom115 values given for a verylarge ~umber of samples of different types of food range
from 0.1 per cent up to about S per cent (0.76 µ.µ.c
K• 0/g up to about 38 µ.µ.c K.o/g). Co~sequently potassium intake will be very dependent on diet and may show
large variations between countries. For instance, Scott
Russel1 116 has pointed out that in the United Kingdom
23 per cent of the tot;;J potassium in diet originates .fro~
dairy produce and 3;, per cent from pot~toes, while m
the United States the figures have been gwen as 38 percent and 19 per cent respectively. The potassium intake
for the United States based on per capita food consumption has been calculated to be approximately 2300µ.µ.c/d.111, us

cent of the a-emitting radio-active material is in the soft
tissues. 107
RAnIUM-226

VI. Natural radio-acthity in the human body

70. Ram is taken into the body through food, water
and, to a lesser e.-.;tent, air (para. 36). The total Ra 226
content of normal human bodies has been determined bya number of workers, and values ranging from 3-1400µ.µ.c obtained. These results are summarized in table XVI,
along with data regarding the number of samples measured, and the average Ra 326 content of dri?king waterin the area from which the samples were obtained. Where
results are reported in terms of activity per gram ash,and individual total ash values are not given, it is assumed that a 70 kg man produces 2600 g skeletal ash and
400 g tissue ash. The results. show5 ' some co~relation
with the Ra 226 content of drinking water when thts source
is predominant.

67. The e."'(tremely low levels of naturally occurring
radio-activity normally present in the human body makemeasurement of the individual radio-isotopes very difficult. In vivo, measurement of gamma rays is often used
to measure the body potassium content. The total bodyRa 226 content can be estimated by measuring the rate ofexhalation of radon and assuming a general value forthe fraction of the total radon formed which escapes inthe breath. This fraction is not accurately known andmay indeed vary under different conditions. Ra226 andother nuclides can also be estimated by the analyses of
autopsy samples.

71. Wal ton et a/. 121 measured the Ra228 concentrations
in samples from up to 11 bones from each of 11 bodies
in order to determine the variation within the skeleton.
They concluded that there is no systematic difference inthe radium content of the various bones of the averageskeleton at least to within -+- 15 per cent. Departuresfrom th~ mean of up to SO per cent do occur in a few
specimens. However, this degree of consistency within
the various bones was not confirmed by Holtzmanu 2 inhis measurements of both the Ram and Pb 210 content
of five bones from each of three persons who had beenborn in different states in the United States. These result? are given in table XVI!.

TOTAL ALPHA-ACTIVITY

68. Turner et al. 119 measured the total a-activity ofbones of persons native to Cornwall, London and Cumberland. The average value is 0.38 µ.µ.c/g ash, but individual results show large variations (figure 3). Thereappears to be a significant difference between values forCornish bones and those from the London area or from
Cumberland. The total a-activity in 10 Eskimo bones 107
showed a range from 0.18-0.97 µ.µ.c/g ash with an average of 0.61, and the rib of an Egyptian107 who died almost
4,000 years ago gave a value of 0.34 P.J!'C/g ash. Figure 3
indicates that for persons not occupationally e.-.;posed toa-activity, the concentration does not vary with age, but
as the weight of the skeleton increases from birth toadult so the total a-activity in the skeleton increases inthis period and then stays constant.

'! 1.0

•

s
.a

.

1"I

8. ..

~

o.s

•

•

:f)
i:

•

•

0

x ox~ o •
~ 8x
Xx

I
"l$'

~

•
•
• • ~•• ••

x

0
lfl

·:o

30

4JJ

50

60

70

•

80

90

100

72. There is a distinct possibility that measurementson teeth may be used as an indicator of Ra 228 bone levels,
particularly if water concentrations are constant in thearea. Lucas 64 found a value of 0.10 µ.µ.c/g ash for the
average of Ra 226 levels in teeth for nine persons which
was almost identical to the 0.11 µ.µ.c/g ash found for bonefrom residents from the same city. The total a-activity
levels in teeth obtained from the Royal Dental Hospitalwere also very similar to those in bones from persons
who had lived in London. 107 Further, the activity of teeth
from the inhabitants of Niue Island, 123 an area of highnatural radiation (see section VII below), is of the orderof ten times that of teeth from the inhabitants of normal
areas.
73. The relative concentrations of radium in the skeleton and body tissues is uncertain. Muth et al. 62 suggestthat 25 per cent of the total body radium is contained in
the skeleton whereas Hursh et al.m give a figure of 78
per cent and LucasG• 80-85 per cent. Results given by
Hi11110 also tend to support this higher figure. The results for bone and muscle ash and wet tissue are given
in table XVIII. No explanation has been given for the
relatively high tissue values obtained by Muth, but total
a-activity values in bone and soft tissue (para. 69)
favour a skeletal content of about 80 per cent of the total
body value.

74. Consideration of the above information indicatesthat the world average for the Ra226 total body burden is
likely to be closer to 50 µ.µ.c than 100 µ.µ.c. In subsequentconsiderations, we will assume a conservative value of
75 µ.µ.c, of which 80 per cent ( 60 µ.µ.c) is in the skeleton.

·Age (years)

Figure 3. Human bone ash, total a activity. e. Cornwall;
X, London; 0. Cumberland

69. Mayneord120 finds a large variation of activity for
different soft tissues. 0.15 to 1.00 µ.µ.c/g ash, but the
average value of 0.52 µ.µ.c/g ash agrees very well withthat obtained for skeleton ash. This leads Mayneord toconclude that in the normal human being, about 25 per

THORIU:M

75. The presence of Th 228 in human tissues125 has been
demonstrated by means of a-ray spectroscopy, but, as215

with plant tissues (para. 64), the parent isotope of thethorium series, Th 232 , has not yet been detected. It istherefore thought 12 ~ that the Th 228 originates from themetabolic uptake of radium in the form of Ra228 rather
than uptake of thorium. Because the half-life of Ram
is considerably less than that of Ra226 , it may be expectedthat the Ra 228/Ra226 activity ratio will be a maximum in
newly fomed bone and will be less than this value inolder bone. The magnitude of this effect is not known
and, indeed, it does not appear to be sufficient to introduce an age effect into the total a-activity content ofbones (figure 3). Mayneord et al. 125 suggest that 40 per
cent of the total a-activity in adult bone is due to radiothorium, i.e., Th 228jRa226 series activity ratio is approximately 0.7. Measurements reported by Stehney128 onashed bone samples from six subjects (average Ra226
skeletal content of about 90 µ.µ.c) gave an average
Th 228jRa226 series activity ratio of 0.4. This value israther uncertain owing to the large fractional errors in
the Th 228 measurements. Using thoron in breath technique, Cullen121 has found indications of much higher
Th 228 content of normal persons. It will be assumed thatthe world average Ra228 total body content is 50 µ.µ.c, of
which 40 µ.µ.c is in the skeleton.

the bone. The results for the average Ra 226 and Ra228
contents, suggested in paragraph 77 and assuming 35 percent and 100 per cent equilibrium respectively, are given
in table XIX. Also included in the table are the estimateddose-rates to the same tissues resulting from a skeletal
Pb 210 content of 200 J.Lp.C ( 50 per cent equilibrium). The
average dose-rates to the body tissues other than bone,
assuming that the Ra 226 , Ra228 and Pb 210 activity is uniformly distributed and that the activity levels are 25 percent of the values assumed for the skeleton of an average
individual, are about 0.5, 0.8 and 0.3 mrem/y respectively from each of the above radio-isotopes. 130
POTASSIUM -40

79. In viva measurements of total body potassium
content have been made by a number of workers. The
results of measurements by Anderson et al.1 31 for L590
males and females as a function of age of the subject are
given in figure 4. The concentrations vary considerablywith age, and above an age of twelve years, a sex difference appears. Beyond twenty years of age, the percentage
content in both males and females decreases in a similarmanner but the male level is about 20 per cent higher
than the female.

Pnz10, B121om AND Po210
76. Various workers have determined Pb 210 , Bimmand Po210 concentrations in human bone in excess of that
expected from the Ra226 content. Holtzman122 mademeasurements on samples of individual bones fromforty-four humans and found an average skeletal Pb210
content of 360 µ.µ.c (corresponding mean Ra!?26 content
was 100 µ.µ.c).He concluded that the origin of this Pb 210
was mainly from food, to a slightly smaller e.."{tent fromthe atmosphere and a minor contribution only fromdrinking water. Hursh128 obtained a value of 105 µ.µc
for the mean skeletal Pb 210 content of eighteen cadavers
obtained in the New York area (average Ra 220 content
was 120 JLP.C). Hill and Jaworowski129 measured thePb 210 content of bone samples from six subjects andfound an average skeletal content of 160 µ.µ.c. It will beassumed that 200µ.J.LC Pb210 is the skeletal content of an
average person.
DOSE-RATES FOR NATURALLY OCCURRINGU AND TH SERIES

77. From the available data on natural radio-activity
in humans, the average skeletal content of Ra 226 , Ra228
and Pb 210, each in various states of equilibrium with its
daughter products, has been chosen as 60 p.J.LC, 40 p.J.LC and200 µ.µ.c respectively (paras. 74-76). The range of values
for individuals is extremely large, e.g. for Ra226 it may
be higher or lower than the average value by a factor
of at least 25 (table XVI). However, for a population
in a given small area, the range is likely to be muchsmaller.
78. The dose-rate to bone due to the naturally occurring uranium and thorium series is mainly due to thealpha-emitting components, and hence the irradiation
pattern is extremely variable and depends on the size ofthe particular tissues being considered, their relation to
the radio-actiYe deposit and the ranges of the alpha particles. Spiers130 has calculated the dose-rates to the osteocytes, the connective tissue lining the walls of the Haversian canal and the bone marrow originating from theRa 226 and Ra 226 content of bone on the assumption that35 per cent of the Rn 222 and Rn220 formed is retained in

2.5

.i

..

~ 2.0 0
0

'::I

~
"

~

~ 1.s

.

l!
0
p..

•

o Males• Females

1.0 L.L.L.&..&..L.L.L.JL.L.J!..l..lu...&..L...L.........................................'-'-'...............................
0

10

20

30

40
50
Age (years)

60

70

80

Figure 4. Average body potassium concentration of males andfemales as a function of age of subject

80. The potassium content of the various body organs
varies considerably from about 0.05 to about 0.31 per
cent, and the average for the whole body is about 0.2 per
cent. 132 There is evidence that the potassium content ofgonadal tissue is close to 020 per cent by weight, andusing this figure, Rundo133 estimates that the dose-rate
to the testes is 17 and 2 mrem per year from the /3- andy-radiation respectively. This is in good agreement withthe values of 16.5 and 2.3 mrem/y given in the 1958 report of the Committee and 18 and 2 mrem/y by Spiers. ~ 2
81. In trabecular bone, Spiers53 quotes the potassium
content as being between a value of 0.05 per cent formineral bone and a value near to 0.2 per cent for bonemarrow, and gives the mean dose-rate as 15 mrem peryear.
CARBON-14

82. The tissue dose rate due to natural C14 has been
given as 1.0 mrem/y, 52 1.5 mrem/y13 ' and 1.6mrem/y, 135
the difference between these values being essentially due
to the values assumed for the specific disintegration rate216

of natural CH and the average beta energy per C 14 disintegration. Taking 14 dpm/g carbon as the specific disintegration rate (para. 51), 50 keV as the average C1'beta energy136- 138 18 per cent1 as the average carbon content of the \vhole body of 70 kg weight, REE equal to 1,
then the average dose throughout the human body due
to natural cu is 1.06 mrem/y. The corresponding average dose-rate to soft tissue, with a carbon content of
12 per cent, 139 is 0.71 mrem/y, and to bone, with a carbon
content of 27.8 per cent, 139 is 1.64 mrem/y.
83. Owing to the Suess Effect (F I 68) the dose reduction during the period 1850-1954 was approximately
one mrem (about 0.01 mrem/y). If the use of fossil
fuels up to year 2000 is as has been estimated,1' 0 theSuess Effect will then be nearly 10 per cent and the dose
reduction over the period 1850-2000 would be approximately four mrem.
TRITIUM84. The natural level of tritium in water in the middle
latitude regions prior to the introduction of tritium due
to weapon testing was of the order of 0.005-0.02 µ.µ.c/g
H.Hl-'.l·u Assuming soft tissue to be 100 per cent water,
and that the average energy of tritium beta rays is 6 keV,
this implies an average dose-rate to soft tissue of about
0.003 mrem/y (REE= 1.7) or 0.006 mrem/y if an
REE of 3 is used (para. 3).6
VII. High natural radiation areas
85. In a small number of areas the dose-rate from natural background radiation is considerably higher thanthat experienced by populations in the major portion of
the world. This high radiation background is due to thepresence of larger than normal amounts of naturally
occurring radio-active materials in the soil, drinki~gwater, air, building materials, etc., and al~o to th.e cosmic
ray altitude effect {paras. 1_3 an~ 14). It 1s cons1der~145
that studies of the populations m these areas are hkely
to contribute to the fund of biological knowledge and theultimate specification of the genetic risks accruing fromincreasing exposure to ionizing radiation. This type ofstudy is one of the few ways of studying the effects ofionizing radiation on human hereditary material.

represent a continuous source of radiation exposure tolarge populations.
90. In those areas where the drinking water is ofhigher than normal activity, the populations are receiving
additional radiation exposure and may be of interest forstudy of possible biological effects. One such area wherea detailed survey is currently being made is in the Middle
vVest region of the United States. Some of the drinking
water in this area originates from wells which penetrate
the deep sandstone formations and the water has concentrations up to 37 µ.µ.c Ra 220Jl. Results reported so
farm indicate that drinking water containing more than
1 µ.µ.c Ra226/l is consumed by approximately 800,000
people, of whom about one half consume water containing more than 4 µµ.c Ra 226jl. Of these, about 30,000
people consume water with activity in the range 10-37µµ.c Ra226Jl. The resulting range of Ram skeletal burdensM in people who have been consuming this water forlong periods of time is given in table XVI.
HIGH NATURAL RADIO-ACTIVITY IN THE AIR

91. The Rn 222 and Rn 220 content of air will generally
be higher in areas of higher than normal natural radioactivity. For instance, the average Rn 222 concentration at
Bad Gastein, 148 which is situated in a deep valley containing many radio-active springs, is about 1 µ.µ.c/1 comparedwith the average value of about 0.1 µ.µ.c/l for the European continent. Also, concentrations in confined volumes
such as buildings will be considerably higher if ventilation is poor or absent. Under certain meteorological conditions, e.g., during fog, the natural radio-activity concentration in the air may increase by several factors often.
HIGH NATURAL RADIO-ACTIVITY IN BUILDI~GS

92. Aside from high radiation in buildings due to theincreased Rn 222 and Rn 220 content of the air (para. 91),
dose-rates may be increased owing to the high naturalradio-activity of the construction materials. Granite andlight-weight concrete containing alum shale are common
building materials which often result in particularly highradiation levels inside buildings, as can be seen from thedose-rates give in table V.
HIGH ALTITUDE AREAS

li:rGH NATURAL RADIO-ACTIVITY IN THE EARTH'S CRUST

93. As discussed in paragraphs 13 and 14, the cosmic
ray intensity increases markedly with altitude. This raises
the possibility of study of populations living at al~tudesof the order of 3,000 metres where the total cosnuc ray
dose-rate due to the neutron and ionizing components
may be of the order of 50-150 mrem/y. Table XXI gi"."essome of the high altitude areas in the world ~long with
their altitude, latitude, population us and cosmtc ~y contribution to tissue dose-rate estimated on the basis of the
figures given in table I.

86. There are five known major inhabited areas where
there is increased radiation from soil or rock-these arein Brazil, France, India, Niue Island and the United
Arab Republic. Data on the size, population and doserates of these areas are given in table XX.
87. The Kerala radiation measurements1 '° were madeinside three main types of houses in ten villages in thearea. The results did not show any clear relation between
radiation levels and structural differences in these houses.
The average gamma dose-rates in the .viJ!ages includedin the survey revealed a twenty-fold variation (131-2,814
mrad/y), and .the. average value of 1,_300 mrad/y. is
obtained by we1ghtmg values for each village according
to its population.
88. There also exists the possibility of an additionalsignificant radiation dos~ ~o the ~opula.tions ~n these ar~asdue to internal deposition ot radio-active material.
No published material on this aspect is available atpresent.
89. Certain natural springs have a very high naturalradio-activity content and some of these are listed intable VII. However, these springs are not generally used
as a permanent source of drinking water and so do not

VIII. Summary of exposure data
94. The mean gonad and skeletal dose-rates from natural sources of irradiation under "normal" conditions
are given in table XXII. (For information on highnatural radiation areas, reference should be made tosection VII above.) The suggested typical value for ~etotal cosmic radiation tissue dose-rate, 50 mrem/y.. 1s
the value at sea level for middle latitudes (para. 8 andtable I). The terrestrial gamma-radiation results fromthe gamma activities present in the soil, buildings andair and the average tissue dose-rate of 50 mrem/y takes
int~ account absorption of radiation by the outer tissues
217

and also the relative time spent indoors and outdoors.
Internal irradiation of man arising from the presencein the body organs of naturally occurring radio-active
nuclides-K.o, C1 4, H 3 and various decay products of
the uranium and thorium series-is extremely dependent
on geometrical considerations and average dose-rates invarious tissues are given in table XXII. The dose-rate
to the lungs due to the natural radio-activity content of
the air is not presented in table XXII but, as mentioned
in paragraph 42 above, this dose-rate is higher than thatto any other body tissue. The dose-rates due to H 3 arevery small in comparison with those due to the radionuclides given.
95. The total dose-rates in the body tissues given intable XXII may be considerably in error owing to uncertainties of the individual components. These uncertainties are discussed in the text of the present annex,
and it is anticipated that more truly representative values
will become apparent as further investigations are made.
It is felt that where a representative value for the natural background dose-rate to individuals in "normal"
TABLE II.

areas is required, the best value which can be recommended at the present time is about 130 mrem/y.
TABLE I.

VARIATION OF TOTAL COSMIC RAY COZ.."TRIBUTION TO
TISSUE DOSE-RATE WITH ALTITUDE AND L.<\.TITUDi:

Total cosmie radiasion tisme
dos• ras. in mrem/:I"

Altilauk(km)

0 •••.......•...•........
1. ..................... .
2 •.••••.••••••••...•..•.
3 ..•.•.•.•..............
4 •.••.....•.............
5 .........•.............
10 ...................... .
15 .•.....................
20 .......•..•............

35
60
100
170
26-0
400
1,400
3,000
3,500

40
70
130
220
360
580
2,300
5,000
6,000

50
90
170
300
500'
800
~.500

11,00014,000*See annex A for RBE values used.
•• Distinction between geographical and geomagnetic latitudes
is not justified.

PHYSICAL DATA FOR RADIATION FROM CERTAIN NATURALLY OCCURRING RADIO-ACTIVE NUa.IDES 149

NuclithCommonSymbolHa .. ••····

Be7 ••••••••

cu ........

Na 12 •••••••

pn ........

5" ........
K'o ........
Rbn •••••.•
1..a1n .•.•..
Sm1u •.•.••
Lune.• ....

u=• .......

ThS3• •.••••
Pa•mi •.••.

u:u• .......

Th:UO. • • • • •Rat21 •..•.•
Rn:ll, •.•.•
Po"'· •.••.
Pb 114 ••••••
Bin• •••...•

Po114 ••••••
Pb 118 ••••••
Bi:10m .•••••
p 0 210 • • • • • •Th:t1 2 ••••••
Ratn •••.••
Ac121 ••••••
Th:n •••.••
Rasu •••••.
Rnno •.....
Pone ...•.•
Pb 211 • • • • • •Bi:U ...•••.

pons ......
TklDI •• •, • •u:w .......
Nps"' ..••..
Pu 21 ~ • • • • • •nameTritium
Beryllium-7
Carbon-14
Sodium-22
Phosphorus-32
Sulphur-35
Potassium-40
Rubidium-87
Lanthanum-138
Samarium-147
Lutecium-176
Uranium I
Uranium X1
Uranium X2
Uranium II
IoniumRadiumRadon
Radium A
Radium B
Radium C
Radium C1
Radium D
Radium E
Radium F
Thorium
Mesothorium I
Mesothorium II
Radiotliorium
Thorium X
ThoronThorium A
Thorium B
Thorium C
Thorium C1
Thorium C 11
Uranium-235
Neptunium-237
Plutonium-239

Radio-utir1
half-life

12.26 y53 d5,760 y2.58 y14.3 d87 d
1.3 x 10'y
4.8 x 101Dy
1.1 x l()lly
1.2 x l()lly
2.2 x 101 8y
4.51 x 10'y24.1 d
1.18 m2.50 x 10'y
8 x 10'y1,620 y3.823 d3.05 m26.2 m19.7 m
1.6 X 10- 4s
20y
5.0 d
138.4 d1.41 x 101Dy
6.7 y
6.13 h
1.91 y3.64 d55 a0.16 s10.64 h60.5 ~
3 X 10-1s
3.1 m
7.1 x 108y
2.2 x lO'y
24,300 y

Parlicl• enerties in MeV
and percentaies 'IJ'Me .i:..own*

p- 0.0186(100)EC
p- 0.165(100)p+ 0.54(90)EC(10)p- 1.71
p- 0.167
p- 1.32(89)EC(ll)p- 0.27
EC(70), p- 0.20(30)a2.20
p- 0.42(100)a4.19, -, CE, SF
p- 0.19(65), 0.10(35)p- 2.31, -(99), IT(!)
a4.77(72), 4.72(28), -, SF
a4.68(76) 4.61(24)a4.78(95), 4.59(4), a5.49(99+), 4.98(0.08), 4.83
a6.00(99 +) p- (0.02)
P-1.03(6), P- 3.18, -(99+)a5.51, -(0.04)
a7.68
fr 0.017(85),0.063(15)P- 1.16(99+ )a(0.02)
a.5.30, a4.01 (76), 3.95(24)p-<0.02
p- 1.11 (53), 0.45-2.18
a5.42(71), 5.34(28), a5.68(95), 5.44(5)a6.28(99+ ), 5.74(0.3)
a6.78{3- 0.34(84), 0.58(12), p- 2.25, -(64), a6.09, -(36)a8.78
p- 1.80(47), 1.~2.38
a4.18-4.56, SF
a4.52-4.87
a5.15(i2), 5.13(17), 5.10(11), -, SF'Y energi., ;,. MeV andfleruntaiu trlaere knoins*

No.,,••
0.477(12)No 'Y
1.28(100)
No 'Y
No 'Y
1.46(11)
No 'Y
1.43(70), 0.81 (30)No 'Y
0.31 (100), 0.20(100), 0.088(100)0.048(23)0.092, 0.063, 0.029
0.043, 0.23-1.83
0.053, 0.118
0.068, 0.142-0.254
0.187(4), 0.51 (0.08).
No 'Y
0.352, 0.295, 0.053-0.259
0.61, 1.12, I. 76, 0.45-2.43
No 'Y
0.046(15)No.,,
0.80(0.001)
0.059(24)No 'Y
0.057' 0.10, 0.91, 0.078-1.64
0.084, 0.212, 0.137, 0.169
0.241 (5)0.54(0.3)
No 'Y
0.239(84), 0.30, 0.115-0.41
0.040(25), 0.73(6), 1.62, 0.124-22
No 'Y
2.61 (100), 0.58(77), 0.51 (30), 0.040--1.09
0.185(55), 0.143(12), 0.095(9), 0.074-0.38
0.087(14), 0.029(14), 0.057-0.200
0.013(17), 0.051. 0.038-0.42( <0.001)

inten!itiei rather than photon intensities; they also include conversion-electron intensities.
•• "No 'Y" means that gammas have been searched for but notfound (excepti~ perhaps X-rays from electron capture).
C E =conversion electron.
E C=electron capture.
I T=isomcric transition.
SF ~spontaneous fission.

•Beta and gamma energies (MeV) are limited to four plus a
range, given in order of decreasing intensity. When known, thepercenta~ of disintegration (intensitv) giving a particular energy
appears m parenthesis following the energy. The dash between
two energies indicates that there are three or more radiations inthat range of leeser intensities than those already given. A dashfollowing several energies indicates additional energies of lesser
intensity. Percentages applied to gamma energies are transition

218

TAllLE III.

u:ss, Tg232, RA 226 AND K•O CONTENTS IN µ.p.c/G
IN VARIOUS ROCKS (MEAN VALUES)

Type of rockU'"

Igneous rocks •........................ ·{

1.4

Tli"'

Ram

K"

1.3
3.5
2.3

1.3

22
25
29
30

0.5

Granite• ••.•...•.....•.....•••.....•.

·l

3.7
3.1

1.4

3

2.6
13
1.0

1.1

Basalts .••.....•.........••••. , .....• ·{11

8

TABLE IV.

0.9
5......, 3
""15
0.25

0.4

0.7

0.5

0.15
0.1

0.5

22
40
20
4
8

0.1
0.17
0.14

0.7
0.3
0.4
0.7
1
60
60
0.4

38
150
151
41
57
152

153
154
41
57

153

0.5

Volcanic rocks:
Basic lavas ...••......•••..•..•......
Acidic lavas •......................••
Sedimentary rocks ..•......••••.....•..
Sandstones ..•..........•..••........
Sandstones •.•..•.•.••.•.••••.•••.•.•
Limestone .••••......••.••...•..•.•••
Limestone ..•.......•.••••..•........
Limestone •••...........•.•••.••....•
Alum shales, Sweden •........•.•••...
Alum shales, Sweden •.•...•••........
Shales .•............•••.•••..•...••.
Bituminous shale, U.S.A....••••..•...
Phosphate rocks, Florida ...•.....••..•
Phosphate rocks, Nauru •.•...••..•..•
Phosphate rocks, N. Africa .••••.......
Phosphate rocks, N. Africa •••..•......

&/treriu

9

2.3
2.5

2.5
29
2.3

155
155
153
150
41
150
41
42
41
42
150

152
152
156
153
57

0.8
1.0

MEASURED TERRESTRIAL GAMMA DOSE-ii.ATES OUT OF DOORSIN VARIOUS COUNTRIESCountry

Austria .......•.•.••....•.......
France •.•.........•.........•...
Japan •.•............•.....••••••
Sweden• .•.•••...••...•.••....••
UK .•.•....••..•.....•...•...•.•
USA* ...•••••••...•.•••...•..•.

Dou rau in air
mra'IY

Commenl

47-56
45-90
{180-350
23-37{ 79-11970-10060-120{ 50
18-01{ 77-15545-130Limestone
Granites and shales
Kanto loam
Granite areas
Stockholm street
Igneous rocks
Clay
Sedimentary rock or clay
Granite areas
Measurements in 23 States

157
158
159
159
160
160
160
53
53

161

•Values obtained by subtraction of an experimentally determined value of 28 mrad/y toallow for cosmic radiation at sea level and appropriately larger quantities at various altitudes.
TABLE V.

Counlr1

Austria .••••••.•MEASURED TERRESTRIAL GAMMA DOSE-RATES IN AIR INSIDEBUILDINGS IN VARIOUS COUNTRIESDose rale in air
mrad/y{ 47-56
65-75

75-112
Japan ••••..••...
Sweden* .•......
UK ••••.........
USA .........•.

{ 48-68
29-1-180-100{ 48-57
99-112158-202{ 85-300
32-57
29-90

Commenl&fere11U

Wooden house
Brick or conc.-ete
GraniteConcrete
Wooden (Tokyo)
Wooden (Kyoto)
WoodenBrickLight weight concrete (containing alum shale)
GraniteOther than granite
17 houses in New York area

157
157
157
162
159
159
42
42
42
163
163
161

*Values obtained by subtraction of 28 mrad/y to allow for cosmic radiation (but this correction is probably too large in the case of multistorey buildings).

219

TABLE VI.

MEAN DOSE·R...TES FROM TERRESTRIAL GAM:!>fA-RADIATIO:-l 01'.L.Y
IN FOUR LOCALITIES IN UNITED KINGDO:!>f53.1-ftan dose•ral<in air.Uean dose-rak in h11man
tissues
mrad/-ymrad/yL«a1ily

Edinburgh ....................... .
Dundee .......................... .
Aberdeenshire .................... .
Aberdeen .....•.................•.

TABLE VII.

0..1 of doers

In houses

48.5
63.0
69.5
104.0

60.0
67.2
81.5
85.3

36
42
50
57

37
43
51
58

NATURALLY OCCURRING RADIO-ACTMTY IN PlJl!LIC WATER SUPPLIES

Water source

RD"' co1uentralion µµc/l

Austria Bad Gastein ......... .
Germany, 7 cities ........... .
Sv.-eden, 2 cities ............. .
UK, ground andsurface v;ater ............. .
Cornish waters ............ .
Devon waters •........•....
USA, tap waterfor 41 cities .•..............
Deep sandstone well, Ill.* .. .
Surface water, III .......... .
USSR, freshwater, (mean) .... .

0.6
0.03-0.3
0.2-1
Up to 0.7
Up to 2.4

Rnm concentration ,,µc/l&/erenu

Up to 220

167
62
169

Up to 200
Up to 3,000
Up to 13,000

61
61
170

Up to 0.2 (average 0.04)
Up to 37
< 0.2

171
172
56
173

•See section VII.
TABLE VIII.

NATURALLY OCCURRING RAD!O-AC!MTY OF NATURAL WATERS AND SPRINGS

um

Ran•
conuntralionµµc/l

conuntration
pµ&/l

Wakr source

Germany, river water •........
UK, river water .•............
US.>\, river water ............ .
Lake water ................ .
Ground water ............. .
Austria, springs ..•............
France, springs .............. .
Germany, springs ............ .
Japan, springs ............... .
Lebanon, springs ............. .
UK, springs ................. .
USA, springs ................ .
USSR, springs and brooks ••....

TABLE IX.

0.07-0.8
0.01
0.03 (1-3)31

0.005-0.01
1.7
Up to 40
Up to 4Rnm
concentration
pµc/l

0.2-0.3

Up to 22Up to 1390.07-18

Up to 0.3 17
Up to 12Up to 10'
Up to 10'
Up to !OSUp to 7 X Hl'
Up to 6 X !OSUp to 7 X 10:
Up to 3 X 105

Up to 3

Reference

62
164
57
57
165
166, 167
158
62
153
39
61
153
168

CoNCENTRATIONS OF RNU2 AND RN220 L"i FREE All!.
AT GROUND LEVEL IN VARIOUS REGIONS

Average co11ce11tratio11 in µµc/l
Rn"' (radon)

Country

Austria ................................. .
Czechoslovakia .......................... .
France ............................ ···· ..
Holland (Amsterdam) .................... .
Sweden ................................. .
UK .......................••.............
USA ..•................................. {USSR ••........................•....•...

0.1-0.3
0.03
0.2
0.13
0.1
0.3
Up to 3(smog conditions)
0.25
0.005-0.5

220

Rn"' thoron

0.002
0.006

0.004
0.05

Re/ere nu

157
69
158
174
42
53
175
175
173

TABLE X. AVERAGE CONCENTRATIONS OF R.N~ 22 AND R.N22D IN AIR OF VENTILATED A2'1l
U!.'VENTILATED SWEDISH APARTMENTS AND THE CORRESPONDING CALCULATED
AVER....GE DOSE RATES TO LUNGS~2
Awage concentralion in p,,,:/lArerate dose rak IO lungs in mrem/yRnU•

Wood .•....•••.•.........•.....•
Brick .•••••...•..................
Light weight concrete(containing alum shale) ...•...••.

R11 2n

Rn"'

A•

,a-

A•

sea

0.527
0.909

0.537
0.913

0.02780.0910

0.136
0.450

263
453

73
128

185
582

52
173

1.86

1.86

0.0959

0.461

930

262

640

178

**Condition B: High ventilation rate, 10-1 sec. -1,• Condition A: As..-uming equilibrium.

TABLE XI. AVERAGE RN222 CONTENT INDOORS AT v.uious LOCAUTIES42
A rerage Rn concentration

Counlry and locakA•erate Rx conunkalUmp,,,:/lCounlry and local.

Canada, laboratory ••••.•.•••••••••
UK .•....••.•••••...........•...

0.05-30.08

Sweden:Wooden apartments ••.••..••••..

0.5

Brick apartments .....•••.....••
Concrete apartments ••.•....•..•
USA, laboratory ••••.•..•......•..
USA, laboratory .••••••...•.•.....
USA, laboratory ••••••••.••.....•.

,,.,,.e/I

0.9
1.9
0.9-1.0<0.1
0.13

TABLE XII. AVERAGE CONCENTRATION OF PB210, BI21om AND Po21D IN AIR AT GROUND LEVEL IN VARIOUS REGIONS
Regi<mRnlll tloS<ghld #oducl

A oerate coneentralion
in air ,,.,,ell

Referenee

Pbno
Pb SIDPb210

3 x 10-1
10-li
5 x 10-1

176
70
173

UK •••••••.•....
USA •••••••.••..
USSR •••••••••••

RegionRn"' tlowihler #oducl

Arerage coneentrationin air p.p&/l

Rt:/ermu

Binom
Pono

4 x 10-1
0.4 x 10-1

173
176

USSR ••••.•••..•'CK ••.•...••....

TABLE XIII. RADIUM-226 IN FOODSTUFFS (µµc RA226 PER KG ORIGINAL MATERIAL)

Food 1ype

Whole wheat bread .••...
White bread ••••••••.••••
Flour-white •••••••••••.
Milk-liquid .••••••..•..
Potatoes .•••.•.•..•..•••
Macaroni. .••.••••.•.••.
Dried beans .............
Canned vegetables .•••..•
Fresh vegetables •••••••.•
Root vegetables •••••••.••
Canned fruit ............
Fruit juices ••••.••.•.••.
Fresh fruit •.•••...••.•••
Rice •••.••••••••...•.•••
Eggs ........•..••••..•.
Fresh fish ..•....••..•..•
Shellfish ••••.••..••..•••
Meat ........••..•.•.•.•
Poultry .•...••.••.•• • .•.

San Francisco

Chicaio

N<VJ York Cily

SJUWY 2
Ju,..1960

Surwy J
Otl. 1960

Swney 1
!Jay 1960

3.2
3.2
2.7
0.25
2.0
2.1
6.1
2.2
2.4
3.4
0.37
1.6
1.5
1.5
4.1
1.2
1.2
0.44
0.73

1.2
1.5
1.7
0.24
2.5
1.8
3.2
0.54
1.2
2.3
0.37
0.49
2.8
1.0
7.9
0.68

3.5
3.3
2.4
0.24
1.4
1.6

Sunty 2
&pl.1960

Suney 2
Aut.1960

Suney J
Jan.1961

2.9
2.0
2.0
0.22
0.77
1.9
2.5
1.1
0.57
1.8
0.26
0.86
0.57
0.37
2.1••
1.0
1.7
0.64
1.4

2.8 ..
2.9
1.34
0.22
1.0*
1.2
2.3
0.91
0.66
2.6*
0.5
0.71
0.91
0.63
2.6
0.8
2.0
0.81
1.9

2.8
2.5
0.83
0.2
2.0
1.7
4.1
1.0
0.84
2.4
0.73
0.62
0.65
0.8
1.9
1.2
1.0
0.55
0.49

1.0•
1.8
2.2
2.0•
1.2
0.68
1.4
0.7
2.7
0.71
2.5
0.45
0.79

1.1

0.47
0.86

•Data corrected by barium recovery as well as strontium recovery.
••Missing sample. Paired value used for computing sums.
TABLE XIV. RAz26 CONTENT OF VAJUous FOODS rn GEIW.ANYilz
Food

Bread ...•....•..••...•.......••.•\\''bite bread •••.......•...•......••
Wheat flour .••••••••....•••......•
l\lilk ..............•.....••.••...•
Potatoes ........................ ..
Cabbage .•••••••.•••.•••••••••••••

l'IJ&/k/l

food

food

,,.,,.;kg food

2.6
1.7, 3.3
2.7
0.3
0.6, 1.0
1.0, 2.4

Carrots
ApplesEggs
Fish
Pork, beef
Tap water

1.6, 1.7, 6.1
0.9
3.1
2.8, 4.0, 4.0, 6.3
0.8, 1.5, 0.8, 0.8
0.03-0.34 (av 0.19)

221

T ABU: XV.

RA22G COh"TENT ot VARIOUS FOODS IN UNITED KINGDOMle>eFood

ppe/l<tfood

Food

25, 62, 68
1.1
2.0

Cereal .•••...•..•.....•.•................•.•.
Tinned pears .............................••..
Egg., ........................•.•.......••.•.

TABLE XVI.

Sa111pli111 locality

N um/Jar of bo4ies

USA, Rochester, N.Y.................
USA, Rochester, N.Y.................
USA, Rochester, N.Y.................
USA, Northwest Pacific area •••.......
Germany, Frankfurt on Main ••.•.....
Germany, Frankfurt on Main ......... ,

20•
14•

p.p.e/lt.t foodFresh fish (plaice) .••.•.......••.............•
Cockles and mussels .•.•....••....•.......•...
Veal, Sausage ••••.•...............•••..••••..

TorAL B-ODY RA!2B CONTENTS

Co11U1tlTalionRa"'ix lap uattr

950
15
Up to 56

Ra"' body coalelll p.p&

ppe/I

Raxte

Mean

0.04
0.04
0.04
0.001
0.14--0.31
0.2

38-35347-13015-Q513-139130-790

0.04

3-150

118
87
30
47
330
130
(35 inekeleton)
24

USA, Prisoners, 4 mo. detention •.•..••

140
21
499
15 samples
11

3.4

100

USA, Prisoners, 7.6 yr. detention .•••.•

8

3.4

202

US..\, Prisoners, 19.7 yr. detention •...•

11

3.4

236

US..\, Lockport boys .................

8

8

368

USA, Chicago boys .••..•...•.......•

7

0.03

36

USA, low activity water ..•..••.......
USA, high activity water .•...•.......

42
34

< 0.1

USA, New York •••••••.••••....•••••
Six different countries .•••.••.•...•..•
13 different countries., •..•.•.....••..

1.5
18.2, 5.7
0.9, 2.0

ro
33

15-81
36-1400

0.1-10.5

36

TYP• of sample

Rl/n-tnu

Whole body ash
Whole body ash
Body organ ash
Whole body ash
Body organ ash
Body organ ash

177
178
124
179
180
62

Whole skeleton ash
Single bone ash
Bone ashcomposite sample
In vi1Jo, radon inbreathIn rivo, radon inbreathIn vi1Jo, radon inbreathIn vi1Jo, radon inbreathIn vivo, radon inbreathSingle bone ash
Single bone ash

121
121
121
181
181
181
181
181
54
54

" Check series using different methods of measurement.
TABLE XVI!.

RA 2 26 AND PB 2 10 IN B-ONES OF SUBJECTS FROM ROCHESTER, N.Y., USA1 2Z

Concentralio11 ir: (ppc/1 ash :I: 90 Pa cenJ e<n<fidence Intl) X /()I

Barn in Nebraska,
lil!ed in Rochester,

Born in Con1'eclicul,
liw:d in RocliMter,agts 14-43

agu t-68

Skull •..•...•..•.••.....•••
Tibia •••..•••...••.••••••.•
Joint ..........•••••.......
Jaw .•...•.•.•••••.•.••.•..
T11eth ••.....•..••••••.•••.•

Pblll

RatH

Ra"'

Pb"'

70 ::1::4
70 ::1::4
12 ±3
16 ::!:: l
12 ::!:: 1
19 ::1::3

201 ::!:: 15
419::!::14
296 ::!:: 13
152 ::!:: 7

51::!::2
100 ::!:: 7
25 ::!:: 2
25 ::!:: 2
28 ::!:: 2

93 ±5

Born in Florida,
lioed in Roches/a',
aies 49-52

Ra"'

131::!::932 ±3
27 ::1::3
26 ::1::2
27 ::!:: 330 ::!:: 3

90 ::1::9
83 ::!:: 8
49 ::1::4

18 ±4

TABLE XVIII.

RA2H CONTE!'."T OF BONE AND l!USC:U

Vertebraem ...•...............
C!avicle114 ••••••••••••••••••••
Skeletal muscle 114 • • • • • • • • • • • • •Tibia shaft°. . . . . .. .. . .. . . . . ..
FemurG ...•.................•
Muscle&11:1.....................
Bone56 •••••••••••••••••••••••?-.f uscle" . . • . .• , • . . . • • • • . . • . . .

Ra'" conlent/r
ashlo-•""')

Ra"' COflUnl/t.rd tisJue ()( 10-1 p.,.c)

10.7
9.2

3.4
1.1
0.05
5.4
4.8
2.5

ex

Timu

10
10

l0

5

56
37
12
3
3

12
11
245
14.6
12.2

222

Pb"'

366 ::!:: 19
1,330 ::!:: 21
78 ::!:: 6 "71 ::!:: 777 ::!:: 6

TABLE XIX.

MEAN DOSE-RATES (MREM/Y, RBE=lO) TO VARIOUS TISSUESOF NORM.AL HUMANs130

Sz.eklalRa"'
and dauiltl<Ts

Skeklal Ra"'•nd dDughterJ

Sktklal Pli'"and dau1hlers(JS3 equilibrium)(eguilibr•um)(50% eguilibrixm)(60 pµC)

Body lis•""s

Osteocytes (5 µdiameter) ................. .
Haversian canal (10 µlining, 50 µdiameter) .. .
Trabecular marrow ...............••.......

TABLE XX.

(40 µ.µ.c)

10

16

5.4
0.6

8.6

(ZOO µpc)

6.6
3.6
0.4

1.0

5PECI.AL ARE.AS OF HIGH EXTERN.AL RADIATION TO RADIO-ACTIVITY FROM SOIL OR ROCK

E::krnal dose-rau ;,. air(Cosniic plus !4rreslria1)

Ionization chamber
scintillation
counter

1 village with 350 Average 1,600 mrad/y,peak 12,000 mrad/yan
inhabitants,
pasture land andscattered farms
180-350 mrad/yin
7,000,000

Primitive granitic, schistous and sandstone
areas of France-area includes about
one-sixth of French population

Monazite area in Kerala and Madras
5ta~ India-approximately 200 km
Jong and several hundred metres wide
Niue Island, Pacific-volcanic soil andunusually high radio-active content
of plants

Geiger counter and

4,500

Population weighted mean 1,300
mrad/y plus about 200 mrad/ybeta rays148
Maximum external radiation 1,000
mrad/y. High total a-radio-activity
content 50-360 µµc/g in the main
foodstuff-tarom"Hj.ghly
populated"

300 and 400 mrad/y in 2 villages;
4 other villages in same area 110 to
150 mrad/y1"

100,000

Monazite area• of Northern Nile Delta
region, UAR

TABLE XXI.

Ionization chamber
scintillation
counter

Average 500 mrad/y,peak 1,000 mrad/ym

30,000Monazite area in States of Rio de Janeiro
and Espirito Santo, Brazil-sequence ofcoastal strips, each several km long andseveral hundred metres wide
Mineralized volcanic intrusives in States ofMinas Gerais and Goias, Brazil--0 km 2
in a dozen scattered places

CosM1c RAY oosE-R.AT!s IN HIGH .ALTITUDE AREAS AND
CORRESPONDING POPULATIONSH~

Area

La Paz, Bolivia ..•..•..••...
Quito, Ecuador ..•.••.•.••••
Bogota, Colombia .. , •...•...
Cerro de Pasco, Peru .•.....•
Lhasa, Himalayan Area .....

(metres)

Lalilu.U

Cosmic rayconlribulion
to Jissuc doserote )bastd
labk ) mremh

3,630

16°5

270

2,850
2,640

O"
4°N

160

4,259

10°5

3,684

30°N

Altitude

223

°"

150
330
310

P~iox

319,600
212,873
325,658
19,187-20,000

scintillation
counter (Na. I
and plastic
phosphor)
Ionization chamber

Scintillation
counterTABLE XXII.

BODY TISSUE DOSE-JI.ATES DUE TO EXTERNAL AND INTERN AL IRRADIATION FROM
N.4.TURAL SOURCES OF RADIATION IN "NORMAL" REGIONS

rllU mr'Rh,E raliu.s)Douin(see paraira/Jhs Z-3 forSource of irradiation

Gonad

Ha~ersian

canal

Bone
ma"°'°&ference
in tatParagraph 8,
Table I
Paragraph 31

External irradiation:
Cosmic rays (including neutrons} ..•

50

50

50

Terrestrial radiation (including air).

50

50

50

Internal irradiation:
K'o ••.........•.................

20

15

15

Paragraphs
80-81

0.5

5.4

0.6

Paragraph 78

0.8

8.6

1.0

Paragraph 78

0.3
0.7
3

3.6
1.6
3

0.4
1.6
3

Paragraph 78
Paragraph 82
Paragraph 41

Ra 121 and decay products (35 per centequilibrium) ..•.....•..........
Ram and decay products (equilibrium) ..•........•.. ·. · · · · · · · · •Pbiio and decay products• (50 per
cent equilibrium) .•............•

cu .............................
Rnm (absorbed into bloodstream) ••TOTAL ......................

137

125

122

• Pb21° in excess of that expected from Ra:t:a and decay products in 35 per cent equilibrium.

''
I

224

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230

ANNEX FENVIRONMENTAL CONTAMINATION
Content&
Page
INTRODUCTION•••• •• • • • • • •• • •• ••• • •• • •• •• • • •• ••• • •• •• • • •• • •• •• • ••• • •

233

Part

I. PRODUCTION AND TRANSPORT OF NUCLEAR WEAPON DEBRIS •••••• , , •••• , • 234
II. TRANSFER OF RADIO-ACTIVE MATERIAL THROUGH FOOD CHAINS INTO THE
HUMAN BODY • , , • , •• , , , • , •• , ••• , , , , , • , •• , , • , , • , • , •• , • , • , • , • • • • • • 287
III. EXPOSURE DATA • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • 347
IV. DISPOSAL OF RADIO-ACTIVE WASTES AND RELEASES FROM ACCIDENTS IN
NUCLEAR REACTORS • , • , , •••••••• , •• , •••••••••••• , • , • • • • • • • • • • • • • •365

ANNEX FENVIRONMENTAL CONTA..~IINATION

Introduction

andPART I

Production and transport of nuclear weapon debris

CONTENTS
P1Jragraphs

lnir!Jduction ...•.. , ....•..••.••..•.•.••.. , • • . • . • . . •Part I. Production and transport of nuclear weapon
debris ...........•••••••.•..........•.•....... , • .

I. PRODUCTION OF RADIO-ACTIVE DEBRIS IN NUCLEAREXPLOSIONS ••...••.•.•••.•. , • , •........••. , • .
Fission products • . . . • . . . . • • • . . • . . • . .. . • • .. • . . • •Production . . . . . • . . . . . . . . • . . . . . . . . . • . . . . . . . . .
Decay characteristics . . . • . . . . • . • . . . . . . .. .. . • . •Fissionable materials and induced activity. • . • • • • •General . . . . . .. .•• . .• • .. .. •• .. . . . . . . . .. . . . . . •Fissionable materials • • . • . . . . • . . . • . . • . • • • • . . • .
Tritium .. . . . . . . .. .. . .. ... .•• .. . •. . • .. •• . . . . .
Induction in the bomb casing..................
Induction in the environment........... . • • • . . •Carbon-14 • . . . . . . • • • . . . • . • . . . . . . . • • . . . . . • • • . .
Physical properties of substances present in theradio-active debris .•...•... , , .......••• , • , •• ,Atmospheric explosions . . . . . • .. . . . . . .. • . . .. . . .
Near surface explosions ........ ,..............
Surface or shallow underground explosions....
Other explosion types. • • • • • • • • • • • . . • . . • . . • • • • .
Chemical properties of weapon debris and fractionation . . . . . • . . • . . • . • • . . • • • . . . . . . . . . . • • • . • .
Debris solubility . • • . . • . . . . . . . . . . . . . . . . . . . . . . .
Fractionation • . . . . • . • . . . . . . . . . . . . . . . . . . . . • • . .
II. INJECTION AND TRAXSPORT OF RADIO-ACTIVE DEBRIS..
Introduction . . • . . . . . • . . . . . • . . . . . . . • . . . . . . • . • • . .
The atmosphere..............................
Types of fall-out........................ • • . . •Injection of radio-active debris into the atmosphere
Partitioning . . • . . . . . . . . . . . . . . . . . . . . . • . . . . . . . .
Injection •..••••.•..... , .•..... , .•.•.. , .. , , • .
Movement of debris in the stratosphere...........
General . . . . .. . .•. . ••. .•. •••••.•.... .. . • . • • . .
Gravitational settling • .. • .. • • • • . • • • . • • .. . • • • • .
Diffusion . . • . . . . . • • . . • • • • • • • . • • • . . • . • • • • • . • • .
The stratospheric reservoir....................
The Brewer-Dobson model....................
The Spar-Feely model . . • . . • . . • • . . . . • . . . . . . . . •Half-removal times . • . . . • . • . .. . .. . . . . . . . . . .. .
Stratospheric aerosols . .. • . . • • . . . . . . • . • . . • . . . .
Transport from stratosphere into troposphere. . . . .
Transport through the tropopause. . . . . . . . • . . . • •Tropopause movements . . . . . . . . . . . • . . . . . . . . . . •Disturbance of the tropopause........... • • • • . •Transport through the tropopause gaps .. ,......

P1Jragraphs

1-6

The troposphere . . . • . . . . • . . . . . • . . . . • • . • . . . . . . . .
Horizontal movements • . . • • . • . . • • • . • . • • • . . • . •Survey of air measurements...................
Air concentrations above ground level. . . . • . . • . .
Air concentrations at ground level..............
Capture of debris in precipitation..............
Dry removal of debris.........................
Half-removal time . . • . . . . . . . • . . . • • • . . . • • . . • . •Carbon-14 .....•.. , .. . • . .. . . • • . • • • • • • .. • • • • . . . .
CH in the stratosphere . . . • • . . . • • • . • • . . . • . . . . . .
CH in the troposphere. • . . . • • • • . • • • . . • . • . . . • . . .
Carbon cycle in nature... . . . . . • • • • • • • . . . . . . . . •Movement of carbon in the carbon cycle •••.... ,

7-120
7-30
11-15
11-13
14-15
16-22
16
17
18
19
20
21-22

III. DErosrrION OF BADIO-ACTIV"E FALL-OUT •.•..•••••..•
Rate of fall-out deposition ........•...•.•• , ••••.•
Methods of measurement ..........••.•.•.••...
Relation to airborne activity •••...••.•.•••••...
Relation to debris concentration in rain •••••...
Relation to total precipitation ...•••.•.•••.••...
Dry deposition .•.•.....••.•••.••..••••..••••.
Measurements of Srllo and Csl.31 ••••••.•••.••..
Measurements of short-lived nuclides ..•.......
Tritium ..••••. , ...••.......•.•..........•..•
Accumulated fall-out deposit .....••.•.....•.....
Deposition of Sroo ........................••..
Other nuclides .•. , .......•..•..•.............
Local factors influencing deposition •••.•.•.....
Deposition and transport in water ..•..••.....••..
The oceans .........•.•.....••......•...•••.•
Lakes and rivers ......•....•...••..........•..

23-26
23
24
25
26
27-30
27
28-30
31-71
31-33
31
32-33
34-37
34-35
36-37
38-47
38
39

53-60
53

54
55

56
57-58
59
60
61-71
61
62-64
65-67

68-71
72-93
74-83
74
75
76
77

78-79
80-81
82
83

84-89
84-87
88

89
90-93
90-92
93

IV. PREDICTIONS OF FUTURE LEVELS ••••• , ••••••••••••• 94-120
Inventory of SrDo .• , ...•.•...•.. , ..••. , .....•... 97-99
100
Other inventories ..........•....•..............
CH inventory ...•.......•....•.••.••...... · · • · · 101-1()4
Prediction of future fall-out. ................... . 105-120
General •...•............•••.......•.......•. 105-106
Sr 9 o and Cs 13T ............•.•................. 107-108
Deposition of Sr9o and Csl.31 from tests up to the109
end of 1960 ..........••....•.••............•A model illustrating deposition of Sr9o and Cs131
from a pattern of tests subsequent to 1960 ..•. 110-114
CH from tests up to the end of 1960 .•....•.•... 115-118
cu from continued testing .................... . 119-120

40
41
42-43
44
45-46
47
48-52
48-49
50
51
52

TABLESREFERENCES

Introduction

1. The explosion of nuclear weapons results in the release of radio-active debris. In the case of a nuclear
explosion in the atmosphere much of this debris will forsome time be found as airborne activity usually aggregated into small particles although some gaseous activity
is also present. The airborne activity is gradually de233

herent complexity of the subject and the incompletenessof our knowledge of the mechanisms involved and theexact conditions of testing. However, since the previous
report of the Committee, much information has beenobtained relating to the dissemination and passage ofdebris from nuclear weapon tests through the biosphere.

posited on the surface of the earth and this deposit isusually referred to as fall-out. Fall-out constitutes themost important source of environmental contaminationfrom nuclear weapons tests. Other sources, e.g. the pollution of the atmosphere by airborne activity and the oceans
by water soluble debris will also be discussed in thisannex.

6. This annex has been arranged as follows :2. The first nuclear explosion occurred in 1945. The
rate of testing was especially high over the years 1954
to 1958; from November 1958 to August 1961, on theother hand, the rate was extremely low. The environmental contamination arising from this testing is themain subject of study in this annex. Data relating to thelarge-scale testing after 1 September 1961 are still too
incomplete to permit a detailed evaluation of the consequent contamination.
3. The contamination of the environment !Ubjects man
to radiation from sources which may be categorized conveniently as follows :(a) External source! consisting of the accumulated
deposit of fall-out on the earth's surface;( b) Internal sources arising from : ( 1) the ingestionof certain radio-nuclides which enter readily into foodchains and are absorbed by man to a relatively great
extent; and (2) the inhalation of airborne particulatematerial which is deposited in the lungs.

!. PRODUCTION AND TRANSPORT OF NUCLEAR WEAPONDEBRISThis section deals with the production and dissemination of radio-active debris from nuclear weapons, withsuch measured rates of deposition and total amounts ofdebris accumulated in the atmosphere and on the earth
as are necessary to evaluate the irradiation from externalsources and from inhalation, and with estimates of rates
and amounts to be expected in the future under specified
conditions.
II. TRANSFER OF RADIO-ACTIVE MATERIAL THROUGH
FOOD CHAINS INTO THE HUMAN BODY

This section summarizes measured levels of radionuclides in food and the human body as well as the present knowledge regarding the mechanisms through whichthese radio-nuclides are transferred from fall-out deposits to the human body and their possible future concentrations in the body.

III. EXPOSURE DATA

4. The discharge of radio-activity from atomic energy installations, hospitals and other premises, may also
cause external and internal irradiation of certain populations. These populations are small and localized compared with those exposed to contamination from nuclear
weapons.

This section evaluates the irradiation of human populations as calculated from the data in the previous sections.

5. This annex presents the available data and estimates the present and future levels of the environmental
contamination and the doses received. The estimates are
subject to considerable uncertainty because of the in-Both routine and accidental releases are described, including type and amount of wastes, and the ensuing doses
to human populations are estimated.

IV. DISPOSAL OF RADIO-ACTIVE WASTES AND ACCIDENTALRELEASES OF RADIO-ACTIVITYPART I

Production and transport of nuclear weapon debris
10. The main contamination of the environment iscaused by the radio-active fall-out deposited on the
ground. An important characteristic of most fall-out is
its particulate nature. These particles are formed when
the fire-ball created by a nuclear explosion cools off andthe processes and materials involved determine to a large
extent the physical and chemical properties of the fallout.

I. Production of radio-active debris in nuclear
explosions
7. The radio-active components of nuclear weapon
debris are mainly produced through the process of fission. Certain heavy nuclei, like those of U 235 and Pum,
disintegrate (fission) into two lighter nuclei under the
influence of neutrons. These fission products are mostly
unstable and undergo radio-active decay. During theprocess of fusion (i.e., the collision and fusing of lightnuclei giving a release of energy) used in large-size
nuclear weapons, essentially only one radio-active product is released, namely tritium.
8. The fissionable materials themselves are radioactive, as also is tritium, sometimes used in explosives
based on nuclear fusion. Not all of these materials areused up in an explosion and they thus will be found in
the radio-active debris.
9 .. An ~xcess of free neutrons is produced in connexion with both fission and fusion reactions. Within a~raction _of <: s~cond these neutrons are captured eitherm matena~s 1ns1de the weapon or in the environment of
the explosion. In this way a variety of induced radioactive materials are formed.

FISSION PRODUCTS

Production

11. When a heavy nucleus undergoes fission, two
new nuclei are usually formed, which in the majority ofcases are of unequal mass. This splitting of a heavy
nucleus may occur in a number of ways and as a result
the fission products formed range in mass from about
70 to 170 atomic mass units. The primary products
formed are as a rule unstable and decay to form new
nuclides which in turn may be unstable. The fission reaction thus results in the formation of a large number ofdecay chains, 1 three examples of which are given below
for future reference (para. 28) :234

/153 2.8 hr Kr 88 +neutron
Chain 89: 4.4 sec Br'\.853 3.2 min Kr-+15.4 min Rb-+50.5 day Sr-+Stable Y
4.59
4. 78
4. 79
/153 3.2 min Kr 59 + neutron
Chain 90: 1.6 sec Br'\.853 3.3 sec Kr-+2. 7 min Rb-+28 y Sr-+64.3 hr Y-+Stable Zr
5.0
5. 77
5. 77
/43 Xe 138+ neutron

Chain 137: 24.4 sec I/'\.963 3.9 min
6.00

923 2.57 min Ba

Xe-+30 yCs!
6· 15 '\. 83 stable Ba(1)

The half-life of each nuclide is given immediately preceding its symbol. The figure below some of the symbols
refers to the fission yield (i.e., the per cent probability
per fission of forming the nuclide) in thermal neutron
fission of U 235 •whereA, = activity of the fission-fragment mixture t unitsof time after the explosion;
A1 = activity of the same mixture when t = 1 unit oftime;n = a parameter which depends on the age of thefission products.

12. In most cases the last two or three members of adecay chain are formed mainly from the decay of precursors, i.e., these products have only small independent
yields (they are not readily formed as primary fission
products). As a consequence the total yield of these latemembers is close to the chain yield except in those cases
where branching occurs, as in chain 137.

Formula ( 1) is approximately valid for a mixture offission products formed in a single e.xplosion. For simultaneous thermal neutron fissions of um, for example,
the law describes the gross beta decay to within 15 percent over the time period from one hour to two hundreddays if a value n = 1.15 is chosen.H For the fission
products in weapon debris however, much larger deviations are observed, especially for the gross y-decay. 16- 20

13. The yield of any given fission fragment varies
considerably according to the nature of the fissionable
nucleus and the energy of the neutrons causing thefission. 1 - 9 Table I gives numerical values for the fission
yields of certain radio-nuclides resulting from the fissionof nuclei of various heavy atoms. The table shows, forexample, that the fission yield of Sr110 varies from 2.2
per cent for Pu239 to 6.8 for Th 232 • Since a combinationof different fissionable materials may be used in experimental atomic devices, the actual fission yields are likely
to be somewhat different when such devices are exploded.
The last two columns in table I give data from measurements on particular examples of weapon debris. 1- 9 Fromdata like these the production of Sr90 and Cs187 in past
weapon tests has been calculated. Figures of 1.00 Mc Sr00
and 1.70 Mc Cs13 ' per 10 megaton of fission energy areusually assumed. Later measurements 9 indicate valuesof 1.09 and 1.73 Mc respectively. Individual tests may
show fairly large deviations from these values.

Decay characteristics
14. As has been mentioned, the explosion of nuclear
devices based on fission of heavy nuclei produces a mixture of nuclides with a wide range of mass numbers.
In all, more than 200 nuclides are formed, 10- 14 most ofthem radio-active, having half-lives ranging from lessthan a second up to many years (in a few cases millionsof years, i.e., essentially non-radio-active nuclides). Thisfission product mixture decays under the emission ofbeta and gamma rays, the gross activity thus decreasing
with time. Since the decay constants of the various
nuclides differ widely (figure 1), it is obvious that thevariation with time of the mixture's activity cannot be
expressed by a simple exponential law. It has been foundthat the gross decay varies inversely with a power of thetime elapsed from the moment of explosion (fission),
i.e., according to the empirical law of Way and Wigner 1 ~:°"7•

Figure 1. Decay of a fission product mLxture

235

The Way-Wigner law is still useful though, as a simple
method of distinguishing nuclear weapon debris fromnatural radio-activity and as a rough means of estimating
the age of fresh debris.
15. The radiation from fission product mixtures has
been studied in some detail theoretically 4 • u, 2 0-2 s and experimentally.29-32 It has been found that they-spectrum
gives a reasonably accurate identification of a fission
product mixture, its age and in some cases its mode oforigin. The average y-energy is usually within 0.64 +0.10 MeV but the intensity of individual y-energies mayvary to a large extent, for example three years after
fission, the total number of gamma quanta per minutefrom 14 MeV neutron fission of U 238 is 80 per centhigher than the value from thermal neutron fission of
U 235 • The theoretical ratio of beta to gamma decays isfound to be close to 1 for fission products less than one
month old, but rises to a maximum of between 3 and 7
three years after fission.'
FISSIONABLE MATERIALS AND INDUCED ACTIVITY

General16. In a nuclear explosion a large number of neutrons

U238 +n----+

U239·---~

24 minThe induced activity of Np 239 is often found to be of
the same order as the gross beta activity of the fission
product mixture in fresh weapons debris.18120• 33 For thesame time period, i.e., ten to twenty ·days after an explosion, it has also been demonstrated 3' that another induced
activity is present in some debris, namely um formed
through a ( n, 2n) reaction in U 238 in certain weapons.
The presence of this nuclide may be taken as an indication of the explosion of a thermo-nuclear weapon. 33
Finally, multiple neutron capture may occur in the fissionable materials, giving rise to small amounts of transuranium elements of atomic number as high as 100.35 • 116

are released. All of these neutrons are very short-lived,
being captured immediately by surrounding nuclei. This
property of the neutrons, apart from being essential forthe creation of the chain reaction that produces the energy in the explosion, gives rise to various types of induced radio-activity-in the fissionable materials, in thebomb case and in the environment of the e..xplosion. Mostof the induced activities are of little biological significance, either because of short half-life or low yield.
Those of importance will be treated in detail in the following paragraphs.
Fissionable materials

17. Weapons based on nuclear fission contain· materials which are alpha-emitters, e.g. U 235, Pu239 and U 238 •Plutonium is the most important among these from thepoint of view of its possible biological effects. In aweapon in which the fissile material is plutonium, muchof this remains unchanged after an explosion. Plutonium
may also be produced in a nuclear explosion by thereaction :33

N J>229'----+
2.3 daysaPu 239---~24,000 yearth's surface, about 50 per cent of the neutrons may
reach the earth's surface and react with the nuclei of
elements in the soil. As a result radio-nuclides of many
elements are formed. 23 ,-1 3 ,+i. They include Si3 1, Al~ 8 andNau which have short half-lives and also the comparatively long-lived Zn65 , Fe55 , Fe59 and Mn 5' etc. This
neutron capture in mineral substances is predominant in
an underground explosion. In the case of an undenvater
explosion, most of the neutrons will be absorbed by thewater and by substances dissolved in it. The major
product is inactive H 2 but radio-active isotopes of Na,
K, P, Cl, Mg, Sand Cd are also formed as well as Zn85
etc. mentioned above."' 3 • 45 When the explosion occurs
high in the atmosphere, practically all the neutrons areabsorbed by the nuclei of nitrogen with the formation of
the long-lived radio-nuclide cu.

T ritimn

18. Tritium may either be present as such in a weapon
or be produced in the explosion by one of the thermonuclear reactions involved.37 • 38 Although the maximum
energy of the tritium /3-decay is only 18 KeV, the long
half-life of 12.5 years and the biological significance ofhydrogen makes some consideration of its importancedesirable.

Carbon-14
21. The quantity of C1 • formed in a nuclear explosion/is determined by the number of surplus neutrons enter!
ing the atmosphere. The production of C14 will depend
therefore on the type of nuclear device exploded andalso on whether the explosion took place on the surfaceof the earth or high in the atmosphere. A "surface" test
will produce approximately 50 per cent of the CH thatwould be produced by the same device in the "air" test,
because about one half of the escaping neutrons will be
captured in the soil or water rather than in the atmosphere. Practically all tht; neutrons escaping from the
exploding nuclear device will produce C14 when they areabsorbed by the atmosphere ..w
22. Estimates of the neutron yield per megaton offission in fission devices have ranged from about 1.5 to
3 X 1026 for various fissionable materials. A value of
2 X l0 2 a neutrons per megaton has been adopted in thisannex. An even wider range of values has been estimatedfor fusion devices depending on their design. Leipunsky37•4' has found a range of 1.5 to 22 neutrons for anenergy release of 180 Me V for different fusion reactions.
This may be estimated as 2.2 - 32 X 1026 neutrons per

Induction in the bomb casing

19. Neutrons captured in the bomb casing and othernon-fissile materials in a nuclear weapon induce a number of other activities. Radio-active iron and zincnuclides have been found in weapon debris 39 as haveamounts of Mn 5' , Co57 , Co 58 and Co60.•a-. 2 These substances are of little biological importance in comparison
with the fission products. In some weapon tests, sufficient characteristic activities of Rh 102 and W 185 have been
produced to serve as tracers for the movement of airborne debris.
Induction in the environment

20. The nature of the activity induced in the environment of a nuclear e..xplosion depends on the nature of theenvi;onment. In a ground surface explosion, or an explosion at such a low height that the fireball touches the236megaton. Libby4 8 • • 9 suggests a value of 3.2 X 10:s neutrons per megaton of fission and fusion, weighted according to nuclear testing prior to 1958. Machta50 gives
a figure, based on United States test experience, of
2 X 1026 neutrons per megaton of total (fission andfusion) yield for an air burst and 1 X 1026 neutrons per
megaton for a ground burst. These latter values are
based on the assumption that equal yields of fission andfusion were employed and are estimated by Machta tohave an uncertainty of a factor of 2. For explosions prior
to 1959, an assumption that 2 X 102° atoms of C14 areformed per megaton of total yield agrees closely withexperimental data on the increase of atmospheric C 1-t.

place, huge amounts of soil or water are mixed into thefireball. The particles formed are usually large (up to2 mm) with an irregular distribution of the radioactivity, sometimes on the surface and sometimes
throughout the volume of the particle. The specificactivity is lower than in the previous cases. 60 However
some small (0.1 µ.) high specific activity particles are als~
to be found. 51

Other explosion types
26. An underwater e.xplosion in deep water initiallycreates the same type of particles as those found after
an atmospheric explosion. Many of the particles are
however soon captured by water to form slurry drops(para. 24). In an underground explosion where thefireball is contained and does not break through to thesurface to form a crater, it has hitherto been found thatthe fireball vapour condenses and mixes with melted
ground material which subsequently solidifies. The resultfor 1-20 kiloton weapons is that 200-500 tons of rockfuse with every kiloton yield of fission products. 61 Someof the gaseous debris does not take part in this process
and has occasionally been found to vent to the surface
and enter the atmosphere. In a very high altitude e.xplosion it is to be expected that the fireball vapour leaves thepoint of the e..xplosion too rapidly for appreciable nucleation or particle formation to occur. The weapon
debris will therefore be either gaseous or made up of
extremely small particles, e.g. clusters of some hundredsof atoms. 62

PHYSICAL PROPERTIES OF SUBSTANCES PRESENTIN THE RADIO-ACTIVE DEBRIS

Atmospheric explosions
23. When a nuclear weapon is exploded, an aerosolof radio-active particles is usually formed. Two processes
are involved in this particle formation :51 the heating ofmaterials brought into the fireball and the condensationof vaporized materials. The relative importance of thesetwo processes varies with the weapon yield and the environment of the explosion. In an atmospheric e..xplosion,i.e., an explosion in the atmosphere at such an altitude
that the fireball does not touch the ground, the condensation process is all-important. The contents of the fireball
will consist of the ·vapours of the fissionable elements
and their products and of other materials used in building the atomic device. As the fireball cools down, thesevapours oxidize and then condense to form tiny, solid
aerosol particles. 52 • 53 A prominent constituent of thefireball is often iron vapour, and then many of the particles formed are small, black spheres of magnetite(Fe3 0 4 ) that are homogeneously radio-active as a resultof the incorporation of mainly fission products. The size
distribution ranges from 10 µ. down to 0.01 µ., the mostprobable size perhaps being 0.2 p.54 for a kiloton explosion. The specific activity is high, in one case a 4 µ.
particle has been found having an activity of 5 X 10-9
curie 40 days after its formation. 55

Near smface explosions
24. The situation becomes more complicated in thecase of a near surface explosion, i.e., when the fireballintersects the ground or water surface to a small extent(e.g. a tower shot), because large amounts of soil, wateror iron are included in the fireball. 51 The same kind ofparticles present in an air explosion are found, but they
are often attached to the surfaces of much larger irregular particles of unaltered soil material, or in the case of
a water explosion they have been captured by water toform slurry drops ranging in diameter from about 50
to 250 µ.. Often, these larger particles have been heated tothe melting point and the originally surface-bound radioactivity then distributes more or less homogeneously
through the volume of the particle, which is spherical inshape with a diameter of about J4 to 1 mm. The colour ofthese particles varies from black (iron) to transparent(silicate) with intermediary examples of red or brownish
colours (indicating a mixed composition).111. The specificactivity is again high and may range up to the values
found in air explosions.17• sa-a 9

CHEMICAL PROPERTIES OF WEAPON DEBRIS AND
FRACTIONATION

Debris solubility
27. The solubility of the debris is very sensitive to thecomposition of the explosion environment, including thestructural materials of the device. Regardless of theweapon yields, 63 air explosions produce small particles
with high solubility. Solubilities in water of up to 30
per cent and in 0.1 N HCL of close to 100 per cent havebeen found. 19 Ground surface explosions produce a large
fraction which is highly insoluble but also a smaller
amount of particles similar to those from an air explosion.19 Explosions in deep water give particles which arehighly soluble (i.e., more than 90 per cent) whether thedebris is associated with large amounts of water andfalls close in or is more widely dispersed. 51 Shallow
water explosions finally give particle solubilities intermediately to these extremes. In general, stratosphericdebris is completely soluble and has been shown to becompletely available to animals.M-66

Fractionation
28. The process of particle formation takes place in
only one or a few seconds after the e.xplosion of a kiloton
weapon, and even in a megaton e..xplosion the delay isless than a minute. As has been pointed out earlier(para. 11) some of the fission chains start out with agaseous or volatile precursor (e.g. isotopes of Kr, I or
Xe). Table II shows the percentage of some mass chainsthat may be in gaseous form during the early period
after an explosion.67 • 68 Substantial fractions of somemass chains are gaseous and this has an important effe~ 9on the distribution of individual nuclides among theaerosol particles that grow out of the supersaturated
vapours of the rising cloud. Such distribution differences
are referred to as fractionation. This phenomenon is

Surface or shallow underground explosions
25. In the case of a surface or shallow underground
explosion, i.e., when appreciable crater formation takes
237

very complex and not completely understood, although
it has been studied both theoretically10 and experimentally.11, 19, s2, s1, sa,68, 61-s9, 11-1s It is to be expected in general that fractionation would increase with a decrease ineither the explosion yield or the height of burst. 68 Exceptions to this rule have, however, been found.
29. Considering specific radio-nuclides it has been
observed03 that the ratio of Sr90 to total fission productactivity increases with decreasing particle size, and that
Sr90 associated with large particles is concentrated in athin surface layer. As a result, all of the Sr90 may bewater soluble even when appreciable fractions of otherradio-nuclides are not. Sr8 9 , 1131 and Csm are likely to
fractionate even more strongly than Sr90 (table II) andthis bas also been found to be the case. 68 Correspondingly,
nuclides such as Zr90 + Nb 95 concentrate preferentiallyin large particles of refractory material, e.g. iron oxide
or silica.
30. In table II the percentage of some induced radionuclides that is in gaseous form is also shown together
with the fission products. From the data it is to be expected thatand Np 239 will not fractionate, whereas
tritium and C14 will. This is especially true for C1' as it
is formed outside the fireball to a large extent. It is also
likely that this C1'' is rapidly converted to CO and C02
which will then move upwards with the hot gases fromthe explosion.

um

II. Injection and transport of radio-active debris
INTRODUCTION

The atmosphere
31. The structure and characteristics of the earth's
atmosphere strongly influence the transport and deposition of injected radio-active debris. Figure 2 gives a very
schematic picture of the structure of the atmosphere. In

the troposphere, cloud formation, precipitation andturbulent mixing are important phenomena. The stratosphere has a more stable structure because of the temperature distribution. The boundary between troposphereand stratosphere is known as the tropopause and lies at
an altitude of about 16 km in equatorial zones and 11 km
in temperate and polar regions. There are always two
main breaks in the tropopause of each hemisphere (onlyone breal{ is shown in figure 2), the first one between thepolar and middle latitude tropopause and the second
between the middle and tropical tropopause. In association with each gap there is a jet stream, a zonal windof high velocity.
Types of fall-out
32. Particulate radio-active debris injected into theatmosphere is to a large extent deposited on the earth's
surface as fall-out. Gaseous debris, e.g. P 31, Kr85 andCH02 may also reach the surface of the earth. Conventionally, three different types of radio-active fall-out arerecognized-local (or close-in), tropospheric, and stratospheric:(a) Local fall-out takes place near the point of explosion and within about one day. It is significant especially in connexion with surface or near-surface bursts;(b) Radio-active debris that is injected into thetroposphere and carried around the world is depositedon the earth's surface as tropospheric fall-out. As longas this activity is airborne (about one month) it is referred to as tropospheric debris ;( c) When debris injected above the tropopause is
finally deposited on the ground (which may take one orseveral years) it is referred to as stratospheric fall-out.
Stratospheric debris will naturally be observed in the
troposphere some time before it deposits.

33. Gaseous debris usually resides in the atmosphere
for a longer time than does particulate debris injected at
the same time and place. The atmospheric processes ofremoval are complex and variable; for instance, !181 mayreach the ground absorbed on particles, dissolved inprecipitation. through gaseous impaction or direct absorption in the pulmonary tract from inhalation of air.
INJECTION OF RADIO-ACTIVE DEBRIS INTO THE
ATMOSPHERE

Partitioning
34. The partitioning of the radio-active debris between
local, tropospheric and stratospheric fall-out depends
upon three factors governing the injection: weapon
yield, height of burst, and the meteorological conditions.
Figure 3 gives some dimensions of the radio-active cloud
as seen about ten minutes after a surface explosion. 74 • 7 5
The figure shows that the radio-active aerosols fromsurface explosions with yields greater than 100 kilotonsof TNT may rise considerably higher than the tropopause. This becomes true for even smaller weapon yields
when the explosion takes place high up in the air, andfor an atmospheric explosion above the tropopause ofcourse all the activity is stratospheric.

TROPO$Ft!ERE

-30"C

90
N

60

Degrees latltiJ.ii11
Figure 2. Structure of atmosphere in July90s

35. Direct measurements of the partitioning of debris
between local, tropospheric and stratospheric fall-out arevery few and uncertain. Some values have however been
postulated"6 • 49 • • 0 -•s and a summary of these is given intable III.7 9 The data are very approximate in nature.
They apply only to the gross activity and not to individual
radio-nudides like Sr90 and Cs 137 -..vhich may partitioninjection. Based on the limited data available, one approach is to compare the activity levels from the injections of the autumn of 1958 with those of 1961. However, the first months of deposition are not typical of theannual pattern of fall-out because it is expected that thecharacteristic peak of debris \vill appear only in thespring of 1962. Only after the measurement of thisspring peak at many places of the globe and the evaluations of these results can the 1961 injections be reliably
estimated. Data available (as of March 1962) include
measurements of deposition of Sr90 for three months of1961 (October, November, December) in Tokyo84 andfor one month (October) in Abingdon (United Kingdom)85 and in four towns of the United States. 811 Mostof these measurements showed that the rate of Sr90 deposition in 1961 is less than in the same months of 1958.
There are data about the Cs137 deposition only in Toh.70
in the same months. The rate of Cs 137 deposition for twomonths was higher and for one month less thm in 1958.
Measurements of short-lived activity in air, e.g. in the
United Kingdom 85 and Japan, 87 showed that levels rose
sharply in September 1961 to levels of the same order
as in corresponding months in 1958. Notwithstanding
the obvious scarcity of data as a basis for long-term
extrapolations, the similarity of the character of fall-out
levels from the tests in 1958 and 1961 permit an estimateof the 1961 injection as near to the 1958 autumn injection. During 1959, a global integral from monthly
collecting sites gave 0.86 Mc Sr90 from the autumn tests. 88
This, combined with an estimate of the corresponding
portion of the stratospheric reservoir, gave a total of
about 1 Mc Sr90 ( 10 MT fission) ; a figure in reasonableagreement with injection estimates of 0.6 Mc8~ and 1.2
Mc.~ One might assume that this figure of 1 Mc is anunder estimate of the 1961 injection, bearing in mind
that fall-out could be distributed over a longer time than
was the case after the 1958 injection.

60'i-:- 50
r

j

~

;

~

'ii

E

II
~

..

ll

~ :io
l

l

50

100 :200 • -'ODi:2·

s I 10 . J)

M.rot...
T...1--n yiald (TNT f'l\llYal.nl) •Figure 3. Approximate nuclear cloud dimcnsionsTs

differently because of fractionation phenomena, giving
smaller contributions to the local fall-out in relation to
the gross activity. For induced activities, even more
extreme conditions may apply. Tritium and C14 , forexample, contribute a different proportion to the close-incontamination than does activity induced in the soil.
Injection
36. For theoretical predictions of fall-out from
nuclear e..xplosions, it is necessary to know the quantityof radio-active products injected into the atmosphere.
This quantity is determined not only by the energy yieldof an explosion, but also by two quantities dependent on
the construction of the nuclear weapon concerned: thefi~sion-fttsio!l r_atio which gives the amount of fission
products, and the .Ileutron yield per unit of thermonuclear energy which gives the C14 production. Suchvalues of these coefficients which have been published are
not supported by published experimental and theoreticalevidence. Therefore, at present, the Committee's calculations of past injections are based on the measurementof deposition of debris and of inventories of the atmosphere during sufficient periods of time after the explosion. With respect to the explosions produced before
1961, an estimate has been published 46 • 80• 81 of the fission
and neutron yields of all the explosions based on postulated values of fission-fusion ratio and neutron yield.
This estimate is given in table IV. With the help ofcoefficients from table III, the stratospheric injection of
explosions prior to 1961 is estimated as 68 megaton offission energy yield, i.e., 6.8 Mc Sr90 and the quantityof cu atoms as 24 X 1027 • The amounts of Sr90 and CH
agree reasonably well with the measured Sr90 deposit(table XIV) and in the atmosphere (table XVI) as wellas with the amount of ea appearing in the atmosphere(table XVII). This shows that the over-all values ofcoefficients and energy yield accepted in references.e• 80 • 81
are not in contradiction with experimental figures for
Sr110 and C1 "' although other combinations are possible.
There are estimates of the yield from the 1961 e..xplosions(total energy yield-120 megaton, fission energy yield25 megaton).82 • 83 The correctness of this estimate of thestratospheric injection from the 1961 explosions is as yet
unknown, as sufficient time has not elapsed to allow
measurement and evaluation of the inventory. The
principal considerations given at the beginning of thisparagraph ·are applicable to this estimate.
37. At present there are not sufficient data on fall-out
from the 1961 tests to make an accurate estimate of the

MOVEMENT OF DEBRIS IN THE STRATOSPHERE

General38. Different theories have been put fonvard in recent
years regarding the mechanisms responsible for thetransport of radio-active debris within the stratosphere.
It is generally agreed, however, that the factors that are
most important comprise advection, diffusion (usually
turbulent) and gravitational settling of particles. The
first of these processes, the mass movement of air, is themost rapid with wind speeds of even more than 100
km/hr90 in the east-west directions. These zonal winds
distribute radio-active debris in a latitudinal band of thestratosphere circling the earth within a few days to si..,..
weeks after the injection. Vertical movement is notnearly as rapid because of the thermal stability of thestratosphere, and horizontal movement of stratospheric
air streams from north to south (and the reverse) is also
insignificant in comparison. This will be discussed further in paragraph 42.
Gravitational settling

39. Gravitational settling of debris particles may be
important during the first one to two months after an
injection but there are indications that it plays a roleeven for older debris. 01 • 92 One estimate93 shows that atheights of about 20-30 km the fission product activity
may be associated with very small aerosol particles offrom 0.055-0.095 microns. According to another estimate, 94 the particle dimensions at these altitudes vary239

between 0.02-0.2 microns. Direct measurements 95 haveshown most particles to be less than 0.2 i:iicrons and it isthus in general to be expected that the size range shouldbe 0.01-1.0 microns some months after injection.06 • 97
Below 30 km such small particles settle extremely slowly
by the action of gravitati~nal forces and. it maY: therefoi:ebe inferred that the particles move mamly with the air
masses in which they are suspended. 18 Above 30 km, on
the other hand, settling may occur more rapidly owing,among other things, to the low air density. 62

Diffusion
40. With regard to the importance of diffusion as atransfer mechanism of nuclear weapon debris, there
seems to be rather firm evidence that the rate of diffusive
mbcing is smaller in the stratosphere than in the troposphere. 7s, o8

The stratospheric reservoir
41. Apart from the early time period, when gravitational settling may remove some of the activity, the different processes of removal thus all appear to be rather
slow in comparison with the zonal advection. It is therefore generally agreed that radio-active debris injected
into the stratosphere may remain there for some time,
constituting a reservoir that is only gradually depleted
when activity moves down into the troposphere and fromthere to the surface of the earth. If rapid mixing andconstant fractional removal per year is assumed, therate of depletion may be expressed by giving a hal~­removal time of the stratosphere, T 0 . 5 (the mean residence time Tm is often used alternatively, the relation
being Tm X ln 2 = To.~). Only data of a very approximate nature 33 •9 g were available for the 1958 report, and it
was stated that "the mechanism of transfer from thestratosphere to the troposphere is not completely understood" .100 As no direct measurements of the stratosphericreservoir were available, its size was estimated from themeasured rate of fall-out and an assumption of 10 year~
was made for the mean residence time. This value wasrecognized as an upper limit ( 5 years being more probable) and was adopted mainly because it gave a conservative estimate of the size of the reservoir. The situation has improved in subsequent years to a large extent
through studies of the atmospheric transport of weapon
debris. These studies will be described in the following
paragraphs.
The Brewer-Dobson model

43. Several modifications of the Brewer-Dobson
model have been proposed. 741 • 107-m Clearly the only wayof resolving the question of stratospheric transport isthrough actual measurements in the stratosphere. Many
results of such measurements have now been reported. si, s3, 8s, 1os, 11._1 s1 Using the nuclear weapon debris
as a tracer it has been possible to map the meridional
movement up to altitudes of about 30 km. This information is gathered both through measurements of actual
concentrations of such fission products as Sr~, Sr81\
Ce 1 « and of induced activities such as C14 , W1 85 andRh 102 • Studies of the change with time of the ratio ofthese activities have also proved useful in evaluating thetransport mechanisms. The ratio Sr89/Sr9° for instancedecreases in a known way with time after fission andits measured value is therefore a better indication of thedebris age than are data on nuclide concentrations only.
In figures 4 and S the stratospheric distribution of Sr90
and W1 85 in the period May-June 1959 and 1960 are
shown. 152 It is apparent that the ma.ximum Sr9° concentration in 1959 over the equatorial tropopause had vanished in 1960 and there were instead less intense maxima
in the polar regions. Although this is consistent with one
version105 of the Bre\ver-Dobson model, the data on W1 85(figure 5) are not. This nuclide was injected in thetropical stratosphere in 1958 and since then (as of themost recent measurements in June 1960) the maximum
concentration has remained stationary over the equatorial region. In addition measurements on Rh102 shown 2that the polar maxima of Sr'° in 1960 were to someextent due to debris injected in 1958 with one explosion
at 30 km (this injection was about 3.0 Mc of Rh102 andthe nuclear cloud rose much above 30 km and probably
into the mesosphere). This debris has gradually moved
downward and poleward. The modified Brewer-Dobsonmode1 105 has therefore met some additional objections

100

.,

eo--._,.I"""'----"

42. The first efforts to explain the mechanism ofstratospheric transport of radio-active debris were madeby Machta 101 and Stewart. 102 Their proposal is based ona model originally proposed by Brewer103 and Dobson 104
to explain the stratospheric distribution of water vapour
and ozone. This model assumes that besides the rapid
zonal air movement there is a slower meridional circulation of tropospheric air. This air is heated in the tropical regions and carried up into the stratosphere whereat altitudes around 30 km105 it moves polewards, sinks
and re-enters the troposphere in late winter and spring.
This model is consistent with such experimental findings
about the ground deposition of fall-out as: (a) a seasonalvariation of fall-out rate: ( b) a maximum fall-out deposition in middle latitudes; ( c) a greater deposition in the
ported. 31, 33, 8 8 , 1 0 5 , 11...1u Using the nuclear weapon debris
injected into the lower polar as compared to the lower
tropical stratosphere. Supporting evidence has also beenfound in measurements of the deposition of naturally
produced Be 7 • 106-108!IO

UTITllDC

Fig"re 4a. Stratospheric distribution of Sr90 in dpm/103 SCF(= 0.016 µµ.c/m3) during May-June 19591 5 2

10

ICJ"'

a

.,.

za-

""

'"°"™
LATITU:lE
Fig"re 4b. Stratospheric distribution of Sr90 in dpm/10 3 SCF(= 0.016 flµc/m3) during May-June 19601:;2240

basis for describing the removal of weapon debris fromthe stratosphere. There are three parameters that govern the removal of injected debris: altitude, latitude andtime of explosion. If the measurements are interpreted
in terms of half-removal times these are found to varyalso with time after injection, becoming increasingly
longer. This is indeed to be ex.pected as the stratosphereis not uniformly mixed and as the rate of removal isseasonal and localized rather than uniform in time andspace. The concepts of half-removal time and mean residence time thus have very limited usefulness. A numberof estimates of half-removal times have been given in
the literature. 12s, l 53- 155 Some estimates (pertaining to removal of the first half of the injection) have been proposed based on stratospheric measurements : 1~• 1. 52

lO
~

""

LATITUOfi

l!O'

Figure Sa. Stratospheric distribution of w1s5 in dpm/103 SCF(= 0.016 /l/lc/m3) corrected to 15 August 1958, during MayJune 1959152

MimthsLower polar stratosphere (autumn injections)5Higher polar stratosphere ......................... 12
Tropical stratosphere up to 20 km .•.............. 10
Tropical stratosphere 20-30 km .................... 20
Tropical stratosphere 30-45 km. . . . . . . . . . . . . . • . . . . . 30
Mesosphere above 45 km ....•..................... 60

The uncertainty of these figures is great, at least SO percent and sometimes maybe 100 per cent. Until there is amore complete understanding of the meteorologicalfactors that influence stratospheric transport of debris
the values cited above should be considered tentative andused with caution. It has, for example, been pointed
out153 that debris injected into the lower, temperate
stratosphere may be removed within a matter of hours
under exceptional circumstances. The figures for altitudes above 30 km are based only on extrapolations ofmeasured data. Despite these uncertainties it has been
said that the upper limit is probably ten years for debris
injected anywhere in (or falling on top of) the atmosphere.152 Similar values are not available for the southern hemisphere, since the northern hemisphere stratosphere acts as a continuing source of debris passing into
the southern hemisphere. Two seasonal trends may also
be emphasized: the more rapid transport of debris fromthe tropics into the winter hemisphere than the summer
hemisphere and a downward transport of high altitudedebris to the vicinity of the polar tropopause in late
winter. That much is still unknown about the transportmechanisms at high altitudes can be inferred from thefact that there is only one observation published on therise of a cloud from a high altitude explosion. 156

10 ....

.

I
20'

""

LATITUO~

20'

Figure Sb. Stratospheric distribution of w1s5 in dpm/103 SCF(= 0.016 µµ.c/m 3 ) corrected to 15 August 1958, during MayJune 1960152

as a result of the high altitude samplings. Possibly theseand other objections may be overcome through the further modifications suggested by Goldsmith and Brown. 113
A basic uncertainty in dealing with this problem is thelack of data from above 30 km altitude.

The Spar-Feely model
44. One difficulty with the unidirectional poleward
flow postulated in the Brewer-Dobson model is the finding that although an injection of debris into the tropicalstratosphere is noticed after some months in temperate
and higher latitudes, there is also a southward movementfrom polar injections. 152 Evidence of this151 was the collection at 20 km at 30° N on 4 October 1961 of debris
from an explosion injected in the polar region sometime between 10 and 15 September 1961. The total
beta activity was about 40,000 dpm/m 3 and later samples
showed even higher concentrations. In order to explain
this and other results discussed previously, Spar andFeely'141 • 144• 145 have proposed the existence of a bidirectional, diffusive e,'{change rather than a unidirectional,
mass flow in the stratosphere. Actually two phenomena
may be involved in this model, only one of which is diffusion, the second being that the zonal winds are notstrictly zonal but show a meandering pattern, the effectbeing larger in temperate and especially polar latitudes
than close to the equator.

46. Although the half-removal time is based on a simplified concept of the mechanism of atmospheric decontamination, some estin1ate is useful in determining which
short-lived fission products may reach the earth's surface before they have fully disintegrated in the stratosphere. The percentage of relatively short-lived radioisotopes (Sr811 , Y 91 , Zr95 , Ru106, !1 31 , Ba140, Ce1 -n, Ce1~)
falling out from the stratosphere onto the earth's surface
increases as the stratospheric half-removal time diminishes.

Stratospheric aerosols
47. In connexion with the measurements on stratospheric debris it has been found157-uo that there exists anatural aerosol layer extending from the tropopause up
to about 25 km with a ma-ximum concentration around
20 km of aboot 1 particle/cm 3 • The particles are mostly
composed of ammonium sulfate or persulfate and haveradii in the range from less than 0.1 to 1.5 microns.
It has been estimated161 that weapon debris has a coagu-

Half-removal times

45. Present meteorological evidence is evidently insufficient to permit a definite choice as to what model best
represents the characteristics of the stratosphere. However, the measurements referred to have given a better
241

Ia.tion half-life with this natural aerosol at 20 kill of 20,
80 and 280 days for particle sizes of 0.005, 0.01 and 0.02
microns. It may thus be that small radio-active particles
are incorporated into the natural dust background before
they are removed from the stratosphere. This may havesome effect on the rate of removal, especially of debris
from high-altitude explosions that is of very small particle size. It has also been suggested that the influenceof~olar rad_iatig_n on particle transport may be decisive,
especially in the ~rly_ex~atl_sion stages_of_ the- radioac~clo_ud.162 The significance of these two processes
can at present not be evaluated from experimental data,
however.
TRANSPORT l"ROM STRATOSPHERE INTO TROPOSPHERE

Transport through the tropopause

48. The characteristics of the tropopause probably
play a crucial role in the stratosphere to tropospheretransfer of radio-active debris. Danielsen163 has madean extensive study of the tropopause concept and demonstrated that it is not that of a "membrane" preventing
mass flow of air. Rather, the tropopause should be defined as a surface lying between one high-stability region(the stratosphere where the temperature increases withaltitude) and a region with low stability (the troposphere
where the temperature decreases with altitude). If isentropic surfaces are calculated from measured data on
temperature and pressure, it is found that these surfaces
may intersect the tropopause. 153 This means that mass
movement of air is possible across the tropopause, although this may not occur to the extent necessary to
explain quantitatively the transport of debris from thestratosphere to the troposphere. However, isentropic airtransfer in combination with rapid vertical diffusion may
explain the steep gradient of airborne activity concentration immediately above the tropopause (figure 6).10530...............
25..................

.........~,.
.....,.
I

20.........

iaos

49. Diffusion across the tropopause may occur but isprobably of little importance.143 It has been shown17 thatfor fresh debris, gravitational settling of 5 micron size
particles is faster than diffusion into the troposphere.
As the debris gets older, gravitation plays less of a role,
although the existence of the natural aerosol layer(para. 47) may still promote some settling of debris.
Tropopause movements

50. There is a seasonal movement of the tropopause(figure 2) that could account for much of the transfer
of debris to the troposphere. This movement is noticeable
in the temperate latitudes and of particular importancein the polar regions where the tropopause vanishes during
arctic and antarctic winters.164 It is then sometimes notedthat the temperature continues to decrease with altitude
even above 10 km and turbulent mixing may therefore
take place to very high altitudes. In the polar and temperate regions large volumes of the lower stratosphere
may thus be incorporated each spring within the troposphere. This trend is reversed in the autumn.
Disturbances of the tropopause

51. Staley153 has pointed out that in connexion withlarge-scale atmospheric disturbances in temperate andpolar latitudes, vertical air transport may occur from thelower stratosphere and down to an altitude of 1-2 km,
i.e., the lower troposphere. Although this observation isbased on only one example of an e>.."tratropical storm thatwas considered typical, there is some evidence in supportof Staley's finding. Miyake et al.m-i<1s have found a goodcorrelation both between the incidence of an extratropical disturbance and high radio-activity in air and rain
and between the frequency of such disturbances (asmeasured at the 500 mb level) and the global Sr9° deposit (figure 7). For the second correlation to be meaningful the stratospheric concentration of debris close to
the tropopause should be fairly constant with latitude.
This assumption seems reasonable from figures 4 and 5.
Additional support may be found in the fact that a stuayof the stratosphere between 30°-90° N in the spring of195958 showed the net zonal removal to be approximately
pro~ortional to the area of the zone, i.e., a curve of ashape similar to figure 7 (except between 30°-40° N).
Transport through the tropopause gaps.....

52. The possibility of mass transfer of air and debris
through the tropopause discontinuities or "gaps" (figure 2) ~as been extensively referred to in the literature.
Accordmg to Staley, 153 however, "there is no meteorological evidence that jet streams must flow downward" .
Direct sampling in the gap region 116 shows some mixingof stratospheric and tropospheric air but the magnitudeof the phenomenon is not impressive as judged fromthese data.

1i

~

l< 15

.!:

THE TROPOSPHERE

7.5

H orizo1ital movements

53. The transport of radio-active aerosol clouds within
the troposphere has been extensively studied. 169 It has
been found that the radio-active clouds from e.xplosionsof comparatively low power, reaching altitudes of between 7 and 11 kilometres, enter the zone of persistenthorizontal winds. Horizontal air stream speeds in thiszone are usually so high that radio-active clouds can circle
the earth within two or three weeks, or even less. Direct
observation from aircraft of the movements of a corn-

Sr90 d/mln/m3 air

Figure 6. Vertical distribution of Sr11o at various latitudes
July 1957-June 195g1os'

242

sr-90mc/km.2°lo30

Sr 90 depoeition

0

W 0 E
20

00

--){--

25·---A---- OOO 'IC
15

15
10

10
5

I

I

I

I

I

I

_.,.. .P

0

0

90

80

70

60

JI)

50

30

20

10

0

°H
LatitudeFigure 7. Frequency distribution of trough at SOO mb and fall-outlsa(45'0 N), 182 in Panama (10° N),183 and in England(52° N) 181 on 23, 24 and 28 February respectively, andfinally in Sweden ( 60° N) 185 and Czechoslovakia( 50° N) 158 on 1 March 1960. In another case it has
been suggested that tropospheric debris from injections
at about 70° N appeared in about a month in Australia( 15° S). 187 It is perhaps possible to generalize about the
average distribution from repeated tests at the same siteand say that tropospheric debris tends to produce a maximum air concentration displaced towards temperate latitudes irrespective of the test site location. 76 • 1 88 But itshould in any case be realized that only evaluations of thesynoptic situation can give a detailed explanation of results such as those shown in figure 9. 189

pact radio-active cloud170 • 111 has shown that the cloud
lengthens in the direction of movement and in some cases
may divide into independent sections where there is asteep wind speed gradient with altitude (figure 8).m
The assertion is sometimes made that tropospheric debris
distributes in the general latitude in which the e..-..;:plosion
occurred.*8 • 4n,irs,m As is evident from figure 8, this is agreat oversimplification. Recent measurements haveshown that a tropospheric injection at latitude 27° N
on 13 February 1960 was found in the ground level airin Ghana (5° N) on 14 February, 175 in Cairo (30° N)
the next day, 110 • 177 in Bombay (20° N), 178 and Crimea(45° N) 179 on 16 February, in Japan (35° N) 180 and
Israel (32° N) 151 on 17 February, in Romania

Figure 8. Early history of the Mike cloudHZ

243

Figure 9. Total beta activity in surface air (µµc/mS)189244

Survey of air mearnrements

Air concentrations above ground level
55. There are at present relatively fe\v data on activity concentrations in tropospheric air above groWld
level.aa, 1u, 118, 1ss, 20•, 2s3, 201,21s Table yi9s, 201 gives somedata on the average concentration of Sr90 and Csu• in theatmosphere over the USSR in 1955 and 1956. Figure 10
shows the variation of Cs137 with altitude and time, giving
some stratospheric and ground level measurements forcomparison. 115 • 211 • 2 • 5 A seasonal variation of airborne
debris is clearly demonstrated as well as an increase inconcentration with altitude.

