ECRR
2010 Recommendationsof the European Committeeon Radiation Risk

The Health Effects of Exposure to Low
Doses of Ionizing Radiation

Regulators’ Edition: Brussels 2010

2010 Recommendations of the ECRR
The Health Effects of Exposure to Low Doses of
Ionizing Radiation
Regulators' Edition
Edited by Chris Busby
with
Rosalie Bertell, Inge Schmitz-Feuerhake,
Molly Scott Cato and Alexey Yablokov

Published on behalf of the European Committee on
Radiation Risk
Comité Européen sur le Risque de l’Irradiation
Green Audit 2010

European Committee on Radiation Risk
Comité Européen sur le Risque de l’Irradiation
Secretary: Grattan Healy
Scientific Secretary: C.C.Busby
Website: www.euradcom.org
2010 Recommendations of the ECRR
The Health Effects of Exposure to Low Doses of Ionising Radiation
Edited by:
Chris Busby, with Rosalie Bertell, Inge Schmitz Feuerhake Molly Scott Catoand Alexey Yablokov
Published for the ECRR by:
Green Audit Press, Castle Cottage, Aberystwyth, SY23 1DZ, United Kingdom
Copyright 2010: The European Committee on Radiation Risk
The European Committee on Radiation Risk encourages the publication oftranslations of this report. Permission for such translations and their publication
will normally be given free of charge. No part of this publication may be
reproduced, stored in a retrieval system, or transmitted in any form, or by anymeans, electronic, electrostatic, magnetic tape, mechanical, photocopying,recording or otherwise or republished in any form, without permission inwriting from the copyright owner.
The ECRR acknowledges support from:The International Foundation for Research on Radiation Risk,
Stockholm, Sweden ( www.ifrrr.org)

ISBN: 978-1-897761-16-8
A catalogue for this book is available from the British Library
Printed in Wales by Cambrian Printers(Cover picture: XY projection of secondary photoelectron tracks induced in a 20nm
diameter Uranium nanoparticle by 1000 natural background radiation photons ofenergy 100keV;in a water particle of the same size this exposure would produce 0.04
tracks in the same XY plane. FLUKA Monte Carlo code. Elsaessar et al. 2009)

The ECRR acknowledges the assistance of the following individuals, including
contributors to its 2009 Lesvos Greece International conference where thedevelopment of its 2010 recommendations was discussed:
Prof. Elena Burlakova, Russian Federation
Dr Sebastian Pflugbeil, Germany
Prof. Shoji Sawada, JapanDr Cecilia Busby, UK
Prof. Mikhail Malko, Belarus
Prof. Angelina Nyagu, Ukraine
Prof. Alexey Nesterenko, Belarus
Dr Alfred Koerblein, Germany
Prof. Roza Goncharova, Belarus
Dr VT Padmanabhan, India
Dr Joe Mangano, USA
Prof. Carmel Mothershill, Ireland/Canada
Prof. Daniil Gluzman, Ukraine
Prof. Hagen Scherb, Germany
Prof. Yuri Bandashevsky, Belarus
Dr Alecsandra Fucic, Croatia
Prof. Michel Fernex, France/Switzerland
Prof. Inge Schmitz Feuerhake, Germany
Prof. Alexey V Yablokov, Russian Federation
Prof. Vyvyan Howard, UK
Mr Andreas Elsaesser, UK
Prof. Chris Busby, UK
Mm Mireille de Messieres, UK/France
Mr Grattan Healy, Ireland
The agenda Committee of the ECRR comprises:
Prof. Inge Schmizt Feuerhake (Chair), Prof. Alexey V Yablokov, Dr SebastianPfugbeil, Prof. Chris Busby (Scientific Secretary) Mr Grattan Healy (Secretary)
Contact: scisec@euradcom.org

Contents
Preface
1. The ECRR.

1

2. Basis and scope of this report6

3. Scientific principles

9

4. Radiation risk and ethical principles

19

5. The risk assessment black box: ICRP

36

6. Units and definitions: extension of the ICRP system44

7. Establishing the health effects at low dose: risk

63

8. Establishing the health effects at low dose: epidemiology

75

9. Establishing the health effects at low dose: mechanisms

84

10. Risks of cancer following exposure. Part I: early evidence

107

11. Risks of cancer following exposure. Part II: recent evidence

121

12. Uranium

144

13. Non-cancer risks

163

14. Examples of application

173

15. Summary of risk assessment, principles and recommendations

180

16. List of ECRR members and other contributors to this report183

All References

189

Executive Summary
Annex A: Dose coefficients
Appendix: The Lesvos Declaration

239
244
246

ECRR 2010

ECRR 2003 was dedicated to Prof. Alice M Stewart, the first scientist
to demonstrate the exquisite sensitivity of the human organism toionizing radiation. The Committee dedicates this present volume to thememory of:Prof. Edward P Radford,
Physician and Epidemiologist“There is no safe dose of radiation”
Radford was appointed Chair of the BEIR III committee of the US
National Academy of Sciences. His BEIR report in 1979 drew attention
to the inadequacies of the then-current radiation risk model. It waswithdrawn and suppressed but he resigned and published a dissenting
report. His career was destroyed.
In 2009 the ECRR awarded the Ed Radford Memorial Prize, donated by
his widow Jennifer and the Radford family in the USA to
Prof. Yuri I Bandashevsky
Physician and Epidemiologist
Bandashevsky drew attention, through his scientific research and self
publications in English, to the effects of internal radioactivity from
Chernobyl on the health of the children of Belarus and was rewarded byarrest and imprisonment.

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Preface
The presentation in 2003 of the new radiation exposure model of the European
Committee on Radiation Risk caused something of a revolution in the focus ofscientists and politicians on the adequacy of previous scientific theories of theeffects of radiation on living systems. This was long overdue, of course, sinceevidence has been available for more than 40 years that it was unsafe to use
studies of external acute radiation to inform about risk from internal chronic
exposures to evolutionarily novel radionuclides. Such a scientific paradigm
shift is not easy: the course and direction of the nuclear, military, economic andpolitical machine dedicated to the development of nuclear energy and its
military applications is monolithic and has massive inertia. It was therefore
surprising and encouraging that ECRR2003 received such attention, andeffectively brought about a new and intense interest in the flaw in the thencurrent philosophy of radiation risk: the physics-based concept of absorbed
dose. The support and encouragement for the new model, and its success inmany court cases (where it was invariably set against the ICRP model) was
perhaps assisted by the increasing evidence from Chernobyl fallout exposuresand from examination of Depleted Uranium effects which were emerging at thetime of ECRR2003. The success of the ECRR model is that it gives the correct
answer to the question about the numbers of cancers or other illnesses that
follow an exposure to internal fission products. This is immediately clear toanyone: to juries and judges as well as ordinary members of the public. It
received powerful support from reports of increases in cancer in Belarus after
Chernobyl and also from the epidemiological studies of Martin Tondel ofcancer in northern Sweden published in 2004: Tondel’s findings of astatistically significant 11% increase in cancer per 100kBq/m2 of Cs-137
contamination from Chernobyl are almost exactly predicted by the ECRR2003
model.
There have also been developments in laboratory science that can be
explained in the new model but are quite impossible to explain in the old ICRP
model. One of these is the understanding that elements of high atomic number,
like Uranium (but also non-radioactive elements like Platinum, Gold etc.) havethe ability to alter the absorption characteristics of tissues in which they areembedded. Uranium is the central element around which the nuclear fuel cycle
revolves, and huge quantities of the substance have been contaminating thebiosphere since early in the last century. It is therefore necessary to update the
ECRR risk model and include consideration of these ‘phantom radiation
effects’. The widespread dispersion of Uranium from weapons usage has madeit necessary to add a chapter on Uranium weapons. Since its founding in
Brussels in 1998, the ECRR has been joined by many eminent radiation
scientists from many countries. It will be clear from this new revised edition
that the pressure on politicians and scientists to change their understanding of
the health effects of ionizing radiation is now too great to ignore.

ECRR 2010

1
The ECRR
1.1 The background
The European Committee on Radiation Risk is a spontaneous creation of Civil
Society which was faced with clear and alarming evidence of the failure of its
democratic institutions to protect it from the effects of radioactive pollution.
Predictably, the engine which generated this development was the Green
movement, the result of another and earlier Civil Society reassessment of theaims and ideologies behind the systematic exploitation and contamination of
the planet. The ECRR was formed in 1997 following a resolution made at aconference in Brussels arranged by the Green Group in the European
Parliament. The meeting was called specifically to discuss the details of the
Directive Euratom 96/29, now known as the Basic Safety Standards Directive.
This Directive has, since May 2000, been EU Law regulating exposure toradiation and to releases to the environment of radioactivity in most countriesof the Union. The Euratom Treaty preceded the Treaty of Rome and so oncethe document had been passed by the Council of Ministers there was no legal
requirement for the European Parliament to address it. It was thus cleared
without significant amendment although, astonishingly, it contained a statutory
framework for the recycling of radioactive waste into consumer goods so longas the concentrations of itemised radionuclides were below certain levels.
The Greens, who had attempted to amend the draft with only limited
success, were concerned about the lack of democratic control over such aseemingly important issue and wished for some scientific advice regarding thehealth effects which might follow the recycling of man-made radioactivity. The
feeling of the meeting was that there was considerable disagreement over thehealth effects of low-level radiation and that this issue should be explored on aformal level. To this end the meeting decided to set up a new body which they
named the European Committee on Radiation Risk (ECRR). The remit of thisgroup was to investigate and ultimately report on the issue in a way thatconsidered all the available scientific evidence. In particular, the Committee’s
remit was to make no assumptions whatever about preceding science and toremain independent from the previous risk assessment committees such as theInternational Commission on Radiological Protection (ICRP), the United
Nations Scientific Committee on the Effects of Atomic Radiation(UNSCEAR), the European Commission and risk agencies in any EU member
State.
The ECRR's remit was and is:
1. To independently estimate, based on its own evaluation of all scientificsources, in as much detail as necessary, using the most appropriatescientific framework, all of the risks arising from exposure to radiation,
taking a precautionary approach.

