REPORT OF THE

UNITED-NAXI-ONS .

SCIENT1ft&~f'iMfttTTEE"'\."'\., /'l
IrN.
~·:·~.: rrn:iE. -~t· lI .
O.,..._~ ''.l:Il=-~ .: . ·• •--' . '.-, . ~.lo .···,,· ;o-?,·~i

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,.

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.