54. A large number of measurements of weapon debris
in tropospheric air are now available. 33 • 69 • 8 s,u._ru,:ia5uo,154·1•S-218 niiost of these data relate to measurementsof the total beta-activity of fission products. The principal shortcoming of these latter studies is that the age ofthe investigated activity, with rare exceptions, remains
unknown ; the energy spectrum of the radiation and thenuclide composition of the activity is then also unknown.
It is therefore impossible to utilize these data either foran accurate evaluation of health hazards (F III) or foran explanation of tropospheric transport of debris. Inview of the large amount of work that has been done
the world over in measuring total ,8-activity of air (andrain, para. 74) one might express the hope that the general uselessness of total ft-measurements might be more
widely realized and modifications introduced in future
measurement programmes so as to yield meaningful
results. In consequence, the data on airborne activity
reviewed here will pertain only to measurements giving
some indication of the age or composition of the fission
product mixture.

J1)1C cs

137

Air concentrations at ground level
56. Measurements of air concentrations at groundlevel are much more numerous than those at higher altitudes. Existing determinations of Sr9° show the same
seasonal variations as observed for Cs 137 (figure 10)
although the effect is much less marked for the southernhemisphere. Go, 121,154, 192, 20s, 21s, 21s, 220-221, 220, 231, 2a3, 2a• It isalso evident that the northern hemisphere has a considerably higher amount of airborne activity than thesouthern part of the globe, but this difference decreased..
.

per kg ol air:•

lOr-~~~-r~~~-r~~~--.~~~~...-~~~-r~~~-r~~~---:·~·~~~-.-~~~.....-~~~--.

..
-::.. ··:.

:': :.

:::

P :

..

···......
:1'" ·•. . :. :. :... .,....... .

...
: ··:
::··. .
: \f

: :. :····: ··: !\f ·:\._.JV-

V,;.·...

.

:··

w

./ {\
•

•

V
LOt-~~~-+~~~~1--~-:-:-·~·-r-~~~~1-11--~~-1-~~~--li----4l--~-1-~-1-1-....;...--4~~~~..i.-~~~~
A~

12-14 km---=-¥.
..

:.
o,01r-~~~-r-~~~-+~·~~~--:.:-:l"""-l--\f--+-r~--11---"'11-1-~+-~+1~--!1t.HL-J-~~-'"·~·::.i..~--4~,__-k'--~.:.---1::·.....::··.

~

1.2. Groundkm-; \:

.fi..

level
~001'-----:=:~...L....-~~~.J_~~~...l...-~~~....L.~~~-1-~~~-L~~~--1~~~--l~~~:.......IL-~~--'

1952

1953

1954

F ig"re

1955

1956

1957

1958

10. Cs137 in air over the United Kingdom 115, :r.r, 21s

245

1959

1960

1961

from 1959 to 1960, presumably because of the rapid
fall-out of the debris injected in the polar stratospherein 1958. As the number and distribution of the sampling stations does not represent a truly world-wide
network a detailed evaluation of the global situation isdifficult. The latitudinal distribution of different nuclides has been studied in some detail and results of themeasurements are given in figure 11 212 • 220•25 o,u 2 whichshows a minimum close to the equator and higher concentrations in temperate latitudes. The time variation of
Cs 137 was exemplified in figure 10 and a large number ofstudies are now available both on this nuclide1H, 115 •186•
205, 211-2:8, 2so and on others.120, 1s5, 20s, 2111-22r, 233, :ro wisi
and W 185 produced in the summer 1958 equatorial tests
and Rh102 produced in the 1958 high-altitude equatorial
tests provided unique tracers and made possible the subsequent identification of debris from these tests. Using
this technique, it has sometimes been possible to partition
the airborne activity between different stratospheric injections. Fi~re 12 shows such data281 for Cs137 in air
in the vicinity of Chicago. It is of interest to note thatdebris from injections into the very high equatorial
stratosphere was not observed in appreciable quantities
at ground level until more than a year281 •zs 2 after injection.

100

ME
8

..

10

CD

a.

c

~
'V
0.1

Total
Hcrdtcell

SowietOC~btrHieh AltitQde

M

~

.!

a
:::;
.

u

.

... ,,
0,,c c3
..

0

-::

0

~~

10-•r....._......_......_......._.'-'--'......._........_...._......_........._........................,.....,.............._........_........_._._.........,
J
1958
J
1959
J
1960
J
1961

Figure 12.Partition of Cstar in surface air near Chicago, USA:s1(a) Aerosol particles may act as condensation nuclei
for water vapour. 290•291 This effect has been shown to bei;mall at least for debris consisting mainly of silicates oriron oxide ;292
( b) The vapour pressure gradient arou~d a growing
raindrop or snow crystal may induce capture of aerosol
particles. Facy293 - 295 has shown that this phenomenon
may be important for particles smaller than 0.1 micron;( c) Inertial capture of particles through impaction\irith falling raindrops and snowBakes.2EH;- 29 s This effecthas been shown to be of importance only for particle sizes
greater than 5 microns ;299 •3 00(d) Capture by Brownian motion has been demonstrated to be very effective for particles less than 0.01
micron but becomes unimportant for sizes over 0.1
micron ;isr
( e) Other alternatives have also been discussed 7e but
seem to be of negligible interest.
Evidently aerosol particles in the range of 0.1-5. microns
may not be removed by scavenging as efficiently as areother sizes. Independent evidence of this is furnished bymeasurements on tropospheric aerosols. 301- 304
58. Attempts to establish a correlation- between theconcentrations of debris in ground level air and in rain
have met with varying success. There is usually little or
no reduction in the ground level air concentration duringrain, 213 • 801 · 305 •306 but prolonged, heavy precipitation canlower the air concentration appreciably. 301 · 308 Furthermore, the activity of raindrops from a natural rain cloudhas been found to be the same at an altitude of about
2 km as at ground level. 309 This means that the mechanism whereby fine aerosol particles are captured by falling raindrops is not very efficient. The scavenging effectof falling snow may, however, be greater. Effective
scavenging by aerosol capture apparently occurs during
the formation and subsequent growth of the raindrops.
Other data in figures 13 310 and 14166 show that there is a
general tendency for the activity concentration to decrease as the amount of precipitation in a sample inincreases.102 This can be e..xplained either by assuming
nucleation to be of primary importance and the larger
drop size of a heavy rain giving more diluted concentrations than in a slight rain, or it may be postulated
that drop growth is more important, a greater rate of

Figurt 11. Latitudinal distribution of some fission products inground level air212,220,2so,•12

Capture of debris in precipitation
57. A relationspip has been established between meteorological factors and the concentration of debris intropospherical air and rain.153 • 10 s-168•283- 286 It has beenshown for instance that increased concentrations of fission product ratio-activity in ground level air has accompanied the passage of anti-cyclones. i.e., higher pressures and descending air currents. The formation of"stagnant zones" at the confluence of cyclonic and anticyclonic currents is also conducive to more intense deposition of aerosols on the earth's surface. It is apparent
from this and other work 33 •10 that removal of aerosol
particles occurs much more rapidly than in the stratosphere. The main reason for this is the scavenging effectof tropospheric precipitation. Although the effect is notunderstood in detail, several mechanisms have beenrecognized as possible explanations of the scavenging
process :1s,281-2s9

246

£.
E

.s
....tJc

July 3, 1g5s
15

s..

~
:~

....u

"'

c

f

i

!

10

20

Figure 13. Fluctuations in rainfall rate (mm/h, upper curve)
and fluctuations in specific activity (arbitrary units, lower
curve) versus time in the Netherlandsa10.: . . :. ""°" "''-'
.:
''
'

..
:

May 1954 - February 1956
C 40p14c of sr90/IDJ.
cold front

o warm front
x

..:

tcatp

''

t

®

i
!. """'""" .....-,.
~,

l.C:l»I...

~!

Figure 15. Results of measurements of fall-out materials during
the period September 1956-January 19602~3
Curve A: Concentration of fall-out materials in the lower
stratosphere over SE Norway. Each point represents the resultof one measurement.
Curve B: Monthly average concentrations of fall-out materials in air near ground level. Each point represents an averagevalue of measurements from 9 stations.
Curve C: Monthly average concentrations of fall-out materials in precipitation. Each point represents an average value of
measurements from 12 stations.

=

•

H57

!HT

i

typhoonRa.1nfall amount (mm)Figure 14. Variation in specific activity of rainwater withamount of precipitation in JapanlM

rainfall depleting the airborne activity inside the rain
cloud. A third possibility is that the evaporation of falling raindrops is greater in a heavy than in a light rain.
Whatever the detailed explanation, it is found that on
the average over a long time there is a good correlation
between ground level air and rain concentrations (figures
15 and l6). 2 s3 ,m This is a reflection of the fact (figures
10 and 16) that the concentration of debris in the air at
ground level closely follows the activity fluctuations inhigher tropospheric air most of the time.

Dry removal of debris
59. The scavenging action of precipitation is not the
only process that removes radio-active debris from thetroposphere. Gravitational settling may occur, especiallyfor freshly injected debris. It may also be of some importance even for older debris, however, since there isindication that the presence of natural or industrial
aerosols in the ground level air increases the concentration of airborne activity9 7 • 311 • 312 presumably through coagulation which, as discussed previously (para. 47), may
be quite rapid for submicron particles. This conclusion
is only tentative, as other e.xplanations are possible313
and the effect sometimes is absent.135 Impaction, verticalmass movement and eddy diffusion of air are other
247

.....

Gl!!lUllO Ll'l·ll.
C.Jl\11.TOH-~

a ClPOSITIOH ~l.l.ll.15£0 'TO Mi-'H ..INU.ll. 0.tMf.lLL

05ca.

Figure 16. Annual variation of Cs1s1 in air and rain27SC14 in the tropospherefactors contributing to the removal of debris from thetroposphere. All these factors are, however, best discussed in connexion with measurements of fall-out deposition on the ground (para. 78).
Half-removal time
60. The rate at which tropospheric air is cleared ofaerosols is conveniently expressed in terms of a halfremoval time. Because of the greater rate of mixing in
the troposphere, this concept is more applicable here
than in the case of the stratosphere. A summary of available evidence76 indicates a value of about twenty toforty days as a realistic half-removal time for debris injected in the troposphere above the rain-bearing layers,i.e., about 4 km.

CARBON-14*

CH i1I the stratosphere
61. An extensive series of stratospheric C02 samples/
have been collected by the United States Atomic Energy
Commission150 in conjunction with the ASHCAN
project. The stratospheric contents of C14 at various
periods of time ,have been computed from these data
and are given in table VI. The estimated accuracy is + 30
per cent.
•For discussion of C14 see also annex E.

62. The first experimental verification of increased C14
levels due to nuclear tests \vas reported in 1957 ;314 thedelay behveen substantial production in 1954 and experimental verification of an increase in specific activityof the troposphere being due to the hold-up in the stratosphere. Subsequently, this increase has been followed byvarious workers 31 ~ 829 who have shown that by mid-1959
the increase in the northern hemisphere troposphere wasabout 27 per cent and in the southern hemisphere troposphere 18 per cent. The rate of increase with time in
the troposphere of the two hemispheres, is shown infigure 17 and is consistent with that expected from mixing into the troposphere from a stratospheric reservoirof 04, the content of which has been increasing withtime. In 1960 a decrease in cu levels was reported. 3 <ro,ss.z
The C14 produced from high yield explosions is virtually
all transferred to the stratosphere as shown by the measurements of C14 activity of ground level air in the Philippines before and after the United States Castle test series
in early 1954.333
6~. The measurements of 0 4 activity of tropospheric

air have been made cither by direct separation and collection of C02 from the air _9r by using contemporaryplant material It has been generally assumed that the
0 4 activity of contemporary plant material' reflects directly the activity in the troposphere but this may not+30

4
NORTHERN HEMISPHERE
TROPOSPHERE

3

+20

x

0

~

>
-f
0

;r:::
.,.

2

+10
SOUTHERN HEMISPHERE
TROPOSPHERE

1956

1957
YEAR

Figure 17. Tropospheric inventory of artificial CH

248

necessarily be so for trees, since it is possible that significant fractions of the carbon in the young leaves has
been derived from sources which have been stored forsignificant periods in the trunks or roots. 3 ,z 7 Although
little information is available, it may perhaps be concluded that analyses of annual plants provides more
information on the current C1' activity in the troposphere. Thus, while CH activity measurements of contemporary biospheric materials usually give the samevalue as obtained for ground level air, care is needed in
the interpretation of this type of measurement.
64. The greater increase observed in the troposphereof the northern hemisphere compared to the southernhemisphere is as e.xpected, because all large-scale injections of artificial C14 have been into the northern hemisphere stratosphere. However, the present difference
between the tropospheric C14 levels in the two hemispheres would level out in the absence of testing in a
few more years owing to the inter'-hemispheric exchangeof air masses. 319• 334 Evidence also exists for a small but
positive latitudinal effect in ea levels of the northernhemisphere troposphere during the period 1956-1959 335
Carbon cycle in nature
65. Considerable study of the carbon cycle in natureand the distribution of cu 334 • 33s- 353 has been undertaken in the last decade. As a result of biological processes
and of circulation in the oceans, the carbon which is contained in the atmosphere, in living matter and in theoceans is cycled at a rate that is very rapid on a geologic
time seale (time scale of the order of a few hundred toa few thousand years). The main reservoirs of carbon
that are generally considered in order to determine thepresent and the future distribution of cu, and the relative sizes of these reservoirs, are given in table VII.
66. The amount of carbon in the atmosphere and thetotal amount of carbon in the carbon cycle are knownwith reasonable accuracy (within 10 per cent); however, the figures given in table VII for the amounts ofcarbon involved in the biosphere, humus and surface
waters of the ocean could be subject to considerable error(up to 50 per cent).
67. The rate of carbon e.xchange between the reservoirs of the exchangeable system varies from three toseven years for the mean life of a carbon dioxide molecule in the atmosphere 315 • 316 • 3 :w. 350 • 351 • 361 to approximately 1,000 years for the mean life of a carbon dioxide
molecule in average deep ocean water before its transfer
back to the atmosphere317 • 350 (para. 71). In the case of
the sedimentary system, e.xchange of the carbon withthat of the atmosphere takes place only very slowlytime scale of the order of millions of years 334 • 343-andhence the C 14 content of the sedimentary system is negligible.

M oveme11t of carbon itt the carbot1 cycle
68. Prior to 1900, the C14 distribution within the carbon cycle was in a ''steady state", for although the carbon
in the various reservoirs did not have the same cu
specific activity. the cu specific activity in any given
reservoir was constant with time. Since 1900, however,
mankind has upset this steady state situation in two ways.
First, the combustion of coal and oil has added to theatmosphere an enormous amount of "CH-free" C02
which has reduced the C1' specific activity of the atmosphere and those reservoirs in rapid exchange with it(~~ffect). 339 • 3 e. Secondly, in recent years the testing of atomic weapons has added noticeable amounts ofCH02 to the atmosphere, thereby increasing the C1 ' specific activity of the atmosphere and those reservoirs in
rapid e.xchange with it.
69. There are, therefore, three time periods over whichmeasurements of C14 specific activity may be used toassist in the determination of the dynamics of carbon
cycle. These time periods are :(a) Prior to 1900, steady state distribution of ci..;( b) 1900 to 1952, Suess Effect decrease of C14 specific activity;( c) 1952 to the present, C14 incorporated from nuclear weapons and a smaller fraction incorporated fromtlie operation of reactors.
70. A convenient method of investigating the dynamics of the carbon cycle33 'i 35 <>--352 • 363• 365-367 is by mathematical analysis of a model consisting of various reservoirs in the e.xchangeable system between \vhich transfer
of carbon is assumed to be determined by first order rate
constant and within which mixing rates are assumed to
be rapid compared to the transfer rates. The values ofthe various exchange constants are not known accurately,
so there is corresponding uncertainty in predicted levels.
71. The exchange of carbon between the atmosphereand the surface ocean·· is the main process which determines the distribution of added o• in the carbon
cycle. Considerations of the three separate time
periods3u, 35o, 862 • 368 referred to in paragraph 69 lead toestimates of the mean life of a C02 molecule in theatmosphere, before transfer to the ocean, ranging fromthree to seven years. A less important role is played by
the transfer of carbon from the atmosphere to the land
biosphere. Investigations of the process of photosynthesis in the biosphere 3 •:1-345 suggest that the mean life ofa C02 molecule in the atmosphere before its entry into thebiosphere is of the order of thirty years. The average ageof deep ocean water relative to surface ocean water isoi the order of 1,000 years.31e,n1,aa~nm. Deposition of radio-active fall-out
72. Data on air concentrations were given in the previous section and here experimental values of fall-out
deposited in soil and water will be reviewed. These concentrations vary with time and from region to region.
Whenever possible, therefore, data on the concentrationof radio-isotopes include reference to the geographicalco-ordinates and the time of collection. The curves andgraphs attached may be used for rough quantitative
assessments.
73. The process of fall-out deposition is in generalterms the result of the action of atmospheric phenomena(precipitation and wind) at the ground surface. It is
customary to distinguish between wet and dry deposition,
the first process comprising the impaction of debris contained in rain, snow, etc., on the surface of the earth, thesecond being the impaction of the debris particles themselves. The wet deposition is usually the more important
process except in arid regions where the dry deposit may
predominate.
RATE OF FALL-OUT DEPOSITION

Methods of measitrement

74. Fall-out rates have been studied in many parts of
the world for many years using a variety of methods.
Sampling techniques have included funnel and pot col249

lectors, often in combination with an ion exchanger,
sticky paper and gauze trays, to mention the more important methods used for the collection of wet and dry
depositions. Sampling techniques were discussed in theprevious report of the Committee and the differences incollection efficiency described. Subsequent measurementson these samples have employed both advanced techniques of radio-chemistry and gamma-spectrometry as
well as simpler measurements of total ,8-activity. As inconnexion with airborne activity (para. 54) it may again
be stated that measurements that give only the total [Jactivity with no indication of the age or composition of
the fall-out are of little value for the interpretation of theresulting health hazards. 312 Again, therefore, greater
emphasis will be placed upon data specifying fall-out
composition.

fairly good correlation with airborne activity (figures
15 and 16). This fact and the assumption made in theprevious paragraph of a relation between airborne
activity and fall-out rate suggest that only a poor correlation should exist between fall-out rate ( approximately equal to amount of rain X concentration in rain)
and the total amount of precipitation. This is indeed
found to be the case when data are studied as a functionof time at one place. 202• 505 Figure 18 shows monthly datafrom the United States 374 and figure 19 gives yearly
averages from the United Kingdom m both based on
measurements of Sr9° in rain. In addition tables VIII
and IX give values for Sr9° and some other nuclides. It isof special interest to compare figure 19 with the data on
airborne activity from the same place (Milford Haven)shown in figure 10. The approximately uniform increasein Sr9° accumulation over the period 1956-1958 corresponded to a uniform air concentration over these same
years. In 1959 there was a threefold increase in the airconcentration corresponding to a sharp rise in Sr9° deposition rate in spite of the fact that the yearly precipitation was almost constant. The low air values in late 1959
and 1960 finally gave rise to an abrupt decrease in thefall-out rate.

Relation to airborne activity

75. The deposition of fall-out has been shown veryclearly to result mainly through precipitation falling onto the earth's surface. 33 • 120• 144 • 373 As most precipitation
originates in the lower troposphere, the rate of fall-out
in any particular region should as a rule be determinedby the tropospheric airborne activity. It is important inthis connexion to distinguish between short- and longterm conditions. Short-term (daily) variations in deposition do not correspond too closely to the short-term
variations of the same nuclides in the air. In certain
cases, a decline in the fall-out rate of Ce1 H, Cs137 and
Sr-8° coincided with an increase of their concentration in
air. 226 If, on the other hand, long-term conditions are
considered, one would expect an averaging out of mostchance fluctuations in the concentration of airborne
activity and of most differences in the properties andorigin of the clouds bringing rain to the area concerned.

Relation to total precipitation

77. If there is thus a poor correlation between total
rainfall and fall-out rate at one place as a function oftime, there exists- a good correlation between the sametwo quantities for different places over the same time
period.120 • 876 • 377 This is true at least for limited areas ofhomogeneous climatic conditions, but the conclusion may
also hold when points at great distances are compared.
Miyake et al. 187 • 168 have shown that it may be possible todescribe global deposition of Sr90 with an empiricalformula:Fd = C(l - e-2P + 0.06P)
where Fd is the deposition, C is the amount of airborne
radio-activity in the rain-bearing air column above unit
surface area and P the rainfall amount. If C is taken as
0.054 me Sr9°jkm 2 in the northern temperate zone and as

Relatio~i to debris concentration in rain

76. As was shown earlier (para. 58) the specific concentration of activity in rain varies with the amount ofprecipitation in the individual rainfall (figures 13 and14). Yet, taking monthly averages, this effect was foundto be less important, the rain concentrations showing a

zoo

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3

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ii:

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IV

v

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VII

VIII

IX

x

XI

XII

II

1958

Ill

IV

V

VI

VII

VIII

IX

X

1959

Figure 18. Rainfall (dashed line) and rate of fall-out in Westwood, New Jersey, USASH ·

250

XI

XII

1956

1957

1958

1959

1960

0.18 mcfkm2 cm

25

0.01 mcfkm2 cm

20

!

15

.....
0

II)

0,03 mcfkm2 cm

0

E

10

s

•
Figure 19. Cumulative Sr 90 as a function of cumulative rainfall (Milford Haven, United Kingdom) sr 5

0.007 me Sr90jkm2 in the tropical region between 15° N
and 20° S then the fit between theory and data is as shownin figure 20. Examples of limited areas 376 •371 are shownin figures 21 and 22 based on quarterly data of SrS-O andin figure 23 relating the fall-out of Cs137 over several
years with the precipitation in that same period.120 The
points in figure 23 correspond to different places in
Nonvay and Sweden. Even within limited areas exceptions to this rule have however been found, giving forexample 3 T 8 in 1958 monthly averages of 54 and 69
mc/km 2 of beta activity in two places where the averagemonthly rainfall was 306 and 47 mm respectively. Thisparticular finding, however, is not conclusive, as it isbased only on a total beta measurement.

I0al Winter

0
v

30

~

0

8

ff' 0 0~00

o ooooli;, C oCf3
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i "values

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0

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10000

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nn preclpllatiQn 19SJ.19S9

500

Figure 20. World-wide Sr9o fall-out and amountof precipitation1er, 1es
I : C 0.054 me Sr&ojlan2 in temperate zone
II: C = 0.007 me Sr 9 0/km 2 in tropical zone

.

1,000

Rainfall mm /. 3 month

Figure 21. The relation between the quantity of Srl>O and thequantity of rain deposited per unit area. of ground during
three months (United Kingdom, 1958)376=

251

measuredvaluesa: esll7Jla1

a 1 Winterx 2 Spring!

• 3 Summer

t. 4 Autumn£ 3.0

6 i::0

IO

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7D

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E 2·0
•

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E

Cll

1.0

50

40

1.000

500

311

Rainfall mm/ 3 month

Figure 22. The relation between the quantity of Sr9 0 and thequantity of rain deposited per unit area of ground during
three months (Japan, 1958)3TT

Dry deposition
78. Dry deposition of fall-out may occur in at least
three different ways. Gravitational deposition may be important for fresh fall-out. Observations in Cairo 178 • 177
two days after a tropospheric injection and in Bombay 178
one day later showed intense fall-out ( 100 and 170
mcjkm2 of total beta activity respectively) despite thecomplete absence of rain. The calculated amount of longlived activity was very small, however, for example lessthan 0.01 mcjkm2 of Cs131 • Another dry process is theinertial deposition of aerosol particles associated with theflow of air over objects on the ground37 9 • 381 mainly grass
and leaves of trees. A third mechanism, finally has been
described by Facy 2 u1 • 293 • 295 proposing that deposition
may take place by the nocturnal diffusion of water

10

icoo

ZaJJ

•axi

m1

!ilXl

~ •

7lllJ

am

mi

- plCipibtiol f!Oll l J_, 1955 Ill Amllii• dal9

Figure 23. Correlation between Cs137 soil activity andrainfall in Swedenuo

vapour from the atmosphere into the soil 382 • 383 or on toherbage.
79. The quantitative relationship between "dry" and"wet" fall-out of radio-active aerosols on different partsof the earth's surface depends on climatic conditions. For
example, in an area with comparatively heavy precipitation, such as Norway, the average monthly proportion

2.5

2.0

~

g

... 1.5
E

a.

rt

e

;.. 1.0
Cl)

u

E

0.5

1954

1955

1956

1958

1957

Figure 24. Monthly fall-out rate of Sr

252

90

1959

in New York City9

1960

1961

1.6 .

l.S
l •.f

1.3
·1.2

1.1

1.0

..;:

c
0
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.

0.9

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Q.

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.u
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o._._i...._.~-"...L...L...L...i....._.i.-..__1...1-.1...J.....1....1...&...L..i.-.i....__~~~........__....._..._.._-.~""""'--....................

v Vl ·VU VIII· ix x XI X11
1957

l II Illj

wv

VIVIIVlll lX

1958

x xi Xll I 11 m IV v VI VIIVIIl IX x· XI XII.

IFigure 25. Average monthly fall-out rate of Sr90 in USA11of "dry" fall-out between November 1958 and September 1959 ranged from about 10 to 72 per cent. This is
likely to have included some gravitational settling of thelarger particles present shortly after a test. The average
proportion of "dry" fall-out during that period was about
30 per cent.120

f

1959

2.0

I II ll1 IV v· VI vuvm IX x Xl XIl

t960 -

Months and years

7

e. o.c..0or ma-Fol>nqy 1959

!

-

.;;

Adval doposltlQQ
Riilnfoll Cl>rlec!l<rl~ 1.0

Measurements of S~ 0 and Cs137

80. The Committee has received a large number ofreports giving data on the fall-out rate. The following
references give measurements Of Sr9°. 31 •50•1Al 2 , 115-llll, lM,
l Ta, 214, 1&2, 1ae, 200, 2o.s. 201, 2oe, 21-s, 224, 22s-2-41, 3T5-31s. a&5-•13 Some
examples will be found in figures 24 and 25 and tables X
and XI. For Cs137 the following references may becited :so, 102, 11e, 224, 22e, 221, 232, 234, 235, s15, 376,384-3$4 and forother nuclides, like Sr' 9 , Ce1"", Zr95 etc. :50• 1° 2· us, 11 9 • 20s,
21e, 220, 221, 2ao, 232-235 Tables XII and XIII containsome of these data. A survey 88 • 116 •138 •276 of the average global distribution of Sr9° is given in figures 26
and 27. The latitudinal variation of the fall-out rate
shows changes with time that are consistent with a short
residence time of polar injections. Spring maxima areevident in both hemispheres, occurring in March to May
in the northern and in September to November in thesouthern hemisphere. As the number of sampling stations within each latitude band does not constitute a representative selection with regard to geographic differences in annual rainfall, two curves are shown for eachtime period, one giving the arithmetic mean of observed
values, the other a mean weighted for annual rainfall.

3.0'

1.0

O_;LI.-,1--L...-L--:l,--..J..~.1.---1~..J..~.1.,_-,,1,-~i--.I...~~

90° 60°

30° •

South

Figure 26a,b. Global distribution of SrBo ss,11e,13s,.2TG

253

c,

June~st 1959

Actual deposition
Corrected for mean :raintall

2.0

l.O

e. December l959-FebN&17 1960

f. March-Hq 1960---------g, May-June 1960--------h.· July-August 1960

i. September-October 1960

j, November-December 191$>

North

South

Figu,.e 26c-j. Global distribution ·of Sreo 88,110,l38,2rs

From figure 27 a fairly good correlation between airborne activity and fall-out rate can be inferred, as was
suggested in the previous discussion (paras. 75 and 76).
81. Measurements of Sr90 and Cs131 could be complementary if the ratio Cs 131/Sr9° were known. This ratio
usually lies between 1.5 and 2.0 although occasional
values lying outside these limits have been observed. The
determination of Sr90 involves a complicated chemical
analysis and Cs 131 samples have been found to requireconsiderable care in the collection technique if errors
larger than 50 per cent are to be avoided.11 5 It is therefore not surprising that the Cs181/Sr90 ratio, which according to some measurements has an average value of
1.7,283 • sa,.n•,• 15 in other cases has been reported to be
2.8 with single values up around 8. 885 All of these deviations need not be analytical errors, as it is evident fromtable I that the Cs187/Sru 0 ratio may vary between 0.93
and 3.05 for different modes of fission. In addition it
has been shown that fractionation 185 and differing transport properties of different size particles may play anunportant role. iii., 2so, :a1254

M easm·ements of short-lived nuclides

82. The seasonal variations observed in the Sr90 andCs137 fall-out rate are not necessarily found with respect
to more short-lived nuclides like Zr9 5 , Sr8 9 or Ba1 • 0 •Here the time of injection becomes more important since
the deposition is largely tropospheric. In the case of pn
no deposition may be observed later than about twomonths after injection. Figure 28160 • 416 shows the variation of Sr89 fall-out from 1956 to 1959.
Tritium

83. A number of studies have been made on the atmospheric transport and deposition of tritium.'11- ' 28
It has been found that tritium is deposited mainly
through the action of precipitation, rain and snow containing tritiated water. In figure 29'17.-us the fall-out rateof tritium from 1951 to 1960 in the vicinity of Ottawa,
Canada, is shown. The values for 1951-1953 correspondto the natural background (E 56) whereas in 1954 themaximum found in individual rains is more than 100

19!581953

1960

ACCUMULATED FALL-OUT DEPOSIT

0.2 J F M A II J J A 5 0 N 0 J F M A M J J A S 0 N D J F II A M J J A S O N D

Deposition of Sr90
..:

c
l
.....

..
..e

0.1

84. The cumulative deposit of different nuclides iscustomarily measured in either of two ways, throughextended measurements of fall-out rate or through radio-chemical separation of the activity in soil samples.
The first method is preferred for short-lived nuclides
like !1 31 and Ba140 ; the second method is considered tobe more precise for Sr90 and Cs 13 ', but most often both
sources of information are used for the latter nuclides.
Extended measurements of fall-out rate have been presented in previous paragraphs. Integrating the rate gives
the deposit and the results of such a procedure are shownin figures 30-32.166 • 226 •ms, 375 • 378 • 430•431 There is a large
amount of data currently available (December 1961) on
radio-chemical analyses of soils for Sr80 content. 9 e, 10 2.119 ,SURFACE DEPOSITION~ 0.05
0

2'
cl'i
0.01

0.009
10

.

-

North9r" H1mhpb1:re- - · Southern Htlftltpb:u•-a0u ;, 174, ie2, 196, 201, 2u-221. 236-239,2-'2-2•4, 38-t, as1. 393 1 s9e, 402, •oa-...11.
NRL. AVERAGE AIR
CONCENTRATION

8:;;:
c

e.....

.

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JFWAMJJASONDJFMAMJJASONDJFWAMJJASOHD

1958

1959

432443 The error of most of these data is considered
not to e..""<ceed + 10 per cent as a result of the radiochemical separation. On the basis of 1960-61 data aneffort has been made to draw a map of the world-wide
distribution (figure 33). Only in North America are thedata numerous enough to allow the drawing of isolines.
85. If the soil data are extrapolated through the useof rainfall values and the correlation between rainfall
and fall-out rate (para. 77) it is possible to constructmore detailed maps, 390 but the accuracy of this procedure
is perhaps not too great. For North America it has beenpossible in this way to showff' higher Sr9° levels due totropospheric fall-out from the Nevada Test Site injections. Figure 34 shows the Sr9° e..'Ccess above the world
average from this cause. The figures have been arrived
at through subtracting from the total Sr110 deposit a constant value corresponding to the stratospheric fall-out.
Recent observations 445 indicate that this procedure maylead to an overestimate of the tropospheric fall-out.
86. The Sr90 data may be combined in 10° latitudinalbands to show the average world-wide distribution(table XIV). The data of table XIV is shown in figure 35. This obviously gives a less detailed picture than
413

1960

Figure 27. Global fall-out rate and surface
air concentration210

times higher. From data like these it has been concluded418' 424 • 428 that the atmospheric half-removal time
is no greater than thirty-five or forty days for tritium.
Essentially this conclusion holds only for tritium contained in water molecules, but the existence of a large
stratospheric reservoir of tritium in the form of hydrogen molecules is not likely as judged from measurements
on stratospheric hydrogen.429

•

30

20
N

E

~
~
u

E

Figure 28. Rate of fall-out of Sr89 in Milford Haven, United Kingdom102, 31'5, 3T6, au

255

sooo

!!

·c:::>

1000
1100
800
700

e

SOO

:s:

400

~

·=t!

300

"c
.::

200

~

0

too

CJ

u

c
0

u

e

~

jE

100
90
80
70

eo
so
Three-month average tritium
concentration in rainfall

40
30
3'SfE

Tritium concentrationin river water (Ottawa River)-e-0-

Measured tritium concentrationsin individual rainfalls

20

101-------1------_,;1----_:_--(-S!._----l-------if-------il-------il-------i-------;~-----1951

1952

!953

1954

1955

1956

1958

1957

1959

l~O

Years

Figure 29. Tritium in rain and river waters in Canada417,ns

taken, for example, at twelve different points of therelatively small island of Hokkaido differed in Sr9° content by a factor of more than ten.436 Such variations could
arise in two ways. Topographic factors may cause
marked differences in the deposition of rain and hence offall-out over small areas; furthermore, after it has been
deposited, activity may be displaced by the movement of
surface water and wind.

a map, the high values, for example, on the west coastsof Norway and the state of Washington, United States,
raising the latitudinal mean only slightly. In addition,
the values in some latitude bands are based on highly
limited numbers of measurements and consequently theerror in the average may considerably exceed the 10 per
cent396 error in measurement.
87. It is finally possible to integrate the latitude distributions of Sr90 for different years and to arrive at
values for the total deposition as a function of time.
This yields for 1956 a figure of 1.4 ± 0.4 Mc Sr9°, whilefor 1958 the value is 3.1+1.0, for 1959 5.4 + 1.6 and5.4 + 1.6 for 1960. The uncertainty is obviously great
and a much closer network of sampling stations (outside
North America) is needed if better data are wanted.
It has been found that a correction factor of 1.18 applies
to such determinations of Sr90 as only 85 per cent of thestrontium present is extracted on the average. Thisfactor applies to broad average values but should not
be used to correct individual values. Here, therefore, it
has been used in giving the average figures above but allother Srti0 data given are uncorrected.

DEPOSITION AND TRANSPORT IN WATER

The oceans

90. The fall-out activity in the oceans arises mainly
from three sources : deposition of tropospheric andstratospheric fall-out, close-in fall-out from land andwater surface explosions, and rainwater run-off carriedby rivers into the oceans. The two first effects presumably dominate the deposition of fall-out over the sea, thefirst perhaps being 1.5-2 times greater per surface area
than over land, as judged from measurements in theBlack Sea region. 311 Activity deposited on the water surface rapidly mixes down to about 100 m depth.• 5 ° From
there downwards the rate of exchange is much slower.4 51
For this reason and because of the surface movementof ocean water, the variation of water concentrations offall-out with time, place and depth is extremely complex.

Other nuclides

88. Soil data on nuclides other than Sr90 may be foundin the literature 431 • -Hs-u9 and some are given in table
XV. These values are based on gamma spectrometricalmethods.

91. Measurements of total ,8-activity as well as Sr90
and other nuclides have been reported. 224 , 201• ~M, 2ss, atia,
4 4 5
r.i s Values 451 ··"61 of around 4 µ.µ.c Sr1°/100 1 in thenorthern Atlantic and a corresponding value of 2 in thesouthern Atlantic have been reported. The concentration
at 50-1.000 m was about half the surface values but

Local factors infiuen.cing deposition'89. It should finally be pointed out that local differences of fall-out deposition may be found. Soil samples

256

100

NEW YORK(276)

30

N

E

~

!:?

u

so

u

E

2S

TOKY0(166)

1957

1958

1959

1960

YEARS

Fig11re 32. Accumulation of Cs131 in soil of Japan•a1

20

...

1959 in the eastern Pacific. Similar results have beenfound for Cs1 :r..462 • 463
92. Variations in tritium concentration were also observed in seawater.418 In samples collected from the surface of the sea at a number of widely-spaced points
ranging from Arctic latitudes (74° N, 91° W) to 47° N,
47° W, the tritium concentration in the second half of1954 and the beginning of 1955 fluctuated between 4.2
and about 3 tritium units.* The data are too limited toallow any conclusions to be drawn about the world-wide
conditions.
Lakes and rivers
93. Data also exist for lake and river waters the world
over. 211, 225, 230-2as, 2•2-2H, 203-210, 4o~s In general values
around 0.1-1 p.p.c Sr90 and 0.05-0.2 µ.p.c Cs 137 per litre
water are found, 237 • 468 but both higher and lower values
are occasionally observed. There is a trend in concentration similar to that of the fall-out rate. but the variations
with time in any one lake or river are smaller, as could
be expected. It has been estimatedm·• 89 that the run-offof Sr9° by rivers to the sea is about 1-10 per cent andthat of Cs 137 2-6 per cent of the yearly deposition but thi3
value is likely to vary between different water sheds.
The amount of Sr9° in ground water, finally. is usually
too small to be detectable. 488 l\ Ieasurements of tritium
concentrations in ground water samples collected frombores at a depth of 40-50 mm showed that, between
February 1954 and July 1959, the tritium concentration
fluctuated behveen about 1.4 and 0.4 tritium units, i.e.,
was appreciably lower than in sea water and very much
lower than in rain water.

I!

$.

°j;
u
E

15

LENINGRAo(226l

10.

BOMBAy(430)

s

1957

1958

1959

1960

YEARS

Figure 30. Variation with time in the cumulative Sroo fall-out

1

Zll

~Ill

..

~

~:

IV. Predictions of future levels

K1oi--~-t~~-t-~~-t----1t-'tt:zdllll'l----r-T~;-~--,zo(

Figure 31. Cumulative deposition at Milford Haven,
United Kingdom 3 7 5 , 37 6

further down at 2,000-3,000 m no strontium was discovered. Higher values have been found in the western
Pacificm varying between 80-310 µ.µ.c/100 l of surface
water in 1957-59. At 5,000 m' 53 the values were about
one-tenth those at the surface while at 6,000 and 8,000 m
no Sr90 was found. .m, • 03 Lower values were found in

94. It is obvious from the discussion in the three previous sections that the process of fall-out deposition on
the earth's surface is e.xtremely complex. It therefore
follows that the task of forecasting the deposition is very
difficult. This has indeed been found to be the casealready in connexion with predictions of local fall-out
although this phenomenon is of short range and duration in comparison with the world-wide fall-out. There
are two separate problems to consider in this conne.xion :• (a) prediction of future fall-out from past testing;( b) prediction of future fall-out from hypothetical
future testing.
*I tritium unit = 10-1 8 H3 atoms/hydrogen atom.
257

~~ ..~o

N
tTt

00

.;'

.....

y

\Jl5.B..

J) 6.J~.6- •~••"'d•f""'" ,,....,..,..,,., •r •e«pla11c•
ln1ranut. fl11•1I",.,,.i1..r:1ro-. '""'•"a- Jm,PJ.,
kl' lh• Un1'"1 N•''"'"'
er• nnf, fn "''"'

The- ...,,.,.,.,.

nol

MAP NO, 1154 REV.I

MA'I'

Ullllf.D NATIONS

llflt

Figure 33. Sroo mc/km2 in 1960-1961

dtf#tmol"ird mul '"'''

30

1950

20

.........

10

•1958

Figure 34. Srll<> in USA soils from tropospheric fall-out4H

95. The first problem can be given an approximate
solution on the basis of experimental measurements.
An inventory of present activity levels in the atmosphere,on the ground and in the oceans can be established towithin about a factor of 2. The future changes in thesereservoirs may then be forecast to give a picture of theaverage world-wide deposition of fall-out in years tocome ..Also 0e .lati~udinal and to a ce~ain extent the geographical distnbubon may be described in an approximate manner.

20
Sou1h

60

Fig1tre 35. Mean concentration of Sreo in soil at
different terrestrial latitudes

Because so many assumptions must be made, no precise
calculation is possible, especially as any nuclear devices
t~sted in the future and the conditions of these tests may
differ substantially from the past atomic tests with which
we are familiar. These considerations must be clearly
realized before any conclusions can be drawn from thefuture predictions that are presented in the following
paragraphs.
INVENTORY OF SR90
97. Measurements of the atmospheric concentrations
from close to the ground up to 30 km have been evaluatedto give the inventories shown in table XVI.162 • 470 Dataon deposition may be taken from soil measurements(para. 84) and integrations of the fall-out rate. 880 11a, u8,
152 278•
All these data are summarized in figure 36. Owing

96. T~e second problem cannot be solved in this way;
the solution has to be based on assumptions. And a large
number of assumptions are necessary to give an answer.
To mention the more important ones:(a) Total amount of testing;( b) Types of weapons;( c) Weapon yields ;( d) Heights of burst;( e) Season when bursts take place;(f) Test site latitudes;(g) Meteorological conditions.
Megacurie Sr90

io40

0 Soil measureu:ents
f?j Atmosphere measurements·TotaJ.

_,..,,Precipitation.measurements

[. •

5

[J

Figure 36. Inventory of Sr&a

259

to radio-active decay the total amount of Sr>° continuously decreases with time at a rate of 2.5 per cent peryear.
98. A closer analysis of the data in figure 36 reveals
that from the end of 1958 to mid-1961 the stratosphericreservoir diminished from 1.5 to 1.0 Mc of Sr9°, i.e.,a difference of 0.5 Mc. Over the same period of time aworld-wide deposition of about 1.5 Mc can be inferredfrom soil and rain measurements. As there were noappreciable injections of Sr90 during this time, the data
are inconsistent. If, as has been suggested, there is ahigher deposition over the oceans than over dry land,
this discrepancy would be even greater.

102. The data shown in figure 17 for the increase of
the C14 activity in the tropospherrwere obtained bymeasurement of the increase of C1 activity relative tonatural C14 activity. No measurements above 30 km areavailable however. Conversion to atoms of C14 was doneon the following basis: the troposphere contains fivesixths of the mass of the atmosphere, the C02 content of
the atmosphere is 310 ppm by volume, and the specificactivity of natural carbon. is 14 + 1 dpm/g. The troposphere of each hemisphere thus contains 15 X 10 21 atomsof cosmic ray produced C14 and each 1 per cent increase
corresponds to the addition of 0.15 X 102 7 atoms of C1'
to the troposphere.

99. The discrepancy in the inventory data is most
likely explained by inadequacies in the sampling system:(a) No samples taken above 30 km in the stratosphere;(b) Too few samples in the northern polar stratosphere in 1958 and 1959;( c) No deposition samples reported for large areasof the world, especially the oceans (figure 33).

103. The amount of artificial C14 in the biosphere andsurface ocean;(:annot be accurately determined by direct
measurements at the present time and hence must be
calculated using e..xchange constants and reservoir size
data as deduced from the studies of the carbon cycle.
Computed values for the C14 content of the biosphere andocean, along with the stratospheric and tropospheric contents as indicated by experimental data, are given intable XVII for 1 July 1957, 1958, 1959, and May-June
1961.

Thus it is possible only to speculate about the actual
situation. One possibility is that the stratosphere above
30 km contains older debris than hitherto assumed. This
assumption is supported by the observation 277 • 281 thatabout 50 per cent of the Cs 137 in ground level air in lc.te
1960 could be from injections earlier than 1958. On theother hand, stratospheric measurements152 of the ratio
Cem/Sr90 (which varies with the age of the debris) do
not show any appreciable influx of older debris fromabove30km.

104. The value of 14 X 102 7 atoms for the total artificial C14 inventory for 1 July 1958-appears reasonably
well established. 3111• m An estimate of the C14 production
from that date up to 31 October 1958 may be obtained
from the data given· in the hearings of the United States
Joint Committee on Atomic Energy. 80 This leads to an
expected production of an additional 5-8 x 1027 ea
atoms in that period, i.e., a total inventory of 19 to
22 X 102 7 C 14 atoms as of October 1958. Using theexperimentally determined value of 9 X 102 7 C1 4 atoms
as of 1 January 1957, Hagemann et al. 411 estimate a total
inventory of 25 X 102 7 C14 atoms for 31 October 1958.

OTHER INVENTORIES

100. The measurements reported on Cs137 are too few
and limited in scope to allow the establishment of an
inventory similar to the one for Sr9°. The same can also
be said for a number of other nuclides, like Sr89, Zr9 5and eem, that are of some importance as possible healthhazards. In the case of Cs 137 the production in relation
to Sr110 can be estimated within fairly narrow limits andas this ratio stays almost constant with time, an inventoryof Csu 1 may be arrived at in an indirect way. This procedure is however open to question both because of varying production ratios (table I) and because of the possible importance of fractionation phenomena. Yet thisapproach is the only possible one at present. For
Cs137/Sr90 a value of 1.7 is usually assumed and thisvalue is also adopted here. A simple multiplication of all
srio data by 1.7 will therefore describe the Cs137 inventory according to paragraphs 97-99.

PREDICTION OF FUTURE FALL-OUT

General105. The first requisite of an accurate prediction isan accurate inventory. A second necessary condition is arealistic model that describes the complex transport situation. As is apparent from the foregoing discussions,
there is appreciable uncertainty on both of these points.
Any future prediction will of course inevitably beaffected by this. One conclusion may therefore at thepresent time be that there is no need for adopting a complicated, mathematical treatment of the prediction
problem. A simple approach, although more approximate, will be in better line with the uncertainties in thedata.

cu INVENTORY
101. From the measurements of cu levels in the tropo-106. In the 1958 report of the Committee the prediction of future fall-out was based on the simple exponential model, i.e., assuming a constant fractional removalof debris from the atmosphere. The deposition F d ( t)and the rate of fall-out Fr(t) were determined by theequations:sphere and the stratosphere;the artificial C14 inventory
may be computed and compared to that calculated fromdata on the total energy yield of nuclear weapons, as
given in paragraphs 36 and 37.

Fr(t) = Fr(O) • e->.t • e-i;+

1260+\Tm [ 1 - e->-t • e--:f-..

lwhere Fd(O), Fr(O) and Q(O) give the deposit, fallout rate and atmospheric inventory at the start of theprediction period (t = 0). Tm is the atmospheric mean
residence time, ;\ the radio-active decay constant and n
the rate of injection of debris.

35

30

Sr9° and Cs 131• soil dai.
90
- - - 6McS1,-,1

107. For nuclides like Sr90 and Cs 137 which have halflives much longer than the mean residence time in thestratosphere, the ultimate deposition on the ground isrelatively independent of the value assumed for the residence time. Effects that depend only on the magnitudeof the total deposit (e.g. uptake by plant roots) thus
vary only little with the assumed residence time.
108. Rate-dependent processes (e.g. uptake by plantleaves and plant base absorption) are directly affectedby the residence time. Assuming a short residence time,
there will practically be only one year that is characterized by a marked effect. For a longer residence time,several years would show a less marked effect. The overall dose delivered over several years will not vary appreciably with different residence times.

10

Deposition of SrR 0 and C~J 7 from tests up to
the end of 1960s109. The deposition of Sr90 from these tests waslargely completed by mid-1960 and was about 5.4 Mc
Sr90 (para. 87) and the atmospheric reservoir was about
1.2 Mc ·(table XVI). The injections of 1959 and 1960
were small enough not noticeably to influence the global
distribution of Cs137 and Sr90 • The Sr9° deposit from
weapon tests carried out up to 1960 is predicted to reacha ma."Cimum value of 5.8 Mc Sr90 in 1964 and then to
decay with a 28-year half-life (figures 37 and 38).

"

I
I

D

19SO

'

1960

1970

1980

l!/90

2000

2010

2020

110. As was pointed out in paragraph 36, for theoretical predictions of fall-out from nuclear explosions
it is necessary to know the quantity of radio-active products injected into the atmosphere. At present there are
not sufficient data on fall-out from the 1961 tests (para.
37) to make an accurate estimate of the injection fromthose tests. In addition, there is no way in which theCommittee can predict the pattern of future testing andtherefore no way of predicting the actual fall-out levels
from any such tests. Accordingly, as an illustration, theCommittee has chosen a model for the estimation of-.

lojoction,---------------------' ------------~~~~~----------

I
I•I

fqullibrhm fall-I rate

.,.,.

II

~

":;;
u

"" 0.5
-=-

~

•

I
I
I

I
I
I
I
I
I
I

roln data- - - 6·McSr90;sy
Tosts 1nding end al

1960

•

:zo.co ,_fall-out from tests conducted after the end of 1960, in
which large-scale testing is resumed in the year 1961
with an injection of 1 Mc Sr90 and 1028 atoms of C1'
and continues for specified periods with the same annual
injections of Sr90 and cu. Within this context, fourcases are considered :(a) Tests are discontinued at the end of 1961 ;( b) Tests are discontinued at the end of 1962;( c) Tests are discontinued at the end of 1965;( d) Tests are continued indefinitely.
111. It is assumed that the stratosphere is cleared
according to an exponential law with a half-removal timeequal to 2~ years. The results of calculations for Sr"I'
are given in figures 37 and 38. Cs 137 activity is calculated
assuming it to be 1.7 times the Srio activity.

A model illustrating deposition of SrR 0 and csin from apattern of tests subseq1tent to 1960

1.0

2030

Figu,.e 37. Future deposition of Sr-90

1961
1967

oL-~'~..L.~~:t.::::=-:::::-.JL..-~-l~~.....L~~...l-~~..L.~~J.-~--l---~1'11\0
1970
19110
1990
2opo
2010
:mo

1950

Figure 38. Future fall-out rate of Sr90

261

112. The latitudinal distribution of future fall-out
would be expected to follow the general pattern of
figure 35. A larger fraction of debris from polar andtemperate latitude injections is deposited in the northernhemisphere. In the past this has amounted to about 15
per cent more for polar injections than for equatorial
injections.

(c) There will be a further fall with a half-period of
about 1,000 years-owing to equilibration with the deep
ocean. When equilibration is complete, the C1• level inthe troposphere will be approximately 1 per cent above
normal;( d) This 1 per cent increase above norm:l will thendecay with the mean life of C14-8,000 years.

113. On these assumptions the maximum deposit
from tests completed by the end of 1961 should occur
in 1966 and be about 6.5 Mc. The rate of fall-out couldin 1962, however, be higher than 0.7 Mc (figure 38)
but would then be correspondingly less in subsequent
years. In figures 37 and 38 curves have been drav.-n corresponding to tests being discontinued at the end of 1961,
1962 and 1965. These curves give no indication whatsoever of the actual extent of future weapon testing.

117. Figure 39 shows the biospheric level of artificial
C14 expected on the basis of both a 5 and a 2 reservoir
model for the following conditions : addition of 22 X ion
atoms of C14 ; average residence time of C1• in thestratosphere before transfer to the troposphere-fiveyears; average residence time of cu in the troposphere
before entrance into the biosphere-thirty years; average residence time in the troposphere before transfer tothe surface ocean-five years ; average residence time inthe surface ocean before transfer to the deep ocean1,000 years. The value of 22 X 102 7 atoms of 0,* represents a probable value for what has been injected as ofthe end of 1960 (para. 104 ).

114. For short-lived nuclides, a long delay between
injection and deposition will give time for considerable
radio-active decay. Early deposition will however bring
down measurable amounts of short-lived nuclides. This
early deposition has taken place largely in the hemisphereof injection. Probably the residence times for polar andtemperate injections are shorter than for equatorial injections, and the doses from short-lived isotopes will
be greater for polar and temperate injections than forequatorial injection. Radiation doses from the fall-outof these isotopes have been calculated in annex F,part III.

400

200
100
60
40

C1 ' from tests up to the end of 1960

115. The present distribution of the inventory of artificial cu from tests of nuclear devices to date.'is knownwith an accuracy of probably + 20 per cent. Before thedose received by biospheric material from this added cu
can be calculated, future biospheric levels of artificial
C 14 must be deduced. This can be done mathematically,
but the accuracy is limited by the uncertainty in theknowledge of the exchange rates between reservoirs andthe total C14 content of these reservoirs.

.

u-;; 10!i~

0.6116. A limited ,amount of data on ea troposphericlevels for 1960 47~ has come to the attention of the Committee. From the available information, it now appears
that the tropospheric levels resulting from the injectionof CH by nuclear testing up to the end of October 1958
may be described as follows:(a) A peak C1 4 increase of about 30 per cent above
normal-was reached in the northern hemisphere troposphere in late 1959, and levels are now decreasing, being
about 25 per cent above normal in the troposphere ofboth hemispheres in late 1960;( b) There will be a fall with a half-period of several
years to between 10 and 20 per cent above normalowing to equilibration with the biosphere and surface
ocean;

0.9
0:2

y.... altfl 19sg,
0;1
0 ·S 10

Nro

40

100

200

400·

1000

2000

4000

10;000118. In the simpler 2 reservoir model, the exchangeof carbon between stratosphere, troposphere and surface
oceaiY'is assumed to be rapid and they are considered asa siiigle reservoir which is in exchange with the deep
ocean. The resulting mathematical expression, according
to this mode, for the future atmospheric and biosphericlevels will be :K 1 , Ku are the exchange rates of reservoirs I and II.
Index o stands for natural C 14
Q = number of atoms formed
or in numerical form, the addition of 22 x 102 7 C 14
atoms to the atmosphere can be expressed as

If all quantities of C14 are to be expressed as fractionsof the natural C14 level. we shall, dividing by N 10 ,obtain the following results:§

20

Figure 39. Future levels of CH from nuclear tests= _Q_. f(t)

Nro
where
N r. N 11 are the total number of atoms of C 14 in reservoirs I and II+

N = 25 (0.96 e-o· 0209 t
0.04 e-o.oooim)
where N is expressed as a percentage of the natural
C 14 level.

262

C1 • from contimted testing
119. The rate of testing and/or the rate of injectionof cu atoms into the atmospher~ varied considerably inthe period before cessation of nuclear testing. In paragraph 103 and table XVII we see that the total C14 inventory as of 1 July 1957, 1 July 1958 and 1 July 1959
was 10.5, 13.8 and 21 X 102 ' atoms respectively. We
shall now consider a hypothetical case of continued testing which results in an average annual production of 1~ 8
CH atoms per year.

If the quantity of cu is expressed as a fraction of thenatural C 14 level we shall, dividing by N 10 , get aformula, as follows:
N1 (t)
N10

where N is expressed as a percentage of the natural c1 4
level. This means that under these conditions, the biospheric level would be expected to increase over the next
one or two hundred years to a value of about four times
its natural C14 content, and then increase much more
slowly over tens of thousands of years to a value of theorder of thirty times the natural C14 level (figure 39).

owhere B = annual injection of C 14 , or in numericalform with an annual rate of production of 1028 atoms

cu

TABLE I.

+ 3,650 (1 - e-<>.ooowt)

N = 525 (1 - e-<>.0209 1)= ~ Jtf(t)dt
N10120. The future distribution of this additional C1"'/
could be found by estimating the content of each rese~voir at some future time on the assumption that it contains the CH from each of the previous years as estimated by either the 5 reservoir or 2 reservoir model
analysis (paras. 117 and 118). On the basis of the tworeservoir model and continued injection of C1\ the futureatmospheric and biospheric levels at any time ( t)will be:FISSION YIELD OF CERTAIN RADIO-NUCLIDES RESULTING FROM THE FISSION OF
HEAVY NUCLEI BY THERMAL AND FAST NEUTRONsl- 9

Fissi<m ;ykl;J (3) from fisrims by thermal neutrcms, fisrims ~mneutrons Uast) and uulrOns 111ilh enern of 14.6 Me

Fissitmprodut:I

Kra •....•.••
Sr" .........
Sr10 •••••••••
ye1 ••...•••..
Zr15 •••••••••
Ru101. • ••.•••
Ru1°' ••••••••
Sbll' .•.•.....
1m ...•.•••..
Te 112 ••••••••
Jlil ••••••••••

Ce117 ••••••••
BaU0 0 • • • • • • •eeu1 •••.••..
CelH •• ••••••

Half.life

10.6
50.5
28
58
65

uu•

UU'
(fas()Pu"'(fas()

0.30
4.79
5.77
5.4
6.2
3.0
0.38
0.011
3.1
4.7
6.9
6.15
6.35
6.0
6.0

0.25
4.15
4.38
. 5.21
6.72
3.97
0.47
0.059
3.11
4.44
6.02
6.18

0.07
1.44
2.23
2.69
5.12
6.25
6.17
0.123
4.85
6.32
6.19
6.8
5.0
4.65
3.66

(thermal)

years
days
years
days
days
days

7
1.01 years
2.0 years
8.05 days
77 hours
20.8 days
years
30
12.8 days
days
33
days
288

TABLE II.

5.79
5.29

4.76

um

um

um

(fast)

Th"'(fast)(14 MeV)(14 MeV)

0.14
2.81
3.2
3.68

6.7
6.8
7.2

0.42
4.2
4.5
4.64
4.69

0.25
3.2
3.1
3.78
5.40
4.89
3.11
0.65
5.29
4.7

S.7

6.6
2.7
0.024
3.33

4.7
5.72
6.2
5.7
S.62

4.5

0.16
0.042

3.5

1.58
0.48
4.02
4.2
5.4
5.10
4.16
4.47
3.3

1.2
2.4
6.3
6.2
9.0
7.1

TID SSSS

5.71
4.65
4.45
3.3

Ti= aftn fisrims

89 ...•....••.••••..•...........•......•.•••..............
90 ...•....•............•.........••....••••.........•..•.
95 • ••••••••••••.••••••..•.......•....••.••••......•.••...

103 ..•..•..•.•.•.•..•...•.......•........•.........••.....
131 .......•.•...•..•...............•...•.•.•....•....•..•.
132 ......•................•...............••.•.•..••..••...
137 •.•••.•..•....•.........••••......•....•..............•
140 .......•..........•..................•.................
141 ..•.•.••...•.................•..........•....•..••...••
144 .....•...........•.•..................................•

Other nuclides
Ha ••••••.•••.......•.•....••.•..•••...•.......••..••.•.

cu .................................................... .

U"'r ...•..................................•••..•..•..•..•
Np2:n •••••••••.•.•...•....••..•••••.....•••••.•.•••..•..

263

17 sec.

35 see.

100
100
20

100

100
94
0

100

99

0
65
100

10

100
90
30
0

100
100
0
0

100
100
0
0

100
96

2.56
3.50
3.76
5.07
5.20
2.44
0.29
2.89
4.24

5.76

5.57
5.18
4.58
4.69

4.42

J sec.

100
60
100
75

15
0
100
100
0
0

(117)

2.93
3.5
3.65
5.17

4.88

PERCENTAGE ~·RACTION OF MASS CRAIN IN GASEOUS OR VOLATILE FOR~7,68

HASL

TABLE Ill.

ESTIMATED PARTITION PERCENTAGE OF DE.BRIS (FISSIO~ PRODUCTS) BECOllU!iG LOCAL,
TROPOSPHERIC AND STRATOSPHERIC FALL-OUT BY TYPE OF SHQT79

Troposphaic

Loeal

Air.....................................
Land surface. . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Water surface. . . . . . . . . . . . . . . . . . . . . . . . . . . .
Deep underwater. . . . . . . . . . . . . . . . . . . . . . . . .
Contained underground .................. .
Low tower .............................. .
High tower ............................. .
Balloon •.......•........................

TABLE JV.

O
79
20
100

Shol siu under I MT

sphaicLoeal

Troposphaic

99
20
79
0

0
80
20
100
100
80
80
0

100
20
80
0
0
20
20
100

Stralo-1
1
1

0

FISSION AND FUSION ENERGY YIELDS OF NUCLEAR DEVICES46, 81
Fission 'Yield (mttatons)

Fusion :yi<ld (meialon.r)

Air usu

Sur/au U.uAir U.ts

Sur/ate um

0.19

0.57
37
7.5
9
0.07

5.4
26

22
9.5
19

31.4

50.5

1945-1951 ................................. .
1952-1954 •.•...............................
1955-1956 ......•...........................
1957-1958 ................................. .
1959-1960 ................................. .
TOTAL

TABLE

°""

Shcl siu equal lo or
I MT

T'YPe of shcl

1

5.6
31
37.79

54.14

v. MEAN CONCENTRATIONS OF Cs13195T AND
SrUO IN THE ATMOSPHERE
20OVER THE USSR•

T

Conctn·Dau ofsamplinc

May 1955 ............... .
July-August 1956 ......... .
March-April 1954 ........ .
March-May 1955 ......... .
December 1955 .••........
April·July 1956 ..•........
August-December 1956 .....

esm

eew

of air

Sr"

Sr''(0.005)*5(0.006)*3.5µµ curiu/111' µµ curies/m•of air(in mdres)Over European USSR
From 3,000 to 7,000
0.026Over Far Eastern USSR
From 3,000 to 7,000
0.020
Average over USSR
From 3,000 to 7,000
From 3,000 to 7,000
7,000
7,000
5,000

Rislio of numbdof aloms

Conctn·lralion a/lrtUion of
caesium-137 slronlium-90

Allihl4e of
IJdiril'Y
sample0.0014
0.014
0.013
0.018
0.011

0.34
0.44
0.25
0.35-0.74
0.4•Values in parentheses are calculated.

TABLE VJ.

STRATOSPHERIC CONTENT OF ARTIFICIAL R..o\IJIO-cABBON1so

Rlldiotarbos

Radiocarbon

conln&I

conltnl(10'' cu

(I<F' CH

Dale

1 July 1955,.....................................
1January1956 ....................•.............
1 July 1956......................................
1 January 1957.... . . . . . . . . . . • . . . . . . . . . . . . . . . . • . . .

Datealoms)

8.6
8.0
5.6
6.6

1 July 1957......................................
1 January 1958... . . . . • . . . • . . . . . . . . . . . . • . • . • . • • • .
1 July 1958......................................
May-June 1961 (preliminary data)..................

264

alanu)

7.4
6.1
8.4
8.0

TABLE VII.

DISTRIBUTION OF CARBON ON THE EARTH AND CH CONTENT OF RESERVOIRSIN THE EXCHANGE.ABLE CARBON CYCLE

Carbon rtsenofr

Resnwir

Atmosphere ..•............................
Biosphere (terrestrial) ..................... .
Humus ..........•........................
Surface waters of ocean (above thermocline). . . .
Remainder of ocean (deep ocean water). . . . . . .

Mass of c1>rbon(g/cm' ofearth's surfau)

Normal invenlor:Jof 0' aJom.s

0.125
0.06
0.20
0.18
7.50

36 x 1027
18 x 1017
x 10 2750 x 10"
1,950 x ion

TOTAL, in "exchangeable" system

8.1,...,z,100 x lon

Sedimentary carbon ................................. .
Organic carbon in sediments .......................... .
Coal, oil, etc ...........................•.... , ....... .

3,500
1,300
1.4

I
II

TOTAL, carbon in ("sedimentary'' systems)

so

4,800

TABLE VIII. DATA ON THE SPECIFIC CONCENTRATION OF Sr90 AND THE RELATIVE CONCENTRATIONOF CAESIUM-137, STRONTIUY-89 AND CERIUY-144 rn RAINFAU. IN THE UNITED KlNGJ>0!\£278,375,3114
Milford Haven area

Time

Rainfallcm

Speci/Uconuntralionof strontium-90
in rainwala
miaomicrocMries
litre

Up to the end of1954 .........
1955 •..••.•.. 82.51
1956 .•.•..... 78.77
1957 ......... 90.21
1958 ......... 115.37
1959
I ..........
II ..........
III ..........
IV ..........

8.00
1.30
8.18
5.84
v .......... 1.83
VI. .........
3.02
VII ..........
6.12
VIII ...•......
3.07
IX ..........
0.71
x .......... 21.91
XI .......... 29.03
XII .......... 16.23
TOTAL, in 1959 105.24

1960
I. .........
II ..........
III. .........
IV ..........

13.58
8.94
4.52
7.54
v .......... 3.84
VI. .........
2.64
VII .......... 10.30
VIII. .........
8.48
IX .......... 20.42
x .......... 14.42
XI .•........ 20.37
XII. . . . . . . . . . 13.45
TOTAL, in 1960 128.50

1961
I. .........
ll ..........

III ..........
IV ..........

v ..........

VI ..........
VII ..........
VIII •••....••.

11.55
6.93
3.99
11.94
4.56
4.95
4.44
10.46

AmounJ ofstron!ium-90.
fall-outon earlh's·i:1r

me km'

Pr~tionPr",J.jjiow

35
23
16
13
8.1
4.6
2.9
1.6
0.7
0.5
0.4

Cs /Sr.,S/SrM

Pr~ionCe"/S,.1

1.97
2.42
2.47
2.60
5.04
6.1
25
12.2
16.8
29.3
25.8
10.2
5.9
8.0
1.21
1.01
1.18

0.49
0.33
1.00
0.98
0.54
0.78
0.62
0.18
0.056
0.27
0.29
0.19
5.73

1.8
1.3
1.7
1.7
1.4
1.3
1.6
2.0
1.0
1.9
1.9
2.1

1.22
1.62
2.34
2.78
5.54
3.71
2.0
1.65
1.00
0.54
0.59
0.60

0.166
0.15
0.11
0.21
0.21
0.098
0.20
0.14
0.20
0.078
0.12
0.080
1.77

1.7
1.9
1.4
1.7
1.7
1.5
1.5
1.1
1.6
1.7
1.6
1.8

0.95
1.88
2.2
2.3
3.4
1.66
1.80
1.10

0.110
0.130
0.088
0.27
0.153
0.083
0.08
0.115

1.8
1.4
1.8
1.6
1.7
1.9
1.6
1.7

265

0.5
2.0
0.4

19
24
17
20
25
43
11
11
12

7
8
7.5
4.0
5.3
6.3
4.9
2.3
3.3
5.1
3.4
3.6

3.0
2.7
3.0
2.0
"'3.6
3.4
3.0
2.9

TADLE IX.

AvlmAGE CONCENTRATION OF STRONTIUM-90 IN RAINFALL PER QUARTER278 • 8 7 6A•eTat•

No.

1
2
3
4
5

6
7
8
N

~

9

10
11

12
13
14
15
16
17
18
19
20
21
22
23
M

slalionLalil11deLongilud1

Tromso ......•.............
Do<lo ...............•..•...
Reykjavik ..................
Kinloss ....•................
Sylt .......................
Liverpool ...................
Snowdon L ..................
Abingdon ...•............•..
.Milford Haven ..............
Felixstowe ..................
Esquimalt ..................
Linz .......................
Gosausce .............••....
Ollawa .....................
Gibraltar .............•••...
Akrotiri (Cyprus) ...........
Cacnwood ..................
Palisadoes ..................
Lagos (Nigeria) ........•••..
Singapore ...............•..
Suva (Fiji) .............•..•
Melbourne ..................
Ohakca ..................•.
Port Stanley, ...•..... , ... , ,69°42'N
67°17'N
64°10'N
57°39'N
54°54'N
53°04'N
53°04'N
51°41'N
51°41'N
51°58'N
48°30'N
48°20'N
47°40'N
45°20'N
36°10'N
35°00'N
18°1.3'N17°56'N
06°30'N
01°19'N
18°05'S
37°45'540012'551°42'5!9°0l'E
14°22'E
22°00'W
03°34'W
08°17'E
04°01'W
04°01'\V
01°18'\V
05°09'W
01°02'E
123°00'W
14°30'E
13°30'E
75°41'W
05°21'W
33°23'E
76°35'W
76°47'W
03°40'E
103°49'E
178°28'E
144°50'E
175°23'Es1°s21w

precipitat ion
tm

70
90
80
70
50
85
350
65

µµc Sr"/lilreµµc Sr"/lilroµµc Sr"/litro

I

II

III

IV

I

II

III

IV

I

II

24.5
20.8
13.5
9.5

21.8
52.9
15.6
17.8
24.6
18.9
20.7
18.6
20.3
22.2
28.8

4.4
5.8
3.4
8.9
7.7
8.3
8.3
7.4
7.7
6.3

1.4
2.6
1.2
1.16

2.89
4.42
3.0
1.79

4.5
5.4
3.6
5.1

2.12
3.4

1.41
1.0

1.0
1.38

3.8

1.62

0.61

1.10

2.4

1.36
1.44
1.69

1.51
1.60
1.71
2.02

4.0
2.60
3.50

1.22
1.90
2.00
3.20
2.0
2.2

0.52
0.74
0.60
0.97
0.58
1.17
0.97
0.82
1.3
0.68
1.64
0.37
0.11
0.25
0.10
0.4
2.3
1.31
1.02

0.80

5.6

1.63
1.61
1.52
1.55
1.80
2.6
2.1
2.3
2.6
15.8
No rain
0.68
0.32
0.59
0.15
0.56
0.91
0.79
0.89

11.4
14.6
11.2

95

13.4

55

14.9
8.8

80
80
250
100

1961

1960

1959

annualSampletalleelion

12.8

90

11.7
13.8
17.8

40
280
80
250
240
290
65
100
65

8.3
13.5
3.6
1.1
<0.3
1.6
1.1
1.1

9.8
28.1
32.8
90.0
9.0
7.2
2.0
0.45
<0.3
5.0
1.0
1.3

5.4
5.7
2.9
9.4
No rain
1.4
8.0
0.83
0.35
0.25
1.0
1.2
1.4

1.62

1.22
1.75
1.72
5.8
2.2
1.99
1.14

0.6
0.47
0.06
0.37
1.7
1.1

0.64

0.62
1.06
0.10
0.19
1.2
0.72
0.76

3.6

5.1
6.2
4.0
3.9
4.4
5.2
2.9
1.23
0.58
0.36
0.09
<0.2
0.43
0.63
0.60

1.20

1.14
1.12
1.31
1.09
1.86
1.91
2.3
3.4
2.7
<1
0.6
0.16
2.2
1.4
1.0

2.7
1.35
2.5

1.95

TAllLE

Ritlunond
USA

MilfordllavenUK

x. RA1·E OF S~O FALl.·OUT mcjkm2 AND MONTH 207, 226, 281, 2BU, 278, 873, 880, sg,, u.oa

/Jpra
llaly

[41nfo:rad
USSR

-

0.25
0.21

BuenosAius
A111nli><a1957
I. •...............

II .................
III .................
IV .................

v................

N

0\
'l

VI .................
VII .................
VIII •..•..•..........
IX ..•..............
x .................
XI..o •.............
XII .................
1958
I. ................

II .................
III. ................

IV .................
V .................
VI •................
VII .................
VIII .................
IX .................
x .................
XI .................
XII .................

-

-

0.23
0.22
0.45
0.6
0.16
0.28
0.24
0.12
0.36
0.30
0.03
0.15

-

-

-

-

0.33

-

0.10
0.11

-

-

-

0.09
0.13
0.22
0.53

-

-

-

Richmond
USA

Japar<

-

~

-

-

0.03
0.21
0.14
0.07
0.11

1959
I. ................
II. ................
III .................
IV ...•.............

v.................

VI ...•.............
VII .................
VIII .................
IX ..•..............
x ...••............
xI .................
XII .. : ..............

Milford
UK

Jspra
//aJy

unln1rad
US R

0.57
0.52
0.23
0.13
0.06
0.01
0.02
0.00
0.02
0.01
0.00
0.03

0.49
0.33
1.00
0.98
0.54
0.78
0.62
0.18
0.06
0.27
0.29
0.19

0.63
1.66
3.90
6.20
3.10
0.80
0.15
0.20
0.08
0.05
0.08
0.10

0.45
0.28
0.15

0.10
0.11
0.12
0.02
0.02
0.00
0.01
0.01
0.00
0.01
0.03

0.17
0.15
0.11
0.21
0.21
0.10
0.20
0.14
0.20
0.08
0.12
0.08

-

-

HaPaK

-

-

Bue Hos
Airti
Arienli><a

-

1960

-

-

0.21
0.34
0.15
0.28
0.94
0.52
0.62
0.51
0.58
0.35
0.29
0.61

o.55}
0.60
0.50
1.60
1.45
1.25
1.10
0.25
1.05
0.46
0.40

0.48
0.16
0.72
1.16
0.78
0.25
0.23
0.30
0.44
0.20

{
-

-

-

0.15
0.13
0.13
0.22
0.65
0.33
0.46
0.34
0.14
0.44
0.32
0.49

I. ................

II .................
III .................
IV .................

v.................
VI ...••.......•....
vn .................

VIII. ................
IX ..•..............
x .................
XI ..................
XII .................

-

-

-

-

-

-

-

-

0.05
0.05
0.09
0.04
0.02
0.03
0.04
0.04
0.11
0.18
0.07
0.07

Japan

0.33
0.12
1.02
1.12
1.86
0.78
0.14
0.17

TADLE XI.

N

83

AVERAGE QUARTERLY FALL-OUT OF STll.ONTIUM-90 ON THE EA.R.TH'S SUIU'ACESTa

No.

Sampling station

Latit1<deLongitudecm

1

Tromso ........................
Bodo .•........................
Reykjavik .....................
Kinloss ...............•........
Sylt .••...................•....
Liverpool. .....................
Snowdon L .....................
Snowdon U ....................
Abingdon .•...•...•.•...•......
Milford Haven .................
Felixstowe .....................
Esquimalt. ....................
Linz ..........................
Gosausce ......................
Ottawa ........................
Gilbraltar ......................
Akrotiki. ......................
Cacnwood ...............•.....
Palisadocs .....................
Lagos .........................
Singapore ......................
Suva ..........................
Melbourne •....................
Ohakea ...................... ·.
Port Stanley ............•......

69°42'N
67°17'N
64°10'N
57°39'N
54°54'N
53°21'N
53°04'N

19°01'E
14°22'E
22°00'W
03•34•w
08°t 7'E
02°58'W
04°01•w

70
90
80
70
50
85
350

51°41'N
51°41'N
51°58'N
48°30'N
48"20'N
47°40'N
45°20'N
36°10'N35° N
17°13'N
17°56'N
06°30'N
01°19'N
18°05'537°45'540°12'551°42'501°18'W
05°09'W
01°02'E
123°oo•w
14°30'E
13°30'E
75°41'W
05°21'W
33°23'E
76°35'W
76°47'W
03°40'E
103°49'E
t78°28'E
144°50'E
175°23'E
57°52'W

65
95
55
80
80
250
100
90
40
280
80
250
240
290
65
100
65

2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25

A•.raie caesium-137 /slronlium-90 ratio Ptr auarurAi•era11• Jironlium-90 fall-oul Per auarler me/km•

Ar.rageann1<alprecipitation

19(}0

1959

10.6
4.57

II

Ill

IV

1

4.6

1.78
2.7
1.29
0.76
0.68
1.02
2.46
1.97
0.74
0.76
0.51
0.39

0.25
0.48
0.52
0.19

0.86
1.03
0.37
0.27

0.38
2.18
3.32
0.34
1.09

0.31
1.70
1.73
0.26
0.55

10.7

2.59
2.14
1.61
3.55
1.28
9.40
9.91
9.46
6.62
1.75
1.73
2.34
2.21
0.97
1.28
1.4
4.54
-5.06.3
3.6
2.26
4.69
2.89
8.39
0.27
10.8
3.25
0.32
1.06
1.85
0.70
0.28
0.95
0.25
0.4
0.24
o.54
0.23
0.33
0.28
0.18
1.13

1.5
3.3
0.77
0.47
0.12
0.2
0.51
0.17
0.22
0.17
0.17
0.14

0.35
0.47
0.26
0.24
0.65
0.53
0.69
1.4
1.18
0.49
0.37
-2.590.16
0.085
p.19
0.11
0.0:>
0.046
0.21
0.20
0.12
0.29
0.15
0.17
0.11
0.09

II

0.98
0.74
0.40
1.35
1.41
0.54
0.50
0.28
0.40
0.97
2.00
0.70
0.28

19<f0

Strontium·
90 fall-out in
1959 me/km'

1

II

1/1

IV

I

17.23
19.14

1.7
1.5
1.4

1.9
1.6
2.0
1.7
1.6
1.6
1.4
1.2
1.8
1.7
1.9
2.3
1.8
2.0
2.9
2.0

1.8
2.7
1.9
2.4

1.7
1.5

4.22

1.4
1.4
1.3
1.6
1.6
1.6

1.1
2.1

1.6
1.4

1.7
1.8
1.5
1.3
1.5

2.1
1.9
1.4
1.9
1.5

1.6
1.8
1.6
1.8
1.7
1.4
1.1
1.5
1.8
1.5
2.6

6.23
23.95
21.37
4.56
6.40
6.80
13.73
8.41
12.34
15.46
1.74
3.17
1.85
1.07
1.24
0.90
0.69

1959

1.6
1.5
1.4
1.7
1.6
1.4
1.8
1.7
1.6
t.9
1.5
1.7
1.5
-1.61.5
1.7
1.8
1.4
t.7
1.6
1.0
1.6
. 1.6
1.9
1.4
2.0
1.3
1.5
1.4
1.9
1.8
1.6

1.6
1.4
L9

1.9
0.9
1.5
t.7
2.2
1.8
1.4
1.7

2.0
2.4
1.7
1.8
1.7
2.3
1.9
1.6
4.0
2.1
1.6
-1.41.7
1.5
2.0
2.4
1.4
1.4
2.2
1.7
1.9
2.2
1.5
1.6
1.9
2.5

II

TABLE XII A.

EXPERIMENTAL DATA ON FALL-OUT OF CERTAIN RADIO-ISOTOPES IN 1957 ON THE EARTH'S SURFACE
IN THE LENINGRAD AREA201

Total
beta-

CeTium-141

Fall·ovl sampli"t period

1957
I ......................................
II ......................................
Ill ......................................
IV ......................................

v ......................................

VI ......................................
VII ......................................
VIII ......................................
IX ......................................

x ......................................

XI ......................................
XII ......................................

me/km'

me/km'

21.4
23.7
20.4
118.4
70.0
34.5
19.5
39.3
119.5
92.8
18.9
27.9

2.49
9.73

Average fall-out per month, 1958 .............

TABLE XII B.

Fall-cul samplinr /!triad

50.5

total

me/km•

11.06
8.2

22.5
9.63
1.86

Total for year with extrapolation for missing
months ..................................

YUrium-91

3 ofatlii,.ily

18.9
10.4
9.9

Stro1ltium-89

CeTium-144

3

me/km'

3

me/km I

3

0.8

3.7

0.12

5.9
9.5
1.43
4.3
20.2
15.4
12.2
7.2
3.9
9.9

2.4
1.6
1.1
3.8
12.6
0.64
3.1
3.77
27.3
4.47

11.2
6.9
5.6
3.2
18.0
1.86
15.9
9.6
22.8
4.8

7.58
1.87

7.9

5.91
9.40
3.03

5.0
13.4
8.8

3.96

14.2

3.22
6.10
4.08
1.37
4.8

8.2
5.1
5.2
7.3
17.2

1.1

1.0
1.5
3.9
6.0
14.4
6.6
7.4
2.7

75.0

49.7

70.7

57.7

6.25

4.14

5.89

4.81

EXPERIMENTAL DATA ON FALL-OUT OF CERTAIN RADIO-ISOTOPES ON THE EARTH'S SURFACE
IN THE LENINGRAD AREA IN 1958207

Ccrium-141

Total belo·
actiPilyme/km•

me/km•

3

3.47
4.04
3.34
8.14
12.50
29.60
9.86
5.67
2.31
13.30
18.76
2.68

11.2
15.7
7.9
14.3
9.3
15.2
10.5
10.2
7.8
6.2
8.0
2.2

Ruthenium-103

Zirconium

Cerium-144

me/km'

3

me/km'

3

3.43
3.57
2.14
3.76
7.77
13.80
5.87
3.71
1.45
6.66
12.85
3.42

11.1
13.9
5.1
6.6
5.8
7.1
6.3
6.7
4.9
3.1
5.5
2.8

3.02
4.03
3.36
7.00
12.71
21.47
7.58
4.20
2.31
10.42
16.67
5.81

9.7
15.7
7.9
12.3
9.5
11.1
8.1
7.6
7.8
4.8
7.2
4.7

me/km•

Ccusium-137

3

me/km'

3

1.33
2.03
1.19
0.90
1.53
0.94
0.46

0.99
1.05
1.30
1.60
5.20
0.40
0.20

1958
I .......................
II .......................

III .......................
IV .......................

v .......................

VI .......................
VII .......................
VIII .......................
IX .......................

x .......................

XI .......................
XII .......................

31.0
25.7
42.3
56.87
134.2
194.2
93.5

55.5
29.64
216.2
233.3
124.0

Total for year with extrapolation for missing months .....

Fall-out
sampli"t
9aiod

Total

wto-

4.94

5.0 {

5.21
14.90
10.58
4.82
3.20
2.04
5.21
8.59
3.01

9.2
11.1

5.5
5.2
5.8
6.9
2.4
3.7
2.4

113.7

68.4

98.6

62.5

14.4

9.47

5.70

8.21

5.21

1.20

Average fall-out per month,
1958 ...................... 103.00

TABLE XII c.

}

EXPERIMENTAL DATA ON FALL-OUT or CERTAIN RADIO-ISOTOPES ON THE EARTH'S SURFACE
IN THE l.E.."'!INGRAD AREA IN 1959207

C<rium-141

actirity
me/km'

me/km'

155.9
89.3
42.4

19.20
6.60
1.23

Ruthe1lium·IOJ

3

me/km'

12.3
7.4
2.9

22.97
6.67
2.63

Zircanium-95

3

me/km'

14.7
7.5
6.2

22.89
10.66
4.36

Cerium-144

3

me/km'

14.7
11.9
10.3

10.95
8.31
4.05

Ccurium-137

3

me/Inn'3~li<ni
/Sr"

7.0
9.3
9.6

1.54
1.07
0.57

0.99
1.20
1.34

3.4
3.8
3.8

1959
I. .............
II ..............

III ..............
Total for firstquarter 1959 ....

Average fall-out
per month in firstquarter 1959 .... ,...,, 0.95

270.03

322.7

379.1

23.31

3.18

0.90

-1.01

,..., 1.26,..., 0.77

1.05

269

TABLE XIII. MEAN MONTHLY FALL-OUT OF SOME RADIO-ISOTOPl!:S IN THE VICU.""1TY
OF RICHMOND (USA) 396
me/km'
Dole of so,,.plt

1959
I. ............
II .•...........
Ill .............
IV .............

v.............

VI. ............
VII •............
VIII. .•..........
IX ..............

x .............

XI .............
XII .............

srn

Sr•/Sr11

(:elU

Pu"'

14.7
17.2
2.6
1.2
0.37
0.029
0.058
0.009
0.024
0.004
0.003
0.021

1960
!. ............

0.080
0.075
0.56
0.012
0.005
0.001

II .............
Ill. ............
IV ..•..........

v.............

VI. ............
VII •............
VIII •..•.........
IX .........•.••

0.84
0.74
0.83
0.15
0.12
0.029
0.038
0.054
0.018
0.098
0.13

0.00290.00150.00170.00050.00050.00090.00060.00120.00020.00030.0017x .............

XI. ............

3.8
2.3
0.85
0.39
0.31
0.12
0.050
0.015
0.018
0.014
0.012
0.016

30
31
13
10
6.9
6.0

0.043
0.021
0.017
0.005
0.005

0.90
0.81
0.10
0.58
0.33

2.6
1.5
0.96
3.0
0.74

1.00

TABI.EXIV. VAJUATIONS IN THE MEAN STIW?."TIUM·90 CONCENTRATION IN THE SOIL AT DIFFE.RE~"T LATTrUDES
r,.creose In
quo11lity ofslro11lium-90
dmn1 periodfrom1956 to 1958

Q~antityofslronlium-90
at the firsthalf of 1958

Quantity a/slrontium-90
al themiddle of. 195901<01<li!y ofstronlium·90
attlsemiddle of1960

Area af~°'znu/aceNo.

Latitude

Aleta cme/km'

Megac

me/km'

Mega cme/km'

Meiac

me/km•

10' km•

1
2
3
4
5
6
7

80°-70°N .................
70°-60°N .................
60°-50°N •................
50°-40°N .................
40°-30°N .................
30°-20°N •................
20°-10°N •................
10°- O"N .................
0°-10°5 •................
10·-20°s .................
20°-30°s .................
30°-40°5 .................
40°-50°5 .................
50°-60°s .................
ToTAt. Mcgacuries

0.03
0.08
0.16
0.23
0.19
0.24
0.09
0.03
0.04
0.06
0.06
0.07
0.09
0.07
1.43

2.2
4.1
6.4
7.4
5.3
6.0
2.2
0.8
1.0
1.3
1.4
1.8
2.9
2.9

0.03
0.17
0.26
0.43
0.36
0.47
0.17
0.10
0.12
0.08
0.10
0.11
0.12
0.09
2.60

3.1
9.5
10.3
13.6
10.1
11.6
4.1
2.3
2.7
1.8
2.4
3.1
3.8
3.6

0.22
0.30
0.76
0.81
1.04
0.40
0.22
0.27
0.12
0.14
0.15
0.15

11.6
11.8
24.1
22.3
25.9
9.4
5.0
6.1
2.8
3.5
4.1
4.7

0.25
0.43
0.76
0.87
0.93
0.33
0.17
0.24
0.13
0.17
0.18
0.15

13.2
16.9
24.1
24.0
23.2
7.7
3.8
5.4
3.0
4.2
5.0
4.7

11.1
18.9
25.4
31.6
36.3
40.1
42.7
44.3
44.3
42.7
40.1
36.3
31.6
25.4

8
9
10
11
12
13
14

270

4.58

4.61

TABLE

xv. CONCENTRATIONS (mc/km2) OF GAltMA-RADIATING FISSION FRAGMENTS IN son. SAltPLESCOLLECTED IX THE VICINITY OF CHICAGO, USAUS
CsUT

Radi&-mulidt

Zr" - Nb"
65-35 days

JO :years

Ru1Dt
1 :yearv .......................
x .......................

69
75
89

13.5
13.0
14

80

36
120

38

XL ......................
XII. ......................

280
380
400
360
290
230
170
140
100
77

49
52
54
57
58
61
66
74
72

1960
II .......................
III ••......•..............
IV •......................

58
43
35

Ru'"

c,111

Ce"'

40 daysJZ daysZ90 days

69
69

67
77
92

42
46
54

100
106

17

65

50

25

58
81

13
31

23
6
15

96
83
104

127
89
71
46

223
156
103
70
43
29
19

435
560
590

72

240
310
340
450
463
340
385
370
380
390

76
75
76

380
365
350

1957

VII .......................

67

cJ2

1958
III. ......................
VI ............ ···········IX .......................

1959
III. ......................
IV •......................

v .......................

VI. ......................
VII .......................
VIII .......................
IX ........•....•...•...•.

x .......................

TABLE XVI.

35
20
11

655
700
655
680
740
710
660
615
620

635

APPROXIMATE $r9<> ATMOSPHERE INVENTORIES (IN MEGACURIES)162,4TO

HeithlNor. 57-Dee. 58

Jan. 59-Aui. 59

StPI. 59-Dte. 59

Jan. 60-May 60

May60

Nor. 60

May61

Above 30 km .•..•........
20-30 km ................
Tropopause-20 km •..•.••

0.20 ± 0.04
0.15 ± 0.05
0.61±0.09

Northern hemisphere0.17 ± 0.04
0.20 ± 0.04
0.27 ± 0.08
0.30 ± 0.08
0.38 ± 0.06
0.33 ± 0.05

0.13 ± 0.04
0.25 ± 0.10
0.37 ± 0.06

0.14
0.23
0.25

0.13
0.20
0.24

0.12
0.14
0.19

TOT.IJ.

0.96 ± 0.20

0.85 ± 0.16

0.80 ± 0.15

0.75 ± 0.15

0.62

0.57

0.45

Above 30 km ...••........
20-30 km•••••...•.......
Tropopause-20 km .•.....

0.20 ± 0.04
0.11±0.03
0.22 ± 0.03

Southern 'hemb.pliere
0.16 ± 0.04
0.19 ± 0.04
0.17 ± 0.06
0.15 ± 0.05
0.13 ± 0.02
0.16 ± 0.08

0.12 ± 0.04
0.13 ± 0.05
0.27 ± 0.08

0.14
0.23
0.19

0.13
0.20
0.24

0.12
0.14
0.26

TOTAL

0.53 ± 0.13

0.47 ± 0.10

0.52 ± 0.13

0.56

0.57

0.52

0.03

0.03

0.03

0.03

0.02

0.03

1.52 ± 0.33

1.35 ± 0.26

1.30 ± 0.28

1.21

1.16

1.00

TABLE XVI!.

0.49 ± 0.13

GWbal troposphere
0.03
World total
1.32 ± 0.28

DISTRIBUTION OF CH BETWEEN RESERVOIRS AND TOTAL INVENTORYAS OF JULY 1957, 1958, 1959, AND MAY-JUNE, 1961
CH conltnl In units of 10" ""'"'~&senoir

1Jxly1957

J July 1958

I July 1959

Ma-y.Ju'M 1961.,..

Stratosphere ................
Troposphere ................
Ocean .••••................
Biosphere ..................

7.4
2.5
(0.5)
(0.1)

8.4
4.0
(1.2)
(0.2)

(10-13)
6.7
(2.2)
(0.4)

8.0
13.0
(6.2)

TOTAL

10.5

13.8

(19-22)(27)• Computed values in brackets, other experimental data.

'"* Preliminary data.

271

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pap;noaITTmm:mrn

11e~ecTBan.

285

MocIIBa (1961); v. ~o:itpreJIT OOH A/AC.82/G/L.704.
455. Miyake, Y., On the distribution of radioactivity inthe sea around Bikini Atoll in June 1954. Pap.
Meteorol. Geophys. 5: 253 ( 1954).
456. Miyake, Y., Y. Sugiura, Radiochemical analysis ofradionuclides in sea water collected near Bikini
Atoll. Papers Meteorol. and Geophys. (Japan) 6:
33-37 ( 1955).
457. Bowen, V. T., T. T. Sugihara Strontium-90 in
North Atlantic surface waters.' Proc. Nat. Acad.
Sci. 43: 576-580 ( 1957).
458. Yamagata, N., S. Matsuda, Cesium-137 in the
coastal waters of Japan. Bull. Chem. Soc. Japan
32: 497 (1957).
459. Miyake, Y., K. Saruhashi, Distribution of manmade radioactivity in the North Pacific throughsummer 1955. J. Mar. Res. 17: 383 (1958).
460. Sugihara, T. T., H. E. James, E. J. Troianello
et al., Radiochemical separation of fission products
from large volumes of sea water. Anal. Chem. 31:
44-49 (1959).
461. Bowen, V. T., T. T. Sugihara, Strontium-90 in themixed layer of the Atlantic Ocean. Nature 186:
71-72 (1960).
462. Folsom, T. R., G. J. Mohanrao, P. Winchell, Fallout caesium in surface sea water off the California
coast (1959-60) by gamma-ray measurements.
Nature 187: 480-483 (1960).
463. Folsom, T. R., G. J. Mohanrao, Measurement of
fallout cesium in the Pacific Ocean and in terrestrial effluents likely to alter coastal waters. Intern.
Assn. Phys. Oceanography (1960).
464. Miyake, Y., Strontium-90 in Western North
Pacific surface waters. Pap. Meteor. Geophys. 11 :
188 (1960).
465. Bowen, V. T., "Statement of Dr. Vaughan 'f.
Bowen, Woods Hole Oceanographic Institution,
Woods Hole, Mass.", pp. 234-251 in Applicationsof Radioisotopes and Radiation in the Life Sciences. Hearings before the Subcommittee on
Research, Development and Radiation. Congressof the United States, Eighty-Seventh Congress,
United States Government Printing Office, Wash.
(1961).
466. Bizollon, C., J. Moret, P. Berger, Deux ans decontrole de la radio-activite du Rhone et de la
nappe phreatique. Bull. Inst. Nat. d'Hygiene 16:643-664 (1961); v.e. United Nations document
A/AC.82/G/L.658.
467. Mahmoud, K. A., M. K Molokhia, A. T. A. Abdel
Fattah, Strontium-90, stable strontium and stable
calcium in soil, food items, water and human bonein Egypt. United Nations document A/AC.82/G/
L.665.
468. Yamagata, N., The concentration of Sr90 and
Cs187 in land waters in Japan. United Nations document A/AC.82/G/L.690.
469. Menzel, R. G., Transport of strontium-90 in runoff. Science 131 : 499 ( 1960).
470. Machta, L., A survey of radioactive fallout from
nuclear tests. J. Geophys. Res., in press.

471. Hageman, F., J. Gray, L. Machta et al., Stratospheric carbon-14, carbon dioxide and tritium. Sci-·
ence 130: 542-552 (1959); v.e. United Nations
document A/AC.82/G/L.280.
472. Lockhart, L. B., Jr., Air concentration of radioactive materials at ground level along the 80th W

286

meridian. ·wMO Technical Note No. 43: 35-45(1961).
473. Broecker, W. 5. Personal communication.
Rafter, T. A. Personal communication.
Willis, E. H. Personal communicati.on.
Olsson, I. Personal communication.

ANNEX F

Ei"lVIRONMENTAL CONTAMINATION (continued)
PART IITransfer of radio-active material through footl. chains into the human body
CONTENTSParagrapli.r

I. INTRODUCTION ••••••••••••••••••••••••••••••••••
Radio-nuclides of importance •..•...............
Methods of investigation ....................... .