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ECRR 2010

2. To develop its best scientific predictive model of detriment following
exposure to radiation, presenting observations which appear to support orchallenge this model, and highlighting areas of research which are needed
to further complete the picture.
3. To develop an ethical analysis and philosophical framework to form thebasis of its policy recommendations, related to the state of scientificknowledge, lived experience and the Precautionary Principle.
4. To present the risks and the detriment model, with the supporting analysis,
in a manner to enable and assist transparent policy decisions to be made onradiation protection of the public and the wider environment.
Shortly after the ECRR was formalised, the Scientific Options
Assessment (STOA) Unit of the European Parliament arranged (on the 5th Feb.
1998) a meeting in Brussels to consider criticisms of the 'Basic Safety
Standards' for the public and workers from exposure to ionising radiation. At
this meeting the eminent Canadian scientist Dr. Bertell argued that the ICRP,
for historical reasons to do with the development of nuclear weapons andnuclear power during the Cold War period, were biased in favour of the nuclear
industry and that their conclusions and advice in the area of low-level radiationand health were insecure.
Unfortunately, the STOA rapporteur, the late Prof. Assimakopoulos,
did not accurately report the presentation of Dr Bertell, which was wideranging and extremely critical of the ICRP and its advice (Asssimakopoulos
1998). Responding for the ICRP, Dr.Valentin, its scientific secretary, told theworkshop that the ICRP was an independent body which gave advice onradiation safety, but that those who considered this advice unsafe orquestionable were entirely free to consult any other group or organisation.
Members of the European Parliament who attended this meeting took note ofthis suggestion and agreed to support the preparation of a new report by the
ECRR which would address the issue of the health effects of radiation exposureand could provide an alternative analysis to the one which underpins present
legislation.
It was a widely held view, both at the initial meeting of the ECRR andat the STOA meeting, that enough evidence was available then showing that
low-level exposure to man-made radioactive material caused ill health, and thatthe conventional models of the ICRP and other agencies, which used the sameradiation risk models, entirely failed to predict these effects. A fresh approachto the problem was thus necessary, and in 2001 various members of theEuropean Parliament together with two charitable Trusts supported the draftingof the 2003 report.
1.2 Developments since 2003
The presentation in Berlin in 2003 of the first ECRR recommendations(ECRR2003: the 2003 Recommendations of the European Committee on

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ECRR 2010

Radiation Risk. The health effects of radiation exposure at low doses forradiation protection purposes) represented a watershed in the perception of thehazards of exposures to ionizing radiation. The ECRR published the newpragmatic risk model for calculating the effects of exposure to ionizing
radiation. The application of this model, which was based on epidemiological
data and scientific reasoning using historic absorbed dose data and known
physico-chemical behaviour of elements, gave results which explained andpredicted observations of exposed populations. It received significant attention.
The report was reprinted three times and has been translated into Japanese,
Russian, French and Spanish. A Czech edition is being prepared. It wasaddressed by the UK National Radiological Protection Board (NRPB), which
dismissed it. At the same time the UK Environment Minister Michael Meacher
founded an official government committee CERRIE to discuss the implicationsof the arguments and the evidence which supported them (CERRIE 2004,
2004a). These arguments were also addressed over the two years following the
publication of ECRR2003 by the French IRSN which put a team of scientists toreview the model. The resulting IRSN report (IRSN2005) concluded that theconcerns of the ECRR regarding the scientific basis of the current ICRP model(and all similar models) were well-founded, although IRSN took issue with thescientific basis of the model itself. It was unlikely that ECRR’s arguments
would be accepted universally: this was and is a political issue, a matter which
is discussed briefly in the present report.
In the period since 2003 and the CERRIE Committee, the radiationrisk landscape has altered totally. When the ECRR began, questions about
internal exposures and their anisotropy of effect at the cellular target, the DNA,
were largely new, or at least had been avoided by the ICRP. The
epidemiological basis of the risk model at the time was solidly that of external
exposures at high doses: the Japanese A-Bomb survivors study and its
interpretation in ICRP1990. Since then, the health effects of the Chernobyl
accident have become all too apparent, although these data seem to have been
ignored by ICRP and the UNSCEAR which have shrilly continued tocategorize such alarming reports as ‘radiophobia’. Nevertheless, radiophobia
cannot affect generations of bank voles, wheat plants, and other life forms
whose genetic developments were described by eminent research scientists
contributing to ECRR2006 and ECRR2009.
The results of real data on Chernobyl affected territories (both in the
ex-Soviet Union countries and in European countries) bore out the predictionsof the ECRR2003 model. Since then there have also been reports of anomalous
effects of exposure to the element Uranium, in molecular and in particulate
forms, as it exists in the fallout from the use of Uranium weapons, so-called
Depleted Uranium. This has led to significant effort into research on the effects
of internal exposures to Uranium. The questions raised by this research are also
those posed by ECRR in 1997 and which have formed the basis of the
ECRR2003 model, the development of weighting factors for internal exposures

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ECRR 2010

to certain isotopes based on their chemical affinity for DNA and their mode of
decay.
In 2004, Dr Okeanov of the Belarus cancer registry visited Switzerlandand presented data on increased incidence rates which were in line with thosepredicted by ECRR2003. Also in 2004, a study of cancer in northern Sweden
showed that there was a statistically significant 11% increase per 100kBq m-2
Caesium-137 contamination the 5 years following the Chernobyl fallout(Tondel et al 2004). This can be shown to demonstrate a 600-fold error in the
ICRP model, and supports the evidence given in ECRR2003 that the weapons
test fallout had a similar effect with a similar error factor. The data from
Belarus and the findings in Sweden 2004 could therefore be seen as aconfirmation of the new model.
In 2007, the latest of a long series of childhood leukemia studies was
published: this one from the German Childhood Cancer Registry, showing astatistically significant effect on child cancer in those living within 5km of
nuclear plants (KiKK 2007). The size of this study, and the affiliation of theauthors, made it impossible to conclude that this was anything but proof of acausal relationship between childhood cancer and nuclear plant exposures toradioactive releases. This study thus added to those highlighted in ECRR2003
which collectively put the error in the ICRP model as about 500 to 1000-fold.
In 2009, in an update of the study reported in ECRR2003, a metaanalysis of data on the epidemiology of infant leukemia after Chernobyl,
showed a statistically significant 43% excess in those children who were inutero at the time of the Chernobyl fallout: the error that this highlighted incomparing external and internal exposures was a 600-fold error (Busby 2009)
None of these issues were incorporated into the 2007 ICRP reportwhich ignored all the evidence and cited a selection of research papers which
supported its own model. The ICRP took its evidence from UNSCEAR 2006
which in turn failed to cite any evidence that showed that the ICRP risk model
was falsified by data.
Further, it has been increasingly clear that the internal exposures tofission product fallout and to Uranium from atmospheric weapons tests has
been the principle cause of the current cancer epidemic, a matter which waspresented in ECRR2003. Legal cases and test veteran tribunals are now
routinely won on the basis of ECRR2003 and its arguments (e.g. Dyson 2009)
Government agencies increasingly employ the model to scope the outcomes of
new practice, placing the outdated ICRP model at one extreme and the ECRR
model at the other.
The embarrassment of the ICRP came to a head with the matter of
Uranium photoelectron enhancement, a new development which is discussed in
the present report. This idea, which considers the absorbing medium and its
atomic variability, rather than assuming uniform tissue-equivalent material,
shows Uranium to be hundreds of times more dangerous that is currently
modelled by ICRP due to its high atomic number. ICRP and other satellite

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ECRR 2010

agencies have been unable to respond credibly to this development yet nothing
has changed and Uranium exposures continue to be sanctioned. Over the period
many studies of epigenetic effects, such as bystander signalling and genomic
instability have continued to falsify the scientific basis of the ICRP model, theclonal expansion theory of cancer. The model is now bankrupt.
In early 2009, the Scientific Secretary of ICRP, and editor of both its
1990 and 2007 reports, Dr Jack Valentin, resigned. At an open discussion in
Stockholm between him and Prof Chris Busby of ECRR on April 21st 2009 hestated that the ICRP risk model could not be employed to predict or explain thehealth effects of exposures to human populations. This was, he continued,
because the uncertainties for internal exposures were too great, a matter insome cases of two orders of magnitude. This has been the contention of ECRR
since its formation, and is written down in ECRR2003. Valentin also stated (inthis video interview) that since he was no longer employed by ICRP he could
say that he thought it was wrong for ICRP and UNSCEAR to ignore theChernobyl and other effects raised by the literature reports and by ECRR..
In May 2009, ECRR held an international conference in Greece,
Lesvos Island, attended by physicians and radiation specialists from eight
countries. At this conference, the ECRR2003 risk model and its development
were intensively discussed, including new evidence which has emerged since2003, as well as incorporation of the phenomenon of photoelectron
enhancement by elements of high atomic number and with a discussion of theeffects of Uranium exposure. A concluding statement, the Lesvos Declaration,
was formulated (see Appendix). The statement called for the urgent
abandonment of the ICRP risk model by governments and, as an interim
measure, the adoption of the ECRR2003 model. This model is updated here in2010 with addition of new evidence which has emerged since 2003, and theincorporation of the phenomenon of photoelectron enhancement by elements ofhigh atomic number, and with a discussion of the effects of Uranium exposure.
Since it is clear to the Committee that political and lobbying
opposition to the adoption of new rules which have massive political,
economic, military and legal implications is likely to be (and has been)significant, the area of the science-policy interface requires discussion. New
approaches must be developed with a view to obtaining secure policy fromscientific advice. Such a discussion has been added to Chapter 3. This isextremely relevant to the event which founded the ECRR. Although the Greens
were unable to significantly affect the Basic Safety Standards Directive 96/29,
they were able to amend it so that Article 6.2 required that:
Member States must review Justifications of all classes of practice
involving exposures if new and important evidence emerges.
Such is now clearly the case on both epidemiological and theoreticalgrounds.