1-7
2-3
4-7
II. STRONTIUM-90 •••••••••••••••••••••••••••••••••
9-121
SrDO in food chains .•.......................•... 9-36
9-12
Relationships between strontium and calcium ..•Soils and plants .••.••....•...•............... 13-25
Absorption of Sr9o from the soil •........•.. 14-20
Direct contamination of plants ..•.•••...•... 21-24
Relative importance of different routes of con25
tamination ........••.........•....•......
26
Aquatic food chains ...•..•................•..
Milk and animal products .................... . 27-30
Metabolic behaviour in man ...........••...... 31-36
Measured levels of Sr9o in diet ...............•.. 37-79
General considerations ...................... . 37-40
Estimates of the ratio of Sr9° to calcium in the
total diet .•..................•............•. 41-49
Contributions of Srso by individual components
to the total intake •..•......•.•...••.......•
50
Factors causing intake to vary from the average 51-61
SrDo in individual foods ••.•..•..•.•.••...••... 62-79
Mille .......•••..•.......•..••.......•..•.• 63-66
Cereals .....••.......••..••..••.•.•.••.•... 67-73
Vegetables ..••...••......•......•......... 74-76
Fruit .•.•.••.•...•..••.••.••.......•.••....
77
Meat, eggs and fish .......••.•..•....•.•...•
78
Tea ••••.•.••.•....••.••..••..•••...•.•...•
79
Measured levels of Srso in human bone •....•.... 80-91
Effect of age ...••••..••..•..•••...•.•.....•. 82-84
Geographical location •........•••• , .•.•.•.•.. 85-87
Trends with time ••.••..••.........•.••.•... , 88-89
Observed ratio (bone/diet) from measurementsof Sr 9o in bone ••..........•••.....•.••.•.• 90-91

Paragraphs

Evaluation of mean levels of Sr9o in diet andbone . . . . • • • . • . . . . . • . • • • • . . . . . . . . . . . . . . . . . . . . 92-102
Evaluation of Sr9° to calcium ratios in total diet,
1958-1960 . . . . . . . . . . . . . . • . . . . . . • • • . . . • . . . . • . 94-99
Comparison of calculated and measured Sr9o inbone ...................•.....••........... 100-102
Future levels of Srso in diet and man ..•......... 103-121
Method of evaluation ......................... 105-107
Estimated values of proportionality factors .... 108-119
Calculated future levels ...................... 120-121

III. CAESIUM-137 •.........•.••................•... 122-150
Cs131 in food chains ............................ 122-132
Relationships between caesium and potassium . . 122
Soils and plants .............................. 123-127
128
Aquatic food chains . . . . • . . . . . . . . . . . • . . . . . . . . .
Transference into millc . . • . . . .. . . . . . . . . . . . . . . 129
Metabolic behaviour in man and mammals .... 130-132
Measured levels of Cs1ar ....................... 133-145
Cs1a1 in the total diet . • .. • • . . . . • • . • . . . . . . . . . . 134-135
Cs1a1 in millc • . • . • • . . . • • . • . . . . . • • • • . . . . . . • . • . 136-138
Cs1s1 in other foods • . . . . . . . • • • . • . . • . • . . • . • • . 139
Measured levels of Cs1s1 in the human body •.. 140-144
Evaluation of mean levels of Cs137 in the humanbody . . . . . . . • . . . . • • . •. . . . . . . • . . . . • • . . • . . . • . 145
Future levels of Csl37 in diet and man ••..••.•••• 146-150

IV. SHORT-LIVED RADIO-NUCUDES •••••••••••••••••••• 151-156
Radio-nuclides of importance •.••••...••..••.•••• 153-154
Measured levels •.•.•.•..•.•••••..•.•.••••••••• 155
156
Future levels .......•.••......••••••...••..••.•TABLESREFERENCES

I. Introduction

R.ADIO-NUCLIDES OF IMPORTANCE

1. Since the Committee's 1958 report, much information has been obtained on the levels of radio-nuclides in
man and in foodstuffs and on the mechanisms by which
they are transmitted through food chains. Many countries publish information on the former regularly, anddetailed reviews of some aspects of the passage of fission
products ~rough food chains are available. 19 •119 Thispart of the annex summarizes the present state of knowledge in this field, emphasizing those factors which are
relevant to the assessment of the exposure of humanpopulations. While the measured levels of radio-nuclides
described in this section apply only to fall-out from
nuclear e..'i:plosions, it will be appreciated that the generaldescription of food chain behaviour is applicable also
to other releases of the radio-nuclides treated. These
releases are described in part IV of the present annex
and the behaviour of 0 4 is discussed in parts I and III.

2. Many radio-nuclides are produced by the explosionof nuclear weapons (FI, 11-13) and a limited numberof them are important as sources of internal radiation in
the human body. The potential importance of radionuclides in this respect is determined by:(a) Their production yield and half-life. Radionuclides with relatively high yields and moderate to long
half-lives include those of the rare earths, zirconiumniobium. ruthenium-rhodium. iodine. caesium and thealkaline. earths, especially strontium ·and barium;(b) The rate at which they enter into food chains
after being deposited on the earth's surface. All radionuclides may be ingested by man or by domestic animals
after direct deposition onto the aerial parts of plants
but the isotopes of strontium are more readily absorbed
from soils by plants than are other fission products. Thishas been shown by experiments with separated radio-287isotopes and with debris from nuclear weapons ;153 • 1°"·1611-167( c) The extmt to which they enter into foods of animal origin. Strontium, caesium and iodine are relatively
readily transferred into milk and caesium into meat.
This also has been demonstrated by experiments withseparated isotopes182•187•220 • 223 •287 and with debris from
nuclear weapons. 219 The importance of these radionuclides is also emphasized by experience with fall-out
distributed worldwide as a result of the testing of nuclear
weapons ;19( d) The extent to which they are absorbed from thegastro-intestinal tract of man. Strontium, iodine andcaesium are well absorbed but radio-isotopes of the rareearths, the actinides and noble metals are absorbed to avery small degree. 19 All radio-nuclides in the diet,whether or not they are absorbed, will contribute to theirradiation of the gastro-intestinal tract;( e) The fraction deposited in the critical organ in
man and the time for which it is retained. Radiostrontium is deposited in bones and some part is retained
there for a period of years. Sr90 is the strontium nuclideof major biological significance because of its long halflife, but it may be necessary to give some consideration
to Sr8 9 in periods when the major part of the fall-out
is of relatively recent origin. Caesium-137 is generally
distributed throughout the body and the major portionis retained with a half-life of some months. Iodine
isotopes are concentrated in the thyroid gland but, owing
to their short half-lives, are of importance only inperiods of fresh fall-out. Major attention is devoted to
Sr&0 and Cs 137 when long-term effects are being considered.
3. Pu= 311 is not considered in detail because it is absorbed to a negligible e>..i:ent from soil by plantsm andis very poorly absorbed from the gastro-intestinal tractof animals and man. 288 Estimates made in the United
Kingdom in 1959 at the period of highest air contamination suggested that the ingestion of Pu 2311 in food was
negligible, while the Pu239 inhaled amounted to 10-2µJLC
per day per person. 98 Similarly it was calculated that in
the United States over the period 1954-1958, the amountof Pu m entering· the diet was only 1/3,000 of that inhaled."120in the body can be measured by in vivo counting but thelimited number of whole body counters and the factthat they are usually immobile have hitherto made itdifficult to obtain representative information for large
populations; the introduction of mobile counters may
reduce this limitation. The measurement of Cs137 in postmortem samples may enable the radiation dose to individual tissues to be more precisely determined.
6. The measurement of the levels in diet provides corroborative evidence of the levels in the body. When therelationship between the level of the radio-nuclide in thediet and in the body has been well established for a few
areas, body levels for other areas where direct measurements are inadequate or unavailable can be estimatedfrom analyses of the diet. It has recently been suggested
that the monitoring of urine can serve as an alternative
method for estimating the current intake of Sr 00 andCs 137 , but the practical value of this procedure has not
yet been established. m, 21e, 2so
7. The sampling of food also offers a method of rapidly detecting changes in the levels of intake and ofdetermining the chief contributors of radio-activity t~
the diet. The levels of radio-nuclides in fall-out andfoodstuffs can be correlated and the results related toparticular local agricultural and climatic conditions. By
relating levels in the body and in diet to the pattern andamount of fall-out some estimate can be made of possible future levels.

8. In order that these relationships should not be
purely empirical, knowledge is required of the mannerin which the radio-nuclides of interest behave in biological systems and pass through food chains into man. In
the following sections, therefore, a summary of the present knowledge of these subjects is described before thepresent and predicted future levels are given.
D. Strontium-90
Sr90 IN FOOD CHAINS

Relationships between strontium and calcium
9. Sr90 (and Sr89 ) behave in the same manner as thestable strontium normally present in biological systems
and in a manner generally similar to that of calcium, towhich it is related chemically. Stable strontium is present in nature in very small and variable amounts relative
to calcium, and the transfer of Sr110 through food chainsis largely determined by the amount of calcium which
is present. For this reason the concentration of Sr90 inbiological materials is frequently reported as a ratio ofstrontium to calcium (expressed as micromicrocuries of
Sr9° per gram of calcium). This mode of expression isconvenient, as the calcium content of bone and that ofmany other important tissues are relatively constant, andtissue doses can therefore be inferred from the ratio.
Furthermore, because the ratio in bone is largely determined by the ratio in diet, the content of Sr90 in the
total diet, or in its major constituents, is appropriately
expressed in these terms. In other circumstances, however, the expression of results in terms of unit weightor volume is to be preferred.

METHODS OF INVESTIGATION

4. In order to calculate the radiation dose to man, it
is necessary to estimate the content of radio-nuclides inthe body. This can be done directly by the analysis of
post-mortem samples or for gamma-emitting radionuclides by whole body counting, or it can be ascertaiaedindirectly by the analysis of the diet or excreta.
5. Direct measurement can provide more certain information for the calculation of dose and the values
obtained for Sr90 and Cs 137 in man in many areas areadequate for the necessary dose computation. There aresome practical difficulties in sampling the population ina fully representative manner. For Sr90 , samples ofhuman bone must be obtained. In interpreting the results it should be remembered that samples may nothave been obtained from the whole area of interest, andthat, while samples obtained as a result of accidental
death may be assumed to be representative of the population with respect to diet, those from individuals dying
from other causes may not be representative either indiet or in calcium metabolism. The total content of Cs181.JO. While the behaviour of Sr90 is similar to that of
calcium, it is not identical with it and this has led to
the need to express quantitatively in a clearly definedmanner, the relative rates of transfer or utilization ofstrontium and calcium in biological systems. In the pres288

ent report the over-all discrimination is expressed by the"observed ratio" or OR (sample/precursor):*
OR= Sr/Ca ratio in sample
Sr/Ca ratio in precursor
The term "discrimination factor" (DF) is used to express the contribution of individual physiological processes to the over-all discrimination. 124 • 288 The OR may
be a result of any number of discriminatory stages. Thus,
OR= (DF1) (DF2) (DFa) .... (DFn)
The DF values are given appropriate specific names.
When a single stage process is being studied the OR and
DF are, of course, identical, but the OR (milk/diet),
for example, expresses the result of discriminatory processes in gut, udder and kidney. 187 • ~ 2 •11. The true OR can be measured only in systems insteady state or where the strontium and calcium being
introduced cannot be confused with that already present
in the system. It is especially important also to ensurethat the strontium to calcium ratios as measured in the
precursors truly represent the ratios available to theorganism. While the OR obtained in practice may depend to some extent on the method used, it appears thatgenerally comparable results are obtained by the various
possible methods. Three principal methods have been
used: 1 u(a) The measurement of the ratio of stable stro1itimn
to calcium in the prernrsor and sample. This has foundparticular application in determining the OR (bone/diet) in humans where Sr 90 has been present in the dietfor only a short period of time, and where tracer e.xperiments can only be performed with difficulty. The value
obtained reflects any changes in the ratio of stable strontium to calcium in the precursor or in the OR which
may have occurred in the life history; it represents alifetime integrated value. The difficulty of making precise measurements of stable strontium in the presenceof large amounts of calcium and of using this procedureexperimentally has limited its application;(b) The measurement of the ratios of radio-strontimn
and stable calcium. If this method is to be used experimentally it is necessary to supply the radio-strontium
and calcium over the entire life history in order to prevent interpretation from being complicated by the presence of calcium absorbed before the radio-strontium was
supplied. Studies with fall-out Sr90 belong in this category; the difficulties in the derivation of OR (bone/diet values from measurements of fall-out Sr90 are discussed in a subsequent section (para. 90). This method
has been used successfully for the determination of theOR (milk/diet) on the assumption that the Sr90 andcalcium in milk come largely from that ingested in theprevious few days;( c) Alternatively, radio-isotopes of both strontium
and calcium may be used. The radio-isotopes can be distinguished from the stable nuclides which have previously entered the system being studied. Hence the result
is unaffected by the previous nutritional history of thesubject and the necessary feeding time is short. However, the value represents the behaviour only during the*The following nomenclature was adopted in the 1958
report:91
DF (precursor/sample) = Sr/Ca rat_io _in sample
Sr/Ca ratio in precursor
The over-all discrimination factor was considered to be theresult of several individual factors corresponding to separate
stages. However, the alternative nomenclature is widely usedand possesses some advantages.

experimental period. This technique has many advantages in case of measurement by radio-chemistry.
12. Some criticism has been made of the use of observed ratios on the grounds that they may vary whenexperime.ntal conditions are changed. 193 • 19 ' However,the practical use of the OR concept is considered justified178• 201 since in many processes (for example, absorption by plants, secretion into milk, absorption into thebody and deposition in bone) the OR may be very nearlyc.onstant and predi~tabl:. On the other hand, the quantities of Sr90 per urut weight or volume of tissue mav bemuch more variable. In particular, the OR (bone/diet)reflects the contamination in local areas of bone which
are active at the time and is comparable at all ages, except perhaps in the very young. In contrast, the actual
retention of radio-strontium varies markedly with age
and diet and with the degree of attainment of steadv•
state conditions.
Soils and plants
90

13. Sr may enter plants either through their roots
from the soil or by the direct contamination of theirabove-ground tissues. It is important to distinguish between these two modes of entry because the amountabsorbed from the soil is determined by the cumulative
total deposition, while the extent of direct contamination
depends on the magnitude of the recent deposit.
Absorption of Sr0 from the soil
14. Field experiments in the United Kingdom andSweden indicate that, depending on soil type, the ratioof strontium to calcium in plants is likely to be in therange of 1-10 µµc Sr90/g Ca if 1 me Sr90 per km2 ispresent in the soil.135- 137 • 2 °'• 283 The quantity entering
crops each year is usually in the range 0.2 to 3 per centof that in the soil, 19 • 135- 137• 142 • 147• 283 depending on thefactors discussed in the following paragraphs.
15. The effect of calcimn. The quantity of labile* calcium in soil is the most important of the factors determining the extent to which Sr90 is absorbed by plants.
Experiments in Sweden,13 s-138 the United States, 139• uo,m, 145 • 151 the United KingdomH 2 • 147 and the Union ofSoviet Socialist Republics1 H show that the uptake ofSr 90 is greatest in soils of low calcium content. The uptake of Sr9° from these soils is reduced by the additionof lime, but usually not by a factor exceeding 3.19• 129
When soils contain adequate calcium for the growth ofcrops and the cation exchange capacity is largely saturated with calcium, the addition of lime has little or noeffect. Although wide differences exist in the ability ofvarious species to absorb Sr90 , it is well established that
this character is correlated with the ability to absorb
calcium.
16. The results of experiments in water culture showthat the OR (plant shoot/solution) is close to 1 (table 1).
This is also generally true of plants growing in soil
when the strontium is uniformly distributed or whendifferences in the rooting depth of plants are taken into
account. 1 u, 128 Some apparent differences between theratio of strontium to calcium in different species growing under the same conditions have been reported143 butthese are not accepted as typical. 136 Variations in ratiosof strontium to calcium, however, occur between different tissues of the plant. Somewhat higher ratios areusually found in roots and stems than in the leaf tissue
in which the major part of both strontium and calcium*Labile calcium consists of calcium present in the soil solution
together with readily exchangeable calcium with which the solution can be replenished.

289

is normally contain~d. 125 • 126 Th?se f?r fruits are !ewer;
the ratios of strontmm to calcium m wheat gram andedible legumes are about 0.5 of that in leaf ~ssue ;136 ' m
the ratio in wheat flour is about 0.7 of that m the wholegrain.~ 82

17. Varying values for the OR (plant shoot/soil)
have been reported133 •135 but it _is no~ clear t?at 0e
variation was mainly due to the difficulties ?f estimatmg
the relative availability to plants of strontium and calcium in the soil. The conventional extraction procedureswith ammonium acetate may give. inaccurate in_fc;mnation especially in soi}s wh~ch contam lar_g~ quantities ofslightly soluble calcium; m other conditions, however,
useful comparative data ea~ be obtained.12~ The ratios
in which the two ions are available C!1n be e?timated ~o~e
precisely by analysing solution~ with whi.ch ~e s~il 1s
in equilibrium or by equilibratmg the soil with dilute
solutions of calcium chloride. 85 • 131•132•m• 263 Under field
conditions, however, the non-uniform distribution of
the two ions in the soil will normally prevent proper
evaluation.
18. The influence of soil facto~s other than ~alcium.
The extent to which both strontium and calcmm areabsorbed from the soil varies depending on the clay andhumus content. the pH, the concentration of electrolytes
other than calcium, and the moisture content.19•134•144 •u 5
Soil conditions which encourage shallow root development usually cause the absorption of Sr110 to be increased.
. • 144 •146
The addition of organic matter •m.1arge quantities
and of fertilizers may have varymg and complex effects12s, ia1, 1u, u5, 1M, 2se which are, however, usually n?tlarge when these materials are applied at normal agncultural levels.
19. Movement of Sr" 0 in soil. When soil is not disturbed the downward penetration of Sr90 is slow, andeven after several years most of it remains in the upper
few centimetres. 10 · 14° The rate of downward movement
varies with soil type; a low content of ~lay and humus,
a 'high content of elect~olytes and a rapid 1?ovement ofwater increase penetration19•1 63 The mechamsm of movement is uncertain but both mass flow in water and self
diffusion may be involved.m A horizontal movement ~f
Sr96 due to transmission through the roots of plants 1sreported. 157 The repeated cultivation of .soils causes ~edistribution of Sr90 to become progressively more umform throughout the plough layer ;148 the depth to which
it is incorporated in this wa.Y m::y have a marked .effecton the ratio of Sr00 to calcmm m plants. Ploughmg tothe depth of 20 to 30 cm has been four_id to reduce theratio by a factor of up to 3 compared with placement on
the surface, when shallow rooted crops such as rye
grass or kale \Vere grown.m, ur, 253 With more de~plyrooted crops, the effect was sm~ller. Marked reductions
in uptake by several crops with mcreased depth o_f placement have also been noted on a podsol1H and with soybeans in a loamy soil. 145 In laboratory- experiments,
lowland rice, which is normally grown m flooded fields
with a strong development of surface roots, absorbed
more Sr90 when the activity was placed on the surface
than \vhen it was mixed in the upper soil layer. The
reverse was found with upland rice, which is grown in
conditions similar to those in which wheat is grownY 1 • m
20. Changes with time in the availabilit:y of Sr 90 for
absorption. Considerable attention has been given to thepossibility that with the passage of time Sr90 may _be
slowly converted into sparinglv soluble forms whichcause it to be more slowly abso1:bed relative to cakiur:i.
Some i.'lvestigators have found no evidence of this290

effect.151 However, in other soils it has been shown t!iat
a small per cent of Sr90 may cease to be _labile durm_g
three or more years 1 ~ 2 .m and. it is P?ssibl: ~ ~t thiseffect is considerably greater m certain soils. 5 The
present evidence suggests that the fixat~on of. Sr90 is oflittle practical significance from the viewpomt o~ thecontamination of human diet but results over considerably longer periods are necessary for a final evaluation.
Direct contamination of plants
21. Three routes of direct contamination have been
distinguished: Sr90 may be retained on the leaves or on
inflorescences of plants (termed foliar or floral contamination respectively), or it may be trapped by thebasal parts of plants from which it is absorbed without
being incorporated in the soiI (plant .base absOTJ?tion) .10 • 201 These three mechanisms of direct contamination lead to contrasting distributions of Sr90 in different types of edible tissue. Sr90 which enters by plantbase absorption moves upwards through the stem to allaerial tissues like material absorbed through the roots,
but little of that which enters leaves or inflorescences
is redistributed to other tissues.
22. Foliar contamination. The extent to which Sr90
is retained on vegetation depends on both the extent andduration of rainfall and the extent and form of the
exposed leaf tissue.121 •122• 123 Experimental studies usi~gspraying equipment suggest that w~en Sr~0 ?~scends mrain about one-quarter of the deposit may miti~y lodge
on the leaf tissue of permanent pastures which cattle
consume. 227 Absorption into the leaves is relatively ~lowand the superficial material can readily be lost, especiallyin rain.122 In the United Kingdom this may cause only
about one-tenth of the initial deposit to remain after twomonths. 221
23. Floral contamination. Attention was first directedto this process by the fact that the ratio of 90 to calcium
in grain and flour usually exceeded that m vegetabl~
by a considerable factor (tables XI-XYII): C?mpansons of the ratio of Sr9° to stable strontium m different
tissues of wheat grain provided evidence on the mechanism of entry. 84 • 201 · 210 · =~ 5 Since the soil is the sole sourceof stable strontium this ratio would be constant throughout tissues formed at the same time if Sr90 entered only
from the soil. It was found, however, that this ratio wasconsiderably greater in bran than in flour, and this was
ascribed to direct contamination of the outer layers of
the wheat grain. It was calculated that in the United
Kingdom in 1957, an average of 66 per cent ~ad enteredby direct absorption, 84 •:oi while in the Umted Statesvalues of 20 and 90 per cent were obtained in 1959. 210 • 235
An investigation in Japan, where the levels of Sr90 inwheat flour in two years were compared with the fall-out
rate and deposit, suggested that, while in 1959_ 50 per
cent or more of the Sr90 in wheat flour was attnbutable
to the recent deposit, the corresponding figure for 1960
may have been less than 15 per cent. 327 These. results
are consistent with those of experimental studies thatshow that higher concentrations of radio-st:ontium. arefound in the grain of wheat plants spray~d with solutionsof Sr90 after the ears have emerged than m those sprayedearlier· this could be prevented if the ears were protectedfrom the spray by small caps. 159 The much h_igher val~es
which were recorded up to 1960 for the ratio of Sr9 to
calcium in husked (brown) rice tha~ in milled (wli!te)rice have also been attributed to direct uptake. smce
tracer experiments and the measurement of stable stro:i;tium indicate that such a difference could not occur 1f
only soil.uptake were involved. 127 •195S:

24. Plant-base absorption. Some of the material not
directly retained on leans, or leached downwards fromthem, may be washed into the axils of leaves or into
the crown of plants, or the root mat. It may also be
trapped on decaying vegetation where it is available forabsorption by the surface roots. Retention in this way isparticularly likely to occur in permanent pastures. The
Sr90 so trapped is relatively undiluted with the calciumin the soil and in a particularly favourable position forabsorption.19 • :oi•

Relative importance of different routes of contamfoation
25. The rapidity with which Sr9° is transferred fromrain into food chains provides evidence on the magnitudeof direct contamination, because entry by these routes isdependent on the recent deposit, while absorption fromsoil is determined by the cumulative total deposit, though
not necessarily in a simple manner. The extent to which
short-lived nuclides (P 31, Sr5 9 , Ba140 ) were transferred
to milk when relatinly fresh fission products were present in fall-out underlined the importance of direct contamination. 2g1• 251 However, quantitative assessment of
the relative importance of the recent dep06it and of the
cumulative total deposit is rendered difficult by fluctuations in the rate of deposition of Sr90 , differing soil
characteristics, the changing availability of Sr90 as it
penetrates the 1;oil, seasonal and annual variations inagricultural practices, delays between the production andconsumption of food, climatic differences among various
areas, and variable weather at individual locations. These
problems have been discussed elsewhere. 19 The calculations and the validity of quantitative estimates derived
from available survey data are discussed in subsequent
sections (paras. 103-119) .
Aquatic food chains
26. Aquatic food chains have attracted comparatively
little study in relation to worldwide fall-out since aquatic
products provide 'little Sr9° to most diets, even when the
calcium intake from fish is appreciable (see tables V
and XIX). 19 • 33 ·m-m However, information is available
from Japan83 • m, 266 and extensive studielii have been carried out in relation to discharges from nuclear facilities2 65
and to the sites of nuclear weapons tests. 269 These haveshown that Sr9° is accumulated by the calcareous partsof marine organisms-bones, scales, shells-up to a concentration many times that of the environment, but noconcentration of Sr9'> occurs in the flesh of marine organisms even under conditions of chronic exposure. 261• 269
The equilibrium concentration in flesh is usually less than
one-tenth of that in the surrounding water.19• 267 A value
for the OR (flesh or bone/water) of 0.4 was observed
experimentally in fresh water fish and an OR (whole
body/water) of 0.2-0.3 for marine fish can be estimatedby comparing the ratio of stable strontium to calcium infish bone and water. 30 The level of Sr00 in fresh waterorganisms is generally higher than that in marine organisms from corresponding areas (tab le XIX) . A detailed bibliography on this subject is available. 281
Milk and animal products
27. The chief practical interest in the metabolism of
Sr 90 in animals is in the extent to which it may be transferred into milk, and the possible concentrations that
may be found in meat. Experimental studies with animals
can, however, contribute to the understanding of its
metabolism in man.
28. Quantity rransferred into milk. The total quantityof ingested Sr90 secreted into the milk of cows is variable;

291

like the quantity of calcium it is related to the milkyield. 229 • m, m Values ranging from 0.5 to 2 per cent ofa single administration are found.m. 2 w. 2 2J, 2 2'! In comparison with continuous ingestion under normal conditions of feeding, several independent investigations haveshovm that about 0.08 per cent of the amount given daily
is secreted per litre of milk.1 ss,m,m The amount of ingested calcium and strontium appearing in the milk isinversely related to the dietary calcium leveF 2 '1 since theconcentration of calcium in. milk varies little, regardlessof the dietary intake. It may be noted that the percentage
of ingested radio-strontium secreted per litre of goat's
milk is more than ten times the amount in cow's milkowing to the greater proportion of the dietary calcium
secreted into the former.m In man, it was shown in one
investigation with five women that an average of 0.27
per cent of the dietary Sr90 was secreted per kilogramof milk. 168
29. Observed ratio (milk/diet). Knowledge of the OR(milk/diet) is more useful for many purposes than thatof absolute quantities. The available data for this ratio
are summarized in table II. Values range from 0.08 to
0.16 but the majority of more recent experimental measurements fall close to 0.1 and this value may be adopted
for practical purposes. The values are similar in cows
and goats and also in man. The OR (milk/diet) in cows
and goats does not vary significantly with calcium levelsin the diet from one-half to three times the normal level,
nor with increased levels of stable strontium.m The
ratio in milk appears to be about half that in plasma. 124 •m,1sa,u 7• 22 • Hence, it may be assumed for practical purposes that the ratio of Sr90 to calcium in meat is twicethat of milk, if dairy and beef animals have feed with asimilar ratio of Sr9° to calcium.
30. Observed ratios in poultry. OR (sample/diet)values of 0.5-0.6 were found for bone, egg shell and egg
yolk of laying hens; plasma and egg white, however, had
OR values of about 1.5. 2113
Metabolic behaviour in man
31. Absorption and retention of Sr"°. Ingested radiostrontium is absorbed from the gastro-intestinal tract
into the bloodstream, where some of it forms a loose
comple..""< with p~oteins. It e_nter~ bone by excfiange andaccretion; some 1s excreted rn urme and some 1s excreted
in faeces after secretion from the bloodstream into thegastro-intestinal tract. For practical purposes it is important to distinguish ~etween the assi~ila~ion of Sr90
over short periods of time, when retention 111 th~ bo~ywill be governed to some e..'{i:ent by e..'<change reactions m
the skeleton, and over longer periods in which the bones
will approach a state of complete labelling and e..'<change
reactions will cause no net retention. In an adult exposed
to dietary Sr90 , about 20 per cent of ingested radiostrontium may be retained initially but the net retention
decreases to zero as the skeleton becomes labelled underconstant intake. The amount retained therefore depends
on the previous history of the subject in relation todietary intake of radio-strontium.
32. Experimental studies with Sr55 in man haveshown that a mean of 20 per cent of orally administeredstrontium is absorbed from the gastro-intestinal tract;
this compares with 40-50 per cent of Ca45 • However,much variation occurred between individuals. 224 The
kinetics of removal of injected radio-strontium in normal
man has been studied by means of a whole body c?unter;the excretion was characterized at least by three different
rate processes :214

(a) A rapid excretion within twenty to thirty days
ciated with considerable reformation of bone, is of shortaccounting for some 70 per cent of the dose;
duration. Thus, over a period of several years it isprobable that an OR (bone/diet) of about 0.25 would( b) One of intermediate rate, with a half period of
be obtained. This conclusion is supported by the results
about fifty days accounting for 15 per cent;of surveys of Sr90 in diet and bone reviewed later in( c) A stage of chronic retention in which excretion
this annex (table XXIV and para. 100); the average
was low. The findings are consistent with the general
ratio of Sr90 to calcium in the bone of children has been
concepts of the manner in which calcium and strontium
close to, and often slightly less than, one-quarter of thatare deposited in or removed from the skeleton. The
in their diet. Accordingly a value of the OR (bone/diet)over-all data could also be fitted by a power functionof 0.25 is used for prediction of levels in bone.
and are very similar to those previously described forsheep. 223 This type of information is especially important
35. Processes of discrimination from diet to body.
in understanding situations involving accidental shortIt is of interest to estimate the magnitude of the principal
term e.-..::posures. It also forms a basis for interpreting
processes of discrimination which bring about the OR
relationships between the intake of Sr00 and the resultant(body/diet). The measured e.-..::cretion in faeces of Sr85
irradiation of body tissues.
and Ca• 5 orally administered, 218 or studies of stablestrontium and calcium balances811 suggest an approxi33. Observed ratio (body./ diet).* When it is necessary
matelytwofold discrimination in absorption by theto consider chronic ingestion the evaluation of the OR
gastro-intestinal
tract. There is evidence however that(body/diet) appears to be more useful than estimating
this may not occur in infants. 208 From measurements
actual retention. This ratio has been studied for man
following intravenous injection, the I'l<' urinary can bewith a variety of techniques based on different asestimated as 0.70. Thus the OR (body/diet) of about
sumptions:0.25 is mainly brought about by a twofold discrimination(a) Direct experimental observations on the retention
in the gastro-intestinal tract and one of somewhat lessof Sr85 and Ca' 5 have been made. Recent results with . than twofold in the kidney. The OR (bone/plasma) is
213
si>-teen•.
patients suggest an OR (body/diet) of 0.29;
close to unity. 12 •. u 9
earlier measurements based on measurements of blood
36. Observed ratio (foetus/mother). A further implasma gave values of 0.44 and 0.54 for groups of
portant discriminatory process is in placental transportpatients on two different types of diet ;189from mother to foetus. Direct experimental evidence of( b) The measurement of stable strontium to calcium
discrimination
across the placenta is not available forratios in representative samples of bone and diet in
man but values of OR (foetus/mother) for rats andseveral countries gave values for the OR (bone/diet)
rabbits of about 0.5 are reported. 257 Calculation frcm
ranging from 0.16 to 0.25 (table III);extensive measurements of stable strontium in the bones( c) The ratios of Sr9° from fall-out to stable calciumof newborn in the United Kingdom gave a value ofin body tissues or fluids and in diet have also been
about 0.6. 256
examined. The use of the measured values in bone isdiscussed in a later section when a detailed presentation
MEASURED LEVELS OF Sr90 IN DIETof the bone and diet data has been made. An indirect
General considerations
estimate can be made from the OR (milk/diet) of 0.11
measured in women.168 If the OR (milk/plasma) has a
37. Two considerations are of primary importance.
value of about 0.5 in man as in animals (para. 29), an
First, while the experience of the past years has shown
OR (body/diet) of about 0.25 is suggested. The measthat the concentration of Sr00 in foodstuffs may fluctuateurement of the Sr00 to calcium ratio in large samples ofover short periods of time owing to the varying rates
human plasma, though subject to considerable uncerof fall-out, it is more important to consider mean levels
tainty, gave a result consistent with an OR (body/diet)of intake over extended periods. For this reason dataof 0.25.192
in the following tables are summarized where possible
over calendar years. Second, in order to estimate the34. While the OR (body/diet) is reasonably constantratio of Sr00 to calcium in new bone, the total intake ofwith ordinary diets it may change with unusual dietary
19 178Sr90 and calcium in the complete diet or at least in themodifications or age. • In rats, the presence of large
most important components must be h."Tiown. It is therequantities of milk, lactose or lysine or nutritionally abfore necessary to examine the composition of diet and,normal ratios of calcium to phosphorus have been shownfor comparing the intake of Sr00 m different parts ofto alter the OR. 19 • 178 • 288 • 291 • 292 However, double tracer
the world, it is convenient to identify broad dietary
experiments in man do not suggest that the OR is afclasses.
fected by the presence or absence of milk. 189 • 218 Consistent differences in OR, as measured by stable stron38. Diets might be classified in any of the followingtium and calcium, between countries with very different
manners:
diets cannot be established on the limited data available(a) On the basis of the most important contributors(table III). In very young rats124 and calves 223 a higherof Sr 90 • However, the relative contribution of different
OR is observed than in later life. The observed ratios offoods is dependent on the relative quantities of current
strontium to calcium in the bones of very young children
and accumulated fall-out and consequently may varysuggests that the OR may be higher in infants than inconsiderably;
adults. 258 However, their juvenile state, which is asso( b) On the basis of quantities consumed by weight.
• The term OR (body/diet) is more appropriate when the
Frequently, however, certain foods consumed in quite
amount of strontium and calcium retained in the body are estilarge quantities may contribute little Sr00 or calcium tomated from measurements of strontium and calcium in diet andthe diet;in excretions, the term OR (bone/diet) being reserved for thoseestimates based on direct measurement of the concentrations in( c) On the basis of the amount of calciimi contributed
bone. Since by far the greater part of the strontium and calcium
by different foods to the diet. The quantity of Sr00 inin the body are in bone, the values of the OR (bone/diet) anddifferent articles of diet cannot be inferred directly fromof the OR (body/diet) will be closely similar under steadystate conditions.
their content of calcium both because of the variable292•

extent to which plants may be subject to direct contamination (para. 25) and because of discrimination
between strontium and calcium in their passage to animal
products. Nevertheless, the classification of diets interms of the principal sources of calcium has been foundthe most convenient way of examining the effects of
dietary composition on the intake of Sr90 and of predicting future concentrations in diet and hence in bone(paras. 103-121). Hence this method of classificationis adopted in the present report.
39. Information on the calcium content of diets isavailable. 19• 115 For the present purpose, it is more important to consider the relative quantities of calcium
provided by different foods than the absolute amountingested per day. Wide variations exist between different
countries, but three broad dietary classes can be identified, namely:
Class I diets. Dairy produce is the predominant sourceof calcium; this applies to the greater part of North
America, Europe and Oceania. Calcium intakes in theseareas are generally from 800 to more than 1,000 mg perday. In Southern Europe and Latin America, calcium
intakes may be only of the order of 600-700 mg;
Class II diets. Milk provides less than half total dietarycalcium and vegetables approach it in importance, forexample, India, Turkey and Egypt. The total calcium
intake may be only 300-450 mg per day;Class III diets. Dairy produce is a minor source of
calcium, for example, in Japan and other countries of
the Far East. The calcium is derived mainly from vegetables, with cereals and fish making significant contributions. The calcium intake may vary from 200-400 mg
per day.
Approximate model diets for these three classes havebeen calculated from the food survey data from theprincipal countries where they are consumed (table
XXIII) and are used for subsequent calculations. With
only a few exceptions the composition of the diet of othercountries lies between the limits set by these three classes.
40. The data from which these groupings were derived are in most cases derived from gross figures for
production and consumption of individual foods, combined with average values for the calcium content ofthese foods. However, in some cases, the actual calcium
content of the diet may greatly exceed that expected on
this basis.19 • 172 This may be caused by the use of unusual
sources of calcium, for example, the use of crude sea
salt containing calcium for cooking in Ceylon and South
India or the enrichment of bread with mineral calcium(United Kingdom), with groundnut meal and fish flour(Union of South Africa), and with non-fat milk solids(United States).19 Calcium propionate may also be
added to bread as a mould inhibitor. 199 Com (maize)
grain is very low in calcium but when used for tortillamaking in Central America, is boiled with lime water in
the initial stages of preparation. This process greatly
enriches the diet in calcium: in some areas 75 per centof the total calcium in the diet may be obtained in thisway. 19 The chewing of betel leaves may also contribute
substantial amounts of calcium to the diet. When cereals
such as ragi or quinoa, which are rich in calcium, areused, the contribution of calcium to the diet is muchgreater than with other cereals.

The period of time and geographical area covered, thefrequency of sampling, the number of foods sampled
and the method used have varied very considerably andthus the precision also varies. In tabulating the resultsa primary distinction has been drawn behveen thoseanalyses based on continuing sampling and those basedon a single limited sampling over a short period of time.
42. To provide further information on the nature of
the samples and to assist in the evaluation of the results.
the meth~ds .used have been distinguished as follows, 171
and also mdicated in table IV:-(a) The use of values, often countrywide averages,
obtained from separate surveys of the Sr9° content of
the most important dietary constituents, together withestimates of the quantities of these foods consumed, tocalculate the Sr90 content of the complete diet;( b) The calculation of the content in the total dieton the basis of data obtained from the analysis of foods
purchased locally in stores. This method may often be
used in relatively small areas and therefore some caution
must be exercised in applying the results to larger areas;( c) The analysis of composite samples of complete
diet often based on local purchases. The composition of
the diet may be based on dietary surveys or local estimates of "typical" consumption;17( d) The analysis of samples of the complete dietactually consumed by certain individuals or groupsmilitary forces, hospital patients, or volunteers in metabolic studies. These diets may. or may not resemble theaverage diet of the community.
43. In the first two methods the major sources oferror, when accurate knowledge of the average quantities
consumed is available, may be inadequacies in the representativeness of the sampling of the foodstuff for Sr90 •In the last two methods an additional bias may be introduced when estimates of "typical' diets or duplicate
samples of the actual diets of individuals or groups areused, its magnitude depending on the extent to which
the composition of the diet analysed is representative ofthat of the population as a whole. However, the values
from the United States suggest that comparable results
may be obtained by the various methods. 74 • 171
44. North America and Europe. Amongst countries
in which milk is the major calcium source in the diet,the most complete series of estimates of the Sr90 to
calcium ratio in the diet is available from the United
Kingdom and the United States. Variation by a factorof three in the values from different areas of the UnitedStates in 1959 was observed, particularly low values
being observed on the West Coast. The values from
Europe in 1959 and 1960 fell within the same limits.
In the United Kingdom and the United States a rise wasshown from 1957 to 1959 followed by a marked dropin 1960 and early 1%1. This fall was also shown in
Denmark. Values for 1959 and 1960 in Canada werecomparable with the higher values from the UnitedStates.
45. Asia and the Far East. An extended series of estimates is available for Japan. Although the diet of Japanis not typical of that of the Far East. the results forthat country are of particular interest because it is the
only area in which regular surveys have been carriedout where the diet is not of class I. The mean value forthe ratio of Sr00 to calcium in diet rose from 1957 to
1960. No decrease occurred in 1960, probably owing to

Estimates of the ratio of Sr9° to calcium in the total diet
41. Since the previous report, many values for the
Sr9° and calcium content in diet have been published.

293the storage time of the large cereal component. The
values for Japan were lower than those in Europe andNorth America in 1957 but in 1960 were rather greater.
Samples of composite diets, collected over a short periodof time were taken in Viet-Nam in 1959, and Thailand
and Taiwan in 1960. Though wide variation was observed the mean values are comparable with or lower
than those in Europe in the same period and lower thanthose in Japan. In 1%1 the average Sr9° to calcium ratiosof vegetarian meals in India was comparable with theaverage value for total diet in the United States.
46. Africa. In Africa a series of samples, consisting
principally of cereals, legumes and milk, was taken in
1958 in a number of cities. From these the ratio of Sr90
to calcium in the total diet has been estimated, including
and excluding milk. 38 It is suggested that the latter willapproximate the diet of those groups of the African
population who consume little milk. 38 The limited area
and time covered by the survey indicate the need forcaution in using the values. They appear, however, tobe lower than those in Europe and in the United States.
A limited sampling of the diet of the African populationof Southern Rhodesia was made in 1959-1960. The
values were comparable to those found in North America
and Europe in the same period. The mean value for thecomposite diets in the Delta region of the United Arab
Republic in late 1961 was comparable with that foundin the United States earlier in the year.
47. Central America. A series of estimates was
also made for Central America in 1958. The values
found were very low, of the order < 1-2 µ.µ.c Sr90 per g
Ca. The calculations for the total diet were based only
on the analyses of corn, beans and milk. No analyses ofleafy vegetables or fruit were made, so that the dietcannot be regarded as completely examined, but thevalues indicate the general level of Sr90 in the area. The
values of the ratio of Sr90 to calcium calculated for the
total diet for Guatemala and Honduras were particularly low owing to the practice already mentioned ofpreparing maize for tortilla-making by boiling in lime
water. 19• 29 • 55 • 56 This is particularly common in ruralcommunities. In urban communities the values are likely
to be higher since more wheat and rice, or maize boiled
with wood ash, may be used, and therefore the extra
calcium contribution is not obtained.
48. South America. Results from surveys of brief
duration in several countries of South America in 1957
and 1958 are available, as well as analyses of composite
military rations, based on local foods, in two countries
in 1959. Composite diet samples were obtained fromlocal communities in Colombia and Chile in 1960. The
wide variation in the Sr90 to calcium ratios of different
samples is attributed to differences in climate. 319 This isparticularly well shown in Chile where the average forthe dry northern districts (2.4) is only one quarter ofthat from the wetter southern districts (9.6). 319 In
general values for the Sr00 to calcium ratio of total dietin South America are lower than in Europe and North
America.

Contributions of Sr90 by individual components
to the total intake

50. The relative contributions from different components of the diet in 1959 and 1960 in the few countries from which a detailed breakdown is available isshown in table V. In all the countries listed, except forJapan, the diet is of class I and about three quarters of
the calcium (excluding mineral calcium) is supplied
from milk. In contrast, milk usually supplied only froma quarter to a half of the Sr9°, owing to the discrimination against Sr00 in passage into milk (para. 29). The
value was higher in Canada. Cereals, which are particularly subject to direct contamination by fall-out (para.
23). also supplied a major fraction, especially in Denmark and Austria. In these class I diets, leaf and root
vegetables together contributed from 6 to about 30 per
cent of the Sr90 , and meat, fish, egg5 and drinking water
very small proportions. In Japan, where the diet is ofclass III, milk supplies only a small proportion of thecalcium in the diet. and even less of the Sr9°. In 1960
cereals supplied one quarter of the Sr 90 in the Japanesediet and some 65 per cent was attributed to vegetables
and fruit.
Factors causing intake to vary from the average

51. The foregoing estimates are fotthe average intake of the population as a whole. However, there isinterest in the intake of special groups or of individuals,
depending on their dietary habits. Unfortunately, very
little information is available on the variation of dietary
habits among special groups on which estimates might
be based. 19
52. Age. The diet of very young children is of particular interest and in some countries analyses of prepared baby foods have been made. The results are shownin table VI. The values are comparable with those of
normal samples of similar foods. The intake in the dietof infants has been calculated in Germanv. 24 the United
Kingdom, 85 • 2 z7 and the United States,7 1,ios and composite diets have been analysed in the United States. 312
The results indicate that the Sr9° to calcium ratio in thediet of young children, when they are fed on preparedbaby foods or cow's milk. differs relatively little fromthat in the diet of adults (table IV). The same applies
also to older children. 24 • 312 The Sr90 to calcium ratio in
the diet of breast-fed infants will however be considerably lower than that of other groups,2 4 since this ratio
in human milk is approximately one-tenth of that in themother's diet.108 There may also be metabolic differences
between breast-fed infants and those fed on cow's
milk.Zll
53. Quantity of food consumed. Differences in theintake of Sr90 of adults may arise through normal variations in the amount of different foods consumed. Dietary
estimates in the United States suggest that high consumption of the major components of the diet may betaken as approximately twice the average amounts. 112
When the ratio of Sr90 to calcium in an individual fooddiffers little from that in the total diet, alteration in theamount consumed has little effect on the ratio in the
total diet. This is generally the case with milk in countries where substantial quantities of milk are consumed.
54. The effect of increasing the quantity consumed ofcomponents in which the Sr90 to calcium ratio exceedsthat in the total diet is roughly in proportion to the Sr9°
contribution; this is small in diets containing reasonable
quantities of milk. In the United Kingdom it was esti-

49. Oceania. The Sr90 to calcium ratio in the total dietin Australia has been estimated from analyses of milk,
cabbages and wheat. 320 Little change occurred in thelevel between 1957 and 1960. Values were always below
the average for North America and Europe which areregions of similar diet. No marked rise in the level in1959 comparable with that which occurred in the Northern Hemisphere was detected.
294

mated that doubling the intake of root or leaf vegetables
or fruit would have increased the Sr90 to calcium ratioof the total diet in 1959 by only a few per cent. 85 Inspection of the detailed analyses of diet in the UnitedStates195 shows that the highest contribution of Sr90
from any of these three items is only 15 per cent;doubling the quantity of the food consumed would therefore increase the ratio of Sr00 to calcium in the diet by
only a small amount. Where milk consumption is normally small. increasing the quantity of milk consumed
may reduce the average ratio of Sr 90 to calcium in thediet since the ratio in the milk is generally less than thatin other components.
SS. S pec-ial dietary habits. Certain groups may havespecial dietary habits which affect Sr00 intake, One suchis the consumption of unmilled cereals. Attention has
been paid to this particular habit since the ratio of Sr90
to calcium is often much higher in unmilled than inmilled grain (see tables XI-XIV).
56. Because the ratio of Sr00 to calcium is higher inwholemeal bread or flour than in white bread or flour 73 •85 • 2 ~• the replacement of white bread by wholemeal breadin the diet causes the dietary intake of Sr90 to be increased. The effect, however, appears to be relatively
small 198 • 111 except in countries, such as the United Kingdom, where mineral calcium is added to all white flour, 84 •85 227•but not necessarily to wholemeal flour. It may be
noted that cereals supply a relatively high proportion of
the dietary Sr90 in Denmark and Austria, where theproportion of wholemeal flour consumed is greater thanin the United Kingdom or the United States (table V).
57. The milling of rice also has a considerable effecton the Sr90 to calcium ratio of the diet in those countries
where rice is an important food. A total diet sample inViet-Nam containing "unpolished" (presumably unmilled) rice was three times as high in Sr9° per g ofcalcium as was a diet sample containing milled rice. 110

60. The source of drinking water. The concentrationof Sr90 in drinking water may vary according to its
source. The radio-nuclide concentration in rain is reduced by contact with absorptive surfaces and purification in rivers and lakes occurs by sedimentation or
percolation. Conventional processes of water purification
do not remove radio-nuclides to any great extent. 174 A
survey in the United Kingdom showed that well water( 0.02 µ.µ.c/l) was very low in Sr 90 compared with surface
waters (0.3-0.9 µ.µ.c/l) ,169 • 1700 303 Concentrations similar
to the latter ·were measured in suriace \Vater in the
United States 05 • 73 • 1 ' 3 and Japan. 304 Higher concentrations were shown in 1959 following heavy fall-out thanat other timesm, 303 • 30'1 but the intake of Sr90 in drinking
water is unlikely to have exceeded 1 µ.µ.c per day formost of the period and variations in this quantity due tothe nature of the water supply are unlikely to havecaused large differences in the total dietary intake.
61. People drinking water which has not had contact
with the ground surface may have higher intakes of Sr90 •Mean values for Sr90 in cistern water for periods ofsome months ranging from 2-6 µ.µ.cfl have been reported
from the Federal Republic of Germany (1959-1960),
Japan (1954-1957) and the United States (1958-1959).
22 33 78 173
If it is assumed that no decontamination of• • •the rainwater occurs in the collecting system, the concentrations reported for rainwater (F I, table IX) can
also be considered. Comparison of these data with anestimated daily intake of Sr9° in 1959-1960 of the orderof 10 µ.µ.c (tables IV and XXIV) suggests that thedrinking of rainwater would have appreciably increased
the daily intake of Sr90 for short periods in 1959 when
the rate of fall-out was high. However, expressed as anannual average, the increase would have been smallerin 1959, and in 1960 smaller still.

Sr90 in individual foods

62. The limited number of areas from which estimates of the Sr00 content in total diet are available makes
58. Geographical location. Differences in the total
it necessary to find some basis for extrapolation if levels
dietary content of Sr00 , owing to variation in the degree
in other areas are to be inferred. Measurements of indiof contamination of foodstuffs produced in different
vidual foods, when considered in relation to the diet typeareas are difficult to assess since it is unlikely than any
and general distribution of fall-out provide the bestindividual would receive all his intake from the mostopportunity.
highly contaminated sources. In many countries the variation is likely to be largely controlled by the levels inMilk
milk, since it contributes a large proportion of the Sr9°.
Further, variations due to geographical position will be
63. Since milk is a major calcium source in many
more readily reflected in milk which is consumed relaareas of the world and is easy to sample, it has received
tively locally, especially in rural areas, while other foodmore attention than any other component of the diet.
stuffs, such as cereals, are often distributed over very
In some areas regular surveys are in progress or widelarge areas.
spread surveys have been made. Results of these are
given in table VII and descriptions of the surveys in
59. Inspection of the range of values for milk withintable VIII. From many other areas only isolated samples
countries (table VII) suggests that a variation between
are available, sufficient to give some indication of thesites by a factor of 4 is common in moderate-sized areas,
relative levels. These data are summarized in table IX.
with narrower ranges in smaller areas. In larger countries, such as the USSR or the United States, variation _ Values are available from areas accounting for more.
than 90 per cent of the world production.
by a factor of up to 10 may occur. The ratio in the total
diet may be expected to show a less extreme range
64. Data from some regular surveys are plotted inbecause of more uniform contributions from otherfigure 1. In the N orthem Hemisphere, a more or less,sources. A study of twenty-five 'cities in the Unitedsteady rise from 1954 to 1957 was followed by sharper
States in 1959 showed that the Sr90 to calcium ratio inrises in 1958 and especially in 1959. It is interesting to.
the diet ranged from 4.9 to 16.7 with a mean of 11.8.11
note that the increment was roughly similar in most of,Calculation in the United Kingdom in 1959 and 1960
the countries although the 1958 level differed by a factor:
based on the most pessimistic assumption that all items
as much as 5. Subsequently in 1960 the levels £ell off,
often by an amount comparable to the rise in 1959. Inin an individual's diet were obtained from the areas
where highest contamination was found suggested that
1961, levels continued to fall by a variable amount.i
These observations show the partial dependence ~f the.
the average level would not be exceeded by a factor as
Sr90 in milk on the rate of fall-out and are cons1stent1
much as 10. 85• 227
295

Year

Figure 1. Yearly mean concentrations of Srso per g of calcium in milk from
9 countries (from table VII). For details of the surveys see table VIII

with the heavy deposition in the Northern Hemispherein late 1958 and early 1959. In contrast with thesechanges, the levels in Australia and Argentina changed
only slightly. The Southern Hemisphere was not subjected to the heavy increase in the rate of fall-out in
1958-1959.
65. Detailed comparisons of the data in table VII may
be misleading because, even within regular programmes,
the data from year to year are rarely strictly comparable,
since the areas covered and techniques of sampling havechanged as the programmes developed. The values ofspot samples may be greatly affected by the season atwhich they are taken and all values will be affected by
local agricultural and climatic factors. Consequently, inorder to summarize the data so as to show the broad
trends, mean values for large geographical areas havebeen calculated for the years up to 1960 (table X). Meansfor each country have been weighted for production in
calculating the area-wide average in order to represent
more closely the true average in the milk over the wider
area. Sufficient data are not yet available for 1961 to
calculate comparable mean values.
66. Tables VII, IX and X show that a correlation
exists between geographical latitude and the level of
Sr9° in milk. Between 1955 and 1960 the mean values
for the ratio of Sr90 to calcium in milk in each year wereof very much the same order in most of North America
and Europe, including the USSR. The scattered values
from the Mediterranean area, and data from India andJapan were lower than those of North America andEurope. Very low values were recorded in Central
America, especially in its southernmost region. Unfortunately, no data from comparable latitudes are avail-able from Africa or Asia. Low average values were
found in South America, but in the Republic of South
Africa, Australia and New Zealand, the levels were
somewhat higher. On the average, t11erefore, the highest
values were recorded from the mid-northern latitudes,
and tile lowest in the equatorial region, with intermediate
values further south. This general correlation witll latitude is consistent with the known variation with latitudeof the intensity of deposition of Sr00 •Cereals
67. The comparison of cereal data is complicated by
the number of species, differing in structure, growing
season and dietary importance. The range of values isgenerally very wide. General points that may be noted
are that milled cereals normally contain less Sr9° perunit weight or per g of calcium than unmilled, and that
the Sr90 to calcium ratio of both is considerably higher
than that of milk from the same area.
68. Wheat. The major wheat-producing areas of theworld are North America, Europe, the USSR and theFar East. 20 Sufficient data are available to provide a
reasonable estimate of the levels of Sr00 in wheat andwheat products from all these regions e.."X:cept the Far
East (table XI). In the latter the only detailed data arefrom Japan which is responsible for only a very small
proportion of the total production. The most widespread sampling was carried out in 1959. Values werecomparable in the USSR and in Western Europe butwere higher by a factor of 2 or more in North America
and in Ja pan. In the Souiliern Hemisphere. values werehalf or less than those in Europe. Trends from year toyear are difficult to interpret; in the USSR and Canada
296

values changed only slightly from 1956-1959, but in the
United Kingdom they were markedly higher in 1958
than in 1957 or 1959. The reverse was true in Japan, but
a lower value in 1959 than 1958 was recorded also in
the United States and Australia. These inconsistencies
are probably related to the high degree of dependenceof the level of contamination on current fall-out, during
the time the grain is developing.in Little data for 1960
is yet available but markedly lower values than in 1959
were recorded in the United States and Canada. No
significant fall was noted in Denmark and the Federal
Republic of Germany.
69. Wheat floltr. The ratio of Sr90 to calcium is lessin wheat flour than in the whole wheat grain. This is
illustrated in table XIII >vhere the Sr90 content of milling products from Canada, the United Kingdom and theUnited States are tabulated. The Sr90 calcium ratio inflour was approximately one-third to one-half of thatin whole grain and one-quarter of that in bran. All theavailable values for flour are tabulated in table XII.
Differences are shown between areas comparable to thosefound in the whole grain.
·70. Rye, barley and oats. Rye is an important cerealin Northern and Eastern Europe. Data on the Sr90 content are available for Germany, Denmark and the USSR
which are responsible for a major share of the world's
production 20 (table XIV). Mean values were very similar to those for wheat and this encourages the view that
this may also be true in North America for which values
are not available. 'World production of barley is spreadover a large part of the Northern Hemisphere, with someproduction in Oceania and Africa. Only scatteredanalyses are available, probably because in rriany areasbarley is not used directly for human food. Mean values
for barley in Denmark in 1959 were similar to those forwheat; this was also approximately true in the Federal
Republic of Germany in 1956-1958. Values for barleyfrom South America and Africa are very considerably
lower than in the Northern Hemisphere. Few analysesof oats are available, again probably because of the much
lower importance of this cereal in the diet.
71. Maize. Maize is grown in many areas but is ofminor importance in the average diet of North Americanand European countries and extensive sampling has notbeen carried out (table XIV). Analyses in the UnitedStates in 1958-1959 indicate values per kg very much
lower than those in wheat. However, since the calcium
content of maize is very low, the calculated ratio of Sr90
to calcium is lower than that in wheat by a factor of
only 2-3. Comparable values were recorded in Rhodesia
in 1959 and it was calculated that maize may have supplied about half the Sr90 in the total diet of the African
population. 227 In Central America, where maize is also
important in the diet, the ratio of Sr90 to calcium wasvery low in 1958.
72. Rice. Rice is a staple cereal in the diet of many
populations but has been sampled systematically only inJapan (table XIV). The ratio of Sr90 to calcium inbrown rice ( unmilled or under-milled rice) is roughly
comparable to that of wheat from the same area. Millingmarkedly reduced the ratio of Sr90 to calcium in ricegrain in 1956-1957, but in 1960 the Sr9° to calcium ratio
in milled and unmilled rice was similar. In 1960 the Sr90
content of brown rice had decreased to about one-quarterof that in the immediately preceding years because theamount of direct contamination was greatly reduced. The
few values which are given in table XIV for rice fromother areas in Asia are consistent with lower fall-out
rates in tropical latitudes.
297

73. Other cereals. Millet, quinoa and native grainsfrom a few areas where these are used commonly in thediet have been analysed but no wide-spread samplinghas been carried out. None of the samples is particularlyhigh in Sr90 (table XIV).
Vegetables
74. Green vegetables. Recent and extensive measurements of green vegetables are available only for North
America, Europe and Australia (table XV). In 1959 and1960 the mean values in the Northern Hemisphere weregenerally comparable. They were significantly lower inAustralia. The ratio of Sr90 to calcium is normally somewhat higher than that of milk from the same area.
75. Legumes. In many countries where leguminous
vegetables are eaten fresh and are not major items inthe diet, there is no real necessity to consider them separately from other green vegetables. The available resultsfrom the Federal Republic of Germany and the UnitedStates show that mean ratios of Sr90 to calcium in pea
and bean crops are similar to those in leafy vegetables.
In many other areas, however, dried legumes contributea substantial fraction of the total calories and this justifies separate treatment (table XVI). Surveys conductedin Africa and South and Central America in 1957-1958
show that in these areas the ratio of Sr90 to calcium inbeans and other legumes did not exceed 4 and was often
below 2 µ.µ.c Sr90 per g calcium.
76. Potatoes and starchy roots. The available values
for potatoes are given in table XVII. Like green vegetables they normally show ratios of Sr90 greater thanthose of milk from the same area. In 1957-1960, meanlevels of Sr 00 in potatoes in the United States, the United
Kingdom, the USSR and the Federal Republic of Germany were of the same order. Comparison of the Sr90
content per kg and per g of calcium indicates that themean calcium content is very variable. There is wide
variation in the Sr90 content according to region in individual countries ; this shows some correlation with
rainfall. 84 The data from other areas are too few to permit any comparisons to be made. Analyses of types ofstarchy roots which are important in the diet in SouthAmerica have been made (table XVII). A wide-spread
survey in Venezuela in 1958 indicated a mean value foryucca (cassava, manioc) of 22 µ.µ.c Sr 90 per g of calcium with a very wide range. The wide range may haveresulted from a deliberate attempt to discover extreme
values ; the median value of these figures was only 12.
Samples of potato and sweet potato from the same areagave lower mean values.

Fruit
77. The few available data for fruit are summarizedin table XVIII. They are derived from analyses madein only a few countries and include home grown andimported fruits. The nature of the fruits is so variedthat summarization and comparison is difficult. In theFederal Republic of Germany, Denmark and Australia,
mean values of the ratio of Sr90 to calcium for locallygrown fruits appear to be rather higher than for vegetables. Imported fruits, coming from tropical or subtropical areas were often lower in Sr 90 than those from
north temperate latitudes.
lvf eat, eggs and fish

78. Meat, eggs and fish have not been extensively examined because they generally contribute only a little
Sr90 to the diet. Some data are presented in table XIX.
They indicate values of the ratio of Sr90 to calcium in83. The ratio of Sr90 to calcium in newly formed boneof all age gi:oups should be similar, .except possibly invery young mfants (para. 34) provided that the ratioof Sr 00 to calcium in their diet is the same. However.
the ratio in the whole skeleton of adults is considerably
lower than that for children because of the absence ofgrowth and differences in turnover rates. Analyses of thebones of children may be used to give a direct measureof the concentration in newly formed bone. The bonesof the newb.orn have special value since they reflect the
average ratio of Sr90 to calcium in the mother's dietduring the later months of pregnancy. While the dietof pregnant women may differ from that of the average
adult, this difference may be less than between adultand very y~ung children. The variation with age in the
average ratio of Sr90 to calcium in bones is shown infigure 2 which utilizes the very extensive data obtainedin the United Kingdom in 1959. The concentration in
the newborn was a little over 1 µ.µ.c Sr90 per g of calcium.
The highest mean values, in the bones of children 1 to
2 years old, were about four times higher than in the
newborn. The concentration was less in older children
and at the age of 8 years was about the same as irt the
newborn. In adults the value was very low, about' onequarter of that in the newborn if the normalization factorof 0.45 from femur, the bone analysed, to whole skeleton
is adopted.
84. Less detailed data are available from most otherareas so that wider age groups have been used in showing similar data for eight countries in figure 3. It canbe seen that the highest values always obtain in the 0-4
year age group and the lowest in adults but the relative
difference between the 0-4 year age group and adolescents in different countr:ies is variable. Figure 3 also
shows that, between Japan, the United Kingdom and the
USSR, the values for the newborn are more nearlycomparable than are those for the 0-4 year age group.
These apparent differences between countries in therelative concentrations in bones from different age
groups may be due to unavoidable sampling errors but
may also represent real differences in Sr9° and calcium
intake caused by differences in dietary habits in theyoung. In particular, the extent of breast feeding will
have a great influence on the Sr90 to calcium ratio of thediet owing to the discrimination in passage from mother's
diet to milk (para. 28).

meat and eggs generally comparable to or lower than in
milk. The value in marine fish is particularly low· inriver fish it is higher.
'
Tea
79. A beverage which might appear to contributemuch Sr90 to the diet is tea, since some high values for
the Sr90 to calcium ratio in tea have been reported.ss, 1o,s5
However, laboratory experiments suggest that only asmall percentage of the Sr 00 is released into the infusion.8~·~27 The estimated contribution to the diet is small
and comparable to that from drinking water (table V) '.
MEASURED LEVELS OF SR90 IN HUMAN BONE

80. The Sr90 content of a sample of human bone depends on:(a) The rate of deposition of Sr90 in the bone, which~as. ~en determined hitherto primarily by the age of the
md1v1duals. However, when fall-out has continued fora longer period, this factor will be less important;( b) The dietary intake of Sr90 which in turn depends
on the composition of the diet and on the variation intime, and between geographical areas, of the Sr90 in
fall-out. It is thus related to the year of death and thegeographical location.
81. Values for the concentration of Sr 00 in bone froman_y given area show a wide range (table XX). This
anses from the natural biological variation, which also
occurs with stable strontium and the error associatedwith the measurement of the small quantities of Sr90 in
the bone. In the accompanying comprehensive table(table XX), the range of values is shown in those cases
where detailed information is available. Because thenumber of samples is rarely as many as 100, only generalcomparisons can be made between different areas, andthe significance of differences based on small numbersof samples is doubtful.

Effect of age
82. Sr has been present in the environment for a
relatively short period so that a large amount of preformed bone existed in adults and, to a lesser extent, inolder children. In addition to true growth which occurs
only in children, in both children and adults existingbone is, to a variable extent, replaced by new bone; theproportion of bone undergoing such changes is likely
to be very much smaller in adults than in children. A
recent estimate:~& based on the comparison of Sr9° tostable strontium and Sr00 to calcium ratios in different
age groups suggests that the annual skeletal turnoveris nearly 100 per cent in the first year of life and very
high in the second. It falls to about 10 per cent in thethird to eighth year, and to very low values during thesecond burst of growth around puberty. In adults, rateof turnover in ivory bones such as the femur shaft is~:mly about 1 per cent but may be as high as 8 per centm vertebrae.*90

Geographical location

85. The geographical origin of a bone sample may
affect its Sr00 concentration because of variation in thefall-out deposit in different areas or because there areregional differences in dietary habit. In table XXI thedetailed data for 1959-1960 have been summarized forbroad geographical areas, the mean values from individual countries being weighted for total population. The
mean values in table XXI suggest that the Sr~ to calcium ratio in the bones of adults, adolescents and newborn is similar in areas above the latitude of 30°N; thatis, in North America, Europe and Japan. The value for
the 0-4 year old group in Japan, however, appears to berather lower than that of other areas above this latitude.
This may be due to differences in the extent of breast
feeding, but it may be noted that the levels of Sr&° inmilk from Ja pan also appeared to be lower than in North_1\merica and Europe (table VII).
86. For Central America, data are available from only
two countries and a marked difference is shown between
them. Values for Puerto Rico are comparable with those• The difference in turnover rates means that the particularbone chosen for analysis is not important in the case of young
children since the ratio of Sruo to calcium differs little between
different bones but this is not so in adults.35, 98 Analyses of anumber of whole adult skeletons have shown that the relative
c?ncentrations of Sr9o are as follows: vertebra/skeleton 2.1;
n~/skeleton 1.4; femur/skeleton 0.45.so These values were obb:'nc;d from whole skeletons in New York in the years 1958-1959.
S1m1lar values ~ave been .o.btained in the United Kingdom.2M
It has .been considered legitimate to use these factors for otherareas m order to facilitate comparison where different bones
have be.en used for analysis. In table XX, adult bones have been
nom:ialized by the use of these factors, where identification was
possible.

298

..
5

3

3

5

4

3

...~
()

cc
()

tlO
J.<

&

.,,
0

Ji
()

2

::i..
;:I..

1

0

5

10

15

20

20+

AGE AT DEATH, YEAR!
Figure 2. The concentration~£ Sr•o in human bone in the United Kingdom in 1959 in relation to age at death. · ·The number of samples (n) is shown above each age group256

in which regular sampling has been carried out. Similarrises were shown from 1956-1958 in four countries ofNorth America and Europe. Thereafter the time courses
were divergent, with a marked rise in 1959 being shown
only in the United Kingdom. The value for Canada in1960 (no data are available for 1959) was distinctly
lower than that in the United States, both values being
based on a large number of samples. This order is thereverse of that shown by the milk levels in the preceding
years. Only a slight rise was shown in Japan. No consistent change was observed in Australia or Chile. The
general differences in trend between northern and southern hemispheres are consistent with the differences indeposition of Sr90 • The more detailed differences may
depend in part on lack of representativeness in sampling
but may well arise from genuine differences in dietary
habit in the young.
89. Detailed information from the United Kingdom(figure 5) shows a marked increase with time in thevalues for children but no signmcant change withadults. 98 The data in table XX suggest that this was
generally true in other areas.

in the United States, but those for Guatemala are distinctly lower. The latter corresponds with the low intake
of Sr 90 calculated from dietary information (table IV).
From Africa in the latitude band 0-30° N no information is available, but a few values from the Near East
(Israel) suggest levels rather below those in Europe.
Frnm South-East Asia data are few but again suggest
levels lower than or comparable with those from countries further north. Mean values from the Southern
Hemisphere (South America, Australia, Republic ofSouth Africa) are generally lower by a factor of two
or more than those in North America and Europe.
87. Such differences between areas in the Sr90 content of bone correspond roughly with what is to be e.xpected from latitudinal differences in the deposition of
fall-out. It has been noted, however, that the difference
in bone levels are rather less than those in deposition. 319
A major contributory reason is likely to be difference!
in diet, but this cannot be invoked in a comparison of,for example, Australia and North America where thediets are similar. The transport of food from one region
to another may also be important in producing more
unifonn bone levels.

Observed ratio (bone/diet) frotft measurementsof S~ 0 in bone
90. It is not possible to calculate the OR (bone/diet)for adults from fall-out data because of the short time

Trends urith ti1U
88. In figure 4 values for the Sr>° content of the boneof 0-4 year old children are shown for some countries

299

3·

2

1

____

---._

....,

__ ,

r---

I
I

.____ _ o ._____ oUKUSA____ o
Japan

USSR

1

0

Fed. Rep. Germany
PolandBraz.11
Australia.
Figure 3. Concentrations of Sreo per g of calcium in bones from different age groups in 1959, from 8 countries. In each histogramfrom left to right 0-4, 5-19 and> 19 years. Dotted line in 0-4 group shows the level in the new-born (data from table XX)

3
UK

USA
Fed. Rep,
1~~--,-­------

Germany'--""'() Canada.

l-"---+ Chile
1955

1956

1957

f

1958

1959

1960

Year

Figure 4. Sr&o in the bones of young children 0-4 years old 1955-1960 (data from table XX)

which it has been present in the environment, relative
to the period during which the bones of adults have been
formed. This difficulty does not arise with respect toyoung children, but the composition of their diet is veryvaried and is often not well known, so that no detailed
evaluation of the OR froi:n survey data is justified at
the present time.

91. The bones of the newborn, or still births, however, provide an opportunity for estimating the OR(foetus/mother's diet) since relatively large numbersof bones of the newborn have been analysed and muchinformation is available on the adult diet. For different
countries in Europe and North America (table XXV)the values range from about 0.1 to 0.13. This result is
300

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A NEONATESB ADlH.TS

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Figure S. The concentration (µp.c per g of calcium) of Sr9o in human bone,
1955-1959, in the United Kingdom
Notes:(i) In each group the mean values are linked by a continuous line and the maximum values by an interrupted line. In the first category the lower continuousline (B) relates to the bones of adults and no maxima are drawn as theydiffer so little from the mean; the upper continuous line (A) relates to themean values and the interrupted line to the maximum values for still-born
infants whose bones are formed indirectly from the maternal plasmas.
(ii) The subscript tables for each category give: (n) the number of individuals;{m) the mean value in µµc per g calcium; (s.d.) the standard deviation of
the values in µµc per g cakium9s

in bone in different areas appear to vary in a generally
similar manner to the levels of Sr90 deposition, particularly in regard to geographical latitude.

in good agreement with that which can be inferred fromexperimental studies on animals; the OR (foetus/
mother) is about 0.5 and when this is combined with
the OR bone/diet of 0.25 a value of 0.125 is obtained.
The variable values for Japan shown in this table may
have been due either to the small number of samples ordifferences in the composition of diet.

93. An attempt is now made to summarize these dataand compare the values found in bone with those predicted from diet. The data are considered as means,weighted appropriately for production or population
over broad areas. A comparison is made between the
Sr90 to calcium ratio in the bones of young children andnewborn in 1959-1960 as representing the newly formed
bone in the population, and the dietary levels in 19581960. It would be preferable to use bone data from 1960
only for comparison but this is not yet available fromall areas. Such data as we have suggest that the increase

EVALUATION OF MEAN LEVELS OF Sr90 IN DIET AND BONE

92. In the previous sections of the present annex,
measurements of Sr90 in individual foods, in total dietand in bone have been presented and discussed. Attention has been drawn to the fact that the Sr90 to calcium
ratios in individual foods, in diets of similar types and301

from 1959 to 1960 was small and that the use of the1959 values for these areas i:3 a reasonable approximation. Values for diet before 1958 are not used because
they are fewer than in later years. It is, in any case,probable that the age distribution of samples of bone in
the 0-4 age group is generally biased to younger ages
owing to the higher mortality rate in the first years oflife; consequently, much of this bone would have been
formed in the period 1958-1960.

Evaliwtion of S~ to calcium ratio in total diet,
1958-1960

94. Measurements for the total diet are available only
from limited areas (table IV). However, by adopting
one food as a reference standard and comparing withit the level in total diet or in other foods, extrapolation
to wider areas is pos;sible. Milk has been chosen as thereference standard not because it necessarily supplies alarge proportion of the dietary Sr9° but because it has
been most widely sampled.
95. Two approaches have been used:(a) A comparison of the estimated levels in total
diet from table IV with those in milk from the same
countries from table VII. The results are given in table
XXII. In diets of class I the Sr0 • to calcium ratio in the
total diet ranged from 0.9 to 2.9 times that in the milk.
The average of all results (excluding Denmark, thevalue for whidi fell outside the usual range) is 1.4. In
Japan (class III) the ratio total diet/milk increased
from 1.4 in 1957 to 3.6 in 1960, since the level in the
total diet increased more than did that in the milk overthis period. From the limited surveys in Central andSouth America values for the ratio of total diet tomilk from 0.9-3.3 are suggested. The single value for
Africa ( 10-13, based on limited sampling in Rhodesia
in 1959-1960) is comparatively high. The diet in thisarea, however, shows quite distinct features.n 1( b) A comparison of the Sr00 to calcium ratio in milk
and in cereals, vegetables and fish, where measurements
were availabl& from the same area in 1958-1960 and
subsequently to compile ratios for the ratio total diet/milk for a number of different types of diet. This calculation may be justified on the basis that while actuallevels of Sr9° in foodstuffs in different areas will depend on the extent of deposition, t:he relative degree ofcontamination of different types of crops may be expected to bear some roughly constant relationship to one
another. Considerable variation may occur because ofdifferences in agricultural conditions and practices, but
if comparisons are made oYer sufficiently large areas,
useful relationships may be established.

96. Three types of diet have been used, based on theclassification according to calcium contributions preTiously established (para. 39). Attention should be
drawn to the fact that this classification applies only tothe diets for which detailed information on the calcium
contributions was available and is not necessarily complete. Since the Sr90 to calcium ratio in unmilled cereal
is much higher than in milled cereal, additional calculations have been made for diets in which 30 per cent or
all of the cereal is unmilled. (This would in fact change
the calcium contribution from cereals to some extent
but this has not been taken into account owing to theapproximate nature of the calculation.)
97. Details of the diets and values obtained are set
out in table XXIII. Values for the calculated ratio total
diet/milk range from 1.5 for diets of class I to 4.2 for302

a diet of class II in which a high proportion of the calcium is derived from unmilled cereal. These values are of
the same order as those calculated from measured levels
in total diet. It must be pointed out, however, that thetwo methods are not entirely independent since someof the data used have already been used in the calcula-.
tion of the total diet values. However, this second
method does permit the inclusion of many more data.
98. This calculation provides an opportunity of estimating the differences that might have occurred in the
Sr90 to calcium ratio in different types of diet. It suggests that in areas of similar deposition of SrP0 the ratio
in diets of classes II anCi III, which have relatively little
mill.::, may have been only about twice that in diets ofclass I. In fact. since much of the area of Asia andAfrica, where diets low in milk are common, has been
one of low deposition of Sr• 0 , the differences are likely
to be much smaller. This is borne out by the measured
levels in total diets in Viet-Nam and Africa comparedwith those for Europe• and North America (table IV).

99. The substitution of unmilled cereal for milled
cereals appears to increase the ratio of Sr9° to calciumin the total diet by at most about 50 per cent; this is arather smaller effect than has been noted for some individual countries (paras. 56 and 57). Mention should bemade here of diets not included in the classification
above in which up to 80 per cent of the calcium in thediet comes from cereals and the rest from vegetables.1 nCalculation from the values given in table XXIII suggest that even in this case the ratio total diet/milk would
not exceed 5-10, the exact value depending on the proportion of the cereal which was milled.

Comparison of calculated and measured S~ in bone100. Table XXIV sets out:(a) Production weighted mean levels in milk for theperiod 1958-1960, based on tables VII, IX and X;(b) Mean levels ia diet for 1958-1960, based ontable IV;( c) Calculated levels in total diet, using the weighted
mean levels in milk and the ratios total diet/milk derived from measured levels in the total diet (table
XXII). Since milk values, other than those used in calculating this ratio, are anilable only in Europe andNorth America, this method cannot be applied to otherareas;( d) Calculated levels in total diet based on mean
worldwide ratios of the Sr9° to calcium ratios in individual foods to milk and the approximate diets, assuming that the cereal was all milled (table XXII). Thishas been applied to all areas except Central America,
where the diet has special features (para. 40) and appears not to be classifiable on this basis ;( e) Calculated ratios of Sr 00 to calcium in new boneon the assumption of an OR (bone/diet) of 0.25. The
basis for this value has been previously discussed ;(f) Calculated ratios of Sr00 to calcium in new boneusing observed values in newborn (table XXI) and assuming that the Sr90 to calcium ratio in foetal bone would
be one-half that in new bone of the mother owing toplacental discrimination (para. 36);(g) Observed levels of Sr90 in the bones of children
0-4 years old in 1959-1960 (table XXI).
101. The approximate nature of these calculations
must be stressed. Nevertheless a very reasonable correspondence of calculated and measured bone levels isfound. In general, measured bone levels are somewhat
iower than those predicted from the diet. Greatest uncertainty must attach to the calculations for Asia and theFar East \vhere systematic surveys are few and wherelarge populations are unrepresented by data. However,
the measured values in bone from these areas are lmver
than in North America and Europe.
102. The generally good agreement between values inbone predicted from dietary surveys and the observed
levels (table XXIV) is of considerable importance fromthe viewpoint of design of surveys of Sr90 in the humandiet. The conduct of survevs which confom1 to strict
statistical principles is labo;ious and expensive even inhighly organized countries; and it is likely to be impossible elsewhere. Present results encourage the view thatthe standard of sampling which has been adopted inmany areas is adequate to show the approximate averagelevel of Sr110 in the bones of large population groups;
furthermore it appears that especially when milk constitutes an appreciable part of the diet, the ratio of Sr9°
to calcium in bone could have been predicted reasonably
from the assay of milk alone. Considerably more elaborate surveys are, however, necessary to elucidate foodchain mechanisms.
FUTURE LEVELS OF Sr90 IN DIET AND MAN

103. In the detailed description of the routes of entry
into food chains described previously (paras. 13-24) attention has been drawn to the importance of alternativeroutes of entry of Sr9-0 into vegetation in addition toabsorption from the soil. This is emphasized by thechanging degree of contamination of milk, vegetables andcereals between 1958, 1959 and 1960 (paras. 62-76)
which can be seen to have been related to the changing
rate of fall-out. Some estimates of the relative magnitudeof direct contamination and of absorption from the soil
have been made. In the United Kingdom, for example,
absorption from the soil was estimated to have contributed only about 40 per cent of the Sr00 in milk in 1958
and 1959, but some 75 per cent in 1960 when the rate offall-out was considerably lower. 247 Estimates of theamount of Sr90 in wheat due to direct contamination
range from 20-90 per cent. 84 • 210 • 236 It is clear then thatboth factors must be taken into account in estimating
future levels in diet and bone under specified conditions.
104. The many factors affecting the relative importance of the rate of fall-out and the cumulative deposition in the contamination of food have been stressed
previously (para. 25). Because of these factors it appears preferable to attempt evaluation for world-wide
predictions on a country-wide basis so that local fluctuations assume less importance.

Method of evaluation

105. In the previous report of the committee and inother publications, 203 • 204 • 247 attempts have been made to
predict the future. levels of Sr90 in diet on the basis ofan expression of the following general form:c = pdFd + PrFr
where
C is the concentration of Sr&0 (µ.µ.c) per gram of calcium
in a food,
Fd is the cumulative deposition of Sr00 (mc/km2 )Fr is the current rate of deposition of Sr90 ( mc/km 2/y)and pd and Pr are proportionality factors.
303

They can conveniently be termed the "cumulative" and"rate" factor respectively. Neither factor can be regarded as a true constant. The cumulative factor willvary with location depending on soil type, and will varywith time a£ the distribution of Sr90 in soil changes(paras. 14-20). It will decrease as leaching and possibly
fixation occurs (paras. 19 and 20). The rate factor isdependent on the many variables affecting foliar retention and contamination, and on the e.xtent of plant baseabsorption (paras. 23 and 24). The reliability of theestimates of the proportionality factors is discussed inparagraph 118.
106. The factors were evaluated for the previous report by means of regression techniques, using data formilk, and preliminary results of experiments in which
Sr90 uptake by crops growing in the field was measured.
There are now considerably more data available forlonger periods of time during which the fall-out ratevaried considerably. More e.xperimental evidence is alsoavailable.
107. A number of methods can be used to evaluate
the two factors using the data set out in tables VII to
XVI! and the estimates of fall-out rate and deposit( F I, figures 37 and 38). The principal method used is to
assume that in late 1960 when the fall-out rate was low,
the contribution of the fall-out currently being deposited to Sr90 in food was insignificant. Thus the cumulative factor may be determined by dividing the measured ratio of Sr90 to calcium in foodstuffs bv the accumulated deposit. Since the fall-out rate was 'not zero,a maximum value is obtained. Where possible, meanvalues for wide areas have been used. This method enables values to be obtained for a considerable numberof areas, especially for milk. The rate factor can thenbe determined by applying the calculated value of the
cumulative factor to the results of previous years when
the rate of fall-out was considerably greater relative tothe cumulative total in the soil. This method has been
preferred as the general basis for evaluation because it
makes it possible to use survey results from wide areas.
Supplementary information can however be obtained inother ways:(a) By regression analysis providing adequate dataon the rate of fall-out, the cumulative deposit and thelevel of contamination in the foodstuff are available.
Such data are available only for milk and in relatively
few areas;( b) By calculating the cumulative factor from theresults of experimental investigations of the absorptionof radio-strontium by crops growing under field conditions. This can be the most precise method for evaluating the situation in any one locality. However, since
results are available only for Sweden136 and the United
Kingdom, 142• 247 they do not provide an adequate basis
for assessing the world-wide situation;( c) By assuming that, in the absence of direct contamination, the ratio of srso to stable strontium in allparts of the plant should be the same. The existence ofa higher ratio in whole grain than in roots, 235 or in brancompared with flour, 84 • 210 indicates direct contamination.
This fraction can be evaluated and compared with theannual fall-out deposit to obtain the rate factor. The
value of the cumulative factor may be determined fromthe difference. Si.nee the assumption must also be madethat none of the Sr90 in flour is due to direct contamination, this method gives ma..ximum values for the cumulative factor and minimum values for the rate factor;( d) The approximate value of the rate factor is also

indicated by laboratory experiments in which radiostrontium was deposited on crops in various stages ofgrowth and the amount in the edible parts determinedat maturity. 159

crimination against strontium in passage into the cereal
grain (para. 16) in adopting a value of 0.5. This issimilar to the mean value from field experiments in the
United Kingdom and Sweden. 158 • 142 Adoption of a valueof 1 would not increase the over-all cumulative factor
for any of the diet types by more than about 10 per cent.

Estimated values of proportionality factors

115. Using this value of the cumulative factor, therate factor has been calculated from the available data
for wheat and rice by the methods described in paragraph 107. Considerable variation between different
years and different areas may be e.xpected since thevalues are based on crude estimates of annual fall-out
rates, while the concentration in the grain is dependent
on the rate during a short period before harvest. For
calculation the rate factor is taken as 20 for whole grain
and 7 for milled cereal. These values are assumed toapply for all cereals.
116. Total diet. The values of the cumulative andrate factors adopted for individual foods are set out in
table XXVII. They have been used to calculate factors
for the total diet weighted according to the calcium
sources in the diet types previously used for evaluationof present and past levels. It should be noted from thistable that the rate and cumulative factors for the various
diets differ only by a factor of about 2. For calculating
future levels a rate factor assuming 20 per cent of thecereal is unmilled has been adopted as a conservative
estimate.
117. Because of the delay in consuming such foods
as cereals and potatoes, these weighted factors will beapplicable only if the rate of fall-out is reasonably constant from year to year. Owing to such delays and thepresence of considerable amounts of imported foods inmany diets, direct determination of the proportionality
factors from measurements of total diet, though theoretically possible, is unlikely to give reliable results at
the present time, since the rate of fall-out has varied
very considerably over the few years (1957-1960) for
which such measurements are available. Such an evaluation will be more useful when data are available for aperiod which is long in comparison with the lag in consumption. However, approximate comparisons can bemade, realizing their limitations. Total diet measurements in the United States in early 1961 indicated anaverage level of 6.7 µ.µ.c Sr90 per g of calcium in total
diet, which on the basis of a deposition of 27 mcfkm2
indicates the cumulative factor for total diet in the
United States to be about 0.25 (diet I), compared withthe previously calculated value of 0.4. In Ja pan, thelatest values in 1960 show a value of 19.3 µ.µ.c Sr9{)/g Ca
in total diet and a deposit of 25 mcjkm2 • Hence thecumulative factor for total diet is 0.77 (diet III). These
values must however include some component from thefall-out rate; this suggests that the values calculated
from the individual foods lead to conservative estimatesof the factors for total diet.

108. Milk. By assuming that in late 1960 or in early
1961 the contribution of Sr00 to milk from current fallout was insignificant, values of the cumulative factor
for several areas have been calculated. Table XXVI
shows that they range from 0.2-0.8. Comparison of thevalues calculated in this manner with the results of regression analysis for areas in the United States and theUnited Kingdom, and the values calculated from field
experiments in the United Kingdom, show that good correspondence between the different methods is obtained.
For the purposes of calculation, a world-wide mean valueof 0.3 will be assumed. Values close to this are achievedfor broad regions by comparing the weighted meanvalues in milk for 1960 (table X) with the average
cumulative depositions in appropriate latitudinal bands(F I, table XIV).
109. The value of the rate factor obtained by comparison with previous years or from regression analyses
when the rate of fall-out was comparatively high, ranges
from 0.3-1.2. A value of 0.8 will be used for calculation.
110. At present, much of the Sr90 in unploughed pasture land remains in the upper centimetres of soil. Field
experiments indicate that with deeper penetration of Sr90
in the soil, the value of the cumulative factor will be
reduced by about one-third. 247 Hence, for the long-term
situation a value of 0.2 is adopted.
111. It may be noted that these estimates show thatthe rate factor is considerably greater relative to the
cumulative factor than appeared from the very limited
data available to the Committee at the time of the previous report, when the rate factor for Perry, New York,was estimated as 0.23 and the cumulative factor as 0.34.
112. Green vegetables. Direct estimates of the cumulative factor for vegetables, calculated from the limited
data available for late 1960 (table XXVI) and fromfield experiments,136 • 142 indicate values ranging from 0.5
to a little greater than 1. The value of the rate factor
from the comparison of 1960 values with those in previous years ranges from zero to 0.8.
113. Potatoes and starchy roots. The values of the
cumulative factor calculated from the limited data for
1960 available, range from 1-3 (table XXVI). Field
experiments.in the United Kingdom and Sweden suggest
a range of 0.7-1.4. The value of the rate factor from acomparison of 1960 values with those of earlier years
is indicated as close to zero. For calculation, thecumulative factor will be taken as 1, the rate factor as
zero. The adoption of somewhat higher values for thesefactors has little influence on the over-all prediction since
the contribution of calcium from this source in all theapproximate diets is very small.

118. Reliability of the values adopted. Before attempting to calculate future levels of Sr90 in the total diet, theaccuracy of these forecasts should be considered. Inaccuracies may arise from:(a) The error associated with the measurement of
Sr90 in foodstuffs and in fall-out deposits, particularly
in regard to the representativeness of the samples;( b) The lack of coverage for certain large areas of
the world which leads to the necessity for ex-trapolation;( c) The fact that annual fall-out values are used
whereas vegetables and cereals are subject to contamina-

114. Cereals. The value of the cumulative factor cannot be derived from the 1960 data because of the extent
of floral contamination (para. 23) which was significant
in 1960 in spite of the low fall-out rate. However, because the rooting depth of cereals and vegetables is often
similar, and the soil is prepared in the same way forboth crops, the value for cereals has been derived fromthat for vegetables. Allowance has been made for dis-

304

~s

tion for only short periods, and the rate of fall-out hasvaried considerably throughout the year;( d) The uncertain pattern of future fall-out particularly in regard to distribution throughout the year.
119. However, the reasonable agreement between estimates made by different methods and for different
areas suggests that the values adopted may provide asatisfactory basis for estimating possible future e..xposures of populations, at least in those regions from which
the basic data were obtained. The values should beapplied only to large regions. They may be open to
considerably greater error if applied to particular
localities.
Calrnlated fitture levels
120. In calculating the levels of Sr90 which may occur
in the future, on the basis of proportionality factors(tables XXVI and XXVII) and predicted levels of
deposition (F I, figures 37 and 38), account must be
taken of the fact that some Sr90 will be lost from the soil
by run-off, leaching and removal in crops; part of the
Sr90 which crops absorb may, however, be returned to theland in organic manure. Moreover, slow fi..xation processes may lead to some reduction in the availability of
Sr9°. These processes are discussed in paragraphs 14-25.
For predicting the world-wide levels of Sr90 in diet, it
is assumed that the net losses of Sr90 will be 2 per centper annum. This is considered to be an adequately cautious average which will not under-estimate the generallevel of dietary contamination. Between different regions. wide variation is to be expected; considerablylarger losses have been estimated for some areas 98 but
elsewhere it seems possible that losses may be considerably lower.
121. Estimated future levels of Sr90 in the threeclasses of diet adopted are given in figure 6 for two of
the cases considered in part I of this annex (FI, 110).
These levels are calculated for the mean diet of large
populations; smaller groups may have intakes differingfrom the average as discussed in paragraphs 51-61. The
levels are calculated for the average world fall-out(F I, 33). If the present pattern of latitudinal distribution were observed in the future, the mean levels in thetemperate zone of the Northern Hemisphere would be
about twice those in the figure, whereas the levels in theSouthern Hemisphere would be lower than in the figure.
A discussion of the factors to be used to calculate values
for different latitudes and to calculate a population
weighted mean diet value for the world is given in annex
F, part III, paragraph 33.
(a) Tests ended in 1961. Figure 6 shows that after
a slight rise the levels in diet will quickly fall off untilvalues of less than 2 p.p.c Sr90 per g of calcium arereached by the year 2000. If tests continued until 1965
the levels in the year 2000 would be near to or less than
3 µ.p.c Sr90 per g of calcium. Thereafter radio-active
decay and removal would cause the level to drop by about
5 per cent per year;(b) Continued testing. Under continued testing thelevels would rise until at equilibrium the levels would
be about three times those calculated for 1960.

30

20

!
~

::.E
~

"

~

Continued fesfing

1 Mc Sr90 per ye11r

~

.

;;;;

.:
§

u

-;;
u

..."'~

-;;-

....

-3

.,._
0

No festing after 1961

"'
10

Ill
II

5

1~60

1970

1980

ma

2000

Equilibrium

Figiire 6. Calculated levels of Sr9o in three diet types (para.

39) under two conditions of testing, following the model
adopted (FI, 110, 114). The values are calculated for world
average fall-out. For values in particular latitudes, see discussion in paragraph 119 and F III, 33.

trometer to make simultaneous measurements of Cs137
and the naturally radio-active K"' 0 has encouraged theexpression of Cs137 concentrations in terms of potassiumin a manner analogous to that used for strontium andcalcium (para. 9). However, while strontium and calcium are interdependent and behave in a relatively similar and regular manner in biological systems, this isapparently not true of caesium and potassium. For example, in absorption by plants, the OR (plant/solution)
may increase by a factor of 2-10 as the concentrationof potassium in the external solution is increased.rn'• 117
Similarly in rats, it has been found that a ninefoldchange in the dietary potassium level causes an almost
proportional change in the OR (tissues/diet). 290 It has
also been shown that, in the animal body, Cs137 andpotassium may be distributed in quite different ratios in
different tissues and organs. 262 • 290•m Since the observed
ratio changes markedly under different conditions, itappears that this concept cannot usefully be applied
for this pair of elements. However, as a matter of practical necessity, values for the Cs137 content of diet andman in the following tables are expressed in terms of
the ratio of caesium to potassium, since this is the method

ill. Caesium-137

CAESIUM-137 IN FOOD CHAINS
Relationships between caesium and potassium
122. The chemical similarity of caesium and potas-sium and the opportunity offered by the gamma spec-305

of presentation in many publications.* The ratio of
Cs137 to potassium is, in fact, the preferable unit in which
to express the content in man, since it correlates betterwith lean body mass, and hence with organ dose, thandoes Cs137 per kg of body weight. This, however, is quite
independent of considerations of the similarity of metabolic behaviour of Cs137 and potassium.
Soils and plants

123. Cs137 , like Sr90 , can enter plants both by directcontamination and from the soil. However, Cs137 is absorbed from the soil to a considerably lesser extent than
Sr00 • Once absorbed, unlike Sr90 , it is readily redistributed within plants, its distribution being relatively
similar to that of potassium.
124. Absorption from soil. Large-scale field experiments, comparable to those with Sr1'0, have not been
carried out for Cs137 • However, the relative uptakes of
Sr00 and Cs137 have been compared in many laboratory
experiments and these may be used as a basis from which
the behaviour of Cs131 in the field may be inferred. Theseexperiments show that Cs137 is less well absorbed fromsoil by plants than Sr00 ; the relative amounts vary withthe soil type. In short-term experiments, with typicalsoils of temperate regions, Cs 137 is absorbed to an extent
only 1/10 or less of that of Sr90 •19 • 135• 149 With the passage of time the absorption of Cs137 relative to Sr 90
decreases, and after three years the quantity absorbed
may be about 1/25, or less, of that of Sr00 • 149 • 283 Marked
differences, however, occur between soils and in somesoils of tropical origin the absorption of Cs137 is considerably greater.283 High uptake of Cs 137 relative toSr90 was also found in lowland rice growing in paddy
soil ;118 this was ascribed to the presence of nitrogen in
the form of ammonium ions.
125. Reaction of Cs1 31 with soil a11d downward movement. The relatively low absorption of Cs137 by plants
is due to chemical reactions which tend to bind it to soil
constituents. 19• 1 35 • 179 Cs137 enters into the crystal structure of micaceous minerals in a manner similar to but notnecessarily identical with that of potassium.135 • 179 • 180
Once bound, caesium is replaced from soils to only asmall e.'\.'i:ent by divalent cations, but more readily bycaesium, ammonium or potassium ions. 180 The additionof carrier caesium can increase the uptake of Cs137 byplants. 118• 135 The addition of potassium may decrease
the absorption of Cs 137 in soils low in available ~otas­
sium; it may, however, have no effect when the available
potassium is high.13'• 135 Owing to this strong binding,the downward movement of Cs137 in soils is considerablyslower than that of Sr1'0 •221 • 212
126. Direct contamination of plaiits with Cs137• Cs137 ,like Sr90 , may enter plants by foliar, floral or plant baseabsorption. Cs137 is retained by the plant surfaces on
which it lodges directly to about the same extent or perhaps a little better than Sr90 , 122 • 158 • 159 and the factors
affecting retention appear to be generally similar. The
relative rates of penetration of Sr00 and Cs137 into tissues
are not known. A very marked difference in behaviour
occurs after absorption because of the ready redistribution of caesium throughout the plant.1 ==· 196
127. Plant base absorption. Little is known regarding
the extent to which Cs137 enters plants by plant baseabsorption. However, it may be noted that although in* These may be approximately converted to other units since
the potassium content is roughly constant in milk (1.4 g/I) andin the human body (2 g per kg of body weight).

306

many areas the ratio of Cs137 to Sr90 in milk decreased
owing to the low rate of fall-out in 1960, 251 in others theratio remained relatively constant from 1959-1960. 2270 242
This may be interpreted as due to differences in pasturemanagement affecting the degree of retention in the root
mat and of incorporation of Cs137 in the soil. It suggeststhat retention of Cs137 in the root mat of permanentpastures may cause Cs 137 to be relatively available toplants for a period of a year or more.
Aquatic food chains128. Experimental studies have shown that Cs 137 may
be concentrated by the flesh of aquatic organisms to adegree one or more orders of magnitude higher than thesurrounding water. 267 However, analyses of Cs137 in fish
do not suggest a very large contribution to the total
content of the diet (table XXXI). 33 • 108 Consequently,
detailed discussion of this aspect is unwarranted.
Transference into milk
129. The metabolism of Cs13 ' in animals has been lesswell studied than that of Sr90 • However, it has beenshown that some 10 per cent of orally ingested Cs187
is secreted into the milk of dairy cows ; this corresponds
to about 1.3 per cent of the amount ingested per litre of
milk. 181 • 182 • 207• 221 The amount of Cs 137 transferred into
milk is slightly greater than that of potassium. 207 • 2 ~ No
information is available on the secretion of Cs187 into
human milk.
Metabolic behaviour in man and mammals
130. Cs137 and potassium are absorbed from the gut
virtually completely, and are mainly distributed in thesoft tissues in the body. The distribution of Cs137 fromfall-out in human tissues has been studied in a numberof post-mortem samples. The results indicated a concentration of Cs137 in rib bones which were free ofmuscle but not of marrow, comparable with that in soft
tissues. 222 • 226 The results were variable and further information is necessary before firm conclusions can be
drawn. When Cs137 was injected into patients, the bones
at autopsy had somewhat lower concentrations of Cs137
than the soft tissue. 297 Studies with mice have indicatedthat Cs 137 concentrates in cartilage. 295
131. At least two exponential processes can be recognized in the excretion of Cs137 from the bodv of most
species including man,• 0 • 2118 • 314 following the administration of a single dose. In man two components are wellestablished : a small fraction ( 10 to 15 per cent) is
excreted with a short half-life (1.0 to 1.5 days) while
the remainder is excreted more slowly. There is considerable variation among individuals, and half-lives as
low as 50 to 60 days 287 • 298 and as high as 150 to 160
days 298 • 314 have been reported. The average appears to
be in the region of 100 to 120 days. 217 • 298 •m This contrasts with the more rapid turnover of potassium, theapparent half-life of which depends very largely on the
dietary intake. •o, 1os,2G•, 2ss132. The rate of turnover in different species is generally related to body size, being particularly rapid insmall animals such as the mouse and rat. :e 3 • 115 Ruminants
form an exception to this rule, however, having a relatively rapid biological half-life.m,m The level of dietary
potassium has little effect on the rate of removal of Cs1111
from the human body ;• 0 an increase in daily potassium
intake produces only a transitory increase in the urinary
excretion of Cs137 , and it subsequently returns to its
former rate.264

MEASURED unLs OF Cs137

133. The gamma-radiation associated with Cs137 can'be distinguished from that emitted by the naturally
radio-active K 40 using a scintillation spectrometer.
Direct estimates of Cs13 ' and potassium contents of living
subject:i, of large samples of diet and of samples ofbuman excreta can be obtained. Since the biological halflife of Cs13 ' in the human body is relatively short, there
is comparatively little variation in the concentration ofCs137 (per kg of body weight or per g of potassium)
between different age groups. Thus measurements on
adult subjects can be used for estimating the dose to thewhole population. It will be recalled that for Srg0 ,measurements on adults were of very limited use, andemphasis was placed on measurements of the concentration in the bones of children and in the total diet. For
Cs13 ' much less importance attaches to the analysis ofdiet or to other indirect methods of estimating body-content, and comparafrv-ely few values are available.
Cs137 in the total diet134. Few estimates of the concentration of Cs187 in
the total diet have been made. Estimates available fromthe United States in 1956-1957 and Canada iri 1959,~ 0 • 108(table XXVIII) indicated an intake of about 60 µ.µ.c per
day and a ratio of Cs 137 to potassium of about 20 µ.µ.c/g
K. In mid-1961, analysis of composite diets in the UnitedStates of America indicated an intake of only 33 µµ.c per<lay.siz In these countries some 60 per cent of the Cs 137
was supplied from milk and 25-35 per cent from meats.
In Japan, analyses on composite diets indicate a total
daily intake of close to 50 µ.µ.c Cs137 per day in 1959 and1960. 330 Approximate calculation from the levels of Csm
in foodstuffs at Gunma (table XXXI) suggests thatperhaps half of the Cs137 was derived from cereals andthat vegetables. milk and meat were other important contributors. In Argentina in 1961 the total daily intake ofCs137 was estimated as 40 f'-µC. 44
135. An alternative to analysis or estimation of
dietary Cs 137 is analy.sis of the mean daily excretion ofCs137 • A few data are available far the United States316
and the United Kingdom.~ 98 In 1957 two American subjects excreted 33 and 40 µ.µ.c Cs 137 per day in the urine ;316
the daily total excretion of one subject in the United
Kingdom was 81 µ.µ.c and 36 µ.µ.c in April 1959 and April
1961 respectively. Two other men excreted 42 µ.µ.c and51 µ.µ.c in April 1961. 298 These values are very similar
to those quoted above as estimates or measurements ofdaily diets.

?erved following those in the rate of fall-out. This is
illustrated. in figure 7 which shows the quarterly meanc~:mc~ntrat1on of Cs131 in milk in several areas. Sharp
nses m the concentration of Cs 137 in milk were shovm in
the United States, Nonvay and India following heavy
fall-out in the spring of 1959. That the peak value was
not as high as in 1958 in the United States in spite ofheavier fall-out may indicate the importance of the distributi~n. of fall-ou~ in ~elation to ~e grazing period indetermmmg levels m milk. Following the drop in fallout rate a sharp decline occurred in the concentrationof Cs137 in milk in the United States and India. whichreached low levels in late 1960. In N onvay the pattern
was different. Although a sharp rise in 1959 was shown
the concentration showed no consistent fall until la.t~1960. This type of difference must be ascribed to differing climatic and agricultural conditions; in particular,
it raiies the possibility of a lengthy hold-up of Cs137 in
the root mat of certain types of permanent pasture.
138. The wide variation with time in the concentration of Cs137 in milk from a single area, and the scarcity
of really representative data which cover a complete
year make comparisons between different areas difficult.
The limited data in table XXIX indicate that levels inNorth America and Europe are comparable, with rather
low levels being shown in Denmark and very high onesin Norway. Values from Japan are also somewhat higher
than in North America; in India and Australia they
are distinctly lower.
Cs13 ' in other foods

139. Some data for Cs 137 in foods other than milk
have already been presented in table XXVIII. Other
data chiefly from a single location in Japan are presented
in table XXXI. It may be noted that wheat from Canada
and cereals from Japan have a ratio of Cs187 to potassiumof the same order of magnitude. The vegetables fromJapan, however, have higher ratios of Cs181 to potassium
than those from North America (table XXVIII). A
comparison of values based on such limited sampling is,however, of doubtful significance. Meat from Norwayshows high contents of Cs137 which are in proportion
to those in milk from the same areas.m Not enough is
known about the metabolism of Cs137 in the cow for theconcentration in meat to be deduced from that measured
in milk, but there will certainly be a correlation assuming
similar feed for dairy and beef animals. The ex:ceptionally high values which are recorded in reindeer meat are
attributed to the grazing of lichens 276
Measured levels of Cs131 in the human body

Cs131 in milk

140. Few whole body counters have been available inrecent years; in consequence, determinations of Cs137
in large numbers of individuals have been restricted to
North America and 'Western Europe. Measurementi
have been made recently also in Japan. \Vhile manyother countries are represented in table XXXIL thedeterminations were carried out on relatively few individuals who were visitors to a laboratory where a counter
was situated. The extent to which such visitors are
representative of their native population depends on theinterval between leaving their country and being measured. and also on the extent to which socio-economic
differences in diet exist. Neither factor can be evaluatedwith the available information. Consequently. in table
XXXII results for visitors to each laboratory have beengrouped together in broad geographicaf regions. Resultsfor indigenous populations of countries in which the136. Measurement of Cs13 ' in food has with few exceptiom been confined to milk, because of its importanceas a supplier of Cs137 to some diets, and because of theease with which it can be sampled. Mean values for Cs137
in milk are set out in tables XXIX and XXX. Regularsurveys of milk have been carried out for some years inNorth America, and have been started recently in a number of countries in Europe. Surveys are also carried onin India, Japan and Australia. The rest of the world isrepresented by isolated samples; no recent results areavailable for large areas of Asia, South America andAfrica.
137. The Cs137 content of milk may be regarded aslargely determined by the current rate of fall-out or therate in the recent past owing to the small quantity of
Cs 137 absorbed from the soil. Large fluctuations are ob307

...4-........
.. ..
..: " .. ... .
.: ~. .· .·•... ....~ :.
.:· :. .l
! L;.
.
:

~

A

15

•

~
~

/:::;..

~

~

•

•

•

==:.

.

...

0

....

..

..
.
.
.A.

0

0

!:
~
0

... 10=~.s

A Norway

....

...

(')

"

t)

5

1957

1959

1958

Y6ll1'

1960

1961

concentrations in milk in three countries
India (Bombay)!"• · · · • · Norway (mean of 3 sites)=· w- - - - · · USA (mean of 10-12 sites)Ul

Figure 7.

Cs117

measurements are carried out are presented separately.
It may be seen that there is good correspondence between
the results of different laboratories where reasonable
numbers of samples are available. Consequently, all results have been summarized by broad geographicalregions in table XXXIII.
141. Geographical variation. The mean values for
those areas in the N orthem Hemisphere where large
numbers of measurements have been made are very
similar. Far fewer values are available for persons representative of the Southern Hemisphere, but the meanvalues (for South America, for example) appear to be
somewhat lower than those from the Northern Hemisphere. There is thus some suggestion of a correlation
with the latitudinal distribution of fall-out, although thisis much less clearly established than for Sr90 in bone.
142. Some local groups have been reported with bodycontents consistently in excess of the averages reported
here. 21 6-= 17 Small groups from Oslo and Bergen in Norway were measured in Sweden: their body contents were
184 and 477 µ.µ.c/g K respectively in 1960. It may be
noted that the Cs 137 in milk in Norway was also foundto be higher than in other areas of Europe (tableXXIX). There is also the possibility that high consumption of goat's cheese may have led to higher body contents.277 Considerably higher values have also been foundin people living in the north of Sweden. m, m Thesehigher values can be ascribed to the eating of reindeer
meat, which is high in Cs137 (table XXXI). It may be

noted that in countries with diets high in milk, a correlation exists between the quantity of milk drunk and the
CslST Content Of the body.lOB, lH, 2'H
143. Trend with time. The trend with time in several
groups of subjects is shown in figure 8. Repeated measurements on two groups of persons have been carriedout in Chicago (United States) and Berkshire (England). They follow an almost identical trend. Meanvalues for random samplings in New Mexico and Germany are higher but in all cases the pattern is similar, arise from 1956 to 1959 followed by a distinct fall through1960 to early 1961. This is consistent with a dependenceof the body content on the rate of fall-out since thelatter declined sharply in 1960. In contrast, the considerable rise in cumulative fall-out over this period was notaccompanied by any comparable rise in body content.
144. The rate of response of the content in the bodyis slow compared with the rate at which changes in fallout occur. This is well illustrated in figure 9 which shows
the changes in Cs131 content of the body and the fall-out
rate in Berkshire (England) during 1956-1960. It resultsfrom at least two factors. The first is the time necessary
for changes in the rate of fall-out to be reflected in thediet. This may be quite short for foods such as milk during the grazing season, but will obviously be much longer
when stored foodstuffs. both animal and human, areinvolved. The second factor is the time necessary forthe body to reach equilibrium with the diet. This isdetermined by the b:ological half-life, which is of the
308

so

60

i.:

.

~
0

.. 40

.

~

tJ

20

l956

1S57

1959

1958

l96D

1961

Tear

Figure 8. Trends with time of es1n in man
X--X: 8 subjects measured repeatedly at Chicagoll'• :u0--0: Subjects measured in Berkshire, England (in later years repeated measurements on the same subjects)m, Ha!::,,.--!::,,.: Subjects living in New Mexico 1
0-0: Subjects from USA; measured at Walter Reed Army Research Centerlll• :1111
e--e : Subjects living in Germany (Fed. Rep. of)

3

120

t..

~
~

:::!.

'<

0
::i.
::i.

e-:

0

§ 80
s::s·

2

~

0
....

Cl

...

,::;

to

.a
t-

c.>

..,
...

et

..

E?

a

?.,,

t,)

1

40

1956

1957

1958

1959

1960

<•--•) and the1961

Figure 9. The relationship between Cst37 in the human body2H,29s
rate of fall-out(--) in Berkshire, England205,2oe,aoo

indicate that over the period 1958-1960 the mean annual
level of Cs137 in the human body did not change morethan ± 25 per cent from the value in 1958. Bearing in
mind the limitations of the data for subjects from regions
other than North America and Western Europe (para.
140), it seems likely that the average values for thebroad geographical regions would also fall within thisrange. Allowing for the number of observations and theorder of four months. Marked changes in fall-out rate
may occur in shorter periods than this.

Evaluation of mean levels of Cs13 " in the human body145. The paucity of data from many areas prevents
any detailed comparison of the levels of Cs137 in diet andcorresponding levels in the human body. The summary
table XXXIII, together with the data set out in figure 8,309

greater proportion of the world's population in the
Northern Hemisphere, it appears reasonable to suggestthat the world average in this period was 60 µ.µ.c Cs13 r
per g of potassium ( + 25 per cent).
FUTURE LEVELS OF Cs137 IN DIET AND M.iu.'l'as!n 1959 when the highest levels of dietary contami-~atton were observed (a calculation on this basis is given

m annex F, part III, paragraph 41).
IV. Short-lived radio-nuclides

146. The levels of Cs13 ' in diet and in the body werelargely determined up to 1960 by the rate of fall-out.
The contribution from the accumulated deposit has beensmall but it will become proportionately larger, either
when the rate of fall-out is very low some time after
the cessation of weapon testing, or if the accumulated
deposit becomes larger in comparison with the rate offall-out owing to continued testing.
147. Present data are insufficient to justify the prediction of future levels of Cs137 in diet by methods similar
to those w~ed for Sr00 • Considerably less experimental
information is available. Moreover, the contribution
from the soil cannot be estimated from the results ofsurveys by assuming an insignificant contribution fromthe fall-out deposit during 1960, as was done for Sr90 ,because the rate factor for Cs 187 is very large relative
to the cumulative factor. The delay which can occur
between the deposition of Cs 131 and its incorporation in
the soil is a further cause of uncertainty (para. 136).
148. In view of these difficulties, alternative approaches have been examined. The approximate estimates of the future doses from C5137 , which are madein the following paragraphs, are based on the relationship between the internal and external dose rates. They
take into account the facts that the accuracy with which
it is necessary to estimate the contribution to the internal
dose from Cs137 absorbed from the soil should be considered in relation to the total dose from this nuclide, andthat the e."(ternal dose depends on the total deposit.

151. Radio-nuclides of 5hort half-life reach measurable concentrations in food only during or shortly aftera series of nuclear weapons tests. The levels reacheddepend very much on the size and altitude of the explosions. Tropospheric debris, which is deposited relatively
quickly, gives rise to proportionately greater levels, particularly of those radio-nuclides with very short halflives, than debris injected into the stratosphere.

152. The amount actually present in the diet will ~greatly affected by the seasonal nature of agricultural
production and the delay between consumption and production of many foods. Because of the short half-lives,
absorption from the soil is unimportant and entry inte
food chains occurs mainly through direct contamination.
Deposition in winter months, if dairy animals are not
grazing and if few crops are exposed, is of less significance than comparable deposition in the summer. Foodstuffs other than those consumed very soon after production contribute a negligible quantity of short-lived
radio-nuclides to the diet. Milk is the major source of
these radio-nuclides in many areas. In other areas where
less milk is consumed, fresh vegetables will be the major
source.
RADIO-NUCLIDES OF IMPORTANCE

153. The following radio-nuclides must be considered:(a) Strontium-89. Sr89 (half-life 51 days) behanssimilarily to Sr90 in food chains. It has a special importance in that comparative measurements of Sr8 9 andSr90 lead to valuable information on the rate of passage
through food chains ;(b) Barium-140. Ba140 ( 12.8 days) is also an alkaline
earth element and is deposited in bone in a similar manner to Sr90 and calcium. However, it is relatively poorly
absorbed from the gastro-intestinal tract. About 0.4 percent of ingested Ba140 is secreted into cow's milk 19 withan OR (milk/diet) of 0.06. 18 ' The OR (bone/diet) in
humans has been estimated as 0.06 ;m( c) I odille. Several radio-nuclides of iodine areformed in fission but, owing to the very short half-livesof most of them, only !1 81 (8.1 days) is of importanceat times more than a few days after fission. psi isreadily absorbed by the gastro-intestinal tract and concentrates in the thyroid gland. About 5-10 per cent of
the ingested dose is secreted in cow's milk.19 • 220 • 2 : 3149. On the cessation of the testing of nuclear weapons. the levels of Cs 137 in diet and in the body would
decline in a manner similar to that observed in late 1959
through 1960. Estimates of the amount of Cs137 absorbed from soil suggest that the level in the diet andbody would within a few years fall to less than 1/10of the levels observed in the year of maximum fall-out.
The external dose-rate would decrease considerably
more slowly.
150. If the effect of continued testing on the contamination of diet is to be evaluated, account must be
taken of the contribution of the increasing levels of
Cs 137 in the soil. Because of the difficulties referred toin paragraph 147, no precise estimate of the actual
dietary levels can be made. However, limits can be set
to the magnitude of the resultant internal radiation dosein relation to the external dose from this nuclide. If fallout were to continue at a steady rate the components ofboth internal and external dose due to the cumulative
deposit must show the same proportional increase. Whilethe cumulative deposit determines the external dose it
has hitherto been responsible for only a very small fraction of the internal dose* (para. 146). It follows therefore that, as the cumulative deposit increases. the internal
dose from Cs13 ' will tend to become smaller relative tothe external dose. Thus an upper limit can be set to the
future internal dose by assuming that the relationshipbetween this and the external dose will remain the same

154. Many other short-lived radio-nuclides passthrough terrestrial food chains to only a small extent
and are not absorbed by man in appreciable amount.
However, some consideration has been given to the possibilities of Ce1 " , Zn 65 or Fe55 , which may be concentrated in marine products, reaching man through thisroute. 19 On the most pessimistic assumptions, however.
the amount absorbed appears to be only a very small
fraction of the total intake of Sr90 •* In some cases, however, absorption from the soil may beconsiderably greater than the average (para. 124) ; in theseareas the cumulative deposit would make a greater contribution
tg the internal dose.

MEASURED LEVELS

155. Measurements of short-lived radio-nuclides infood have been made in comparatively few areas, and310

are mainly concerned with milk. Measurements of these
nuclides in foods such as cereals or root crops, which
are stored for an appreciable period before consumption,is unimportant. The most comprehensive sampling of
milk has been carried out in the United States. Annual
mean levels from 1957-1960 are shown in table XXXIV.
Figure 10 shows the variation of levels with time atthree sites in the United States. The generally similarfluctuations in the levels of the three nuclides measured(Sr8 9 , !131 and Ba140 ) were related to the timina of
nuclear explosions and to the fact that in some a~eas
during the winter, the cattle eat mainly stored food inwhich the short-lived activities have decayed.
(a) Strontium-89. The mean levels of Sr8 9 in milkin the latter half of 1957 and in 1958 in the United States
are shown in table XXXIV. During this period ratiosof Sr8° to Sr 00 in milk, comparable to those in the UnitedStates, were recorded in Canada (1957-1958) and in the
United Kingdom (1958).m By the latter part of 1959
the Sr8 9 had fallen below detectable levels (fig. 9).
Information of Sr89 levels in milk following the renewed
testing of nuclear weapons in 1961 is not yet available.
Some measurements in the United Kingdom in 1958
showed that an appreciable contribution of Sr89 could bemade to the diet by leafy vegetables ;8•' - 1,000(b) Iodine-131. The levels of !1 31 in milk in the
United States which were relatively high in 1957-1958(table XXXIV) rapidly fell, so that the average for1959 was below detectable levels. In September 1961,
the resumption of nuclear testing resulted in appreciablelevels in milk. Measurements made in the United Kingdom and the United States are shown in figure 11. The
initial levels were higher in the United States, but overa ten-week period an average value of a little more than
100 µ.µ.cfl was recorded for both countries;

-...
u

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1,000,....,...T"T"'T"'T"'T"'T"'T"'T"'T"'T""T"T"T"T"T"'T"T"T.....-r..............,...,...,...................,.....,

Figure 11. Weekly average concentration of !1 3 1 in milk in the
United Kingdom ( - - ) 305 and United States (- - - ) 3 z2 -a 2 •in late 1961

...
u

~

(c) Barium-140. The time course of Bauo in milk
resembled that of !131 in 1957-1959 (fig. 10). The average level in 1959 was below the limits of detection. In
late 1961, levels of up to 300 µ.µ.cjl of milk were recordedin the United Kingdom 305

>-

!::
>

;::
u

<

.
0

0

a:

FunrRE LEVELS

156. In the absence of testing these short-lived radionuclides quickly decay and become of no significance.
Under conditions of continued testing. an equilibrium
between deposit and decay would be quickly established.
The levels reached in diet would depend on factors relating to the type of explosion and agriculuiral factors, as
discussed in paragraphs 151-152.

10....._........._._.L...L.............................................................'-L.l....L.1....L.lc..J'-Jl(.LJU...L...L-I
JFMAMJJA$0HOJFMAMJJA50KDJ~MAMJJA$010

I

1957
•

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1959

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WEAPONS TESTS

Ii lliii1tY8'111\11 !OM!!!!Mtll.li ~':i~s~~U.S.A.
~

4

S

07

SIZ.

Figure 10. Concentrations of short half-life radio-nuclides inmilk from t.'iree sites in the USA (1957-1959)323

311

TABLE I. STRONTIUM-c.ALCIUM OllSERVED RATIOS IN ABSORPTION BY PLANTS
OR

Aftlhod(J>lanl/solulion)&/t:rttlU

~1

126
124
125
202

Barley •••••••••••••••••• , •••••••••••
Sr", Ca"Ten species ••••••••••••••••••••••••
Sr11, Ca"
Stable Sr, Ca
Tomato •••••••••••••••••••••••••••••
Five species •••••••••••••• ~ ••••••••
Sr", stable Ca
Wheat ••••••••••••••.••••••••••••.• ·} Sr' 0, stable Ca insand culture
Pea •••••..•...••..••••..............

0.7-1.3
~1

1.1

1.0}
{0.9

144

TABLE II. STRONTIUM-cALCIUM OBSERVED RATIOS (MILK/DIET)
Numberqf
svbjalsOR&/erel<U

Sr'' assay
Sr'° assay
Sr'• assay

Herd
Herd
Herd

0.16
0.09
0.08

184, 185
148
8

Stable strontium,
calcium

Herd
Herd

0.13
0.11

209
148

Radio-strontium, calcium
in different experiments

3-5

0.14

223

Simultaneous dosage
Sr 0 , Ca"

8
2
4

0.11
0.11
0.15

224
187
188

Goat •••••••••••.•••....•.•.•

Double tracer daily
Sr", Ca"

2
8

0.09
0.12

186
224

Man ••••••••••••••••••••••••

Sr" assay

4

0.10

168

MtlhodSptdu

Cow .••••••••.••.•..•..•••.•TABLE III. STll.ONTIUM-c.ALCIUM OBSERVED RATIQS (BONF,/Dn:r) IN MAN
Dt14ilMtlhodStable strontium and calcium in dietand bone •••••••••••••••••••••.••••.

Sr•, Ca", single oral dose •••••••••••••••

Canada •••••••••••••
USA ••..••.•••••••••
United Kingdom .••••
Japan •••.•••••.•••••
16 patients •••.•.•...

312

OR

0.24-0.26
0.18
0.23-0.25
0.16
0.29

284
209

10, 84, 149
101
213

TABLE IV.

RATIOS OF Sr90 TO CALCIUM IN THE TOI'AL DIET

Expressed as µp.c sroo;g calcium
Courdry

Lalilu.U.AreaA.
N. America .•••..••.•.•..••....••••>30°N

Europe .•..... , ... , .• , .......•.•.••> 30°N

T011111

CanadaUSA

Central America ••••.. , ..•.• , •••••.•

S. America •• ; •.••.•••....•..••••.• ,Afdra .............................

j

19S8

19S9

1960

16.1
11.8
(4.9-16.7)
17.7

13.1

A
25 citiesc

New York
ChicagoSan Francisco

A, B (6<Hi1)
B
B

6.5

12.6

A
A
D
A
A

5.5

5.9

c
D
c

2.8

5.2

14.2

19.5

A

3.8

4.1

4.8

4.4

UK
Fed. Rep. Germany

3-4 cities
BombayDelta region> 30°N<30°N<30°N> 20°S

Japan
India
Egypt
Australia< 30°N<30°N<30°N

Viet-Nam, Rep. of
ThailandChina (Taiwan}DDD< 20°N

Costa Rica
GuatemalaHonduras
Nicaragua
PanamaA
A
A
A
A< 10°N< 10°N
<5°s< 20°S< 20°s> 2o•s> 20°sColumbia
Venezuela
Ecuador
Peru
Bolivia
Argentina
Chile

D
A
A(58) D(59}A(57) D(59)< 30°N<30°N
5"N-5°s< 2o•s> 2o·s

UAR
Sudan
Kenya
S, Rhodesia
S. Africa

B.
w
.....
w Asia and Far East •• , ........ , •••• ·{

J9S7

1961

R./ermu

6.7

301
17,273

10.2
7.4
3.4

35, 74
198
237, 308, 309

Valw:s based on continued, often widespread, samplirig

Denmark
Austria
Asia and Far East ...•..•.•.•••.•••. {Africa ..•....•..••......•••••....••
Oceania ..••.•.•••.••.•...•.•..•..•

JJ1/lw4"

9.0
13.6•
11.5
10.6•

11.2
9.2
4.4
6.4

10, 84, 85, 227
24
24, 241
228

11.6
7.0
16.8

255

19.6
4.9°
5.6

28, 243
302
329
320

Values based on single, often very limited, sampling

9.4
7.0
5.2
2.2
0,2b
0.2-0.5
1.2
0.8

1.5

2.3
2.6

6.6
2.8
D
Cairo
Khartoum
Nairobi
Salisbury
Johannesburg•Methods. A: Calculated from widespread sampling of major foods. B: Calculated fromlocalized sampling of major foods. C: Composite diet analysed. D: Actual diet of individuals
or groups analysed. (For fuller descrieion see text, paragraph 39.)b These values have been recalcu ated after consultation with the original author.
• Values representative of composite vegetarian meals.

BB

B
8(58) A(59)B

4.8
3.9(4.7)d2.8(4.l)d3.0(4.9)d
5.1 (8.5)d
3.1 (7.4)d

319

38

4.7
2.0b
6

110
319

319
38
38, 11038, 110
38
38
319
38

10-13'

38, 227
38

d The higher figure is calculated for a diet including no milk.
"The Sr• 0 content of some types of food is estimated by assuming values similar to
those in the UK and USA.
1 This was stated to be an upper limit.

TABLE V,

THE PERCENTAGE CONTRIBUTION OF INDIVIDUAL FOODSTUFFS TO THE TOTAL YEARLY HITAAE OF SrDO
m SEVERAL COUNTRIES, 1959-1960

Values in parentheses are based on indirect evidenceF•d. &p,of
USA (71,zm

Milk product! •••••••••••••..•
Root vegetables and potatoes ••Leaf vegetables ••.•••••••••••
Fruit ••••••••••..•..•.•.••..
Meat •••••••••.•••••.••.••.•Fish ••••.••.•••.••.•.•••••••
Eggs •••••••••••.••...••••.••
Cereals ••••••••••••••••••••••
Tea •••...••••••••....•..•..•
Water ••••••••••••••••••.••..
TOTAL, Sr'° p.µe
TOTAL, Ca g
Sr'° µ.p.e/g Ca ••••.•••...••••.

German~UK (85, ZZ7)

Denmark (2Z8)(Z4)

Avs:NaCanada(301)

Japa11•

(ZSS)

(JJO)

1959

1960

1959

1960

1959

1960

1959

1960

1959

1960

39
3.1
29
7.7

29-51
3-16
7-22•
1-14
2-8b
0.1-0.7
1-4
16-32

57
5.9
5.5
(3.5)

38
3.2
{10.6)
(8.1)
(2.8)

27
4.7
11.3
3.7
1.5

26
12
14
24

51
2.7
3.1
1.6

(0.8)
35
(0.8)

1.0
49
(1.2)

2.3

72
3.8
4.6
4.0
5.2
0.1
0.7
6.6
0.6
1.8

2

13
4.4
4.4

53
7.1
4.6
(2.9)
(3.5)
(0.1)
1.7
15.4
6.5
5.2

6,534
370
17.7

1,349-4,760 3,568
396
383
3.1-12.3
9.0

2,529
396
6.4

1.8
17

(5.6)

6,125
4,040
580
580
10.6
7.0

5,800

4,020
239
16.8

Sr90 m BABY FOODS AND THE DIET OF mFANTSµp.c Sr 90/g Ca
USA•

UKb

Fed.&p.of
Germa1'Jf" 1959

1959

1960

13
18
19

5.4

18

l'.1ilk .......••....•••••.

13

9.8

6.4

Infant diet •••..........•
Adult diet (table IV) .••••

12
13.6

9
9.0

8
6.4

Food based on:
Cereals •..••.........•
Fruits .••.•..•..••••.•
Vegetables •••.••...•••

42

6,170
383
16.1

65
(l)d
(4)
25
3

3,650
187
19.5

vegetables and fruit was found by difference. (Recalculated
from 330.)
d Including eggs.

• Including dried beans and canned vegetables.
b Including poultry.
e The value for the composite diet and for milk, cereals andwater are based on direct measurement; the percentage for the

TABLE VI.

24}

1959 (Aug.)1960 (Jan.)

2.8
26

25

Meats .••••.......•...

1.0
25d
14•
14
11.2

1960 (Aug.)

1.9
16
23
8.1
12d
10•
8.8
10.2

• l'.Ieans of 9-13 samples.71 Total diet value for infants 0.1 years old." l'.!ilk value is for
manufactured food based on milk.
7
b :Means of representative samples of five different types of cereal based foods."· !: The
milk value is the countrywide average for fresh milk. The total diet value is an approximate
upper limit.
e Means of number of samples of different brands and types.n• 118
d Formula milk.
•Evaporated milk.

314

TADLEVII. Sr•o IN MILK

Regular or widspread s11rveys (for description, see table VIII)
The nronb11r of sites isgivm in parentheses, followed, tvhen available, by mariu1um a11d 1ninimum arrnual means. All valtces are oive11 as µµ.o Sroo per g calci11111,
Retioll, COUll/rj/ CW Or«J

LoliluiU

N. America •..••..•.

> 30°N
1.0•

Canada ..........
USA
Desert areas ....
Mid-West ......
Centrnl States ..
East. ....•.....
N. W. coa5t ....
Countrywide
average ......

Europe •.•.......••.

1914

1.4 (I)
1.2

,_..

tn

Ireland ...•.......
France •..........
Fe1d. R11p. Germany
Switzerland .......
Austria ..........
Italy .............
Denmark: .........
Norway ........ ,.
Sweden ..........
Finland ..........
Poland,, .•.......
Czechoslovakia ... ,USSR .•.•....•..•(Moscow) ......

Far East ..•.....•..

1. 7 (!)

1957

1'S9

1959

1960

1961

&f<r•n<1(16, 5-18)•8.7 (Jan.-Mar.)26, 13, 14,258-261

4.3 (5, 2.8-4.0)
11.0 (13, 4.1-26)
10.0 (18, 5.3-18)
14 (10, 8.4-18)
22 (4, 8.8-24)

3.4 (5, 2.7-4.0)
7.6 (12, 3.0-18)
7.2 (28, 3.8-15)
8.2 (19, 4.1-13)
8.8 (2, 8.1-9.4)•3.4 (4, 0.8-6.9)•6.2 (9, 1.8-12)•6.5 (27, 1.5-14)•1.5 (18, 3.3-19)•8.5 (.1, 4.5-12)

8.0

11.3

7.3

*6.6 (Jan.-Aug.)4, 39, 62,
65-73,
75-83,
198, 237,
110-112,248-253,
308, 309

6.3 (6, 4.1-8.2) 5.6 (9, 4.2-7.6)

7.0 (•, 5.2-11)

9.8 (•, 7.3-15)

6.4 (•, 4.2-9.9)*5.9•(Jan.-June)

4 (-, 2-8)
6.7 (1)8
14•s.5 ( < 6)
6.2 (50)
12 (2)

10.4 (< 5)
7.6 (150)
12 (2)•2.1 (1)*6.4 (5, 5.2-7.7)*4.6 (1)}84, 85, 227, 11,115, 305
227,24032
21-25, 241, 310
246
255
31,296
18,22849, 230, 242
27, 11354
233
51
37,50,234

5.5°

6.2°

7.9°

11.6 (13, 5.4-19)

14

7.2 (1)
2. 7 (5, 2.2-4.2)
2.7 (1)
3.8 (1)

8.8 {1)4.0 (4, 2.9-5.5)
3.9 (1)4.8 (1)2.0 (6, 1.1-3.0)
5.8 (9, 2.l-16)
5.0 (U, 2.4-8.5)
6.4 (9, 4.5-9.5)
9.9 (2, 7.4-12)

3.2 (5, 1.7-4.7)
8.0 (12, 3.0-20)
7.9 (24, 3.0-12)
8.7 (12, 6.1-13)
13.0 (4, 8.7-15)

3.4

4.7

5.2

4.1 (1)

3 f-, 3-5)
2.0 (!)(-, 3-14)(I)

3.1 (2)*5.2 (8, 2.2-8.0)> 30°N

Japan:.• ....... ,.

Pacific ......... ••··

19Sd

(14, 6.1-21)12> 30°N

UK ..•...........

(,.)

19JS

•1.9 (6, 1.0-5. 7)•11.0 (1)
*6.8 (1)
6.5
6.3 (2)•3.8 (6, 0.8-5.4)•6.0 (4, 5.0-7.4)
15 (3, 10-29)•*9.7 (1)5.1 (9, 3.4-6.0)
7.2
4.8 (2)•10.0 (9, 2-23)*9.4*9.2 ( < 5)
6.4 (150)
9 (2)10 (26, 8-14)
21 (•. 17-31)
4.0 (4, 2.8-4.7)
15 (11, 9.5-29)b*8.2 (7, 2.S-20)*6.7*6.2 (6, 1.4-12)*5.4 (6, 3-10)*4.4 (13, 2.6-6.3)(Dec. only)

57,243,331*5.o (2)*3.2 (2)*2.3 (2)(J an.-Aug.)70, 71, 237' 309*5.9 c21, o.3-33).(..9 (1)•2.3 (16, 0.6-8.8):Z.6 (1)•o.4 (1)(J an.-J uly)}87, 244,302

0.8

0.8 (Sprin!,!)

270

1.9

2.6 (Jan.-Dec.)

5,6, 7*4.6• (July-Dae.)

.129

20°N

USA (Hawaii) ....

Asia
India ............
(Bombay) .....•

5-30°N
20°N

Central America . ...•

< 30°N

2.3 (1)

Mexico ..• , .......

South America . ••..•> 30°S

1.7d

Argentina ...•....

AfricaUAR (Delta region)
S. Rhodesia(Salisbury) ....•

Oceania .......•••..
Australia •......••New Zealand .....

< 30°N,...., 20"S
> 20°s*3.8 (5)•Not a complete year.
•Samples from manr dekots represe11ting 40 per cent of the country's milk supply.
b Assuming 1 litre o mi! contains 1.2 g of calcium.

*3. 7 (5)

•1.3

•o.9

*4.1 (5)3.7 (5)*3.9 (7)227*4.5 \1)(J an.-j une)

12,239,320
309•Adjusted to be comparable with 13 station~ ~ampled later.
d Results for the first 9 months are from powdered milk, not the regular survey of liquid

milk (S).
•Weighted average for Delta region.

TABLE VIII.

Cou "''" or area

Dot. s/arled
or d11ralio11

Nucli"4smeas11,,d

DESCRIPTIONS OF MAJOR SURVEYS FOR RADIO-ACTIVITY IN MILK

Area

Number ofsiles

Type of sompu

ReJ>orkd bySingle monthly sample from dried milk factory
Daily purchases from store compositedmonthly
Weekly samples of dried milk compositedmonthlyMonthly samples from liquid milk collecting
centreDistributing centres

Radiological Protection Division, Dept.
National Health and Welfare
US Atomic Energy Commission, Health and
Safety Laboratory
US Atomic Energy Commission, Health and
Safety Laboratory
Radiological Health Data, Dept. of Health,
Education and WelfareRadiological Health Data, Dept. of Health,
Education and Welfare
Annual Reports, Lamont Geological Observation, Columbia University (Sr 90 ), Los
Alamos Scientific Laboratory (Cs117 )A.E.R.E., Harwell
Ref. (8)Radiobiological Laboratory, Agricultural
Research Council

Canada ..................... Late 1955

Sr Do

Widespread

USA........................

1954

Sr Do

New York City

1954
1955
1957

Sr DO
Sr'o
Sr'o

Perry, New York
Mandan, N. Dak.
Widespread

5-12

1960

Sr• 0
Cs117
SrDo

Widespread

60

Widespread

25-54

Weekly samples of powdered milk compositedmonthly

1-9
9
Many

1-3

Monthly samples of powdered milkMonthly samples from factory
Liquid milk depots providing 40% of country's milk supply: two weekly samples
composited every 6 or 12 weeks
Liquid milk, representative of production;
two weekly samples composited every 6
weeks
Daily samples of powdered milk compositedmonthly
Samples from dairy composited monthly
Two per week
Powder from 1954, then liquid

Federal Minister of Nuclear Energy andWater Economy
Federal Commission of Radioactivity

4

1-2 samples per month, collecting depot

National Committee for Nuclear Research

6-16

n

csm

1957
UK ......................... 1955-57
1957-58
1958

Cs117
Sr 00
Cs117
Sr 00

Widespread
Widespread
Countrywide

Ireland. . . . . . . . . . . . . . . . . • • . . .

1960

Sr'o

Dublin, Cork

France......................

1958

Sr 10

Widespread

Unknown::;: Federal Republic of Germany.,

Sr'oWidespread
LindauLowlandFew-150

Switzerland..................
Italy........................

1957
1960
1954
1960

Denmark.... . . . . . . . . . . . . . . . .

1959

CH

Norway ...............•...•. 1957-59
1958-59
1960

l

es1sr

Sr 00

c 5 111
Sr•o
Sr• 0
Cs117
Sr• 0
Cs111
Cs117

l

Czechoslovakia...............
USSR.......................

1957
1960

Poland......................
India (buffalo milk) . . . • . . . • . .

1958
1958

Hawaii......................

1959
1959

Sr'°
Cs117
Sr• 0
Cst11
Sr 10
10
Sr }
Cs117
Sr• 0
Sr•0 }
Cs111
Cs117
Sr 80

?vlexlco..... . . . . . . . . . . . . . . .. .
Argentina...................
Australia....................

1960
1959
1957

Sr• 0
Sr• 0
Sr• 0

Sweden .•...............•... 1957-59

N. Italy1}

An Roinn Sainte, Dublin
Ref. (32)Widespread

4Monthly samples of powdered milk

Danish Atomic Energy Commission

S. Norway

1-4

Norwegian Defence Research Establishment

S. Norway

2

Several samples per month from dairies composited monthly
Monthly samples from factoryCountrywide

11

Local purchase from shop

Norwegian Defence Research Establishment

Powdered milk from factory, irregularsamples

Research Institute of National Defence

Daily samples from dairy composited monthly
Farms: all year

Ref. (51)State Committee of the USSR on the usesof atomic energy
Ref. (233)
Indian Atomic Energy Commission

Mid-Sweden
2

Moscow

2

Lowland regions
Bombay5

Widespread
Honolulu

21
2

MexicoBuenos Aires Province
5 capital cities

5

1

Powder and liquid milk samples
Daily samples from milk depot compositedmonthly
Irregular
Weekly samples from dairy compositedmonthly
1-2 samples per week composited monthly
1-2 samples per year representative of bulk
supplies

Ref. (43)

US Atomic Energy Commission, Health and
Safety Laboratory
Ref. (270)
Argentine Atomic Energy Commission
Australian Atomic Weapons Tests Safety
Committee

TABLE VIII.
Doh Jlar'4dor duration

NudidullltaJUTld

1960
1957
1959
1960
1961

USSR ....................... 1957-59
1960

Sr• 0

Counlry or arta

New Zealand ••.•••....•.•.•.
Rhodesia .........•.•.••....•
UAR ..••.••......•.....•..•

Finland ............••....•..

1959

Japan •.•....•...............
India ••.....................

1957
1959

DESCRIPTIONS OF MAJOR SURVEYS FOR RADIO-ACTMTY IN MILK (conti11utd)
Number of

Area

JiUJ

Sr'°
Cs117
Sr'°

Widespread
Sydney71

Sr•0

Delta regionl

T:tP• of sample

Liquid and powder
Irregular samples from factory
Bulk supplies
Dried milk
Liquid milk composite samples

Dominion X-ray and Radium Laboratory
Los Alamos Scientific Laboratory
United Kingdom
United Kingdom
UAR Scientific Committee on the Effects ofAtomic Radiation

Widespread surveys for a limited period of the year

USSR Academy of Sciences

Widespread

8

Samples of powdered milk

s,•
esm

Widespread

9

Samples of powdered milk

Sr 90
Cs117
Sr• 0
10
Sr }
Cs111

Widespread

6-9

From dairies and factories

State Institute for Technical Research

Widespread

6

Powdered milk from factory

Ref. (57, 243)

Widespread

16-21

Liquid milk

Indian Atomic Energy Commission

TABLE IX.

SrDD IN MILK AND CHEESE: IN~UENT OJI. 51'00" SAMPUNG
Results presented as p.p.c Sr1Hl per g Ca

Figures in parentheses indicate number of samples: C indicates cheese
Recio11

Latilud~Coun.lry or area

>30°N

USSR., ••.••••••••
Norway •••.....•••
Denmark •••••••••.•
France .....•..••..
Switzerland .•...•..
Italy,,, .•.•••..••.
Spain .•.•.•.•.•.••

Europe ........•........••>30°N

Asia ................•.....

w.......

0.7 (2)....

1.09 (1)0.8 (1)2.1 (12){ 10°-20°N

Pakistan •....•. , •.
India ••.••.....•.•
Thailand .. , .. , .••.

0.14 (1)0.4 (1)0-20°sS. America ................
>Z0°S

{

>Z0°S

......

o.z (Z)

Union of South
Africa •••........

•Monthly or quarterly samples for all or part of year (38, 318).

3.4

11.9

2.8•
7.9•
7.7•
5.1 (2)4.8•
109.04.4 (2)4.3 (7)

6.4•
11.611.3•
7.3 (1)C2 (1)

C4 (2)
C2.3 (2)2.2 (6)

3.5 (4)
3.3•

19110

2.7 (2)C13 (1)2.5 (1)3.0 (6)
1.7•
1.2

2.1•

4.5 (1)7.2•

5.0 (1)

19111&fer•"''

59
65
38,31838, 65, 318
38, 31867, 71
67
65
66
66
66
66
71
4, 65, 67, 33
38, 318
65
66, 6771
2,45,38,318

4.6•

1.2 (5)

1.1

)

1.4

Bolivia .•.....•.•.•
Argentina •••..••••
Chile ••••...•.•••.

>Z0°S

(

3.2

1.3

0.05 (1)Tanganyika,,,, ••..

2.9 (6)

1.2 (4)

Colombia ..........
Venezuela .••.••...
Peru ..•••...•..•..
Ecuador ••••..•.••.
Brazil., •..........

0-zo·s

1959

C6.5 (2)Mexico ••••••••••..

Australia ••••••...•New Zealand ••••.•1958

CS (1)
CS.5 (4)Guatemala •••.•••.
Honduras .....•.•.
El Salvador .••.....
Nicaragua ••.....•.
Costa Rica •..•...•
Cuba ...•.....••••
Panama •...•.•••••
0-l0°N

1957

14.6 (1)Japan.; •••••... , ..

C. America ................

19511

1.35 (1)>30°N

5°-30°N

Africa .•••............••.••

1.5 (1)

3.6 (2)00

Oceania .............. , ....

1955

Turkey ••..•.•••..•
Cyprus •.•... ,·-··.
Lebanon •••... , ...
Jordan ............
Tunis ••••.......•.
Iran ••••.......•..

Mediterranean-Near Easl. .

Far East .........•........

1954

o.z (1)

1.7 (3)0.7 (Z)....
0.60.6•
0.4 (4)
1.1 (7)2.7 (3)2.9•
1.7
1.5 (3)Z.4 (3)5.04.0 (Z)

2.3•
2.3 (2)
0.4
0.9•
0.7•
3.1•
1.7 (Z)
1.5 (3)3.4•
2.6 (6)3.3•
1.8 (4)5.7 (2)

71
38

3.0•

38,31838, 31865, 6738, 32053, 38, 318

1.2 (3)5.3
z.o (2)4.6•
3.0 (1)

3.5•

Z.6•

38
65, 67, 71
67
38,31871
3871

12 (1)
C3.6 (1)0.4(Z)

38, 318

71
66
Z.6•

38, 318

TABLE X.

'.REGIONAL AVERAGES FOR THE RATIO OF Sr90 TO Ca IN MILK"

Lalitudes

1954

1955

1956

1957

1958

1959

1960

N.Amerlca ..••..•••••.......•.••...••.....•..........•••.
\V. Europe .......•••••......••....•...•...•.•......•.•••.
E. Europe (USSR) ••••••••.•••••••••••••••.••••••••••••.•.
Far East Gapan) ••.•••.••.••••••.•••.•...••...•...•.....•> 30°N> 30°N> 30°N> 30°N

1.2

3.7
3

4.9
5.0

5.5
6.4
5.2
1.9

8.5
7.2
3.8

12.2
8.6
10
6.2

7.9
8.6
8.2
5.4

Asia (India) ...•.••••••.•..••.•..........••.......•...•.•.
Central America •••••••••...•.•••••••..••.....•.•.••••••.•

0--30cN
10°N-30°N

2.3
1.9

5.9

2.8

2.3
0.8

s. America...............................................

10°N-so 0 s

1.8

1.9

3.3

1.9

Oceania (Australia) •• ,.....................................

> 20°5

3.8

3.7

4.1

S.7

Africa. • • • • • . . • • • • • • • . • • • • . • • • • • • • . . . • • • . . . . . • • . . • • • • • • • .

> 10°s

2.6°

2.6b• Mean values have been calculated utilizinf primarily thedata from the regular surveys shown in table VI , but using also
the data from table IX where necessary. The means have been
weighted by the quantity of milk produced in each country. It is

important to note that varying numbers of countries are repre·
sented in different years.
b Union of South Africa.
0 Rhodesia.

319

1.2

1.0•

TADLE XI. SrUO IN WROLE WHEAT GRAIN
Results as µµc 1icr g Ca or, italicized, as µµc SrDo per kg
Fig11res fo parentheses indicate the number of samples a11d range

Re1ion

LaUluda> 30°NCountry

Arca

1951

1958

1959

103 ± 10•125 ± 13•

37±4

44±5

124 ± 37
39 ±10114b

1956

CanadaN. America .•......

Minnesota

107 (7, 74-169)
45 {17-76)

217 (7. 105-606)
66 (47-112)

Widespread

156 (8, 111-213)
44 {35-60)
164b {19)105 (1)129b (41-377)
53 (14-198)
67 (12, 9-271)
44 (9-96)
125 (1)

160

100-130

71 (11, 40-126)
Z6 (14-58)

83 (12, 42-220)
39 (18-54)
64 (8, 15-87)
30 (7-47)
70 (7, 51-90)
34 (19-54)
100 (6, 61-213)
39 (19-89)
88 {43, 29-280)
JZ (9-97)
53 (9, 29-85)
zo (12-32)
79 (2, 60-98)
35 (30-40)

6Z

Alaska23 (1)

Mean

E. E"'opo ........

·l> 30°N> 30°N(A

USSR

Widespread

70 (10, 28-140)
Z6 (14-45)

UK

38 (7, 21-49)
Z5 (13-46)

Denmark

Widespread

Fed. Rep.
of Germany
FranceWidespread

131 (7, 109-174)
66 (54-75)l~0

W. Europe .•••..••

GreeceMean

Reference

114, 198
56b
15

86

USA

1960

32 (20-72)
Zl (4-48)

}301
67

j'•·

73, 1474

38, 58j"·'··
227

73

84,85
227
89 (8, 48-212)
3Z (19-71)
92 (23, 42-146)
4() (18-63)

18,22846,30773
73

65

fo Ea" .......

·l> 30°NJapan

Widespread

145 (1)36

141 (4, 120-170)
44 {34-48)

89 (4, 43-114)

Manchuria

242 (8, 116-375)
78 {29-133)
155 (1)64· ......•....•• {5°N-10°S
Africa0°-60°5

Congo(Leopoldville)
Bolivia
Peru

Z.5

}66

•16 (2)• 4 (2)

38
65

Argentina• 8 (4, 0.7-18)

Chile
Oceania .......... , {•6 (1)

1958-59

S. America .....••.

> 20°5!243
73

Australia•Year of reccipt:or samples.
·.Weighted composite samples.

1959-60

31 {14, 21-48)
16 (12-33)•4,5 (2, 4.4-4.6)
1Z.3 (1)
25 (5, 15-42)
9.5 (6-13)

9.6 (5, 0.4-39)

19 (6, 14-27)
7.0 (4-8)

b Countrywide means, weighted for production.

}65, 7366
319}227,239)
320

TABLE XII.

Sro 0 IN WHF..AT FLOUR

Results as µµc Sroo per g Ca or, italiciud, as µµc Sr" per kg
Figures in parentheses indicate tlie number of samples and range
&iion

I

> 30°N

N. Am•dra.............

Country or area

Canada •....•.•...••...••.•...•

USSR .•...•...............•.•••> 30°N

UK............................

·l

1958

31±3•
4.6

38 ± 4•
5.4
69 (19)b
9.5

62b
11

70, 7385 (1)
23

30 (8, 7-43)
7.4 (47-13)

85,22748 (6, 28-90)
12 (8--19)•15 (1)3

24 (6, 13-48)
5.4 (2.8-8.9)

84,85,227

USA ••...•...••..•.....••....•.

E. Europe ............. ·{ > 30°N

W. E"ro"' ............

1957

13 (7, 5-26)
2 (1-4)

France .........•.....•......•..
Austria ••.•.•••.•••••••.•••...••Far East .... , ......... ·{ > 30"N

Japan..........................

< 30°N

UAR .•.••...••••••••....•...•..

Kenya .........•...............

< 20°5

S. Rhodesia •••••..••...••.••...•> 20°5

Union of South Africa .•••..•....•

1960

Re/ere nu

114

40 (47)7.3
160 (1)30 (1)

53 (1)
9

95 (1)
18

*16
7.2
• 8.4
3.8
• 4.9
2.8
• 7.5
3.3

Sudan ..........•........•.•....

~..... Africa ......•..... , • • • . 5"N-5"S

1959

84
255
33,30
38
38
38
38

• 7.4

38

1.6
1957-58

S. America ............. {> 20°S

Argentina •••..•••.•••••..•..•. •Oceania ............... ·{> 2o•sAustralia.......................

•Year of sampling, not necessarily production.
•From production weighted composite samples.

7 (3, 4-12)
1 (1-2)

1958-59

1959-60*19 (2, 7-31)
3 (1-5)13.2 (1)84319

10.7 (5, 7-16)
2.0 (1-3)

7.5 (6, 5-10)
1.4 (1-2)

84,85,227239

b Weighted mean representing production from main growing areas.

TABLE XIII.

DrsTIUBUTION or Sr"° IN MILLING PllODUCTS OF WHEAT

Results presented as µµ.c/g Ca or, italicized, as µµc/kg

Range shown in parentheses
BranF,,,.,.

RDtw
flow/rrain

Rifer~

1957
Canadab,.................... •• . . . . . . • . • •. . . .

103:!:10
37 :!: 4
38 (21-49)
zs (13-46)

134 :!: 15
118 :!: 15
93 (49-136)
87 (42-158)

31 :l: 3
4.6 :!: 0.5
13 (5-26)
z (1-4)

0.40

114

0.34

84

Canadab, ..•••••• ,...........................

125 :!: 13
44 :!: 5

114

164
6Z

38 :!: 4
S.4 :!: 0.5
69
IS
48 (28-90)
12 (8-19)

0.30

USAd,,, .....................................

163 :!: 20
141 :!: 20
201
231
160 (133-224)
262 (162-433)

0.42

70, 73

0.37

85

142
163
93 (68-134)
94 (54-171)62
11
24 (13-48)
5.4 (2.8-8-9)

0.48

73

0.34

227

UK•.........................................
1958

UK•......................................... 131 (109-174)
66 (54-75)

1959
USAd,............ .. • . • • • . . . • . . . . . . . . . • • • . . . . 129

UK..........................................

53
70 (51-90)
34 (19-54)• Of about 70 per cent extraction.

0

Mean of seven samples from various parts of country.

d Weighted means for a number of sta~.

b Calculated from composite whole grain samples and average

distribution in milling products.

322

TABLE XIV. Sr110 IN WHOLE CEREAL GRAINS (other than wheat)
Upper figure is p.µc Srvo/g Ca; lower figure (italicized) is µp.c Sr&0/kg
Figures in paretitheses indicate the tmmber of samples and range<dai11Reg/ot1, country or area

1956

E11rope
USSR .........................
Rye ......•....•.

67 (5, 57-90)
27 (19-33)
87 (1)

128 (1)45

Far East
Japan,, ....•......••...•••••••......

E1irop1;
Denmark., .........••..•••••••I--

Germany, Fed. Rep. of ••.••.•••.

55 (3)

64 (2)

AfricaSyria .•...........•..•••••.•••w

Oats .............

,.....,

Germany, Fed. Rep. of ..........

,......

S. America
Argentina •.•...•••.••.•....•..

Maize ............

88 (7, 64-137)
33 (24-45)
84 (24, 42-185)
44 (19-63)

180 (1)63

101 (1)5330

80 (9, 44-130)
35 (2Q-62)

58 (7, 47-94)
25

18, 228

18, 228
34, 6624, 30734, 666638
38

2.5 (1)
3.4 (2)6538
46 (9, 13-111)
34 (9-65)

42 (8, 25-64)
38 (23-62)

18, 228

155 (1)
1066*8 (1)
4.5

66

N. America
USA .....•..........•.••.•.•••
C. America
Costa Rica .....•..•••...•••••.
Guatemala .......•.....•.•.•..
Honduras ..•.•.•.•...•...•...•
Nicaragua .........•.....•.....

142 (8, 93-188)
55 (37-74)
82 (24, 29-236)
36 (12-101)

0.7•
2.1
•6.S•
3.8

S. America
Peru ........•••.•.••..•••...••
Bolivia, ........•.......•.....•
E11ropeDenmark ......................

&fer.nee37, 60•10 (1)
5

Union of South Africa .•...•...•.
N

1960

124 (3)

Sudan .••......••..••••.••.••..

Vl

1959

93 (4, 51-121)
33 (22-48)

Denmark ......................
Germany, Fed. Rep. of..........

Barley ....•......

1958

1951

0

69
4.8 (8, 1.0-18)••47
3.3 (4, 0.2-4.6)

1.0 (1)

38,31838
38, 31838*2.4 (1)
3.5 (1)•1.0 (1)

S. America
Ecuador •••........•....•••...•
Venezuela .......•......•..•..•
Peru .•.........•.••..........•
Bolivia •......•...••.••...•.••••3,1 (1)*1.4 (2)AfricaUnion of South Africa ••••••••••
Rhodesia .•.•.•.•.•••••.•••••••-....

4.1 (1)

318
38
65
.)8

*6.1 (7, 1.9-13)•tt.3•

63

< 38•
< J

38
38
227

TABLE XIV.

Grain

19S6

SrDo IN WHOLE CEREAL GRAINS (other than wheat) (co11ti1med)

19S7

19SI

19S9

1960

&/trenc•

N. America
USA ••••.••.••••••••••••••••••

37 (1)
8.9

22EuropeItaly,,, •••••••..••••••••••••••

280 (1)22zz

AfricaUAR •••••..••••••••••••••••••

•1.8•

38

Sudan •• , .•..••••••••••••••..••

•6.6•
0.8

38

o.z

Asia and Far East
Ceylon(brown) .......•....•••.....••150 (1)

66

41

India
(paddy) ••••.••.•...•.••.•.••

302

23
Z.1

(boiled) ..•....•...•••••..••.

22(surty) ..................... .

15

1.5

Rice .••....•..•.•

Durma ....................... .

0.8- - - - - •19 (2) - - - - -Thailand •.•.......••.•••••••.•

1.J- - - - - •54 (2) - - - - -0.9

China (Taiwan) .•••••••.•••••••
Viet-Nam (Rep. of)(unmillcd) .•...•.•.••..•..•.•(milled) •.•....••.....•.••...
Japan ........................ .
•••(brown) .......•..•••.....
(milled) ..•..•....•.•...•••.•

171 (8, 81-250)
22 (15-43)
31 (4, 12-62)
z.o (1.3-2.6)

242 (5, 103-270)
40 (1!~80)
24 (2, 20-28)
1.6 (1.4-1.7)

S. America
Venezuela ••••.•.•.•••••.•••.••

Millet,,,.........

JZ (10-58)

18 (3, 6.3-24)
4.3 (1.7-6.4)
16 (1)
8.8

22, 319319
319, 11062 (12, 28-98)
5.7 (2.6-9.0)
62 (12, 19-99)
8.6 (1.0-5.4)

30, 33, 127, 243
33,127,243,32538
22•2.8 (1)- - - - 5 0 (1) - - - 5

Surinam •.•••.•.•••..•.•..•••..

Colombia •...•.••••••••••.••••
Dolivia •• , ••••••.••.•..•••••••.
Ecuador.,, .•.••.••••..••..•...
Afri'ca
Sudan •••••.••...•••...••••••.•

239 (8, 78-425)

26 (1)
6.6 (1)264 (21, 52-448)
29 (4-54)

22

10.5 (1)•14 (5)< 2 (3)

319
38
318
38
38

Kenya ••••.••••.••••••••••••••

S. America
Peru, ••••..•••..••••••••••...•
Quinoa.,.........

S. America

Native grain......

AfricaSudan .•. , .•••.•.•••..•••••.•..

Bolivia ••...•....•.••••.••.•••.

• Indicates year of samples, not necessarily the year of harvest.
••On the asaumption that maize arain rnntAln• ')' m" rn 1tnn - tu

7.7 (1)65

2.7 (2)38
38••• !Jri;i_wn rice is undermitled rice (with crerm rPmnVf'<ilTABLE XV.

SrOO IN GREEN LEAFY VEGETABLES

Results presented as µµ.c Sr90 per gram calcium, or italicized, as flflC SrDOfkg
Fig11res in parentheses i11dicate the t11m1ber of samples a11d maxirlmm and 111irii11111m values
R41ionCountry

Ducriplion

19S6

USA ..........•....•.•

Simple means of samples of cabbages
from several states ••....•.••••••

8.1 (9, 1-29)

1958

1959

74, 35241 (8, 21-461)

35,
76
198, 237

Fed. Rep. of Gemmny ..
(,,>

N

(.ft

21 (9, 6-50)
7 (2-18)

Weighted means of countrywide
sampling of brassicas ••....•.•••••
Simple mean of miscellaneous
samples .................•.• .a•.,.

Europe •••••.

...

17 (6, 7-30)
9 (1-22)

IU/uenco

17 (12, 1-76)
16 (2-48)

From Tricity study •.•......••••••UK ...•...............

1960

7.1 (5, 1.2-14)

Spinach ...••.••••.•••••••.••••••

N. America ••1957

8.7 (5-47)
7.5 (3-17)

14 (4-42)
10 (2-40)

8.5 (7.3-19)
4.9 (1-12)

84, 85,227

30 (6, 3-80)
14 (2-49)

13 (22, 6-39)
4.5 (1-12)

14.5 (16, 1.3-30)
8.9 (3.1-19)
11.3 (9-16)
13 (2-34)

66, 24,71, 310228

Denmark .•.•.•..••....

Composite samples of 8 types •.••-~ ...

Austria .•••••.•.•.••••.

Cabbages, composite i;amplPR ••••••

9.8 (5)

255

France •••.•.......•.•.

Cabbage, spinach •.••.•.....•.••••

5.1
5.9 (2)232

Africa •. , •.•. UAR •••............•.

Spinach, molokhia• ....•.....•....

Asia. . . • . . . . China (Taiwan) ........
Thailand ............•.

Leafy vegetables ••••..•.••••.•••.
Miscellaneous samples .•••••..••••
Lettuce •••.•••.••.•..•••..••••••

S. America .. {Venezuela .............
Chile ••••••..•..••....

Cabbage ••••••.•••••••••••••••••''Greens•• •. ..........•.•.....•••.

6.1 (1)3.1 (7, 1.5-7.2)
0.5 (1)

Oceania .•..• Australia ...•....•••....

Composite samples of cabbage
at 5 sites •••.•••••••••••••••.••

2.6 (2.1-4.0)

5.9 (4.0-9.4)

r. . . . . . . . . .

21 (6, 10-62)

8 (2)14 (6, 4-23)
19 (10, 2-60)•Values for 1961 of 3.4-4.2 µµc Sr10 /g calcium were obtained for bulked samples representing the Delta reg!on. 11114 21

35 (7, 0-82)

33
65, 6766

32 (4, 6-58)
10 (1)
66

38
65, 66

4.9 (3.9-8.6)

8.5 (10)12, 239320

TA1U.E XVI. Sroo IN LEGUMINOUS VEGETABLES-PEAS AND BE.A....,.,S
Results presented as p.µc Sr&o per gram calcium, or italicized, as p.µc Sr&Ojkg

Figures in parentheses indicate the twmber of samples and the maximum and minimum values
Region, cou711ry Of' area

1956

1957

N. Ame1'ica
USA...............

8.7 (14, 1-21)

8.8 (5, 4.6-14)

1958

1960

1959

18 (3.4-88)b

6.0 (3-12)•

49 (9-178)

4.0 (2-7)

20 (30, 1-100)
7.5 (1-27)

10.5 (6, 9-12)
6.4 (4-8)
15 (2, 15-16)
6.5 (5-8)R4erenu

35, 74
198

EuropeFed. Rep. of Germany

22 (8, 12-47)
61 (7-100)

Denmark ........•..

Far East ..•.•......••.
Japan.............. 4.5 (1)C. America
Costa Rica ..• ,., .•.•
Guatemala .....•...•
Honduras ..••..•....
Nicaragua ......... .
Panama ....••......

69, 71, 70
24, 22, 310
228

33

2.8•

38
38
38
38
38

o.s0.So.s0.3•

S. America
Bolivia ............ .
Venezuela .•••••.•.••
Colombia ..........•

Africa
UAR ............ : ..
Sudan •...••..•..•..
Kenya ............. .
S. Rhodesia .........
Union of South Africa

1.2 (1, 0.3-22)
3.4 (18, 0.7-18)
3.0 (1)0.8 (4, 0.2-1.4)
1.6 (l.0-2.3)
1.7 (1)
6.J
1.1 (5, 0.3-2.0)(0.9-6.8)
3.7 (3, 2.2-5.2)
4.7 (2.0-7.5)
2.0 (4, 0.3-3.9)
6.1 (l.6-8.6)

z.sb Composite samp,les from 10 states.

• Samples collected and analysed by Lamont GeologicalObservatory.

•From "Tri-city ' study.us

326

38
38
319

38
38
38
38
38

TABLE XVII.

Srso IN POTATOES AND STARCHY ROOTS

Results presented as µµc. Srao per g Ca or, italicized, as µµc. SrBOjkg

The figures in parentheses indicate niimber of samples and the maximum and minimum values
Region and country

1957

1958

1959

1960

POTATOES
r~ N. America

USA ............................. .
(Alaska) •........•...•..••. , ... .

EuropeUK ............................. .
Fed. Rep. of Germany..............

11 (10, 2-22)
Z.6 (0.7-5)

14 (4-32)•
1.6 (0.7-3.6)
28 (10, 6-36)
7.6 (2-15)

Denmark .•...•......•.••.•.•..•..

25 (12, 1-61)
J.7 (0.8-8.2)
7.8 (1)39 (5-130)•
4.0 (0.6-10)

23 (4-85)•
1.9 (0.5-7.1)
25(1)
2.5
33 (9, 12-63)
1.4 (0.6-2.3)

20 (5-62)•
1.6 (0.5-4.8)
27 (15, 11-65)
4.1 (1.9-8.2}
47 (9, 14-83)
1.8 (0.7-3.1)
25 (16)
1.5

Austria .•••.•...•.••.•...•...•....

USSR............................ 17 (3, 9-33)
0.8 (0.5-1.3)

36 (3, 24-46)
1.7 (0.9-2.4)

74, 198
39, 5884, 85
227
69, 71
241, 307
228
255
59

42 (3, 34-52)
2.3 (1.5-3.0)

AfricaUARd ........................... .

38

5.4b
1.1

S. America
Colombia •....•..••..•••...•..••••
Venezuela •......••.......•.•.•.•..
Chile. • . • . . . . . . . • . . . • . . . • . . • . • . . • .

38

2.1b
0.5

Sudan ••.•••••..•....•...•..•..•••

28 (3, 14-35)
5.4 (2.5-7.8)

319
38
65, 66319

21 (4, 1.5-70)

38
38
319

6.1 (1)0.5 (1)4.2 (2)10 (3, 1-24)

YucA (CASSAVA, MANIOC)

S. America
Venezuela •....•.•..•••••..•.•..••.
Bolivia ..•..••..•.•....••.•••.....
Colombia .••.....•••••••••......•.

22 (21, 0.5-182)
5.9 (4, 4-9)

d Values for potatoes of 17 µp.c Sr90 /g Ca and for colcasia of
9.4 µp.c Sr' 0 /g Ca were found for the Delta region of the UAR
in late 1961.m• Wei~hted mean from samples representative of countrywide
production.
b Composite samples.
• From Tricity study: year consumed.

327

TABLE XVIII. Sre 0 IN FRUIT
Sr"
Re1W.. and country or area of orl1in

Total number

Fruit

Year

ApplesPeaches: canned
Peaches: canned
Raisins
Strawberries
Apricots: dry

1959
1959
1959
1958-59
1959
1959

4.3
2.2
117
8
24
17

Eight types
Eight types
Peaches
Berries
Strawberries
Tree fruits
Apples and pears
Soft fruits
Imported fruit(12 kinds)
Nuts
Apples
Pears
Plums
Oranges
Figs
Figs
Hazelnuts

1958
1959
1959
1959
1959
1959
1960
1960
1960

9.3 (2-29)
14 (3-35)
12.9
4.3 (1.7-8.3)
19 (7.1-37)
3.3 (0.4-6.1)
2.0 (0.7-5.1)
4.1 (1.9-10)
0.4-22

1960
1960
1960
1960
1957
1958
1958
1957

7-122
1.8
4.1
1.9
6
12
13
14

Dates
MelonsApples

1958
1958
1958

8 (5-11)
5.4
2.7

Pineapples
Pineapple juice

1958
1958

143•
6.4

82

66
66

Bananas

1957

1.5

4.8

66

Peanuts
Dates
Pecan nuts
Mixed nuts
Plums

1958
1958
1958
1958
1957

14.4
0.8
3.2
12.8
2

6.5
1.0
4.7
5.7
4.5

p.p&/k1

f'll&!t Ca

of sam~lu

N. America

USA ••••••••••.••••.••••.•.

EuropeFed. Rep. of Germany ••••••. ,Denmark ••••.••••.•••••••••

Austria ••.••••••..•••••...••
Spain ••••.•••...•...•....••.
Portugal .•....•.•••••.•..••.

Greece .•.••••.....••..••.••.
Italy (Sicily) ••......•.......
Near EasJ
Iraq .••.......••••..•••.•.••.
Iran ••••••••..••••••••••••••
Asia
Fed. of Malaya ..•••.•••••..•
CaribbeanWest Indies ...••..•••.......
AfricaSudan .............••..••••.

Union of South Africa ...•••••

5
4
1
2Composite1
47 (16-96)
42 (18-90)
162
36 (8.4-81}
69 (25-130)
23 (4.3-42)
22 (6.5-67)
16 (7.7-30)
5.o-48

13
8
1

7
4
22
10
17
Composite

9.~56

49
80
12
10

4
3
1
1

3
1

5.3
4
4.9
35

97

1 Composite
1 Composite
1 Composite
1 Composite

76

69, 7170, 71
70
24
22
24
228
228
228
228
255
255
255
66
76
76
66
76
66
66

38
38
38
38
66

• Dry weight.
TABLE XIX.

Sr90 IN MEAT, POULTRY, EGGS, AND FISH-1958·1960

CountTy

l'tST

fSp&fk1

USA .•.....•........•.••....

1960

1.0 (0.5-1.9)

10 (1-14)

Tri-city studya

198

USA •••••...••••••....•••.•• 1960
Eggs
USA ..••.•••..••••••••••.••• 1960
UK ..•........•..•.•••••..•• 1959
1960
Australia ••••••.•••..•••.••••. 1959

1.7 (0.7-2.5)

3.0 (1.6-4.5)

Tri-city studya

198

3.8 (1.9-11)
5.2
4.0

4.6 (3.5-5.9)
9
6.3
7.3

Tri-city study•
Countryside sampling
Countryside sampling
Eight samples from New South Wales

198
85
227
61

1960

0.35 (0.1-1.0)

0.3 (0.1-0.6)

Tri-city studya

198

1960
1958
1959
1958
1959
1959
1959

0.8 (0.5-1.8)
18
0.6

1.0 (0.6-1.5)
0.1

Tri-city study•
Samples from North Sea
Tunsa analysed in USA
Tunsa analysed in USA
Deep sea, 4 samples
Coastal, 2 samples
Fresh water, 9 samples

198
66
76
76
243
243
243

/'P&/1 Co

Re/ettn&4

Meal
PouUry

Fi.$~

Fresh
USA ........•.•...........
Shell
USA •..•.•.....••.•..•••••
Fed. Rep. of Germany .......
Spain ..•...•..•............
Japan ..•..................

0.4
3.2
15

• These results arise from an extensive survey of the total diet carried out in three cities in the USA.m

328

TABLEXX.

SrUO JN HUMAN BONE, 1955-1960

Values are given as µµc SrUO/g calci1m1 wit/1 the ntm1ber of samples and tlie range in parenthesest>-4 years

N111J1born
R.eiion, country or area

N. America .•..........•...

Latitu.U

1956

1957

1958

1959

1960

0.6(30)USA ..•.••••••.•..•..•..

0.9(179)

0.44(5)The Netherlands .........
Denmark ................

1.2(241)

1.1 (80)

J.feditnranean .•••••••.•••.•

1.6(2)
1.6 (9)(0.2-5.9)
1.2(74)

1.8 (6)0.89(0.5-2.4)
2.0(38)0.6(17)2.3(24)0.78(24) 1.2(49)(0.15-1.6) (0.3-3.2)
0.4(13)
1.3(16)

1.4(51)(0.2-3.1)
2.0(21)1.9(14)
1.6(8)
3.1 (69)(0.4-9.5)
2.0(47)

1.9(3)(t.0-3.7)
2.1 (5)1.0(3)(0.5-1.6)

1.8(3)(1.0-3.1)

0.7(16)

0.6(50)0.65(114) 1.2(148)(0.25-1.1) (0.3-1.4) (0.55-2.9)
1.6(14)1.0(15)(0.4-2.1) (0.4-5.3)
8.2(3)
4.0(1)(1.2-16.6)
1.0(20)0.64(5)(0.5-0.8) (0.6-1.5)

3.2(15)0.89(101) 1.2(1)(0.5-1.6)
1.3(22)0.4(13)(0.6-2.7)
0.8(8)(0.6-1.0)

Switzerland ..............

N

0.5(2)

1958

1.5(32)

1.6(10)Fed. Rep. of Germany ....

\00.4(2)

0.3(1)

0.8(5)

0.6(4)

0.9(9)

1.6(6)
1.1 (13)
1.2(8)(0.02-4.8) (0.02-5.3) (0.2-3.2)

C. America ••.•••.•••••••.•
Puerto Rico .••.•....•..•
Guatemala .....•........

10-20"NAsia •....................•
India ...•.••.....•...•..
China (Taiwan) ..•.......
Hong Kong ..............

<30°N

0.04(1)1.1 (2)1.0(9)

1.5(123)319•
13, 299

2.4(66)319•

2.9(73)(0.9-5.5)
2.0(28)37, 245233
98, 99, 238,
321
93, 319•0.5(10)0.7(1)
0.8(1)> 20°s0.35(10),...., o•> 20°s0.60(35)

0.51 (73)97
96, 319•0.5(10)0.4(1)

0.82(5)(0.4-1.5)

0.70(13)(0.2-1.7)

0.83(3)(0.4-1.2)

1.0(5)
1.1 (6)(0.22-1.17) (0.2-1.5)

330

0.8(7)
0.3(5)

0.7(34)0.6(1)

2.1 (5)0.6(2)

2.7(10)0.6(28)319•
319•

1.6(13)0.8(1)
0.7(4)
1.7(18)94, 319•319•
313

0.9(18)0.3(1)
0.4(5)

0.6(10)0.8(3)

0.5(1)
0.6(4)
0.6(11)

319•

319•
319•
6, 5

1.0(34)

1.1 (20)0.6(8)

0.4(21)0.73(6)0.85(20)(0.55-0.82)
0.4(33)319•

0.65(42)0.9(226)1.0(124)0.6(114)0.96(172)319•
95,3200.9(55)319•
319•

0.8(3)> 20°sAustralia ..•.......•.....
Congo (Leopoldville) ..•..
Union of South Africa ...•&/ere nee

1.4(3)

1.2(13)

Chile .•.•••..•..••••.•..

Africa0.5(1)

0.5(1)
0.8(1)

0.5(17)

S. America ................ 10°N-10°s

Oceania .....•.•...•...•..•

1961

319•

> 30°N

Japan ••.........••.•..•.

Venezuela .•.............
Brazil .•••....•..........
Argentina ...............

1960

1.3(6)> 30°N

Israel .•..•.........••.•.

Far East. •.•.•.....••....•

1959

1957

> 30°NUSSR ••••.•.•........•..
Poland ..............•...
UK •......•...•...••....

e,,,,

1956

> 30°N

Canada ....••.......•...

E11rope •.•.••.••••••.••••••

1955

t.2(2)TABLE

xx. Sr90 IN HUMAN BONE, 1955-1960 (continued)

5-19 y1ars
IU1io11. co1mlry flf' or1a

Lolilwd1

1951

1956

1951

1951

0.6(14)0.45(4)(0.2-0.6}
0.6(67)0.76(12)(0.4-1.0}
1.0(42)

N. America • •••.•..•. >30°N
Canada .•.........
USA ..............
Europe • ••.••.•...... > 30°N
USSR ......•......
Poland ............
UK ...............

Fed. Rep.ofGennany
The Netherlands ...
Denmark ..........
France ............
Switzerland ........
Italy ..............
Near East .... ........ > 30°N
Iran ...............
Israel .............
UAR .............
Far East ...•.. ....... > 30°N
Japan .............

0.5(16)

1.4(35)
1.1 (17)t.5(79)

1961

195S

0.4(8)

0.16(9)0.19(7)0.6(22)0.3(1)

1956

1951

1951

1959

1960

0.29(30}0.38(27)0.53(113}(0.05-0.6} (0.07-0.8)
0.07(125) 0.06(187) 0.12(335) 0.19(227) 0.27(271) 0.23(31)0.12(60)

0.22(7)0.08(11)0.4(3)

0.2(1)
0.2(5)

China (Taiwan) ....
0.5(3)
Thailand ..•.......
Viet-Nam, Rep. of.
S. America .... •••.•.. I 0°N-10°S
0.1 (1)
Colombia ..........
0.3(21}
Venezuela .........
0.3(4)
Brazil. ............
Ecuador ...........
Argentina .......... > 20°5
0.2(18)Chile ..............
Oceania ...... ........ > 20°5
Australia ..........

0.1 (4)0.2(3)

0.5(10)0.4(9)

0.9(11)0.4(3)

0.2(54)0.3(2)

1.1 (2)0.3(1)

0.7(4)
0.4(1)

1.0(24)0.55(3)
1.1 (1}0.4(3)
1.0{1}

0.13(9)0.1 (7)0.16(29)0.16(8)96, 319•
319•
319•
319•

0.17(17)0.12(4)0.22(3)0.12(58) 0.16(20)319•
0.90(20) 0.41 (4)0.58(36) 0.46(39} 101, 330(0.1-2.5) (0.1-0.7) (0.1-2.8) (0.1-1.0}

0.18(4)0.18(47)0.15(34)0.13(49)

0.21 (151) 0.24(134) 0.34(14)0.14(56)0.15(34)

319•
319•

0.14(33)

0.11(31)0.18(22)0.13(1)0.52(2)

319•
94
319•
319•
319•

0.15(10}0.14(6)0.28(33)
0.07(3)0.17(11) 0.12(8)0.15(23}0.15(130) 0.24(70)0.10(59)

0.08(4}0.08(2)0.11 (19)0.06(24)<0.1 (13)0.19(37)0.10(49)0.15(460) 0.22(247)0.16(247) 0.19(346)0.17(7)0.3{1}

0.4(1·2}

0.5(17)

0.7(6)

0.10(7)0.1(1)
0.16(35} 0.2(3)O.l.1(13) 0.08(40)0.2(13}0.3(37)0.4(10)0.4(22)0.4(25)0.20(40)0.6(3)

0.5(2)
0.34(25)0.6(141)0.53(81)0.5(52)0.62(93)0.9(32)0.13(9)0.43(12)0.8(78)1.0(73)•Values from refl'rence 319 below 1 pµc/g. Ca arc often stated as "less than" the value
quoted.

0.13(28)0.18(3)0.18(25)0.18(360.2(2}

0.4(24)319•
319•
20.01 (2} 229

0.14(38)0.22{38)(0.1-0.8)

0.1 (2)0.4(6)
0.2(4)

0.4(1)

93, 319•97

0.16(19)0.25(3)0.4(1)
0.2(3)
0.1 (9)1.2(4)

319•

0.12(65)0.2(2)

0.2 {2}13, 299

0.18(33}

0.96(41) 1.2(34} 3.0(2)(0.1-2.6) (0.3-3}
1.2(17)0.5(10)&/erenc~

37, 245
233
98,99,238

0.5(1}

0.7(2)
0.6(1)
0.6(9)
0.67(6}0.62(12) . 0.59(3}(10.2-1.8) (0.8-1.5} (0.2-1.0}

1961

0.40(82)0.38(63}0.22(3)0.24(4)0.31 (11) 0.29(28) 0.66(20)(0.13-0.29) (0.11-0.44) (0.04-1.4) (0.07-0.7)
0.22(26)0.14(29)0.36(105) 0.45(145) 0.51 (42)0.2(1)

0.06(1)0.5 (7)0AfricaCongo(Leopoldville) .... ....., 0°
Liberia ............
Union of South
Africa ........... > 2o•s

1960

1.4(5)
1.2(7)
0.27(4)0.78(24) 0.44(18) 0.75(20) 0.90(23) l.t (54)(0.15-0.4) (0.15-1.6) (0.3-0.75) (0.2-1.7} (0.13-2. 7) (0.3-2.0}
0.2(19)0.2(14)0.3(4)
0.7(11)0.9(33)1.2(36)
1.5(9)
0.4(4}
0.37(2)(0.14-0.6) (0.35-4.0) (0.5-0. 7)
1.3(3)
0.4(3)
0.3(7)
0.5(4}w
w

C. A muica .......... 10-20°N
Puerto Rico ........
Guatemala .........
Asia ................ < 30°N
India ..•...........

19 11arsb
1959

0.1 (7)0.18(39)0.23(36)
0.5 (7)0.22(46)
0.4 {9)0.4(3)

0.14(2)

319•
319•
319•
319•
319•
319•
319"
95, 320319•
319•

0.24(125)319•

b Normalized in accordance with footnote to paragraph 81 except Japan, USSR, Poland,in which the bone sampled was not specified.

TABLE XXI.

Sm.!MARY OF THE REGIONAL :lo!E..\NS OF Sr90 CONCENTRATION IN BUMAN BO!>'ES, 1959-1960(pµc Sf'90/g calcium)
At~•OTI

o--4

Newlxml

5-19

>19

A"a

Lalil,,,U

1959

1960

1959

1960

1959

1960

1959

1960

N. America .•.••••..
W. Europe .••......
E. Europe •••..•...•
Near East •....•••.•Far East .•.•.•..•..
Asia .••......•.....
Central America .•...
S. America .....•...

> 30°N> 30°N> 30°N> 30°N> 30°N< 30°N< 30°N

1.2
1.4
1.5

1.1
1.1

2.3
2.5
1.9
0.4
0.8

2.3
2.5

1.1

1.5
1.2

0.3
0.4
0.4
0.1
0.3
0.3

0.3
0.6

Australia .•.•...•...
Africa .••...........

10°N-10°s> 20°5> 2o•s> 20°5TABLE X.XI!.

1.2
1.1

0.6

1.2
0.6
1.0
0.4
0.9

0.5

0.9
1.3
0.5
0.6
0.5

1.0
1.7
0.6

0.5
0.4
0.6
0.8

1.1

0.6
0.8
0.9

0.9
0.3
0.5
0.7
0.4
0.6
1.0

A COMPARISON OF MEASURED RATIOS OF SrDO TO CALCIUM (p.pc/g) IN TOTALDIET (TABLE IV) .V."D :MILK (TABLE VII)
Year

Ralio (m4a11)

Total diet/milk(ra11e-)(a) Values based cm cominued, often 'Uoidespread, dia sampling

N. America
Canada •.•..•....•...................

1959-1960
1957-1960

1.1

USA ..••...........................•

1.3

0.9-1.7

EuroptJUK• .•......•.......................
Fed. Rep. Germany .•...••............
Denmark• ...•.......................
Austria ............................. .

1957-1960
1959
1959-1960
1960

1.2
1.8
2.9
1.7

1.2-1.3

Oceania
Australia............................

1957-1960

1.1

Far East
Japan...............................

1957-1960

2.2

1.4-3.6(b) Values based on single, often fiery limited, diet samples

Central America
Five countries•• b,....................

1957-1958

1.3

0.9-2.0

S. America
Four countriesb.......................

1957-1959

2.7

1.9-3.3

Africa
Rhodesiab...........................

1959-1960

10-13•Excluding mineral calcium.
on limited sampling.

b Based

331

0.1
0.2

0.6
0.2
0.2
0.3
0.2
0.2

TABLE XXIII.

CAI.cm.ATED RATIOS OF THE RATIO OF Sr• 0 TO CALCIUM IN THE TOTAL DIET TO THATIN Mll.K FOR VARIOUS APPROXIMATE DIET TYPES FOR 1958-1960
Peruntage conlribuJion a/ calcium lo the diet
Cereal>

Milk

Cam~

Ratio to milk. " ••••••••.
No. of observations ••••..
Range •••••..•.••....•.•(a) .••..•••••.•
Diet ld (b} •••••••••.••(c) ••..••.••.•.
(a) .•.••••••..•
Diet Ild (b} .••••••••.••(c) ••••••••••••(a} ••••••••••••
Diet III (b) •••.••••••••(c} ••••••••••••

MilledUnmilled

513
33(1-43)
0
1.5

10(2-10)
80
80
80
40
40
40
10
10
10

5
3.5

0
20
14
0
15
10
0

5

0
6
20
0
5
15

Vet.b

Fish•

3

<0.1
3

35

(1-12)
15
15
15
40
40
40
60
60
60

Ralio Jolal
diel lo milk

1.5
1.6
1.9
2.6
3.1
4.2
2.6
3.0
3.8

15
15
15

• Including wheat, rye, maize and rice.
b Vegetables of all kinds and fruit.

•Marine fish only. If all the fish were from fresh water the ratio of total diet to milk might
be increased by about 0.4. (Based on Japanese data, table XIX.)
d Diet (a) contains only milled cereal, (b) 30 per cent unmilled cereal, (c) all unmilled cereal.

TABLE XXIV. CoMPAJUSON OF MEASURED Sr&0 TO CALCIUM IN BO?-.""£, 1959-1960, WITH LEVELS IN
NEW BONE CALCULATED FROM DIET MEASUREMENTS, 1959-1960 (see text, para. 100)All units /1/LC SrOo/g Ca
New bone 1959-60

Total didCaktll4hd

Assumeddiel l~P•

N. America.................
W. Europe.................
E. Europe..................
Near East..................
Far East...................

I
I
I
II
III
Asia •••.•••••••••••••.•••.• II-III

Central America,, ......•....

S. America,.................

I-II

Africa......................

II

Oceania....................

I

Mi/Jt
(a)

> 30°N.Measured(labu IV)
(b)

9.5

12
11

8.1
9.1
< 30°N< 30°N> o•s> 20°s> 20°s

13
11
13

3
13°
7
1
4
4•
3-8

5.1•
3.5•
1.6
2.3
3.8
2.6

JI,cm

diel
( R • O.ZS)

(t)

14
12
14

Calculmed
from bones
af newbons
(/)

3
3
3
1
3
2
0.3
1-2
1
1-2

13
9
3-6
6
7

2.3
2.5
3.0
2.4
2.3
1.1

M<JUUred asmean Ind i•<>-4-ycar~

(rj

2.3
2.5
1.9
0.4
1.0
1.7
0.6
0.6-1.0
0.8
0.9

b Based on the weighted mean of milk and the ratios of total
diet to milk for the approximate model diets (from table XXIII).
• Based on one country only.

• Based on the weighted mean of milk and measured ratio of
total diet to milk in some countries (from table XXII).

TABLE XXV.

Calcul4Ud
(c)•
(d)b

A COMPAJUSON OF THE RATIOS OF SrDO TO Ca IN AVERAGE ADULTDIET AND BONE OF NEW-BORN OR FOETUS

The ra11ge of values is shown in parentheses. The data are taken fromtable IV (diet) and table XX (bone)
OR (foelus/molher'z diel)

Coulllr;yUSA (New York) ••••.......•.••••••••••••••.•
UK ••••..••••..•...•..•...•.............••..
Denmark ••...•...•...•••..•.....••.•.•...•..
Fed. Rep. of Germany ••.•.•...•.•...•.•...•..
Australia .....•...•...••.... , .........•.....•
Japan ...................................... .

332

1957-1960
1957-1960
1959-1960
1959-1960
1958-1960
1957
1958
1959

0.09 (0.07--0.10}
0.12 (0.11--0.13)
0.10 (0.09-0.11)
0.12 (0.11--0.12)
0.10 (0.08-0.12)
0.56
0.21
0.08

TABLE XXVI.

ESTIMATED PROPORTIO:SALITY FACTORS FOR THE CALCUL.\TION OF FUTURE I.EY"ELSDERIVED FR01>i SURVEY MEASUREMENTS TO 1960
Milk

Veietabksp,Countr:y

Pd

P,

Pd

Argentina •..••.•.
Australia .........
Canada ...•.•.•..
Denmark .••.•...
Germanyb ..•..•..
Japan •••...•••••
India ............
New Zealand •...•
Norway ....•.•.•
S. Rhodesia ••.•..
USSR •••..•.•...
UK .••••.•.••..•
USA .•••.•.••••.

0.24
0.71
0.30
0.23
0.29
0.23
0.26
0.80
0.52
0.30
0.40
0.21
0.27

0.54
1.5
0.66

1.5

1.1
0.9
0.7

Value adopted ••••

0.3

0.8

Starchy roots
Pd

Cereals-P,

Unmilkd
P,

Milkd
P,

30
3

0.8
0.6

18
20
19, 148

0

9
6

1.1

0.3
0.7

34 (47)•

0.6

0.5
1

0.8
0

•Mainly based on wheat; Pd is assumed as 0.5.
b The value of F d is assumed to be the same as

1.2
0.8

0
1

20
16

25

4
5
16

0

20

7

in the UK.

•Rice.

T •.\BLE XXV!I.

SUMMARY OF PROPORTIONALITY FACTORS FOR PREDICTING FUTURE RATIOS OF
SrDo TO Ca IN THE TOTAL DIET
p,b

p,b
Did

conlribulion

pd
immediahsituation

I and II ..••.............
III ......................
IV ..•......•..........•.

80:5:13:2
40:20:38:2
13:15:50:7

0.4
0.6
0.7

Cakium•Pd
lont·l<rm
zilsustion

0.35
0.6
0.7

(unlh milkd (Vlilh unmilkd
weal
eerealOllly)
Ollly)

1.8
4.7

1.1
1.9
1.7

3.6

•From milk: cereals: green vegetables: starchy roots (based on potatoes). The contribution
from fish has not been taken into account since, because of dilution of Sr 90 in the sea, the contribution is likely to remain small.
b For calculation it has been assumed that 20 per cent of the cereal in the diet is unmilled.

TABLE XXVII!.

SOME ESTIMATES OF TIIE MEAN DAILY I~'TAKE OF Cs1 87 IN THE TOTAL DIET
Canada 19S9 (108)

USA.-19S6-19S7 (40)

Milk and milk products .••.••.••.•..•.•.
Vegetables except potatoes• ••.•.••••••.•
Potatoes ............................. .
Fruit- ............................... .
Meat• •..••...•.••.....•...••.••..••.•
Fish• •••••••••••••••..•••.•.••.•.•••.•
Flour and cereals-. •...•.•.•.•••...•••••

Cs1" /K total diet ••••.•..••••••••••••••
Whole body •••••••.•••••..•••....•

l'/J& Cs"'li K

K inlah lpp&

Per cenl

pp& Cs"'/i K

K l111ak1 i

pp&

Per ual

32
5

37

60

1.0
0.78
0.41
0.47

55

0.8
0.0
1.0

1

3
25

35
1
0
2.5

35

2.9
0
2.5
14.7

5

0
25
32

1.16
0.57
0.60
0.10
0.46

2.0

0.40

2I.8b

34

24

0.20

4.8

7

0.22

5.1

8

3.09

61.9

3.28

63.7

20
40

6~ }
23

19.5

57
b Assuming one-fifth of the potassium is from fish.

• Sampled on a very limited scale.

333

TABLE XXIX.

CsUT IN MILK

Reg11/ar or widespread surveys (for description see table VIII)
Results as µµc
R~gionN. America

EuropeLaliludt

Country>30° N

Canada .......
USA ..........

>30° NUSSR .........

UK ...•.......
Fed. Rep. of
Germany ....
Italy ..........
Denmark ......
Norway .......

(,.)
(,.)

.j>..

Sweden .......
Finland .......

Csts 7 per g potassium, or as µµc/litre
1957

Arta

Widespread
Widespread

Mid-Sweden
Widespread

1958

1960

1959

61 (12, 28-100)
33 (38, 12-59)•
42 (33, 2-70)•
52 (33, 20-97)•
34 (J)b tki.o&.liS. ~fi.1, 44 (5)'~~.i~i .54 (JZ, 30-86)

Widespread
MoscowWidespread
LindauN. Italy
Widespread
S. Norway(italicized). Number of sites and range, where available, in parentheses.

36 (9, 22-54)b

19 (4, 12-2J)b

31 (2, 25-38)

27 (1 )b40 (l)b15 (11-22)b
27 (2, 23-30)
149 (3, 47-270)
46 (1 )b40 (22-80)b55 (10, 26-115)
32 (38, 7-70)•
Z8 (9)

15 (9, 10-Z5)>30° N

Japan .........

18 (2)bAsia

10-20° N

India .........

Widespread
Dom hay

S. America>20"S

Argentina .....

Oceania>20° sAustralia ......

Main production
zone
Sydney18 (1)•Upper figure Los Alamos survey, lower figure U.S.P.H.S. stations.
Not a complete year, or samplccl irregularly.

b3, 40, 69, 71, 72
3, 40, 69, 71,
72, 251234

30 (9, 13-59)
13 (2)
19°

8, 22723 (t)b24, 25, 241

12 (4, 8-14)
150 (11, 39-397)

18,22849,42,43
231,242
41
54
191
243

55 (19-ZZO)

Far East&ftrtnc.

1961

52 (4, 22-118)b88 (10, 21-19J)b

77 (8, l 6-117)b

9.4 (1)18 (1)
17 (21, 3-160) 1'

11 (1)
5.5 (16, 1.5-lJ)b

10 (1)
5.6 (7, 4-9)

88, 8989, 244, 302

19°

20•

44

12 (1)~

18 (1)

19 (1)• Countrywide bulked samples for part of year.
Composite samples.

d40, 69, 71, 72, 73

TABLE XXX.

Cs1 37 IN :MILK; INFREQUENT OR SPOT SAMPLING

Results expressed as µµc Cs137 per g potassium

Figures in parentheses indicate number of samples
Country

Europe> 30°NFar East> 30°N

Central America
S. America

1957

Denmark .........•......••..
France ..................•...
Switzerland ...........•....•.
Fed. Rep. of Germany .•.. ,,..
Japan ..........•........... ,.Mexico .......•.......••...•.
Colombia ................•••.
Venezuela .................. .
Brazil ...................... .
Chile ....................•...

10-20°N
10°N-10'S> 10°5TABLE XXXI.

54 (1)
80 (3)

1959

1958

1960

39 (2)
34 (2)
77 (2)
54 (1)
39 (1)
29 (1)
74 (2)
20 (2)
16 (1)6 (1)
1.2 (2)26 (2)
36 (1)
66 (6)
40 (1)

1961

50 (4)

69
69
69
23
33,69, 72

69
69, 72
69
71, 7269, 72

THE Cs1s1 co:NTE.NT OF SOME FOODS ,Cs"'

Coktt:JrY aiul lyJ>eYear

cou,.1ry

CerealWheat grain .•.........•............•. Canada
Japan (widespread)
Rice (brown) .•........•......•.......• Japan (Gunma)Rice(brown) ....••...•....•............. Japan (widespread)(milled) ........•.......•.......•... Japan
Barley ...•.•......................... Japan (Gunma),
Rice(boiled) •...••.......•..•..•......•• India(surty) .•.•..•.........••.••.•.••••• India

VegeJables
Cabbage, etc. ........•...•..........•. Japan (Gunma)
Root vegetables, .•.........••....•.•.•• Japan (Gunma)
Meat
Beef .••.•........••.••......•.•.....• Japan (Gunma)
Pork ........ , .......•.•..........•..• Japan (Gunma)

Beef .•.••...•.••.....••••.•.......... Norway
Reindeer., ••. , •.•..................... Sweden
Fish
Cuttle fish .............••.••.......... Japan (Pacific)

Skipjack ...........•..............•... Japan (Pacific)•The Csm/K ratio in.flour is not significantly different.

335

p.p.e/kt

p.p.e/iK

Ref.,.nsu

35•
47•

1957
1958
1960
1961
1956
1957
1958
1959

55

44

108
63

63
37

114
114
326
326
90
90
90
90

1959
1960
1956
1957
1958
1959

143
31
80
48
89
401

139
36
34
22
35
146

326
326
t90
90
I 90
J,90

1959
1959

0.3
10.4

0.2
4.9

309
309

1957
1960
1957
1960

13
26
18
36

6.0
12
7
15

90
90
90
90

1960
1957
1960
1960
1960

92
98
207
24,000

1957
1960
1957
1960

21
26
16
87

265
90
38

54
31

32
36
90
180-1,760 (3)

90
90
90
231
276

11

90
90
90
90

28
9
43

T •.\l!LE XXXII.

THE Cs187 CONTENT OF MAN, MEASURED BY WHOLE BODY COUNTER

Results as µ.µc Cs1s1 per g potassium

The figures in parentheses indicate the tiumber of observatiotis
Name or numba-

RetionLatuutk

N. America> 30°N""'"""iarepruenled

of

1956

1957

1958

1959

1960

1961

USA

so (279)

51 (294)62 (461)69 (576)
Quly-Dec.)
51 (30)(Dec.)
64 (2)

74 (280)
67 (777)

67 (279)
51 (646)

31 (245)57 (20)(Spring)
94 (4)
79 (8)
58 (30)*48 (94)49 (21)(Dec.)
92 (2)
55 (1)
49 (47)•45 (88)
63 (1566)

Canada> 30°N

Europe32 (14)UK

48 (14)37 (18)Fed. Republicof Germany
SwedenNear Eai;tFar East
Asia

C. America
Caribbean
S. America
AfricaAsia
Oceania

66 (46)73 (-}

25 (1)

62 (1)
60 (2)
44( 2)
75 {16)54 (1)
64 (2)
67 (70)47 (1)
78 (1)
75 (1)

14 {2)
14( 9)

35 (5)
52 (2)
11 (2)so (1)

42 (3)
60 (12)99 (2)
49 (9)
60 (3)
47 (10)49 (5)
62 (1)
45 (2)103 (2)54 (3)

L.A.

W.R.
107, 108
117
L.A.

W.R.
42 (807)274, 298
104
116, 250, 253

55 (87)105276

36 (26)

L. A.
51 (43)

W.R.
L. A.

49 (2)W.R.
L.A.

29 (31)
29 {11)51 (2)

W.R.
278
L. A.

W.R.
L. A.

27 (4)
54 (5)
68 (1)

28 (1)
25 (4)

W.R.
W.R.
L. A.
W.R.
L.A.

35 (1)

W.R.
L.A.
L.A.

68 (1)
34 (1)

36 (1)

W.R.

W.R. from the Walter Reed Army Institute of Research. 111 •• Measurements made on former luminizers (female).
L.A. indicates data from the Los Alamos Scientific Laboratory.'· G, n, n, 102

TABLE XXXIII.

87 (10)83 (122)66 (3)

20 (2).

76 (47)70 (22)32 (4)

7
11
2> 20°N4> 30°N25
Japan
0-30"N 4
6
10°-30°N 3
3
20°N
5
7
< 10°N5
2< lO"N2
2< 10°N< 10°s22

65 (-)Gune)
85 (9)
67 (208)57 (2)
32 (5)109 (1)49 (145)

Refermuuo.w

11EAN CONCENTRATIONS OF Cs18 7 (µ.µc/PD. G POTASSIUM) IN THE HUMAN BODY AS MEASUREDBY WHOLE BODY COUNTING (from table XXXV)The figures in parentheses i11dicale the number of observations
Re1io11

Latitude

1956

1951

North America .........•.•.•.•...
Europe •••...........•........
Near East •........•.............
Far East ........................
Asia .•....•.•.••..•..•••••....••
Central America .•.............•.
South America ...................
Africa ••.•...•..............•....
Oceania .....................•.•

>30°N
>30°N
>30°N
>30°N
<30°N
<10°N

so (279)

51 (294)
37 {18)>20°s

TABLE XXX!V.

32 (18)

19)9

1958

25 (1)
16 (4)
14 (2)
14 (9)

65 (1,069)
69 (83)61 (3)
71 (18)66 (3)
66 (3)
35 (5)
52 (2)

50 (1)

1960

55 (949)
63 (1,891)
39 (7)
50 (146)
51 (2)
45 (10)69 (1,089)
65 (302)54 (1)
67 (72)56 (15)59 (14)48 (15)51 (3)
74 (5)

51 (2)

MEAN CONC:ENTR...TION OF SHORT LIVED FISSIO!i PRODUCTS
IN MILK IN THE USA, 1957-1960

Values, expressed in p.µc/litre, are from 5-12 stations of the US Public Health Service~51
5,u

Ytor

1957 (second half)...............................
1958...........................................
1959.................................... •. • • • . .
1960...........................................