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2
Basis and Scope of the 2010 Report
2.1 Objectivity
For reasons based on the principles outlined in the previous chapter, theCommittee takes the view that its analysis should be based on all available
information. The Committee believes that in the search for scientific objectivity
it should ‘look out of the window’, rather than following the trend of increasing
dependence on desktop mathematical modelling. Thus the Committee has
considered the results of studies published in the peer-review literature and also
reports, books and articles which have not been submitted for peer review. The
Committee believes that the approach adopted by scientific risk committees of
only accommodating evidence with accurate dose-response data published inpeer-review scientific journals has resulted in the propagation of a model whichis increasingly seen to be unsafe (Carson 1962, Bertell 1986, Nussbaum andKoehnlein 1994, Busby 1995, 2006, 2009, Sawada 2007). Furthermore, theCommittee believes that discussions in the area of radiation risk must involve
all groups in society. Therefore, although primarily consisting of scientists, theCommittee and its advisors include those physicians and specialists who must
deal with medical problems of exposed persons. For example, risk assessment
should include physicians trained in public health, occupational health,oncology, pediatrics, and scientists trained in genetics, epidemiology andbiochemistry. These disciplines are not represented in the Main Committee of
the ICRP. The regulations on membership as posted by ICRP includes:
physicists, medical regulators, radiologists, biophysicists, etc. Among thoseincluded as advisors to the ECRR are specialists such as ecologists, zoologists,botanists, risk sociologists, lawyers, politicians and members of nongovernmental organizations and pressure groups.
2.2 Basis of the report
The present report, like the 2003 report, is intended to be accessible to and to
inform decision makers who need to assess health risks to workers andmembers of the public who may be exposed as a result of practices which
involve ionising radiation. The basis of the report is a perceived failure of thepresent radiation-risk model (referred to in this report as the ICRP model) to
explain or predict real increases in ill health in a large number of groups
exposed to ionising radiation at low doses and low dose rates. Most of theexamples where this has occurred will be referred to in the body of the report
but the position of the Committee has also been affected by much that cannot
be included, for reasons of space.
This includes reports which have been published in the peer-review
literature, and reports which have not, or which started life as television
documentaries and ended as court cases. It includes consideration of those who

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voted with their feet and left areas where there were nuclear sites, regions
which slowly became wastelands where only the poorest people would live andwhere the beaches were deserted by holidaymakers and fish were increasingly
difficult either to catch or sell. It includes the stories of ordinary people whohave been affected by man-made radioactivity, in India, Namibia, Kazakhstan,
Nevada, Australia, Belarus and the Pacific Islands. It includes the massive
literature, both peer-reviewed and so-called grey literature, that surrounds thephenomena of exposure to Uranium weapons, from the Atomic Bomb test
veterans to the populations of Iraq and the Balkans and veterans of those
Uranium wars.
2.3 Scope of the report
The report will critically review the present methodology for assessing
radiation risk. It will argue that its dependence on averaging, in the area ofenergy deposition in tissue in space as well as in time, and also its dependence
on epidemiological studies involving external exposure, has resulted in major
errors in its quantification of risk from internal irradiation. It is intended thatthe report should convey sufficient evidence that the present radiological safetymodels are largely accurate for external irradiation situations involving doses
greater than 100 mSv so long as the exposures are well defined and uniform,
but break down where calculations involving averaging methods are used to
examine non-uniform doses in microscopic tissue volumes. It is the
microscopic distribution of ionizing events in tissue, from the point of view
both of the external field and of the medium of absorption, which is the criticalfactor in radiobiological damage and this has not been modelled by the physicsbased ICRP model which largely ignores molecular interactions, dealing rather
with average energy transfer.
The report will examine the historical origin of the ICRP model andwill review epidemiological evidence for its successes and failures. The reportwill consider the philosophical and methodological aspects of the science ofradiation risk and make a distinction between the inductive and deductive
approaches to establishing objective risk estimates. It will discuss the current
science-policy interface and the opportunity for (and evidence of) bias in thetranslation of scientific (experimental) knowledge into changes in policy. It
will present evidence for quantitative ranges of error in the ICRP models as
highlighted by various authors and studies and will assemble these into a set ofhazard enhancement weighting factors which form the basis of a pragmatic
approach to the problem of assessing radiation risk using the present units andquantities. It will extend radiological protection to non-cancer illnesses, lensdestruction, neurological illnesses, diabetes, immunologies and several otherradiogenic illnesses and will now specifically include a risk factor for heartdisease.

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Finally, the report will briefly outline some examples of the applicationof such a system for assessing radiation risk. A calculation of the mortality
yield of the post-war nuclear age based upon ICRP and modified ICRP risk
factors will also be presented. The approach is necessarily pragmatic. Data onradiation exposures and activities has historically been tabulated and recorded
using units of absorbed dose devised from within the ICRP system: it istherefore necessary to provide factors which may be used with this system andthis is what the Committee has striven to achieve. These factors are provided as
central estimates of hazard-enhancement for certain types of exposure and may
be used as multipliers of risk for the risk factors presently used by ICRP.
However, the Committee believes that the use of the average energy dose units
Gray and Sievert places too many constraints on the science of risk assessment
for internal isotopes and that a different, more rational system of assessing such
exposures is required. Some suggestions were made towards achieving such asystem were made at the 2009 ECRR conference in Lesvos, Greece, but theconsensus was that major difficulties existed in developing such a system andthat the bases of such a system were best employed in developing semiempirical weighting factors for the current system of absorbed doses.
2.4 References
In ECRR2003 the Committee carefully considered the question of whether theeditors should attempt to reference every statement made in this Regulators'
Edition. On the one hand, the ICRP, whose handbook ICRP90 the ECRR2003
volume was intended to supplant, provided no references. On the other hand,
the more lengthy reviews of the United Nations (UNSCEAR) and the US
Academy of Sciences (BEIR) carry selected references which support theirstatements whilst failing to cite work which either falsified or did not support
their statements. The new 2007 ICRP Publication 103 contains 286 references.
However, as the analysis in Chapter 5 shows, 90 of these are to non-peerreviewed reports by ICRP itself, whilst only 120 are in peer-reviewed journals
and these are reports mostly written by individuals associated with the riskorganizations themselves. There are no references to any effects of Chernobyl
or to childhood leukemia clusters near nuclear sites or to Uranium effects.
In ECRR 2003 the Committee considered the constraints that would beplaced on the size of the edition if all statements were fully referenced, and theloss of flow of the argument which would follow the considerable expansion of
the text. As a compromise, it decided to attach a list of the main works onwhich its beliefs are founded, without attaching each to some piece of the text.
There was some criticism of the 2003 report on the matter of references and soin this 2010 report many references are now linked to text where it is felt thatsuch a link would be valuable to the reader.

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3
Scientific Principles
Since a wise man may be wrong, or a hundred men, or several Nations, andsince even human nature, as we know it, goes wrong for several centuries on
this matter or on that, how can we be certain that it occasionally stops goingwrong and that in this century it is not mistaken?
Montaigne 1533-92, The Essays
3.1 Radiation Risk and Scientific Method
The Committee believes that it is instructive to examine the scientific basis of
the method which has been historically developed to create the radiation risk
models.
The classical exposition of the scientific, or inductive method(originally due to William of Occam) is what is now called Mill’s Canons, thetwo most important of which are:
 The Canon of Agreement, which states that whatever there is incommon between the antecedent conditions of a phenomenon can besupposed to be the cause, or related to the cause, of the phenomenon.
 The Canon of Difference, which states that the difference in theconditions under which an effect occurs and those under which it does
not must be the cause or related to the cause of that effect.
 In addition, the method relies upon the Principle of Accumulation,
which states that scientific knowledge grows additively by thediscovery of independent laws, and the Principle of InstanceConfirmation, that the degree of belief in the truth of a law is
proportional to the number of favourable instances of the law.
Finally, to the methods of inductive reasoning we should add
considerations of plausibility of mechanism.
These are the basic methods of science (Mill, 1879; Harre, 1985;
Papineau, 1996)
The questions of interest here are:
 What are the health consequences of exposure to external radiation
doses at levels below 2mSv, the approximate annual dose received
from natural background?
 What are the health consequences of exposure to novel internal
radioisotope exposures at whole organism and individual organ doselevels below 2mSv?
 Is the concept of dose applicable to internal radiation exposures?
Although risks from exposure to high levels of ionising radiation are
generally accepted, since they are fairly immediate and visible, the situation
with regard to low-level exposure is curious. There are now two mutually
exclusive models describing the health consequences of such exposure. There

9

ECRR 2010is the ICRP one, based on reductionist physics-based arguments and which ispresently used to set legislation on exposure limits and argue that low-level
radiation is safe, and one which is espoused by concerned independent publicdomain organisations and their associated scientists. These two models areshown schematically in Fig 3.1.
They arise from two different scientific methods. The conventionalmodel is a physics-based one, developed by physicists prior to the discovery ofDNA. Like all such models it is mathematical, reductionist and simplistic, andconsequently has a powerful descriptive utility. Its quantities, dose, are averageenergy per unit mass or dE/dM and in its application, the masses used are
greater than 1kg. Thus it would not distinguish between the average energy
transferred to a man warming himself in front of a fire and a man eating a red
hot coal. In its application to the problem at hand, the internal, low-level,
isotopic or particulate exposure, it has been used entirely deductively. The
basis of this application is that the cancer and leukemia yield per dose has been
determined following the external acute high-dose irradiation by gamma raysof a large number of Japanese inhabitants of the towns of Hiroshima andNagasaki. Together with this, other arguments based on averaging have beenused to maintain that there is a simple linear relationship (in the low-dose
region) between dose and cancer yield. This Linear No Threshold (LNT)
assumption enables easy calculations to be made of the cancer yield of any
given external irradiation.
By comparison, the mechanistic/epidemiological model shown at thebottom of Fig. 3.1 arises from an inductive process. There have been manyobservations of anomalously high levels of cancer and leukemia in populations
living near nuclear sites, especially those where the measurements show that
there is contamination from man-made radioisotopes, e.g. reprocessing plants.
In addition there are populations who have been exposed to man-maderadioisotopes from global weapons tests, downwinders living near nuclear
weapon test sites, and those exposed to these materials because of accidents(like the Chernobyl infant leukemia cohort), or because of work in the nuclear
industry or military. More recently, research has addressed those exposed to thefallout from the use of Uranium weapons: these have shown a wide range ofgenetic and neurological effects. A review of these findings is given later inthis report. In contrast to the averaging approach of the conventional model, thebiological model preferred by the ECRR considers each type of exposure
according to its cellular radiation track structure in space and in time. Since
ECRR2003 the effect of the absorbing element in the body has also become
important. It is not easily possible to employ such a model to predict risks
from unspecified ‘radiation dose’ to ‘populations’; rather it is concerned withmicroscopically described doses from specific isotopes or particles whose
decay fractionations are considered to interact with cells which themselves
respond biologically and biochemically to the insults and may be in various

10

ECRR 2010stages of their biological development. The dose-response relationshipfollowing from this kind of analysis might be expected to be quite complex.
In examining radiation risk, the Committee finds that thesephilosophical models are mutually exclusive and has to decide which one iscorrect. In making such a decision the Committee has employed the basic rulesof scientific method.
The Committee believes that the Linear No Threshold (LNT) model isfundamentally acceptable (with some reservations) in its application to acute,high dose, external irradiation, although it notes that the ICRP, UNSCEAR
and BEIR Committees introduce a reduction of the modelled risk by a factor of
2 for low-dose-rate exposure, which breaks the assumption of linearity. The
Committee believes that the extension of LNT to acute, external, low level
radiation may be justified on the basis of theory, since the plausibility of themodel rests on the idea of uniform density of radiation track events in
microscopic tissue volumes. For chronic external irradiation, the Committee
does not believe that the scientific method has been properly used to show that
there is either epidemiological or theoretical justification for assuming a linear
response at low doses. This is because the complex ways in which the organism
responds to low-dose radiation both at the cell and at the organism level havebeen overlooked. However, the Committee believes that the errors introducedby the assumption are unlikely to be more than an order of magnitude.
The Committee is also concerned that the assumption of linearity ofdose response is used to inform epidemiological studies of trend. A number of
epidemiological studies have shown decreasing health effects at the highest
doses and this finding has been used to suggest that radiation exposure cannot
be responsible for the effects studied, although several plausible reasons forsuch a result (e.g. high-dose cell killing) may exist. The range of error for
external irradiation effects and the mechanisms involved will be addressed in
Chapter 9.
With regard to internal radiation doses, the Committee identifies a
serious misuse of scientific method in the extension and application of the
ICRP external model. Such a process involves deductive reasoning. It falsely
uses data from one set of conditions— high-level, acute, external exposure— tomodel low-level, chronic, internal exposure. The procedure is scientificallybankrupt, and were it not for political considerations, would have been rejectedlong ago. On the other hand, it should be clear that the radical model shown in
Fig 3.1, suggesting high risk, conforms to all the requirements of the scientificmethod listed at the beginning of this chapter. Man-made radioisotopes, often
in the form of ‘hot particles’, are common contaminants of the areas near
nuclear sites where there are cancer and leukemia clusters, and of nuclear site
and test site downwinders, and of fallout-exposed populations. This satisfies
the Canon of Agreement. The contingency analysis tables with control
populations for such studies show that the Canon of Difference is also satisfied:people living in more remote regions than the downwinders show lower levels

11

ECRR 2010of illness. The Principle of Instance Confirmation is fulfilled since so manystudies have shown that increases in cancer and leukemia follow exposure
regimes at low dose. We are left only with Plausibility of Mechanism, which
will be addressed later in this report.
The Committee's position on the scientific applicability of the ICRP
model to the yield of fatal cancer in a range of exposure types is outlined inTable 3.1.
It is important to note that science and scientific conclusions are not thesame as conclusions based on legal styles of evidential analysis. Science is nota simple question of weighing evidence for and against a theory or model ofreality as it might be in a court of law or in everyday decision-making. The
rules are strict. If one single piece of experimental evidence cannot be
explained or incorporated into a theory, the theory has to be discarded (Kuhn
1962, Popper 1962). Therefore the existence of the nuclear site child leukemia
clusters alone is enough to falsify (to prove wrong) the ICRP risk model; yetnothing has been done despite these data emerging in the 1980s. The
Committee feels that it may be illuminating to ask how such a state of affairs,
once set up in ignorance, becomes crystallised and difficult to challenge, evenwhen large numbers of sick and dying draw attention to the existence of an
insecure model. The conservative nature of science and its systems wasconsidered in the late 1950s by an eminent and past member of the British
Royal Society, the Nobel-Prize winner, chemist and economist Michael
Polanyi.
Table 3.1 Errors associated with ICRP extension of acute high dose externalstudies to other types of exposure
Type ofexposure
External
acute>100mSv
External<100mSv
Internal<100mSv
Internal
High Z
elements

Is ICRP model applicable?
Yes

Uncertainty in error factor for
fatal cancer identified by ECRR
0.5 to 25

Very approximately but
problems with cell and organism
responses.
No

1 to 2000

No

1 to 2000

1 to 50

Polanyi, was interested in the scientific method, and in scientists: his writings
pre-dated the Science War philosophers like Kuhn and Latour. He was awarethat at any time, the scientific world view might be completely wrong. In

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asking how we know anything at all and how we build up a picture of the ‘realworld’ Polanyi saw many similarities between scientists and primitive witchdoctors like the Azande who had been studied in the 1930s by theanthropologist Evans Pritchard who wrote:
They reason excellently in the idiom of their beliefs, but they cannot reason
outside, or against their beliefs, because they have no other idiom in which toexpress their thoughts. The contradiction between experience and one mystical
notion is explained by reference to other mystical notions.
E. Evans Pritchard, Witchcraft, Oracles and Magic among the Azande,
1937
Addressing the supposedly scientific world view, Polanyi concluded:[For] the stability of the naturalistic system we currently accept, instead, restson the same logical structure as Azande witchcraft beliefs. Any contradiction
between a particular scientific notion and the facts of experience will be
explained by other scientific notions. There is a ready reserve of possible
scientific hypotheses available to explain any conceivable event. Secured by its
circularity and defended by its epicyclical reserves science may deny or at least
cast aside as of no scientific interest, whole ranges of experience which to theunscientific mind appear both massive and vital.
M. Polanyi FRS, Personal Knowledge, 1958
The Committee has concluded that the ICRP scientists and risk models aregood examples of such systems of closed scientific communities andepicyclical logic. Polanyi’s comparisons with Azande witch-doctors arefamiliar territory to those who have registered the sequences of denials andimplausible explanations which have followed discovery of the Sellafield(Seascale) child leukemia cluster and many other examples of the failure of the
ICRP risk models. In the following chapter we examine the origin of the ICRP
risk model and see how it has become the deductively based interpretative
machine that rejects automatically and epicyclically any experience which toordinary people seem both massive and vital.
3.2 The Science Policy Interface and Bias: CERRIE
The Azande problem is what psychologists term group-think. (Janis and Mann
1977). It is not restricted to the ICRP and those supporting the ICRP approache.g. UNSCEAR, NCRP, and BEIR. Since the UK Mad Cow Disease episode in
the 1990s it has become increasingly clear that scientific advice on policy canbe seriously biased in this way. In the Mad Cow episode, a scientific committee
advised the government (against outside scientific advice and experimental
evidence) that the agent could not cross the species barrier. They were wrong

13

ECRR 2010and many members of the public have died because of their error. Interestingly,
the Chair of the Committee which gave that wrong advice was at the same time
the Chair of the UK National Radiological Protection Board, Sir Richard
Southwood.
The Policy Information Network on Child Health and Environment,
PINCHE, an EU-funded network of 30 or more eminent doctors and scientists
from several countries of Europe, spent 4 years discussing this issue of the
Science Policy Interface to produce a report which was commissioned by the
EU. The PINCHE concluded that science advice from selected committees wasregularly biased by the selection process of references to support theconclusions. These conclusions were generally biased by the affiliations of thecommittee members and secretariat and tended to support, in economic healthas opposed to human health, those decisions which resulted in least damage totheir affiliated institutions or industries (Van den Hazel et al 2006). The
solution to this, PINCHE agreed, was to found oppositional committees wherescientists were funded to support both sides of any argument which informedon environmental risk, an idea which was suggested by Scott Cato et al 2000.
The groupthink concept is now widely accepted: the US Pentagon trains askeptics corps to battle decisions and planning errors made through groupthink,a process called Red Teaming.
The Committee on Radiation Risk from Internal Emitters CERRIE was
set up by the UK Environment Minister Michael Meacher in 2001 along justthese lines. Its remit was to discuss the evidence for the failure of the ICRP
model for internal emitters and present both evidence which supported andopposed such a belief. In the event, this process failed when the Minister was
removed in 2003 before the final report was published and a new Environment
Minister, Elliot Morley, was appointed by Tony Blair. Morley shut down theCommittee before it could carry out the key research which had been agreed todecide the issue and legal threats were used to prevent the oppositional reportbeing included (see endnote Morley 2010). The minority oppositional report(which was excluded by the legal treats) was separately published in 2004
(CERRIE 2004b).
3.3 The scientific basis of ICRP2007
Naturally, bias extends to ICRP 2007 which cites the main CERRIE report but
not the oppositional report. With the results of PINCHE on biased selection ofreferences in mind it is quite informative to examine the reference base for
ICRP2007. There are 286 references: their general description is shown in
Table 3.2.