336

Bo1H

pn

65
80
250
50
15
40
20
Not detectable- - - Not detectable - - -1961

31 (245)43 (963)
49 (2)
29 (42)26 (5)
35 (1)
36 (1)

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n paaHEIX pattonax CCCP B 1960 roM. rocyAap-

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275. Andersson, I. 0., I. Nilsson, Radioactivity in people
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·
137
276. Liden, K., Cs burdens in Swedish Laplanders
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279. Argonne National Laboratory, Radiological Physics
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280. Morgan, A., G. M. Arkell, Determination of
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282. Russell, R. S. To be published.
283. Fredericksson, L. To be published.
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285. Jacobson, L., R. Overstreet, The uptake by plantsof plutonium and some products of nuclear fission
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286. International Commission on Radiological Protection, ICRP Publ. 2. Report of Committee II on
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287. Lengemann, F. W., C. L. Comar, The secretion of
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288. Comar, C. L., R. H. Wasserman, M. M. Nold,
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289. Visek, W. J., R. A. Monroe, E. W. Swanson et al.,Calcium metabolism in dairy cows studied with
Ca45 , J. Dairy Sci. 36: 373-384 (1953).
290. Wasserman, R. H., C. L. Comar, The influence of
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291. Wasserman, R.H., C. L. Comar, M. M. Nold, The
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59: 371-383 (1956).
292. Wasserman, R.H., C. L. Comar, Effect of dietarycalcium and phosphorus levels on body burdens ofingested radiostrontium. Proc. Soc. Exp. Biol. and1vied. 103: 124-129 (1960).
293. Monroe, R. A., R. H. Wasserman, C. L. Comar,
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200: 535-538 (1961).
294. Wasserman, R.H., C. L. Comar, A. R. Twardock,
Metabolic behavior of Cs137-Ba137"' in the lactating
goat. Int. J. Rad. Biol. In press.
295. Nelson, Arne, S. Ullberg, H. Kristoffersson et al.,Distribution of radiocesium in mice. Acta Radiologica 55: 374-384 (1961).
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on environmental radioactivity, collected in Italy
July-December 1960, BI0/03/61; v.e. United
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297. Rosoff, B., A Feldstein, F. Stand, et al., Cesium137 excretion and distribution in man. Abstract.
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298. Rundo, J. To be published.
299. Canadian Department of National Health and Welfare. To be published.
300. Stewart, N. G., R. G. D. Osmond, R. N. Crooks,
et al., The deposition of long lived fission products
from nuclear test explosions. Results up to the
middle of 1958. U.K. Atomic Energy Authority
report AERE HP/R 2790; v.e. United Nations
document A/AC.82/G/L.241.
301. Grummitt, W. E. To be published.
302. Rao, A. S. To be published.
303. Crooks, R. N., R. G. D. Osmond, T. J. Webber.
Radiostrontium and radiocaesium in drinking
water in the United Kingdom. Results to December
1960. U.K. Atomic Energy Authority report AERE
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A/AC.82/GjL.676.
304. Yamagata, N., T. Hanya, S. Nagayama. The concentrations of Sr-90 and Cs-137 in land waters inJapan. Government of Japan (August 1961); v.e.
United Nations document A/AC.82/G/L.690.
305. U.K. Agricultural Research Council, Radioactivity
in milk in the United Kingdom 1961: Preliminary
report (December 1961); v.e. United Nations
document A/AC.82/G/L.722.
306. Miller, C. E. To be published.
307. Merten, D. To be published.
308. United States Atomic Energy Commission, Healthand Safety Laboratory, Fallout program quarterly
summary report (Oct. 1, 1961), HASL-115; v.e.
United Nations document A/AC.82/GjL.679.
309. United States Atomic Energy Commission, Healthand Safety Laboratory, Fallout program quarterly
summary report (December 30, 1961), HASL117; v.e. United Nations document A/AC.82/G/
L.737.
310. Der Bundesminister fiir Atomkernenergie undWasserwirtschaft, Umweltradioaktivitat undStrahlenbelastung. Bericht I/61. C. Brandt, Bonn
(1961).
311. Harrison, G. E., W. H. A. Raymond, H. C. Tretheway, The metabolism of strontium in man. Clinical
Science 14: 681-694 (1955).
312. Michelson, I. To be published.
313. Bryant, F., J. F. Loutit: Sr90 in the Bones of Infants in Hong Kong. United Nations document
A/AC.82/GjL.718.
314. Richmond, C.R., J.E. Furchner, W. H. Langham.
Long-term retention of radiocesium by man.
USAEC report LAMS-2627, p. 163 (1961).

346

315. Richmond, C.R., Retention and excretion of radionuclides of the alkali metals by five mammalian
species. USAEC report LA-2207 (1958).
316. Miller, C. E., L. D. Marinelli. In vivo measurements of Cs137 • Argonne National Laboratory report ANL-5755, p. 47 (1957).
317. Kulp, J. L., A R. Schulert, Sr9° in man and his
environment. Vol. I. USAEC report NY0-9934.
318. Kulp, J. L., A. R. Schulert, Sr90 in man and his environment-Volume II : Analytical data. USAEC
report NY0-9934. United Nations document A/
AC.82/G/L.739.
319. Kulp, J. L., A. R. Schulert, Sr90 in man and his environment-Volume III: Publications. USAEC
report NY0-9934. United Nations document A/
AC.82/GjL.738.
320. Bryant, F. J., L. J. Dwyer, D. J. Stevens et al.,Measurements of strontium-90 in the Australianenvironment up to December 1960. Nature 193:
188-189 (1962).
321. Medical Research Council, Monitoring Report
Series No. 3, Assay of strontium-90 in humanbone in the United Kingdom. Results for 1960,
Part II. HMSO London (1961).
322. U.S. Department of Health, Education and Welfare, Radiological Health Data. Monthly Report,
Vol. II, No. 11 (November 1961); v.e. United
Nations document A/AC.82/G/L.714.
323. U.S. Department of Health, Education and \Velfare, Radiological Health Data. Vol. II, No. 12(December 1961); v.e. United Nations document
A/AC.82/GjL.740.
324. U.S. Department of Health, Education and Welfare, Radiological Health Data. Vol. III, No. 1(January 1%2); v.e. United Nations document
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325. Kodaira, K. To be published.
326. Kodaira, K., N. Yamagata. To be published.
327. Ichikawa, R., M. Abe, E. Masako, Evaluation oforigins of strontium-90 contained in wheat plant.
Science 133: 2017-2018 (1961).
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A/AC.82/GjL.765.
329. Mahmoud, K. A., A. T. A. Abdel Fattah, F. Henry,
Wide survey of Sr9° in soil, food items and dietin the delta region of UAR during the period Julyto December 1961. U.A.R. S.C.E.A.R., Vol. 4, No.
3 (1962).
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Res. 3 (1): 61-67 (1961); v.e. United Nations
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331. Asari, T. To be published.

ANNE.X F

ENVIRONMENTAL CONTAMINATION (continued)
PART IIIEx po&ure data

CONTENTS
Par4t1rap1's

ParaqroPM

1-3

Dose commitment from Sr&-0 which would be received under conditions of continued testing .• 35-36
Cs13 7 in whole body and bone ••••• , ............ 37-41
Dose commitment from internal e.'tposure to
es1s1 due to testing up to the end of 1960 andthe end of 1961 ............................ 39-40
Dose commitment from internal exposure to
Cs1 s1 under conditions of continued testing... 41
C14 in whole body •..••.•••••.••••••..• , • , , • . . • 42-48
Dose commitment from CH due to testing up to
the end of 1960 and the end of 1961.......... 44
Dose commitment from cu due to continued
testing • . •• • . . . . . • • •• • • • . • . •• •. • . • . • • •• . • • • 45
Reduction of dose from C14 due to combustionof fuels • • . • • • • • . • . . • • • • • • • • • • • • • • • • • • • • • • • 46-48
H 3 in the body . . • • . • • . . . . . • • . • • • • • • • • • • • • • • • • . • 49
Short-lived isotopes . • . . . • • • . .. • • • • • . • • • • . . . • • • • 50
Sr-89 in bone .••••••.•..•.••••••••••••.••••••••• 51-54
BaHo and t.auo in bone • • • • • • . . . • • • . • • • . • . • • . • • 55
11 31 in thyroid . . • • .. • . • .. • • • • • .. • • • • • • .. • • • • • • • 56-58
Mixed fission products in the GI tract. • • • • • • • • • • 59-61
Entry of radio-activity into the body through inhalation . . . • . . • • • • • . • . . • . • . . . . . . • • . • • • • • • • • . • . • 62-66
Summary of radiation doses to tissues due to fall-out 67

I. INTRODUCI'ION • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • •II. ExTE:llNAL EXPOSURE • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • 4-25
World averages of fall-out deposit. ....•••.•••.. ,.. 4-5
Methods of dose estimation • • • • . • . • • . • • • • • . . . • . • . 6-13
Direct determination ••..•....•••.•••.•.•••• , . . . 7
Indirect methods ...•.••• , ......•.••••.•••• , • • • . 8-11
Theoretical calculations of the total external dose •• 12-13
Factors affecting dose to tissues •.•.........•.••... 14-19
Weathering . . . • • . . . • . . • • • • . . . . . • . . • . • . • • . • . . • . • 15
Shielding by building structures ••..•....•...••.. 16-17
Screening by the human body • • • . • . . . . . • . . • • • • • . 18
Combined shielding and screening factors.,...... 19
Doses due to external sources .•.•.....•....•.••..•• 20-25
Total external dose in air received from testingfrom 1954 to August 1961 • • • . . • . . . • . . • . • • • • • • • 22
Total external dose commitment from testing up
to the end of 1960 and the end of 1961.......... 23
Total external dose commitment which would bereceived under conditions of continued testing .• 24-25
III. INTER..'iAL EXPOSURE •••••••••••••••••••••••••••••• 26-67
Ingested radio-nuclides ••••••..••••••.....••.•..•• 27-61
Strontium-90 •••••..•••..•.•..•..•• , , •.••••...• 28-36
Concentrations in diet and bone . . . • . . . . • . • . . • . 28
Dose from Srso in bone ••.•..•..•...••.••• , . . 29
Method of estimation of mean population dose., 30-31
Dose commitment from Sr9o due to testing carried out up to the end of 1960 and the end of1961 •..•.•••••••••••••.••••••.•..••••.••••• 32-34

TABLESR£n:ttNCES

resumed in 1961, at an assumed constant annual rate of
injection of 1 Mc of Sr9° and 1()25 atoms of cu. On thatbasis, calculations have been made for tests up to theend of 1960 and up to the end of 1961, as well as forcontinued testing. Since the doses are necessarily basedon many assumptions, they must be c0nsidered as estimates rather than precise determinations.

I. Introduction

1. The purpose of this section of the annex is to estimate the average doses of radiation received by theworld population from fall-out.
2. Fall-out materials deposited on the ground are an
external source of e."'l:posure to man. In addition to this,some radio-nuclides are taken into the body and become
an internal source of radiation. Information on these
two sources has been given in parts I and II of thepresent anne..'C. To determine the average radiation dose
received, a considerable amount of dosimetric and demographic data is also required.

II. External exposureWORLD AVERAGES OF FALL-OUT DEPOSIT

4. The average fall-out deposit per square km of thesurface of the earth, Fd, is obtained by integrating the
local values of fall-out, Fd, over the total surface of theearth, S 0 , i.e. :3. This section of the annex presents "dose commitments"-the total doses which will be received by mankind in all generations (H 15-21 )-from given periodsof weapon testing. In addition, that fraction of the dose
commitment that will be reached by the year 2000 isalso given. The calculations have been based on the factthat testing was carried out from 1954-1958, and was-Fd = S1
o

1

FddS

So

In order to get a measure of the mean effect of the global

347

5. The values of the population weighted mean worldgeographical factor have risen from 1.6 to 1.9 in theyears 1955-1960 owing to changes in the pattern offall-out. It is therefore possible to use measurements
in certain latitudes where Fd/F°.i is equal to about 1.9 toestimate the doses to the average member of the world
population. This avoids the problem of attempting a
total summation over the world's surface when insufficient data are available.

fall-out, a population weighted average fall-out can be
defined as_ fe,NFddS
G F d - fs.NdS
where N is the population density, and G is called "themean geographical factor" (figure 1).
3.0-· - · 1959

Populal!cn- - · 1950

METHODS OF DOSE ESTIMATION.........
/',. / ;-:,...\

I /
' .

2,0

/// /

~..

//

I

4

/i

3

I

1.0

6. Various methods have been used to estimate thedose in air in the open from which the dose in specificorgans of the body may be deduced. These may besummarized as :(a) Direct measurements using ionization chambers
and counters mounted about 1 metre above the ground;( b) Indirect methods based on the determination of
the radio-active fall-out products in soil either by gammaray spectroscopy or by chemical analysis. The cumulative deposition may also be deduced through similar
analyses of fission products in rainfall, making allowance for radio-active decay;( c) Calculations based on the fission product yields
of nuclides and assumed residence times (paras. 12 and13).

Pop 'x106ll1O'--~...L...~......L.~~L....~...L...~-.1..~__:c=::::....l.._~_J

N

ao

~o

'o

20

o

20

40

so

so

Lailtudo

8

For both ( b) and ( c) above, one requires information regarding the dose from infinite plane sources of nuclides,

Figure L Geographical factor fall-out deposit

9.Ref'.
-

1,2

SWeden83• - • } UK norma.llsed••••••• May 1956
4

7

- - Japan

5

6

5

A

[\

4

I\

3

I·

I

2

I

l

1950

I(
1951

1952

1953

1954

1955

1956

1957

1958

1959

1960

years

Fiaure 2a. Direct measurements-external dose measurements (100 mrad/y = 11.4 µrad/hr)

348

1961

1962

9

Bef.
8

--Argonne

7,8--·New York

13

9 -11
x Leningrad (deduced)

7

•

UK

14

6

5

4

3

2
,.
"

\

~":-

x\

1

·~

x •
1950

1951

1952

1953

1954

1955

1956
years

1957

1958

1959

Figure 2b. Indirect measurements-external dose measurements (100 mrad/yallowing for the scatter and absorption in the air andsoil, and the relevant calculations of these are given inparagraphs 9-11.

1960

1961

1962

= 11.4 .arad/hr)

noted may be due to dry deposition of fall-out or to nonuniformity of site drainage.
9. To derive the values reported in figure 2b it isnecessary to deduce the dose-rate of the particulargamma-emitting radio-isotopes when they are uniformly spread on an infinite plane in the concentrations derived by gamma-spectroscopy or other methods.
These are based on calculations by several workers. 15• 211
The dose-rate in air due to a deposit FJ(t) of a certain
gamma-emitting radio-isotope (j) spread uniformly on
an infinite plane, can be considered as being governedby the relation :Direct determination
7. The most comprehensive survey has been carriedout in Sweden1 • 2 where high pressure ionization chambers have registered dose-rates from fission products
since 1951. Measurements have also been made elsewhere3-s using high pressure ionization chambers, geiger
counters and plastic scintillators, respectively. These
measurements are shown in figure 2a. The rapid fall in
the Japanese measurements in 1959 indicates that thesehigh levels were due to short-lived products.

dd~ 1 = k 1B1FJ(t) mrad/y

(1)

where

Indirect methods

d~i = dose-ratein airfrom thedeposit FJ(t) (mrad/y)

8. Many measurements&-13 using gamma-ray spectroscopy or chemical analysis have been reported andare shown in figure 2b. A comparison of figures 2a and2b shows that there is reasonable agreement between
direct and indirect estimates for the years 1954-1961.
The Swedish data1 • 2 are lower than the others, as themeasurements are made at a latitude higher than thatof the peak shown in figure 1. Pearson and Salmon12
have shown that calculations based on the cumulative
deposition in rainfall of Cs137 and Zr9 5 + Nb 95 give results which are 70 per cent of those obtained using
gamma-ray spectroscopy of soil, and other calculations
on the same data show closer agreement.14 The difference

k1=

dose-rate from primary radiation(mrad/y/mc/km2)

B1= ratio of total/primary radiation dose-rate(build-up factor)

FJ(t) = deposit of isotope j (mc/km 2 )The constants k 1 and B 1 have been considered for eachof the important radio-nuclides and quite a wide rangeof values has been reported (table I). The values incolumns 4 and 5 do not include the factor Bj and thevalues in column 6 have been chosen taking this into349

account. The variations in the values are due to: (a) the
variation of the gamma-ray spectrum used in deriving
the values for each nuclide; ( b) the values of the buildup factor and the methods of applying them; and ( c)the assumption made as to whether Zr 95 and its daughter
product Nb 95 are in secular equilibrium on the ground,or in a state of transient equilibrium.

s. 0

'

4

Ml!On time in the utmcspher~. weeks
I IO 12 14 16 18 20 22 '~4 2650
6\'

10. The determination of the build-up factor whichshould be used for each particular isotope has been based
mainly on the work of Goldstein et al. 21 However, certain experimental investigations have been carried out
using Cs137 and Co60 P• 23 Davis22 compared scintillation
counter measurements made about 1 m from the groundwith the theoretically derived dose-rates after correcting
for air absorption and build-up. The experimental values
were 6 and 16 per cent lower than the theoreticallyderived values for Cs187 and Co60 respectively. The variation of the build-up factor with altitude was also measured and gave values at 1 m from the ground, e."'\'.trapolated from about 100 m, of 0.8, 1.4 and 2.4 for P 31 , Cs137
and Co60 respectively. Solon 23 obtained a value of 1.25
for Co 60 from sources on the surface. Values of backscatter from a broad beam from infinite sources of theorder of 20 per cent for radiation in the range 0.4-1
MeV have been computed. 24 • 25

11. Lindel119 quotes a figure of build-up factor of 2
for Cs131 but this and other estimates are apparently all
based on a homogeneous medium, and do not take into
account the change of medium from earth to air. It would
seem that the value of 2 used by some workers for thebuild-up factor may be an over-estimate when fall-out
penetrates into the upper layers of the earth's surface.
However, Gustafson18 in his determinations has taken
account of both air absorption and the absorption by
the soil due to penetration of the isotopes into the upper
soil layers. The penetration of fall-out products into thesoil has been estimated on the basis of measurements
made in Chicago : 77 per cent activity for a depth up to
3.8 cm, 16 per cent for 3.8-7.6 cm and 7 per cent for
7.6-11.4 cm. Gustafson's method has been used toobtain the values for Sb125 , psi and Ba140 + La140 given
in table I. The constants given in table I are calculated
for a height above the ground equal to 1 m. The dose-ratechanges little with height, being about 15 per cent higher
at 0.5 m than at 1 m from the ground. 19
Theoretical calrnlations of the total external dose
12. From the values of table I and the concentrationsof individual nuclides on the ground the dose-rate fromeach nuclide may be estimated. The relative contributions to the total external dose from the nuclides present
on the ground depend upon:(a) The fission product yield of the particular nuclide. This may vary with both the fission element andthe neutron energy. The yields of some nuclides, especially Ru106 and Sb125 may vary by a factor of up to
25 (F I, table I) ;( b) The residence time in the atmosphere which determines whether any short-lived products that areformed at the time of the explosion will contribute to
the ground level gamma-ray dose.H As has been shownby Dunning26 (figure 3) the ratio of the dose due toshort-lived nuclides to the Cs181 dose over 30 years mayvary from 10 to 0.4, depending upon whether the residence time is two weeks or ten years. The dose contributions are equal if the mean residence time is about 2.6
years;

0...,.,

\
...

T

E

'

- ...

'

t--usa top ---.s.--riohl scoleII

u~ ~llomot>d·~.....,.1efl scale-.i>.,.

.."

~

u
10

~

.,,"

I

0

li.

....
·-...,"::

-- --

5.0

·~

.:.,,
1
j
U)

0J

0

2345678910
Mean time in the olmosphere, yeatS~

Figure 3. Theoretical relative 30-year doses for(short-lived fission products)/cesium-137( c) The gamma-ray energy as well as the half-lifeof the particular isotope. The energy will also determine
the relative importance of products present in the deeper
soil layers since the greater the energy the less the absorption within the soil ;(d) The latitudinal variation of fall-out. The distribution of fall-out from the troposphere is not the sameas that from the stratosphere (F I, 53).
13. To illustrate these effects on the dose at groundlevel, theoretical calculations of the dose-rates fromvarious nuclides at equilibrium have been carried out
for various atmospheric residence times. The yields given
by Katcoff21 for fast neutron fission of U 238 have been
assumed and the calculations are based on a constantfall-out rate of Sr00 of 2 me per km 2/y which is approximately the world average over the surface of the earth
for 1959. Assuming further that the rate of deposition ofCs137 is 1.7 times higher than that of Sr9° (FI, 81) andthat the geographical factor is 1.9, this leads to a world
population weighted mean fall-out rate of Cs137 in 1959
of approximately 6 me per km2/y. Table II gives thedose-rates in air which would arise from various nuclides
if this fall-out rate continued until equilibrium conditions are set up on the ground. It will be seen that the
shorter the atmospheric residence time the higher thedose-rate because of the effect of the short-lived products,
especially Zr 95
Nb95 • Concentrations equal to 90 per
cent of the equilibrium value will be reached in about one
year or so for most of these short-lived products, whereas
the equilibrium for Cs137 would only be reached after
33 or 100 years, depending on the assumption made as
to the effective half-life of Cs1 s7 on the ground.

+

FACTORS AFFECTING DOSE TO TISStJES

14. The doses reported so far give the external doserates measured in air. To estimate the actual doses thathave been received or will be received by individuals, thefollowing factors must be taken into consideration.

Weathering
15. Some of the fall-out material on the surface ofthe earth is transferred by rain into lower layers of soil
and also washed off hard surfaces such as roads andpavements. Measurements made in the United King350

dom14 showed that the slow penetration of Cs131 into
undisturbed soil reduced the external dose-rate by 20 to30 per cent over four to five years; thus the external
dose-rate decreased with an effective half-life of about
ten years. Agricultural procedures which cause fission
products to become uniformly mixed in the first 20 to 30
cm of soil will cause a considerable reduction in the total
external dose from Cs 137 but the dose will subsequently
decrease with the 30-year half-life of the nuclide. The
attenuation of the external exposure due to cultivation
is not however taken into account in this assessment.
The effect of weathering will not be so important in thecase of the short-lived fission products which will havedecayed before any appreciable penetration into the soil.
Snow will reduce the dose-rate of external radiation,and measurements carried out by Sievert2 are shown infigure 4. Calculations of this effect have also been carriedout.19,2s

17. The shielding factors may be slightly larger for
fall-out, as the average gamma energy from fall-out is
O.i Me V 33 • 3 ·1 whilst the energy from Co60 is 1.1-1.3
MeV. To estimate the reduction in daily dose due tothis shielding, an assumption must be made regarding thetime spent in and out of doors. According to the information given in the United Nations Demographic Yearbook, 1960, 35 it is estimated that one-third of the world's
population live in urban and two-thirds in rural communities. Assuming that the time spent out of doors isthree and nine hours per day, respectively, a world average time out of doors of 7 hours per day is obtained. A
shielding factor of 5 has been taken as the world averagevalue, and with an average time spent indoors of 17 hours
the over-all reduction of dose due to shielding has beentaken as 0:4.
Screening by the httman body
18. To obtain the doses received by different bodyorgans it is necessary to allow for the attenuation by
the intervening body tissues. Measurements conductedby Spiers 36 using sources over a 371' geometry gave values
as in table IV. This shows the screening factors tomarrow, testes, and ovary for different energies of radiation. The factors agreed well with those theoreticallyderived by O'Brien. 37 The values of the screening factor
for the gonads and bone marrow given in table IV are
sufficiently similar for the mean energy of fission products of 0.7 MeV to justify applying an average value of
0.6 both to gonads and to bone marrow.

Shielding by building structures

16. External radiation is absorbed by building materials, and therefore doses received inside buildings willbe less than those outside. This dose reduction factor
has been estimated by making measurements in manydifferent places inside buildings, whilst a Co60 source waspassed through a continuous polythene tube laid over theroof of and ground adjacent to several different typesof buildings. w- 31 Fixed arrays of cobalt and caesium
sources have also been used.H Table III shows the wide
range of shielding factors which have been experimentally derived and indicate the importance of thecontribution to the dose on the top floor of a building
due to the fall-out products on the roof.

Combined shielding and screening factors
19. The combined effect of shielding and screening
therefore produces a dose reduction factor of 0.2 which
Station A2

13

13

12

12

.
.
,'
.

11

11

,

c
E
E 10
c 8 ...

10

10

0

;;

"'

5
j

.~
c.

'u 4~

l!! 2 (/)

0...

11

1

21

Nov. 1960
Figure 4a. Variations of the dose-rate during thefalling of the snow

11

M~y 1961

21-

Figure 4b. Variations of the dose-rate during themelting of the snow layer

351

31

\Vill be used to convert air doses to doses to the gonads
and to the bone marrow. The value of 0.2 may be considered as a world average, and it must be emphasizedthat a wide range of values up to the maximum of 0.6
would obtain in particular countries, depending on thetypes of dwelling houses and the average time spent outof doors.

Combining the dose commitments from Cs 137 and shortlived products, the total dose commitment due to externalradiation would be 27 mrem and 30 mrem for testing
ending 1960 and 1961 respectively.

DosES DUE TO EXTERNAL SOURCES

24. (a) Caesium131 • From the continued testing conditions postulated in F I, 110 of 1 Mc Sr90 injected peryear and allowing for an effective half-life of 10 years
for Cs187 on the ground, an equilibrium deposit on the
ground would exist when the fall-out rate of Cs13T equals
the effective rate of removal of Cs137 from the superficial layer of the ground, i.e.
Fr=(µ+X)Fd(oo)whereµ= effective weathering constantX= radio-active transformation constant
Fd ( oo) = fall-out deposit averaged over the surface ofthe earth

20. Comparison of published reports on doses isdifficult owing to differing methods of calculation. The
dose and dose-rate from fall-out have been given either
from the total deposition on the ground or from theportion which has fallen out during a fixed period,
ignoring past depositions.
21. The doses reported in the following sections are
the population world average doses measured in air,and after presenting these the tissue doses will be derived
by applying the shielding and screening factor of 0.2.

Total extenuzl dose in air received from testingfrom 1954 to August 1961
22. The measurements of the total external dose in
Sweden and the United Kingdom given in figure 2ahave been used to derive a population weighted external
dose during this period. Graphical integration of thesecurves gives total air doses of 46 and 68 mrad respectively. These measurements were taken for areas inwhich the values for Fd/Fd were approximately 1.5 and
1.9 for Sweden and the United Kingdom respectively.
The mean population weighted external dose in air (forG = 1.9) is therefore 63 mrad during this period. The
total dose to the gonads and bone marrow during thisperiod is therefore 13 mrem.

Total external dose commitment from testing up to
the end of 1960 and the end of 1961
23. This estimate is made in two parts-the contribution from Cs 137 and from short-lived products.
(a) Caesium131 • The estimate of ground level concentration of Cs187 may be deduced from annex F,part I, figure 37, which shows the total Sr90 deposit on
the ground,* by using a relative yield factor for Cs137
of 1.7 and a geographical factor of 1.9. The air dose
received up to the end of 1960 from Cs187 iS therefore
10 mrad. Assuming an effective half-life of 10 years for
Cs 137 on the ground, the air dose received by m~dover all generations would be 80 and 92 mrad for testmg
ending in 1960 and 1961 respectively. The dose commitment for the gonads and bone marrow would therefore be 16 and 18 mrem for tests ending 1960 and 1961
respectively, and 92 and 94 per cent of these dose commitments would have been received by the year 2000.
(b) Short-lived products. It has been shown that the
air dose up to August 1961 was 63 mrad and that Cs187
contributed 10 mrad, therefore it may be assumed thatthe dose commitment from short-lived products is 53 X
0.2 = 10.6 r.J 11 mrem for testing up to the end of 1960.
The dose from short-lived products may be approximately calculated for further testing by using the ratiosof the yields of Sr90 • Therefore the short-lived contribution due to testing up to the end of 1%1, whenaccording to the proposed model a further 1 Mc of Sr90
had been injected, would be 10.6 X 7.6/6.6 ,_, 12 mrem.

* The Sr90 deposits have been estimated for a partial area ofthe earth of 471 X 106 sq km. F I, table XIV.

Total external dose commitment which would bereceived imder conditions of continued testingi.e., 3.4 = -~~ F c1 ( oo)3

Therefore F 4 ( oo ) = 49 mc/km2
Assuming that the geographical factor is 1.9 and thatthe external dose rate from 1 mcflan2 of Cs 137 is 0.12
mrad/y, the air dose-rate would be 11 mrad/y. Therefore the dose commitment due to one year's testing would
be 2.2 mrem (H 48).
(b) Short-lived products. The dose commitment of
10.6 mrem has been received (paragraph 23) from theinjection of 6.6 Mc Sr90 and therefore the annual injection of 1 Mc Sr9° will give a dose commitment of 1.6
mrem from short-lived external deposit. No weatheringfactor needs to be used.
25. Therefore the total dose commitment from external radiation per year of testing is 3.8 mrem. It should
be noted that the dose from short-lived products isreceived in the immediately following years whereas thedose from Cs 137 will extend over many years (table V).

m. Internal exposure
26. Three types of internal exposure must be considered:{a) Ingested radio-nuclides which are absorbed fromthe gastro-intestinal tract. The important fission products
from this viewpoint are Sr90 and Cs137 and the sbortlived radio-nuclides Sr89 , Ba140 and 1131 • The manner inwhich they are absorbed and retained in the body is discussed in annex F, part II, paragraphs 2. 9-12, 31-36,
130-132, 153-154. In addition to fission products, theneutron induced radio-nuclides cu and H 3 must be considered, although the latter is of less importance;( b) Ingested radio-nuclides in passage through thegastro-intestinal tract. These comprise those radionuclides which are either not, or only partially, absorbed,
and which cause irradiation of the mucosa! lining of
the GI tract;( c) Inhaled radio-active particles. These \Vill be deposited, depending on their size, into the upper or lower
portions of the lungs where, if they are not removedby exhalation or ciliary action, they will irradiate thelung tissue and particularly those cells in the immediateneighbourhood.
352

INGESTED RADIO-NUCLIDES

27. The appropriate basis for assessing tht? exposureof populations is discussed in anne.--< H. ~ hnear do~erelationship is assumed; .thus the mean tt~sue dose !sused for estimating the nsk to the population. On thisbasis the variation between individuals need not be considered. Ho\vever, this would become important if athreshold concept were accepted. 58 Information on variability in intakes of Sr 90 and Cs137 is given in annex F,part II, paragraphs 51-61. T.he pro~lems associated "":ithlong-term retention and distnbut10n. of. bone-seeki?gradio-nuclides in the skeleton, and with mhomogeneityof dose in individual bones are discussed in annex H.
Observed variations in the concentration of Sr90 withage and in individual bones of the adult skeleton are
described in annex F, part II, paragraphs 82-84.

Strontitem-90
Concentrations in diet and bone
28. The data available up to the present time on theconcentration of Sr90 in bone in children up to four yearsof age (F II, 80-89, tables XX, XXI) h~ve been take!1 torepresent the concentration in new bone m the population.
It has been shown (F II, 31-36, 90, 91, table XXIV)
that the ratio of Sr90 to calcium in this bone is about
one quarter of that in diet. The OR (bone/di~t) is. therefore taken as 0.25. Hence future concentrations m newbone can be derived from the predicted levels in diet
(F II, 103-107, 120, 121) which have been calculated
from the models described previously (F I, 110).
Dose from Sr90 in bone
29. Several theoretical estimations of the dose received
in bone and bone marrow from 1 µ.µ.c of Sr90 per gramof calcium have been reported, 39- 45 These show that thedose to compact bone is about 2.7 mrem/y.. The dos~­
rate at various distances from bone surfaces is shown mfigure 5. For the purpose of the estimation of the f3. doseto cells lining bone surfaces it has been assumed m thepresent report that the f3 dos; re~eived is one hal! of the
f3 dose within bone. The estimation ~f the_ dose m_bi;memarrow cavities due to the incorporation ot a µ-em1tt1?gnuclide in the surrounding bone is complex. The energiesof the f3 particles are distributed over a broad spectrum,and for each energy a specific range in bone and }n soft
tissues or a combination of the two must be considered.
The dose to the bone marrow also depends on the sizeof the marrow cavity and of the bone trabeculae. Whenthe thicknesses of the trabeculae are less than the rangeof the f3 particles, electronic equilibrium conditions within the bone will not exist. The mean size of the marrowcavities in different bones varies, depending on the site,
between 400-700 µ. \vith maximum sizes as large as 1 mm
in the vertebral bodies ...-i Table VI shows the comparisonof bone marrow doses to bone doses for a 500 µ. marrowcavity and three different trabeculae thicknesses. For
Sra 0 + yuo the mean value of the ratio bone marrow
dose: compact bone dose for this size of marrow space
is taken as 0.25. and the dose to bone marrow from 1 µ.µ.c
Sr90/g calcium is taken as 0.7 mrem/y.

Met hod of estimation of mean population dose
30. Methods of estimation of the mean populationdose due to long-term ingestion of Sr90 have been reported.19• 2 s. ' 7· ' 8 The estimation of mean pop~lation
weighted doses to th: above tiss_ues has.been earned out
on the following basis. The maJOr portion of the strontium is laid down during the growth years 0-20 and once
deposited remains fixed after about the age of 2, except
for the turnover of 1-10%/y due to exchange processes
and bone resorption (F II, 81). Sr90 i;icorporated in theearly years will therefore decay, leadm~ !o a to~l doselower than if a constant new bone acbv1ty durmg thewhole of the life is assumed. A factor F, called the dose
increment factor is introduced to take into account therate of bone acc;etion and the radio-active decay of thenuclide. The factor F for Sr90 has been derive~ by
Lindell,19 and figure 6 shows the val1;1es for various
conditions of bone growth and resorption. A value of
F = 0.6 is used in this report for Sr9°, representing the
average value of the resorptio~ ra~e~. Therefore ~e bonedose actually received by an md1vidual over his wholeF'lOM

1111 k0 • ~Sr•Ill ka•~••o.y,..,.

F;o
u

0

211

40

60,....

021)•go ol~F.,oMId) k.·

lfsr• 02.Q

0Figure 6. The dose increment factor F,.(u) ~oran expected life span of 70 years, as a functionof age of uptake.
(a) Extreme case of instantaneous equilibrium
between bone and environmental Sr90 , with
infinite turnover constant.
(b) Biological half life for Sr and Ca assumed
to be 7 years (ks,=0.1/year).
(c) Biological half life for Sr and Ca assumed
to be 50 years (ks,=0.014/year). Note theincreasing importance of uptake and ret~­tion in childhood, and the reduced uptake m
the adult.
(d) Essentially no Sr and Ca turn-over. Uptake
only d~ring bone growth in childhood.

BONE
MARROW
500
IHTERSPACE MICRONS

1000

Fig1ire S. Central dose rates for in~nite s~dwich c;if bone slabs
labelled with Sr9o, interleaved w1tp d micron thick sheets.. ofbone marrow.-H The full lines give the date of En_gstrom,
Bjiirnerstedt, Clemedson and Nelso11,• 6 the dotted hnes thedata of Libby• 5353

lifetime, assuming a constant contamination, may be
deduced from the following expression which also gives
the dose commitment from any given pattern of contamination.

De = F"Y J~ c(t) dt

(2)

where
D, =total dose in mrem
F = dose increment factor (assumed average value 0.6)
"Y
= dose-rate for unit concentration (2. 7 mrem/y /µ.µ.c Sr9°/g Ca to bone, 0.7 mrem/y/µ.µ.c Sr'°/g Ca to bone marrow)c(t) = Ratio Sr90/Ca in the salts entering bone (µ.µ.c
Sr90jg Ca, assumed equal to 0.25 X diet concentration)
31. Estimates of doses from Sr90 are based on data
to be found in other sections of this annex. The total
depositions and fall-out rates arising after various
periods of testing are shown in annex F, part I, figures
37 and 38 respectively. The levels of Sr110 in bone in
the years 1954-1960 are reported in annex F, part II,
tables XX and XXIV. Future concentration in the three
types of diet and in bone are given in annex F, part II,
paragraph 121, and are based on the proportionality
factors given in annex F, part II, table XXVII, and thefuture levels of Sr9° fall-out rate and deposit, assumingthat for the latter there will be a 2%/y reduction due
to the effects of weathering and agricultural procedures
and to the removal of strontium from the soil by crops(F II, 120).
Dose commitment from Sr90 due to testing carried out
up to the end of 1960 and the end of 1961

32. The bone dose received up to August 1961 has
been estimated on the basis of the population weighted
average values of the Sr90 to calcium ratio in the bonesof children up to four years of age for each year from
1959-1960. These values have been calculated from thedata of annex F, part II, table XX, and are given intable VII. Allowance has been made for the number ofsamples and the populations represented. The approximate nature of these values, in view of the large populations unrepresented, or represented by very few values,
must however be recognized. The contribution to thedose commitment-formula (2)-received by bone cells
is 12 mrem, by cells lining bone surfaces 6 mrem, andby the bone marrow 3 mrem.

~ N

so

U,5

'I
I

l

0

{0

10

(1
~

.....,

f

I
l

i..

30

!

,0

~

10

f.S

i3

.£

~

l..

1941

g
g

~:

u

...
Cl

~

0

asa

195ll

1'10

1910

lffO

1000

Eqodlibrl=> n1..

0[

Figure 7. Population weighted concentrations of Sreo in diet andbone for testing up to the end of 1960 and to the end of 1961
X Measured Sr 00 in the bones of children
0-4 years old (F II, table XX)

34. The dose commitments to bone cells, to cells liningbone surfaces, and to the bone marrow, have been calculated using formula (2) and the graphically integrated
curve of bone concentration given in figure 7. \Vhen combined with the contribution to the dose commitment derived from measured data up to 1960 (para. 32), thedose commitments to bone cells, cells lining bone surfaces
and bone marrow are 133, 67, and 33 respectively, for
testing up to the end of 1960. The dose commitments
are 158, 79, and 40, respectively, for testing carried out
up to the end of 1961 at the assumed rate. By the year
2000 some 91 and 92 per cent of the dose commitment
would have been reached for tests ending in 1960 and1961 respectively.
Dose commitment from Sr 90 which would be received
under conditions of continued testing
35. The population weighted world average concentration in diet and bone resulting from continued testinghas been calculated from the predicted levels in thethree approximate model diets using the method described previously, and is given in figure 7.

36. The dose commitment from one year of testing
to bone cells, to cells lining bone surfaces, and to thebone marrow would be 21, 11 and 5 mrem, respectively.
The dose commitments from Sr90 for the three conditionsof testing are summarized in table XL

33. Future levels of Sr90 in the approximate model
diets are given in annex F, part II, paragraph 120, fortests up to 1960 and 1961. From these a world average
concentration has been obtained by weighting the values
for each diet by population and geographical distribution,
assuming that the latitudinal distribution of fall-out will
repeat the pattern observed so far. The diet types for
populations and the F .i/Fd ratios used are shown intable VIII. Obviously some gross assumptions have had
to be made in view of the lack of more exact information,
but it may be noted that the values of concentration
calculated for different diets do not differ by more thana factor of 2 (F II, figure 6). The population weighted
average diet is derived by adding together for each dietthe values obtained by the following formula:::!:: N1 X

The composite population weighted diet and the corresponding bone concentrations in different years are
given in figure 7.

Cs1 17 in whole body and bone

37. The biological half-life of Cs131 is four months,
and therefore the body will reach an equilibrium withthe diet after a few months' delay. The distribution isreasonably uniform throughout the whole of the soft
tissues, but a slightly higher concentration in bone has
been observed ( F II, 130-133, 140-145). Dose estimates
are therefore required both for the gonad dose and forthe bone and bone marrow dose. Measurements• 9 of thecontent of Cs 137 in specimens from 114 subjects haveshown a ratio of 2.2 between bone (including marrow)and muscle. This higher concentration of Cs 137 in boneleads to a bone marrow dose 30 per cent higher than soft
tissue doses if the same model of marrow cavity size
as in paragraph 29 is used. The difference in concentration, however, has not been confirmed in other repo.rts.

Fd/ff'.i Concentrat1on. D"1et1·where N 1 is population given in table VIII, column 3,
and FJF'd, given in column 4, is defined in paragraph 4.
354

38. The dose calculations may be carried out in termsof the dose-rate from 1 p.p.c Cs 187/g of soft tissue or thatfrom 1 p.µ.c Cs131/g of potassium. Values have been reported for the former in the range 7.3-11 mrem/19 • 28 • 60
and a mean value of 10 mrem/y will be used in thepresent report. The differences between these figures arc
due to the method of calculation of the gamma-ray contribution to the body dose. The dose-rates to bone cells
and to bone marrow are therefore 22 and 13 mrem/y on
the basis of the measurements reported49 and the dose tocells lining bone surfaces has been taken as 18 mrem/y.
Since there are about 140 g of potassium in a 70 kg man,
1 p.µ.c Cs 137/g potassium will deliver 0.044, 0.036 and0.026 mrem/y to bone cells, cells lining bone surfaces
and bone marrow respectively.
Dose commitment from internal exposure to Cs d1te to
testing up to the end of 1960 and the end of 1961
131

39. The mean value of the whole body measurements
for the years 1958-1960 was 60 p.p.c Cs137/g K (F II, table
XXXIII). Assuming that this level had been maintainedfor five years, the contribution to the dose commitment
to bone cells, cells lining bone surfaces, bone marrow,and to the gonads are 13, 11, 8 and 6 mrem respectively.

paragraph 82. The average dose to the whole body is
1.06 mrem/y, and, as a consequence of their different
carbon contents, the dose to bone is 1.64 mrem/y andthat to soft tissue 0.71 mrem/y. Therefore the dose produced by a known amount of ea formed during weapon
testing may be estimated by direct comparison with therates of production of naturally occurring ci. and withthe resulting doses.47• 51 - 5 • The dose commitment, which
may be estimated with reasonable accuracy this way,,'
will be received over many generations, as the mean lifeof C14 is 8,000 years, but estimates of the dose to thisgeneration necessitate the use of the limited data described in annex F, part I, paragraph 118, regarding
the distribution of C14 in nature.
43. The dose-rate r from N 1 atoms of artificially produced O• in reservoir I (i.e., the atmosphere and surface
waters of the ocean) therefore will beNIQ
r = ro -N = ~ f(t)
(3)
lo

N10

where
r 0 = annual dose from naturally occurring C 14
N 10 = number of C 14 atoms in reservoir I= 86 x 1027 atoms c 1•
Q = number of atoms formedf(t) = distribution of C 14 into the other ( 14 reservoirs
with time

40. With a discontinuation of the tests, the levels of
Cs 137 in the body would be expected to decline in a man·ner similar to that observed in late 1959 and in 1960
( F II, 146-149). By extrapolation from the data in annex
F, part II, figure 8, it can be estimated that the concentration of Cs137 in the body will be reduced to one-tenthin about 3 years after the cessation of tests. This corresponds to an effective mean life of Cs137 of 1.4 years.
Therefore the dose commitment from Cs137 for testing
up to the end of 1960 was 17, 14, 10 and 8 mrem forbone cells, cells lining bone surfaces, bone marrow andgonads, respectively. The dose commitment from testing
up to the end of 1961 may be estimated by adding thedose commitment from one year of testing to thesevalues (para. 41).

Therefore the dose in a given time t may be obtainedby integration(4)
J~ f(t)dt is expressed algebraically in F I, 118, on thebasis of the observed distribution of cu innature.

Dose commitment from ea dtte to testing up to the endof 1960 and the end of 1961

44. The total C1 4 formed by weapon testing up to
August 196:yis estimated as 22 X 1027 atoms (FI, table
XVII). Therefore the dose commitment may be calculated from the naturally occurring C1 4 formation rateand consequent dose-rates. Using the symbols given inparagraph 43

Dose commitment from internal exposure to Cs 131 1,nderconditions of continued testing
41. In anne..""C F, part II, paragraph 150, limits havebeen set to the magnitude of the resultant internal radi~­tion dose in relation to the external dose from thisnuclide. The dose commitment for internal Cs137 fromone year of testing is assumed to be equal to

D . . = r 0 Q.
{3

Cs 137 deposit at equilibrium
csm deposit 1959

(5)

42. The natural rate of formation of CH is 3.22 X 1028
atoms C14/y. The radiation doses to tissues from naturally occurring CH in nature are given in annex E,

where f3 = 3.22 X 1026 atoms C1'/y. Therefore the dose
commitment due to testing up to the end of 1960 to thebone cells, cells lining bone surfaces, bone i:iarrow .an.d
gonads is 111, 80, 48 and 48 mrem respectively. S1m1larly, the dose commitment due to testing to the end of1961 when, according to the model, a further 1028 C1'
atoms have been injected, would be 162, 116, 70 and
70 mrem respectively to the same tissues. The portionof the dose commitment received in any period of time_,
may be estimated by using formula ( 4). It is shown inannex F, part I, paragraph 118, that for an injection of
22 X 1027 atoms this equation is as follows:This expression can only be C."'{pected to give approximate values, as it is based on a highly simplified modelof the transport of the C14 in the atmosphere and oceans.
The gonad dose given by formula (6), which will be_Internal Cs137 dose 19~9 X

The dose commitment from one year of testing is therefore 6.6, 5.3, 3.9, 3.1 mrem for bone cells, cells liningbone surfaces, bone marrow and gonads.
C 1.. in whole body355

received by the year 2000, is 5 mrem, i.e., 10 per cent of
the dose commitment.

Dose commitment fromci' due to continued testing

45. Under conditions of continued testing/it is assumed in annex F, part I, paragraph 119, that 10 28 C14
atoms are injected annually. From one such injection thedose commitment is 51, 37, 22, 22 mrem to the bone cells,
cells lining bone surfaces, bone marrow and gonads respectively. Only 10 per cent of this dose however will
be received in the next fifty years.

ci

Reductio1i of dose from 4 due to combustion of fttels
46. The increasing combustion of fossilized fuels,
such as oil and coal, results in a reduction in the specificactivity of the C1 4 in the atmosphere due to the additionof "C14 -free" carbon dioxide. This effect is called theSuess effect and is described in annex F, part I, paragraph 68.
47. According to Suess 55 the average rate of combustion of these fuels since 1950 is 82 X 1011 kg/y. Thisrate is increasing with a doubling time of 20 years sothat by the year 2000 the rate may be 5-6 times higher.
48. The total C0 2 content of the atmosphw/is 21 X
1014 kg, and, since the start of industrial co;/ combustion, some 14 per cent of this amount has been injected
into the atmosphere. With the above input rates).t isestimated that the total amount of carbon added by theyear 2ooq :will be 50 per cent of the atmospheric reservoir. The average residence time given by Suess for a
carbon atom in the atmosphere is only 10 years before
it is transferred to the ocean. Therefore the present decrease in specific activity of the atmosphere due to thiscause is only about 2 per cent which corresponds to a
total input of 14 per cent. By integration, it is calculated
that the decrease in specie activity by the year 2000
will be about 6 per cent corresponding to the 50 per centtotal input. This effect would therefore cause a corresponding reduction in the gonad doses from C14 which
may be received by the year 2000.

H' in the body
49. The natural level of tritium in water is 5 X l0-18
tritium atoms per hydrogen atom, and the soft tissue
dose corresponding to this level is 1.8 X l<r3 mrem/y.
Tritium is formed in the process of the explosion of afusion type weapon (FI, 18). On several occasions since
1953, in the northern hemisphere the tropospheric concentration of tritium in rain water56- 59 has been obsen•ed
to be approximately a hundred times greater than thenormal. However, these levels are greatly reduced bydilution in the mixed surface layers of the ocean. Thiseffect, as well as the relative· short half-life of 12 years
and the low energy beta-radiation of tritium, accounts
for the dose levels to soft tissue being very low. 41

the estimated levels of these nuclides in the diet.
sru in bone

51. Because the metabolism of Sr89 is the same as thatof Sr110 , the radiation dose from Sr89 can be estimatedfrom that for Sr90 on the basis of the ratio of the two
nuclides in diet and the relative magnitude of the tissue
doses caused by the ingestion of 1 µ.c of each nuclide.
52. The radiation dose-rate from 1 p.p.c Sr89/g Ca
maintained in bone is 1.5 mrem/y and 0.33 mrem/y tobone marrow. This latter value is interpolated from thedata given by Bjomerstedt46 who showed that for a 0.5
MeV ~-emitter the average dose to bone marrow is
17 per cent of the dose to bone, whilst for Sr90
Y 90
it is 25 per cent (para. 29). The mean dose increment
factor F for Sr8' is .005.
53. During the years 1955-1960 the mean concentration of Sr9° in bone was 1.3 µµc/g Ca and the averageworld concentration of Sr89 in rainfall was about ten
times that of Sr00 • 65 The Sr89/Sr>° ratio in milk measured in the United Kingdom, Canada and the UnitedStates during 1958 showed that the activity in milk
approached half of that in rain. 64 Assuming the level inmilk corresponds to that in diet type I, and that the concentration in bone depends mainly on the rate of fall-out,
the total dose can be calculated from formula (2) (para.
30) for the years 1954-1960 in which 6.6 Mc Sr90 were
injected into the stratosphere. The resulting population
weighted dose to bone due to Sr9 9 from an injection of
1 Mc Sr9° would be 0.05 mrem and that to bone marrow
0.01 mrem. These values represent the dose commitment
from Sr 89 since the total dose from this isotope is received in one year. They are less than 1 per cent of thedose commitment from Sr90 •54. There are very few data on the Sr8 9/Sr9° ratio inbone. A series of United Kingdom measurements forthe latter half of 1957 showed an average value of 2.3
for post-mortem specimens from some 60 children inage range 0-4 years. 65 At the time of death the resulting
dose-rate from Sr8 9 in this bone was therefore approximately equal to that from Sr 0 • In view of the ratios of
their half-lives, the dose commitment for Sr8° would
thus be less than 1 per cent of that for Sr9°. This is inreasonable conformity with the dietary estimates givenin the previous paragraph.

+

Ba140 and Lauo in bone
55. Since the metabolism of barium is very similar
to that of strontium, the dose to bone from Ba140 and
La140 can be considered in the manner adopted for Sr89
in paragraph 53. The fission yields of Ba140 and Sr89 arevery similar, although the disintegration energy of
BaH0 + l..a140 is about twice that of Sr8 9 • However, theuptake of barium from the GI tract both in the cow andin man is much smaller than that for strontium and theshorter half-life will make for greater decay before its
entry into diet. 61 • 6 ' On account of these considerations,the dose commitment from Ba140
La140 is much
9
smaller than that from Sr8 and is accordingly neglected.

Short-lived isotopes+

50. Consideration is given here to the doses to the
GI tract, to the lungs, as well as to the concentrations in
the body of SrS 9 , BaH 0
La140 and l1 31 • 60-e 2 These have
half-lives of 51, 12. 8 days respectively. The concentrations of the short-lived isotopes in milk follow the pattern of weapons testing (F II, 151-155) but vary depending on the time involved between the explosion and contamination of the vegetation. The available informationon the levels of short-lived fission products in man is not
sufficient for accurate estimation of the radiation doses.
Many of the following dose calculations are based on+

Jm in thyroid

56. Measurable levels of P 31 have been found in the
thyroid glands of man and animals soon after the detonation of nuclear weapons. 6 s- 7o !1 31 enters the body
mainly in fresh foods; milk is the predominant source
in many areas. As a result of tests conducted in theautumn of 1961, the average concentrations in milk
produced in the United Kingdom 11 and the United
356

States 72 • 7 3 were 110 and 135 p.p.c/1 respectively over a
period of ten weeks. Thereafter the levels declined rapidly (F II, figure 11).

that the dose to the lower large intestine from this cause
is negligible.
61. An alternative approach would be to use the factthat during 1958-1959 in the United Kingdom less than
10 per cent of the body intake of Sr 90 arose from contamination of water and air. If it is assumed that the:ntake of strontium arising from air and water was accompanied by mixed fission products of age greater than
one month. the dose to the GI tract can be computed by
the method of Greitz 75 as about 1 mrem/y. This value
is in conformity with that derived in the previous paragraph.

57. The radiation dose to the thyroid varies greatly
depending on the age of the subject and the nature of
the diet. Because of their higher absorption of iodine
and of the smaller size of their thyroid glands infantsreceive a considerably larger dose than adults from thesame intake of !1 31 .1" Furthermore. if infants are fed on
fresh milk, their intake of 1131 may exceed that of adults.
However, even in countries where milk is a major component of their diet, many children are fed largely or
entirely on prepared milk products in which the 11 31 will
have decayed so that the exposure of their thyroid glands
is correspondingly reduced.

58. The pattern of distribution of short-lived activities
is very different from that of long-lived materials andconsideration is here confined to areas where the deposition of iodine is appreciable. Moreover. the pattern ofdeposition of iodine may be very different for different
conditions of explosion. For reasons explained in annex
F, part I, paragraph 37, it is assumed that the patternof deposition of !1 31 observed in the autumn of 1961
will occur with each annual injection of 1 Mc Sr90 . Thisdeposition led to a mean level of 125 p.p.cjl, as averaged
over a period of ten weeks in the United States and theUnited Kingdom, and this figure is used as a basis forcalculation (table IX). Children under the age of one
year who consumed 0.5 litre per day of fresh milk may
have received a total dose of about 170 mrem, while
adults taking half this quantity of milk have received
only 4 mrem. In some countries the intake of fresh milk
by young children appreciably exceeds the value assumed
in table IX though elsewhere their intake is considerably
lower.

ENTRY OF RADIO-ACTIVITY INTO THE BODY THROUGHINHALATION

62. The average daily inhalation of certain fission
products in the United Kingdom during the years 19571960 is given in table X 14 and the concentration in groundlevel air is presented in anne..'C F, part I, figures 10 and
11. The average daily amounts of Cem, Ce1 "" and Zr95
inhaled in March to June 1958 have been reported as
8.8, 6.6 and 8.9 p.p.c respectively. 76- 78
63. When particles are inhaled into tht lungs. someare exhaled again, whilst of the remaining ones the larger
are mainly swallowed and ingested and the finer may beretained within the lung tissues for considerable periodsof time. Knowledge of their movement within the lungs,
however. is very limited. Because of the small range of/3-rays, very high doses occur in tissue in contact withthese particles. 70
64. The average dose-rates to the lungs may be deduced following the approach used by the ICRP. 50 The
average dose to the lungs from the concentrations ofCe141 , Ce1H and Zr95 reported above would be 0.14, 2.6
and 0.7 mrem/y respectively. From the world average
concentration of Sr90 in ground level air (FI, 56) the annual dose-rate would be about 1 mrem/y. Analyses of an'.lmber of post-mortem specimens 80 • 51 showed in 1959
that lungs contained total activities of Zr95 , Ru103 , Ce1 H
of 0.36, 0.6 and 0.02 p.p.c/g respectively. These would
give average dose-rates to the lungs of 3.2, 1.3 and .05
rr.rem/y respectively.

Mixed fission products in the GI tract
59. The dose to the GI tract is determined by thequantity of fission products entering the body by ingestion and inhalation. No direct measurements of thisquantity are available, however. Some gamma spectrometer measurements of faecal samples74 were carriedout in the United Kingdom in April-May 1959, which
was the period of highest fall-out contamination in air
in that year. The United Kingdom measurements showed
an average daily excretion of 150 p.p.c/day in214 g faeces
in addition to the total natural potassium activity of
577 p.p.c/day. Allowing for there being some beta-active
nuclides that are not gamma-emitters, the dose-rate in the
faecal material would be about 10 p.rad/day and about
half this for the adjacent tissue in the lower large intestine, which is the part of the GI tract sustaining thegreatest dose. The estimated excretion of Zr9 \ which is
not appreciably taken up through the GI tract, was
10 p.p.c/day and it is noteworthy that the average inhalation of this isotope over the period January-June 1959
was 12 µ.p.c/day. During this period also the total inhalation averaged 100 µ.µ.c/day beta activity compared withthe estimated e..'Ccretion of 150 p.p.c/day of gamma activity in the two-week period of the measurements; theintake during this period may well have been higher
than the av;erage.

65. A dose-rate to the lungs of 5 mrem/y may occur
during periods of testing but further information isrequired to obtain the average dose over prolonged
periods of time.
66. Some measurements have also been made of concentrations in pulmonary lymph nodes,1 4 and concentrations 12-64 times those of lung tissue have been rep-0rted.81
Su~n!ARY OF RADIATION DOSES TO TISSUESDUE TO FALL-OUT

67. Table XI shows the dose commitments to the population (H 15-21) for the periods of testing 1954-1960
and 1954-1961. respectively. The values for these two
periods differ owing to the assumption made in the illustrative model proposed in annex F, part I, paragraphs
110 and 119 that an injection of 11k Sr9° and the formation of 1028 atoms of C1 4 occurred in the year 1%1. The
fraction of the dose commitment reached by the year
2000 is also given. This fraction represents the dose
received by a particular tissue to that date plus the dosethat will be received from radio-active materials which

60. The measurements suggest that the dose-rate to
the lower large intestine was less than 2 mrem/y during
this period of very high air contamination, and that the
average dose over the five-year period 1955-1959 wasless than 1 mrem per year. These calculations suggest
357

are already incorporated within the tissue. It excludes
however any dose due to radio-active materials in theenvironment which have not yet been incorporated into
body tissues. The last column of the table gives the dose
commitments due to one year's injection according to
the proposed model. These may therefore be used as

TABLE l.

units to derive dose commitments from a given practiceof testing when the actual injections of Sr90 and formation of C14 are known. The values given in the table must
be considered as indicative rather than as accurate estimates because of the many assumptions on which their
computation rests.

PRODUCT OF GAMMA-RAY DOSE CONSTANTS ki X Bi FOR CERTAIN
RADIO-ISOTOPES BY VARIOUS WORKERS

k; X Bi in mradb Per mc/Jmi>

Lou:it"et al.

Mahmoud' ..

0.129
0.137
(0.46)
0.091
0.031

0.082
0.085
(0.29)
0.055
0.018

0.35

0.11

0.06

0.077

0.008
0.009

0.008
0.003

0.008

IsotopeZr•:~· · · · · · · · · · • · · · · ·}o.14**
Nb ....•............

+°" ..........•.....•

Zr95
NbH•** ........ .
Ruto3 .•....•...•...... 0.046
Ru 1
0.019
SbtU .. : ............... 1m ..••...............

Collins,,.
et al.

0.5
0.1
0.04
0.06
0.05
0.12
0.13
0.03
0.01
0.01

0.025

-

Csll 7 •• , ••••••••••••••• 0.056
Ba1'°La1'°. . . . . . . . . . eeu1 ••••.............. 0.005
Ce"' ................. 0.004++• Does not include contribution due to build-up factor, i.e., values are fork; only.

** Contribution due to 1 me Zr'6 plus 1 me Nb111•*** Contribution due to 1 me Zr" plus 2.4 me Nb" (transient equilibrium conditions).

TABLE II.

AIR DOSE-RATES AT 1 !l!ETRE FRO!\! GROUND FRO!\! RADIO·NUCLIDES IN EQUIUBRIUM FOR V..\RIOUS
ATMOSPHERIC RESIDENCE TIMES AND CONSTANT Csl3T FALL-OUT RATE OF 6 mcjkm=/y.

AlmosplierU:
residence time

mrem/yHalfdays

Mean-

'ears

Zr"-"111095

RulP

Ru'"

Sb.,._

25 ...............
63 ...............
126 ...............
247 ...............
2.5y ..............

0.1
0.25
0.5
1.0
3.6

85.7
45.5
17.3
2.5

15.7
5.8
1.2
0.5

4.3
3.9
3.3
2.3
0.4

0.58
0.55
0.51
0.43
0.18

0.3

0.6

0.4

3.3

6.7

0.07

903 equilibrium
set up after years

ee•«
5.3
0.3

0.12

1.7

1.7

0.7
0.1

1.6
1.3
0.8
0.1

0.3

2.6

Total

Cs!Sl

"'']

31.2.
or
12

58.4
23.7
6.5
0.7

100 or
33•**The value used for the yield of Sbl!.5 is 0.24 which is a meanvalue of the yield between the fission neutron and 14 l\IeV neutron
fission of um (FI, table I).

*These values depend on whether a 30 y or a 10 y half-life isassumed fori.e., if weathering is not or is allowed for. The
equilibrium concentrations would be 261 and 97 mc/km1 respectively.

esw,

358

TABLE III.

SHIU..DING FACTORS

Wall thickness

Large buiUJingio•

Basement
FirsttSecondThird

Roof lhick,.,,ss

41cm concrete
20cm concrete 11 cm
brick
20cm concrete 11 cm
brick
20cm concrete 11 cm
brick

500-10,000
80-100200-300
250

Floor directly
under roof

20cm concrete
5cm insulation
10cm concrete
5cm insulation

HousesConcrete blockit
Brick14
Cemesto and woodll ..

100
50

Basement
Firstt? 15crn concrete

Basement

4cm concrete and2.5cm asphalt paper

1.3cm wood, or
4cm wood above
windows
5cm wood

2.5cm insulation
1.3cm plaster14
3.9
8-35 (av. 20)
12.2

22cm brickFirsttWood frame 11•••

Basement
Firstt2.5
13
2.5

Light shielding
Japanese house=

1-2

t The first floor is the floor at ground level or just above incase of semi-basement house.
•Average conditions exist beyond 8 ft. from inner surface exterior wall. Dose rate X 5-10 times hi~her inside of window opening + 2 on first floor below window-sill level.
TABLE**Average of 4 houses assuming contribution from infinity.
•••Average of two houses.
pi;~fl...-;
No~: The effect of sloping ground has little effect on theshielding factors. The effect of having sources close to buildings
only, ignoring remote sources, increases the figures up to plus.:.1.

IV.

5ou:ENING FACTORS OF THE HUMAN BODY DETERYI:t."EDBY 3-:r GEOMETRY WITH OMNIDIRECTIONAL RADIATION
MeV

o.z

o.s

J.D

J.S

Z.D

Marrow ............ 0.57
Testes .••..••.•..•.. 0.5 7
Ovary ............•. 0.47

0.61
0.61
0.50

0.65
0.67
0.56

0.69
0.73
0.61

0.75
0.78
0.66

TABLE V.

POPULATION WEIGHTED GON.-ill AND BONE-MARROW DOSES (ASSUMED EQUAL) DUE TO
EXTER..'\'AL RADIATION FROM FALL-OUT (G= 1.9)

Doses received from 1954-August 1961 (based on
measurements). . . . . . . . . . . . . . . • . . . . • . . . . . . . • . . .
Estimated dose commitment from testing up to theend of 1960...................................
Fraction by year 2000. . . . • . . . . . . . . . . . . . . . . . .
Estimated dose commitment from testing up to theend of 1961...................................
Fraction by year 2000. . . • . . . . . . . . . . . . • . . • • . .
Total dose received by mankind in all generations per
year of testing (1 Mc Sr"/y)...................

TABLE VI.

csm

Short-lired
mrem

mrem

Total
mrem

11

2

13

11
1.0

16
0.94

27
0.97

12
1.0

18
0.92

30
0.95

1.6

2.2

3.8

RATIO OF MARROW DOSE TO BONE DOSE FOR BONE CONTAINING Srso
Thicknessof trabeadae

500"'
500"'
SOOµ

70 µ.
125 µ.
100 µ.

0.23
0.26
0.28-0.31

359

Bjornerstedt (Theoretical) 15
Spiers (Experimenta1) 39
Libby (Theoretical) 41

TABLE VII.

THE CONCENTRATION OF Srso IN 0-4 y OLD BONE BASED ox
ANNEX F, PART II, '!'ABLExxµµc/g Ca

ppc/gCa

1955.............................
1956.............................

0.6
0.7

1958................ •. . . . . . . . . . . .
1959.............................

1.4
1.8

1957.............................

1.2

1960.............................

1.8

TABLE VIII. ASSUMED DIET TYPES, POPULATIONS AND FdJFd RATIOS USED TO COMPUTE
A POPULATION \VEIGHTED WORLD DIET (F II, table XXIV)
Anumeddidt:,ipePopu/alimt N;

x 10'

FJFd

EuropeOceania

220
622
15

2.3
2.0
0.5

II

Near East
Asia (India)
S. America
Africa

65
400
136
247

2.3
2.3
0.5
0.6

III

Asia and Far East

765

2.3

C. America

40

1.5

Area

N. America

From these values a population weighted world average diet is derived as the sum of concentration diet 1 X 0.7, concentration diet II X 0.5, concentration diet III X 0.7.

TABLE IX.

ESTIMATED DOSES TO THE THYROID GLAND FROM 1181

It is assumed that the average level of 1181 in milk is 125 µµ.c/I over a period of ten weeks (para. 58).
Age

..,.

0.5 .....•........
3 .•...•.........

Quantity of fresh milk
consumLd per da:,iQ1<0nlil:,i of fresh milk
consumed per da:,i(litres)

Th:,iroid
dase
mrem

0.5
0.25

170

10 .....•.........

0.25

25

45

Adult •.•••...••••

0.25

4

TABLE

,,.

Age

x. AVE.RAGE DAILY INHALATION OF FALL-OUT NUCLIDES IN
VARIOUS YEARS IN THE UNITED KINGDOM
Micro-microcuries per da',1

1955

Total beta fission
products ••••. 13.3
Cs137 • • • • • • • • • • •0.22

Sr8° (calc.) ......

0.13

1956

20
0.24
0.14

Zrll' .•........•.

1957

0.00200.0021

1959
Jan.-Jur.e

1959
J uJ,,.Sept.

1959
Ocl.-Dec.

17

4
0.12
0.07

32
0.26
0.15

57
0.36
0.21

100
0.65

0.43
0.25

3.9•

6.2
3b

12

0.8

0.06

0.00230.00320.010

0.00380.0011

IUl •.••.......•
Pu!l3 9 (calc.) .....

1958•August-December.

1.1

b October-November.

360Thr)toiddase
mrem(lilTes)TABLE XI.

DosE COMMITMENT FROM NUCLEAR TESTING
Dose commitment for
Dose eommilmenJ for
puiod of testing 1954-1960 period of lestini 1954-1961
Fraaion of
doJe commitment

Tiss~

Gonads ......................

Internal

Cells lining bone surfaces •..•..

External
Internal

Short-lived
Cs131
Cs137

c11

Short-lived
Cs137
Sr 90
Csm

c11

Sr89

Bone marrow ...........•..•.•

External

Short-lived

Internal

Sr 90
Cs117

es•rz

c11

Srll

Dose
commitmenJ

Per :ltt>r of

Para.

Total mrem

Z,000

Total mremz.ooo

teslini•
mrtrn

23,24
23,24
39-41
44,45

11
16
8
48

1.0
0.92
1.0
0.10

12
18
11
70

1.0
0.94
1.0
0.10

1.6
2.2
3.1
22

83

0.47

111

0.42

29

11
16
67
14
80
0.15

1.0
0.92
0.92
1.0
0.10
1.0

12
18
79
19
116
0.17

1.0
0.94
0.91
1.0
0.10
1.0

1.6
2.2
10.5
5.3
37
0.03

188

0.58

244

0.54

57

11
16
33
10
48
0.07

1.0
0.92
0.92
1.0
0.10
1.0

12
18
40
14
70
0.08

1.0
0.94
0.91
1.0
0.10
1.0

1.6
2.2
5.3
3.9
22
0.01

118

0.61

154

0.56

35

Soo.1rce of radiation

External

Frtulion ofdose com-mi177".enl

23,24
23,24
32-36
39-41
44,45
53

23,24
23,24
32-36
39-41
44,45
53

•For details of model see anne.i: F, part I, paragraphs 110 and 119.

361

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364

ANNEX FENVIR01'~IENTAL CONTAI\IINATION (continued)
PART IV

Disposal of radio-actire wastes and releases from accidents in nuclear reactors

CONTENTSParagraphs

Paragraplu

I. DISPOSAL OF RADIO-ACTIVE WASTES • • • • • • • . • • • • • • • • • 1-33
Introduction • . . . . • . • • • . . . . . . . . . . . . . . . . . • . . . . . . . 1
Classification of radio-active wastes. . . . . . . . . . • . . . 2
Methods oi disposal. . . . . . . . . . . . . . . . • . . . . . . .. • . . . 3
Origin and nature of radio-active wastes........
4
Gaseous and airborne wastes.. . . . . . • . . . . . . . . . . . . . 5-7
High-level radio-active liquid wastes............. 8-10
Liquid wastes of intermediate and low-level activity 11
Solid wastes ............••...••...........•..... 12-13
Disposal of radio-active wastes into rivers •...•.•.. 14-16
Disposal of radio-active wastes into seas and oceans 17-18

Mixing process between deep-water and surfacewater of the oceans and "biocirculation" ....•.•.. 19-23
Disposal of radio-active wastes on land........... 24
Direct disposal of low activity wastes into superficial permeable layers of the ground ..•........• 25-26
Isolation in special geological formations .......... 27-29
Conclusion •...........•....•••................. 30-33
II. RELEASES FROM ACCIDENTS IN NUCLEAR REACTORS. • • • 34-39

I. Disposal of radio-active wastes

far as practicable, the radiation dose to man. Two basic
methods are available to achieve this aim. The first is tocontain the waste in shielded areas and to absorb most of
the radiation in the shield. If special attention is paid tothe problems of siting, containment and shielding, any
quantity of radio-activity can be dealt with in this way.
The second method is to disperse the radio-activity in theenvironment so that most of the radiation energy isabsorbed by the diluting material, and again the radiationdose to man can be kept low. There is, however, a limit
to the capacity of the environment to accept wastes without causing excessive radiation dose to man. Broadly
speaking, therefore, the first method is the appropriate
one for high-level wastes, and the second is satisfactoryfor low-level wastes. Intermediate-level wastes must be
considered on their merits and are usually partly contained and partly dispersed.

TABLESREFERENCESINTRODUCTION

1. The problems of waste disposal have arisen withcivilization and have become increasingly complex withits development. The use of atomic energy has increased
the already complicated problems of disposing of thewastes arising from human communities. Radio-active
materials could be transmuted into non-radio-active materials by further neutron capture, but this procedure
would not be economic. Chemical treatment merely transfers wastes to a more convenient form while leaving alower concentration of radio-activity in the treatedwastes. With the continuing extension of isotope technology in industry and medicine and the development of
nuclear power, there will be larger quantities of radioactivity to be stored and there will also be an increase in
the amount of low activity wastes released into man's
environment. It will therefore become more and more
important to control these releases and to assess the contribution they make to man's exposure to radiation.

ORIGIN AND NATURE OF RADIO-ACTIVE WASTES5-15

4. Radio-isotopes originate from three different
sources: natural radio-active isotopes with their decay
products, fission products and radio-isotopes obtained asa result of activation. By far the greatest quantity ofradio-activity in the form of wastes produced at thepresent time originates from the reactor-fuel cycle. A
general flow-sheet indicating the types of waste produced
during the nuclear fuel cycle complex is given in figure
1.7 Smaller amounts of radio-activity occur in the wastes
from medical and industrial uses of isotopes. Althoughthese releases are small, they take place in a very large
number of establishments and the disposal problems thus
posed are by no µieans negligible.

CLASSIFICATION OF RADIO-ACTIVE WASTES

2. According to their physical state, radio-active
wastes are classified as solid, liquid and gaseous. Though
no fixed classification system has been agreed upon, liquid
wastes can be arbitrarily divided into three groups
according to their specific activity: low-, intermediateand high-level wastes. 1 - ' These terms are used to describe the approximate concentration of activity in theparticular waste materials and their quantitative definition varies from one establishment to another. Low-level
wastes are those having a range of activity from a trace
amount up to one microcurie per litre; intermediate-level
wastes have concentration up to three curies per litre;and high-level wastes have specific activities up to hundreds of curies per litre. 1

GASEOUS AND AIRBORNE WAST ES

5. Gaseous and airborne radio-active wastes are produced during feed material production. isotope separation, fuel element fabrication, fuel reprocessing andreactor operation. During the re-processing of shortlycooled fuel elements, fission product gases are released,

METHODS OF DISPOSAL

3. Methods of waste disposal must aim at reducing, as

365

ISOTOPES

1, U OUST
2. RAOOH

1, U OUSTI, U OUST
2. ·RADON
3. FUTURE: ciHAZAROS

I. NOW: U, Pu 23 P
2, RJTURE: u2U
Pullt,40,CI, lh2J2

A~ 1, N14, FP'1,

2. RAOOHPARTICULATES

12 Xe, kr, FP'•,PARTICULATES,HEAVY ELEMENTSIGNIFICANCE

LOCAL

LOCAL

LOCAL

TOTAL CONTAIN-·MENT REQ'O
FOR OUSTGASES DECAY
RAPIDLY; NO
GENERAL CON·TAMINATION

MAJOR POTENTIAL
SOURCE OF AIR
Cetl TAMI NATION

"'"'
5~
~~

~'It

U, Pu, 1h•

MILLINGMINING

0.3"
ORE

STRIP
HARD ROCK~FEED MA TERI AL PREP,

J, LEACH
I. 'SOLVENT EXTRACTION
70"
2, SOLIDS~ 2. UF, PRODUCTIONREMOVAL
3. MET AL REOUCTIOH
U30 1
3. EXTRACTION
4. OXIDE PREPARATION
4. PRECIPITATIOH
5. UF 6 PRODUCTION

t

I

I

FUEL FABRICATION_.... 1, METALOXIDES2.
3. CLADDIHG
4. ASSEMBLY

FUEL
ELEMENTEJFUEL REPROCESSINGCOOLING

I. OECLAOOING
2. DISSOLUTION
3. SE PARA TJON
4. PRODUCT RECYCLE·
5. WASTE TREATMENTrF6
ISOTOPE SEPARATION
UF 6 DIFFUSIONISOTOPES'UF 6 ·ENR.
ENRICHEDU +DAUGHTERS

U + DAUGHTERS

1. U + DALGHTERS
2. FUTURE: Pu &HEAVY ELEMENTS

U, Pu 239
unJ, Pu2•0,i1
Th232

No2'; Cose, Co60
Zr 95, FP'1

FP'1, HEAVY ELEMENTS
INACTIVE SALTS

NOHE

NONE

NetlE

NONE AT PRESENTNONE

1000 gal/Ion(100) gal/Ion
10 2 - 103 c/gal

MINES
ARE
DRY

600,000 gol/IO<I.. 100,000 gal/ton

UNKNOWN

MAX: 10-6 c/gal

MAX: 10- 6 c/vol

VERY LOW

:J

"'w
~;:;
"'-'
~~

a:::;o3i5..
~

HA, (1) val/ton U.. c/galLA, (l) gal/Ion.. c/gal(1) HIGH ACTIVITY WASTE: ACTIVITY IS ORDER OF W.GHITUDE ESTIMATE, CURIES/GAL(2) LOW ACTIVITY WASTE;

Fig11re 1. Schematic flowshcct for origin of wastes

COOLINGCIRCUITS
CLOSED,
LOW VOLUMESPISCHARGED.. 2000 - 10,000 gol/lcn":6 x 10- 5 c/gol

including Kr85 , Xe133 and !1°1 • Where air is used as acoolant for reactor cores or shields, the short-lived isotope Au appears in large quantities. C14 may be produced
in a reactor by irradiation of the graphite moderator, orof the carbon dioxide used as a coolant, and by irradiation of nitrogen.

problems are posed by the presence of alpha-emitting
transuranic isotopes of long half-life. 21

6. Before being discharged into the atmosphere, airborne and gaseous wastes may have to be partly decontaminated through various dev;ces. 16 Isotopes of thenoble gases are diluted by meteorological processes andthe dose to man can be adequately controlled by the selection of a suitable stack height. Kr85 may in the future
give rise to significant exposures if improved methods oftreating gaseous effluents are not developed. Other materials, notably isotopes of iodine, are deposited from theair and may be substantially reconcentrated by agricultural processes. This introduction of radio-activity into
the food chain is usually likely to contribute more to theradiation dose to man than direct exposure to the airborne waste.

11. Low activity wastes can often be disposed of
directly in the soil, rivers or seas. The quantity of waste
which can be disposed of in this way depends on theradio-active components of the waste and on the capacityof the environment to absorb or disperse these components without causing excessive radiation dose to man
or harm to the environment. If the amount of waste for
disposal exceeds the estimated capacity of the environment, then the waste must be treated to remove part of
the radio-activity through concentration. The concentrate
can then be stored or transferred to other parts of theenvironment better able to receive the radio-activity.
Intermediate-level wastes almost always require treatment in this way. A relatively complete decontamination
can be achieved only by using a combination of methods,
the choice of which depends on the composition of thewastes. The efficiency of decontamination methods is
given in table IV. 22

7. Quantitative information on the amounts of radioactivity discharged in gaseous wastes is extremely sparse,
but both the United Kingdom and the United States havepublished some information relating to atomic energy
installations. Some of these data are summarized intable I.17 Because of the various ways in which gaseousdischarges can cause radiation e..xposure to man, the discharge figures in table I cannot be used directly to assess
the environmental consequences of the discharges. However, in many cases, detailed assessments have been madeof the resultant radiation doses to man and it has beenfound that these are very small. 18 It is reasonably certainthat gaseous wastes from all sources make a very small
contribution to man's total radiation dose.
HIGH-LEVEL RADIO-ACTIVE LIQUID WASTES

8. Wastes of high activity must be stored for long
periods of time so as to prevent their release into theenvironment. At present, all high-level activity wastes
from the re-processing of reactor fuel are kept in a concentrated liquid state in tanks. These tanks are either
placed in buildings above ground or, more commonly,
underground.
9. Despite a number of shortcomings, such as selfheating, radiolysis and corrosion with leakage as a possible consequence, storage of liquid high-level activity
wastes in tanks can be considered as satisfactory. Nevertheless, research is being carried out to make possible thestorage and disposal of high-level activity wastes in thesolid state. as this will provide their safe fi.xation for along period. The conversion of high activity wastes tothe solid form has some disadvantages including particularly the production of additional low- and intermediatelevel wastes and of gaseous wastes. The additional proc~
essing required also causes additional radiation doses.
However, the increased safety of the finally stored or
disposed waste may well outweigh these disadvantages.
The methods of conversion of liquid wastes into solid
substances are given in table II. 19

LIQUID WASTES OF INTERMEDIATE- AND
LOW-LEVEL ACTIVITYSOLID WASTES

12. Solid wastes include contaminated equipment,
process wastes such as slags, contaminated laboratory
wastes, and the concentrates from some types of treatment of liquid wastes. Depending on the activity and theavailable environmental conditions, solid wastes areeither permanently stored, e.g. in concrete-lined trenches,or buried witl1 or without containers, or dumped on thesea-bed in drums or concrete containers. They are often
processed to reduce their volume and to simplify thesubsequent disposal operations. Such processing includes
incineration and baling and usually produces secondary
gaseous or liquid wastes which have proved to be oflittle hazard.
13. Typical quantities of liquid and solid radio-active
wastes discharged into rivers, seas and oceans from someof the establishments of the United Kingdom Atomic
Energy Authority and United States Atomic Energy
Commission are given in table V.17
DISPOSAL OF RADIO-ACTIVE WASTES INTO RIVERS

14. Studies of the biology of river waters into whichradio-active wastes are discharged have indicated thatradio-nuclides are strongly concentrated by river organisms, both plant and animal. As e..xamples. observations
made at Hanford and at Chalk River will be reported. 2 a-25
15. Low-activity cooling water from the reactors at
Hanford is discharged, after a short delay. in retention
basins into the Columbia River. The activity decreases atpoints downstream from the discharge point because ofradio-active decay and adsorption onto sediments. 23
Estimates have been made of the radiation doses topeople living in downstream communities and it has beenfound that in spite of some very high concentration
factors 24 in individual river organisms the principal
sources of radiation dose to man are drinking water and a
species of whitefish. The use of the river for irrigationand the transfer of radio-active materials to the sea andtheir reconcentration in marine organisms have beenshown to contribute extremely small radiation doses toman. 23

10. The per cent fraction of total radio-activity contributed by certain fission products of biological interest
after various times of cooling is given in table III. 7
Serious attention should be given to the proposal 20 thatCs 137 , Sr90 and other long-lived isotopes be removed fromhigh-level wastes, so that the residue can be finally disposed of after a period of about fifteen years. Additional367

16. At the Chalk River plant the effluent is diluted bylarge volumes of water used for cooling the reactors
before it enters into the Ottawa River. The concentrationof the beta-gamma emitting radio-nuclides is equal to
2 X 10-s µ.c/cc upstream from the plant; at a distance of
1.6 km downstream from the plant, the concentration is3 X 10-s µ.c/cc. 25 Sr90 in excess of that attributable tofall-out was occasionally observed in fish caught in thelocality of the reactor outfall.
DISPOSAL OF RADIO-ACTIVE WASTES INTO
SEAS AND OCEANS 26

17. Two methods of disposal of radio-active wastes
into seas and oceans are used at the present time. The
first consists of the direct discharge of liquid wastes fromatomic plants into coastal waters ; the second of the
dumping of solid wastes on the bottom of the sea after
sealing in appropriate containers, thus delaying the entrance of radio-active substances into the water masses.
In this connexion the oceans can be considered from two
points of view: as a dilution medium for radio-active
waste and as an area of temporary isolation in whichradio-activity can decay before escaping to the water andultimately returning to man.

cannot be regarded as isolated from the surface waters.
Waste disposal in the deep water in containers must
therefore be treated as a form of temporary storage, thestorage period depending both on the life of the container
and on the rate of transfer to the surface waters. In addition, the process of transfer will result in substantial
dilution.
21. Experiments 31 have indicated that the expected life
period of metal drums because of corrosion in sea waters
is not more than ten years, whereas concrete containers
may last as long as thirty years. One container describedin the literature31 is capable of withstanding high pressures and corrosion, so that its expectation of life at thesea bottom is 1,000 years.
22. Since 1946 the United States Atomic Energy
Commission has been disposing of relatively low-level
radio-active waste products at sea off the Atlantic andPacific coasts of the United States. Most of these wastes
were packaged in 200 1. steel drums with encased concrete drums, and preformed, reinforced concrete boxes
were used in some instances. During three oceanographic
cruises 32 in March, April and November 1960, samplesof sea water. sediments and marine life were collected
for the purpose of measuring their radio-activity level.
Bottom photographs were taken and documentary motion
pictures of the April cruise were filmed. Different seasonsof the year were chosen for the cruises in order to detectseasonal differences in levels of contamination. \Vater
depth at all sites \Vas 1,800 m. or greater. The three areasof survey were two disposal sites and the control area off
Point Arguello, between the two disposal sites. In general, the results indicated that within experimental error,
no radio-activity was detected· in excess of the background levels.

18. While the possibilities of the ocean as a medium
for dilution are great, it is obvious that uniform dilutionof the global quantities of radio-active wastes in the ocean
is highly improbable both because of the slow rate of
mixing of water and because of concentrating effects.
Among the factors which influence the fate of radioactive wastes in sea water are the physical and chemical
state of radio-nuclides and also oceanographic conditions.
The possible physical states of elements in sea water are:ionic, colloidal, and particulate.27 Elements in ionic form
will be diluted better, but as they remain longer in solution they may enter in zoo- and phytoplankton. Elementsin particulate form or those which tend to be absorbed
by particulates in the sea will have a tendency to settle on
the sea-bed, which will lead to a higher concentration ofradio-activity at the bottom as compared with the rest of
the sea. Radio-nuclides in particulate fonn may then be
removed by filter-feeding marine life and so become
available to the larger marine fishes. Thus, radio-active
materials may enter bottom sediments and in some form
become available to bottom-dwelling marine life.

23. At the present time, since many factors are still
unknown to us and few data on the question of disposingof sealed wastes in ocean depths are available, it is difficult to reach definite conclusions on the suitability of suchpractices for all types of waste. At present, however,
only small amounts of radio-active material are being
deposited in the ocean and before this practice could be
extended to the high activity waste from large-scale
nuclear power programmes, much more investigation
would be required into the processes of dispersion andreconcentration. There is still substantial disagreements:i-sa on the validity of deep ocean disposal, but evenwith the assumption of a very rapid mixing of the deep
water and the surface water the present practices have so
far given rise to exceedingly small radiation doses to man.

MIXING PROCESS BETWEEN DEEP WATER AND SURFACEWATER OF THE OCEANS AND "BIOCIRCULATION"

19. In considering disposal of radio-active wastes by
burial in ocean depths, it is necessary to examine thepossibility of exchange between deep and surface watersof the ocean. Two points of view exist. 28 The first maintains that the replacement of deep waters in the ocean
takes place comparatively rapidly, in perhaps forty tofifty years. This point of view is supported by observations and calculations regarding dissolved oxygen andphosphate, and other factors present in the ocean. The
other point of view holds that the replacement of deep
waters in the ocean, and consequently the time required
for any contamination from the depths to come to thesurface, takes place much more slowly. over a period ofseveral hundred years, or even 1,000 or 1,500 years. This
opinion is supported by studies conducted with carbon-14
and radium. In addition to the movement of radio-active
nuclides due to vertical transfer of water layers, "biocirculation"29-3o also must play a role.

DISPOSAL OF RADIO-ACTIVE WASTES ON LAND

24. Like the ocean the land also can be considered bothas a place for ultimate disposal through isolation in special geological formations and as a medium for dispersionof low-level radio-active wastes. In the latter case there
is also some degree of isolation by adsorption of theradio-activity on to the soil as well as dispersion anddilution in the ground water. In rare cases substantially
all the radio-activity is retained by the soil and only apurified waste reaches the ground water. This situation
occurs at Hanford where some quantities of radioactivity are released into the ground and no fission products have been observed to penetrate into the riverwaters. 23 Direct disposal of low-level liquid and solid
wastes into the ground is practised at the present time,
and the isolation into special geological formations is in
the state of development.

20. It is now clear that the deep waters of the oceans
368

DIRECT DISPO!>AL 0.1:" LOW-ACTIVITY WASTES INTO
SUPERFICIAL PERMEABLE L"-YERS OF THE GROUND

25. Disposal of low-level liquid radio-active wastes to
the ground is founded on the ability of various earthmaterials to remove and retain fission product cations.
Some years of practical experience in the controlled disposal of \Vastes to the ground at the Hanford Works,
Oak Ridge National Laboratory, and Savannah River
Plant have demonstrated the feasibility, safety and economy in the disposal of at least limited volumes of some
types of liquid wastes. 37
26. The binding capacity of soil for radio-nuclides
depends on the composition of the soil and on the properties of the discharged wastes. Strontium is well sorbed
by montmorillonite, kaolinite, mica, hydromicas, peat,
phosphorite and nepheline syenites. 38 Caesium, as a rule,
is very well retained by soils, and the extent to which it isretained depends on the mineral content of the soil. It
has been established that the most suitable types of soilcolumns for the decontamination of liquid wastes arethose composed of vermiculite overlaying solid phosphates, which in turn lie on coarse-grained gravel. 39

31. The problem of disposing of radio-active waste
will assume increasing importance with the developmentof atomic energy which is expected in the next few
decades. It has been estimated4 H 8 that the thermal power
produced by atomic plants will reach 700.000 megawatts
by the year 2000 and will be accompanied by billions ofcuries of accumulated radio-activity. Almost all the resulting radio-active material will be sent to permanentstorage and improved storage methods are being investigated. It is also likely that there will be an increase in theamount of radio-activity dispersed into the environment
not only from fuel-reprocessing plants but also from theincreasing uses of isotopes in industry and medicine. The
control of such discharges and the assessment of theresulting radiation doses to man \vill thus become increasingly important.
32. Most of the present practices for the disposal of
low activity wastes are satisfactory provided that they are
subject to close and continued control. In some cases thiscontrol should include appropriate environmental monitoring and the primary aim of this monitoring should beto establish that the disposals cause no unacceptable radiation doses to man. In the case of the majority of theindustrial and medical applications of isotopes, simple
procedures controlled by suitable sanitary standards-1 9- 53
can be used for disposing of radio-active wastes without
the need for a complex environmental monitoring programme.

ISOLATION IN SPECIAL GEOLOGICAL FORMATIONS

27. It has been proposed to discharge liquid wastes
even of high activity into various rocks, salt formations,limestone, shale formations, gypsum, sandstone and otherimpermeable geological formations. 4 0-41 All these methods are at the e..xperimental stage. Of all the indicatedgeological formations, the most promising are sandstoneand salt formations.

33. The release into the environment of the principal
fission-product wastes from the large scale production of
nuclear power cannot be considered until substantiallymore information is available on the behaviour of suchfission products in the environment.

28. Deep well injection's of radio-active materials into
porous geological formations 4 0-43 are suitable for regions
which have porous rock, such as sandstone, under which
is a layer of impermeable material such as shale. Sandstone possesses several desirable properties. such as considerable heat conductivity, stability in acids ; its porosity
reaches 10-30 per cent; it has a fairly high ion-exchange
capacity (20-30 milligram equivalents per 100 g.).

II. Releases from accidents in nuclear reactors

34. The release of radio-active materials as a resultof nuclear accidents represents a situation that must be
considered in connexion with its potential effects on man
and his environment. Of the six major nuclear accidents
to dateH only the accidents at Windscale and at ChalkRiver led to a substantial release of radio-active
nuclides. 55- 5e

29. Disposal into natural salt fonnations provides oneof the most interesting possibilities. 4 4-4 6 The method has
several geological and operational advantages and is expected to provide a high degree of isolation. Analyticalstudies indicate that it is possible to store two-year-old
10,000 megawatt-day/ton, 3,200 litre/ton waste in a
sphere about 3 m. in diameter. Structural properties andthermal conductivity of rock salt are not changed to any
significant extent under the influence of high doses ofradiation. The chemical interaction of liquid wastes withsalt produces chlorine and other gaseous compounds, but
their quantity is not very great.

35. The accident at Windscale was caused by local
overheating of the uranium fuel elements during the annealing of the graphite moderator of an open air-cooled
reactor. The amount of radio-activity released during theaccident is not known precisely, but approximate estimates were made from the measurements of the radioactive iodine deposited on the ground and from measurements on air filters obtained both in the United Kingdom
and in Continental Europe. The following list shows estimates of the amounts of various isotopes released :CONCLUSION

CuriesIodine-131 ................................... 20,000
Tellurium-132 ............•..••.......•...... 12,000
Caesium-137 . . . . . . . . . . . . . . . . . • . . . . . .. .. . . . . . .
600
Strontium-89 . . . . . . . . • . . . . . • . . . . . . . . • . . . . . . . .
80
Strontium-90 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2

30. Information on the contamination of the environment through disposal of radio-active wastes is very
}itnited and only for few areas are relevant data pub1ished periodically. In even fewer cases is the publishedinformation sufficient to allow any assessment of theresultant radiation doses to man. These cases represent
major releases of radio-activity into the environment andit has been shown that the resultant radiation doses to
man are small. 18 Other releases of radio-active waste
result in even smaller doses and present waste disposal
does not make a significant contribution to man's exposure to radiation.

36. During the six weeks after the accident, over 3,000
samples of milk were analysed. The I 131 content of milkrose to a maximum three days after the accident when
the highest levels recorded were 1.4,uc/l. The levels of!131 in samples of drinking water obtained from reservoirs, and from streams feeding reservoirs and watertaps, varied from below the threshold of detection (about369

100 p.p.c/l) to about 1,000 p.p.cj1. Samples of eggs, vegetables and meat from the more highly contaminated areas
were examined. They also were shown to be contaminated with !1 31 , but contributed much less to the diet ofthe population than did milk.
37. Before the accident the ratio of Sr90/Ca was
44 µ.µ.c/g in milk from a farm within a quarter of a mileof the perimeter of the Windscale Works. Shortly after
the accident values up to 115 µ.p.c Sr9°/gCa were observedin milk from the farm nearest the plant. It was also foundthat in the area of highest contamination, the maximum
levels of Cs137 , Ru103 and Ru 100 , and Zr05 in grass were0.25, 0.21 and 0.3, p.c/m2 respectively.
38. The only control measure needed as a result of theaccident was the control of the consumption of milk andvegetables from an area of approximately 500 squa::ekilometres. The opinion was expressed in the official report following the accident that this control measure had
been adequate and that it was highly unlikely that any
harm was done to anybody as a result of the accident.
39. Most reactor accidents have taken place in experimental reactors or in reactors cooled by the old-fashioned
flow-through system rather than in the more modem
power generating facilities where the coolant is recirculated. The probability of other types of accidents
occurring can only be assessed on the basis of past experience. This is still limited but suggests that releases ofsuch a nature as to cause concern for the health of individuals in the population are extremely rare. It is also

likely that carefully planned emergency measures cansubstantially reduce the radiation doses which would
otherwise result from accidental releases.
TABLE l.

SOME EXAMPLES OF RELEASES OF GASEOUS WASTE FROMATOMIC ENERGY PLANTS
Amount of t11asle andradio-aelive ctmk1sl

Site

United Kingdom
Springfields (feed material production
plant) .•..•.••••••....•••..••...•.•• Approx. 1 c/y, alphaCapenhurst (gaseous diffusion plant) •••.. Approx. 0.1 c/y, alpha(uranium)
Calder Hall (nuclear power station) ..•••. 10 c/hr, AU
Chapelcross (nuclear power station) •...•• 10 c/hr, A"
Dounreay (reactor research centre) •••..•• 0.5 rnc/hr, A"
Harwell (nuclear research centre) .••..••• 30rnc/y:beta;1 mc/y,alpha; 50 c/hr, AU
Amersham (isotope production plant) ••••• 15 mc/wk, pn
Aldermaston (nuclear weapon research
centre) ••.••..•••••.•••.••.••.••••.. 20 mc/y, beta;
3 mc/y, alphaUnited States of America
Hanford (plutonium production plant) •••• 1 c/d, 1111
Idaho (reactor testing station) •••••..•••. 100,000 c/y beta,
mainly very shorthalf-life, and noblP
gases
ORNL (reactor development andchemical processing laboratory) ••.•.. 0.25 c/y, alpha(uranium)
Brookhaven (nuclear research centre)
700 c/hr, AU

TABLE II. PossmLE METHODS OF CONVERSION OF w ASTES TO SOLID FORMS
Preparation containing fission
products
Difficulties in the
preparation
process

Metal oxides
dried at200-250°c
Considerable
dust

Metal oxides
calcinated at500-700'C
Dust

Volume variations

Reduction up
to 100 times
Yes

Separation of gaseous
products in radiolysis
High
Heat resistance
0.05
Heat conduction
kilocalorie/metre/h/C°Considerable
Transfer of fission
products into water

Calcinated clays Cement blocks

Molten salts

Must bemixed

Corrosion of the High temperature
equipment(> iooo°C)

Reduction up
to 100 times
No

Limitedexchange
capacity of
clays
Reduction up
to 50 times
No

Increase up to
30-50%
Yes

Reduction up
to 70 times
Yes

Reduction up to
350 times
No

High
0.03

High
0.05

MediumLow
About 1

Very HighUp to 2

Appreciable

S::nall

Small

SolubleVery small

TABLE III. CoMeosmoN OF FISSION PRODUCT MIXTURE AFTER ONE-YEAR IRRADIATION OF FUELELEMENTS BY 3 X lQ3 THERMAL NEUTRON FLUX AND VARIOUS TIMES OF COOLING
Approximate 3 of total F P acJinly afler coolint
lsoloj>e

Half-life

100 days

J Y<4rS

JO years

Cs117
Srto
Pmu1

26.6 years
28.0 years
2.6 years
290 days
10.3 years
8.1 days
63 days12.8 days
41.0 days
1.0 year
54 days5.27 days

<2
<2
3
45
<1
< 1
33
<I
5
2
7
<1

15
15
15
50

"'49
"'49
<I

1

<1

Ceto_pru~Kr" (gas)Jm (gas)Zr95-Nb95
Ba 140-Lauo
Rutlll-Rhto•
RulDLRhtoe
Sr11
Xe 1» (gas)Preparation type
glass

370

3

TABLE IV.