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ECRR 2010

Table 3.2 Distribution of references in ICRP2007
Number of references
91
21
52
103
20

Organisation beingreferenced
ICRP/ ICRU/IAEAUNSCEAR/NCRP
Books and reports
Peer-reviewed journals
ICRP member’s paper

Peer reviewed
No
No
No
Yes
Yes

Of the 123 references to peer-reviewed literature many of them are to personnel
associated with the risk agencies in some way or other publishing in ‘house
journals’ like the Journal of Radiological Protection, whose editor is Richard
Wakeford, until recently Chief Scientist for British Nuclear Fuels. There arereferences to some bizarre journals like the Central European Journal of
Occupational and Environmental Medicine. This latter reference is to work bya member of the ICRP Committee, A. Akleyev. One reference is to The
inheritance of pyloric stenosis by Carter C.O published in the British Medical
Bulletin in 1961. How can this be more valuable or relevant to radiologicalprotection than the many references to Chernobyl effects available to ICRP orprovided in the ICRP 2007 internet consultation by ECRR scientists?
The introduction to ICRP 2007 states: We could not have done it
without your help! referring to an internet dialogue where ICRP canvassed
comments on the draft recommendations. Many of the ECRR scientists
communicated within this ICRP ‘consultation’ process, and theircommunications and references can still be read on the ICRP website.
However, none of these suggestions or references made it into the final edition.
Indeed there was one important and relevant paragraph which was in the 2005
ICRP draft on the internet.
It stated:(50) For radiations emitted by radionuclides residing within the organ or
tissue, so-called internal emitters, the absorbed dose distribution in the organ
depends on the penetration and range of the radiations and the homogeneity of
the activity distribution within the organs or tissues. The absorbed dose
distribution for radionuclides emitting alpha particles, soft beta particles, lowenergy photons, and Auger electrons may be highly heterogeneous. This
heterogeneity is especially significant if radionuclides emitting low –range
radiation are deposited in particular parts of organs or tissues, e.g. Plutonium
on bone surface or Radon daughters in bronchial mucosa and epithelia. In
such situations the organ-averaged absorbed dose may not be a good dose

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quantity for estimating the stochastic damage. The applicability of the conceptof average organ dose and effective dose may, therefore, need to be examined
critically in such cases and sometimes empirical and pragmatic proceduresmust be applied.
But ICRP did nothing to change any of the dose coefficients for isotopes thatcaused such exposures or to apply such empirical and pragmatic procedures.
and the embarrassing paragraph above was quietly dropped from the final
ICRP 2007 report.
This brief review of the 2007 ICRP report demonstrates that there has
essentially been no change in the model from that which was published in
1990, and that new evidence and arguments which scientifically falsify thatmodel have been totally ignored. The ICRP continues to support the same risk
factors for exposures to ionizing radiation and its model is still the basis forlimits to releases to the environment. The ICRP 2007 model does not discuss
the evidence: it is selective and partial and clearly does not conform to thephilosophical requirements of science outlined in this chapter. As the Lesvos
Declaration in the appendix demands, it must now be abandoned.
3.3 Peer review, research funding, and the Scientific Consensus
In responding to concerns about the clear failures of the ICRP model to predictor explain observations, politicians and regulators commonly refer to theconcept of a scientific consensus. The Committee has made it very clear in thischapter and elsewhere that the political understanding of science as some kindof process which goes forward through the mechanisms of research, peer
review of reports and acceptance of change by a ‘scientific community’ which
represents a scientific consensus on any matter is dangerously inaccurate. Oneof the reasons for this which has not been discussed is the control of peerreview publication of research reports. In this model of science, before any
research is believed to be ‘scientific’ it has to be published in a learned journaland subjected to peer-review. The reviewers are anonymous and may dismissthe contribution: in which case the editor usually rejects it. Thus the evidence isinvisible from science and cannot become part of the scientific consensus. The
problem is, of course, that reviewers will generally dismiss any research which
contradicts their own beliefs; and if they do not, often the editor will. This
process has kept many important results from being presented and therefore
being incorporated into any scientific consensus. A good example of this bias isafforded by the Journal of Radiological Protection which appeared in the
1970s, in which those who believe in the ICRP system publish. Their papers
are reviewed by each other, and therefore regularly appear: thus giving theirbeliefs and their model some spurious credibility; naturally, any contributions
which disagree are sent out to referees and dismissed. The current editor of thisjournal, Richard Wakeford, of British Nuclear Fuels, Sellafield, is a champion

16

ECRR 2010of the adequacy of the present approach. The editorial board reads like a list of
those who work for the nuclear regulatory bodies, ICRP. UNSCEAR, IAEA
and so on worldwide with a few nuclear energy workers thrown in. We see
Jack Valentin of ICRP on this board. This process represents one way in which
the evidence that the ICRP model is incorrect is excluded from ‘science’. In a
most recent example, the UK Health Protection Agency (RadiologicalProtection) withdrew from a stakeholder dialogue involving ECRR on theSecondary Photoelectron Amplification Effect (described below). The reason
was that HPA’s initial mathematical treatment was clearly absurd andcontained many basic errors. When these were pointed out, the response wasthat there would be no further discussion on the issue: a paper was to be
published in the peer review literature. The paper, by the Deputy Director of
HPA(RP) John Harrison, is apparently to appear in the Journal of RadiologicalProtection where it will have been reviewed by those with a bias in favour of
accepting it.
And there is another way in which the scientific consensus is skewed.
Researchers who do manage to get dissident results into the scientific media
lose their research funding and often their jobs (see Viel 1998). Politicians anddecision makers should be cautious therefore in dismissing research which is
not published in the peer review system (so-called grey literature). This was theconclusion (for exactly these reasons) of the science–policy group in the EU
funded PINCHE report conclusions (van den Hazel et al 2005).

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ECRR 2010

Fig. 3.1 Mutually exclusive models derive from induction versus deduction.
The “high dose acute A-Bomb survivors” group had mean external doses of
200mSv but are strictly a “high dose rate” group.

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ECRR 2010

4
Radiation risk and ethical principles
4.1 Problem to be addressed
The release of radioactive materials into the environment results in thecontamination of living organisms. This internal radiation exposure andexternal radiation from the same radioactive materials in the environment cause
damage to cells. Recent research into genomic instability and bystander
signalling suggests that such exposure results in death or mutation in roughly athird of all somatic or genetic stem cells intercepted by a radiation track. One
high-impact consequence of this is that a small proportion of the descendants ofthese irradiated cells may become cancerous and kill the individual. Other
consequences are that the general loss of cells to the organism may result inboth specific and general impairment of health. Third, these effects in germline
cells are not restricted to the exposed individual and may be passed on to thenext generation.
The question to be answered is: is it ethically acceptable to sanction theoperation of an industry for which this circumstance is an inevitable outcome?
Two other questions may be asked:
 First, is such a sanction a case of political decision making after
consent has been given by an electorate, and if so, has it followed
adequate debate and full access to accurate information?
 Second, is the answer to the ethical question subject to a de minimis
threshold such that small amounts of harm may be sanctioned if theoutcome is justifiable in terms of a greater good? This latter question
seems to have been implicitly asked and answered, but as theCommittee will argue (para. 4.4.7), the basis of the answer isphilosophically questionable and should be revisited.
4.2 Human chauvinism
Before embarking on an exploration of the case to be made for and against
radioactive emissions from the perspective of different ethical theories theCommittee acknowledges that the major ethical theories presented here
particularly those of rights and utilitarianismare anthropocentric. That is tosay, they agree about the scope of moral decision making, and that it should
include only one species: our own. Routley and Routley have challenged what
they refer to as ‘the inevitability of human chauvinism’ in the following terms.

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In our enlightened times, when most forms of chauvinism have beenabandoned, at least in theory, by those who consider themselves progressive,
Western ethics still appears to retain, at its very heart, a fundamental form ofchauvinism, namely, human chauvinism. For both popular Western thought
and most Western ethical theories assume that both value and morality canultimately be reduced to matters of interest or concern to the class of humans(Routley and Routley, 1979).
The drawing up of guidelines for exposure to ionising radiation as aresult of the civilian nuclear power programme is a typical example of suchhuman chauvinism. All the models are designed to determine doses to people,
despite the obvious fact that all wild and most domestic animals spend moretime outside, and are thus more subject to radiation, than most people.
The ethical problems with routine contamination of people byradionuclides presented in this chapter are fairly compelling in themselves, but
a serious consideration of animal rights would suggest a vast inflation in thelevel of harm caused. The Committee welcomes the efforts that various
agencies (e.g. IAEA 2002, ICRP 2002) have made in exploring various ethicalapproaches to protection of the environment as distinct from protection ofpeople. The Committee does not set out to rehearse them, but notes that there isa general tendency to recognise that the environment has its own moral
standing - i.e. towards recognising the validity of protecting the environment
for its own sake, rather than for the sake of its human utility.
The positions thus taken may be far more rational than they at firstseem to western minds. Major eastern philosophical/religious systems which
are frequently cited (e.g. by IAEA 2002) as the sources of non-anthropocentric
views of environmental protection hold to the law of action, motive and result the idea that harm deliberately done inevitably returns to the perpetrator, almost
always in a future life. The fact that this is seen as an obstacle to thepreeminent goal of achieving enlightenment throws a fresh light on the
supposed non-anthropocentrism of eastern attitudes to the environment. Action,
motive and result also raises questions about the long-term interests of anyone
engaged in radiation protection to the extent that they were deliberately toignore relevant evidence. Ironically, hoping that those responsible might suffer
as a result of the harm their actions caused would itself be a further obstacle toenlightenment.
In view of the difficulties of identifying and quantifying detriment to
the environment at the low levels of dose commonly found and the consequentissue of whether such doses matter, it may be helpful to bear in mind an
important insight from the debate between environmental ethicists. Mary
Midgley (1983) identifies a problem commonly associated with certain
environmentally and socially destructive processes; that although they may begreeted with general moral repugnance it is often difficult to substantiate the20