EFFICIENCY OF DECONTAMINATION METHODS OFUQUIDWASTES

Unspedfkd
clpha-remDNl

Trtalmenl

FeCI, .•.......•.............. 97%
BaCh + Fea (SO;),, .•.......•.• 99%
Lime soda-softening process ...• 70-99%
40-80 ppm AI + activatedsilica (S-10 ppm Si02) ....... , 80%
20 ppm Al + lime or NaaCO, .. , 90%
40 pp~ Na!PO, + lime +tanmc acid. . . . . . . . . . . . . . . . . 98%
100 ppm Na,PO, +lime or NaOH 95%
Phosphate treatment followed bysulphide treatment .•....... , 99%
Phosphate treatment followed byvermiculite columns ......... 99.95%
Precipitation and electrode-ionization ............... 99-100%
Ion-exchange resins............ 1QL1()6
Mixed bed....................
1(}1Evaporation .................• lOLl()f

TABLE V.

Site

Type ofwaste

Uniled Kingdom
Springfields ...........
Capenhurst ..........•
Windscale and Calder ..

LiquidLiquidLiquidChapel cross (1960) .....
Dounreay (19S9-{)0) ....

LiquidLiquid[Liquid
Solid
Harwell ............... ~lSolidU1upecjjkd
be1a-1amma-remof4l

SO%
98%
S0-80%
6S%
70%

75%
7S%

90%
99.36%
99-100%lQLlO•
1()1

lQLlQG

EXAMPLES OF LIQUID AND SOLID WASTE DISPOSAL FROM SOMEATOMIC E."<ERGY DTSTALLATIONS

A mo1n1I and raii~actit•e C011lenl

2.S X 10'm1/y; SO c/y alpha; l ,SOO c/y beta
2 X lO'm'/y; 1 c/y alpha (uranium)
8 X 10'm1/y; 90,000 c/y beta; 40,000 c/y Ru: 1,500 c/y Sr90 ;70 c/y alpha3 X 10'm'/y; 4.S c/y alpha and beta; 80 mc/y Sr90
105m•/y; 40,000 c/y beta; 20 c/y Sr 90 ; S c/y alpha7 X lO'm'/y; lS c/y beta; O.S c/y Sr90 ; 0.02 c/y alpha
800 tons/y; 80 c/y beta; 4 c/y alpha
SO tons/y; 1,000 c/y beta; 200 c/y alpha

rqWd
Solid

S X 10'm1/y; 0.02 c/y beta; 0.06 c/y alpha
400 tons/y; 2 c/y alpha; O.S c/y beta

Solid

SO tons/y; 200 c/y alpha; lS c/y beta

Uniled States of America
Hanford (19S9) ..... , ..
ORNL (19S4-S7) ......

Liquid3,000 c/d beta; 1,200 c/d Cr61 ; 70 c/d Zn 86 ; 0.2 c/d Sr9o

LiquidBrookhaven (19S7-S8) •.

{Liquid
Solid

105m1/y; 2SO c/y beta; SO c/y Sr10
S X lO'm•/y; 0.1 c/y beta
1,000 c/y

Aldermaston ..........

371

J.fahcd of
disJH>sal

Pipeline to tidal estuaryOpen brook to tidal estuary
Pipeline to open sea
Pipeline to tidal estuary
Pipeline to open sea
Pipeline to River Thames
Dump in light drums on bedof English Channel
Dump in strong drums on bedof Atlantic Ocean
Pipeline to River Thames
Dump in light drums oo bed
of English Channel
Dump in strong drums on bedof Atlantic Ocean

Pipeline to river
Discharge to local stream
Discharge to stream
Dump in drums on bed ofAtlantic Ocean

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39. Stru.."<ness, E. G., K. E. Cowser, 'vV. de Laguna et al,"'Waste disposal research and development in the
United States of America", pp. 482-498, in Disposal of Radioactive Wastes. Conf. Proc., Monaco,
16-21 Nov. 1959. IAEA, Vol. 2, Vienna (1960).

27. Greendale, A. E., N. E. Ballou, Physical state offission product elements following their vaporization in distilled water and sea-water. United States
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USNRDL-436 (1954).

40. Nace, R. L., "Contributions of geology to the problem of radioactive waste disposal", pp. 460-480, in
Disposal of Radioactive Wastes. Conf. Proc.,
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28. Fedorov, K. M., "Circulation and mixing in the deep
waters", pp. 303-304, in Disposal of Radioactive
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29. Zenkevich, L. A., "Adsorption and biocirculation in
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1959. IAEA, Vol. 2, Vienna (1960).

41. Simpson, E. S., "Summary of current geologicalresearch in the United States of America pertinent
to radioactive waste disposal on land", pp. 520-531,
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30. Ketchum, B. H .. "Oceanographic research requiredin support of radioactive waste disposal", pp. 285291, in Disposal of Radioactive Wastes. Conf. Proc.
Monaco, 16-21 Nov. 1959. IAEA, Vol. 2, Vienna( 1960).

42. Kaufman, W. J., "The containment of radioactive
wastes in deep geological formations", pp. 535-546,
in Disposal of Radioactive Wastes. Conf. Proc.,
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31. Waldichuk, M., "Containment of radioactive waste
for sea disposal and fisheries off the Canadian
Pacific coast", pp. 60-77, in Disposal of Radioactive
Wastes. Conf. Proc., Monaco. 16-21 Nov. 1959.
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43. Kaufman, W. J., "On investigation of disposal ofradioactive wastes into deep geological formations",
pp. 1218-1226, in Industrial Radioactive Waste Disposal. Hearings before the Special Subcommittee
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Eighty-Sixth Congress. United States Gov't. Printing Office, Vol. 2, Wash. (1959); v.e. United Nations document A/ AC.82/G/L.287.

32. United States Atomic Energy Commission, Surveyof radioactive waste disposal sites. USAEC technical report TID-13665 (1961).

44. Heroy, 'vV. B., "Disposal of high-level waste in natural salt formations", pp. 2028-2035, in Industrial
Radioactive ·waste Disposal. Hearings before theSpecial Subcommittee on Atomic Energy. Congressof the United States, Eighty-Sixth Congress. UnitedStates Gov't. Printing Office, Vol. 3, Wash. ( 1959);
v.e. United Nations document A/AC.82/G/L.287.

33. Pritchard, D. W., ''The application of e.xisting
oceanographic knowledge to the problem of radioactive waste disposal into the sea", pp. 231-248,
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34. Koczy, F. F., "The distribution of elements in thesea", pp. 191-197, in Disposal of Radioactive Wastes.
Conf. Proc., Monaco, 16-21Nov.1959. IAEA, Vol.
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45. Parker, F. L., L. Hemphil, J. Crowell, "Status report on waste disposal in natural salt formations",
pp. 2087-2140 in Industrial Radioactive Waste Disposal. Hearings before the Special Subcommittee on
Atomic Energy, Congress of the United States,
Eighty-Sixth Congress. United States Gov't. Printing Office, Vol. 3, Wash. (1959); v.e. United Nations document A/ AC.82/G/L.287.

35. Moiseev, P.A .. A. V. Kardashev, "The effect of fission products on the radioactivity of some hydrobionts of the Pacific Ocean", pp. 94-96, in Disposalof Radioactive Wastes. Conf. Proc., Monaco, 16-21
Nov. 1959. IAEA, Vol. 2, Vienna (1960).

46. Parker, F. L., W. J. Boegly, R. L. Bradshaw. et al,' "Disposal of radioactive waste in natural salt", pp.
368-384, in Disposal of Radioactive Wastes. Conf.
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Vienna ( 1960).
47. Bruce, F. R.. "Industrial radioactive waste disposal.
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Subcommittee on Atomic Energy, Congress of theUnited States, Eighty-Sixth Congress. United States

36. Bogorov, V. G .. B. A. Tareev, K. N. Fedorov, "Thedepths of the ocean and the question of radioactive
waste disposal in them", pp. 210-217, in Disposalof Radioactive ·wastes. Conf. Proc., Monaco, 16-21
Nov. 1959. IAEA, Vol. 2, Vienna (1960).
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to the ground'', pp. 1205-1217 in Industrial Radioactive Waste Disposal. Hearings before the Special
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Radioactive Waste Disposal. Hearings before theSpecial Subcommittee on Atomic Energy, Congressof the United States, Eighty-Sixth Congress. UnitedStates Gov't. Printing Office, Vol. 3, Wash. ( 1959) ;v.e. United Nations document A/ AC.82/G/L.287.
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EE! publication No. 60-46, New York.

MEDICAL, OCCUPATIONAL AND OTIIER EXPOSURESCONTENTS
Paraoraplu

Paraorap/&s

I. INTRODUCTION • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • •I!. MEDICAL USES OF IONIZING RADIATION • • • • • • • • • • • •The genetically significant dose . . • . . • • . • • • • • . • • . •Definitions and calculations • . • . . . . • • . . . . . . . . • .
Data .. . . .•. . . • . . . . . • . . . .. . . . . . . .. . . •. . • . • • . •X-ray diagnosis . . . . • . . . . . . . . • . . . • . . . . . . • . . .
(a) National surveys • . . . • . . • . . . . . . . . . .. •( b) Other investigations . . • • . . . . • . . . . . . . .
(c} Mass survey examinations of the chest(d} Comments • • • • • . • . . . • • . . . • . . • . . • . . . .
(e) Consideration of the dose-rate effect...
(/) Reduction of the genetically significant
dose . . .. . . . . ... .•. • . . . • . . •. .• . . . • •External radio-therapy by X-rays and sealed
radio-active sources . . . • . • . . • • . . .. .. • . . • .
(a) National surveys • .. .. .. • . • • • • . • • • • • .
(b) Other investigations . . .. ... . . . • . •. . • .
(c} Comments • . . . . . . . .. • . . . . . . . • . . • • . . .
(d) Consideration of the dose-rate effect..
(e) Reduction of the genetically significant
dose • . . . . . . . . • • • . . . . • . . . . . • . • . • . . .
Administration of radio-isotopes • . . . . • . . . . . .
(a) National surveys . . . .. • . . . . . .. . . . .. . •(b} Comments...........................
(c} Consideration of the dose-rate effect • •(d) Reduction of the genetically significant
dose •• ••• • • . • . • .. . . . . . •. . ••• • •• . . .
Summary....................................
Exposure of the bone-marrow • . • • . • • • . • . • • • . . . •Determination of the mean marrow dose . • . . . .
Distn1iution of active bone-marrow . . . • • . . . • . • •Dose data . . . . . • • . • . . . . . . . . . . . . . . . • . • . . • . . . • .
X-ray diagnosis . • . . . . . . . . . . . . . • • . • • • . • . . . . .
External radio-therapy by X-rays and sealed
radio-active sources . . . . • . • . . . . . • . . . . . . . . .
Administration of radio-isotopes . . . . . . . . . . . .
Comments . . . . . . . . • . . • . . . . . . . . . • • . . . . . . . . . . . .

Dose to other organs and tissues of special interest 91-98
General remarks . . . . . . . • • . . . • . . . . • . . . . . • • • • • .
91
Data . . . • •• . .. . • . .. .• . . • . • •. . . •• . • . . • . .. . . . . . 92-97
Foetal tissue . . . . . . • • . . . . . . . • • . . . . • . . • . . • . . .
93
Lens of the eye • . . • . • • • • . • . • . . • • • . . . • • • • . . . •94
Thyroid . . . •. . •..•..•.. ••. . . . . . . .• .• . .• • . . •95
Thymus •.... .... •. ••• •.. .• . ••.•... ••... .. .
96
Liver......................................
97
Reduction of doses to various organs and tissues
including the bone-marrow . • • • . . . . • . . . . . . . •98Fields of research . . • . • • . • • • . . . • . • . • • • . • • . • . . . . •
99

1-6

7-99
9-74
9-12
13
14-43
14-28
29-30
31
32-37
38-4-0Ill. OCCUPATIONAL EXPOSURE . . . . . . . . . . . . . . . . . . . . . . . 100-116
Number of installations and radiation workers •.. 101-103
Recommendations on the conditions of work •.•. 104
Dose information from individual monitoring .••. 105-110
Internal contamination • ; •.••.••.••.••.••••••• 108
Mining: industrial processing of uranium and109
thorium ••••.•••••••.••••••.••••.....••••.•
Luminizing industry .....•..••............••. 110
Estimates of occupational e.'tposure in high altitude
aircraft ..................................... 111-114
Genetically significant dose • • . . . . .. . .. • . • . • .. . .. 115~iean marrow dose . . . • . . • . . . . . . . . . . . . . . . • . • . . .
116

41-43
44-61
46-49
50-53
54-57
58-60
61
62-73
64-69
70
71-72

IV. OTHER EXPOSURES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 117-126
Radiological installations . . • . . . . . • . . • . • • . . • • • • . • 118
X-ray fluoroscopy for shoe fitting . . . . . . • • . . . • . . 119
Luminous markings in clocks and watches........ 120
Television sets ................................. 121-123
Passengers in aircraft • • . . . . . • . . . . . . . . . . . . . • • • • . 124
Use of nuclear power in ships . . . • . . . .. . . . • • • . • . 125
Genetically significant dose • . . . . . . . • . . • . . . . . • . . . . 126

73
74
75-90

76-77
78-79
80-89
81-85

APPENDIX

86-88
89
90

TABLESREFERENCES

I. Introduction

3. The term "occupational exposure" is, in the present
annex, taken to apply to all activities involving exposureof workers to ionizing radiation in the course of theirwork, regardless of whether the workers are directly engaged in radiation work or not.1 • 2

1. This anne.x deals mainly with information and dataon radiation doses to individuals and populations as aresult of exposure to ionizing radiation of:(a) Patients undergoing medical radiological procedures-medical e.xposure;(b) Workers as a consequence of their work-occupational exposure ;( c) Persons from miscellaneous man-made sources
and abnormal exposure to natural radiation, when thee.xposures do not belong to (a) or (b)-other exposures.
2. The term "medical exposure" is taken to apply to
all types of e.xposure (except occupational) resulting
from radiation administered by radiologists, generalpractitioners, dentists, obstetricians, osteopaths, chiropractors, etc.

4. Data concerning radiation doses to specific organs
and tissues, and to the whole body may be used for the
purpose of:(a) Risk estimates; this implies adequate knowledgeof the dose-effect relationship;( b) Education, which, by presenting comparative
data, might result in improved standards of operation
and a reduction of doses ;( c) Guiding epidemiological studies.
5. The concept of significant dose for the evaluationof a specific biological risk was considered by the Com-375

mittee in its 1958 report (chapter II, para. 26) 3 in thefollowing way:
"Any specific biological effect of irradiation mustbe evaluated from physical factors such as the distribution of tissue dose (expressed in rem) in space
and time and from biological factors such as radiosensitivity. latent period, recovery and repair. TJ1e
simplest situation is that in which a dose-effect relation for a biological effect is known, making it possible
for the probability or degree of this effect to be calculated. Whether the effect eventually may manifest
itself in the form of deleterious consequences, however, depends on individual circumstances such as expectation of life, or, in the case of genetic injury,
expectation of children. For this reason, the potential
effect indicated by a direct application of an assumed
dose-effect relation must be weighted according tothese individual circumstances."
As has been pointed out earlier in the present report,
quantitative risk estimates presuppose assumptions regarding the dose-effect relationship. As long as the truemode of dose-effect relationship is not known, any useof the presented dose data for risk estimates must be
made with the recognition of the necessary assumptions
and the awareness of the uncertainty of the result. In
any circumstances only comparative risk estimates may
be made on the basis of the presented data and theyshould be limited to considerations of exposures to thesame organs or tissues.
6. The present annex deals with the following typesof radiation dose:(a) Genetically significant dose;( b) Mean dose to the active bone-marrow;( c) Doses to organs and tissues of special interest.
Data on radiation exposure to the gonads are presented
using the accepted definition of the genetically significant
dose (para. 9) with the intention that they may be used
for comparative risk estimates of the radiation-induced
genetic effect. following the procedures outlined in the1958 report. However, in the cases of radiation e.-x:posures to the bone-marrow and to other organs and tissuesof special interest the data are not given with the intention that they be used for risk estimates but for educational purposes and as a guide for epidemiological studies
as mentioned in paragraph 4 above. Medical exposure
is dealt with in paragraphs 7-99, occupational exposurein paragraphs 100-116 and other exposures in paragraphs 117-126.
II. Medical uses of ionizing radiation

7. Medical exposure arises from the following typesof procedures:(a) X-ray diagnosis ;( b) Radio-therapy by X-rays and sealed radio-active
sources;(c) Administration of unsealed radio-isotopes fordiagnostic, therapeutic and research purposes; radiation
exposures also result from the use of contrast media
containing radio-active materials. e.g. thorium dioxide.

(a) Table I deals with X-ray diagnosis. Alt.hough thefrequencies are based on sample studies, nine of thetwelve countries which had carried out comprehensive
surveys had similar amounts of radiography and fluoroscopy (excluding mass surveys and dental exposures).
Their annual frequencies range between 260 and 410
examinations per 1,000 individuals. The frequency figures in the cities tend to be higher than those based on
the whole country, not only because cities usually havemore X-ray facilities, but also because many patientsare examined there without being residents of the city
itself or the surrounding suburban area.
( b) Table II, which sets out the frequencies of cases
treated with X-rays and sealed radio-active sources,
shows large differences between the various countries
and areas.
( c) Table III gives the frequency of the administration of radio-active isotopes to cases for either diagnostic
or therapeutic reasons. The number of patients undergoing diagnostic procedures is four to ten times higher
than the number undergoing therapeutic procedures. The
table also gives the annual consumption for medical useof !131 , P 32 and Au198 • The contribution to the amountsof radio-active isotopes from the diagnostic use may bedisregarded, as compared to the amounts used for therapeutic purposes. The information usually originatesfrom the distributors. The figures given for the amounts
should be regarded as maximum estimates in view ofthe disintegration of the radio-active isotopes in transit
and because the total amount of requested isotopes may
not have actually been used for medical purposes.
THE GENETICALLY SIGNIFICANT DOSE

Definitions and calculations

9. In the 1958 report the genetically significant dose
was defined (chapter II, para. 27) as" ... the dose which, if received by every member ofthe population, would be expected to produce the same
total genetic injury to the population as do the actual
doses received by the various individuals".
This definition was based upon the following assumptions and considerations :(a) The relevant tissue dose is the accumulated doseto the gonads ;( b) The dose-effect relation is linear, without athreshold;( c) Th~ individ~al gonad dose is weighted with afactor which takes mto account the future number of
cl:ildren expected of the irradiated individual comparedw1~ an average member of the population (in this connex10n the foetus is treated as such an irradiated individual and not as a child to be expected).
10. Evidence ha~ lately been obtained that although
the dose-ef!ect relat~on for the prod.uction of most genetic
damage rrught be linear at any given dose-rate, it has
a lower slope for low dose-rates than for hicrh ones.
(C, 84-87) There are also indications that th~ genetic
damage to future generations at any given dose or doserate may differ with sex and with the cell-stage of agamete, depending on a difference in the radio-sensitivityof the male and female gametes and on a difference in
the J?Ossibili~y of transferring the damage to future generat10ns. This means that the \Veighting of the individual
gonad dose should, in addition to the factor for future
number of children, include weighting factors for thedose-rates to the gonads and for the difference both be-

8. Data on the frequencies of radiological proceduresin various countries and areas are presented in tables I,
II and III. The frequency figures are obtained as theannual number of procedures per 1,000 individuals of
the population under study:
376

tween the se.xes and the cell-stages. Since these newweighting factors are not yet known, it is not possible
to incorporate them in the calculation of the geneticallysignificant dose.
11. It is still justifiable to use the formulas for the calculation of the genetically significant dose as they were
presented in the previous report. The derivations of theseformulas are therefore repeated in the appendix.. *12. Available information on genetically significant
dose and its parameters is given under the heading"Data", with the following subdivisions: X-ray diagnosis; radio-therapy by X-rays and sealed radio-active
sources; administration of radio-active isotopes.
Data
13. During the last few years many investigations
have been performed to determine the genetically significant dose arising from medical exposure. Thoughmost of these were performed along the lines presented
in the appendix. using either formula 8 or 11 for the
calculations. the sampling techniques and the modes ofmeasurement or estimation of the gonad doses vary.
Because of this, short explanatory statements of the investigations presented are given below in paragraphs
17 to 30.
X-ray diagnosis-(a) National surveys
14. Tables XVIII and XIX present the average gonaddose for each of the ten most significant examinations
for each of the countries submitting information, withthe reservations of paragraph 15. Table XVIII gives thevalues for examinations of male patients and table XIX
the information for female patients. Table XX presents
the values for the foetal gonad dose during examinationsof the obstetric abdomen and pelvimetry. Only the Federal Republic of Germany (Hamburg) and the United
Kingdom presented separate values of foetal gonad doses
for the other examinations. Some countries assumed
that the foetal gonad dose was the same as the female
gonad dose for these other examinations. The variationin the values shown in these tables demonstrate that for
any one e.xamination a wide range of gonad doses may
be obtained. This is due to varying techniques, for e.xample the amount of fiuoroscopy carried out as part ofan examination and the size of the incident skin fields.
Reductions in both of these will greatly reduce gonaddose in an examination. Table XXI presents the total
genetic dose contribution for each examination for eachof the countries submitting information. Similarly, table
XXII gives the same information but presented as thepercentage of the total genetic dose of each country,
whilst the totals are summarized in table XXIII.

15. Further details of the genetic dose computations
and data for each country may be obtained by reference
to the national tables presented as tables IV-XVI. In
these tables the ten types of examination which contribute most to the genetically significant dose originatingfrom X-ray diagnosis are set out in descending order of
their contribution. All other types of examination arepresented as a whole. As an exception to this principle,
the two types of obstetrical examination, e.g., pelvimetry
and obstetric abdomen, are always individually presented, although their contribution to the genetically sig-

* Although, for editorial reasons, the pertinent paragraphs
are not directly quoted, they are substantially a quotation fromthe Co=ittee's 1958 report, annex C, para. 6-17.

nificant dose does not always justify this. They are thenplaced at the bottom of the table, replacing the ninth andtenth types of examination. It should be mentioned that
although the genetically significant dose is referred toas the "annual" dose, the validity of the figures is limited
to the year or years to which the surveys relate.
16. The doses to the gonads and the annual geneticallysignificant doses are presented in mrem. The dose-rates
being the dose averaged over the exposure time are presented in mrem per sec and for the purposes of thisanne.x it is assumed that for X-, /3- and y-radiation 1 r
corresponds to 1 rad and to 1 rem.
17. Argentina (Buenos Aires). Table IV is based ona report by Placer. 4 His investigation is limited to radiography. Studies on the numbers of different types ofradiographs and their distribution by sex of the patients
radiographed were undertaken in a total of eighty-si.x
hospitals and medical centres. The dose measurements
were made with ionization chambers and film badges attached to the skin of the patients. Depth dose data wereused for computing the gonad doses. The geneticallysignificant dose was calculated from formula 11. The
mean age of child-bearing was set as thirty. It should beemphasized that Placer's report deals with numbers ofradiographs and not examinations. An estimate of thecontribution to the genetically significant dose caused byradiography in private clinics and practices has been
made, assuming the distribution of the radiographs invarious types of examination to be the same as in thehospitals.
18. Denmark. The figures presented in table V are
taken from the investigation published by HammerJacobsen. 5 The figures on the numbers of various typesof examination are based upon a sample inquiry. Information on sex and age distribution of the patients was
obtained from a special study on 139,000 e..xaminations.
Measurements on the doses to the gonads were madewith ionization chambers on 2,475 patients during theactual course of examination. Data on doses to the foetus
were obtained by measurements in a phantom. The genetically significant dose was calculated by means of formula 8 in the appendix. The fertility factors used were
calculated from the official vital statistics of the population.
19. Federal Republic of Gernumy (Hamburg). The
data in table VI are taken from the investigation published by Holthusen, Leetz and Leppin. 6 The geneticallysignificant dose was calculated by means of formula 8.
Information on the number of examinations of various
types, subdivided by sex and age of the patients, wascollected by means of questionnaires. compiling all examinations during the period from November 1957 toOctober 1958. Measurements were made on the gonad
doses to adults in the course of examinations belonging
to the types which were e..xpected to give the highest
contribution to the genetically significant dose. In addition, gonad doses to children and to adults were takenfrom an investigation made by Seelentag.7 The figuresford; in table VI are, according to the original paper,mean figures including all age groups. They were obtained by means of formula 8 after the detailed calculation of the annual genetically significant dose had beenmade. The fertility factors were computed from theofficial vital statistics of the population. For comparative
purposes figures are presented for the annual geneticallysignificant dose using formula 11 and a figure for theannual per capita dose for the whole population, disregarding fertility factors.

377

20. France. Table VII is based upon data publishedby Reboul et al.s-Hi The sample study of ~he nu~b:r. ofdifferent types of examinat10ns ar_id their subdjv1s1onwith regard to sex and age of the patter_its, was perrorme_d
in Bordeaux during 1957, and compnsed ~6,0~0. exa!111nations. By means of the records of the Secunte soc1ale
the results obtained from the sample study were extrapolated to cover the whole of France. Measurements ofthe gonad doses were made during the examinations.
For the female patients, the ionization chambers wereplaced on t_he skin at the level of.the ovaries. The fac_tors
for the ratio of ovary dose to skm dose were determinedby measurements in cadavers and phanto~s. The genetically significant dose was computed with the use offormula 11.
21. Italy (Ro-me). Table VIII is based on an investigation published by Biagini, Barilla and Montanara.11
The numbers of examinations of various types, subdivided by sex and age of the patients, are based upon ayear-long study of the number of examinations performed in certain selected hospitals and clinics. A special
correction was made, to exclude the e..'Caminations onpatients who were not residents of Rome. Using ionization chambers the authors arrived at gonad doses throughmeasurements in a phantom and in patients during theexaminations. In order to account for the variations in
the gonad doses as a consequence of differences in technique and physical parameter, figures on gonad doses
were obtained as mean figures from pertinent data
presented by ten authors. The genetically significant dose
was calculated from formula 8. The fertility factors werecomputed from official vital statistics of the population.
22. Japan. Table IX is based upon data from a Japanese report.12 This investigation is based upon two
sample studies, the first covered seven districts comprising around 80,000 examinations and the second was
representative of the whole of Japan, in which details of
66,000 examinations were obtained. The sample studies
for the collection of numbers of examinations lasted for
one week each. During this period, information was also
obtained on the sex and age distribution of the patients.
The gonad doses to adults and children were obtained bymeasurements with ionization chambers in body-shaped
phantoms. The influence on the gonad doses as a consequence of variations in physical parameters was investigated. No measurements were made of doses to the
foetal gonads. Fertility factors were determined fromofficial statistics. The genetically significant dose wascalculated according to the principles set out in formula 8.
The contribution to the genetically significant dose fromthe exposure of foetal gonads was computed only for
obstetrical examinations.
23. Netherlands (Leiden). Table X presents data obtained from Beekman and v\Teber. 13 The numbers ofroentgen examinations of various types are based upona study of the records from 30,000 examinations. Information on sex and age distribution in different typesof examination was also collected. The gonad doses wereobtained from measurements with ionization chambers
in a body-shaped phantom. The influence on the gonad
doses was studied in relation to variations in e..'\:amination
techniques and physical dose parameters. The figures
presented for gonad doses are averaged with regard to
the existing ranges of techniques and parameters. The
annual genetically significant dose was calculated bymeans of formula 8. For comparative purposes, formula
11 was used, under the assumption that the mean age ofchild-bearing was thirty years. In addition, a per capita
378

annual gonad dose was calculated without reg~d to thefertility factors. The fertility factors were obtamed fromthe official vital statistics of Leiden.
24. N oriJJay. The data set out in table XI are extracted
from an investigation performed by Flatby.u Information on the numbers of examinations of various types
was obtained during 1957 and 1958 from all the establishments in Norway where X-ray diagnosis was performed. The subdivision of the number of examinations
by sex and age of the patients was based on a study c?mprising four diagnostic departments ( 40,~0 examu~a­tions). The gonad doses were measured directly withionization chambers during the e.~amination. In addition,
doses to the ovaries were also assessed by measurements
in a body-shaped phantom. The dose measurements comprised around 1,300 patient and 100 phantom measurements. The fertility factors were determined from theofficial vital statistics of the population. The geneticallysignificant dose was calculated by means of formula 8.
25. Sweden. Table XII summarizes the data on genetically significant dose presented in the _Comn:iitt~e's
previous report. The data are based on the mvest1gation
published by Larsson. 15 Information on the numbers of
examinations of various types, subdivided by sex andage of 'the patients, was collected from a sample of hospital records ( 40,000 examinations) and corrected by an
estimate of the numbers of examinations performed byprivate practitioners. Only around 5 per cent of the total
number of examinations were carried out by these practitioners. These were mainly chest and small bone
examinations. Around 1.900 measurements of the doses
to the male and female gonads were performed withionization chambers during the actual course of examination. Only the doses to foetal gonads were obtained bymeasurements in a phantom. The fertility factors werecomputed from the official vital statistics of the population. The genetically significant dose was calculated fromformula 8.
26. Switzerland. Table XIII is based on an investigation performed by Zuppinger, Minder, Sarasin and
Schaer.16 Through a sample study, lasting for three
weeks in 1957 and comprisin'g around 65,000 examinations, information was gained regarding the numbers of
examinations of various types, subdivided by sex andage of the patients. The doses to the gonads were obtained partly from the authors' own measurements withionization chambers in patients and a body-shaped
phantom, and partly, when appropriate, from dose data
published in other countries. Since the Swiss investigation started with the original intention of computing thegenetic dose to individuals below the age of forty butlater changed to a determination of the genetically significant dose according to formula 8, the calculations
were not made directly with the use of this formula,although the principles were the same. The fertility factors were determined from official statistics.
27. United Arab Repieblic.17• 18 Investigations carriedout in Ale.'\:andria and Cairo during the years 1955-1961
are presented in tables XIV and XV. They are representative of the whole of Alexandria and the area west
and south-west of Cairo. Phantom measurements werecarried out on a selection of units used in these cities.
The calculations were made on the basis of formulae 8
and 11 and the results presented as a weighted mean.
The survey showed that some 17 per cent of the annual
examinations were for investigations of the urinary
tract. This is due to the investigation of the endemic
disease, schistosomiasis.

28. United Kingdom. The material presented in table
XVI has been taken from the report of the Adrian Committee.19 The comprehensive survey covered all medical
radiology carried out in the United Kingdom, except
Northern Ireland. The numbers of e..xaminations ofvarious types and their distribution by se..x and age ofthe patients are based on t\vo nation-wide sample studies
in 1957, each one lasting for one week, and together
comprising around 310,000 examinations. The wholecountry was divided into nineteen regions and in eachmeasurements were carried out in a sample of six hospitals. The gonad doses were obtained for 5,400 examinations by measurements with ionization chambers. The
methods used for making these measurements were:( i) Male patients: by a direct dose measurement madewith the chamber in contact with the scrotum during theexamination ;(ii) Female patients : by an indirect method, using
the dose to the skin at the level of the iliac crest, measured
during the course of examination. and the ratio of thecorresponding skin dose and the ovary dose, as obtained
from dose measurements in body-shaped phantoms;(iii) Foetus: by calculations based upon dose data
derived from body-shaped phantoms.
The fertility factors were computed from official statistics. A separate statistical investigation was made to
determine the average number of future children to beborn to a pregnant woman. While the accuracy of thisestimation is low, the general indication is that the fertility factor for a pregnant woman is higher than thatfor a woman in the population at large. These higher
fertility factors, although admittedly approximate, havebeen used solely in computations on examinations madein conne..xion with a pregnancy, viz. pelvimetry andobstetric abdomen examinations. The genetically significant dose was calculated by the use of formula 8.

( b) 0 ther investigations
29. United States of America. Most of the national
surveys are performed in countries with small populations. In countries with large populations, a small-scale
study may not truly reflect the situation, especially when
there are great variations within the country in the parameters that determine the genetically significant dose.
For the United States, Laughlin and Pullman 20 made anestimate of the annual genetically significant dose, on thebasis of those data in the literature up to 1955. using
formula 11. They arrived at a figure of SO + 25 mrem
as a minimum estimate and a more probable estimate of
140-+- 100 mrem. With the same formula. Nonvood
et al. 21 calculated the annual genetically significant dose
caused by X-ray diagnosis for the inhabitants of a small
American town to be 45 mrem. Another United States
investigation 22 covers the employees of the Oak Ridge
National Laboratory who were regarded as patients. The
annual genetically significant dose from X-ray diagnosis
was found to be 50 mrem ( 13 mrem caused by e..xposureof male patients and 35 mrem by e..-..cposure of female
patients). The results of the two later investigations arewithin the range of the minimum estimate obtained by
Laughlin and Pullman.
30. USSR. In the USSR no calculations of the genetically significant dose arising from medical X-ray diagnosis have yet been published. However, Pobedinsky23 has
published data on the doses to the gonads during diagnostic X-ray examinations, e.g. chest, stomach (barium·meal), kidneys, gall bladder. pelvic region, lumbar spine
and lumbosacral region. The data, which are based

upon dose measurements in a body-shaped phantom, arewithin the ranges of the individual gonad doses presented in tables XVIII and XIX. Data have also been
published by Vikturina. ~~ Provided there are not significant differences in the age distribution of the patients and in the numbers of examinations of various
types, it is reasonable to believe that the annual genetically significant dose from X-ray diagnosis in the
USSR is of the same order of magnitude as the doses
presented in the summary table, XXIII.
( c) lvlass sitrvey examinations of the chest
31. Since mass survey examinations of the chest are
frequently performed in many countries, current interest
has been devoted to the doses associated with this typeof examination. In table XVI! data have been collectedfrom various countries and areas for gonad exposure inthis type of survey examination. In most countries these
examinations are performed as mass miniature radiography (photo-fluorography). The table shows that theseradiographic examinations, in spite of their high numbers, give a very low genetically significant dose. In somecountries, however, survey e..-..caminations are performedby means of fluoroscopy. These e..xaminations give individual gonad doses which are up to 100 times higher
than those given by mass miniature radiography. Even
if the doses to the gonads are much lower than in manyother types of examination, the high number of these
fluoroscopic examinations among individuals in the prefertile and fertile ages may cause a considerable contribution to the genetically significant dose. Therefore, inorder to reduce the dose, mass miniature radiography
should be used when practicable rather than mass survey
fluoroscopy.
( d) Comments
32. Certain types of examination, mainly those of thepelvic region, together contribute 85-95 per cent of thegenetically significant dose. This is shown in table XXII.
However, in terms of numbers of examinations, these
examinations represent only about 15 per cent of thetotal in those countries where the contributions fromchest and mass survey examinations are small.
33. The following points from the national tables require further explanation:(i) In table VI, relating to Hamburg, the colon examinations are responsible for a third of the total genetically significant dose. Holthus en et al. 6 have e.-..cplained
this as being the result of a special technique used in
Hamburg for colon examinations, involving extensive
fluoroscopy.
(ii) In Japan12 stomach and colon e..xaminations cause
50 per cent of the genetically significant dose. Table IX
shows high gonad doses for the fluoroscopy in these two
types of examination, which form 23 per cent of thetotal number of Japanese examinations.
(iii) In the Netherlands (Leiden) (table X),13 pelvimetric examinations are never performed and the number of obstetrical abdomen examinations is very low.
Although the investigation reflects only Leiden, thisstatement is valid for the whole of the Nether lands.
(iv) Table XII, relating to Sweden, 15 shows a highcontribution to the genetically significant dose caused by
foetal exposure during pelvimetry. Since the investigation was made, the examination technique for pelvimetry
has been changed in Sweden with the result that thedose to the foetal gonads has been decreased to a small
fraction of the previous dose. 25379

(v) Table XVI (United Kingdom) shows that obstetrical abdomen examinations form nearly 70 per centof the genetically significant dose caused by foetal
exposure. 19
34. In table XXIII, the annual genetically significant
doses arising from X-ray diagnostic procedures invarious countries and areas are brought together. The
contributions to the genetically significant dose causedby diagnostic exposures of males, females and foetuses
are given separately. For some countries and areas, estimates are also given of the uncertainty in the determination of the genetically significant dose.

35. Table XXIII gives information covering populations that together comprise over 200,000,000 individuals (6-7 per cent of the total population of theworld).
36. Some estimates of the genetically significant dose
arising from X-ray diagnosis do not include the contribution from dental radiography. However, available
data show that this contribution is very small with values
ranging from 0.01 to 0.15 mrem/y.
37. In the investigations from the Federal Republicof Germany (Hamburg) 6 and from the Netherlands(Leiden) 13 comparisons were made between the genetically significant dose computed according to formulas
8 and 11 in the appendix. The figures are set out in
table XXIII. There is good agreement between the figures derived by the use of fonnula 8, which accounts forthe relative child expectancy of the average individualfor each type of examination, and by the simplified formula 11, which considers only the examinations performed on patients below the mean age of childbearing(usually thirty years). The per capital dose was also computed for Leiden and Hamburg. In these two cities fae
per capita dose is much higher than the genetically significant dose, which means that the relative child expectancy factor ( w i/w) is considerably less than unity
for most of those types of examination that contributemost to the genetically significant dose. In other countries
the per capita gonad dose may be of the same magnitude
as the genetically significant dose as indicated in the lastreport. This depends upon the age distribution of thepatients within the various types of examination and thefuture number of children expected to be conceived after
the exposure.
( e) Consideration of the dose-rate effect
38. As was pointed out in paragraph 10, there is now
experimental evidence with mice and insects that thegenetic effect caused by irradiation is governed not onlyby the magnitude of the dose but also by the rate at
which the dose is delivered. Table XXIV presents probable dose-rates to the gonads during some types of examination and during fluoroscopy and radiography. Because of the difference in the sites of the testes and theovaries. the dose-rate to the ovaries is lower than to thetestes when the gonads are in the primary beam. Since
examinations usually consist of several radiographs ofvarious sites and in different projections, and sometimesof both radiography and fluoroscopy, the dose-rate mayvary considerably during an examination, by a factor of
1,000 and even more. Although table XXIV presents
only probable dose-rates, these range from 0.005 mrem/
sec to 2,000 mrem/sec, which is a difference of a factor
106 • The lowest dose-rate presented in the table is still
1,000 times higher than the dose-rate by which the natural radiation is delivered. The range of dose-rates used
380

by Russell in his experiments are quoted in table XXIV.
These dose-rates, which were used in obtaining experimental evidence for dose-rate dependence, are within
the range of dose-rates which occur in X-ray diagnosis.
39. Except for e..xaminations consisting of only one
radiograph, or continuous fluoroscopy, the dose to thepatient strictly must be regarded as fractionated, eventhough for most examinations the duration is short compared with the time cycle of cells. An exception is thegeneral film series taken over the alimentary tract. This
type of examination may be conducted over a period oftwenty-four hours, during which radiographs are taken
at intervals of minutes or hours. The rate of deliveryof the dose may either be represented by the actual doserate for each exposure, which usually does not last morethan ten seconds, or by the average dose-rate over the
total time for the examinations, e.g. twenty-four hours.
The computed rate will thus differ by a factor of 104,
depending upon the criterion used.
40. Since Russell's experiments were carried out on
mice with continuous irradiation, with a constant rateof dose delivery at doses of 100-1,000 rem, it is not possible to use his results for a quantitative determinationof weighting factors for the dose-rate dependence in thecalculation of the genetically significant dose arisingfrom X-ray diagnosis.Neither is there information sufficient to take into account the variation in the sensitivity
with the cell stage of the gamete.
(£) Reduction of the genetically significant dose
41. It is obvious that efforts to reduce the geneticallysignificant dose should be devoted to the types of examination which give the highest dose contribution.
Since the genetically significant dose (formula 8) caused
by a type j examination (Di) is the product of the frequency of conducting the examination (Ni/N), therelative child expectancy of the individuals e..xamined(wi/w) and the gonad dose (dJ), a decrease in thegenetically significant dose may be achieved by a reduction in NJ, WJ or di:-(i) Ni may be decreased by lowering the number oftype-j examinations, which means more rigorous indications for the examinations ;(ii) WJ may be lowered by a reduction of the numberof examinations of young patients;(iii) In general, however, the greatest effect in the
reduction of the genetically significant dose can be obtained by lowering the dose to the gonads, di.
42. The ways of reducing the gonad dose are wellknown and are recommended in most of the papers on
which the tables are based and they are summarized asfollows :26(i) To reduce the number of radiographs per patient;(ii) To reduce the length of time and the intensity of
exposure;(iii) To avoid, as much as possible, pre-set schemesof radiological e..xaminations;(iv) 'When fluoroscopr is not essential, to take radiographs only;(v) To use the appropriate physical parameters, withspecial emphasis to the use of the smallest field size ;(vi) To avoid the inclusion of gonads within the
primary beam ;(vii) To protect the testicles by adequate shieldingof scrotum during male pelvic radiologic examinations ;and(viii) To train properly the staff engaged in X-ray
diagnostic examinations.
43. The Adrian Committee19 states that the result ofbringing the techniques in the 10 per cent of hospitals

showing the highest doses up to the standard of theaverage technique of all the other hospitals would in
total reduce the genetically significant dose to 70 per
cent of the present one. If the techniques used by the 25
per cent of the hospitals in the survey showing the lowest
doses were used by all hospitals it would mean a reduction of the genetically significant dose to less than 20 per
cent of the present value. For Sweden, Larsson15 estimates that an increased use of already existing examination techniques, which give low gonad doses, would
mean a reduction of the genetically significant dose to
40 per cent of its existing value. Such reduction may
be achieved without detriment to the diagnostic information to be obtained from the e..""{aminations.
External radio-therapy by X-rays and sealed radio-active
sources
44. As compared to those for X-ray diagnosis, there
are few data for gonad doses and genetically significant
dose caused by exposure of patients undergoing external
radio-therapy. One of the reasons for this is that thefirst investigations showed that the contribution fromexternal radio-therapy to the genetically significant dose
was less than the contribution from X-ray diagnosis.
However, detailed data on gonad doses and geneticallysignificant dose arising from external radio-therapy haverecently been obtained from the Federal Republic of
Germany (Hamburg), France and the United Kingdom.
To make estimates of the average gonad dose received
during the treatment of any one disease is more difficult
than for one diagnostic examination since a disease suchas eczema may affect any area of the body and the detailsof the actual treatment are not always available. Therefore details of the treatment of a large number ofpatients are required to get a representative distributionof the sites affected by a particular disease.

45. Radio-therapy is used in the treatment of nonmalignant and malignant conditions. It is necessary toconsider in any calculation of genetically significant dosefrom radio-therapy the effect of the disease itself andthe irradiation on the relative child expectancy. It may
be assumed that neither the non-malignant conditions
nor the radiation doses, with the possible e..""<:ception of
those in the regions of the gonads, affect the fertility ofthe patients. However, for patients suffering frommalignant conditions the life expectancy is usuallyshorter than in the general population and in each age
group of such patients a lesser number of children will
be conceived as compared to the statistics for the whole
population. The irradiation itself may cause decreased
fertility, which would also reflect upon the number ofchildren to be e..""<pected.
(a) National SJ.trveys
46. Federal Republic of Germany (Hamburg): The
investigation performed by Holthusen, Leetz andLeppin6 also covers radio-therapy. The number of patients treated for various conditions, subdivided by sex
and age, and the individual gonad doses were arrived
at by the same methods as were used for X-ray examinations (para. 19). In their calculations Holthusen et al.
have taken the fertility factors to be zero for patients
who have been irradiated for malignant diseases, andpresume that the genetically significant dose caused by
381

external radio-therapy arises only from irradiation for
non-malignant conditions. The annual genetically significant dose is presented in tables XXV and XXIX in
which the genetically significant dose is subdivided byvarious locations of treatment. The individual gonad
doses and the numbers of patients treated are also set out.
The genetically significant dose was calculated fromformula 8. For comparative purposes, Holthusen et al.
also calculated the genetically significant dose, using
formula 11, and the per capita dose for the whole population (para. 19).
47. France. The figures for France in tables XXVI
and XXIX are based upon an investigation by Reboul
et al. 21 who determined the number of patients who undenvent external radio-therapy for various conditions ina large hospital. By means of information from the
Securite sociale, these numbers, subdivided by sex andage, were extrapolated to cover the whole of France. The
doses to the gonads in various types of treatment were
measured with ionization chambers in the same way as
has been described in paragraph 20. The genetically significant dose was calculated according to formula 11. In
the cases of non-malignant conditions, only around 7 percent of the dose, expressed by 1:.N i · dl> was estimated tohave been given to patients below the age of thirty. Whenthe contribution to the genetically significant dose fromthe treatment of malignant conditions was calculated,the cases with the most severe prognoses were disregarded. Also, the cases where the irradiation was expected to have caused sterility were disregarded. From
the remaining cases, the numbers of patients below thirty
years of age were estimated by means of their hospitalrecords. These patients together form around 6 per centof all those treated for malignant conditions.
48. Netherlands. The data presented in tables XXVII
and XXIX are from an investigation by Scholte et al. 28
for the period 1942-1951 based on radio-therapy treatments in three large hospitals in The Hague, Leiden andRotterdam. The survey does not include any contribution
from dermatology. The calculations were made according
to formula 8 and it was possible to use the actual numberof children born to the patients up to 1960. The numberof children conceived by the patients who received highgonad doses from pelvic region irradiation were only
53 per cent of those which would be expected from thenumber of legitimate live births in the period 1955-1959
in the Nether lands. Even though these statistics are notstrictly comparable they emphasize the effect of the diseases and the irradiation itself on the relative child
expectancy compared with that based on average valuesof the population.
49. United Kingdom. The data presented in tables
XXVIII and XXIX have been taken from the report of
the Adrian Committee19 which covers the United Kingdom except Northern Ireland. The numbers of patientstreated for various conditions, subdivided by sex andage, were calculated from a sample study during threemonths in 1957 of all treatments carried out in United
Kingdom hospitals and comprising around 30,000 patients. The doses to the gonads were calculated from information on the dose parameters used in various
hospitals and private clinics and the results of dose
measurements in a phantom under various conditions.
The genetically significant dose was calculated according
to the principles set out in formula 8. In the calculationsof the contribution from radio-therapy of non-malignant
conditions, it was assumed that the child e.,"{pectancy was
zero for all patients in whom an artificial menopause wasOark's figures for the United States of America, 2 P 12
mrem, should be compared with the figures in the lastcolumn of table XXX, which are 6.5, 21 and 9 mrem in
the Federal Republic of Germany (Hamburg), France
and the United Kingdom respectively. The explanation
for the difference between the figures for per capita doseand genetically significant dose is the same as was given
in paragraph 37.

induced. For all other non-malignant conditions the fertility factors obtained from population statistics wereused. In the calculation of the genetically significant dose
caused by external radio-therapy of malignant conditions,due attention was paid to the changes in the fertility factors, as determined from official statistics, that are causedby the shortening of the patients' life expectancy and by
the reduction in fertility, due to the radiation received
by the gonads.

57. Both in the FederalRepublic of Germany (Hamburg) (table XXV) and the United Kingdom (table
XXVIII) the major part of the genetically significant
dose caused by ~ternal radio-therapy for non-malignant
conditions originates from treatments of the skin(around 55 and 75 per cent respectively). In France(table XXVI) the bulk of the corresponding geneticallysignificant dose arises from treatment to the lumbar
spine and the hips.

(b) 0 ther investigations
50. In the United States, Oarki 9 estimated the annual
per capita dose of the total population due to external
radio-therapy to be 12 mrem. He assumed that the gonad
doses arising from irradiation for malignant conditions
were of no genetic significance. A survey of the individual gonad doses received has also been carried out
by Bailey.30( d) Consideratioii of the dose-rate effect
58. For the reasons indicated in paragraphs 10 and
38 the probable dose~rates to the gonads during external
radio-therapy of certain treatment areas, are given intable XXXI. The dose-rates have been calculated assuming a maximum dose-rate at the treatment site of 50
rem per minute. Since high doses to the gonads may
cause sterility or reduced fertility, treatment sites havenot been included in this table when the dose to the
gonads during a complete treatment is estimated to exceed 200 rem. The dose-rates range between 0.002 mrem/
sec and 50 mrem/sec, which means that the highest doserate is around 10' times greater than the lowest one. This
range of dose-rates covers the lower portion of the range
used by Russell in his e.xperiments.

51. A survey by Purser and Qvist31 yields an estimateof the annual genetically significant dose in Denmark(Copenhagen) of 1 mrem. In the Danish estimate, reduced fertility as a consequence of the severity of the
prognosis of the disease and of the actual irradiation
was allowed for by subdividing the patients into threegroups, with the fertility factor being zero, one-fifth ofnormal, and normal, respectively. Twenty-two per centof the genetically significant dose was assumed to arise
from treatments of malignant disease.
52. For Australia, Martin82 • 33 estimated the annual
genetically significant dose from external radio-therapy
to be 28 mrem. The estimate was made using the appropriate survival rates from the Central Cancer Registry.
It \vas assumed that the prospects of parenthood were
not impaired by the treatment, except for those patients
receiving doses which would cause sterilization.

59. In most instances external radio-therapy is administered in fractionated doses. In external therapy fornon-malignant conditions a total dose seldom exceeds
3,000 rem given over a period of two to three weeks,
while for malignant conditions doses to the treated volume of up to 7,000 rem may be given. The period oftreatment is varied, dependent on the total dose, up to
about seven weeks. If the gonad dose-rates are calculated as mean dose-rates over these periods, the figuresin table XXXI should be divided by a factor of around103 • The lowest dose-rates would then be of the same
magnitude as the delivery rate of natural radiation(3.1()-6 rem/sec).

53. In the United Arab Republic (Cairo) a survey
has been carried out in 1959-1960 of the frequency oftreatments by X-rays. 3 '· 3~(c) Comments
54. Compared to the genetically significant dose.originating from X-ray diagnosis (table XXIII) the genetically significant dose from external radio-therapy (tableXXIX) is small. However, the individual gonad doses
received from external radio-therapy are larger thanfrom an X-ray diagnosis examination.

60. In radio-therapy, as in X-ray diagnosis (para. 40),it does not seem possible to use Russell's results for aquantitative determination of weighting factors for thedose-rate dependence in the calculation of the geneticallysignificant dose. Neither is there information sufficient
to take into account the variation in the sensitivity withthe cell-stage of the gamete.

55. It is the practice in some countries to use radiation
for so termed ovarian stimulation in cases of subfertility. Little data are available regarding the numbersof such treatments but a report36 shows that, in 33 institutions surveyed in Buenos Aires, 222 cases were treatedin 1960 representing some 2 per cent of the total numberof patients treated by radio-therapy for non-malignant
and malignant conditions. The radiation used was generated at 200-250 kV and the average dose to the ovary
was 60 rem with a range of doses from 35-110 rem.

( e) Reduction of the genetically significant dose
61. In contra-distinction to X-ray diagnosis, where
the radiation is a means for producing an image on ascreen or a film, the dose in radio-therapy to be delivered
to an actual part of the body is determined with regard
to the effect that is sought by the treatment. With reference to paragraph 41, Ni, Wi and di govern the genetically significant dose. Regarding malignant conditions,where there are strong indications for treatment, NJ andwi cannot be expected to undergo changes in favour of
reduced genetically significant dose. For non-malignant
conditions, it might be possible to reduce Ns and WJ byusing stricter criteria for the treatment of non-malignant

56. In the German investigation6 the annual genetically significant dose was calculated according to bothformula 8 and formula 11. The per capita dose for thewhole population was also calculated. On the basis of
the data from investigations in France27 and the United
Kingdom111 the per capita dose to the population arisingfrom the treatment of non-malignant conditions in eachof the two countries has been estimated. The figures
are set out in table XXX. As expected, the per capita
doses are higher than the genetically significant doses.
382

conditions, especially among young patients. Reductionsin the individual gonad doses, di, when the gonads are
not the sites of the irradiation, may be obtained asfollows:(i) By the use of strictly appropriate physical conditions of exposure, placing emphasis on the smallest possible radiation field and, for instance, the use of low
energy radiation and beta-emitting sources in skintherapy;(ii) By satisfactory shielding against leakage radiation;(iii) By the use of scrotum protection;(iv) By adequate positioning of the patients during
treatment so that the gonads are.as far away as possible
from the primary beam.

are presented in table XXXII. The dose was calculated
according to the principles of formula 11 and the genetical significance of treatment for conditions with severe
prognoses was considered. It >vas estimated that only
the use of P 31 gave a dose of genetical significance.
69. In the national surveys presented above (paras.
65-68), calculation of the gonad doses was basedon existing information regarding deposition in variousorgans and tissues and the effective half-lives of theradio-isotopes in question. In table XXXIV, some results
are presented for gonad doses arising from the administration of 1 me P 31 or paz. 31 • 3 - 1 Weijer et al. 39 obtained their results from measurements on patients withdifferent diseases, thus allowing for disturbances in thenormal distribution of P 31 in the body. Regarding I1 3 1,
Johns and Taylor37 found that the beta and gamma components formed 50 per cent each of the gonad dose. The
figures in table XXXIV, or results from other investigations, can be used for estimating the genetically significant dose arising from the medical use of unsealed
radio-isotopes in various countries.

Administration of radio-isotopes
62. Only a few national surveys exist on the contribution from the medical use of unsealed radio-isotopes to
the genetically significant dose. It is assumed that thiscontribution is even less than the contribution from external radio-therapy. The number of cases to whom theisotopes were administered and the total quantities ofisotopes are given in table III.

(b) Comments
70. The contribution from the administration ofradio-isotopes to the genetically significant dose is small(table XXXII) as compared to X-ray diagnosis (table
XXIII) and .external radio-therapy (table XXIX).
Between S and 15 per cent of the genetically significant
dose caused by the administration of radio-isotopes
originates from their use for diagnostic purposes. The
individual gonad doses are estimated to range between
25 mrem and 200 rem.

63. Since unsealed radio-isotopes are used for bothmalignant and ·non-malignant conditions, the same
allowance described in paragraph 45 has to be made forpossible changes in the fertility factors among patients.
This means, for instance, that Aum, although used inconsiderable quantities for treatment {table III) has
been considered to be of no genetical significance. ·(a) National surveys'
64. In the present anne..x, national surveys and estimates of genetically significant dose are presented from
Canada, the Federal Republic of Germany (Hamburg),
the United Kingdom and the United States of America(table XXXII).
.

· 65. Canada.. The figures in table XXXII are takenfrom an investigation published by Johns and Taylor. 37
They considered patients below thirty years of age(formula 11) but did not make any correction with' regard to severe prognoses for malignant· conditions.
P 31 formed 75 per cent and P 32 25 per cent of the genetically significant dose from the administration of radioi active isotopes.

( c) Consideration of the dose-rate effect
71. The dose to the gonads from a deposited radioisotope is received through continuous irradiation, witha decreasing rate of delivery as a consequence of theexcretion and the decay of the radio-isotope. The initial
dose-rate to the gonads per millicurie administered P 31
or P 32 is of the order of 1()-3 mrem/sec. This estimate
does not allow for differences in dose-rates as a consequence of .various distances from the gonads to thedeposits of activity in the body. Since the administered. amounts of radio-isotopes usually range between around
5 µc in diagnosis and 200 me in therapy, dose-rates may
range between s.10-s mrem/sec to 0.2 mrem/sec.

66. Federal Republic of Germany (Hambiwg). Holthusen et al. 6 have studied t.he genetically significant dosefrom P 31 (table XXXII). The dose was ·calculated: according to fohriula 8 but the malignant conditions weredisregarded ( cf. para. 46).

72. Although these dose-rates should be regarded as
rough estimates, they are lower than the ones used byRussell in his e.xperiments. It is not possible at thepresent time to take into account variations of dose-rateor of the cell-stage of the gamete.
( d) Reduction of the genetically significant dose
73. Since the administration of radio-isotopes contributes only 1 or 2 per cent to the genetically significant
dose caused by medical exposure, there is no urgent needfor improvements aimed at lowering this contribution.
The amounts of radio-isotopes used can be decreased indiagnostic investigation by further improvement of thesensitivity of the measuring instruments and by the useof in vitro rather than in vivo tests. Particular care isnecessary when labelled substances are used \vhich areincorporated into the chromosomes, such as thymidine,
for these may result in high radiation doses to the genetic
material. In therapy, deposits of radio-isotopes in organs
and tissues which are not objects of treatment, can sometimes be reduced by special measures. For instance, highfluid intake following P 31 administration induces fre-

67. United Kingdom. The Adrian Committee's results 10 are presented in .table X.XXIII. The geneticallysignificant dose was calculated from formula 8 and thenormal fertility factors were modified for some of themalignant conditions. In table XXXIII the annual genetically .significant. dose is. subdivided into the diagnostic
use of radio~isotopes and their use for the treatment ofmalignant and non-malignant conditions. P 31 delivers
60 per cent and P 32 40 per cent of the genetically significant dose from the administration of radio-active
isotopes.
68. United States of America. Chamberlain 38 has
estimated the annual genetically significant dose fromthe medical use of unsealed radio-isotopes. His results383

quent micturition, thus reducing the residual time in the
bladder of the excreted radio-isotope. 89 This causes a
decrease in the dose to the gonads.

photon energy 50 keV, there is a 13 per cent increase in
the dose received by soft tissue remote from bone.
Distribution of active bone-marrow
78. The calculation of the mean marrow dose presupposes knowledge of the distribution in the body of
the active bone-marrow. A comprehensive study was
carried out by Mechanik 43 of the quantitative distribution of the total bone-marrow in adults. A summary of
his data has been published by Woodard and Holodny."
These studies do not, however, give any information on
the distribution of the active marrow. Studies on the
distribution of the active marrow have shown that before
birth the liver and spleen are the major erythropoietic
organs, the activity of the liver being equal to that of thebone-marrow at 7~ months. At birth all bones whichcontain marrow have active red marrow: however withincreasing age this is gradually replaced in some bones
by inactive yellow marrow. By the age of eighteen to
twenty years little red bone-marrow exists in the limb
bones, except for the proximal epiphysis of femur andhumerus.' 5 A gradual replacement also takes place in all
adult bones with increasing age and measurements ofthis effect have been given by Custer" 6 for the ribs,
sternum and vertebrae. Ellis 47 has calculated from thedata of Mechanik and Custer the distribution of total
and active marrow in the adult (table XXXV). This
table also gives the set of distribution figures that waspresented in the Committee's 1958 report.
79. Further research on the distribution of the bonemarrow is needed, for it is well known that the distribution of active marrow varies very much between adultindividuals. Also diseases or other conditions which impose a stress on the haematopoietic system cause the redmarrow to reappear in the limb bones. Large radiation
doses to local volumes of active marrow may also cause
variations in the active bone-marrow distribution. 0

Summary
74. The annual genetically significant dose frommedical exposure has been shown to be in the range 6-.58
mrem from diagnostic radiology .for. those countr~es
given in table XXIII. The contnbutton from radiotherapy and the use of radio-active isotopes has beenshown in tables XXIX and XXXII to be in the ranges
2-13 mrem and 0.18-0.42 mrem respectively. Due to themany national and international reports on the sub~ect
which have been issued in the last seven years there 1s agreater awareness of the desirability of reducing thegenetically significant dose. This has resulted i~ many
countries in a downward trend in the levels estimated.
For the purposes of making comparisons of risk inanne......: H it has been accepted according to table XXIII
that a representative value of the genetically significant
dose would be 30 mrem/y from diagnostic exposure and5 mrem/y from radio-therapy.
EXPOSURE OF THE BONE-YARROW

75. This section of the annex summarizes the data
regarding the doses received by the active bone-marrowof patients undergoing radiological examinations ortreatments. This tissue is regarded as the significant one
in respect to the induction of leukaemia by radiation(D, 254-271, 485-489). It has been suggested (H. 8) thatthe mean dose to a tissue should be used, in the light ofpresent kno\\•ledge, for the assessment of the effects ofradiation at these dose levels. The term "mean marrowdose" is defined as the dose received by any portion of theactive marrow averaged over the whole mass of active
marrow. The mean marrow dose can either be given for
an irradiated individual or as a per capita dose for a
population. ·Dose data
80. There are few available data on mean marrowdoses from medical exposure.

Determination of the mean marrcr& dose

X-ray diagnosis
81. In its 1958 report the Committee presented mean
marrow doses calculated on the basis of assumed averagepractice and available information for various types of
examination-number of radiographs, skin doses anddepth dose data. Several of these dose figures are set
out in table xxxvr, together with the results from a
Danish investigation performed by Buhl," 9 and frommeasurements by Epp et al. 50• 51 A national survey has
been conducted in the United Kingdom {para. 28) andextensive phantom measurements at eleven marrow sites
are being used to derive a per capita mean marrow dose.
82. Even though the investigations presented in table
xxxvr show differences between the dose figures ineach of several types of examination, the order of thetypes of e......:amination with regard to the size of the doseis nearly the same in the investigations. These types are
examinations of the upper and lower gastro-intestinal
tract (barium meal and barium enema), the gall bladder,dorsal and lumbar spine, and the lumbosacral region.
Pelvimetry also belongs to those types of examination
giving among the highest mean marrow doses. The differences in the dose figures reported for any one examination are due to the variations in the assumed e.xtent andtechniques of the particular examination and the valuesof percentage depth doses used.

76. The marrow doses presented below are given as
individual mean marrow doses for various types ofradiological procedure. Mean marrow doses are usuallyobtained from dose measurements with small ionizationchambers placed either on the skin in the radiation field
or at the actual site of the primary irradiated bonemarrow. In the latter case, the measurements are madein phantoms which undergo the irradiation procedures.
The phantoms should represent as closely as possible,
in size, shape and material, the radiation conditions
in viva. Since measurements with ionization chambers
express exposure doses in roentgens under given conditions, the absorbed doses have to be calculated with theapplication of appropriate conversion factors. Whencalculations are based on exposure doses to the skin, thedose figures have to be multiplied by the percentage depth
dose at the location of the bone-marrow in question,corrected for the shielding effect of the bone surrounding
the bone-marrow.
77. In soft tissues adjacent to bone, the absorbed doseis increased by secondary electrons, which are generated
in the bone. This should be allowed for in the calculationof the absorbed dose to the bone-marrow. A discussionof this effect is included in the report of the ICRU. 42 A
typical example from this report shows that within amarrow cavity of size 400 µ., irradiated by radiation of384

83. It is obvious that the mean marrow dose will depend upon the field size and the incident skin dose.
Another parameter that influences the magnitude of themean marrow dose is the quality of the radiation used.
For radiography of the chest, Epp, Weiss and Laughlin50
showed that a low kilovoltage technique ( 60 keV, 1-2 mm
Al filter) gives 50 per cent greater mean marrow dosethan kilovoltages between 80 and 120 (2-3 mm Al filter),for which the mean marrow dose is nearly constant.
Weber 52 has reported similar results for radiography ofthe stomach (barium meal) and abdomen. He found
50 per cent higher mean marrow doses at 70 ke V ( 2 mm
Al filter) than at 90 ke V ( 3 mm Al filter).

of the bone-marrow. They calculated the mean marrowdoses by means of Ellis's distribution figures for active
marrow.
88. Mean marrow doses to children below two yearsof age who were treated with radium skin applicators forhaemangioma have been reported by Nordberg. 57 Dosemeas~rements were made in a phantom which, in shapeand size, corresponded to a child below the age of two.
It was assumed that the active bone-marrow is distributed throughout the skeleton. The mean marrowdoses were calculated by means of the data on the distribution of marrow space given by 'Woodard andHolodny« assuming that the distribution of marrow
space in children is the same as in adults. The results
are given in table XXXVIII and the distribution figures
used are presented in a footnote to the table.

84. In paragraph 31 it was pointed out that in somecountries mass survey examinations of the chest are
performed by means of either fluoroscopy or radiography (table XVII). Skin doses to patients from f!uoroscopy may amount to more than 100 times the skin dosewhen radiography is used. 53 While reported mean marrow doses for mass survey examinations of the chest
using radiography range between 50 and 100 mrem,
it has been calculated that mass survey f!uoroscopy inAustria, France and Spain gives mean marrow doses
averaging 1,900, 1,200 and 1,300 mrem respectively. 53
For Belgium and Switzerland, the corresponding doses
were reported to be 380 and 230 mrem respectively. The
doses are set out in table XXX:VII. Owing to differences
between apparatuses and the duration of the fluoroscopy,
the individual mean marrow doses range from around
200 mrem up to around 4,000 mrem. Since many of theexaminations in France10 are made on young people( 40 per cent on individuals below the age of twenty)
the figures for the mean marrow doses, calculated bymeans of distribution figures for the active marrow in
adults, may be rather uncertain (para. 78). It is obvious
from this table that in order to reduce the dose, massminiature radiography should be used rather than mass
survey fluoroscopy (d. para. 31).
85. In the 1958 report of the Committee (annex C,
para. 50) an estimate of the population per capita bonemarrow dose was made and it was suggested that it
might be of the order of 50-100 mrem/y. The Committee
has no reason to alter this estimate, as little information
has been obtained since the last report.

Administration of radio-isotopes
89. The data at present available to the Committee on
relevant parameters for !131 , P 3 ~ and Au198 do not sufficefor estimating the individual mean marrow doses withany certainty. The estimates of the total dose to theblood following administration of these isotopes give afirst approximation of the mean marrow dose. 37• 39
Comments
90. The mean marrow doses caused by external radiotherapy are, of course, much higher than the ones caused
through X-ray diagnosis. A diagnostic examination of
the lumbar spine results in a mean marrow dose of 100400 mrem . but the treatment of this site for non-malignant conditions may give a mean marrow dose that is
100 times greater. In certain types of radio-therapy formalignant conditions, the mean marrow doses may beeven higher.
DOSE TO OTHER ORGANS AND TISSUES OF
SPECIAL INTEREST

General rem.arks
91. The organs and tissues which, in addition to the
gonads and the bone-marrow, are usually considered of
special interest with regard to radiation doses are thefoetal tissue, the lenses of the eyes, the thyroid, skin,and the liver. Information regarding the effects causedby the irradiation of these organs are given in anne..x D
together with analyses of the radiation doses which havecaused them. Other information is given in the reportof the meeting, held at the Committee's invitation, of the
ICRPJICRU Study Group in 1960.58

External radio-therapy by X-rays and sealed radioactive sources
86. Few data on bone-marrow doses are available atpresent for patients who have undergone radio-therapy.
Comprehensive measurements of the radiation doses tothe spinal marrow in a phantom were carried out by
Jones and Ellis 5' as part of the survey by Court Brown
and Doll54 on patients irradiated for ankylosing spondylitis. Maudal 55 has also made measurements of doses toorgans and tissues for several sites of treatment. The
latter investigation also gives data regarding the dose
received by sites outside the primary beam. Further
measurements have also been conducted in the United
Kingdom as part of the national survey. All these measurements give the dose at the particular site in terms of
100 rem incident at the skin. Table XXXVIII gives representative values of the mean marrow dose received
during such treatment.
87. Holodny, Lechtman and Laughlin56 have reported
mean marrow doses arising from the treatment of cervix
carcinoma ·with radium applicators. Their results, presented in table X..XXVIIL are based on measurementsof the doses in a body-shaped phantom at different sites

Data
92. Table XXXIX gives a few e..xamples of the radiation doses which may be received by these selected tissues
as a consequence of various radiological procedures. The
doses must not be considered as being the results ofextreme circumstances but as figures obtained fromradiological procedures at present or recently used invarious countries. Particular points regarding each tissue
are given in the following paragraphs.
Foetal tissue
93. During the first two months after conception, it
may happen. because of unawareness of pregnancy, thatwomen undergo various kinds of radiological procedures
which would not have been performed if the pregnancy
had been known. Because of the small dimensions of the385foetus at this stage, the foetal dose can be regarded as
the same as the dose to the maternal gonads. Data regarding the incidence of malignancies following irradiationin utero are given in annex D, paragraphs 277-285, andtable VII.

Lens of the eye
94. Full mouth examination and encephalography are
two X-ray diagnostic procedures which may give substantial doses to the lens of the eye. Similarly, treatmentof lesions of the eye, or in the region of the eye, mayalso contribute high doses. Data regarding the formationof cataract or lens opacity is given in annex D, paragraphs 91-93, 289-307 and 443-445.
Thyroid
95. Tests of thyroid functions are frequently performed in most countries. The dose to the normal adultthyroid is about 1.5 rem per µ.c administered !1 31 • Barium
swallow and examination of the cervical spine are assumed to be the two types of commonly performed
X-ray diagnostic procedure which give the highest doseto the thyroid. The treatment of hyperthyroid conditions
and heart conditions with !1 31 gives doses of the orderof 10,000 rem to the thyroid (see para. 96 below)(D, 286, 402-404).
Thymi's%. In some countries enlarged thymus glands havebeen treated by radiation with doses of the order of 200
rem. In annex D, paragraphs 263-272, 485 and table VI,
data are given regarding surveys carried out on theincidence of leukaemia and thyroid cancer in thesepatients.
Liver
97. The use of thorotrast as a contrast medium indiagnostic radiology has been curtailed since its possible
deleterious effects have been recognized. The effects
observed are sequelae at the site of injection and theinduction of liver malignancies. Reports of surveys ofpatients injected with thorotrast have been given by
Hursh et al., 59 Baserga,60 Looney 61 and Blomberg et aZ. 62
Studies of the radiation doses received have been carriedout by Rotblat and 'lv ard63 and Rundo. 64 • 85 A comparisonof the doses to various body tissues over twenty years
from an injection of 20 ml thorotrast is given in table XLfrom Marine!li. 66
Reduction of doses to various organs and tissites
including the bone-marrow
98. Earlier in this annex (paragraphs 41, 42, 61) the
Committee has considered ways of reducing the doses to
the gonads. Most of these measures are also applicablefor the reduction of doses to other organs and tissues
and can be summarized as follows :(a) Improved methods of radiological procedure ;( b) The use of strictly appropriate physical conditions of exposure, including the smallest possible radiation field and good collimation of the beam ;( c) The reduction of the incident skin dose, e.g. by
reducing fiuoroscopy time ;( d) Satisfactory shielding against leakage radiation;( e) The use of radio-active isotopes in diagnostic investigations utilizing in vitro rather than in viva tests andthe use of the nuclide with the shortest half life consistent with the requirements of the investigation; forexample, 1132 may be used rather than !1 31 for some thyroid investigations.
(f) Well-trained staff of all categories for the performance of the procedures.
FIELDS OF RESEARCH

99. The present state of knowledge requires that consideration should be given to the following items andthat research in these fields should be encouraged:(a) The promotion of statistical studies concerning
the number of people medically exposed;( b) Follow-up studies on the offspring of pregnant
patients having radiological examinations or treatmentsof the pelvic region;( c) Follow-up studies of patients having had ( i)radio-therapy for non-malignant conditions such asankylosing spondylitis and enlarged thymus ; (ii) pu
treatment, or (iii) diagnostic e..xaminations using thorotrast as a contrast medium ;( d) Investigations aimed at defining good practices
in diagnostic radiology so that minimum gonad doses arereceived;( e) Investigations of the effect of dose-rate on the
production of mutation;(f) More quantitative information on the distribution of active marrow and how it varies with age;(g) Investigations of the dose received by the bonemarrow during radiological procedures.

ID. Occupational exposure100. In the introduction to the present annex (para.
3) the Committee considered the term "occupational exposure" as being applicable to all activities involving
exposure of individuals to ionizing radiation in thecourse of their work, regardless of whether they are
directly engaged in radiation work or not.
NUMBER OF INSTALLATIONS AND RADIATION WORKERS

101. Work with ionizing radiation is usually subdivided with regard to the purpose of the work as follows :!Dedi~ (diagnosis and therapy), dental, veterinary,industnal, research and educational, and atomic energy.
!able ~LI gives the range of the number of X-ray
installat10ns* per thousand of total population for these
purposes in th~ Netherlands, 67 New Zealand, 68 Norway, 6 P
Sweden, 70 Sw1tzerland,16 and two areas of the UnitedStates of America, New York City71 and Califomia. 72
Most of the installations for medical and dental purposes
have ~-ray apparatus o~ly. Th~ number of X-ray installat10ns used for veterinary, mdustrial, and researchand educational purposes, is at present very small compared \vith those used for medical purposes.
102. Only a few data exist on the number of installations where radio-isotopes are used. In Californi;hwith radio-isotopes is performed in, 6. :Per,';~ent ·of ·tjle
total number of installations and most of this .work.is
done w?ere X-ray work al~o.i~ p~~for,in~d~72 :~ven~1f
work w!th radio-iso_topes i~ ·cafrie:~ PBt.fn ·}h~jfuijorityof hospitals and of md~stnal and research installations
the large number of' pri~ate m~qical ~4 ·derib! practi~

work* "~nstallation''. cove·r~ ~ny d~pi;~eni:~~ ~rl~~~·e p~ctid~,If ·~~os~1tal h~~ ..a. cent~al .x-.r:ai. depanr.iert:.as \a,·e!La~ X~!;ay fadli-

t1es m vanous ·other sections of the hospital each· one· is counted
as an installation: :; . .'.· ·:·r! i >. :;c:• · , , ~:· ", '., . , _tioners using X-ray apparatuses: e.."<clusively, keeps thefigure low as :compared to X-ray installations. It does.
not· seein likely that in any c9untiy the number! of in-_stallations where radio•isotopes are used . would , sur-·mount 10-20 per cent of-the total number ofinstall~ticins.103. Table XLI also·giv'es the r~nges cif the numbersof individuals per 1,0QO of the p9pulation directly occupied in radiation work· in the· countries listed in paragraph lOl. . - ' '.
.
··: · ; 1 ntenu1l.c011tcimination:

RECOMMENDATIONS.ON
THE CONDITIONS
OF ·woRK.
'.

104. '~ecom~endations regar.ding .the ~~p~sure . ofworkers. to iqnizing ra\iiation have been 01ac).e by the,
ICRP. 1 The doses to whi.ch th~i~.siiggesfed.ligi'its apply
do not include the contributions from natural sources ofradiation, or. f1:qm th,e exposure, of, tl-w. workers for medical reasons. The' ma."<imum permissibfe.levefa of exposure
are . ~ept under .constant ·~urveillance and. the· present
recommendations state that for the dose "accumulated:
in· the gonads; the bl09di forming organs and· the lenses·of the, eyes;· at: any age over 18; shall be g6verned· by the:relatiomn;:::: 5 .(NL..,...18) 'rem;,vhere'D:is1ti~sue dose in·rem.'and N: is age in years'~. TheICRPgoes on::'.'.To_ thee."ttent·the forroUla.1peimits, an ·occupationally e."<posed:
person :mai accumulate, the mafilmum. permissible dose•
a:t.a:rate nbt in· excess :of:3 rem,during~any per~odc:of·
13 consecutive weeks"·~ Exposure·Iimited to• certain parts,of therbody,: stich as. the •extreniities,r orto single·.di-gans;:
as<in:the cas!! 6f internal e.."<posure, .is· subject.to· speciali
recommend~tions '.allowing:,' ~somewhat ·higher' 'doses.:B.ased on these·recommeridations, many national ,arid fo";ternational organizations have produced thei.r own: rules:
and recommendations.

. P9?P i,l:t'.FOR,MA;TIQNFl}IJ¥ J;!-<:D~V!DUAL¥<?1:1'.l'.f,ORJ;N.q'• •• ,' ' . ' , '
I

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107. For: atomic energy work; detailed _results hav~
been ,published:·on the .extensive,.mo11itqririg- of i11;d_i"';vic;luals for· occupational ·exposure. Table -xin_r gives;
data on occupational. exposure from penetr~ting radia-:tion at Oak Ridge National Labotatory:,,l]nited Stat~s, 78
the establishments of ,the iUnited Kingdom Atomic:
Energy Authority/ 5 I Argentinaj 36 . Canad~ 79 a,nd , the;United Arab Republic. 80·• ~'' 10s: Table XLII·seis out averagediguresAor the arr•(
nuaVoccupationaf..exposure to' individuals from. external:?<"'and- y-~~,Y sources ;in: various :~inds" of radiation 1w~rk:
in Argentmar Canada/·~ the Netherlands;~ 1 1 Norway/:':and the United:Kingdom. 1S:In Norway:and the=United;
Kingdom; for.which doses'a:re given 'separately for diag-:
riosis ·and .therapy; 'the; anriual dbs'es-in •therapeutic work:
are :higher: than,· in diagnosis~·This •may be •ex:plained"by'
the fact that therapeutic work involves the handling:Of ~radium applicators . .It.~.~ nc:!.Cc:!Ssary that there be a continuous improvement ofpfot~ctlciri devices, especially forworkwithradiumapplicators ... ,, •:·; .. :-T;I :·i·1· \':ia

; J 06: .::Even' :=tho'tigh! •tb'e' . verake" va'.Iti~s' ( received. 'by:.i-f

. 1os: As. fat a'.s .occupatiqna! .e.,.;{posur:e, ca~s·e~ )y in- I
teriial 'cpritarhihation qf. lhe body .by radio-isotopes· is'C<?~C~t;ri~d, ,.s~fX'~Y.S are :fr~q~etjtly fl?-lade. On. t,he .'ni~io:_:activity m the .an~ ~d.\vat~ :;nq by',yhole body C()untmg\
arid unn.e survey~ thb' inhal~~ or~ '.ot.her:-vi~e' ab~orbed I
radjo;-isot6p ~s"t,nay b~ dfilliatec;t P,uring usualW6rkirlg 1
conqitiorts. tl+{ s'urV;eys' 'J:iav~ ;gjven:'. co~~en't_ra.ti?ns far'.
beIO\v the .highest pei:missible' concenfrations,"·cortected'
1

to allo\v Joi-'o.c~hP.at!oriaI, ~#b~ui:f .6§ e.xt'e~ri;i.Iiradfatloll'..}At".'Oak'.· 1s; the letel -'of''afr'·. • .Rid··. 'g·e',National''Laborafo. " ., I '.,.' ' ' ·· .... ry
I · - · ,.. f" .. ' "c6ntaminatiori. itj the Iao1:>~iitories :d·ur~ng~ 1959. 1\'>'.!l~ only{
0.4 per' cent o'f the:a.§sVmed 'ma:X:ihiuiri pbmissible cbii'centration (10-~: JkC)cm 8 .i of, air): ,Regarding. suzyeys: ofbody.burdens of radio~isotopes,,practicallyncu:,ontentra-1
tions ,beyond the maxi~um 'perrr,i~ssible: qnes ha:v;e ...been r
detected for radio-'isotcipes·bther than uranitun-15!: 8~: ,~<;

Mitling: i1i,d~~t'rwl1.p~bcissi~g oj 1!truiiiun '.dnd'tlioriilJi .
' " ' ~ -, •' \. :; ; : '/ \. . ~ .. / ~ ..,.. ' { ' ! , , 1 <I: i : i.
~ ~ J; \1: • ; • ),J.Q9,:, High .~i:incentr;,i.~jon.s, qf1 ~aqo.~ ,~nd:if~qr;on ;~c;l:daughters e."<ist in mines. In areas_. 9f. !P<?OI ~ei;i.ti~t!8~ !
J-

I • :

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: ,

i

i I

where high-grade uranium ores or radium ennchecf residues are stor~q,.ll)e. radoµ c9~centrates 1 m~y! be as highas 1()-i to Hr5 /tc/cm 3"of air.sz':Experieiice has shown,however, tna.t the concentrations of radonrdatigh.ter products", can ;·b'e, ·great}y .-•reduc~d:• by.. Jcircea;, ventilatiOn:s,~ i
DuFing'' thel industrial iprocessing· p£; uranium: and thcH
riumrfine :dusts are often.produced and precautions;must tl:ietaken to prevent inHalatiori-of.them.~h 8 ~,Consideratiop.;o'fi these· hazards is .giveri .in the, reporl i ofth~ rUnited~
States National .Academy::ofa, Science: qµ (the,1eff.ests, of)inhaled,,radio,acti:ve. particles, 83 which also gives data
regarding: the radon": concentration. in_ se:v.et;J.trfiv;e; uranium mines surveyed.ih .Utah. Information• is' als'o ·available for''the Argentillian,~ 6•• Canadian;sa Frerichj8 TJiaiid
S_o11th Af~ic<J,n 88 urapiµi;n_µiin~.~, and!tl~e p~qspl).at~ m~i;ie~ .
in: ilie Un'ited'Ai-!ab' Rg ublic 59· Since' uffi.niuiTi i~-'excf~teHlv~·· ''ia' '1dl":"£~dm:.t11~ 6od? :coti2Jntrlitiat!s."M'
tiled tsb:.
t/~=c:a~"e!sn· . I>h'~det'e'cte<f'!t1i'1ni~ti:· :tn· 1the '\voikeH fo'.(A~ en'tiniaiia<i:~ries·
ffi'e'~!tie~eis' of 'urli.Hh1ni fl1 tlie ufihe::1Il·a.·g:;·frohl
2~29
ritlcrc/r ' 's id:d~te<l. 'e}'24hbtirs'. '. 1 ' " try.Ji•:«:; <c';~:~;;r,·;1( '.'I» ,P n:'·1 ·.y1·;1··l•i': •:•>

wbrkers'at~ oflntei~t, 'the' distiib'utfon 'of dbs'es; and.the~1riiliiiber; M .persolln'etexC:ee'ding i:he r~b:>mmended liiiiioaI 1

Vof· the 1doses reteived··by -the· lZ,QOO workers ·m the'Fed'etaJ '.Republic'df Gerfnatiyha's 1 b~i!ngi~en·W Wkchs:.;
mru;lli16 'ana sho\Vs £6'r the Jears:1952'to, 1959'the·gtadu~lr'~dhctibtl: iri' 'the' riumbet of ;plfr~6ns exceeding the 1 rec~f
drhinended' 'level.' Ji:i 1952;.23 per. ceiit ·e'..xceeded '.0:4/
1
r~m/nib ·while' i;{ i958 bnly '4 pei'615sei.-%Ci/
Tl:ie .divisio'n. ·of ,these irifo riiedicine,' indi.istij :a:nd 're~·s~arcldh6Wea that} I peiceht, ~2 pb: cetit, 'and'J4 pe~'cenh'eipectlvdy 'dfthf.personhel ,vorkµig ur.these fieidre){ceeded' 5'rem/y! It 15 kllowii that' there ha~ !Heen: ·o~er'.
the last decade a great improvement in the doseirniceived·by workers so that r"eportS 6•7! rs ..7 1·show that :only' 0;1'20.5
per .cent of1the.dose· mea:5tirements· 'show. doses :of such ai,
magnitude thatithe individual,: if ~these 4oses continued!
to be· recorded;wotild exceed .the ma.~umi pemiissible:
annual m:"quarterly levels,! ' :.- · :: i, : ;... , , . . , :- , f lthe· tluminizing• in'dustiy hav<i :been .meastired<in:· tthe
United Kingdom.1 ~::Ten of·these were;found•tothave1
body' burdens:in e.{ccess:of• 0,1 ..µ.c.rradii.:ifu;·:the highes~;
being 0.61 ji.c.- Twehty.-"nine persons had, burden's betweeri:
0.05 µ.c and 0.1 µ.c and 234 had burdens lesl:i than '(W5t µ.'c~:
All those persons having burdens above 0.05 µ.c were
employed before the introduction, in 1942, of the first
regulations. An irn;ideqt µivolying t}l~- O!=cupational contamination from Sr110 used in the luminizing industry hasb.~~1?-1~~?i;~~d.rff?1¥.·Sz~irboslqy*,ip.;s~ ,,,,: ,~: :, : ,Jl . <i (Lmninizing
industry_-·:er:.,,., __ ,.{'"!·.:· :1·,:
110. Total body 'burdens' o'f 273 persons employed in

1ev~i. f's ·,of 1HdrT:}~poi;~~~~ • A: '.fompre~e~si~~ '~p41y§i~~
1c'efit were(

,, I

.t

"t

i

·~. ·. '· Jf~. ·•1~.,.:.,.I.~ I.;., ,;·, .,l-:; lj':).J;STIMATE;S,QF.~<;:CpfATIO~Aj:.. ,EXPOSURE,J;~ fiIG;Ei1:'. J..
'·' ..... , . (ALTJ'fpDf.:A~C(JµE,T,.,! ; .,:, "";;.;;;, ",(;·11 L Costrik'' 'radiation· increases ~rith aititi.lde.-' Corti)'

merc~ial jet.a~rcraft.fly.at,~ ;;1ltitude qf&-12,~m,.(25,000-

387:

40,000 feet), while military jet aircraf! may re~ch analtitude of 16 km (50,000 feet). According to estimatesin the United Kingdom 75 and in the United States, 91
the annual radiation dose to a crew at 16 km amounts to
400-500 mrem. At an altitude of 12 km, the corresponding dose is around 300-350 mrem. Dose figures relate
to a northern latitude of around 40°, assuming 80 hours'
flying time per month.

shoe fitting, luminous markings in clocks and watches
and other luminous devices, and television sets. The
public living in the vicinity of radiological installations
and passengers in aircraft may also receive additionalradiation. Some of the more important sources are considered in the following paragraphs.

112. It is anticipated that supersonic transport aircraft, if and when they become commercially available,
may fly at altitudes of up to 26 km (85,000 ft). Aircraftcrews might be e.xpected to fly a maximum of 40 hours
per month at these altitudes. It has recently been calculated by Foelsche92 that at a latitude of N 50° a crew,
under these assumptions, would be exposed to an annual
dose of approximately 1,500 mrem. However, during
intense solar flares a few hours' supersonic flight at analtitude of 24 km may cause· a dose of 8,000 mrem.
If these solar flares can be predicted in advance, aircraft
flying at very high altitude~ would be able to descend tolower altitudes before the peak activity is reached.

118. Members of the general public living near or
having access to these installations may receive small
doses mainly from scattered radiation. The Committee
notes that the ICRP1 has made recommendations thatsuch people should not receive from such exposure morethan 500 mrem per year in the gonads, the blood forming
organs and the lenses of the eyes.

113. The contribution to the dose from contaminationof an aircraft by surrounding radio-active particles canbe disregarded, although the exposure of maintenancestaff has received some consideration.91 • 93
114. Consideration~ has been given to the computation of the radiation likely to be received by space crews
and also to the problem of determining the dose due toprotons in solar flares. 95 • 96
GENETICALLY SIGNIFICANT DOSE

115. By the use of dose information obtained fromindividual monitoring, the genetically significant dosefrom occupational exposure has been reported from anumber of countries. Allowance has been made for theage distribution of the workers. The estimated annual
genetically significant doses calculated from formula 11(see appendix) give the following results :Doumrem Year of Estimatwn

Austrial.19 . . . . . • • . • • • . . . • . • • • . . • . 0.2
N etherlandsB7 . . . . .. • . . . . • . • . . . . • 0.3
Unitea Kingdom75 ..•••..•.....•. 0.4

1955
1960
1959

In the United Kingdom, the contribution to the genetically significant dose from atomic energy establishments
has been calculated to be 0.15 mrem. There is no reason
at present to assume that the genetically significant dosefrom occupational exposure in other countries would
considerably exceed the figures listed above.

RADIOLOGICAL INSTALLATIONS

X-RAY FLUOROSCOPY FOR SHOE FITTING

119. A survey by Seelentag and Peck97 has comprehensively reviewed the literature regarding the doses
received from these machines. They also report measurements on ten different units. The average annual genetic
dose to the population of the Federal Republic of Germany was estimated as 4-7 microrem per year. The
Medical Research Council of the United Kingdom75
estimated in 1956 that the annual genetic dose in thatcountry from this source was not more than 0.1 per centof that received from natural background and that after
the full implementation of present legislation (by 1963)
the dose would be reduced to some 0.01 per cent. In
several countries fluoroscopy for shoe fitting has beenprohibited since it is regarded as causing unnecessary
radiation exposure.
LUMINOUS MARKINGS IN CLOCKS AND WATCHES

120. Reports of the activities of watches and clocks
have been made in Germany, 98 Nonvay,99 Sweden,100
Switzerland101 and the United Kingdom. 75 These showthat there is a wide variation in activities of watches
and clocks up to about 0.5 microgram of radium with amean value of about 0.1 microgram. Estimates of theannual genetically significant dose from this source are
2.6mrem, 98 l-3 mrem,1° 0 8 + 3 mrem, 101 and0.5 mrem. 75
The annual dose to the sales staff has been estimated as
90 mrem. 98
TELEVISION SETS

121. The ICRP 1 has recommended that the dose-rate
at any accessible point 5 cm from the surface of any set
used in the home or place. where the public is likely to
be shall not exceed 0.5 mremjhr under normal operating
conditions. Braestrup and Wycoff102 have shown thatat 15 kV, the normal operating voltage of home televisionsets, the dose-rate at the surface of the screen is about
1 mrjhr. However, most sets are provided with a further
plastic or glass sheet which reduces the dose-rate, but'vhen these sets are operated above normal voltages, for
testing purposes for example, then the dose-rate may
be increased greatly. Operation at 24 kV increased thedose-rate by a factor of 1,000. It has been pointed outthat colour television tubes operate at about this voltage
so that further shielding is required to conform to the
ICRP recommendation.
122. The dose-rates received by the operators of projection TV units working at 80 kV may be of the orderof 10 mremfhr, but high dose-rates of the order of
1 rjhr have been measured close to the tubes. However,these are not in the direction of the audience. 102

MEAN MARROW DOSE

116. No data are available on the actual mean marrowdose from occupational exposure. However, the values
given in table XLII may be regarded as the dose at theskin and therefore the bone marrow doses will be considerably smaller.
IV. Other exposures

117. In addition to the doses received by individuals,
either as patients undergoing medical radiological procedures or by radiation workers during working hours,
irradiation may come from other man-made sources."
These comprise such sources as X-ray fluoroscopy for*Environmental contamination is dealt with in Annex F.

388

123. Braestrup103 has estimated that the average
gonad dose from home television is much less than
1 mrem/yr.
p ASSEKGERS IN AIRCRAFT
124. The enhanced cosmic radiation experienced inaircraft makes a negligible contribution to the total dose
received by the population at the present time.
USE OF KUCLEAR POWER IN SHIPS

125. Information has been given of the predictedradiation levels to the workers and public from the useof nuclear propulsion in ships.104 • 105 The doses received
by occupationally exposed workers were on the average

about 0.5 rem/y and were up to a ma.'(imum of 1-2
rem/y. 130 The activities discharged as waste from thesevessels are unlikely at the present time to make any contribution to the dose received by the general public.
GENETICALLY SIGNIFICAXT DOSE

126. The use of these miscellaneous sources is likely
to contribute about 2 mrem/y, mainly from the use ofluminizing of clocks and watches. However, with theincreasing uses of miscellaneous sources of radiation,none of which individually contribute an appreciabledose, the total genetically significant dose may be expected to increase slightly.

Appendix
1. A general definition of genetically significant
dose has been given in paragraph 9 above. Approximations must be made to calculate this dose, the mostobvious being consideration of groups rather than
individuals. It is convenient to start with the approximate definition*+ N'Ml w<M> d1<M>)+ NiM> wiMl)

w<F>
d<F>
D - 1:I 1:le (.NCF>
Jlc
Jk
lk
-

l: (NiFl wiF>
k

Ji:

Jk

lk

(1)

where
D
(annual) genetically significant dose,
N 1k = (annual) number of individuals of age-class k,
subjected to class j exposure,
Nt = total number of individuals of age-class k,
Wit = future number of children expected by an exposed individual of age-class k subsequent toa class j exposure,
wk = future number of children expected by an average individual of age-class k,
d1k = gonad dose per class j exposure of an individualof age-class k,(F) and (M) denote "female" and "male" respectively.
2. For the practical work, formula 1 can be simplified considerably, the first step being to replace thedenominator by w•N, where
N<Fl
N<M>
w = • w<F>
w~1 >
(2)
N
N
and
1
(3)
w • = N. ~~ Wk• Nt•+-- ·future number of children (w;) of an individual in any
specified age-group.
4. The assumption could be that the average individual will have a future annual child-expectancy
expressed by the present specific annual birth rate.
This makes it possible to calculate, by summation, thetotal future expected number of children of an individual of any age, and hence a~so the mean for any
age-group. If significantly less than unity, the probability of an individual of age a to reach age t should
also be considered. This givesc:ow; = t-a~ c; • At • P: (t)

(4)

where
w:
= expected future number of children of anindividual of age a. With knowledge of thefunction w; of age, the average w~ for any
age-group k can be calculated,c;= age-specific annual birth rate, i.e., annual
expected number of children of an individual of age-group t,
At= number of years included in age-group t,(t) = probability of an individual of age a to reachage (group) t.
5. It must be noted that c; may have a tendency tochange considerably before an average individual of a
specified age has reached the age-group in question.
As it is, however, difficult to predict the values for the
future, c; has been assumed not to vary with time.
6.
= w:-+o is the number of children expectedby the average individual during his whole life. The
range of w· is normally 0.8-2, and the range of w· is
2-4 for most developed countries. The ratio W /w
ranges from 1.5 to 3.
7. The female and male contribution to the genetically significant dose can both be written
1• d.llt
D • = -N ~ ~ N•lli: W1k
(5)

P:

w·

In the last expression, •denotes the sex. N is the total
number of individuals of the population. It should benoticed that w•N is about twice the future number ofchildren expected by the present population eventhough the value of w may be as low as 0.8.
3. As formula 1 has w' in both the numerator anddenominator, the numerical value of w has no direct
relevance, and all terms can be expressed by help of
the ratio wr~/w. For understanding of the demographic
background, however, it is valuable to realize that w
must be calculated from the sum of the age-groupproducts w;·N~ for a population, which means thatan assumption has to be made regarding the expected

v,r

J

k

8. If the gonad dose due to an examination of type jis nearly uriiform for all age-classes k, thend;k = d;(6)
approximately for all k, and formula 5 reduces to1•
D • = -N 1: d.l l: N*Jk WJk(7)
W*The degree of approximation involved in the use of formula
1 depends on the definition of classes j. In theory, there need
be no approximation since the classes may be made so restrictive
as to include only one individual per class.

JorD •l = d.I ' -

k

1

~
\VN k

389

N•Jl< WJt•

:which the'patient is examined: wj can theri be ea!: culated ;from· the: age~d1stribution 'of the patients :andthe normal child-expectancy for each age-gr~up, ... r(c) wj/w\Theoi formula .iis 1iapplitable1:alsbrf ta: .foetal: rexposui;e(w 1 = \V) which must not be overlooked.::': j,,,;,i:,~.-;<:
•

I

•

LI

I

..

.

•

I 1Q·.r:·Qft'eri':d,1 :vanes '.'Considerab)y! ~ftj)t;n:: hospi,t~J. ,to·~hbspi~a1.:·:Mbsf 1 of':t1J~··uncehainfy!'in:'estini!ltesiof;D 1·~iS'prot;iably due'.tq the pi~ci.Jity'of.~sti'ma.Ptig.. a rel~a,~!e''a'\•erage''ofid~;for ·a-'.popiilati'c:>ri·. ~.'· •1c' ", :;: ;.: .. ~·:'.,, w' !

• !i

-1;i 11:;

L1 J1';-,:,nr: .. , ·H, ·~~1.l!!!H/1 :.-:;1~1~;_,·,_:·· ~.;·!nin~~ !·:·it~:irtheye ;tl'e;:~q 9a;ta. ;on: ,th!!,:~hil9~~n,cy; !Qf. :the-.~t11ei:i~1'i 1an iapprQXIJ'.l'l~tene~ttm~t<? :Af .Dj.J~!l-Y.}~e\'. H '1 h'1 I.~! ~e, :uni:leri :th~, ~Sisurript•oi:i .tha,t1tfl~1cl.;i:ilp-e?-peq¥.J;ncy
is not influenced by tlle·;I\~torjei' qf. t)le,:conqitjpn.,for,~ •. -~;~i ·i!i!."1;!ij1 '.::· ·.~:;1:·.1;.;~; Ii<-'. ~:t.;~Hi1•:)(i) ; ~ ~ . 5 / \

(! )

J

~<

:1

I'

,v.'

.... ! .. :.;:f·1 ~;~:'· ·h, ~.'r.fd1!-,>j;1:d ·/(, ·,: l tiJIH (! ;1;;11,1;)
1J,::,;1 .. · ;;k.!'·jo f;: .. ·.~LJ!d·· 'ic1 ·,~.'.:r1~tr!1 ~/:!r:"dJI j.~:.J·,::;.~ ..--~;:!d;J ·~o ~;·:-·!i·./v;n;i/ sl1j\.\ 1 .r ~;.~·'· ·~~; l··~d)ivil1!1i.
0',!JU: ·i:t"J ;.-,', ~.;'' ·,~.\'L !•·~! ,:,;·~; 'ic·; ,•: u:-1il:>f1l! ]

,".'/

f1!·

1 :

_,:

Jl:l J; "ft ::JJ' I';:\;If i •JI/I

j ·'.;i:,,:·., ::r:~.