ECRR 2010

objections to them. To illustrate her point she offers the following entry fromthe diary of Robinson Crusoe:
19 Sept. 1685. This day I set aside to devastate my island. My pinnace being
now ready on the shore, and all things prepared for my departure, Friday’s
people also expecting me, and the wind blowing fresh away from my little
harbour, I had a mind to see how all would burn. So then, setting sparks andpowder craftily among certain dry spinneys which I had chosen, I soon had it
ablaze, nor was there left, by the next dawn, any green stick among the ruins . .
(Midgley, 1983: 89).
Midgley identifies that it is the moral tradition of the (western) Enlightenmentthat has made our objections to such activity unstatable. In her words:
Today this intellectualist bias is often expressed by calling the insights ofcommon morality mere ‘intuitions’. This is quite misleading, since it gives theimpression that they have been reached without thought, and that there is, bycontrast, a scientific solution somewhere else to which they ought to bow—as
there might be if we were contrasting common-sense ‘intuitions’ about thephysical world with physics or astronomy.
(Midgley, 1983: 90).
Interestingly in view of our subject, she sees the model as drawn from atomic
physics.
4.3 The Ethical Basis of the Civilian Nuclear Power Programme
4.3.1 Introduction
Para. 101 of the ICRP 1990 Recommendations represents the closest that theinternational nuclear community has come to providing an ethical basis for its
activities. The paragraph states:
Most decisions about human activities are based on an implicit form ofbalancing benefits against costs and disadvantages, leading to the conclusionthat a particular course of action or practice either is, or is not, worthwhile.
Less commonly, it is also recognised that the conduct of a practice should be
adjusted to maximise the net benefit to the individual or society . . .When thebenefits and detriments do not have the same distribution through the
population, there is bound to be some inequity. Serious inequity can be avoided
by the attention paid to the protection of individuals. It must also be recognisedthat many current practices give rise to doses that will be received in the
future, sometimes the far future. These future doses should be taken into
account in the protection of both populations and individuals.
The ICRP, their satellite committees and those political decision makers thathave come after them appear not to have addressed explicitly the philosophical21

ECRR 2010

and ethical basis of their recommendations or indeed the moral justification forthe health consequences that are an inevitable result of the radioactive
emissions of civilian nuclear power programmes. However, para. 101, cited
above, does identify implicitly the source of the ethical thinking of theCommittee, and it appears to be planted firmly in the utilitarian tradition. The
method of decision making that results from such a philosophical foundation isinevitably that of cost-benefit analysis. The members of the ICRP clearly
assumed that such a moral position was universally accepted, and perhaps the
only source of ethical guidance. This chapter, which outlines the position of the
ECRR, takes a broader view, addressing the issue of the health consequences ofnuclear power and other sources of radioactive contamination from theperspective of a variety of ethical theories, as well as providing a critique of theutilitarian position, especially as applied to nuclear power. It proceeds toaddress specific aspects of decision making that would need to be resolved for
civilian nuclear power to have a firm ethical foundation.
Civilian nuclear power is an interesting case of policy making, since it
appears to have never faced ethical or democratic scrutiny. Although this is notstated, it can only be deduced that such justification was felt unnecessary, due
to the close link between the civilian and military nuclear industries and theorigin of both in the period of the Cold War. In an era when it was believed that
we would be better off dead than red, a few extra deaths as a result of nuclear
processes may have seemed a small price to pay in exchange for our place atthe big table of international diplomacy. Given the changed political situation
an evaluation of the ethical foundation of nuclear power is long overdue.
4.3.2 The Health Consequences of Nuclear Power as Seen from Alternative
Ethical Perspectives
Utilitarianism
Utilitarianism is well known as the moral philosophy that assesses the ethicalrightness of an act or policy on the basis of its ability to maximise the total
aggregated happiness of all the members of society. As one environmental
ethicist expresses it, ‘utilitarians consider an action or a decision to have themoral quality of rightness to the extent that it leads to: . . . the maximisation ofgood consequences, conceived in terms of social welfare or utility, over thelong run (Sagoff: 1988: 171). In other words, the central tenets of utilitarianism
are that results are the key to a moral evaluation of actions and that to assess
their moral rightness we should compare these results in terms of the happinessor unhappiness that they cause (Shaw, 1999).
The objective of this ethical position is the maximisation of total
utility, or happiness. It is important to grasp that it has nothing to say about the
distribution of that happiness (Shaw, 1999). In fact, one of the originalcriticisms of utilitarianism is that it would be quite consistent with a slave
society. Its concern is to maximise well-being on average. This is interesting in

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the context of a discussion of the ethics of nuclear pollution, where doses to the
public are also considered on average, which leads to many of the inaccuraciesof health-risk models identified elsewhere in this report. The policy mechanism
whereby these ‘average well-being’ calculations are translated into policy, thecost-benefit analysis, thus has basic philosophical problems as well as thepractical difficulties explored later in this chapter.
Utilitarianism has always had an immediate appeal, and especially topolicy makers. Shaw (1999:2) considers that ‘utilitarian goals have shaped
public decision-making in the twentieth century’. An important explanation for
the appeal of utilitarianism is its simplicity. It reduces hard moral cases tosimple mathematical equations, which allows policy makers to believe boththat they are in control of a desperately complicated situation, and also thatthey can come up with an answer that is easy to defend.
The downside of the utilitarian calculation is that it yields outcomesthat are morally repugnant to many citizens (see Shaw, 1999). For example,
most citizens believe it would be intolerably callous to allow premature babies
to die, although the costs expended on such a small number of members of the
population are immense. By any rational utilitarian calculation these costs
would increase the sum of human happiness more if they were spent finding
improved means of pain relief or a cure for cancer. Yet the importance thatpeople place on individual moral worth in contrast to the sum of humanhappiness is illustrated by the public horror that was displayed when children
died during surgery by incompetent doctors in Bristol. Although the absolute
number of deaths was small by comparison with the total number of heart
operations carried out annually, the moral outrage was vast. Thus citizens
appear to agree with the conclusion of Anne Maclean, who in a discussion of
the field of bioethics, claims that ‘pure utilitarianism eliminates the essential
ingredients of moral thinking’ (1993).
Perusal of government documents makes it clear that considerations of
average well-being do tend to take precedence over individual rights. For
example, a recent report into the deleterious health consequences of living near
landfill sites was played down by its authors on the basis that the number ofchildren actually born with the defects that had been shown to be related toproximity to a landfill was small. While this follows the logic of the utilitariancalculus it is unacceptable to our moral sentiments, so that the cluster ofcongenital malformations near the Nant-y-Gwyddon tip in South Wales caused
a national outcry.
Utilitarianism allows the death from leukemia of children who live
near nuclear sites to be balanced by the societal gain from the energy source, or
the Plutonium for weapons to defend the country; it can balance the warmthdelivered by electric fires in millions of homes against breast cancer of those
women living downwind of the nuclear power station. It may have an appeal tothe policy maker, but it does not follow the moral sentiments of the citizen.

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This may be part of the explanation for the growing gulf of trust between
politicians and the citizens they are elected to represent.
Rights-based theories
It appears that, implicitly or explicitly, utilitarianism has ruled the ethical roostand provided the philosophical basis for policy making for over a century in the
UK and elsewhere. Its popularity in the United States has been undermined by
the growth in popularity of a new ethical system based on the concept of rights.
If utilitarianism may be characterised as making the right subservient to thegood, then rights-based theories may, by contrast, be considered to hold thatthe good is always subservient to the right. This has far-reaching implications
for policy making in general and for the civilian nuclear power programme inparticular.
The starting-point for such theories is a rejection of the averaging
principle of utilitarianism, which would sacrifice the well-being of any given
individual for the sake of the greater good of the whole community. Rightsbased theories argue that each human being has inviolable rights as anindividual and that the state may only override these with the express
permission of the individual.
Ronald Dworkin, who offers a strong legal defence of rights, argues fortheir fundamental importance in Taking Rights Seriously (1977): ‘the invasionof a relatively important right must be a very serious matter. It means treating aman [sic] as less than a man’. In terms of the conflict between utilitarianism
and rights-based moral theories he argues that the state ‘must not define
citizens’ rights so that these are cut off for supposed reasons of the general
good’.
So, how might we apply rights-based ethical theories to the activities of
the nuclear industry? While debate continues about the level of harmfulness ofemissions, it is accepted by all sides that the production of energy from nuclear
sources will create a fixed amount of radioactive pollutants which will be
released to the environment and will inevitably contaminate the bodies of those
who live in that environment. Such activity, carried out without the fullknowledge of the citizenry, and certainly without their informed consent,
represents an infringement of the most fundamental natural right: the right tothe inviolability of the body. This right is considered basic in rights theory andis used to justify, for example, the use of violence in self-defence if one’s bodyis under attack.
We may find a more specific statement of the individual’s right not tobe contaminated in the UN Declaration of Human Rights where Article 3
states: ‘Everyone has the right to life, liberty and the security of the person’.
Although it has yet to be tested in court, there seems a strong prima facie casethat contamination of citizens’ bodies with nuclear waste represents an
unacceptable threat to the security of the person, and is therefore illegal underinternational law. From a rights perspective, in order for the nuclear industry to

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continue to operate legally, all those who might potentially be contaminatedwould have to be accurately informed about the true risks to their health fromsuch nuclear processes, and would have to agree that the processes should
continue.
Rawls's Theory of Justice
An influential contribution to moral and political philosophy was made by John
Rawls, with the publication of his A Theory of Justice in 1971. While this is nota rights theory as such, Rawls is often discussed in connection with suchtheories since his aim was to determine principles of justice that would ensureethically justifiable distributions. His concern was primarily the distribution of
wealth but we may extend his theory to consider the distribution of ‘illth’
associated with nuclear processes. Rawls’s central intellectual tool is the ‘veil
of ignorance’: he suggests that a distribution is fair if a citizen would choose it
from a range of alternatives without knowing which position in the distribution
she or he would find her- or himself in. Hence the theory stands incontradiction to utilitarianism which only maximises total welfare and hence
could easily admit a small number of very unpleasant situations so long as they
were balanced by pleasant ones. In Rawls’s system, by contrast, an individual
would protect her- or himself against the worst possible outcome. In such amoral universe the question facing the citizen would be, should the nuclear
industry be allowed to continue emitting radioactive waste which will cause asmall number of deaths. The citizen would be behind the ‘veil of ignorance’and hence would not know whether it would be his or her child or grandchildthat might be the one to develop leukemia. The chance would be small, butwould it still be a situation they would potentially accept?
For Rawls, such questions are, in any case, of second order. The
overriding commitment of his moral theory, as with those discussed in theprevious section, is with the absolute right of the person. As he expresses thispoint:
Each person possesses an inviolability founded on justice that even the welfare
of society as a whole cannot override. (Rawls, 1971: 3).
This ‘inviolability’ may be considered to include bodily inviolability, hence thecontamination of citizens with radioactive emissions without their knowledge
or consent would not be possible within a just state, no matter how much theprocess that produced the emissions benefited society as a whole. Since thecitizens of modern nations have never given their consent to the contaminationof their bodies by the routine emissions of nuclear wastes (and are unlikely
even to be aware that such a process occurs on a daily basis) such emissions
are, according to rights-based theories, simply immoral.