.:~'~II:•·!:'. ~l.'''· ·1u fr;1dd ~ih,:; rt?r::., ... ~; '.L r1i L:.~;:if~,t:i r:1'"';,• ·:l~, ·• 1.Jr11;i:1 =•t·.:·•icin;:, : '.

'

1 , ·,.',

:

· .

J

J . .,.

•. ·.. PQJ.ulfJtwn alfl'< "' Oov.n"'1..cwut11 •.ii 1;:1;ruu.qfistudJ1 ·: •!llimeofs1"1Y-' .• ·:·, J ' ' ' . I ' ''1•>

J'"'.':·llJ:·t'.'.': •• • •I•• ~i.I
}(\

,

: .•

,;! L-~i;J:> ! 1:!.', .J<.1 :l1:1JIJ!•1i~\H; 'j·, "1-:._;!i1!U1 1· h•.•·:..-.~; H~: \:d );:.J:>'.•:.::::; 1:··,-1h~i1l·.1 ,,1 ';i. ::,;!111 ~;-JLJ.rJl.j
pj ·:11~ .. !tp:·,~:_:!!" ) i.--•J:> ~;;:'.~ ·:<• f 1.fl!,j-.:;;1::; L:• ·:1 !

! :'.-, 1 . I',._,' J ••. :·. ; : 1 , • ! \ ·; 1. 1-\ • •. ! 1 ·~,1; r · ·I-, r;. .~.·.1•:1. . t.11H1'. . ' ' • 111,r1r.TABLE
I. ANNUAL FREQUENCIES
OF. y -RA~" EXAMINATIONS
I. I ·,
I.
.
·1:11·i;; _~. !;·:<;:.<l• L·:j,'(I!, y.\·' 11 •• 1. ... • : .. ·, ~t·.;.;!l.il i _., !_. 11d.Ii1 ~dIJ11JJ
1

I r;11nr1r;

i ; :.;-J, 01•••'.:'I"'

;"N

,I!

Ann~al. !'um~tr of.:c-raJ!.,exomi~ions pd-.1;0(}(} If! 10iai'p0pui"1icfi" '&aminaJioJs:~~pl'~~}s' .: .. ,.i ..... "·!'··· l' · ._,. ·: ·' . d : ' . .:'"'.:::ifuneys and den,alJ.fass surveys , . ' ·!·, :-=:~~(Rizd;DiraphJI. '.'.FJuo;./,si:0PJ1''. lRaaibvapJ.;,; 111 ·: • Fliwouopy' ;; :· , .. · .: ;D.enJal ;· · 1&ier~q
j

•

·;

.t ' : } ~' " ,1,
"
•
I
I .
. '
t
•
' .
•
:litable' ·, N~ri:lata' ~ .; . 4
c~ep~~.{~~en~~,.A!r~~)F l!?~q.:.195!? '"r !! ,6,000'.QOQa: i .(. 270b ·'"Ng'ciahi' ! ,.,1 80b::i:'J\'Not"a1,~~tfill!a·:. ''.' ;.·;·'.· .. •,:;·, .~-95?:;-1.9~7.. ;, : 9,,5q<) 10<J9, . , }~O: :.: • :.~. ' " ' 190~ · '!'Not'a~~li&ib1e 1 '.···~fo.da'.hi: ·· a2•:$3
310•
25·.:·. '25 · ': · :: '.•No data;""' 53ii19
Austna.... ... . . . . . . . . . . 195571958
6,974,000 ; .
67·BeigiwiL!,:".!.'.'.,':J.. ::.:: '.: '195& ·". ·.: · '8i924,00p'·. 'No.data No data ,, " 130 •.•: . .
(., 21 · · :<No data53:eaiiaaa:.·,.-.:-:.'..::.:-.::.." · '1958' .. , • .11,04s,ooo. :'.220° i'30•.: 90 · , . Not applicable
Nii data 106, 107.neiiffiark.··::L•: .......i.;·.ri :.1956.,, . 4,466;090 .· ·:260-d
140
Not applicable40!u ,, 5Jf~~ ;Republic of. ·: ... '., . 1, • :, • i , . · _. : ,;,-d130/ · .. Not applicable
80
6. !per:n;ia,ny,(l:Iam~\lrg) ..... 1?5~-:-~95~,;•. • 1,75.~.ooo.,
560
.I
. SiO
"
'F
· ... " · ;·.:·.·~••r··~·.
··' · 1'957'1958
OOO OOO··· 1-0-d
40
No data
8-10:.· ran_ce·,·:,·_·, . :-, ,, '~'.. · 42
I j _,I- • ~~1,.110.:.
170
NQt applicable. 151<}~1 : .. ... ; .....·.. .. .. . .. 195,9' . ; 2,06-,000
. 300
. 20
:. ' !~08··1ta'.1y (Rome).'.;·" ..... :-,, · ' q9s1· · ,.
1,875,ooo
500
11N.ot applieable · Nfrdata ,·,•.;:-;f ,, .',.BO·
.
"
'
10~
'
..
'53
' Not appli{;able
Japan................. 1958-1960.· '. 90,000,000'HO-:-:-:", . ;, ;~20
2001 . . '130
4<Jb' ' . . . 13
Not a·pplicable:-~~Fhed~nd,s,(J,eip~~;.··;. 1 ,.,1~~9 ., · !, :.~ 1;0,000. i "350-d .
: ' ' ' 90•"240• ,.
""68· Not applieable
New Zealand.!;:;'.>; ... ::: ", 1951. , , , : , -·.~-~.OOO : ., : i 340°
_d . . ·,210 .
,,:,14
Norway...............
1958 ,
3,~2~,000· 390
Not applicable · d 100:,15
Npt applicable , No data
(Sw7den .......,'.; ..,·:·:~-.:,:·' . .1958,'f\300,000
290
I' . . J30d".~·jg.
.60 ,, I. ..
'. 140'.
·'· ,16·Switzerland ....... :....
1957.
5,160,000
310:c:> .,.,' . '; '. United Arab Republic:· .
. . ... , . . 1 ..
·~d··'·: 17
( :, Alex~ndi'ia'..,.:. 1 .::'.: ,,19S9:1.i?6o'· 1·361700c' · · ,?6
0.3
4
Not applicable;· 5·.: >isCairo ... !'.:!·'.::::.'... 1955-1·901 ,: 1 1 ' 2~640:-00'0~ '"' .. '40·2"
Not ':!Pplicable(~United Kingdom (except ; : . ' ,., , ·' . !''.95.
' .. , :,,19:Not applicable
4.0:
Nsirt'1e,i;111rrl;i.nd~~'l'~' ·.1957-:-1,95&1, . 50,QQQ,ppo:.
280
UnitedStatesofAmenca. 1955-195.6 · ·162;doo,ooo· '"':'z'50° :, ' ,'I :80• •. :400~ .;;• ,. ·; ..20
;135•
.Not applicable0'·I : • : , I

11

ii:

0

l

c.:~

,, . . ,..

•!I'•Including commutorsib Figures relate to films and not to examinations.
·"': D~ta are tak~n frc;>Jll ~he li958 report Q~. f~e Uni~ed. Nations
3
Sc1ent1fic Comm1ttee!on the .Effetts'Of' Atomic Radiaaon.
. d Fluoroscopy is generally' performed only in connexion with.radio~raphy.

'

' J

'

•

~ '

'

l :

, .,
.. .
,
:'':"•Figures· relate tc>'hospitals·only. " ·· · : ··.:., .. . t Fluorosco,py of the cbest rtot connected with radiography out·:not rriass'rurveys.: '"'·· •':• :· ·, .. .: · ' :,:. . ;.. , , :. :• Population sel'Ved ·by" bo~piials 'surveyed.!.. · 1 • • . . . . ..

i.'39oT ..uiu: II. ANNUAL FREQUENCIES OF CASES TREATED BY X-RAYS AND SEALED RADIO-ACTIVE SOURCES

Year of study

Co-"lllry or area

Austria •.. , ......• 1955-1957
Canada •• , •• ,,, .• ,1958
Czechoslovakia(Prague) ...•....
1958
Federal Republic of
Germany(Hamburg) •••.•• 1957-1958
France •••••......
1957
Israel. ............
1959
Italy (Rome) ...•. ,1957
Lebanon ...•..•... 1956-1960
United Arab Republie:
Alexandria.,, •• , 1956-1961
Cairo ........... 1959-1960
United Kingdom(except Northern
Ireland) •••••••.•
1957

Annual 11umber of <asu per J ,OOO of
total popu14Jion

Popvlalion al
lime of study

Maiivsan:6,974,000
17,048,000

410No data

No data

990,000

No data

7.7

1,755,000
42,000,000
2,062,000
1,875,000
1,500,000

4.0
3.7
0.6•.b

12.3
5.9
4.1•,b

0.2

8.3
2.2
3.5•.b
1.3
0.1

0.3

6
27
108
110
111

1,361,700
2,640,000

0.25
0.6

0.21
0.7

0.46
1.3

18
34, 3550,000,000

1.2

1.2

2.4

19

N on-malignanl

No dataTolal&/ertnu

14
1.9•

119
106
109

•Figures relate to hospitals only.
non-malignant conditions around 70 per cent of all cases. For malignant conditions
around 80-85 per cent of all cases.
b For

T.'J!LE III. ANNUAL FREQUE."CIES OF ADMINISTRATIONS OF RADIO-ACTIVE ISOTOPES FOR MEDICAL RE:.ASONSAND THE AN1'"UAL AMOUNT OF pa1, ps2 AND Aul98 FOR MEDICAL USE

Country OT area

Year of study

Population ol
lime of study

Argentina •.•••••.•.....•.•..
Australia ....................
Canada ••••••...•.•....••.•••
Federal Republic of Germany(Hamburg) ••••••••..•.....
Israel .••• , ••••••••.•••......
Lebanon •••••••••••••••••.•.•
Norway .• , .••.••.• , ••.•• , •••United Arab Republic:
Cairo ••••.••••••••.•••.•.•
United Kingdom(except Northern Ireland) ..•United States of America .••••.

1960
1959-1960
1958-1960

20,956,000
9,800,000
17,048,000

1957-19581959
1956-1960
1960

1,755,000
2,062,000
1,500,000
3,500,000

1961
1957
1959

Annual number of tases per
J ,OOO of total populalio11

Annual amounls :{ rodio-aaire isotoPcs
for medic use (turks)•

Diagnosis

TherapyJUl

pn

Aull 1

Re/eren<1

0.30
0.65b

6.0•
8.2
55.0

0.8•
2.1
5.1

No data

No data

0.03
0.09b
0.04•

36
112
106, 113

1,l'd
1.7
0.1

0.2Qd
0.16
0.01

No data

No data

No data

No data

2,640,000
50,000,000
180,000,000

3.4

6
108

No data
5.7

69

1.1

18

4.2•

88•

No data

No data

20
114

No data

2.5
0.3
2.1

0.3
<0.1
0.5

0.33

0.42

1.3

0.07

0.5
1.2

0.08
0.3

SO•
No data• See paragraph 8 (c) above.
b Minimum estimate.

4.4
23.8

d Figures refer to the use of Iut only.

•Figures refer to the quantities actually administered.

•Figures refer to hospitals only.

391

•

11

TABLE IV.

DATA ON THE ANNUAL GENETICALLY SIGNIYICANTDOSE FROM DIAGNOSTIC X-RAY EXPOSURE

Argentina (Buenos Aires)•

Suroey, 1950-1959v•I~ (mrem)MakadultsFemak
adultsFo•lusMok

Femok

Footus

mum

2.2
3.0
2.7
3.7
18•
1.6
1.0•
2.3
0.6•

700
600
300
200
10
600

900
600
450
400
15
700
800
600
900

No data
No data
No data
No data
No data
No data
No data
No data
No data

1.9
1.7
0.8
0.5
1.3
0.7

2.0
1.8
1.2
1.5
0.6
1.1
1.8
1.4
1.2

No data
No data
No data
No data
No data
No data
No data
No data
No data

3.9
3.5
2.0
2.0
1.9
1.8
1.8
1.7
1.2

16
14
8

1.0

0.6

600

800

No data

0.6

0.5

No data

1.1

4

Sun-TOTAL

72

36

7.8

13.1

20.9

83

Other types of examinationb .••

67

56

1.7

2.7

4.4

17

SUB-TOTAL

139

92

9.5

15.8

25.3

100

4.5d

7.5d

12d

14

23

37

Mak

T:YP• of ozaminalionA.

PerUfll..

ate

HOSPITALS AND CITY CENTRES (RADIOGRAPHY)

Urography (descending pyelography) ••••••••••••....•.••
Hip, upper femur •.•.••.••••••
Colon (barium enema) lower GI
Lumbar spine ••.•••••••••••••
Mass miniature radiography •••Pelvis .......................
Obstetrical abdomen ••••••.••.
Lumbosacral region ••.•••..•••
Pelvimetry •••••..•••.•...•.•
Retrograde (ascending)pyelography •••••••••.•••••

B.

F•mal•

2.7
2.8
2.7
2.4
58
1.1
1.2

230

0.3

PRIVATE CLINICS AND PRACTICES (RADIOGRAPHY)dTOTAL• Figures are related to radi~apbs and not to examinations.
b Does not include dental radiography.
• Does not include contribution from foetal exposure.

TABLE

8

7
7
7
7
5

100

d Estimated figures (see para. 1 7).
• Below mean reproductive age, i.e., (nj/n).

v. DATA ON THE ANNUAL GENETICALLY SIGNIFICANTDOSE FROM DIAGNOSTIC X-RAY EXPOSURE

Survey, 1956-1958

Dentnarks
N*
1
N XI,()()()

Typo af e:raminoJio1<

Mak

F•mal1

Intravenous pyelography ••••••
Retrograde pyelography ••.••••
Cystography •••••••.•..•••.••
Hip and femur ••••.......•.•.
Pelvimetry .••••.••.•.••..•..
Urethrography ••.•••••..••...
Pelvis ....•........••••.•....
Spine lumbar ....•...•....•...
Abdomen obstetric .••.........
Abdomen A.P..••..••.•.•...•

4.3
0.9
0.4
2.2

4.3
0.4
0.4
2.5
2.2

0.4

0.7
3.4
2.0
0.4

SUB-TOTAL

15.4

16.3

0.4
2.5
4.3

~ (mrem)MakadultsFemok
adults

1,019
2,580
5,078
980

565
1,136
437
58
822

3,709
567
104
610

210
222
190
85

D~ (mrem)

Foolus

Mak

Femok

4.3
2.3
2.3
2.2

2.4
0.5
0.2
0.1
1.8

Foolusmrem

PerurU-

Ot•J

0.3

0.1
0.7
0.4
0.1

6.7
2.8
2.5
2.3
1.8
1.7
1.5
1.1
0.4.
0.4

24
10
9
8
7
6
5
4
2
2

14.9

6.3

21.2

77

5.0

5.0
1.3

18
5

5.0

27.5

100

1.7
1.4
0.4

Foetal contribution• Other types of examination ..

244

0.7

0.6

TOTAL

260

15.6

6.9

392

D1

TABLE VI.

DATA ON THE ANNU.U. GENETICALLY SIGNIFICANTDOSE FROM DIAGNOSTIC X-RAY EXPOSURE

Survey, 1957-1958

Federal Repiiblic of Germa11y (Hamb11rg)6l~
i x l,ooo~ (mrem)~ (mr<m)Di

adullsFettUJka
adulls

F~!us

Male

FemaleFoetusmrem

P<r«nlate

4.0
3.2

890
1,520

2,530
214

2,740
255

1.87
3.15

4.03
0.17

0.19
0.01

6.09
3.33

34
19

3.6
10.2
3.7
0.32
16.9

241
63
275

439
183
94
680
67

476
178
166
677
63

0.70
0.52
0.90

0.71
0.72
0.24
0.22
0.47

0.04
0.04
. 0.01
0.54
0.02

1.45
1.28
1.15
0.76
0.60

8
7
7
4
3

1.2
4.6

1.1
2.9
0.05

311
88

657
128
600

720
167
2,900

0.21
0.27

0.27
0.20
0.03

0.02
0.01
0.37

0.50
0.48
0.40

3
3
2

SUB-TOTAL

56

46

7.73

7.06

1.25

16.04

90

Other types of examination ..•.

369

299

1.07

0.61

0.02

1.70

10

TOTAL

425

345

8.80

7.67

1.27

17.74

100

T'YP< of aaminaJion

Male

FemaleColon (barium enema) lower GI
Hip, upper femur ......•.....•
Urography (descending
pyelography) ...............
Lumbar spine ................
Pelvis •....••................
Obstetrical abdomen .....•....
Stomach (barium meal) upper GI
Retrograde (ascending
pyelography) ..............
Abdomen .•........•.••..••••
Pelvimetry ..•••••............

3.7
2.6

5.1
11.2
3.8
23.9

Mai<"

65

0.11

•Denotes mean figures of gonad dose. After detailed calculation of D; formula 8 was used for obtaining d;.

TABLE VII.

DATA ON THE ANNUAL GENETICALLY SIGNIFICANTDOSE FROM DIAGNOSTIC X-RAY EXPOSURE

Frances-10

Survey, 1957-1958~ x l,oooN'Tn• of aaminalion

Male

Chest (heart, lung) •....•.•••.
Abdomen •..•...•.•.....••...
Hip, upper femur ...•...•.....
Urography ..•........•....•..
Lumbar spine •.......•..•...•
Obstetrical abdomen ..........
Urethrocystography ....•.••.••
Stomach (barium meal) upper GI
Colon (barium enema) lower GI
Pelvimetry ...................

340
3.7
2.1
2.1
3.0
0.7
5.9
2.0

SUB-TOTAL 360~ (m1em)Maleadults

230
4.4

1.7
1.8
2.4
0.2
0.5
3.8
2.5
0.02

Foetiu

1,300
180
4,500
700
1,600
1,800
300
264
1,200

No data
No data
No data
No data
No data
No data
No data
No data
No data
No data

30b
1,500
1,200
390
250
1,900
90
134

247

v'J

~ (mrtm)

Femak
adultsMale

FemaleFoetusmrnn

P<runJage

4.62
0.23
2.30
0.80
0.80
0.23
0.29
0.23
0.02

No data
No data
No data
No data
No data
No data
No data
No data
No data
No data

38
10.20
2.84
2.62
1.28
0.80
0.47
0.43
0.37
0.02

65
18
5
4
2
1
1
1
1
0

9.52

57.03

98

0.96

1.18

2

10.48

58.21

100

38•
5.58
2.61
0.32
0.48
0.24
0.14
0.14
9.51
38•

84

65

0.22

TOTAL 444

312

9.73

Other types of examinationd •..

38°
figure cannot be split into male and female dose.
d Does not include dental radiography.

• Does not include contribution from foetal exposure.
b !\lean value for the dose to testes and ovaries.

• Since di is given only as mean figure for the gonads the dose393

TABLE VIII. DATA ON THE ANNUAL GENETICALLY SIGNIFICANTDOSE FROM DIAGNOSTIC X-RAY EXPOSURE

Italy (Rome)ll

Survey, 1957

Nj
N

•

X 1,000

D * (rnrern)d (mrern)
1Di

1Type of eumin<Uion

Mak

Femak

adulU

FemaleadullsDigestive tract ...............
Hip, femur .•..••............
Urography (descending
pyelography) .......•.•...•.
Pelvis ...••............•.....
Lumbar spine ................
Barium enema ......••.......
Cholecystography .•.•.•••••.•.
Abdomen ............•.......
Obstetrical abdomen ..•.•.....
Pelvimetry •.•........ ; .•.....

27.8
6.1

14.2
7.0

123
586

411
223

No data
No data

3.08
3.93

5.25
1.09

8.33
5.02

5.2
5.0
7.9
4.7
9.1
5.2

3.4
4.7
4.8
2.4
11.6
3.4
0.8
0.1

940
1,130
234
239
12
141

1,060
330
570.
1,050
156
210.
399
1,250

No data
No data
No data
No data
No data
No data
No data
No data

2.44
3.38
2.03
1.01
0.12
0.66

2.52
1.40
2.19
2.27
1.27
0.64
0.59
0.23

4.96
4.78
4.22
3.28
1.39
1.30
0.59
0.23

Sun-TOTAL

71

.52

16.65

17.45

34.10

79

Foetal contribmion• .•..•• ;, •••.•
Other types of examination• ••

2.59
276

174

4.15

2.57

2.59
6.72

6
15

TOTAL 347

226

20.80

20.02

2.59

43.41

100

Mak

Fodus

Mak

Female• No figures subdivided into various types of examination areavailable.
bThe figures for D; are the sum of the male and female

TABLE IX.

Foe!us•mrtmb

Pauftl-

ate

19
12

u
11
10

8
3
3
1
1

contributions.
• Does not include dental radiography.

DATA ON THE AN~UAL GEN'ETICALLY SIGNIFICANTDOSE FROM DIAGNOSTIC X-RAY EXPOSURE

Japan 12

Sur-.;ey, 1958-1960

N*cl'; (rnrem)

Nl X 1,000
Type of examination

Male

FemaleStomach (barium meal) ui;i!ler GI

53

33

Colon (barium enema) lower GI

5.0

4.5

Lumbar spine ................
Lumbosacral region ....... ; ...
Hip, upper femur .............
Pelvis .......................
Chest (heart, lung) ...........

7.6
3.7
4.7
1.6
103

3.6
1.6
6.0
1.5
65

3.6

2.6
1.1
0.15

Urography (descending
pyelography) ...............
Obstetrical abdomen ..........
Pelvimetry ...................

SCB-TOTAL 182

Mak
adulU

Femaleadults

4.3•
74~ '(28) (2,660)
81 •220(2,390) (4,320)
121
767
1,700
116
30.5
691
1,490
80
8:0•
1.0(78)
(0.6)
631

92
162
322

~ (mrern)

D1
PtrU'ltl-

FoetusMak

Female

Fodus

mrem

age

No data

0.69

10.92

No data

11.61

30

No data

4.01

4.28

No data

8.29

21

No data
No data
No data
No data
No data

4.36
4.44
1.93
1.58
0.41

0.19
0.06
0.46
0.08
1.07

No data
No data
No data
No data
No data

4.55
4.50
2.39
1.66
1.48

12
12
6

No data
162b
322b

1.27

0.13
0.12
0.03

No data
0.30
0.09

1.40
0.42
0.12

4

4
4

1
0.3

119

18.69

17.34

0.39d

36.42d96

Other types of examination' ....

74

37

1.82

0.79

No data

2.61

4

TOTAL

256

156

20.51

18.1

0.39d

39.Qd

100

graphy and fluoroscopy.
b The dose is assumed to be the same as to the maternal ovaries.
0
Does not include mass miniature and dental radiography.
d The figure implies contribution from foetal e.xposure only
from obstetrical examination.

• Dose figures relate only to the radiographical part of theexamination. In around 8 per cent of chest, 38 per cent of stomach
and SO per cent of colon examinations, fluoroscopy is performed.
The figure ,,;thin brackets denote the gonad doses arising fromfluoroscopy. The values of Dj refer to the total irom both radio-394

TADLEX.

DAT... ON THE ANNUAL GENETICALLY SIGNIFICANTDOSE FROM DL..G:SOSTIC X-RAY EXPOSURE

Netherlands (Leiden)13

Sur"Jey, 1959-1960~ x 1,000
z;rType o/ e::aminalion

Urography (descending
pyelography) •.•.•••...•.•.
Hip, upper femur ....•....•...
Colon (barium enema) lov.·er GI
Lumbosacral region .......•...
Pelvis .•..••.•••••..•...•.•.•Urethrocystography .••...•..••
Abdomen •••...•.•.••.....•..
Lumbar spine .•.••.•••..••.••
Obstetrical abdomenb •••.•••••
Pelvimetry .••......••..••••.•d'; (mr'111)

Mak

Fnnak

5.6
1.6
3.7
1.9
3.4
1.1
3.7
4.5

3.0
2.1
2.6
1.5
3.4
0.3
2.6
3.3
0.1
0

~ (mrem)Di

MakadultsFtmak
adults

Fot-

Mak

Fcmak

Fotlus

mrcm

Ol<

512
3,323
25
60
157
423
92
16

604
140
613
790
142
1,608

604
140
613
790
142
1,608

1.16
1.48
0.03
0.07
0.35
0.11

132

132

0.18

47
100

47

0.03

0.62
0.04
0.50
0.46
0.19
0.30
0.16
0.06
0.01
0

0.08
n
0.08
0.07
0.01
0.03
0.01
0.01
0.02
0

1.86
1.52
0.61
0.60
0.55
0.44
0.35
0.10
0.03
0

27
22
9
9
8
6
5
2
<1
0

100

Pt7U111-

St:B-TOTAL

26

19

3.41

2.34

0.31

6.06

89

Other types of examination' •••.

282

222

0.32

0.36

0.05

0.73

l1

TOTAL

308

241

3.73

2.70

0.36

6.79

100

• Doses are the same as for female.
b The position is not justified by the magnitude of the dose.
• Does not include mass miniature radiography and dental

TABLE XI.

radiography.
n = negligible.

DATA ON THE ANNUAL GENETICALLY SIGNIFICANTDOSE FR.OM DL-\GNOSTIC X-KAY E..XPOSUR.E

Nor..vayH

Survey, 1958

~ x 1.000z;r

dj (mrem)~ (mrcm)

D;

Mak

Ftmak

:Mak
adultsFemck
adulisFo.Jus•Mak

FemaleFoetusmrem

PercenJate

11.9

9.2

130

592

592

0.78

1.81

0.12

2.71

27

3.0
5.7

3.4
5.9

185
376

2,050
135

2,050
135

0.16
0.92

1.19
0.29

0.09
0.01

1.44
1.22

15
12

3.8
3.4

217
384

159

0.37
0.61

3.3
14.4

3.5
6.0
0.3
1.4
0.3
3.0
11.2

0.12
0.05

0.51
0.20
0.19
0.01
0.10
0.27
0.07

0.03
n
0.50
n
0.34
0.01
n

0.91
0.81
0.69
0.59
0.44
0..10
0.12

9
8
7
6
4
4
1

SUB-TOTAL

47

44

3.59

4.64

1.10

9.33

93

Other types of examination ....

320

294

0.30

0.32

0.02

0.64

7

TOTAL

367

338

3.89

4.96

1.12

9.97

JOO

Type of czamination

Lumbosacral region .••........ }Lumbar spine ••.••..........•
Colon (barium enema) lower GI
Pelvis .••••......•...........
Urography (descending
pyelography) .••..•......•.•
Hip .•.....••••.•.......•...•
Pelvimetry .....•..•.........
Femur •....•....••••........
Obstetrical abdomen ••........
Abdomen ...•.....•.....•....
Stomach (barium meal) upper GI

1.4

407
65
2.8

403
800b
10
400b
178
17.5

403
159
900b
10
600b
178
17.S

0.58

b Estimate and calculation based on e..xposure data.
n = negligible.

• Except for obstetrical examinations, the doses are the same
as for female.

395

TABu;XII. DATA ON THE AN!l.'UAL GE1'"ETICALLY SIGNIFICANTDOSE FROM DIAGNOSTIC X-RAY EXPOSURE

Survey, 1955-1957

Swede1115N*I
N X 1,000

T:H>1 of enmination

Femak

9.1

7.0

940

5.3
4.1
2.5
4.1
2.6
1.0
1.8

0.6
3.8
4.2
2.4
5.0
4.4
0.2
0.9
0.6

Male

Lumbosacral region .••.••••••. }Lumbar spine •.•••••• , •••••••
Pelvimetry •••.•••••••••••••••
Urography ....•..•...•••.••..
Pelvis •.•..••.•..••.•••••....
Abdomen ••••••••••••••••••••
Colon •••••••••••••...•••••••
Hip •••....••.•••.•••.•.•....
Urethrocystography ...........
Femur ••••.•..••••.•••••.•.•
Obstetrical abdomen ••••••.•.•~ (mrem)Maleadulls

1,240
870
1,360
310
1,090
3,700
830

Femak
aduUs

~ (mrem)

D1

Pauni-

mrem

Foe/SU"

Mak

490

490

6.30

1.36

0.14

7.80

21

1,080
925
200
1,150
1,520
260
1,940

4,500
925
200
1,150
1,520
260
1,940
35
910

3.48
2.70
1.78
0.56
2.19
1.57
1.40

0.28
1.77
0.40
0.93
2.03
0.25
0.14
0.02
0.06

6.40
0.16
0.03
0.11
0.21
0.01
0.02
0.01
1.20

6.68
5.41
3.13
2.82
2.80
2.45
1.73
1.43
1.26

18
15
8
7
7
6

35
265

Femak

Foetusare

5
4
3

SUB-TOTAL

31

29

20.0

7.2

8.3

35.5

94

Other types of examinationb •••

186

188

0.3

1.8

0.2

2.3

6

TOTAL 217

217

20.3

9.0

8.5

37.8

100

• Except for obstetrical examinations the doses are the same
as for female.

b Does not include dental radiography.

TABLE XIII. DATA ON THE ANNUAL GENETICALLY SIGNIFIC..\NT
DOSE FROM DIAGNOSTIC X-RAY EXPOSURE

s.L'itzerland16

Survey, 1957
N*1
N

Type of t%amina!ion

Urography (descending
pyelography) ...............
Obstetrical abdomen .•........
Pelvis ...............••......
Lumbar spine ................
Colon (barium enema), lower GI
Retrograde (ascending
pyelography) ..............
Chest .......................
Hip, upper femur .............
Stomach (barium meal), upperGI
Pelvimetry •..•..............

Mak
adults

Femak

4.0
1.1
2.4
7.4
6.9

1,000

1,000
700
300
500
200

1.2
188.0
3.5
26.5
0.24

1,000
2
100
20

Male

Female

3.7
2.8
7.4
6.9
0.8
190.0
4.1
31.1

Sun-TOTAL 247

dj (mrem)

XI,000

1,200
150
150

adults

1,000
1
300
50
700

D* (mre'")FoetusMale

Female

1.93

2.14
1.73
0.55
1.62
1.20

800
2.55
0.48
0.90
0.42
0.69
0.27
0.31
800

1.96

mretn

Pcruntage

4.07
3.69
3.10
2.10
2.10

18
17
14
9
9
5
5
4
4
3

0.38.

1.04
1.04
0.97
0.96
0.72

2.34

19.8

88

2.5

12

22.3

100

7.55

9.90

290

194

I.78

0.73

TOTAL 537

435

9.33

10.63

396

Foetus

0.62
0.35
0.70
0.65
0.34

241

Other types of examination .•..

Di

2.34

TABLE XIV. DATA ON THE ANNUAL GE:SETICALLY SIGNIFICANTDOSE FROM DIAGNOSTIC X-R..\Y E..XPOSURE

Survey, 1956-1960

United Arab Rep:iblic ( Alexandria)11..

N*
Ni X 1,000•d (mrem)D (mrm:)1

T:ype of e.ramir.olion

Mole

FemaleUrinary tract. ................
Lumbosacral spine ............
Lower GI tract ...............
Upper GI tract ...............
Mass radiography ............
Chest .......................
Cervical spine ................

3.7
3.2
2.3
0.7
7.2
3.6
2.4

Skull ••.•••••.•••••.•••..••••

1.1

4.6
3.1
2.2
0.8
10.7
7.4
2.4
1.2

24

32

.\fak
adulls

Fema~

SOO

320
270
600
470
5
5
1
1

255
100
70
5
5

adult;

D;

1

Foel:ts•mrem

Per<enla11

1.47
0.84
1.3
0.36
0.05
0.04
0.002
0.001

3.32
1.66
1.5
0.41
0.09
0.06
0.002
0.001

47
24
21
6
1
1
<1
<1

4.06

7.04

100

--"

--"

__.

_.

2.98

4.06

7.04

100

Mok

Femok

1.85
0.82
0.2
0.05
0.04
0.02

2.98

Foetus•Obstetrical abdomen• ...••....
Pelvimetry• .................•SUB-TOTALOther types of examination ....
36

TOTAL

•No data.

TABLE XV.

DATA ON THE AN?.-UAL GENETICALLY SIGNIFICANT
DO:SE FROM DIAGNOSTIC X-RAY EXPOSURE

United Arab Republic (west and so1ith-west of Cairo)lB

Survey, 1955-1961
N~NI

x 1,()()0

Mak

Femak

Mak

Type of examinaJion

adullsFemaleadultsUrinary tract. ...............
Lower GI tract ...............
Upper GI tract ...............
Lumbosacral spine ............
Mass radiography ............
Chest. ......................
Cervical spine ................

4.1
1.5
1.0
0.9
5.7
5.0
0.9
2.6

5.1
1.8
1.1
0.9
8.4
10.0
0.9
2.9

500
100
70
255
5
5

320
600
470
270
5
5
1
1

SUB-TOTAL

22

31

Other types of examination .•..

22

4

TOTAL

44

35

Skull •••..•••••••••••••••••••~(mrem)~(r:rem)

FoelurDi
mrem

PerU?UOle

1.9
1.10
1.13
0.23
0.04
0.05
0.001
0.003

3.98
1.23
1.18
0.46
0.06
0.07
0.001
0.003

57
17
17
7
1
1
<1
<1

4.45

6.98

100

Mok

Femak

2.08
0.13
0.05
0.23
0.02
0.02

2.53

Foetus•Obstetrical abdomen• .........
Pelvimetry* .•................

--A

2.53

•No data.

397

4.45

6.98

100

TABLE XVJ. DATA ON THE ANNUAL GENETIC.<\LLY SIGNIFICANT.
DOSE FROM DIAGNO,STIC X-RAY !"XPOSURE
Surve)', 1957 ~ ~958

United Kingdom (except Northern lreland)to~ x 1,000
N
Maia

Tl'P• of ezaminalion .

Female•d (mum)1

MakadultsD

Fnn4k
od,,U,

Foetus

367

723
536

Male

• (:r.rem)

D1

1

Percnoi-

Femck

Foe/Ju

mrem

1.12

2.27

3.39

24

1.72

1.17

0.22

3.11

22

0.96

0.69

0.09

1.74

12

1.33

0.01
0.60
0.06
0.04

1.48

ci,22
0.11

0.14
0.55
0.32
0.36

0.60
0.51

11
8
4
4

0.14

0.29

0.05

0.48

3

83

4.48

4.64

3.34

12.46

88

52

40

0.35

0.39

0.04

0.78

6

TOTAL 136

123

4.83

5.03

3.38

13.24

94

0.83
0.01
0.01

6

14.1

100

Gl<

A.· NATION.AL HEALTH SERVICE·, HOSPITALS

Obstetrli:a:I abdomen ••..••....

1.5

Pelvis .•••,;;.'. ..•..•....••.••.
1.8
Lumbosa~I ~gion ••••..•.••• : 2.2
Lumbar sp1ne •.••..•••......• , 3.5' I~
Urography '(descending. •.. 1
2.3
~ pyelogi'aphy) ••••••.•••.•. ·1 ::1,liRetrograde (ascending
pyelography) ...............
0.3
Hip, upper femur .... ·....•.•..
2.0
Pe.lvimetry, •••.••.....•••.••.
Abdomen;;'.~ ••••.•..••••.•.. ' : ·3.0
S.tomach (barium meal), upperGI
6.0
Chest (heart, lung) (excluding, ~ass mi~iature radiography). q3.•:,.. ! •

,,_,
.._.-

370

392

2.0

765

585

740

102
745
183
333

0.4
2.9
0.4
3.0
4.3

ql

105
44
2.75

I

5.4

'"!
154
885
281
448

5.5

1.15

··~

SUB-TOTAL 84
Other types of examination ..••

2.0}
2.3
3.1

B. DIAGNOSTIC X-RAY EXPOSURE OUTSIDE NATIONAL HEALTH SERVICE HOSPITALSGeneral diagnostic examinations
Mass miniature radiography •••Dental radiography ..•••••••••

22
95
40

0.09
0.3

0.09
0.3

TOTAL genetically significant dose

398

0.09
0.3

No data
No data
No dataTAnLE XVII.

DATA FROi.r VARIOUS COUN'J'IUES AND AREAS ON GONAD EXPOSURE FROM MASS SURVEY EXAMINATIONS 01' THE CHEST

Populatiot1 at time of studyt'..>l\0'°Country or area

Total

Below age JO

Argentina (Buenos Aires) ...........
Australia .........................
Austria ...........................

6,000,000
9,500,000
6,984,000

2,770,000

Belgium ......................••.•

Number of examinations
Per 1,000 of
total population

Number of examinations
per 1,<JOO of population
below age JO

Radiography Fluoroscopy

Radiography

Fluoroscopy

-"

_..

2,990,000

76
190
25

25

166
No data
37

8,924,000

3,797,000

128

26

226

48

Canada ............•...•..........
Denmark ........•................
Federal Republic of Germany(Hamburg) .....•...•............
France ...••.................•..•.
Italy (Rome) .••.......•...••......
Japan ...........•..•.•...........
Netherlands (Leiden) ............•..
Norway ...........................
Spain .............. , ..............

17,048,000
4,466,000

9,300,000
2,080,000

90
140

_.

86
120

_..
__.

Sweden ...........................
Switzerland .......................
United Arab Republic:
Alexandria .••..•.............•..
Cairo .....................•.....
United Kingdom (except Northern
Ireland) ..••.•..................
U nitcd States of America ......•....
R = Radiography.
F = Fluoroscopy.

1,755,000
43,600,000
1,875,000
90,000,000
110,000
3,525,000
29,000,000

16,000,000

130
40
77
322
80
211
2

7,300,000
5,160,000

2,300,000

140
130

1,361,700
2,640,000

787,000
1,527,000

4
5

82,000,000

95
135

50,000,000
162,000,000

20,000,000
58,400

_.

_.
_.
_.
5
-"

60

-·

-"

No data71
No dataNu <lata
53
No data4

28-"

Gonad dare adults (mrem)
FemaleMale

Femalt:

Total

Reference10
No data
R 0.3
F 7
R 0.2
F 5
0.7
0.25

15
No data
0.8
18
0.6
13
12
0.15

1.3
No data
No data

0.6
No data
No data

1.9b
0.2"

4
3,33

No data

0.36L
002"l
0.09h

53

No data
0.03
0.03

0.5
0.02

0.45b
0.53"
0.05

0.16

0.32
0.6
11
0.4
0.4
1.0
0.8
31
1.6
0.5
1.5

0.02
No data
0.33
No data
0.01
0.02
No data

0.0:!
No data
0.60
No data
0.01
0.06
No data

0.1
No data

0.3
No data

5

7
7

0.04
0.03

0.05
0.04

0.09
0.07

17
18

0.09
1

0.09
3

No data
0.05

No data
0.13

0.01
0.18"

19
20

R 0.25-"

6

No data
155

70

7
6

-·

No data

_.

-"

90

Ge11etica//y significant dose (111re111)

Male

5.5
0.05
0.4
0.13
R 0.3
F 12
0.8
R 0.2
F 0.6
5

0.05
0.02h
0.93
0.08b
0.02
0.08
0.002''}
0.13"
0.4
0.05}
0.07"

53
107, 115
5
6
3, 10
11
53
13
14
53
15
16, 53• Not applicable.
significant dose calculated according to formula 11, e.g. assuming themean age of child-bearing to be 30.
h Genetically

TABLE XVJll,

GONAD DOSES AS SUDMITIED DY COUNTRIES AND EXAMINATIONS (MALES)(mrem)

Argentina (Buenos Aires)'.... . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Denmark .................•.......... , . . . . . . . . . . . . . . . . . . .
Federal Republic of Germany (Hamburg)... . . . . . • • . . . . . . . . .
France. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Italy...................................................
Japan ...................•........... , . . . . . . . . . . . . . . • . . .
Netherlands (Leiden).. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Norway.................................................
Sweden•. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Switzerland. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
lluited Arab Republic ......... , ........ , ... , , ....... , ... ,United Kingdom.........................................

Mass
suri•ey,chest

Chest,
htart.
luni

10
0.3
0.2

5
0.4
0.5

2

60
2
4
45
12
2
3
3
6

I0
5
3

8

3()d
6

0.5

0.1
0.4
0.1
0.8
0.4

1
2

5

0.1

Cho/eels·
lo1rap y

1

Stomach,bari1tm
meal

Abdomen

150
610
88
250
141
220
92
65
1,360
105

Col011,bari1t111
enema

300
40
890
134
239
1,310
25
185
310
150
100
146

Pel•is

600
567
275
1,500
1,130
1,490
157
376
870
1,200

Lumbarsf>ineLumbasacral

230
200
104
63
555
250
234
767
1,700
60
16
-130h-940h150
255
370

Ilip,

upper
f•mur

Ftmur

600
980
1,520
1,200
-586691
3,233
407
384
1,090
830
100
740

d Estimate fromcontribution due to fluoroscopic examinations in private practit'e.
• Including urethrocystography.

b

TABLEXIX.

Retroerade
pytlotrophy•

600
700
2,580
1,019
311
241
1,900
390
940
631
512
423
15
217
1,240
3,700
1,000
1,000
500
-765-

60
20
65
90
123
13
4
3
14
20
70
44

• Radiographs, 11ot examinations.
In these countries the two types of examinations are combined.
•Hip only; femur 011ly.

Uro1rap/1ydesc.ndint

GONAD DOSES AS SUBMITIED BY COUNTRIES AND EXAMINATIONS (FEMALES)( 111re111)

Argentina (Buenos Aires)• ................
Denmark .. , ....... , .. , ................
Federal Republic of Germany (Hamburg)
France .................................
Italy .............................. · ...
Japan .................................
Netherlands (Leiden) ....................
Norway ..................... ··········
Sweden• ...............................
Switzerland ............................
United Arab Republic ...................
United Kingdom ........................

Masss-uney.
chest

Chest,

15
0.2
0.3

10
0.1
0.7
30d
1.0
13
2

11
0.4
0.4
1
1.6
1.0
5
0.1

heart,

lune

2

4
5
5
5

Choltc:ystovaphy

90
16
35
105
156
80
4
8
17
299

• Ra<lioi;raphs, not examinations.
In these countries the two types of examinations are combined.
•Hip only; femur only.

i.

Sloma.eh,barium
meal

90
9
67
300
411
1,108
6
18
29
50
470
333

Uro1raphy
desetndint

Retroirade
pyelocraphy•

800
900
565
1,136
439
657
4,500
1,800
1,060
92
604
1,608
125
403
925
1,940
1,000
1,000
320
-585-

Abdomen

200
85
128
375
210
49
132
178
1,150
183

Obsl<lrieal
abdomen Ptl•imetr:y

900
822
600
1,200
1,250
322

800
190
680
1,600
399
162
100
400
265
1,500

800
1,080
1,500

367

745

Colon,
bari1on
enema

450
20
2,530
264
1,050
2,200
613
2,050
1,520
200
600
464

Pel•is

700
210
94
1,300
330
80
142
135
200
300

I.um bar
spin1

Lumbasacral

600
400
222
183
402
700
570
121
116
790
47
-592"--490h-

500

Hip,
upper
femur

Femur

600
58
214
180
-22331
140
10
159
35
260
300

270
392

102

d Estimate from contribution due to fluoroscopic examinations in private practice.

• Including urcthrocystography.

T AJJLE XX.

FOETAL GONOD DOSES AS SUBMITIE.D BY COUNTRIES FOR OllSTh'TIUCAL EXAMINATIONS(mrem)
Obsttlri,alabdomenFederal Republic of Germany (Hamburg) •.........•.......•
Netherlands (Leiden) •........•..•..•...••......••........
Norway •.....•...•..................•...........•.•.....

Obstetricalabdomen

677
100

2,900

JiOO

900

Sweden •.••••..••..•••.•..••......•.....•................
Switzerland .........•••....••...•..•.....................
United Kingdom ..••••...•..•••••.•......................

Ptloitntlry

910
800
723

4,500
835

.j>..

0

.......

TABLE XXI.

TOTAL ANNUAL GENETICALl.Y SIGNIFICANT DOSE FROM X-RAY DIAGNOSIS SUBMITTED DY COUNTRIES AND EXAMINATIONS( 111re111)
Alau

Argentinad(Buenos Aires) .......
Denmark ..•..........
Federal Republic of
Germany (Hamburg)
France ...•...........
Italy .................
Japan ................
Netherlands (Leiden) ...
Norway ...............
Sweden ...............
Switzerland ...........
United Arab Republic:
Alexandria ..........
Cairo .•.............
United Kingdom .......

Chl1t,

Stomatli,

Marl.

Clwletys·
lotrapliybariurn

lune

2.8

0.3

0.3

1.2

5.7
6.7

1.6
7.0

1.3
0.4

2.6
0.4

1.8
1.8

0.60
0.43
8.33
11.61

1.45
2.62
4.96

0.50
0.47

0.48
10.2
1.30

0.76
0.80
0.59
0.42
0.03
0.44
1.26
3.69

0.40
0.02
0.23
0.12

38•
1.39
1.48

meal

1.04

0.96

1.86
0.91
5.41
4.07

0.06
0.07
0.48

0.41
1.18
0.51

3.32
3.98
1.53

0.12

0.09
0.06

Urogr°J::h"dtscu1 int• Rounded-off total from national fi~ures.
In these countries the two types o examinations are combined.

hRttrograde
J>ytlouaJ>hy• Abdomensun•ey.
chest

1.40
0.44
1.73
1.04

0.35
0.40
2.82

Obstetricalabdomen Pelvimetry

0.69
6.68
0.72

Colon,
bariumenema

Lumbarsp;,,,

2.9

2.6
1.5

2.9
1.1

2.5

6.09
0.37
3.28
8.29
0.61
1.44
2.80
2.1

1.15

1.28
1.28
4.22
4.55
4.5
0.10
0.60
-2.71b-7.8 "2.1

4.78
1.66
0.55
1.22
3.13
3.1

1.5
l.23
0.21

0.60

1.15

3.39

Lumb~

Pelvissuer al

/UJ>,
"ppa
femur

Femur

Ot/1ers

1'oltll•

5.1
2.3

3.4
6.3

37
27.5

3.33
2.84
5.02
2.39
1.52
0.81
2.45
0.97

1.70
1.18
6.72
2.61
0.73
0.64
2.3
2.5

17.7
58.2
43.4
39.0
6.8
10.0
37.8
22.3

1.63

7.0
7.0
14.1

0.59
1.43

1.66
0.46
-3.11-

1.48

Includes contribution from fluoroscopic examinations in private practice.
These values include the contribution from private clinics and practices.
• Includes urethrocystography.
0dTAnI.E XXII.

Mass

Ciresi,suri•ey,htarl.

chtsl

Argc11lina (!3uenos Aires)
Denmark ...........•..
Federal Republic of
Germany (Hamburg)
France •........•.• , •.••~
0
Iv Italy •.•.•..•.•••••...•
Japa11 ...........•......
Netherlands (Leiden) •••.
Norway •.........•.....
Sweden ••.......•......
Switzerland •...•.•.•.••.
United Arab Republic:
Alexandria .•.........
Cairo ..............•.
United Kingdom ••••.•.•

lun1

Cho/ecystopaphy

8

65•
3

Stomach,bariummeal

COMPARISON OF PERCENTAGE TOTAi. GENETIC IJOSE FROM IJIAGNOSTIC
RAIJIOLOGY BY COUNTRIES AND EXAMINATIONSRetrograde
UroColon,
pytlobarium
1rapl1yObstetrical
descendint iraphy b .A.bdomm abdamtn Ptltim<lry enema

3

15
24

4
25

3

8

1
19
30

4

5

4

1
1
3

17
4

6

Lumbarspine

Lumbasacral

7

Hip,
upper
femur

Subtotal

Others

Total

14
8

92
77

8
23

100
100

89
98
79
96
89
93
94
88

11

7
6
12

100
100
100
100
100
100
100
100

13

100
100
100

Femur

4
2

7
2

5
7

8

7
5

8
4

3

3

34

6

18
3
4
5
4
7

4
1

2

1

1
1
1
4
3
17

1
0.3

7
2
10
12
12
2
9
-2721

19
5
-126
22

9

4

11

4
27
9
15
18

Pcltis

6
5
5

47
57
12

•Includes.contribution from fluoroscopic examination in private practice.

7
18
3

1
8
21
9
15
7
9

11

4
8
12
8
14

21
17
4

24

8

8
6

6

4

2
21
4
11

24
7
22

II Includes urethrocystography.

1087TABLE XX!II.

COMPARISON OF THE AN:SU.... L GENEI'ICALLY SIGNIFICANT DOSE ARISI:sG FROM X-RAY
DIAGNOSTIC EXPOSURE Di VAlUOUS COUNTRIES AND AREAS

Genetically sitnificanl dose (mwn)
JlakCountry or area

Femok

B

A

Argentina (Buenos Aires) ... : ...•.
14•l',io data
Austria ...•....••.•....... ·.,,···
Denmark ••••............•......
Federal Republic of .Germany. ·(Hamburg) .....•.....•.......
8.8
1Qb
France .••......•.......... :.. ' ..
Italy (Rome). . . .. .. .. .. .. .... . • .
21
Japan; ..•..... :;_.,, ......•. ·,·...;..
21:.
Netherlands (Leiden). . . . • . . . . . . .
3. 7
Norway ...•.............. "'.·":.: . ,,-?,?,
Sweden .••.••................ :..
20
Switzerland.....................
lOd
United Arab Republic:
Al.undria ...••...............
3
Cairo .•••.................•..
2.5
United Kingdom (except
Northern Ireland) .•....•......
S.1 •

Total

Foetus

B

A

A

23•
No data.

No data
No data

1Qb

;,1

20
18
2.7

s.o

IV
·16-25

1.J

18

No data
2.6
0.4
0.4

43 ± 35

9
12d

4
4.5
3.6•

v

29

VI
VII

VIII
IX

,\;,')'

6.8•
10 ±.338 ± 1022d

8:s· ;,No data

5.3•

17'
S8

39·~ d

1.1

I·

.. I

lobZ.

37•
28•

7.7

&ft:rtt'M

c

B

x

18.7•

S.7•

XI
. XII
XIII

:.;•J

7
7

XIV

14 ±1

XVI

xv

:;. A)s.coiµput~<\ 1~c;c:ording·P?.t?e,f9£'1lliµ~.O. ;== 1 2:. ~1: .,- 1: ; ·.di':1-;1.:,J11;;(1·.·,.:_ 1 _,;;~:.::.)'~-;•;.

!'1.,';"·~,_!:.j,··~J/!.ilj

B is computed according to the formula D = 2: n · d;..

. ' .: ~ -. ':,_,.'C is computed according to the formula~·":'., ~-~1 .-.p ..,·.. -, ..

I

(!..

l·•·'

1

l·:,,\,')--: ":.·,"

1•Arising from radio'graphy only.
.
.. d lnc!udes 'a' ·cpnt15hution from foetal exposure ansmg from"·Except for.1cbest examinations in private pra~tice· .. which "''obstetr1cal·eµ17Jmations . .,:·
. ,:...... -.
give a contribution of 38 mrem to the genetically significant
c 0.85 mrem, arising from examinations outside the Nationaldose and which cannot be split into male and female .figures. .• ,Health Service hospitals, are distributed among m,ale,. fem;ile•Does not include mass miniature radioizraphy.
' ."";.. ·and foetus.
'.-•·~ ·' · ·.r :r:"(l.1

t.:J:• I (t!'If,! ;:· ! "\ ~~-;~;I;;(..!,)

1( ,(i· l; f ' -!'U,ilo::: .i\i~l~ 1

~ ': .,\I(· 1.::

,

T,

,,:/J

.' 'J.11(ll.f}J ., , : Il}'/i!(;,()

JO.ll

c\'~

0 I

•I

1 .. ,•{;; ~ :···: ~r JI ; ~· •·~' ~~' f;. t ~.' 11; 1 I

c:1t .. ~·(J!!;,,ti_1\:;,(I{.)

f.-i J.t{ ~ .I.I

n.1

I ; 1.t I

IJ;J

"'

i (l

( .. (Io:J:-.,t'•t{~ ~ i ~ "! J i 1.I -'. ~ , i i~I:;'. ~);q''I/.•/ : I ::J';; I•e-;,·:,;.

~:I;;: f ·, I(';:,(l,,;, J;

: .!

l. i

; fl

.. '

..

·"

,.• J

LI.
:~ ;

U!l~

,,

J

j

10.11 1, •• ;,

: 1

· .•

.h

.

TestesChest ................................... .
Stomach (barium meal) ................... .
Colon (barium enema) .........••....•....•

0.00.H>.02
0.05 --0.2
1-lOQo•~I; . I:- • ,\

I '. '•. ,,'0.01--0.04
0.1 --0.3
3- 20!, ·.•

Radiography

1oct-:1 ,.~oey..

Naea'ral radiatiori .' .!'. ........ ·.~.:j ......... '..

. !! . ''.

}AP ......... ;·;; ... .-, ..,: ..

r,.,:,ii'1.:30- so10- so40-20020- 8010-30
4-8 . '.
30-2 00~·
40-siJoaJ.. ·, ·Chest .................................•..
Stomach ..•...................••........•,,. Colon ..... ~ .•.. ;, ............ , ..... ·"" .• ; ..... •.·Lumbar spine.Lumposacral joint :'"·' .. ·. '· ·:,~elvic region .
La~eral ... -, ........... , .
.l:f.D·~~ry blad~.l~r.;~; .::) ..;., ...... ~')), ....... ~'-"

0 ·. •

5~100

r , t 1. ~ 1

0•The testes in the primary beam.
b See:imnex:•C1 ;table·X.:1>.• • ,,~, ;w:-,c With scrotum protection ,.._, 10 mrem/sec. Ii:·:·d With scrotum protection 2-3 mrem/sec.

·'.C403

• '.

1. .

'. ~ ;( I( I ::'; .lt1:

_l
I

'
1'

30-100100-400

b:oi 4-14.00 'irirem/sec,hNole: Russell's experiments cover the following dosb-rate range,{I;: I J: ;.) • ';

'

,

~!·

~

I

L

'

'I

'

I

.,,

'.·

'
. .,1

.1,, ·.!.•,

: \.

l.

_; _;

"' "•'f.l ' ~ l

I •\

l

.'
I

d

Fluoroscopy

. I

i l

~

Dose rau (mum/sec)

Type of":111)

J,TYP~s19~X-R.w'~ici~i~j\TIONs' .·'.,,.. ··;";;,,,;;, :·::;: ...

ezaminalion•.. ~: ''·:.\\ I ;'"'"'' '''"''"' "i.Jii.i XXiV. 'pi«)~Al3il~sE-RA-r'is'~o!.Ali ~~ns~\mu;.d:v.Jubus' ~ . ;.... " .:·"
.:.

;~·

('

:,,1,, •.. ;TABLE XXV.

DATA ON THE ANNUAL GENETIC...\LL Y SIGNIFICANT DOSE FROM EXTEIL'>AL
RADIO-THERAPY FOR NON· MALIGNANT CONDITIONS

Sttrve)•, 1957-1958

Federal Repttblic of Germany (Hambttrg)S
Number of patients
lreoled per J ,OOO
of total
populatio11

Gonad dose (mrem)
Average figures

Annual teuticaUy significant dose
(mrem)

Loeolion

Mak

Femak

Mak

Femak and foetus

Mak

Femak

Fodus

Tol4l

Skin (various conditions) ...•

1.52

1.63

1.40

0.01

1.46

0.46

0.72

0.05

0.25

0.02

0.32

Other sites •••.••••••.•...•.

1.48

2.43

J-a
6,900
6,000
70-10,000

0.05

Spine ..••..•••.••••••.••••

0.1-"
390
800
40-3,000

0.18

0.22

n

0.40

TOTAL

3.5

4.8

0.28

1.87

0.03

2.2

•The dose ranges are due to various conditions and different
sites treated.

n denotes less than 0.005 mrem.

TABLE XXVl. DATA ON THE ANNUAL GENETICALLY SIGh'IFICAh"'T DOSE FROM EXTERNALRADIO-THERAPY FOR NON-MALIGNANT CONDITIONSSurve)', 1957

Fra11ce:1

L<>catwnN•mber of patimls
treald per 1,000of J.olal populaliorr

Gonad dose (mrem)..berage figures

Mak

Femak

Male

Femak

Male

FemaleFoetusTotal

5....h100

20....h200nn

No Data

n

900
2,800
14,2001,500
4,500
49,600

0.02
0.01
0.5

0.04
0.04
1.0

No Data
No Data
No Data

0.06
0.05
1.5

91,500100....h17,00099,500
20....h
8,000

0.5

0.5

No Data

1.0

0.2

0.3

No Data

0.5

1.2

1.9

Skin (various
conditions) .••••••.••••••.
Spine:
Cervical ..••.......•..•.•
Dorsal •.•••••••••••••••.•
Lumbar ..••••••••••••••••

0.31

0.38

0.16
0.04
0.25

0.22

Hip ••••..•••..••...•..•..•

0.04

0.04

Other sites •••••.•.....•.•..

0.26

0.29

TOTAL

1.1

1.2

O.o7
0.16

3.1

b The dose ranges are due to various conditions and different
sites treated.
n denotes less than 0.01 mrem.

• Reboul has calculated that 6.8 per cent of :!:N;d; oriiPnatesfrom patients below age 30. The subdivision into locations ismade under the assumption that this percentage is valid for all
locations.

TABLE XXVII.

Annual geu#cally si1rriji&anl dose
(mrem)•DATA ON THE ANNUAL GENETICALLY SIGNIFICANT DOSE FROM EXTE!L'>AL RADIO-THERAPY:FOR NON· MALIGNA..>\T CONDITIONS

Sm-,;ey, 1942-1951

N etherlands~s~umber of patierrts

treated PCT 1,000
of total
Population

Condi1io11
treatedGorrad dose (n:rem)
A rerate figures

Annual te11eticaUy sitnificant dose
(mrcm)

Mak

FemaleMale

FemaleJ,faleFemaleTotal

High gonad doses •.•.•..•.....

0.65

0.33

70

110

Low gonad doses ............ .

1.4(1.4)o1.16-5.Q3•(2.57-8.02)b
0.17

1.63
(3.i6)b(0.17)

2.79-6.66"(6.33-11. 78)b
0.34

TOTAL

2.1

1.7

(1)•

3.1-12.1• Based on actual number of children born to patients.
on total expected number of children averaged
throughout population.

•Female assumed equal to male.

b Based404

TABLE XX\rnr.

DATA ON THE ANNUAL GENETICALLY SIGNIFICANT DOSE FROM EXTERNALRADIO-THERAPY FOR NON·'..\IALIGNANT CONDITIONS

S11rvey, 195i-1958

U11ited Ki11gdom (except Northern Ireland)l9
Number of patientstreated Per 1,000
of total
pop:1la:io11

Coi:dition

Gonad dost (mrem).4 =erage figures

Annual geneJiccl!y significant dcse
(mrem)

treatedMale

FemaleMalt

Fem ale and foetus

Male

FemaleFoetusTotal

Skin conditions .••......

0.46

0.57

0.93

0.03

2.52

0.03

0.01

300-4
6,000
20,000

1.55

Ankylosing spondylitis ..
Arthritic and rheumatic~.:conditions ..••.......
Other non-malignant
conditions •.....•....

150-4
32,00050,000

1.07

0.08

n

1.15

0.02

0.02

0.18

0.05

0.27

0.07

160,000
20-a
50,0000.04

0.02

23,000
40-a
6,000

0.04

0.49

n

0.53

TOTAL

0.5

0.7

2.70

1.69

0.08

4.47

• The~dose ranges are due to various conditions and different
sites treated.

TABLE XX!X.

n denotes less than 0.005 mrem.

COMPARISON OF THE ANNUAL GENETIC,\LLY SIGNIFICANT DOSE ARISING FROM EXTERNALRADIO-THERAPY IN VARIOUS COUNTRIES AND AREAS
Annual genetically signiji<ant dose (mrem)
Non-malignant conditions

Country or area

Federal Republic of
0.28
Germany (Hamburg).
1.2
Franceb ••.••.•.•......
Netherlands ..•..•..... 1.33-8.19
United Kingdom except
2.70
Northern Ireland ..••

Malignant conditions
FemaleFoetus ·Sub-total

Total

Reference

2.2
3.1
3.1-12.1

O•-2.5"(0.5)d0.5O•No data
No data

0
2.5
1.0

2.2
5.6
4.1-13.1

6
27
28

4.47

0.41

0

0.52

5.0

19

FemaleFoetusSub-total

Malt

1.87
1.9
1.8-3.93

0.03
No data
No data

O•

1.69

0.08

Male

•Not subdivided into sexes.
d Female assumed equal to male.

•Fertility factors regarded as zero.
b Genetically significant dose calculated according

0.11

to formula

11.

TAllLE JL"{X. Cm.IPARISON OF GEJ.'TETICALLY SIGNIFICANT DOSE AND PER CAPITA DOSE CAUSED BY
EXTERNAL RADIO-THERAPY FOR NON-MALIGNANT CONDmONS
Mode of calculalion(doses in mrem)

N1!: ff •Country or area

Federal Republic of Germany (Hamburg). . • . • .
France •.......................•............
United Kingdom (except Northern Ireland)... .

TABLE XXXI."

Wi

w·di

!:

-ff ·d;

6.5
21
9

2.0
3.1

2.0

N

4.5

EsT:U.IATED DOSE-RATES TO THE GONADS FRO:.\! EXTER..'TAL RADIO-THERAPYFOR NON-MALIGNANT AND MALIGNANT CONDITIONSb
Dose role (mrem/ sec)
Orories

TestesLocation

0.01-0.05
2-5
20-50
0.008-1

Head .•••••••...................•.•... ·•···•··· 0.01-0.05
0.5-3
Thorax .•.•........•....•...................... ,5-15
Abdomen and pelvic region .................•.....
Skin (various sites) ...•....•....•.••.......•.•... 0.002-0.5
Natural radiation ..•............• , ............. .

3.10-G•Russell's experiments cover the following dose-rate range-0.014-1400 mrem/sec.
b Estimated on the assumption of 50 rad/min at the treatment site.

405

TABLE XXXI!. CoMPARISON OF THE ANNUAL'GENETICALLY SIGNIFICANT DOSE FROM THE
ADMINISTRATION OF R..o\DIO-ACTIV& ISOTOPES IN VARIOUS COUNTRIES AND AREAS
Gt1tdical1y si111ifi&ant

dose (mrem)Year of study. DiatP<osis

Therapy

1956

0.02•

0.4Qa

1111 , P=

37

195.h'':
1958 .

0.01

0.18

11 11

6

0.15

1111 , pa '

19 .

Jmc

38

Canada ••.. ; ..•.......•••••..
Federal Republic:of Germany._'J.
(Hamburg) .••...••••...•...
United Kingd6~, (except Nortiiern.
Ireland) •.......•..••..••••
U~ited States .
,, 1of America .••.•.•......•...

''<.

1957 ''-

l '.t

0.03. ,, .

'

0.24b

.!

•l

',I

•Computed accordintt to formula 11. No allowance made for the influence on fertility
Crom the severity of the, disease. , .
b Computed according td forffiula fa.':"".' "::
I .
' .
. "
0
Other radio-isotopes considered to be of no significance.

". '.''' . . . i ··.,

'!

.. ,

:1:.

t :·

. i

'

t':

'.

1·•••

..

:- -·.

TABLE.X:XXI!J;ANNUAL GENETICALLY SIGNIFICANT DOSE· FROM THE ADMINISTRATIONOF RADIO-ISOTOPES...... d;·it · •. ' ' I

Use 1 ,'

!

I

·i

' ~ [

:

',(I

tt ! I ' ~

: ·

'

,

I

'

Malignant diseases ......................... .
_· '.

,,,1 ·; . • r •·.

{ 1111pu; ;!·:.i ,,,'"I

Non·malignant conditions ••..••••••.••..•.••~.

Genetically si:nificant dost

Radio-isatopi>. DiagnO~·.·.'
Test doses •..•.•••••. , .•••.•....•.•. , •••••••
Therapy": l.United Kiiigdom (except Northeryi lreland)U;Survey, 1.957

.....

0.016
0.012

.. !

~

.;

:

''··

9

(;i
\,:··i

I

0.049
0.059
0.045

{Im
p=
Jiil

...

'
27
33

25

. o..~8±0.18,

TOTAL
i.,

..'>I•

Note. The contribution fr~m a"ther radio-isotopes is negligible.
·I

!''I

T ADLE XXXIV.

GoNAD DOSES IN MREM PER .WMINISTERED MILLICURIE OF
JlSl OR p32

Radio-isotope

Gonad dose (mrem)

450
450 (130-1,170)
1111 •••••••••••••••••••••••••••

600±300

pa ...........................

l&marksNormal physiologicalconditions
20 patients:
10 thyroid cancer
7 hyperthyroidism
3 others.
Normal physiologicalconditions.

&faen~e

37
39

40

2,600

Normal physiologicalconditions

37

7,000

Normal physiological· condition!

41

406

.'

':.ii.''It•·[

T AllU: XXXV.

MARROW DISTRIBUTION IN THE ADULT
Total

SiJe

Head.;;• •••• .-. •••.•... Cranium, mandible
Upper limb girdle., .... Scapulae, clavicles, head and neck of humeri
Thorax ••.•••..••..... Sternum
Ribs 1 to 12
Spine ................ Cervical vertebrae
Dorsal vertebrae
Lumbar vertebrae
SacrumLower limb girdle ..•... Pelvic bones, coccyx, head and neck of femora.:Mechanik0 , and Woodard and Holodny.~for ribs, sternum and vertebra at age 40. Other
values assumed in study.
• Ellis}7
d Half the contribution of 10 per cent from "other" (e.g. in

actiPeinga

actiPema"ow•

ma."owin g•Ellis"

tu commitkr

182
116
39
20i
47
197
152
194
364

0.75
0.75
0.6
0.4
0.75
0.75
0.75
0.75
0.75

140
85

13
8

10
5m

i.sl

25

25

85
35
150
115
150
270

3.5
14
11

26

Epp ~t al. U .S.A.• 11

Mean marrow doie (mrem)1958 &port oflheCommillee"'

Buhl"
DenmarJ:b

AP

Lal.

200
100

10
30
50

3
90
180

70
35

180

PA 1.3

4.5

50

Head •••...••...•....................
Spine •..•...•.•....•.•.........•.•.. ·Cervical ••.•.............••...•..•..
Dorsal •.......••........••.....••..
Lumbar ..........................•.
Lumbosacral region .. , ......•..•••.....
Pelvis .••..••.....•..•................
Hip, incl. upper femur .............•...
Arm and hand ........•....... , , , .....
Thorax (ribs and sternum) ...•....••..•
Chest (regular) •.....••....•...••......
Gall bladder. •........•........•.•. , ..
Stomach (barium meal), upper GI. •.....
Colon (barium enema), lower GI .•...•..
Abdomen ••••......••...••............
Urography .....••.•..........•.......
Retrograde pyelography ........•.......
Urethrocystography .......•.•....•....
Pelvimetry ...............•........•..
Obstetrical abdomen .........•......•..
Hysterosalpingography ..........•......
Dental. ....•...............•.•...••..

50
400
400
300
20
30
2
200
40
400
500
700
50
200
100
300
800
100
100
20

30
20
0.2
150
20
150
200
200
30
80
30

25

•Radiography only.
.,,J. , ;,•;_l :.,, r·,;1.·.,,.:·1 '.•, '''b In Buhl's investigation the dose calculations are b~~d.. up~h the figures 'for the distribution',. ·of active marrow presented by the Committee 3•
The technical factors used are those of the Memorial Hospital, New York. The doses arethose that arise from well collimated and aligned fields. The dose due to the scatter outside thedirect beam has been included but not the effect due to the photo-electrons from the bone.
0'·,r; ',:,·:/,"-,i_;._ ,;J;·: h::. ,:·:·: 'lq '1'r~_c;1',j,J1,;_ '·:'.
1

'. ~;

, . ;,;::•;:·.:~ :J.):·.'TABLE XXXVI!. INDIVIDUAL AND PEi.CAPlTA iIEAN.:i.JARROW DOSES IN SO~!E COUNTRIES ARISING
FRmI, MASS SU~VEY. ,i.uoROSCOPY .OF :rHE CHEST. AND COMPARlSON WITH C.~CULATED PER
c....Prtli."rxMis'FRoiii:'ilADi:CiGR.~PHY''';'::• \•'\i:.,,.:: ·'·,,;;.;;::· :: i:.! '.··;:··::,,.,; ..«:
1

-'

,, .

· .. ..

, ': '~

Mean marro1D ®se (mrem)<.::)

Per eapila
dose if

Number ofe~arr.inations! fier:1;000
\'

;

.. :

Per eapila

oj lotaf,

1 p·opula/~on•

Au'si:ria ..... .':::~.:: ..•.... 5·.';: .< ..••.•.. ;:;\':·:<. ;,25
I\elgium ..... ~.•..•.•... , . ~ ..• ~ ..•.•.••••.• ._40

14

MEAN MARROW DOSES FROM DL~GNOSTIC X-RAY EXPOSURE(EXCLUDING MASS SURVEYS OF THE CHEST)&:amination

1958 r1por1 of20•

extremities, etc.) in the 1958 report of the Committee (annex C,
para. 44).
•The contribution from pelvis and half the contribution of 10
per cent from ''other" (e.g. in e."<tremities, etc.) in the 1958
report of the Committee (annex C, para. 44).

b Custer's

TAllU: XXXVI.

.A.eti:e manes Per ctnJ

Total

Fra&lion

man-ow'". 26' ;France ..... .':';". ....... :.-:.:·,·; ........ ".';. '''·'570
sP4iln ...... :;;;:'1 . <.......... \'. ............. I. : 5·
Switzerland. ;· ~ ; ~< ! •••••••• L . . . . . . . . . . . . .

60

IIndividual .

2,000
'380
1,200
1,300 '
230••Figures taken from table XVII. . .' · . . ·,'··b Mean marrow dose per examination assumed tci be 100 mrem•;407

radicgraf>h:t· · in total· ·, is used•: ··imlead of

50.10 ....
680. .2~6 ; j. populaJwn · . ftuor,os"'P:I>

... 8
. ,14

2.5

57

.Q,5-".6

I

TABLE XXXVIII.

EXAMPLES OF MEAN MARROW DOSES IN EXTER.."'AL
RADIO-THERAPY"

A!ean marr1r.t1 close (rem)Site or e<>ndition

Cervical spine, 10 X 15

Type of radialion

Per 100 r skin dose

cm................... X-rays (170 keV,

2.6

filter 0.5 mm Cu)
Lumbar spine, 10 X 15 cm .•..••••..••.••.••• X-rays (170 keV,
filter 0.5 mm Cu)
X-rays (170 keV,
Hip, one side, 10 X 15
filter 0.5 mm Cu)
Carcinoma of cervix.. . • . . • • . . • • . • . • • • . . . . • • . • Radium (applicators
containing 50, 75 or
87.5 mg Ra)
Haemangioma•. • • . . • . • . • • . • . • • . . . • • . • . • • . • • • Radium (applicators
containing Ra ranging
between 8(H30 mg)

TABLE XXXIX.

54, 55

5.5

cm ....................

•With the exception of those for haemangioma Ellis's fiiures
for the distribution of active bone-marrow have been used (table
XXXV).
b The values of total skin doses used in references 54 and 55
range from 300 rem to several thousand rem delivered overmore than one course of treatment.
• Children below two years age. According to paragraph 78,
it is assumed that only red bone-marrow exists. The distributionof the active marrow is taken from Woodard and Holodny0

Total treatment

2.5
60-10056

0.5-25d57

under the assumption that the distribution of marrow space inchildren and adults is the same. The following distribution figures
were used: upper limbs 123, lower limbs 393, ribs 7%, head 7o/£!
spine 153, scapulae 23, clavicles 1 %. sternum 1 %. pelvis 16'10
of total marrow space.
d The range covers various sites of the haemangioma. The
highest fi~ures are received when the haemangioma are situatedon the skin of the abodomen and the thigh.

E.Ju.MPLES OF RADIATION DOSES IN VARIOUS KINDS OF RADIOLOGICAL PROCEDURE TO
ORGANS AND TISSUES OF SPECIAL INTEREST

Diagnosis
Examination

TissueFoetal tissue(a) age < 2 months ...•(b} age > 7 months •.•.
Lens of the eye .••..•••

Thyroid ..••••••••.•.•

Thymus •••••••..•...•
Liver •.••.•••••.•••..•

Dose remN on-maliinanl condition

Maliinant condition

Dose rem

See tables in this anne.-..-assume foetal dose is same as maternal gonad dose
1-3
Pelvimetry
Obstetric Abdomen"'°·5
Dental (full mouth)
5-25
Retinoblastoma(dose to unaffected eye)
5-20
Encephalography
Head lesions
Cervical spine
Uptake from40
400-1,200
25 µC 1131
2-10
Tonsillitis
150
Ba Swallow
Thyrotoxicosis JUI
10,000
Enlarged gland"'200
2,100-5,400
20 cc Thorotrast(over 20years)TABLE XL.

ESTIMATES OF RADIATION DOSES IN THOROTRAST PATIENTS(20 ml injection)

Estimates of Th 232 activity111: 0.02l7 µc/ml (German), 0.0244 µc/ml (U.S.A.)

TiSSIUl

Skeleton .......................
l\1arrow ..•....................
Bronchi .•......................
Lungs .........................
Liver ..........................
Spleen •••......................

RadioadiresourceAreragedose-rate
rad/yAca.mulatedrem•(ZO years)

Th=32 + d
Th:!32 + d
Thoron+daughter
Thoron+daughterTh 2!2 + d

1.4-3.0
1.2-2.9

600
580

116

12-19

3,800

117

0.8-1.9
27
71

380
5,400
14,000

117
118
118

Rcfcrt11ce

59•The RBE value used in this report for"' particles is 10, but l\farinelliH suggested that therange of RBE values in this case may be between 4-10.

408.......200
100-1,500

TABLE XLI.

RA:sGE OF NUMBERS OF INSTALI.ATIO:SS AND OCCUPATIONALLY EXPOSEDPERSONS PER 1,000 OF THE POPUL.-\TION
Numbtr of

Number of workers
directly engaged inradiation UJork

installatlon.s
Ptr 1,0CO
of kJtal(tier l ,000 of totaJ
population)

population

Medical:Diagnosis ......... , ......... ,, .... .
Therapy ..........•............. , .•Dental., ............................ .
Veterinary ..•........................
Industrial. ....•.•.............•......
Research and educational ......•....••.
Atomic energy .......••...............

TABLE XLII.

Co1rlribution
kJ Iii< annual
teneticallysigni}kan: dose

0.1-0.7}
0.02-0.1
0.1-0.80.004-0.03
0.003-0.02
0.01-0.03(mrem)

0.3-0.5""'0.90.1-0.3

0.05-0.06""'0.020.1-0.3

0.1-0.2

MEAN ANNUAL DOSES (IN MREM) OF EXTERNAL X- ANDY-RADIATION TO VARIOUS
GROUPS OF OCCUPATIONALLY EXPOSED PERSONS

Uniltd Ki111dom'I
Type of work

ArgenJina•

Canada a(1959-1960)(1959)

Medical:Diagnosis •...... }Therapy ........
Dental •.•••..•...
Veterinary ..••••..
Industrial. •.•.....
Research andeducational .••••
Atomic energy .••••

300-1,400b

70

430

(1960)

Male

Female{50-380
2,000
170
400
110
(1,900)d

440
1,900

500
1,600

1,100•

380

40

27

(1960)

150-225•640

400-1,000b

180}

100-SOOb(1959)NOTVJay"

N elherlandJD{

420•The lower figure concerns private practitioners: the higher, hospitals.
b The range of observed values is given.

• Both X-ray and gamma-radiography.
d The dose within brackets concerns gamma-radiography only.

TABLE XLIII. RESULTS FROM MONITORING RADIATION WORKERS AT THE OAK R.mGE N..\TIO:SAL LAlloRATORY, USA, THE
ESTAllUSHYE...,.TS OF THE UNITED KINGDOM ATOMIC ENERGY AUTHORITY, ARGENTINA, CANADA AND THE UAR(Penetrating radiation)
Oak Ridge NaJional
Lab01atorya(1959)

Artenlina"(1959-1960)

UAR"

CaP1ada"(191$1)(1959)(1959)

person.s

Peru111/J<TS011$

Per cent

No. ofpersoKS

Per "1ll

No. ofNo. of
Person.s Per ""' persoKS Per <enJ

4,695

100

16,374

100

579

100

423

100

600

100

1,492•

9.1

12.4

9

2

4

1

4.5

6°

No.of

Total wearing dose mders or films............

United Kintdom Atomic
Energy Authority"
No.of

Annual dose (rem)> ! ...................................
> 2 ••••••.••••....•.••...•....•.••••••

441

9.4

179

3.8

> 3 •••........•.............•..•....••>4 .•.•...........•............•.•..•.
>5 .................•...•......•...••.

74
35
10

1.6
0.75
0.21

> 6 ••.....................•....•....••

8
2

0.15
0.04

0

0.02
0

> 7 .•.....••...........•..............
>8 ...•..•..............•.............
>9 .••.....•..........................

•Annual dose > 1.5 rem.
l"'\,b Three individuals received annual doses of 17.2, 10.3 and10.7 rem.

2.6
0.81
0.26

417
133
43
22

0.13

6
3
3b

0.04
0.02
0.02

•In range 2.0-4.9 rem.

409

2.0
0.6

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94. Bond, A. F., M. G. Del Duca, A. D. Babinsky.
Methods of predicting radiation dosage in spaceflight. Preprint No. 60-21. Presented at the 6th
Nat. Ann. l\iieeting, Amer. Astronautical Soc.,
18-21 January 1960, New York City. American
Astronautical Society, New York (1960).

110. Biagini, C., M. Barilla, A. Montanara, Survey ofradiation therapy of non-malignant conditions inRome. Preliminary data, 1960. Data submitted to
the ICRP/ICRU Joint Study Group, v. ref. 58.
111. Giaccai, L., Data on radiological data from Lebanon, 1960. Data submitted to the ICRP/ICRU
Joint Study Group . v. ref. 58.
112. Commonwealth X-ray and Radium Laboratory,
Australia, Annual report for the year ended 30th
June 1960.
113. Sowby, D., Personal communication on the amountof radioactive isotopes administered for medical
purposes.
114. Stanford Research Institute, Radioisotopes inmedicine. Research for Industry 12: 6-7 ( 1960) ;v.e. U.S. Dept. of Health, Education and Welfare,Radiological Health Data, Vol. 1, No. S (August1960).
115. Johns, H. E., J. C. Wilson, Gonadal dose frommass miniature chest X-rays. Can. Med. Assn. J.
78: 571-575 (1958).
116. Reynolds, J. C., P. F. Gustafson, L. D. 1farinelli,
Retention and elimination of radium isotopes produced by the decay of thorium parents within thebody-calculations and comparison with experimental findings. Argonne National Laboratory report ANL-5689 ( 1957).
117. Rundo, J., A. H. Ward. P. G. Jensen, Measurement of thoron in the breath. Physics in Med. andBiol. 3: 101-110 (1958) .
118. Rundo, J., The determination of the distributionof internally deposited thorium by means of studies
with a realistic phantom. Acta Radio!. 47: 65-78(1957).
119. Physikalisch-technische Pruefanstalt fuer Radiologie und Elektromedizin, Radiological data; v.e.
United Nations document A/ AC.82/G/R.102

95. United States Naval School of Aviation Medicine,A note on the RBE of proton radiation in space.
Research report, Project MR005. 13-1002, Subtask 1, Report No. 18 (January 1961).
96. United States Naval School of Aviation Medicine,
Dosimetry of proton radiation in space. Research
report, Project MR005. 13-1002, Subtask 1, Report
No. 19 (June 1961).
97. Seelentag, 'vV., S. Pek, Die genetische Belastung
der Bevolkerung bei Durchleuchtungen in Schuhgeschaften. Strahlentherapie 110: 116-132 (1959).
98. Seelentag, W., E. Klotz, Die Strahlenbelastung derBevolkerung durch Leuchtzifferblatter von Uhren.
Strahlentherapie 110: 606-621 ( 1959).
99. Eikodd, A., A. Reistad, A. Storruste, et al., Radioactivity of luminous watches and estimation ofdose to the wrist and the gonads. Phys. Med. Biol.
6: 24-31 ( 1961).
100. Lindell, B., P. A. Wiberg, The radioactivity ofwatches. Personal communication.
101. Joyet, G., La dose-gonades des cagrans lumineux.
IXth Int. Cong. Rad. 2: 1291 only (abstract),
1961. Georg Thieme Verlag, Stuttgart ( 1961).
102. Braestrup, C. B., H. 0. Wyckoff, Radiation Protection, pp. 173-174. Charles C. Thomas, Springfield, Ill. ( 1958).
103. Braestrup, C. B., R. T. Mooney, X-ray emission
from television sets. Science 130 : 1071-1074( 1959).
104. Bumazyan, A. I., I. D. Kamyshenko, Yu. G. Nefedov, The problem of sanitation and hygiene measures in the atomic icebreaker "Lenin". Med. Radio!.

413
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ANNEX H

COMPARISON OF DOSES AND ESTIMATES OF RISKCONTENTSParagraphs

f. INTRODUCTION • • • • • • • • • • • • • • • • • • • • • . • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • •1-2

II. PROBLEMS ASSOCIATED WITH RISK ESTIMATION • • • • • • • • • • • • • • • • • • • • • • • • • • • • •Effects and relevant tissues . . . . . . . • • . . . . . . . . . . . . . . . • . . . . . . . . • . . . • . . . . . . . • •Dose-effect relationship . . . . . . . • . • . . . . . . . • • • . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Basis of risk comparison . . . . . • • . . . . . . • . • . . . • • . . . . • • . . . . . . . . . • . . . . . . . • . • • •Weighting factors for population . . . . . . • • . • • . • . . . . . . . . . . . . . . . . . . . . . . . . . . . .

3-24
5
6-14
15-21
22-24

III. PROBLEMS ASSOCIATED WITH THE EST!MATIO:s' OF THE DOSE RECEIYED BY BODY
The problem of RBE (relative biological effectiveness) . . . . . . . • . • . . . . . . . . . .
Effect of transmutation of CH • • . . . . . . . . . . • • . . . . . • . . . . . • . . . . . . . . . . . . . . . . . .

25-36
34
35-36

IV. CoMPARISON OF DOSES • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • •Doses from natural radiation • . . . . . . . . . • . . • . . • . . • . . . . . . . . . . • . . . . . . . . . . . • . .
Doses from medical exposure . • . . . . . . . . . . . . . . • . . . . . . . • . . . . . . . • • • . . . • . . . • . •Doses from fall-out . . . . . . . . . . . . • . . . . . . . • . . . . . . . . • . • . . . . . . . . . . . . . . . . • . . . .

37-43
38
39
4-0-43

V. COMPARATIVE GENETIC AND SOMATIC RISK ESTIMATES • • • • • • • • • • • • • • • • • • • • • • • •Summary • . . . . . . . . . •• . . ... . . •• •. .•. . .• • .• ••. . . . .. . .. .. . . . . . . .. . . . . . . .. ..

44-49
50

TISSUES •••••••••••••••••••••••••••.••••••••••••••••••••••••••••• , • • • • • • •TABLESREFERENCES

I. Introduction

1. Much information has been reported since 1958 on
dose levels and effects of radiation in animals and man
but there are still many gaps in knowledge. It is notpossible to determine with desired precision the effecton the world population of the doses from natural radiation (annex E), medical and occupational expos?re(annex G) or from fall-out from weapon testmg(annex F, part III).
2. Accurate assessment of the late effects of low dose
exposure requires a full knowledge of the relevant
effects, of the tissue or tissues involved and of the doseresponse relationships. At the present time there is a lackof information with regard to each of these factors andalso, of course, uncertainty regarding future levels ofradiation. In the present annex various of the problems
will be reviewed. The first part of the annex deals withthe general problems involved in making risk estimates,and presents a method for comparing the risks fromvarious sources of exposure. The second part discusses
the problems associated with the assessment of biologically significant doses, estimates of which are presented
in the third part. Finally, genetic and somatic risks fromthe various sources of man's exposure are compared.
11. Problems associated with risk estimation

3. Knowledge of the late effects of radiation comesfrom clinical and experimental data at much higher
levels of dose (and often of dose-rate) than those of414

natural radiation, fall-out and many types of medical
exposure. 1 ""' The types of effect, or their dose-response
relationships, will not necessarily be the same at low as
at high dose levels.
4. The estimation of risk at low dose levels requires
answers to three basic problems :(a) The effects to be considered ;( b) The critical tissue for each of these effects;( c) The function of dose, dose-rate and dose distribution to be taken as the relevant exposure parameterfor each of these effects.
EFFECTS AND RELEVANT TISSUES

5. Both genetic and somatic effects have to be considered. The genetic effect is the production of n:utations
and the critical organs are the gonads. Possible latesomatic effects which have given rise to most concern are
the induction of leukaemia, malignant bone tumours, andthe reduction of life expectancy. The significant tissue
for the induction of leukaemia is generally considered
to be the active bone marrow. With bone tumours, earlypre-malignant changes have been reported 5 in the connective tissue lining endosteal surfaces or trabeculae
and in the loose connective tissue in bone marrow spaces
between trabeculae: these are therefore probably thetissues of importance. There is as yet no information
concerning tissues important in the reduction of life
expectan<.y. Therefore no estimates will be made of therisk associated with this effect. Although limited exposure data are aYailable for other organs such as
thyroid, gastro-intestinal tract and lung. these tissues willnot be used for risk estimates because of uncertainties
in dose-effect and dosimetric parameters. More iniormation. including the specification of the relevant effect,would be required for any careful assessment of risk tofoetal tissue.

30

0

~
~

~

DOSE-EFFECT RELATIONSHIP

6. There are two considerations concerning the exposure parameter to be used : (a) what is theoreticallyjustifiable? ( b) what is practicable? For genetic effects
experimental data justify the use of a linear dose relationship at low doses and dose-rates. No such generalization can be made about late somatic effects of radiation.
In radiation carcinogenesis at high dose levels many different mechanisms may play a part including various
kinds of interactions between damaged cells and tissues,
effects of vascular and hormonal changes, as well as specific radiation-induced changes in cells. Also there may
be several different ways in which the same macroscopic
effect can be brought about, so that the equivalence ofmacroscopic effect does not imply equivalence of primarymechanism. Carcinogenicity, at these high levels of radiation dose, could only be described by a very complex
function of dose and other e,'\:posure factors.

20

10
CC'""..rt3ro-wn
10

:z

10

Yet.rsFigure 1. Time incidence curve of leukaemia

radiation in a time which is short compared with themean life span of an individual (curve 1), a linear doseeffect relationship implies that the area under the curve,i.e., the total incidence of injury, is proportional to dose.
If with a reduction in dose there is an increase in thelength of the shortest latent period or a change in the
shape of the time-incidence curve (curve 2) so that theprobability of induction of the effect has not dropped tozero at the end of life, any statement about the doseeffect relationship-linear or otherwise-cannot be madewithout consideration of life expectancy.

7. One would expect, however, that the mechanismsof production of any late effects are simpler at lower
doses because interactions between damaged cells, as wellas general systemic effects of radiation, will play asmaller part. Although the possible importance of subtle
generalized changes in tissue cannot be ruled out, it islikely that, if serious late effects can arise at these lowdose levels, they will result predominantly from specificchanges induced in individual cells.

1

2

T!1!loFig:ire 2a (see para. 10)

8. If it is assumed that even the smallest dose entails
a finite probability of effect, can any statement be madeabout the shape of the dose-response curve near theorigin? For certain radiobiological effects which have anon-linear relationship at high dose levels (e.g. certain
types of chromosomal change induced by radiation), it
is probable that the slope of the dose-effect curve near
the origin is linear. However, the range of effective
linearity may be very limited. Formally, if the dose
function >vhich determines the incidence of the effectincludes a linear dose term, however small, it is this term
which will be controlling at the lowest doses. The assumption of a linear dose-effect relationship normally
implies that mean accumulated dose, i.e., cell-rad, within
the tissue of interest can be taken as the significant doseparameter for calculation of incidence of late effects.
Protraction of e,'\:posure and non-uniformity of dose
within the tissue of interest can be ignored. However,
if a non-linear dose relationship holds, a mean dosecannot be used to estimate the incidence of effects. Alsowith a non-linear dose-effect relationship. the dose-rate
might be an important factor.

11. Similarly if, whatever the dose, the effect has afinite probability to the end of life (figure 2b), any
simple statement concerning linear relationship can only
be made if the shortest latent period does not changewith the dose, and if the probability of injury at any
later time is proportional to the dose.
Do_"";..-1--~ ~lllp
oaly l>alda If~=.~1 2:::;

milor Z

Dase

Time

Ll!espu

12. In the present state of knowledge, mean tissue
dose is the only parameter that can be used to estimate
risks in populations. If the dose-effect relationship is
non-linear the use of a per capita mean tissue dose will
be inapplicable, and individual dose and dose distribution would need to be considered: this would be a much.
more difficult task.

9. The assessment of risk of specific late somaticeffects on the basis of a given dose-effect relationshipmust take into account the way in which injury is distributed over time. In the time-incidence curve the important parameters will be the shortest latent period L
before any effect is manifest and the subsequent shapeof the curve. For e.xample, figure 1 shows the time-incidence curve deduced from data on the incidence of leukaemia after radiation therapy for ankylosing spondylitis.6

13. So far as an absolute assessment of risk is concerned, that is, an estimate of the actual number of effects
from a given radiation e,'\:posure, a clear distinction must
be made between the genetic and somatic problems. Forradiation-induced genetic changes there is good experimental evidence that the dose-effect relationship islinear; the difficulty of making absolute assessments for

10. If the probability of the induction of a specific lateeffect (figure 2a) has fallen to zero after a given dose of415

a human population lies in lack of knowledge of the slopeof the dose-effect curve under various conditions, anduncertainty about the way in which an increased mutation rate will be expressed in a human population.

than this on the rate of appearance of somatic effects
would require a knowledge of the time-incidence relationships at the relevant levels of dose and dose-rate.
21. In the present annex, dose commitments will bebased on world-wide averages of dose from the various
sources and, for the comparative risk estimation, theratio of the respective dose commitments will be used.

14. For somatic effects there are no experimental data
relevant to the form of the dose-effect curve at low doses
and, even at high doses, as indicated in anne..x D, there
are very few reliable dose-response data for late effects.
Thus, although the assumption of a linear dose-effectrelationship at low doses may be made, there is no meansat present of arriving at the actual value of the slope.
However, even if adequate dose-response data wereavailable at high doses, any extrapolation to low doses
would involve large assumptions on: (a) the dose-effectrelationship; ( b) the latent period for manifestation of
the effects; and ( c) dose-rate dependence. For thesereasons it is felt that the use of mean dose as the risk
parameter can be used only to estimate the comparativerisk from various sources, and not absolute risk.

VlEIGIITING FACTORS FOR POPULATION

15. In using the mean dose in calculations of comparative risk of natural radiation, fall-out and medical
exposure, it is necessary to take into account that: (a)the yearly dose from natural radiation is constant; ( b)the yearly dose from medical exposure is varying; and(c) the yearly dose from fall-out not only varies but theradiation exposure continues long after the event.

22. When considering the genetic effect of uniform
irradiation of the population, each increment of time,
and therefore of dose to the gonads, contributes an equal
number of mutations to the population so long as the age
distribution of the population remains the same. However, when only certain individuals in a population are
irradiated, as in medical radiology, the gonad doses will
have varying importance depending on the age of theindividual, as the probable number of children to be bornto the individual must be taken into account. The term
"genetically significant dose" is defined (G. 9-12) as thatdose which. if received by every member of the population, would be expected to produce the same genetic
injury to the population as do the actual doses received
by the various individuals. This population dose is obtained by weighting the individual gonad doses by a relative child e..xpectancy factor so as to make possible
comparisons with doses from sources to which populations are uniformly exposed.s-12

16. It is suggested that the basis of comparison shouldbe the number of injuries resulting from procedures
carried out during any given period of practice. For
natural radiation and medical exposure the period ofpractice and the period of radiation exposure will coincide. For environmental contamination the period ofradiation exposure will greatly exceed the period ofpractice.

23. It is very probably that there is a considerable age
dependence in the development of late somatic effectsof radiation, but there is at present no information onwhich to base appropriate 'veighting factors. In thepresent calculations it has been assumed that the averagelatent period, for the somatic effects considered, is shortcompared with the normal life span, and has not therefore been taken into account.

17. This method of treatment permits comparison of
total numbers of injuries occurring over all time. To
obtain information on the yearly incidence in a population, or on the risk to a given individual . other methodsof treatment would be required which, in the present
state of knowledge, would involve so many assumptions
as to be of little value.

24. The growth of world population also has to beconsidered. The expression "cell-rad" implies the product of two terms, one related to numbers of cells, andthe other to dose. In the case of the risk comparison
between medical exposure and exposure from naturalradiation the "cell" term will be identical for each dose
commitment, and the comparison can be based solely on
the ratio of the doses. However, the dose commitment
from nuclear testing will be delivered during a period oftime in which the size of population (and thus the number of cells) will increase. Ideally, this increase would
have to be taken into account in the calculation of thedose commitment. In view of the uncertainty of the estimates of future world population, this factor has notbeen taken into account in the comparison of risks.

BASIS OF RISK COMPARISON

18. The term "dose commitment'' is used for the radiation dose resulting from procedures carried out during
a given period of practice. For natural background andmedical exposure the dose commitment will be the dose
actually received during the period of practice. For environmental contamination the dose commitment will be
the dose received during the selected period together
with that received subsequently as a result of event5
during the period, i.e., an integration of dose to infinite
time.

CTI. Problems associated with the estimation of thedose received by body tissues

19. The term "dose commitment" is applied not toindividuals but to populations only and represents themean tissue dose (i.e., the dose to the total pool of specified cells) within the population.

25. As has been explained above, comparative risk
assessments will be made for genetic effects, inductionof leukaemia and induction of bone tumours. Radiation
doses from the various sources must therefore be calculated for the relevant critical tissues.

20. Although the dose commitment from environmental radiation due to a given period of practice involves an integration to infinite time, the major fractionof the dose, apart from the contribution from ea. will
have been deliYered within fifty years. This implies, ofcourse, that a considerable fraction of whatever somaticeffects may arise from a given test will have appeared
within about fifty years. Any more detailed statement

26. The estimation of the radiation doses to any
tissue must include contributions from e..xternal andinternal sources. The conversion of exposure dose
measured outside the bodv to absorbed dose in the relevant tissues can be made.by calculation, but often only416

with major assumptions. Alternatively. measurements
may be made on tissue-equivalent "phantoms", but thesewill also have limitations since phantoms can only approximately simulate man.
27. In determining the contribution from internallydeposited radio-nuclides it is necessary to recognize thatthe mean dose to the relevant tissue will not necessarilybe the same as the mean dose to the organ containing thattissue, if dose distribution throughout the organ is not
uniform.
28. This problem does not arise with the gonads since
it may normally be assumed that the distribution ofradio-nuclides is uniform throughout the gonads and thedose in all parts of the gonads, including the germinal
cells, will be the same.
29. The dose to bone from bone-seeking radionuclides, such as Sr90 , may not be uniform. There is the
additional complication, in estimating dose to bone surfaces, in that the lack of electron equilibrium near thesurface has to be taken into account. \Vith single injections of bone-seeking nuclides the problems of dose
estimation may be very severe since there will be "hotspots", i.e., high local concentrations of radio-activity,
in areas of bone growth and remodelling. However, with
continuous intake of radio-nuclides. non-uniformity will
be much less, particularly with beta-emission of relatively
long range (e.g. Sr90 + yno).
30. For continuous uniform ingestion of radio-active
materials during steady bone growth, as in young children, the distribution of activity in a given bone isrelatively even. In the adult there will be greater nonuniformity, but there is much still to be learned about
the effect of age. The effect of such variations on thedose to bone and bone marrow has been discussed. 7 Thereis evidence from recent studies of a substantial variation
between different bones, but presumably this will becomeless marked with prolonged ingestion.
31. Another factor affecting the calculation of bonedose from internally deposited radio-nuclides in theadult is the degree of mineralization of bone, which also
may change considerably with age. This again is a subject on which much further information is required.
32. In the present calculations the major problem, in
determining the internal dose to the bone surface andbone marrow, is the contribution from Sr90 derived fromfall-out. The~e is some contribution in natural radiationfrom the a-emitters, but this dose represents only about
10 per cent of the total from natural sources.
33. Assuming no gross non-uniformity in dose distribution in bone, the Sr90 contribution to the mean doseat the surface of bone will be approximately one half ofthe mean Sr9° skeletal dose derived in annex F, part III.
With regard to the bone marrow dose from Sr90 in thebone, it is shown in annex F, part III, that the mean bonemarrow dose withir. trabeculae will be approximately
one-quarter of the mean skeletal dose. These factors havebeen used in the present calculations.

well as for each effect under consideration. However,values of RBE that have been obtained experimentally
apply only to the conditions under which the measurement was made. At the present time there is no information on the RBE values appropriate to the production of
specific late effects in man, and without this information
there is no alternative but to use the values adopted by
ICRP. The values of RBE quoted by the ICRP, reproduced in annex A, have been chosen as those which areunlikely to be e.."<ceeded under conditions of occupational
e.xposure.
EFFECT OF TRANSMUTATIO~ OF 0"'

35. One further outstanding problem is that associatedwith the interpretation of the effects of the incorporationof cu into body tissue. Carbon atoms make up about
37 per cent of the deoxyribonucleic acid (DNA) which
is an important constituent of chromosomes and is associated with the genes. Hence if a C14 atom becomes incorporated into a DNA molecule and later distintegrates,
the DNA molecule may be damaged not only by theionizing beta particle emitted and the recoiling nucleus,
but also by the transmutation of the (li atom to Nu, a
process which might also give rise to a gene mutation(anne."< B ).
36. Estimates of the magnitude of the transmutation
effect vary from one tenth to many times the effect due
to ionization 1 0-13 and more e..xperimental data areneeded before a reliable assessment of this effect canbe made.
IY. Comparison of doses

37. With the reservations outlined in the previous
sections and in the relevant sections of the other annexes,
the doses to present and future generations are summarized in the following paragraphs.
DOSES FRO~! NATURAL RADL.\TION

38. Natural radiation includes cosmic rays, radiations
from radio-active nuclides in the earth and in building
materials, and radiations from internal radio-activity.
The yearly population doses to gonads and bone marroware given in table I. These represent only average valuesof natural radiation; they do not reflect the large variations throughout the world.
DOSES FROM .MEDICAL EXPOSU1lE

39. Table I also gives representative values of theyearly dose due to medical e.xposure. During the next
decade the availability of X-ray facilities will be muchgreater throughout the world, and information will be
required regarding the doses to the larger numbers ofpeople being e.xamined or treated. This e.xpansion cannot
be predicted, nor can the possible development of moreconservative procedures. For the purpose of this annex,
the doses to the population will be assumed to be constant.
Although much smaller, the doses from occupational
exposure and miscellaneous sources of radiation are
included in table I.

THE PROBLnr OF RBE (RELATIVE BIOLOGICALEFFECTIVENESS)

34. As has been shown in anne.xes Band D, the valueof the RBE of ionizing radiations of different characteristics, e.g. neutrons and X-rays, depends on the biological effect considered. 8 • 9 For the assessment of any
given biological effect, it is clear that a precise analysis
requires an RBE for each of the radiation conditions as

DosES FROM FALL-OUT

40. The world average doses (weighted for population distribution) resulting from fall-out do not include
the doses from local fall-out within the first few hundred
miles from megaton surface nuclear e.."<plosions.

417

41. The estimation of the dose from current fall-out
is possible \vith some accuracy on the basis of observed
data. However, \vhen one attempts to predict levels ofactivity on the ground or in foodstuffs due to past andfuture testing, and to derive the ensuing doses, theunknowns make any estimate extremely difficult.

table III for the genetic risk and for the selected somatic
risks (induction of leukaemia or bone tumours). These
dose commitments are compared to the dose commitments from natural radiation and medical and occupational exposure during the same period. For these twolatter sources, the dose commitment for any one year isequal to the dose actually experienced durmg the sameyear.

42. In the case of e>..1:ernal exposure and internal exposure from substances with rapid turnover, the dosecommitment from a given period of practice can becalculated as the dose actually received up to the present
date plus the dose to be expected in the future. For
isotopes, such as Sr90 , ·with slow turnover, the same calculation is more difficult. As has been shown in annex F,part III, the dose-commitment from Sr00 can be derived
from an integral of the environmental contamination
D.., = k

46. It can be seen from table III that, for the period
chosen (i.e., 1954-1961), the comparative genetic risk
from fall-out is about one-tenth of that from natural
sources. The genetic risk from medical e.xposures* is
about one-third of that due to natural sources. Fall-out
contributes to the dose commitment for the induction ofleukaemia and bone tumours between one-quarter andone-sixth of that from natural sources.

J"'c (t) dt

47. If no further testing is carried out, the relative
importance of the dose commitment due to previous tests
will decrease in comparison with the accumulated doses
from natural sources and medical exposure. The figuresin table III indicate that the whole series of tests during
1954-1961 will give a dose commitment corresponding
to about one to one and a half years of exposure fromnatural radiation.

toIf experimental data are available for the period to to t1,
the dose commitment can be writtenD., = k(f'c (t) dt + f''c (t) dt)

r..
t,
where the first integral can be evaluated from the measured values of c(t) and the second integral has to be
derived from a predicted future environmental contamination. It should be realized that the dose actually received during the period to to t 1 is only part of the first
integral (F III, 67).

48. In the event of continued testing at a constantrate of injection, equilibrium conditions would obtainin about 100 years, except for C14 • For this nuclide equilibrium conditions would imply many thousands of yearsof testing. The dose commitment from one year of injection is numerically equal to the yearly dose under equilibrium conditions at the same rate of injection. The
dose commitments per year of testing at the assumed
rate are compared with the dose commitments due to one
year of natural irradiation and medical and occupational
exposure in table III, columns 5-7.

43. The dose-commitments given in table II have been
calculated on the following assumptions with regard to
testing conditions :(a) Testing up to the end of 1960. The dose-commitments can partly be derived from experimental data ( cf.
para. 42). The future doses have been calculated on thebasis of a total atmospheric injection of 6.6 Mc Sr90 and
2.2 X 1028 atoms of C14 •(b) Future testing. As a model to be used for the calculation of the doses from possible future testing, it has
been assumed that the yearly rate would involve the injection of 1 Mc Sr9° and 1028 atoms of C14 into theatmosphere;(c) Testing dttring the period 1954 to 1961 inclusive.
Since the experimental data do not permit an assessmentof the atmospheric injection of Sr90 and C14 during 1961,
it has been assumed for the purpose of the dose estimatesthat the total injection during the period 1954-1961 (8years) was (6.6 + 1) = 7.6 Mc Sr90 and (2.2 + 1) 1028
= 3.2 X 1028 atoms of CH. It is shown in annex F,part I, that this is the most reasonable estimate that
the Committee can at present venture to make.

49. If the dose commitment is derived from an integration of future doses to infinite time, the dose from
C14 will be found to contribute more than 60 per centof the total dose from fall-out. If, however, the integration is only carried out to the year 2000, the contribution
from 0 4 is only about 5 per cent of the dose from fall-out.
SUMMARY

50. The assumption of a linear dose-effect relationship and the use of the mean tissue dose have been used
to estimate the comparative risk of the doses from thevarious sources of radiation to which the population is
exposed, but there are insufficient data to make absoluterisk estimates at the present time.
*See table I, footnote.

V. Comparative genetic and somatic risk estimatesT."1lLE

1. AVERAGE YEARLY DOSE TO THE POPULATION
Geneticallysignifican'
do ..

44. The period of practice for which the dose commitments have been calculated is the period 1954-1961(eight years). It has been assumed that all the weapon
tests were carried out during this period and none previously. This period has been used because it is difficult
to analyse the measurements of fall-out to determine theactual doses likely to be received from any one seriesof nuclear testing, but only the doses arising from thetotal testing so far carried out.

Bonemarr<r.#surfausNatural radio-activity. . . . . .

125

122

130

Med.ical exl?osure•D1agnosttc. . • • . . . . . . . . . .
Therapeutic.............

30

50-1005?

• Based on the values reported in annex G.

418

b""4

(mrem)

Occupational and miscellaneous exposure . . . . . . . . . . . . ,..., 2

45. The dose commitments to all generations due tonuclear weapon testing during this period are given in

Cells linin1

dost(mrem)(1!1rem)?

TABLE II. DosE CO!.!MITMENT no!.! NUCLEAR TESTING

Tests 1954-1961
Fr<>t:tion ofDattcommit·men:

Dos~ c.cmtr:i!·

dost commit·(mrem)''""' rt<>t:htd
byZOOOnum p" ycr;rof ttstini(mrtm)

cu...............

41
70

0.97
0.10

7
22

TOTAL

111

0.42

29

cu...............

128
116

0.94
0.10

37

TOTAL

244

0.54

5i

84
70

0.94
0.10

13
22

154

0.56

35

Comrilr.ition

Orion

Gonads ........................ All sources but cu

Cells lining bone surfaces ......... All sources but cu

Bone marrow ................... All sources but cu

cu ..... .

TOTAL

20

T ADU: III. CoMPARISON OF rusx•(Dose commitment to all generations)

Go-U

Tests 1954-1961

Future ttsts

Dost commitment (mrem)

Dose commitment per :;ear of leslini (mrem)Cells linintbone nufau3

Boumcrroe

1,040

1,000

(1.00)

125(1.00)

400-800(0.4-0.8)

37(0.30)

Go-U

Cdls lining
bmre surfaces

Bon.man=(1.00)Natural sources ....

1,000

(1.00)

Medical andoccupationalb ....

300

(0.30)

Fall-out:
All but C 14 ••••••CH ........•....

4170(0.04)(0.07)

128
116(0.12)(0.11)

84
70(0.08)(0.07)

7
22(0.06)(0.18)

37(0.15)(0.28)

13
22(0.10)(0.18)

Total fall-out •.•...

111(0.11)

244(0.23)

154(0.15)

29(0.23)

57(0.43)

35(0.28)(1.00)?

b See table I, footnote.

•Figures in parentheses indicate contribution relative tonatural sources.

419

130

(1.00)?

20

125
5{}-100(0.4-0.8)

REFERENCES
1. Brues, A. M., Critique of the linear theory of carci-

nogenesis. Science 128:693-699 (1958) ;v.e. United
Nations document A/AC.82/GjL.242.
2. Upton, A. C., The dose-response relation in radiation-induced cancer. Cancer Res. 21: 717-729(1961) ; v.e. United Nations document A/AC.82/
G/L.675.
3. Arley, N., R. Eker, Dose-response relationship inradiation carcinogenesis. Nature 189: 151-152(1961).
4. Burch, P. R. J., Radiation carcinogenesis: A new
hypothesis. Nature 185: 135-142 ( 1960).
5. International Atomic Energy Agency, Radiation
damage in bone. Austria (1960). United Nations
document A/AC.82/G/L.446.
6. Court Brown, W. M., R. Doll, Leukaemia and aplastic anaemia in patients irradiated for ankylosing
spondylitis. Medical Research Council Special
Report Series No. 295 (1957) ; v.e. United Nations
document A/AC.82/G/R.105.

7. B jornerstedt, R., A. Engstrom, "Radioisotopes inthe skeleton: Dosage implications based on microscopic distribution'', pp. 401-422, in Radioisotopes

420

in the Biosphere. R. Caldecott and L. Snyder, eds.,
University of Minnesota ( 1960).
8. Storer, J. B ... P. S. Harris. J. E. Furchner, et al. ,The relative biological effectiveness of various ionizing radiations in mammalian systems. Rad. Res. 6:
188-288 (1957).
9. Neary, G. J., R. J. Munson, R. H. Nole, Chronic
radiation hazards. An experimental study with fastneutrons. Pergamon Press, London ( 1957).
10. Pauling, L., Genetic and somatic effects of carbon-14.
Science 128: 1183-1186 (1958); v.e. United Nations
document A/AC.82/G/L.252.
11. Totter, J. R., M. R. Zelle, H . Hollister, Hazard to
man of carbon-14. Science 128: 1490-1495 (1958);
v.e. United Nations document A/AC.82/GjL.249.
12. Kyann, A. M., B. M. llcaeB, B. B. XBocroBa JI ,lijl.,
31fJq>er.Tlll!HocTD 6noJIOrII1lec:&oro AettcTBH.lI C 14 npn
ero ;iix..uo11:eHim n ~file cTpy:&TYJHir. A.Ka~emrn:
HayK GCCP, MocR.Ba (1%0); v.e. ]!;O:&.pi:eHT OOH
A/AC.82/G/L.423.
13. KyanH, A. :M., BnoJiofIIllec:&aJ1 onacnocn OT IIOD'hImeIDIJI 1tonn;eHTpa~II C14 B peaynmTe B3phIBOB
J!AepHm: 6o~r6. A:&a,n:eMJIJI nay:& CCCP, l\locR.Ba(1960); v.e. ~O:&y:YeHT OOH A/AC.82/GJL.413.

ANNEX I

LIST OF OFFERS TO ASSIST L~ MEASUREMENTS OF SA11'IPLES
1. The Governments of the following Member States informed the Committee
before 10 March 1962 that they had made known to other Governments the e.xtent
to which they are prepared, at the request of other Governments, to receive andanalyse samples in accordance with the programme of work of the Committee, in
response to section IV of General Assembly resolution 1376 (XIV) of 17 November
1959: Argentina, Australia, Belgium, Canaea, Denmark, France, India, Israel, Italy,
Japan, Norway, Sweden, Union of Soviet Socialist Republics, United Kingdom ofGreat Britain and Northern Ireland and United States of America.

2. Similar communications were received from the International Atomic Energy
Agency and the World Health Organization.

421

ANNEX J

LIST OF REPORTS SUBI\ITITED TO THE COMMITTEE
1. This annex lists reports received by the Committee from Governments, specialized agencies, the International Conm1ission on Radiological Protection and theInternational Commission on Radiological Units and Measurements.

2. All those reports are included of which a sufficient number of copies for distribution in the A/AC.82/G/R. and A/AC.82/G/L. document series were received
before 10 March 1962.
3. The first 213 reports received by the Committee are listed in annex I of its
first comprehensive report.**Official Records of the General Assembl;y, Thirteenth Session, S"pplement No. 17(A/3838).

422

Document
No.

Document
No.

C011ntry and title

A/AC.82/G/R.

A/AC.82/G /R.
ARGE~TINA

214

Cozmtry and title

BR.-\ZIL

Descontaminaci6n y potabilizaci6n de !asaguas del Rio de la Plata luego de una
explosion nuclear.

228

Radio-active products in the soil and in
the atmosphere.
CZECHOSLOVAKIA

UNITED STATES

215
216
217

218

219
220
221

Detection of radiation effects on hairroots of the human scalp.
Fission product radio-activity in the air
along the 80th meridian January-June
1957.
The biological effects of atomic radiation.
The effects of radiation on oceanography
and fisheries.

229
230
231

Measurements of radio-active fall-out on
the territory of the Czechoslovak Republic.
The role of deoxiribonucleotides in irradiation sickness.
Damage of the liver cell produced by asmall dose of radiation.
U:mTED STATESCANADA

232

Consanguineous matings as a means ofevaluating the effect of deleterious recessive genes on fertility in humans.

233

DEKMARK

234

Gonad-dose-measurements in Denmark.
Risk of parenthood and risk of subsequent
parenthood. Denmark, 1955 and 1956.
Genetically significant radiation doses
from diagnostic radiology in Denmark.

235
236

Common strontium content of the humanskeleton.
Current strontium-90 level in diet in
United States.
Long-term fall-out, a summary of measurements made through June 195 7 by thegummed-film network of the AEC.
Environ men ta! contamination from weapons tests.
The shorter-term biological hazards of afall-out field.

ARGENTINA

222

Distribuci6n geografica de! calcio y potasio solubles del suelo en la Republica
Argentina.

GERMANY

237

Tables of radiological data.

238

Data on radio-active fall-out, collected 'in
Italy (January-June 1958).
·

239

lVIeasurements of radio-active fall-out andairborne radio-activity in \Varsaw andCracow during the year 1957.

ITALY
UNITED STATES

223

Tabulated results of radio-strontium
analyses.
Strontium-90 in man, II.
l\fanual of standard procedures.
Addendum to above document.

PoL~'iD

224
225
225/
Add.1
225/
Addendum to above document.
Add.2
225/
Corrigendum to above document.
Add.2/
Corr.1225/
Addendum to above document.
Add.3
225/
Addendum to above document.
Add.4
225/
Addendum to above document.
Add.5
225/
Addendum to above document.
Add.6
225/
Addendum to above document.
Add.7
226
Leukemiain Hiroshima City atomic bomb
survivors.

Ur-.1TED STATES

240

A/AC.82/G/L.
UNITED KIXGDO!>I241

The deposition of long-lived fission products from nuclear test explosions.
U~ITED STATES

242
243
244

245

UNITED KINGDOM

227

Some measurements of the radio-activityof the air during 1957.

Radio-active and natural strontium mhuman bone. UK results for 1957.

246
423

Critique of the linear theory of carcinogenesis.
Geochemical scavenging of strontium.
Uptake of waste Sr 90 and Cs137 by soirandvegetation.
Beneficiation of soils contaminated:;\vithstrontium-90: beneficial effects ofjiotassium.
The distribution of radio-activity fromram.

Document
No.

Document
No.

Country and title

A/ AC.82/G/L.

A/AC.82/G/L.
UKITED STATES (continued)

247
248
249

UNITED STATES

268

Radiation dose rate and mutation frequency.
Retention of radio-active bone-seekers.
Hazard to man of carbon-14.

269

270
271

U:t-."ITED KINGDOM

250

A preliminary survey of radiostrontium
and radiocaesium in drinking water in the
United Kingdom.

252
253

254
255

256
257
258
259

260
261

Atmospheric aspects of strontium-90 fallout.
Accidental radiation excursion at the
Y-12 Plant.
The acute radiation syndrome.
Strontium program quarterly summary
report.
BELGIUM

272U}>"ITED STATES251

Country and title

Radiation exposures from nuclear tests at
the Nevada test site.
Genetic and somatic effects of carbon-14.
Radiochemical analyses of air-filter samples collected during 1957.
Cs137 biospheric contamination from nuclear weapons tests.
Determination of tungsten-185, strontium-90, barium-140, and cesium-137 in
fall-out samples.
Entry of radio-active fall-out into thebiosphere and man.
Radiocarbon from nuclear tests.
Analysis of stratospheric strontium-90
measurements.
Nuclear-critical accident at the Los Alamos Scientific Laboratory on December 30, 1958.
Atmospheric radio-activity studies at the
US Naval Research Laboratory.
Gamma radio-activity of people and milk.

Mesures des doses aux gonades re!;ues!ors d'examens radiologiques.
UNITED KINGDOM

273

274

Radio-active and natural strontium inhuman bone-UK results for early 1958.
Radio-active and natural strontium inhuman bone-UK results for mid- andlate 1958.
UNITED STATES

275

276

Quarterly statement on fall-out by the
US Atomic Energy Commission-September 1959.
ILO
The protection of workers against ionisingradiations.
UNITED STATES

277

278

Quarterly statement on fall-out by the
US Atomic Energy Commission, October
1959.
Strontium program quarterly summary
report.
GERMA'-'-"Y

ITALY

262

279

Data on radio-active fall-out. collected in
Italy (July-December 1958).

UNITED STATESFRANCE

263

Quelques donnees recentes sur la conversion roentgen-rad clans l'os et le muscle.

280

Stratospheric carbon-14, carbon dioxide,
and tritium.

281

Contamination of the NRU reactor m
May 1958.

282

Data on environmental radio-activity,
collected in Italy (January-June 1959).

CANADABELGIUM264

Comparative sensitivity to radiation ofseeds from a \vild plant grown on uraniferous and non-uraniferous soils.

ITALY

CANADA265

Levels of strontium-90 in Canadian milk
powder samples up to the end of December 1958.

NORWAY

283

Cesium-137 in milk.

284

The analysis of the strontium-90 levels in
Canadian milk up to 1958.

285

Strontium-90 in milk and human bonein India.

UNITED KI!\GDOM

266

Strontium-90 in human diet in the United
Kingdom, 1958.

267

Therapeutic abortion on account of X-ray
examination during pregnancy.

The recent increase in the C 14 content of
the atmosphere, the biosphere and theocean.

CANADA

DEN:>!ARK

L\"DIA424

Document

Document

No.

No.

Cozmtry and title

A/ AC.82/G/L.

A/AC.82/G/L.
UNITED KINGDO~[

286

SWEDEN (continued)

The deposition of fission products fromdistant nuclear test explosions: results to
mid-1959.

306
307

UNITED STATES

287
287/
Add.1
288
288/
Corr.1
289
290
291

292
293

308

Industrial radio-active waste disposal.
Addendum to above document.

295

296

Dosage implications based on microscopic distribution.
A method for determination of the strontium distribution in human bone.
A method for photographic identificationof microscopical radio-active particles.
NORWAY

309

FAO
Radio-active materials in food and agriculture.
Corrigendum to above document.

310

FRA.~CE311

Wet and dry deposition of fall-out materials at Kjeller.
ARGENTINA

Activite de I' atmosphere due au krypton85.
Radioactivite artificieIIe dans la stratosphere.
Modifications de la radioactivite naturelle
due au carbone-14.
Polution de !'air et irradiation au sol dues
au panache d'un reacteur en fonctionnemen t normal.
Mesure du rayonnement 'Y du corps humain.

312

FaII-out en la Republica Argentina durante 1959.
Estudio de. la contaminaci6n de! Prochilodus platensis (Sabalo) con productos defisi6n.
La precipitaci6n radiactiva atmosferica
en la Republica Argentina en el periodo
Enero 1957-Julio 1958.
UNITED STATES

313

Measurements of the air concentration ofgross fission product radio-activity during
the IGY-July 1957-December 1958.
NEW ZEALAND

314
315

INDIA

294

Country and title

Measurements on the ground depositionof fission products from nuclear test explosions.
Airborne fall-out measurements in India.
Measurements of cesium-137 in Indianand foreign milk.

Environmental contamination.
Notes on measurements of alpha-particle
activity of soils, fertilizers, plants andanimals.
AUSTRALIA

316

Strontium-90 in the Australian environment.
UNITED STATESCANADA

297

317

Automatic linkage of vital records.

318
SWEDEN

298

299
300
301
301/
Add.l

302
303
304

305

Gamma radio-activity of Swedish people
measured during May and June 1959.
Fractionation phenomena in nuclear
weapons debris.
Cs137 in Swedish milk and soil.
Determination of sr~ 0 in dried milk, milk
and soil.
Addendum to above document.

319
320

321

Cs 137 in Swedish milk-results up to June
1959.
The fission products Zr 95 and Nb 95 in
Swedish milk.
Recent fall-out measurements in Sweden.
Gamma radiation from nuclear weapons
fall-out.

322
322/

Radiochemical analyses of air-filter samples collected during 1958.
Effect of soil nutrients on plant uptakeof fall-out.
Symposium on occupational health experience and practices in the uranium industry.
Press release HEW-L6. US Dept. of
Health, Education and \Velfare, regarding radio-activity in milk, dated 20
August/59.
Press release HEW-L44. US Dept. of
Health, Education and \Velfare, regarding radio-activity in milk, dated 3 October/59.
Fall-out from nuclear weapons tests, volume 1.
Addendum to above document.

Add.1

322/
Add.2

425

Addendum to above document.

Document
No.

Document
No.

Country and title

A/AC.82/G/L.

A/AC.82/G/L.

UNITED KrNGDO~

USSR

323

Onpe,n;eJremre sarpmnemdl: 6no~eplil'. npoilfi>TilMII ~ep!IhlX IICIIlllTaHH11: ( c6opHIIK
CTaTe.li).

324

0 llyJICTllIITeJILHOCTII nep1mo.!1 CIICT8:IDil K

342

326

343

Onyxo.m y KpiiCc, B03HIIli.IIIne JIOCJre BHryTpn6promnHBoro BB8,ll,8HlI.lI 3.30THO:&lICJIOfo)
mryTOHR.lI (Pu-239).

0 6no;rorrrlJeCKOM ,n;ettcTBIIII IIOllll3IIpyIDII(Oil:pa,!I,IIaJI.IIII B :Mainrr ,n;osax.

328

0 H8KOTOpm sarr.OHO:MepHOCTJIX B03HIIKBOB8HIIJI OCTeoreHHLIX capKOM, IlH)zyJI.IIpOBaHHlill pa)J.IIOil30TOJiaMll.

329

344

HeKOTOpLie ]\aHHLie o nJIIIJIIIIIII IIOHnsnpyrom;nx Il3JlY"'l8HH.lt Ha Hy&JI8IIB0Bhle B8II(8CTBa
B 3illBOM opraHII3Me.

327

345

346

347

ro ,n;eJieHHJI.
BLIIIa)J.enne CTPOHJI.IIJl-90 na noBepxnocTD
TeppIITOpmr CCCP.

331

3a,!\a'ln 1mcnepn..'ieHTam.Hofi TeXHIIKII JiyqeBLIX B03)J.eficTBH.li II HeE.OTOphle p~o6IIO­.!OrIITI8Cli.lie ,11,anHLie.

332)l;eficTBIIe JIOIIIl3IIpyIOII(efi pa,11,HaJI.llII
6a:&Tepna;n,Hhle BnpycLI.

334

348

Estimate of future Sr 90--deposition.
FINLA?\"D349

Ha

lvleasurements of the amount of radioactive fall-out in Finland.
UNITED STATES

350

Radioactivite de !'air et des precipitations
au niveau du sol dans la region parisienne.
Etude autoradiographique du metabolisme du 131 iode chez le rat.

Natural aerosols and nuclear debris studies. Progress Report II.
SWEDEN351

The transfer of strontiurn-90 from motherto fetus in mice.

352

Press release HEW-1\146, dated 4 February 1960.

UNITED STATES

335

An investigation of the late clinical findings following thorotrast (thorium dioxide) administration.
GER31A1'i"YFRANCE333

Physical aspects of the radio-active fallout over Scandinavia, especially during
the period October 1958-0ctober 1959.
The increase of ')'-radiation from theground in Sweden (1950-1959) caused by
fall-out from nuclear weapon tests.
A method for the automatic recording ofionizing radiation.
The radio-active fall-out in Sweden 19571958.
UNITED STATES

0 ne.ttporyMopa;n,nott pery.lIJIIJ;II11 E.18T01IllO-

330

Radio-strontium and radio-caesium indrinking water in the United Kingdom.
SWEDEN

CJia6hrn paAH~OBHIDl Bos,n;e.licTBmrn.

325

CounJry and title

UNITED STATES

Health and Safety Laboratory strontium program quarterly summary report
HASL-77, dated 1January1960.

SWITZERLANDNORWAY336

353

Radio-active fall-out in Norway, 1959.
GER31ANY

337

Sonderaussch uss Radioakti vita t-Radioakti ve Partikel.

UNITED KINGDOM

354

u NlTED STATES
338
339
340

Bericht der eidgenossischen Kommission
zur Uberwachung der Radioaktivitat zuhanden des Bundesrates.

Radio-activity of surface waters of theUnited States.
Press release HEW-:rvl9. US Department
of Health, Education and \Velfare, dated
December 31. 1959.
Quarterly statement on fall-out, by the
US Atomic Energy Commission.

354/
Add.1
355
356

Strontium-90 in milk and agricultural
materials in the United Kingdom. 19581959.
Addendum to above document.
\VHO
Methods of radio-chemical analysis.
Effect of radiation on human heredity:
investigations of areas of high naturalradiation.

FRA?\CE

341

CANADA

Rapport sur le probleme des doses aux
gonades resultant de !'utilisation medicale des radiations ionisantes en France.

35i

426

Gonadal exposure dose to adults in diagnostic radiography.

Document
Z.to.

Document
Country and title

No.

A/AC.82/G/L.

A/ AC.82/G/L.
U:'llITED KIXGDO~! (continued)

UNITED STATES

358
358/
Add.1
359
360

361

The biological effects of atomic radiation.
(Summary reports 1960.)
Addend um to above document.

375

376

377

Evolution de la teneur du lait et desvegetaux en radioelements artificiels clans!'est de la France (periode du 1er janvier
1958 au ler octobre 1959).

378

Strontium-90 in human bone m theUnited Kingdom (1956-1958).

365

379
380

Leukemia in Hiroshima atomic bomb
survivors.

367
368

The genetic background to the reactionsof various mouse strains to X-rays.
Distribution of S 35 in mice after injectionof S 35-cysteamine.
Environmental radio-activity at Riso,
April 1, 1957-March 31, 1958.
Environmental radio-activity at Ris6,
April 1, 1958-March 31, 1959.
Environmental radio-activity at Riso,
Report No. 14, 1959.
ITALY

369

Data on environmental radio-activity,
collected in Italy (July-December 1959).
lNDL-\.

370

Evaluation of future levels of radio-active
fall-out.

371

On the transportation and deposition of
fall-out materials.
Fall-out over Norway from high-yield
nuclear explosions.

NORWAY372

BELGimf

373

Programme "Evolution du Sr 90 clans Jes
sols et les vegetaux".
U!'l"ITED KlNGDO:\l374

Radio-active contamination in the upper
atmosphere.
On the radio-activity and particle analysis
of airborne dust in the troposphere.
Corrigendum to the above document.

380/
Corr.1
Behavior of radio-active fall-out and air381
masses around Japan.
The residence time in the atmosphere of382
the debris from atomic test explosions.
Radio-activity of airborne dusts and383
atmospheric pressure patterns.
384
Sr 90 deposition and meteorological factors.
Depositionof radio-active dust and385
atmospheric conditions.
386
Radio-active fall-out in Japan and its
bearings on meteorological conditions.
Strontium-90 in Western North Pacific387
surface waters.
Cesium-137 and strontium-90 in fall-out
388
deposits.
Local changes in Sr 90 deposition in the389
soil as observed in Hokkaido Island,
Japan.
Neptunium-239 content in the radio390
active rain water collected in Japan during the period 1954-1958.
Recent variation in the atmospheric391
radio-carbon and the problem of transferof radio-carbon into hydrosphere.
Research on radio-activity in stock rain
392
water of lighthouses in Japan.
Radio-active contamination of milk and393
milk products in Japan.
Radio-active contamination of marine
394
products in Japan.

DE!><"?.IARK

366

Radio-active and natural strontium inhuman bone. UK results for 1959. Part l.
Bibliography of papers published in the
United Kingdom from January 1959 to
May 1960 on radio-biological and allied
subjects-MRC.60/735.
JAPAN

SWEDEN364

Fall-out program quarterly summary
report (March 1, 1960 through June 1,1960).
UNITED KINGDOMFRAN"CE

UNITED STATES

363

The radio-activity of the atmosphere nearground level due to distant nuclear test
explosions.
UNITED STATES

Critical analysis of measurements of thegross fission product activity in the air at
ground level.
Health and Safety Laboratory fall-out
program quarterly summary report.

UNITED KINGDOM

362

Country and title

Training in radiological health and safety.
427

Docuiunl
No.

Docuiunt
No.

Cozmtry and title

A/AC.82/G/L.

A/AC.82/G /L.
395
396
397

398
399

400
401

402

403

404

405

406

407
408

409

410

411

412

413
414
415

Ccr.mlry and title

JAPAN (continued)
The rapid radio-chemical determinationof caesium-137.
The concentration of cesium-137 in human tissues and organs.
:\fo1surements of radiation doses due tobackground gamma rays by plastic scintillators.
Cytological effect of hot rain.
Effects of radiations on mitoses studied
by Tradescantia test in vit'O. I. X-ray
irradiations by small doses.
Statistical observations on leukemias inHiroshima during the past fourteen years(1946-1959).
Optimum mutation rate and degree ofdominance as determined by the principleof minimum genetic load.
Relative applicability of the classical andthe balance hypotheses to man, especiallywith respect to quantitative characters.
Human genetic study in Japan.

416

USSR (continued)
reHBTIPieCI\aJI pa)l;IIOlJYBCTBilTCJThHOCTh R.1eTOK pa<iHhlX nnµ;on MJe1wmrraroIIJ,HX.

417

84>qie&r Ma.rrm ](03 pa;1,nau1m na xpoMoCOMHhle rrepeCTpOttim nprr 06..'IYlJCHill:I R-1eTOK B KYJhTypax SM6puo11aJlhHErX n;:anettlJBJIOBeRa.

418

BJirr.mme reHOTIIIla opra!Ill3Ma Ha 'IJBCTI1n'!1l.11>11ocTD H,11;epHoro a1IIIapaTa n. :~rn.lh!M µ;oaaM 11011IIanpyrom;ett pa.n;nan.nu.

419

Po,1h nac.rre,n;cTBeHHhIX oco6e11HocTett n pa,lJ.l!OlJYBCTBIITe:IhIIOCTII ll>llBOTHhIX.

420

421

0.6 i:lKClleprrneHTai1hIJOfi o6paTIDIOCTII .ll,ll,epHhlX lIOBpeir•,n;eHIIfi B o6.:rY'leHHh!X R.Wnrax:MJeIWJIIITaIOIIJ,IIX.
CpanmrreJJuIIoe II3ytJe11IIe 9i(l<f>e1mrnnocm
0AII0Itparnoro II cfipaKIJ,IIOHIIpOBaHHOfO
peaTreaoncr.oro o6.JY11eHirn: ceMerrnmwn
Mblllill.

USSR(}ma.11emme nocJe.n;cTBWI nopan.emrli, Bhl3Bammx B03.n;eficTBIIeM 110Hn311pyrom;efi pa.n;IIarr,nrr.

422

CpanH11Te.11IiHaJIpa,ti;HOlJYBCTBIITeJI1>HOCTh
JllllIHillWB o6e3h.HH M acaca 11mlatta n Mhlmefi rrpu 06JIYlleHIIIl peHTreHOBhlMU ,;ry-423

8i(l<fie1m1BHOCTh 6nOJOrIIl!8CIWfO ,n.ettCTBllJI
C 14 npn ero BE..ilIO''lCBITII B mUBhle CTpYJ>TYPLI •II;moremmrlleCRa.JI paiJ.IIOllfBCTBIITe.'lhHOCTb
no.'!OBhIX K.1eTOK o6e3J:i.!1If u :MLimeii Ha ypOBne Maru:x II ,n;pyrnx .U.03.

424

BJnmme noHII3IIpyrom;nx 113.IY'leHlifi Ha
IllIO,ll,ODIITOCTh ea.MOR neKOTOphlX DII)J;OB rp1,r3J'"HOB.
reHeTIIlJeC:&aJI OJiaCIIOCTh MaJILIX )J;03 pa,!l;llaD,1111 )l;JIJI treJIOBerra II nx acplfle.&T na
nacJe)l;CTileHHOCTL o6e3hml II rphl3J'"HOB.

425

KoHTpOJIIIponanue ecrecTBeHIIoro 1!JraIJ,llonrroro rrpon.ecca.
B.JIImIIIe Mam.u: p;o3 IIOHII3IIpyrom;eii pa)l;IIaIJ,llll Ha lJaCTOTY B03Hll&HOBemrn: cn.emreHHhlX c rroJIOM pen.eccrrnHhlX JieTaJIDHiiIX MY~ii y .n.pooocprrm.
Pa.n;nolJj'BcTBrrre.a1>HocTI> pa3n1>1x cra.n;rrfi
cnep:irnToreneaa y Drosophila melanogaster.

426
427

[.428

3am;IITIIIIB s<pqieKT n;ucrea:mrna (fi-~ep1.amoaTIIJa:mma) na xpoMoco:Mnhle nepeCTpofi1m B TRaRSIX o6e3hml II MbIIIIefi.

429

reHBTH 1IeCKIIfi acpqleKT pa.n;IIaIJ,IIII y MIIKpOopraHU3MOB npu pa3.T[II"IHhlX nepecTpothrnx
JQep11m crpynyp.
06paT1rnocT1> IJ,UTOreHeTI111ecKnx nonpeaq~e­
Hllii, BhI3BaHHhIX pa,n;uan;neii.
BnoJOrIItiec1rnJi orracHocn OT IIOBhlllleHIIJI
KOH1IeHTpai::r.m1 C14 n peaym.mTe B3phlnon
JI;!1;8plib1X 60MO.
Ilpll'IIlHbI pa,11;uoycrofilJIIBOCTII paCTeHIItt.
OTHocuTe.11:r,11a..ir reHeTnqecKaJI pa;nro'IynCTBIITeJJhHOCTI> pa3.i!IllJHhlX Bll,l(OB MJBROilllrarom;nx rr .l{poaoqmm.

430
431

432
433
434

428

.

:U:uTOJOrlllJeCRIIe )l;OR~aTe.llhCTBa <fl113 IIOJOrlllJeCJWfi 3aIIJ,IIIIJ,eHHOCTII ayroTeTpaII.10Ilp;oB rpelJIIXII (Fagopymm esculentum
moenh) OT ,n;efiCTBH.ll llOHII31IpyIOIIJ,ett pap;uaIJ,IIIl.
Pa.,n;naIJ,lloHnoe nopa;r.emrn p1>16.
Oco6eHHOCTII ~onannoro MJI'8.IJ,1IOHHoro npon.ecca y MH&poopra11uaMOB.
SWEDENThe concentration of some fission productnuclides in ground-level air during theperiod September 195i-December 1959.
UNITED STATESSecretion of dietary strontium-90 andcalcium in human milk.
X-ray induced chromosome aberrations
in mammalian cells in t•ivo and in r•it;o,Sex-linked recessh·e lethals in Drosophila
whose express:on is suppressed by the
Y-chromosome.
X-ray sensitivity of primary spermatocytes of the mome.
Summan- of available data on the strontium-90 content of foods and of total dietsin the United States.
l\Iutation frequency at low radiation intensity.

Document

No.

Coimtry and title

Country and title

A/AC.82/G/L.

A/AC.82/G/L.
UNITED STATES (continued)

435

436

43i

438
439
440
441
442
443
444

DEXMARK (continued)

448
449

Factors causing a high frequency of micehaving the XO sex-chromosome constitution.
Genetic control of physiological processes:
The genetics of radiation toxicity in animals.
Radio-activity of invertebrates and otherorganisms at Eniwetok Atoll during 19541955.
Ratio of cesium-137 and strontium-90
radio-activity in soil.
The error hypothesis of mutation.
Strontium-90 in North Atlantic surface
water.
Leukemia in Nagasaki atomic bomb survivors.
Neoplasms among atomic bomb survivors
in Hiroshima City.
Special report on high altitude sampling
program.
Evaluation of radiological conditions in
the vicinity of Hanford for 1959.

450
451
452
453
454

455
456

AUSTRB.

445

445/

457

The 90-strontium content of the diet ofchildren and juveniles in 1959.

458
459

l'vleteorological fractionation of nuclear
bomb debris.
Determination of fall-out radio-activity
in the atmosphere by means of an airborne filter.

460

Fall-out observations in India after the
first French atomic test in Sahara.

NORWAY

INDL~

Addendum to previous document.

Add.2

445/

Addendum to previous document.

Add.3

445/

ARGENTINA

Addendum to previous document.

461

Add.4

445/

Addendum to previous document.

Add.6
445/
Add.i
445/

Add.8
445/

462

Addendum to prev-ious document.

463

Addendum to previous document.
Addendum to previous document.

464

Addendum to pre'll-ious document.

Add.9

IAEA
~46

Radioestroncio en la Leche.
UNITED STATES

Add.5

445/

U XITED STATES
Consanguineous marriages in the Chicago
region.
Radiation dose rate and mutation frequency.
Influence of dose rate on radiation effecton fertility of female mice.
Acute radiation response of mice from across between radio-sensitive and radioresistant strains.
Effects of incorporated radio-carbon, C 14 ,on somatic flower-color variations andmorphological changes in the snapdragon,
A nlirrltinum majus.
Annual report for 1959 on the radioactive fall-out study program.
Quarterly report of the radio-active fallout study program-January-March1960.
GEIUIANY

Data compiled by the Bundesstaatliche
Baktcriologisch-Serologische Un tcrsuchungsanstal t in Linz, the Bundesanstalt
Fuer \Vasserbiologie und Abwasserforschung at Wien-Kaisermuehlem and the
Zentralanstalt fuer lVleteorologie undGeodynamik in Vienna as to the degreeof radio-activity in air and water.
Addendum to previous document.

Add.1

445/

Strontium-90 in human bone.
Information regarding levels of Sr 90 andCs 13i in rainfall up to the end of 1959.

Dependence of mutation rate on radiation intensity.
Some prompt and delayed effects of
X-rays on growth of human amnion cells(strain FL) in tissue culture.
Damage and recovery of mouse testis
after 1,000 r acute localized X-irradiation\Vith reference to restitution cells, sertoli
cell increase, and type A spermatogonial
recovery.
}APA~

Radiation damage in bone.
DEN:\IARK

465

Excerpt from draft-report on the activities of the Danish AEC for the period
from 1 April 1959 to 31 l\larch 1960.

466

429

Delayed radiation effects in sup,;vors of
the atomic bombings.
Further studies in radiation conditioned
behavior.

Document

Document

Cou1'try a1Ul title

No.

A/AC.82/G/L.

A/AC.82/G/L.

ROMANIA (continued)

JAPAN (continued)

467
468

The use of ionizing radiation as a motivating stimulus.
Accumulation of radio-active materials
by fishery organisms.

484

Atmospheric radio-activity in Bucharest
from January to June 1960.

485

Fall-out program quarterly summary report, HASL-95.
Summary of gummed film results throughDecember 1959, HASL-93.

UNITED STATESU:NITED STATES

469

486

Research in radio-biology.
ARGENTI~A

470

Country and tiae

No.

UNITED K!NGDmf

Informe sobre mediciones radioquimicasde la precipitaci6n radioactiva.

487

Strontium-90 in human diet in the United
Kingdom, 1959.

CZECHOSLOVAKIA

471
472

SWEDEN

Action of chloramphenicol on the change
in capacity of Escherichia coli B cells
irradiated with X-rays for phage T3.
The significance of the intensity of metabolic processes and of weight for theradio-sensitivity of the organism.

488

489

AUSTRALIA

JAPAN

473

The summary of researches in Japan particularly related to document A/AC.82/
R.87.

490

Results of strontium-ninety determinations on samples from Lucas Heights andRichmond, N.S.W., 1959-1960.

491

Autoradiographic and microscopic examination of nuclear-weapon debris particles.
Summary report on upper-air radioactivity measurements, 1956-1960.
An approach to the question of computing doses and effects from fall-out.
Radio-active fall-out in Sweden throughMay 1960.

SWEDEN

UNITED STATES

474

Measurement of bone marrow and gonadal dose from the chest X-ray examination
as a function of field size, field alignment,
tube kilovoltage and added filtration.

492

493

SWITZERl.A,.-.."D475

Die Belastung des Menschen durch ionisierende Strahlen.

494

JAPAN

476
477
478
479

UNITED STATESThe concentration of cesium, rubidium
and potassium in human body with reference to cesium-137.
Annual and geographical change of Sr 90
dietary intake of Japanese.
Sr 90 in human bone in Japan, during
1954-1960.
The environmental increase of cesium-137
since 1957 to 1960.

495

496
497

498
499

UNITED STATES

480
481

Interim report of studies of Sr 90 in adultbeagles.
The determination of internally depositedradio-active isotopes.

500
501

DE!-."!>fARK

482

Caesium-137 in spray-dried Danish milk.

483.'\tmospheric radio-activity in Bucharest
and Iassy in the Romanian People's Republic.

The content of esm and (Z r Nb) gs in
Swedish soils.
The Cs137 and Sr 90 content in dried milk
samples from 1958 and 1959, FOA 4,
Rapport A 4141-456, June 1960.

A selected list of references on marine andaquatic radiobiology.
Radiological Health Data, Pb 161371-4,
quarterly report, July 1960.
Radiological Health Data, Pb 161371-7,
quarterly report, October 1960.
Radiological Health Data, Pb 161371-6,
monthly report, September 1960.
Initial depletion and subsequent recoveryof spermatogonia of the mouse after 20 rof gamma rays and 100, 300 and 600 r of
X-rays.
Radiation and the sex ratio in man.
The ORINS human radiation counters,
Orins-38.
CZECHOSLOVAKIA

502

ROMANIA

503

430

The role of cellular cytoplasma in thedevelopment of primary effect of radiation.
Strontium-90 in milk. 1957 to 1960, andits relation to radio-active fall-out in Central Europe.

Document
No.

Docu1Mnt
No.

Country and title

A/AC.82/G /L.

A/AC.82/G/L.

CZECHOSLOVAKIA (continued)

504

505
506
507
508
509
510

511

527

Report to the Danish National Health
Board on the irradiation studies in progress at the Copenhagen University Institute for Human Genetics.

528

UNITED STATES

529

Fuerzas de Wigner y el modclo de capas
de! nucleo.
Fuerzas nucleares con centro repulsive yel modelo de capas del nucleo. Efectos desegundo orden.
El efecto del reflector en los reactores
heterogeneos.
Sohre la generaci6n de funciones transferentes por medio de distribuciones.
La interacci6n spin-6rbita entre nucleones y cl acoplamiento spin-6rbita en elmodelo de capas de! nucleo.
Construcci6n y caracteristicas de contadores de ventana de "Vidrio para la medici6n de rayos beta y gama.
Estudio de los efectos direccionales en la
ruptura electrica de Kcl.
Energy levels of Sc~ and Ca42 •Geomagnetic coordinates and cosmic
radiation.
The simple cones of albedo of cosmic rays.
Short range forces and nuclear shelltheory.
Addendum to above document.

523
524
525
526

DEN')!ARK

lVlEXICORadio-active iodine concentration in the
fetal human thyroid gland from fall-out.
530

513

The deposition of fission products fromdistant nuclear test explosions-results tothe middle of 1960.
IAEA
Dosimetric investigation of the radiation
accident, Vinca, Yugoslavia-Report to
the Director General of the International
Atomic Energy Agency.

515

The uptake of radio-active strontium bycrops under field conditions in the United
Kingdom.

535
536

INDL-\

537
538

Cesium-137 in milk.

538/
Add.1
539

Radio-active fall-out in air and rain.
NORWAY

517

Radio-active fall-out m Norway-July
1959 to July 1960.

519
520
521

522

Velocity-dependent forces and nuclear
structure. II. Spin-dependent forces.
UNITED KINGDOM540

MEXICO

518

532

534

UNITED KINGDOM

516

531

533

UNITED K!NGDm.I

514

l\IEXICO (continued)
Cuarto informe sobre estudios de la precipitaci6n radioactiva.
Contador 4 r. con circuito de anticoincidencia doble.
Analisis quimico empleando protones conenergias de 1.5 mev.
Y odaci6n de la seroalbumina con yodo131.

Changes in o~ consumption by rats during irradiation.
The time dependence of the man-maderadio-activity of atmospheric precipitation.
Polyvalent immunological tolerance inhomologous radiation chimaeras.
A brief survey of results of measurementof fall-out and rainfall strontium-90 in
fall-out and milk.
Report on measurements of man-madeairborne radio-activity in IGY and IGC,
1957-1959.
Changes in the catalase activity of theliver in mice after X-irradiation.
Effect of radiation on bone marrow cells
at various temperatures in vitro.

UNITED K!NGDO.M

512

Country and title

Soluciones de la ecuaci6n de Bhabha parauna particula libre.
Producci6n mes6nica de mesones.
Metodos de calculo de la precipitaci6n
radioactiva.
Resonancia del ps por bombardeo de 0 15
con deuterones.
lVletodos de determinaci6n del estroncio-90.

Bibliography of papers published in the
United Kingdom from June to November 1960 on radiobiological and allied
subjects.
GHANA

541

Radio-active fall-out in Ghana.
BELGIUM542
431

La retombee radioactive a l\fol et au
Congo.

Document
No.

Document
No.

Country and title

A/AC.82/G/L.

A/AC.82/G/L.
BELGIUM (continued)

542/
Add.1
543

544
545

546
547
548

549

550
551
552
553

UNITED STATES

562

Addendum to above document.
USSR
Cop;epmaHne Sr90 B noi:me n pacTnTem.IIOM
rro:&poBe MOC:&OBC:&Ott o6JacTil.
Cop;epiKaHIIe Sr00 n :MO.llOIW pasHI:.IX pattoHOB CCCP B 1959 roey.
lfocJep;oBaHne co,ll;epn>aHnJI Sr90 B sepnoBhIX :&yJinTypax (ypm1mtt 1958 ro.rr.a).
YBe.irnl!eHne co.rr.epa.annJI pa.rr.noyr.llepop;a npeayJihTaTe JI.l(epIU.i!X B3pDIBOB.
E BOIIpocy 06 yBeJIIlllermn CO,Jr.eplKaHIIJI C14
B anrncipepe.
IlccJiep;onanne cop;ep&aIIRJI CTPOHD;IIJI-90 B:&aprocpeJie, :MOJIOKe II paCTIIT6JIDHOY IlOKpOBe .ireIInn:rpap;c1wtt o6;:iacrn (1957-1959
rOAJ:iI).
Pap;noxIDiIIPiec1me MeTOAJ:il ana.rrnsa ncxycCTBeHIThIX pa)l;IIOll30TOIIOB B pa3JlilllThIX
rrpnpop;IrnX o6':be:&rax.
To:&Cll'IHOCTD pap;noaR.TllBH<>ro uo;i;a n xpoHlll!eCl\OM s:&cIIepH:Menre.
06aop nccJie,n;OBann.tt no 6110.rnrnl!ecxo11ryp;ettcwnro pap;na~n B MaJIHX p;osax.
IIpmrnneIDie TJlllTilJI B 6noJ1ornl!ec1mx nccJiep;onaHilJIX.
06 orracHOCTII C14 , o6paayrom,erocJI npn
JI,ll;epmrx Bspmax.

563

564

565
566

567
568
569

5i0
571
572

UmTED KINGDOM

554
555

573

Assay of strontium-90 in human bone in
the United Kingdom (further results for1959).
The hazards to man of nuclear and allied
radiations.

574

SOUTH AFRICA

.556

575

Radio-active fall-out over South Africa.
UNITED KINGDOM

557

Country and title

576Radiological hazards to patients.

Health and Safety Laboratory fall-out
program quarterly summary report,
HASL-105, January 9, 1961.
Radiological Health Data, monthly report, PB 161371-9, Volume 1, No. 9,
December 1960.
Fission product radio-activity in the air
along the 80th meridian (West) during
1959, NRL report 5528, August 15, 1960.
Atmospheric radio-activity in SouthAmerican and Antarctica, NRL report5526, August 15, 1960.
Medical survey of Rongelap people fiveand sLx years after exposure to fall-out(with an addendum on vegetation). BNL
609 (T-179) (Biology and !Vledicine),
September 1960.
Effects of inhaled radio-active particles,
N AS Pub!. 848.
Long-term effects of ionizing radiations
from external sources, NAS Pub!. 849.
Effects of ionizing radiation on the humanhemapoietic system, NAS Pub!. 875.
Cancer Research, Division of Biology andMedicine, TID-11132. November 1960.
Fate of radio-active contaminants inwater, progress report No. 2, technicalreport R60-2. May 1, 1958 to June 1959.
Radiological Health Data, monthly rereport, l\farch 1961, PB 161371-12, Volume II. No. 3.
Radiological Health Data, monthly report, February 1961, PB 161371-12,
Volume II, No. 2.
Health and Safety Laboratory fall-out
program quarterly summary report,
April 1, 1961, HASL-111.
Radiological Health Data, quarterly report, January 1961, PB 161371-10,
Volume II, No. 1.
Radiation research in the life sciences,
November 28, 1960.

SWEDEN

558

559

560

361

GERM'A..1'l"Y

Attempts to influence the elimination ofradio-strontium.

577

ICRP/ICRU
Exposure of man to ioruzmg radiation
arising from medical procedures withspecial reference to radiation-induced
diseases.

The 90-strontium content of human bones
and tissues in 1958, 1959 and 1960.
SWEDEN

578

ICRP
Meeting with experts on somatic andgenetic radiation effects. lVI unich, 1959.

579

WHO
Medical supervision in radiation work.
432

Advcction over Sweden of radio-active
dust from the first French nuclear test
explosion, FOA. 4 Rapport A 4155-4727(Rev.).
Studies on plant accumulation of fission products under Swedish conditions.
I. Plant accumulation of Sr 90 in pot experiments in relation to uptake underfield conditions.

Document
No.

Document
No.

Country and title

A/AC.82/G/L.

A/AC.82/G/L.
u~rTED STATEs

SWEDEX (continued)

580

581

595

Studies on plant accumulation of fission products under Swedish conditions.
II. Influence of lime and phosphate fertilizer on the accumulation of Sr 89 in red
clover grown in 29 different Swedish soils.
Studies on plant accumulation of fission products under Swedish conditions.
III. Accumulation of Sr 90 in the aerial
parts of different weed species at varying
Ca-level in soil.

596

597

NORWAY

582
583

584

Fall-out in Norwegian milk in 1959Report No. S-0003.
Seasonal and latitudinal variations inradio-active fall-out-Report No. F-0412.

598
599

FAO
Dietary levels of strontium-90 andcesium-137.

Radiological Health Data. Volume II,~umber 4, April 1961, quarterly reportUS Department of Health, Educationand Welfare.
Radiological Health Data. Volume II,
Number 5, :\fay 1961, monthly reportUS Department of Health, Educationand Welfare.
Journal of Occupational Medicine-Special Supplement, lVIarch 1961-Acuteradiation death resulting from an accidental nuclear critical excursion.
Atmospheric radio-activity and fall-out
research, TID-12616.
Health and Safety Laboratory fall-out
program quarterly summary report,
July 1, 1961, HASL-113.
FR..-L'<CE

600.ARGENTINA

585

Country and title

Dosis geneticamente significativa debida
al radiodiagn6stico medico.

601

Resultats d'une prerniere enquete sur leseffets somatiques de !'irradiation foetoembryonnaire in utero.
La technique d'autoradiographie anatomique a la temperature de l'azote liquide.

NORWAY586

Caesium-137 in air, precipitation, drinking water, milk and beef in Nonvay during 1959 and 1960.

602

UNITED KINGDOM

587

Strontiurn-90 in milk and agricultural
materials in the United Kingdom, 19591960.

UNITED KINGDOM

603

FRANCE

588

Mesures de la contamination radio-active
de la chaine alimentaire.

604

l:SDIA

589

IAEA
Survey of radio-activity in food consumed
in Austria. Report on first sampling period(June-December 1960).

Strontium-90 in milk and human bone in
India.

605

Bibliography of papers published byUnited Kingdom sources from November
1960 to April 1961 on radiobiological andallied subjects.
Current data on the frequency of humansex chromosome abnormalities. MRC.61/
716.
Relationship between the deposition ofstrontium-90 and the contamination ofmilk in Britain during 1958-1960.

ARGENTINA

590

GERMANY

Contaminaci6n por radioestroncio durante el aiio 1960.

606

UNITED STATES

591

Genetics research program of the Divisionof Biology and Medicine-TID-4041.

UNITED STATES607

CZECHOSLOVAKIA

592
593

608

Delayed changes in children following
irradiation with small X-ray doses.
An investigation of gonad dose exposurein radiotherapy of non-malignant conditions.

609

ITALY

594

The genetically significant do5e in medical
uses of X-rays and radio-active materials.

610

Data on environmental radio-activity,
collected in Italy (July-December 1960).
433

Radio-active fall-out data 1959, dated
May 1960, TID-11851.
The effect of consanguinity on the distribution of continuously variable characteristics.
Radiological Health Data, Volume II,
Number 6, June 1961, monthly report,
US Department of Health, Educationand \Velfare.
Atmospheric transport of artificial radioactivity.

Doettment

Document

No.

No.

Cotmtry and title

A/AC.82/G/L.

A/AC.82/G/L.
Ul'·.-ITED KINGDOM

611
612

Dominant lethal effects of high intensity
X-irradiation of mouse spermatogonia.
Sex chromosome loss in mice following
irradiation of the fertilised egg.

629

INDIA

613

614

615
616

617

618
619

620
621
622
623
624
?~

6 _;,

626

627
628

Country and title

Radiochemical procedures for the assay
of low levels of strontium-90 activity inmilk, human bone and water.

630

USSR
YpoBem, aarp.lI3nenn.a: npllaeMnoro CJIOJI aTMoccpep1I rrpo.u;yitTa!lm ncI111Tanntt Jl,ll,epnoro opya\HJI IIO II3M0p8Hll.IIM B IlO~MOCKOBiie
c 1955 no 1959 roµ;.
I'.no6a.m.noe pacrrpocrpanenrre B arnoccpepen BDIIIa)J;enne na aeM.JIO pa,rr.noa:&THBHiiIX
npO.icyRTOB JI;(0pHL!X B3p.bIBOB.
CocTaB II xo~enrpaD;mr pa.lJ)IOaKTHBIThIX
sarpmrnenntt noaµ;yxa B Iln~cKOY n TnXOM oKeanax B 1959-1960 ro.u;ax no MaTepIIa.rn:M 9KCil0,ll;lIIl;llII Ha 0/C «BIITJI3D>.
Boa.n;eficTBIIe nonnarrpyrom;ett pa11.nan;nn na
ny1rneIIHOill>!ti o6MeH IIOJIOBblX It.'10TOK caMn;on-rrpOII3BO,ll;IITeJefi B CBJI3ll c paaBIITll0M
MY3\CKHX II ffi0HCJ\IIX oco6e.tt B IIX IIOTOMCTBe.
KoJJ.If'I0CTB0HHBJI xapa:&'l'epIICTJIKa 1JYBCTBllT0JIIiHOCTll n;enrpa.ilDHOfi nepnnott CIICTeMiiI:& ll0Illl311pyrom;eMy Il3Jlf'10HIIIO.
0 po.m pa.n;IIan;nonnoro rronpe:aq:i;em1.lI 11nyTp1rn..11eT01IIThIX rronepxrrocTefi pa3p;eJ1a B 6IIo.;10mqecitoM µ;eii:CTDIIII IIOIIJI311pyKl~ II3.l!J'I ennii.
Pnnmn.a OKIIC.mTeJILIIl:JX rrpon;eccoB II eenapymenne rrpn .n;elicTBIIIl pa.u;IIan;nn.
Ilepexop; Sr90 OT MarepII K rroTOMCTBY II TI3MenenIIJI nepnno.tt n cep.n;eqno-cocy,rr.ncTofi
CIICTC:m.l y IIOC.ilC,!J;IIIIX.
Ilprrpo;i;a rrepBII1fI.(IiIX n;nroreaern11ec1mx JIY1IeBblX rroBpe;np;enutt n :&aTaJIIITif'ISC:&aJI aKTIIBHOCTii xpOMOCOM.
0 «KIIClIOpO,!J;HOM acpcpeKT0»' na6JIO,ll;aeMOM
npll JJ1!0BOM rroBpe&;i;emm pacrnre.iThHiiIX
II jKIJBOTHfilX R.ileTOJt.
K Borrpocy 06 o6paTIDiocrn paa.lH1IHiiIX
cpopM paµ;naqnonnoro nopa;Eenn.a: y .n;nm10IIAHhlX !J;pOll\.il\CBhlX R.lJ0TOR.
0 neRorophlx rrpo6.11eMax coBpe:\rnnno:tt pa.n;no6noJorun.
Pea1rn,rrJI ROpROBoro CJIOJI nap;noqe1IHIJROB
nprr B03p;elicrBim na opraHII3M Ma:rnx ,11;03
IIOHII3IIpyK>m;eii: pa.!J;IIaIJ,J!Il B ycJIOBIISIX
BHyTpeHHero 00ll)"I0HIIJI.
AnaJIII3 )J,ettcTBrur OCHOBHDIX cp1131PI8CKIIX
cpaRTOpon, IJ3)IellJIIOm;IIX pa,n;11oqYJlCTBIIT8Jll>IIOCTb.
Pea~Ifll MOaroBoro CJOJI na;ri;rrotJe1IHtIKOB

631

632
633

634
635
636
637

638

639
640

641
642
643
644

645

434

USSR (continued)
rrpn B03)J;0iiCTBIIII Ha opraHII3M :Yamx ,ll;03
IIOHII3rrpymm;ett pa,!l;Ilan;nn B yc.nOBII.lIX BnyTpeHHero o6Jiyqenrur.
<l>JIYopeCIJ,CllTIThle IICCJl0)1,0BaHIIJI II3M0Henntt ny:&JJeonporen,;i;oB n BX µ;epIIBaTOB B
o6JiyqenHiiIX KJJeTKax.
0 µ;efiCTBilII penTreHOBCIWrO o6JiyqenIIJI HaOKIIC.JIJ.ITennoe cpoccpop1rnnpomume B MllTO:XOH)J,pILHX pacrenntt.
,TI;efiCTBIIe MHOron.parnoro peHITeHOBCKOro
06J1yqeIIIIH B ~IaJJhlX jl.03ax na p;e.lITe.lThIIOCTb
Bl>ICIDJIX OT,!1;0.lOB n;enrpaJDHOtt nepnnott CllCTelm: 3\IIBOI'HUX.
3naqeane pereuepan;nonHDIX rrpon;eccon n
peaKD;Jin TEanett na o6JY1IeHIIe.
Il3Mene11n.a: yc.:rnnnopecp.rnKTOpnott ,u;eHTe.n.nocTn co6a:&, Bhl3Ba11Hl>I0 xpOHII1!0CKIIM 06m;mr o6JyqenneM npe.n;e;u,no )J,OIIycrrnro:tt.n;o30.fi peHTI'enonDIX JIYqefi.
EeJIKOBiiili o6Men II ID!JlYHO.!lOrH1!ecR11e
oco6eHHOCTII r...'leT01IHblX opraHOll)J,OB llpH
OCTpott JiyqeBoli 60J03Illl.
0 rro,aaBJennn perenepan;nonnDIX npon;eccoB B xocrn rrpn paaJn'IHblX ycJIOBIIJIX 06JIYtienn.lI 3rnBOTHDIX.
0RCil0pln!0HTaJIDH00 JI3yq0Hll0 IICpBIPIHOrO
Mexaa113Ma ,n;eficTB11H pa,n;naqnn na .H).ij)O:&Jl0TRII.
He:rwTopiiie :aorrpocDI sxcIIepIIMeIITam.no6noJioruq:ecRoro o6ocnoBannH Maxcmra.!IIiIIO-!l;orrycrlllThIX KO.illl1ICCTB pa.n;noaKTHBHHX
ll30IOilOB npn rrorraµ,aHIIII IIX B opra1Tll3M.
CrreR.rpocporoMerplf'Iec1we II pa,ii;IIO~erp11qe­
cKoe IICCJe,:i;onaaJie rrperraparoB ,n;eao&c11prr6onyit.-10HH0Bott KllCJ!OThI, Bl>I,ll;0JI0HHblX ll3
netieHII RphlC IIOC.il0 IIOpaiRSHIIH crponn;neM-90.
0 nal!aJiillhlX :r.rexaHJI3Ma:x 6110JIOrif'!ecxoro µ;eiicTDII.lI 11011113rrpymm;nx 1I3.1yqen11tt.
0 110ROTOphlX Mexanir.rnax BJil.lIHIIJI Ma.'ILIX.n;o3 xpom1qec1wro o6m;ero penrrenonc:&Oro06,1yqenn.lI na BDicmyro nepnayro µ;eJITe;n,nocTii II neRoropDie nererarnnHDie lflyn:&n;un 6eJJhlX RpLIC.
Oco6ennocrn xpOHIPiec:iwro rropaaieHnJI,
BDI3nannoro crpom:~neM-90.
0 xapah."Tepe 113MenennH noJIIDiepnoro
CJieKrpa ,I(HR npn Y-o6Jyqennn ee pacrnopon.
0 .n;Byx BII;i:a:x pa,:i;11an;rroHHoro rrocJe!l;el!:cTBn.lI, BhlJIBJ.lI0Ml>IX y CSMHII JPIM0HJI.
0 rrepe.n;aqn crpoan;nJI-90 caMKalliI Rpnrc.n;eremmal!.
K. norrpocy o xapaRrepncrIIRe cmrreaa 6e;rROB n opranon.ll,ax uero:i;. TRanelt nop:r.ranHDIX II 06JY1!8HHhlX OCJhlX Kpl>IC.

\

Document
No.

Document
No.

C<nintry and :itle

A/ AC.82/G/L.

A/AC.82/G/L.

..\RGEKTINA

646

90

90

La incorporaci6n del Sr -Y en vegetales: estudio radioautografico de dicha
incorporaci6n en Vicia faba.

661
662

GEIUL-L"Y

647

648

Research on fundamental radiobiology
and somatic effects of radiation of Germany. 1954-1960.
Major radiogenetical studies carried out
in the Federal Republic of Germany during 1953 to 1960.

663

664
665

Sv.1'DE-"

649
650
651
652

Distribution of radiocesium in mice. An
autoradiographic study.
Radio-activity in people living in thenorth of Sweden.
Radiocesium and potassium in Norwegians.
Cs 137 burdens in Swedish Laplanders andreindeer.

666

667

Strontium-90 in fall-out and in man m
Australia, January 1959-June 1960.

668

CZECHOSLOVAKIA

654
655

669

658

659

Fall-out in Norwegian milk in 1960. Norwegian Defence Research Establishment,Intern Rapport S-0006.
SWEDEN

670

Bericht der eidgenossischen Kommission
zur Uberwachung der Radioaktivitat zuhanden des Bundesrates.

671

FR...>L'l'CE

657

Assay of strontium-90 in human bone in
the United Kingdom. Results for 1960,
Part I with some further results for 1958
and 1959. Medical Research Council
l\fonitoring Report, Series No. 2.
Human bone metabolism deduced fromstrontium assays.
NORWAY

Chronic occupational exposure to Sr 90
and Ra226 •Results of systematic measurement offall-out in Hradec Kralove and Plzen,
Czechoslovakia.
SWITZERLAND

656

UAR
Gonadal and bone marrO\v dose in medical diagnostic radiology.
Annex to paper of estimation of gonaddose in radiotherapy of benign conditions.
Report on exposure of workers of Atomic
Energy Establishment of United Arab
Republic.
Fall-out over United Arab Republic fromthe fourth French nuclear test over Algerian Sahara.
Strontium-90, stable strontium and stable
calcium in soil. food items, water andhuman bone in Egypt (UAR).
Committee on the Effects of Atomic
Radiation on :\fan. Detailed annual report No. 2, Cairo, July 1961.
UNITED KINGDO~I

Ac:sTR.U.L.\

653

Country and litle

The protective effect of cysteamine
against genetic damages by X-rays inspermatozoa from mice.
Sex-ratio-an unreliable method for estimations of radiation hazards.
UNITED STATES

Determination du rapport rad/r clans l'os
et le muscle par la methode des gaz
equivalents.
Deux ans de controle de la radio-activite
du Rhone et de la nappe phreatique.

672

673

CAi'LillA

674

Strontium-90and cesium-137 in Canadian
wheat (1957-1959).

675

Radiological Health Data, Vol. II, No. 7,
July 1961. quarterly report. US Department of Health, Education and Welfare.
Radiological Health Data, Vol. 22, No. 8,
August 1961, monthly report.
Assessment on the radiation dose due tofall-out.
The dose-response relation in radiationinduced cancer.

UXITED STATES

660

660/
Add.1

UNITED KINGDmt

Applications of radio-isotopes and radiation in the life sciences. Summary-analysisof hearings held on March 27, 28, 29 and30, 1961 before the Sub-committee on
Research, Development and Radiation of
the Joint Committee on Atomic Energy
Congress of the US, June 1961.
Addendum to above document.

676

Radiostrontium and racliocaesium indrinking water in the United Kingdom.
Results to December 1960.
UNITED STATES

677

435

Offsite ecological research of the Divisionof Biology and l\Iedicine-terrestrial andfreshwater.

Document

Document

No.

No.

Country and title

A/AC.82/G/L.

A/AC.82/G/L.
U?-aTED STATES (continued)

678
679

680

681
682

683
684

699

Radiological Health Data, Vol. II, No. 9,
September 1961, monthly report.
US Atomic Energy Commission Healthand Safety Laboratory fall-out program
quarterly summary report for October 1,
1961. HASL-115.
Bioenvironmental features of the Ogotoruk Creek area, Cape Thompson, Alaska.
A first summary by the Committee on
Environmental Studies for Project Chariot. December 1960, TID-12439.
Atmospheric radio-activity at Kodiak
and Wales, Alaska, NRL Report 5658.
Evaluation of the ground-water contamination hazard from undergroundnuclear explosion. UCRL-5538, April 8,
1959.
Distribution of radio-activity from a nuclear excavation. UCRL-6249-T, October 26, 1960.
Proceedings of the Second Plowshare
Symposium May 13-15, 1959, San Francisco, Calif. Part I. Phenomenology ofunderground nuclear explosions. UCRL5675, l\fay 15, 1959.

686
687
688
689
690
691
692

693
694
695
696
697
698

FAO
The organization of surveys for radionuclides in food and agriculture.
UNITED KINGDOM

700
701

702

703
704
705
706
707

jAPAN

685

Country and title

Strontium-90 and cesium-137 in fall-out
deposits and implications of their ratio.
Cesium-131 and strontium-90insea water.
A new method of measurement of absorption dose rate from terrestrial backgroundradiation.
Deposition of Cs137 and Sr 90 in Tokyo.
Measurement of the carbon-14 concentration in essential oil using the liquid scintillation spectrometer.
The concentrations of Srg 0 and Cs137 inland waters in Japan.
Cesium-137 levels in human body, August
1958-August 1960.
l\Ieasurements with a whole body counter.
Natural concentration of krypton-85,
carbon-14 and tritium in recent years.
Physical aspect of fall-out in the troposphere.
Influence of radio-activity of the atomic
explosion in Sahara desert.
The peak in radio-active fall-out in thetemperate zone of the northern hemisphere.
Penetration of artificial radio-activity indeep waters of the Pacific and vertical
diffusion rate of sea water.
Seasonal variation of radio-active fall-out.

Medical X-ray exposure history of .~theparents of children 'vi th Down's syndrome(mongolism).
Surveys of radio-activity in human dietand experimental studies.
USSR
l:I11TeHCHBHOe pa,n;noa1mrnnoe BI:ma,IJ;eHne B
Crure1rne (Kpmr) B pesynrare JI,D;epnoro
B3pnrna B Caxape 13 !J>eBpa.1JI 1960 ro,n;a.
I:Iccj[e,u;onaHHe pa,rornan.TIIB!IbIX 3arp.llllnenntt B pattoHe 1Iepnoro MOp.H B 1959 ro;i;y.
3arp.ll3HeIDIOCTb MOpe.ll: n OReaHOB uc:&ycCTBennmm pa.n;rroa1mrnmYn Bem;ecTBaMH.
Co,n;epiKanrre Sr90 B KOCTHOtt TEann mo.n;ett,
npoa;HBarom;nx Ha repplfl'Opnn CoBercxoro
Corosa.
Bhllla.rr.enna 11.0.ill'OllillBYIIUIX npoµ,y&TOB .rr.e.'Iemm Ha TeppnTopnn GCCP B 1959-1960
ro.n;ax.
Co.n;epamnne Sr90 n Cs137 B rrpo6ax MoJIORa, BSJIThIX B pasnm pattonax CCCP B
1960 ro.n;y.
FRANCE

708
709

Etude de la vocation des sols en place ala retention du radiostrontium.
l\clethode d'etude de la contamination
radioactive des sols en place.
DENMARK

710

Environmental radio-activity m Denmark 1960.

711

La retombee radioactive a l\fol-Rapportd'avancement ler semestre 1960.

BELGIUM

UNITED KINGDOM

712

Radio-active fall-out in air and rain; results to the middle of 1961.
U~ITED STATES

713
714

715

716

Radiological Health Data, Volume II,
Number 10, October 1961, quarterly report.
Radiological Health Data, Volume II,
Number 11, November 1961.
Fall-out from 19Si and 1958 nuclear test
series.
The latent period. incidence, and growthof Sr 90 -induced osteosarcomas in CFI and
CBA mice.
CANADA

717
436

The effect of radiation dose rate upon theDocument

Dowment

No.

No.

Country and title

A/AC.82/G/L.

A/AC.82/G/L.

C..c\.J."'.-\D.-\ (continued)

ilS

719

720

]..\PAN (continued)

production of eye colour mutations in the
Clzalcid dahlbominus.

733

UNITED KlNGDO~f734

Strontium-90 in bones of infants in Hong
Kong.
Bibliography of papers published by theUnited Kingdom sources from l\fay to
October 1961, on radiobiological andallied subjects.
Assav of strontium-90 in human bone in
the United Kingdom-Part II.

735

737

La retombee radioactive a l'vlol-Rapportd'avancement 2eme semestre 1960.

738

UNITED KINGDOM

722
723

739

Radio-activity in milk in the United
Kingdom 1961: preliminary report.
Some provisional estimates of radio-active
fall-out in the United Kingdom-autumn
1961.

740
741

l:NDIA

i24
725

726

727
728

Fission product radio-activity in the air
along the 80th meridian (West) durina0
1960.
Health and Safety Laboratory, fall-out
program, quarterly summary report,
September 1, 1961 through December 1,
1961, HASL-117.
Sr 90 in man and his environment, Volume
I II: Publications.
Sr 90 in man and his environment, Volume
II: Analytical data.
Radiological Health Data, Volume II,
No. 12, December 1961.
HASP second special report on high altitude sampling program.
NORWAY

Observations of fall-out in India during
the period of cessation of nuclear tests.
A study of washout of radio-active fallout and particulate matter in individual
rain showers.
Gamma-ray analysis of fall-out samples
collected in India during October 1958 tol\Iarch 1960.
Cesium-137 and strontium-90 in milk.
Seasonal variations of cesium-137 in the
ground level air.

742

Caesium-137 and strontium-90 in precipitation, soil and animals in Norway.
UNITED STATES

743

744

Radiological Health Data, Volume III,No. 1. January 1962.
Fall-out from USSR 1961 nuclear tests.
AUSTRALIA745

MEXICO

729

The distribution of active marrow in thebones of normal adult.
l\,Iutation rates at low level irradiation in
Drosoplzila melanogaster.
The genetically significant dose by the
X-ray diagnostic examinations in Japan.
UNITED STATES736

BELGJU~I

721

Country and title

Measurements of strontium-90 in theAustralian environment.
ARGENTINA

Quinto informe sobre estudios de la precipitaci6n radioactiva.

746

UNITED STATES747

The effect of deposition rate and cumulative soil level on the concentration ofstrontium-90 in US milk and food supplies. AEC TID-13945.

748

Radiocesio en la dieta humana.
UNITED STATES

730

Criticality accidents in Vinca, Yugoslavia,
and Oak Ridge, Tennes...~e.
Health and Safety Laboratory-Preliminary data on fall-out from the fall 1961
USSR test series. Staff report, February
27, 1962, HASL-121.

JAPAN

731
732

SWEDENA shift of sex-ratio in the progeny from
irradiated males in Drosophila melanogaster (preliminary note).
On the incidence of Jeukernias in Hiroshima during the past fifteen years from1946 to 1960.

749
750

437

Late effects of thorotrast in cerebral angiography.
On the Hiroshima and Nagasaki experience of nuclear weapons initial radiation
LD 60 for man.

ANNEX K

LETTER SE1'T AT THE REQUEST OF THE COMl\IlTTEE BY ITS SECRETARY TO STATES MEMBERS OF THE UNITED NATIONS AND MEMBERS OF THE SPECIALIZED AGENCIES AND OF
THE IAEA ON 7 APRIL 1960
( b) Levels of Sr90 and Cs137 in diet: this involves
measurement of the mean levels in the principal contributing food products and in the total diet. Corresponding data on natural radio-activities would also be desirable:(c) Data "linking" rainfall and deposition of Sr00 •Sir,I have the honour to inform you that the ScientificCommittee on the Effects of Atomic Radiation has now
completed its seventh session. The Committee has received during the course of its past work, and is continuing to receive, substantial data from Goverrunents
and United Nations agencies, and assistance continues tobe rendered to the Committee by them, by international
non-governmental and national scientific organizations
and by individual scientists. The Committee is greatly
indebted to all of these and welcomes all infonnation
relevant to its work on the effects of atomic radiation on
man and his environment. It wishes to ensure continuation of the flow of such material so that nothing significant in the knowledge available in the world as a wholeshould by any mischance escape its notice.

The Committee also noted that Member States in needof assistance in the field of sampling and analysis areable to obtain it from a number of other Member States
or from interested agencies of the United Nations thathave offered such assistance : these offers are listed inannex 1 to the present letter. The Committee recognizedthat it is desirable for close co-operation between theCommittee, Member States and participating agenciesof the United Nations to be maintained in considerationof these arrangements and collation of scientific information obtained. The Committee would appreciate receiving in all cases full information on the manner inwhich data was obtained; and it emphasized that collections should be made by methods which ensure that data
is precise and representative.

A primary objective of the Committee is to assess theeffects of radiation on the world population. In any
attempt at this assessment it is necessary to h."llow theworld-wide levels in food products and in the humanbody of radio-active debris from the testing of nuclear
devices. Data obtained now is of particular value inassessment of the present and prediction of the future
situation, because of the period that has elapsed since thelatest high yield nuclear tests.

The Committee invites all those who can do so to
submit by 31July1960 data on Sr110 and Cs131 levels up
to December 1959.
The Committee was also requested by General Assembly resolution 1376 (XIV) to consider and study
appropriate arrangements for encouraging genetic, biological and other studies that will elucidate the effects ofradiation exposure on the health of human populations.
The Committee recognized that any fundamental advances in knowledge of biological mechanisms will be
relevant to the understanding of the genetic and somaticeffects of ionizing radiation on living tissue. Fundamental advances can be best facilitated by bringing together
scientists of experience and distinction and making themaware of each others' needs for information and data;
progress also requires the provision of necessary equipment to enable ideas to be tested. Whilst new and significant advances in basic science can never be guaranteed,
it is possible nevertheless for scientific institutes andindividual scientists to develop and expand informationin fields where knowledge is lacking. Sometimes this lackcomes about not through a deficiency of method to elicit
information but through paucity of data provided by asingle individual or unit. In its own area, the Committee
is especially conscious that although means have beendeveloped for measuring:(i) The mutation-rate, natural and radiation-induced,
at specific loci in mammals such as the mouse :(ii) The radio-biological effects of radio-active elements such as Sr00 in mammals;(iii) The induction of specific new growths such as
lymphoma by gamma-rays at defined dose-rates,
the accumulation of data in these and related areas adequate for statistical appraisal is e..'\.tremely time-consum-

In pursuit of this aim the Committee on 3 July 1959
addressed an invitation to States Members of the United
Nations and members of the specialized agencies and of
the International Atomic Energy Agency to send any
further data of the type already contained in its comprehensive report, so as to enable this report to be kept up
to date or e.ictended. This invitation outlined the principal
categories of information sought by the Committee, including those of immediate significance to its programme. The Committee was subsequently requested byresolution 1376 (XIV), adopted by the General Assembly on 17 November 1959, to consider and study, in
consultation with certain agencies of the United Nations
and other interested organizations, appropriate arrangements for the purpose of stimulating the flow of suchinformation and data, and for encouraging genetic, biological and other studies.
In the course of its studies of appropriate arrangements for stimulating the flow of relevant informationand data, the Committee noted that at the present time
there is a substantial part of the globe regarding which
there is little information concerning levels of radioactive contamination in soils, water, food products andthe human body. The Committee would like to obtaindata for these areas and would suggest that countries inthem initiate sampling programmes. especially on thefollowing topics :(a) Levels of Sr90 in human bones classified by age
groups: for example-still-born, 0-1. 1-2, 2-3, 3-5, 6-10,
11-20 years ;438

ing and e..xpensive. Thus close collaboration between
laboratories all working within a defined and agreed
framework is eminently desirable.

to obtain reports of all work in relevant fields and is an.xiousthat no results of relevant research carried out in laboratories
of Member States escape its attention, whether or not thoseStates are at present represented on the Committee.

The Committee feels that Governments might wellwish at this time to re-examine the ways and means
whereby its requests for relevant information can best
be channelled. in their respective countries, to the appropriate national scientific organizations and committees,
as well as to individual scientists. It would welcome
information from Governments concerning the namesof individual scientists or members of panels to whom its
requests are referred: such information would enable it
to communicate requests with the specificity and detailappropriate to the scientists concerned, through theusual Go\'ernmental channels.

The Committee is neither carrying on its own research, nor
directly sponsoring research, but rather depends on the workof other scientists which it studies and collates for the guidanceof the United Nations and the information of all scientists.

Conscious of the need to establish and maintain suchcontact with scientists and scientific bodies, the Committee decided to request Governments to bring to theirnotice a statement which it prepared at its seventhsession. This could be done either by direct distribution,by diffusion in scientific journals or by any other appropriate means. This statement is attached to the present
letter as annex 2.
May I, in conne..xion with the Committee's requests
for information, draw your attention to the fact that 150
copies of each report are required for distribution andcirculation to the Committee, as distinct from depositionin the Committee's library. The reports should be addressed to the Secretary of the Scientific Committee on
the Effects of Atomic Radiation, United Nations, NewYork.
ANNEX I
[The list originally given 1'n the present annex has been superseded by the one cotttained in annex I to the report.]

A1''NEX 2
Statement addres~ed lo scientists in the radiation field by theUnited Nations Scientific Committee on the Effects ofAtomic Radiation

The United Nations Scientific Committee on the Effects ofAtomic Radiation• is indebted to the many scientists throughout
the world whose work contributed directly or indirectly to theCommittee's first report published in 1958. It recognizes thatmuch research pertinent to its area of concern is being carriedon now, and that almost any aspect of biology contributes toknowledge of radiation effects in man. The Committee wishes•The General Assembly, at its tenth session, established byresolution 913 (X) the United Nations Scientific Committee
on the Effects of Atomic Radiation consisting of the following members: Argentina, Australia, Belgium, Brazil, Canada,
Czechoslovakia, Egypt (now part of the United Arab Republic),
France, India, Japan, Mexico, Sweden, Union of Soviet Socialist
Republics, United Kingdom of Great Britain and Northern
Ireland, United States of America.

In July 1959 the Committee invited Member States to send
it data on a wide variety of physical and biological topics.
Among these were the following:
1. Physical data relevant to radiation levels and accumulated
doses from both natural and man-made sources:?.fedical, industrial and research uses of ionizing radiations andradio-active materials;
Radio-active fall-out::i\Ieasured contamination of air, ground, foodstuffs and man
by strontium-90 and caesium-137;
Computation of external doses from fall-out deposit, including short-lived isotopes;
Significant disposals of radio-active wastes;
Other significant sources of ionizing radiations;
2. Methods of measurements and radiological standards ;3. Fundamental radiation biology;
4. Somatic effects of ionizing radiation;
5. Genetic effects of ionizing radiation.
At its last meeting the Committee reviewed the present stateof knowledge in its area of concern and discussed certain specificareas where additional information would be particularly welcome at the present stage of its work. In view of the need forthis information the Committee brings to the notice of scientists those areas where an intensification of scientific effort
would seem to be most helpful.

In the biological field the Committee noted the need for more
extensive statistical data concerning:(i) The mutation-rate, natural and radiation-induced, at
specific loci in mammals such as the mouse;(ii) The radio-biological effects of radio-active elements suchas Sr9D in mammals;(iii) The induction of specific new growths such as lymphoma
by gamma-rays at defined dose-rates.
In the physical field the Committee would like to obtain dataon the following topics, especially for those parts of the globe
for which there is little information available at present:(a) Levels of Sr9D in human bones classified by age groups:
for example-still-born, 0-1, 1-2, 2-3, 3-5, 6-10, 11-20 years:( b) Levels of Sr 0 o and Cs1a1 in diet: this involves measurement of the mean levels in the principal contributing food products and in the total diet Corresponding data on natural radioactivities would also be desirable;(c) Data "linking" rainfall and deposition of Sr90.
However, all data pertinent to evaluation of effects of radiation, particularly in the low dose and dose-rate range, remainof interest to this Committee and would be appreciated becauseof the assistance that would thereby be rendered to it in its work.
The Committee receives reports through Governments whichhave been invited to forward them to the Secretary of theCommittee.

439

APPENDIX I

LIST OF SCIE.NTIFIC EXPERTS, MEMBERS OF
NATIONAL DELEGATIONSThe scientific e.xperts who took part in the preparation of the present report
while attending Committee sessions as members of national delegations arelisted below :.ARGENTINA

Dr. D. Beninson (Representative}
Dr. J. Flegenheimcr
Dr. A. Placer

Mr. G. Lambert
Dr. G. Lejeune
Mr.L.Facy
INDL..

AUSTRALIA

Mr. D. J. Stevens (Representative)
Professor A. M. Clark
BELGIUM

Professor J. A. Cohen (Representative)
Professor M. Errera
Professor F. H. Sobels
Dr.J.Blok
Mr. J. F. Bleichrodt
Miss Z. M. Beekman

BR... ZIL
Professor C. Pavan (Representative)
Professor C. Chagas (Representative)
Dr. L. R. Caldas
Dr. 0. Frota-Pessoa
Dr. N. Libanio
Dr. A. Paes Carvalho
Dr. E. Penna Franca
Father F. X. Roser, S.J.
CANADA

Dr. E. A. Watkinson (Representative)
Dr. F. D. Sowby
Dr. W. E. Grummitt
Dr. H. B. Newcombe
Dr. P. M. Bird
Dr. G. H. Josie
Dr. B. B. Migicovsky?Yfr.H.CameronCZECHOSLOVII.KL\

Professor Dr. F. Hercik(Representative)
Professor Dr. F. Behounek
Dr. M. Hasek
Dr.L. Novak
Dr. M. Vojtiskova
FRANCE

Professor L Bugnard (Representative}
Dr.H.Ja=et
Mr. J. Labeyrie

Dr. A. R. Gopal-Ayengar(Representative)
Dr. V. R Khanolkar (Representative)
Mr. A. S. Rao (Representative)
Mr. P. N. Krishnamoorthy
Dr. K. G. Vohra]APA!'

Dr. K. Tsukamoto (Representative)
Dr. M. Tsuzuki (Representative)
Dr. E. Tajima
Dr. Y. Hiyama
Dr. Y. Miyake
Dr. M. Kimura
Dr. R. Ichikawa
Dr. Y. Tajima
MEXICO

Dr. M. Martinez-Baez (Representative)
Dr. F. Alba Andrade
Dr. A. Moreno y Moreno
Dr. H. Zalce
SWEDEN

Professor T. 0. Caspersson(Representative)
Dr. A. Nelson (Representative)
Professor R. M. Sievert(Representative)
Dr. B. Lindell
Dr. B. Aler
Dr. L. Frederiksson
Professor K. G. Liining
Dr. K. Edvarson
UNION OF SoVIET SOCIALIST REPUBLICS

Professor V. A. Engelhardt(Representative)
Professor N. A. Kraevsky(Representative)
Professor A. M. Kuzb
(Representative)

441

Professor V. Klechkovsky
Professor 0. Leipunskii
Dr. K. K. Aglintscv
Dr. A. A. Prokofyeva-Belgovskaya
Dr. Y. M. Shtukkenberg
Dr. M.A. Arsenieva
Dr. V. I. Terentiev
Dr. V. T. Kozlov
Mr. G. I. Apollonov
UNITED .ARAn REPUBLIC
Dr. M. E. A. El Kharadly(Representative)
Dr. K. A. Mahmoud
Dr. llf. M. Mahfouz

UNITED KINGDOM OF GREAT BRIT.UN
AND NORTHERN IRELAND

Dr. E. E. Pochin (Representative)
Dr. W. G. Marley
Dr. A. C. Stevenson
Professor L. F. Lamerton
Dr. R. S. Russell
Dr. J. F. Loutit
Mr. P. J. Meade
UNITED STATES OF AMERICA

Dr. S. Warren (Representative)
Dr. G. W. Beadle
Dr. V.Bowcn
Dr. A. M. Brues
Dr. C. L. Comar
Dr. C. L. Dunham
Mr. M. Eisenbud
Dr. G. Failla
Dr. J. H. Harley
Mr. S. Hendricks
Dr. A. H. Holland, Jr.
Mr. H. Hollister
Dr. L. B. Lockhart
Dr. L. Machta
Dr. E. A. Martell
Dr. W. L. Russell
Dr. A. C. Upton
Dr. M. R. Zelle
Dr. P. Tompkins
Dr. J. Totter

APPENDIX IIIJST OF SCIENTIF1C EXPERTS WHO HAVE CO-OPERATED WlTH
THE COl\~llTIEE IN THE PREPARATION OF TfIB REPORT
Dr. R. K. Appleyard
Dr. R. G. Bjomerstedt
Dr. R. E. Ellis
Dr. G. J. Fergusson
Dr. V. Glisin
Dr. L. D. Hamilton

Dr.A. P.James
Dr. D. W. Kearn
Dr. A. I. Kulak
Dr. L. E. Larsson
Dr. L. J. Middleton
Dr. F. Perrissin

442

Dr. L. D. Sanghvi
Dr. F. Sella
Dr. D. L. Simonenko
Dr. L. Wierzchowski
Dr. K. Zakrzewski

WHERETO

BUY

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GHANA: UNIVERSITY BOOKSHOP
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CEYLON: LAKE HOUSE BOOKSHOP
Assoc. Newspapers of Ceylon, P. O. Box 244,
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CHINA:THE WORLD BOOK COMPANY, LTD.
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THE COMMERCIAL PRESS, LTD.
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HONG KONG: THE SWINDON BOOK COMPANY
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!NOIA:ORIENT LONGMANS
Calcutta, Bombay, Madras, New Delhi
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OXFORD BOOK & STATIONERY COMPANY
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P. VARADACHARY & COMPANY
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INDON.£SIA: PEMBANGUNAN, LTD.
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JJ\PAN: MARUZEN COMPANY, LTD.
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KOREA. REPUBL.IC OF: EUL-YOO PUBLISH·ING CO., LTD.,1', 2-KA, Chongno, Seoul.
PAKISTAN:
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PUBLISHERS UNITED, LTD.
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SINGAPORE: THE CITY BOOK STORE, LTD.
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VIET-NAM, REPUBLIC OF: LIBRAIRIE·f'AP'ETERliXUAN THU ,li5, rue Tu-do, B.I". 283, Sai&:on.

EUROPE
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UNITEDNATIONSBELGIUM: AGENCE ET M~SAGERIESDE LA PRESSE, S. A.
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CZECHOSLOVAKIA: CESKOSLOVENSKYSPISOVATEL,
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DENMARK: EJNAR MUNKSGAARD, LTD.
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FINLAND: AKATEEMINEN KIRJAKAUPPA
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FRANCE: EDITIONS A. PEDONE
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GERMANY, FEDERAL REPUBLIC OF:
R. EISEl'jSCHMIDT
Sehwanthaler Str. 59, Frankfurt/Main.
ELWERT UNO MEURER
H;rnptslr!lsse 101, Berlin-Schtlneberg.
ALEXANDER HORN
Spiegelgassa 9, Wiesbaden.
W. E.SAARBACH
Gertruden5trasse 30, K61n (1).
GREECE: KAUFFMANN BOOKSHOP
28 Stadion Street, Athens.
!CELANO: BOKAVEP.ZLUN SIGFUSAREYMUNOSSONAR H. F.
Austurstraeti 18, Reykjavik.
IRELAND: STATIONERY OFFICE
Dublin.
ITALY: LIBRERIA COMMISSIONARIASANSON I,
Via Gino Capponi 26, Firenze,
and Via D.A. Azuni 15/A, Roma.
LUXEMBOURG: LIBRAIRIE J. TRAUSCH·
SCHUMMER,
Place du Thelltre, Luxembourg.
NETHERLANDS: N.V. MARTINUS NIJHOFF
Lange Voorhout 9, 's·Gravenhage.
NORWAY: JOHAN GRUNDT TANUM
Karl Johansgate, 41, Oslo.
PORTUGAL: LIVRARIA RODRIGUES Y CIA.
186 Rua Aurea-, Lisboa.
SPAIN:LIBRERIA BOSCH
11 Ronda Universidad, Barcelona.
LIBRERIA MUNDl·PRENSA
Caslello 37, Madrid.
SWEDEN: C. E. FRiTZE'S KUNGL HOVBOK·HANDEL A·B
Fredsgatan 2, Stockholm.
SWITZERLAND:LIBRAIRIE PAYOT, S. A.
Lausanne, Gen&ve.
HANS RAUNHAROT
Kirchgas3e 17, Zurich 1.
TURKEY: LIBRAIRIE HACHETTE
469 lstiklai Caddesi, Beyoglu, Istanbul.
UNION OF SOVIET SOCIALIST REPUBLICS:MUHDUNARODNAYA KNYIGA
Smoienskaya Ploshchad, Moskva.
UNITED KINGDOM: H, M. STATIONERYOFFIC!!,
P.O. Box 569, London, S.E.l(and HMSO branches in Belfast, Birmingh;im,
Bristol, Cardiff, Edinburgh, Manchester).
YUGOSLAVJA:CANKA~JEVA ZALOZsA
Ljub~ana, Slovenia.
ORZAVNO PREOUZECE
Jugoslovenska Knjiea, Terazije 27/11,
Beograd,PROSVJETA!5, Trg Bratstva i Jedinstvn, Za&:reb.
PROSVETA PUBLISHING HOUSE
lmport·Export Division, P.O. Box 559,
Terazije 16/1, Beograd.

PUBLICATIONSLATIN AMERICA
ARGENTINA: EDITORIAL SUDAMERICANA, S. A.
Alsina 500, Buenos Aires.
BOLIVIA: LIBRERIA SELECCIONES
Casilla 972, La P<?z.
BRAZIL: LIVRAR IA AGIRRua Mexico 98-B, Caixa Postal 3291,
Rio de Jeneiro.
CHILE:EDITORIAL DEi. PACIFICO
Ahumada 57, Santiago.
LISRERIA IVENS
Casilla 205, Santiago.
COLOMBIA: LIBRERIA BUCHHOLZ
Av. Jimenez de Quesada 8-40, Segota.
COSTA RICA: IMPRENTA Y LIBRERIA TREJOS
Apartado 1313, San Jose.
CUBA: LA CASA BELGA
O'Reilly 455, La Habana.
DOMINICAN REPUBLIC: LIBRERIA DOMINICANA
Mercedes 49, Santo Domingo.
ECUADOR: LIBRERIA CIENTIFICA
Casilla 362, Guayaquil.
EL SALVADOR: MANUEL NAVAS Y CIA.
la. Avenida sur 37, San Salvador.
GUATEMALA: SOCIEOAD ECONOMICAFINANCIERA,
6a. Av. 14·33, Guatemala City.
HAITI: LIBRAIRIE "A LA CARAVELLE"
Port·au-Prince.
HONDURAS: LIBRERIA PANAMERICANA
Tegucigalpa.
IYIEXICO: EDITORIAL HERMES, S. A.
1gnacio Mariscal 41, Mexico, D. F.
PANAMA: JOSE MENENDEZ
Agencia Internacional de Publicaciones,
Apartado 2052, Av. SA, sur 21-58, Panam6.
PARAGUAY: AGENCIA DE LIBRERIASOE SALVADOR NIZZA
Calle Pte. Franco No. 39-43, Asuncion.
PERU: LIBRERIA INTERNACIONAL
DEL PERU, S. A. Casilla 1417, Lima.
URUGUAY: REPRESENTACION DE EDITORIALES,
PROF. H. D'ELIA
Plaza Cagancha 1342, 1 • piso, Montevideo.
VENEZUELA: LIBRERIA DEL ESTE,
Av. Miranda, No. 52, Edf. Galipan, Caracas.

MIDDLE EAST
IRAQ: MACKENZIE'S BOOKSHOP
Baghdad.
ISRAEL: BLUMSTEIN ' S BOOKSTORES
35 Allenby Rd. and 48 Nachlat Benjamin St.,Tel Aviv.
JORDAN: JOSEPH I. BAHOUS & CO.
Dar-ul·Kutub, Box 66, Amman .
LEBANON: KHAYAT'S COLLEGE BOOK
COOPERATIVE.
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8869-August

1962-8,500