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Virtue ethics
The strand of moral philosophy identified as virtue ethics provides analternative view of how we might judge behaviour to be ethical. Rather thanbeing based on a technique involving measurement and calculation, or on aclaim to the fundamental inviolability of rights, it proposes instead that
ethically sound behaviour is behaviour that could be considered virtuous.
Theorists of this school may at first appear vulnerable to the suggestion thatthey are not actually providing useful guidance, since there can be no objective
agreement about which types of behaviour are virtuous. However, a little
consideration makes it clear that in fact such subjectivity problems afflict theother theories also. For example, utilitarianism rests on a no less subjective
judgment about what ‘happiness’ or ‘utility’ may be. And similarly there canbe no absolute agreement about which rights are fundamental and inviolable
when two rights come into conflict. Virtue ethics, by contrast, makes no claim
to objectivity. According to Rosalind Hursthouse (1999), ethics cannot begiven a foundation from a neutral point of view; rather, we all have an acquired
and subjective ethical outlook.
This is a philosophical position with little appeal for policy-makers,
since it does not provide them with water-tight answers to hard cases.
However, we may consider that it is a more accurate reflection of the complex
reality of moral decisions. Although virtue ethics is a system that begins withthe behaviour of the individual, it has important lessons for policy-makers.
First, we may conclude that any system that constrains individual virtue ismorally damaging to the individual. Thus a generalised acceptance of a form ofvicious behaviour, for example lying, will encourage a general cultural
response in the direction of greater dishonesty, encouraging a general decline in
the standard of virtue. By contrast, behaviour that is generally recognised to be
virtuous operates as a kind of moral education to others.
In terms of the nuclear industry we may draw some important lessons
from a virtue ethics approach. The operation of the civilian nuclear power
programme has been founded on some highly dubious moral decisions. Perhaps
most important is that of secrecy. Initially because of the relationship with
nuclear weapons, and now because of the threat of terrorism, it is clear that thenuclear industry has tended to operate in an atmosphere of secrecy anddishonesty. One example is the secrecy over the full extent of and possible
consequences of the radioactive releases following the Windscale reactor fire in
1957. There are many others. From the perspective of virtue ethics this may beconsidered to undermine a virtuous society. The justification of pollution andhealth detriment, and the minimisation of the risks involved, has also appeared
to demonstrate a callousness that is not conducive to a morally sound society.

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4.4 Ethical Considerations for Policy-Makers
4.4.1 Problems with cost-benefit analysis
Cost-benefit analysis is a methodology now favoured by policy-makers inattempting to decide whether a given process should be allowed to be initiated.
It is the method used for deciding whether to grant a licence to build a new
nuclear power station, for example. However, there are considerable problems
with this method as an aid to policy-making.
In the first case it relies on the ability to measure costs and benefits
accurately. It is notoriously difficult to measure environmental costs (see e.g.
Pearce, 1993; Funtowicz and Ravetz, 1994). As is demonstrated elsewhere inthis report, in the case of nuclear power, measurement of the negative healthconsequences is equally intractable. Similarly, the benefits of any process may
often be assessed and given a monetary value in a way which views the processfrom within an existing paradigm. For example, the value of energy is assessed
within a policy framework which plots an inevitable increase in our need forenergy, ignoring the possibilities of energy-saving and demand management.
Behind the assumption that we will always and inevitably need more energy
lies the further assumption that economic growth will continue, an assumption
which has long been the subject of fierce debate (see e.g. Daly, 1973). Withinsuch a set of assumptions the benefits of extra energy are likely to beoverstated.
Cost-benefit analysis has been identified as having its origin in theutilitarian philosophy and this explains its second major flaw: the question of
the equitable distribution of costs and benefits. We have seen that utilitarianism
is based on an averaging process, and cost-benefit analysis similarly averages
costs and benefits across all members of society, considering what it calls the‘social utility function’, which represents the simple addition of all individuals’
utility functions. But the reality of industrial processes is that some segments ofsociety bear a disproportionate share of the cost. This is acknowledged
explicitly in ICRP's para. 101 above, although ICRP ignores the need to justify
it on ethical grounds.
Tietenberg (2000) offers an example from the United States. In 1979 asociologist from Texas wrote a report about a campaign by African-Americans
in Houston to oppose the siting of a hazardous waste site in their community.
They lost the campaign. He suggested that race and not just income was afactor in the land-use decision. A fuller study in 1983 found that 3 of the 4commercial hazardous facilities were in African-American communities; thefourth was in a poor community. A study by the Centre for Policy Alternatives
in 1994 found that the situation had worsened.
One can easily draw parallels with the situation in the UK, where all
the nuclear power-stations were sited in areas of high unemployment. The
reason cited was the attempt to spread the benefits of the technologicalrevolution, yet it can easily be seen that the costs have also been borne unduly

27

ECRR 2010by these people, as evidenced by the Sellafield leukemia cluster. This policy
has since been enshrined in a planning directive which zones areas of highunemployment and allows lower standards of environmental protection there inorder to attract job creators.
The costs of any potentially hazardous industrial process are always
minimised by siting the facility in a poor area for several reasons:Land costs are lower in these areas;
Future legal liabilities would be minimised, since the poor will be less able
to fight legal actions;
Poor communities will require lower compensation, since their potential
future earnings lost through early death are lower.

So the averaging methodology used during cost-benefit analyses ensures thatthe costs of the process under consideration will fall unduly on the poor. But
what about the benefits? Wealthier households have a higher level ofconsumption and therefore make greater demands for the processes thatgenerate environmental pollutants. For example, a home with a dishwashingmachine and central heating will demand more electricity, and hence will be
responsible for a larger share of the pollutants resulting from the production ofenergy. It will have received more of the benefits of energy production, but islikely to have paid less of the costs.
4.4.2 Problems with discounting
A key problem with environmental decision-making, as identified earlier, isthat present actions have effects long into the future; this is a particular concern
in the case of nuclear power, whose waste products will be hazardous for a
future longer than we can reasonably include in our policy-making. In order tomake choices when the benefits and costs may occur at different points in timepolicy-makers use a method known as calculating the present value, which they
achieve by discounting future values using a discount factor based on themonetary interest rate.
In other words, £1 invested today yields £1.10 in a year’s time if theinterest rate is 10%. So the present value of £1.10 received a year from now is£1. We can find the present value of any amount of money x received one year
from now by computing:x/(1+r)where r is the current rate of interest, now referred to as the ‘discount rate’.
What would be the value of your £1 in two year's time at an interest rate of r?
Because of compound interest its value would be:

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2

£1(1+r)(1+r) = £1(1+r)

Hence the present value of x received two years from now is:2x/(1+r)If we follow the same pattern we find that the present value of a one-time net
benefit received n years from now is:PV[Bn] =Bn (1+r)n

The present value of a stream of net benefits [B0, . . ., Bn] received over a
period of years is computed as:nPV [ B0 ..... Bn  (1  r )
i 0

Bi

i

Where r is the interest rate and B0 is the amount of net benefits received
immediately.
This method is used to gain a clearer idea of the present value of somethingwhich will yield future costs and benefits as well as present ones. The values ofbenefits and costs to future generations are greatly affected by the process of
discounting, which has a fairly limited time horizon so that the present value ofa benefit or cost tends to converge to its lower limit of zero within a finite, andquite short time. The process of discounting itself reduces costs and benefits
occurring in the far distant future to virtually zero within a finite time. As
Hussen (2000: 329) states for the benefits:
When the time horizon of a project under consideration is fairly long, as is thecase for many environmental projects, the difference between private andsocial discount rates that are within the range 3 to 5 percent is irrelevant. Thisis because discounting reduces benefits coming in the far distant future to
virtually zero within a finite time, as long as the discounting rate is positive.
What matters is the very fact that a positive discount rate is used.
The same applies to costs, so that the process of discounting radically reduces
the importance of long-lasting costs, thus most of the costs of the nuclear
industry, which will be paid thousands of years into the future, will bemathematically removed from cost-benefit analysis.
The whole process of discounting implies that gains and losses tosociety are valued less the more distant they are in the future. So long as thediscount rate, however small, is positive (implying that jam today is always

29

ECRR 2010preferable to jam tomorrow) then discounting will always imply unequal
weighting of costs and benefits over time. Can we justify this ethically when
we are enforcing costs on future generations? Taking seriously the calls forintergenerational equity would require us to use a discount rate of zero.
4.4.3. The precautionary principle
The precautionary principle suggests that when we are unsure about the risks ofa certain industrial process or its pollutants we should not allow it to proceed
until we can be sure that it is safe. Such a principle has never been applied tothe civilian nuclear power industry. The primary reason for the lack of
precaution was that, in spite of the novelty of the procedures they were engaged
in, nuclear physicists were convinced that they were not a risk to public health,and they convinced policy-makers of this also. However, it is clear from thescientific findings presented elsewhere in this report that there is considerable
doubt about the health effects of radionuclides. Certain areas of scientificdiscovery, particularly cell biology and the study of the immune system, havemade tremendous progress since the inception of the nuclear power
programme. This is illustrated in particular by the fact that the risk model
within which the nuclear programme currently operates was drawn up before
the discovery of DNA. Given this level of scientific insecurity it would seemadvisable in the interests of public health to apply the precautionary principle tothe operation of nuclear stations and to prevent them from releasing further
radioactive emissions until they can prove conclusively, and in accordance withthe most recent physiological discoveries, that they are safe.
4.4.4. Who bears the cost?
In response to a challenge to the ethical foundation of civilian nuclear power
and the cancers caused by licensed emissions, nuclear industry apologists haveoffered comparisons between the number of miners killed as part of the lifecycle of energy production in coal-fired power stations with the number ofcitizens killed by cancers consequent on nuclear releases. However, this is an
ethically flawed position. The miners are well informed about the risky natureof their employment and accept it in return for direct pecuniary gain. Theirsituation is not the same as that of the adult or child who breathes in radioactive
particles released from Sellafield without knowing they are in the air, orwithout benefiting directly from their production. Such people are in effect bystanders and thus have a morally distinct status from those who are engaged in
producing the pollutants. The situation is more analogous to that of the people
in London who died in the smogs caused by coal-fired power stations andindustrial plant. Once the facts about the health risks of such unregulatedburning of coal in cities were known these deaths were considered morally
unacceptable, leading to the introduction of smokeless zones. A similarly strict
moral position needs to be adopted with regard to the nuclear industry and30

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would be if the true levels of emission and their real effects of health weremore widely known.
4.4.5 Accounting for different levels of radiosensitivity
It is accepted as scientific fact that not all human systems respond similarly toradiation; there are variations in levels of radiosensitivity. About 6% of the
population are heterozygous for the ATM gene which confers inefficiency inthe system which identifies DNA damage and enables repair to take place:these people are significantly more sensitive to radiation. A number of othergenetic defects have been identified which make sub-groups exquisitely
sensitive to radiation carcinogenesis. This means that a fixed level of exposure
to ionising radiation represents a much greater risk to some people than others,or, put another way, that a level of licensed discharge that may be consideredsafe for one citizen has a fairly high probability of causing another, moreradiosensitive, citizen to develop cancer.
This presents a very particular ethical problem. In the case of many
genetic susceptibilities, say nut allergy or xeroderma pigmentosum, we canreasonably expect people suffering from such conditions to avoid nuts or stayout of the sun. However, radiosensitive citizens in a modern society face two
insurmountable problems in terms of such self-protection. First, they areunaware of the condition, since there is no medical test. Secondly, even if they
were aware of the condition, they could do nothing to avoid the emissions frompower stations, which are released without warning and spread through the air
and water. The only message to the radiosensitive would be John Gofman’s: ‘Ifyou can’t stand the radiation, you’d better stay out of the environment’. Again,
we are faced with the result of a risk-modelling system that relies on averaging.
In this case, the average radiosensitivity of the human system is used as thebasis of the model. This will inevitably lead to some particularly radiosensitive
members of the population facing very large risks of developing cancer andother radiogenic illnesses. By some accounts the proportion of radiosensitive
individuals is roughly 20%. In addition it seems that different races may havedifferent radiosensitivities, making the basis for radioprotection on theJapanese LSS study inapplicable to different racial groups. Once we take into
account varying radiosensitivity in the population it is difficult to think of amorally acceptable alternative to developing risk models that are based on thehealth risks of the most susceptible citizens. The question is revisited in
Chapter 9.
4.4.6 Cross-border problems
The cost-benefit procedure and the utilitarian philosophy that underpins it areboth based on calculations of human satisfaction within a given community.
Thus, for example, all calculations of doses to the UK public from theproduction of nuclear power are based on the population of the UK. However,31

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it is clear that environmental pollution does not recognise national boundaries.
Pollution from Sellafield has been discovered throughout the North Sea,
leading to complaints from Scandinavian governments. A research institute in
St. Petersburg found evidence that the main source of pollution in the Barents
Sea was from Sellafield, rather than the nuclear submarine Kursk which sankthere. It has also been found as far away as northern Canada. The country mostheavily contaminated with pollution from the UK civilian nuclear programmeis the Republic of Ireland. This has led to furious political activity in a country
which has no nuclear power of its own. The Irish government rightly argues
that a cost-benefit analysis of the Sellafield operation may confer benefits on
the population of the UK but costs are also borne by citizens of the Irish
Republic who receive no benefits.
Thus the methodology of justification of UK nuclear power takes noconsideration of its effect outside the borders of the UK and for it to have asound ethical basis the deleterious consequences for citizens of other countries
need also to be considered. Other examples of serious transboundary problems
are satellite catastrophes like the event of 21 April 1964, when US satellite"Transit-5 BN-3" dispersed 950 g. Pu-238 (about 17 000 Ci) which tripled theamount in the worlds atmosphere.
4.4.7 De minimis and Justification by comparison with natural background
The Committee has considered two justifications for permitting exposures,
namely the de minimis argument and the ‘natural background' argument. The
de minimis argument is based on the legal principle that the ‘law does notconcern itself with trifles’. Thus, an exposure which is assumed to carry a riskof say one death in 100,000 persons exposed is often advanced as a trivial risk
and compared with the much larger risk of being killed in a car accident ordying of cancer following a life of cigarette smoking. Whilst these arguments
may be used to minimise access to the law for compensation for trivial harms
the Committee does not believe that they have any basis in ethics and arelargely pragmatic. For if a madman checked into a hotel in London with ashotgun and informed the police that he intended to shoot dead 60 people (1 in
100,000) or even one person (1 in 6 million), society would naturally expect
him to be arrested and locked up, yet the release of radioactive materials from
nuclear sites attracts no such penalties. Nor would any cost-benefit argument
make an impact on social attitudes towards the hypothetical madman. He
would not be permitted, for example, to shoot only people that he foundmugging old ladies or robbing banks, since even robbers have rights.
The ICRP have clearly considered the problem they have with thisargument and have tiptoed away from the idea of collective dose in favour ofthe concept of protection of (initially) a critical target group and more recently(2007) a target ‘representative individual’. This appears to avoid anyone
multiplying the individual doses by the population receiving them and the32

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associated risk factor to obtain actual numbers of dead people. Of course,
nothing has changed, these dead people still exist; it is just that it is no longer
possible to use the ICRP data to accurately calculate their number. The
radiation is still released and it enters the food chain and the air, so everyone
gets some of it, however small, and receives a health detriment, always finite.
ICRP no longer worries about these people as their dose is less than that of thenominal representative person.
The argument that exposures from nuclear sites are far below natural
background and therefore are somehow acceptable is similarly disposed of on arights basis. For if a branch were to fall off a tree and kill a person walking
underneath, then this would be considered an Act of God. On the other hand, if
someone picked up the selfsame branch and used it to hit someone else on thehead and kill them this would be murder. The release of radioactive materials
capable of causing harm or even death cannot be justified on the basis ofcomparisons with natural analogues.
More importantly, the Committee notes also that the epidemiological
identification of anthropogenic radiation-induced cancer from a putative point
source is dependent upon the statistical comparison of cancer rates acrossexposed and unexposed populations. The Committee points out that thegeneral increase in radiation exposure associated with environmental
accumulation of anthropogenic radionuclides from nuclear sites has made suchcomparisons impossible, since there are no longer any uncontaminatedcontrols. The Committee recommends the employment of methods which are
based on assumptions about background radiation associated with only natural
isotopes at levels which existed prior to the year 1900.
4.5 ICRP: Collective Dose, Controllable Dose and Justification
As noted above, the ICRP has effectively abandoned the earlier concept ofCollective Dose in the low-dose region and has replaced it with a “controllable
dose” process which considers the dose to a nominal Representative Person(ICRP2007). This representative individual has now to be considered within
the Concept of Justification of the practice which is being considered. Everychange in radiation exposure which occurs has to be justified according to thedose to the “representative person”. This person is an average member of what
used to be termed the critical group, those who are to be exposed to radiation asa result of the practice being considered. Thus protection of the public would
be considered adequate so long as the risk to the Representative Person could
be justified in terms of good to that person or to Society. This might bewelcomed as a rights-based change of emphasis were it not for the justificationin terms of “Society”. For there are many situations (indeed all bar medical
exposures) where the Good to Society takes precedence over the Good to theIndividual. Thus the ICRP philosophical basis is still squarely in the Utilitariancamp. Furthermore, the concentration on one individual in the group of those33

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most critically exposed entirely neglects the many thousands, perhaps millions,
who receive doses lower than this quantity yet suffer finite harm. Their harm isreal and though their doses are lower the same risk factors apply and their
numbers are much greater. The Committee believes that the ICRP’s acceptancethat there is no threshold dose for potentially lethal mutation logically andethically demands some measure of collective harm and that, while it may bereasonable to employ the concept of Controllable Dose in the context ofregulating workforce exposures, Collective Dose must be retained as a meansof estimating detriment from radionuclides released into the environment bywhatever route. Abandoning Collective Dose is clearly a political discourse
manipulation and is not compatible with the Justification Principle. It cannot bereconciled with the ICRP’s earlier position that … far future … doses should betaken into account in the protection of both populations and individuals. (ICRP
1990 Para. 101).
Further, the use of the “representative person” (usually ICRP
Reference Man) in methodology involving controllable dose should be changed
to “most at-risk person” in order to include considerations of variation inradiation sensitivity. For example, the foetus or child may have a lower dosethan the 'most exposed person' who might be a high-tension linesman or
farmer, but the foetus is much more sensitive to radiation and could suffer ill
health at lower levels of exposure. Similar considerations apply toradiosensitive individuals.
4.6 Conclusion
In this short chapter the Committee has discussed the ethical basis of thecontamination of the environment which results from an unavoidable byproduct of civilian nuclear power, military nuclear weapons testing and the useof Uranium weapons. The consequent detriment to human health makes the
ethical justification of these activities virtually impossible in all but the mostextreme cases (medical interventions, research and technological uses ofradiation). If the nuclear industry and the military are to continue within asound ethical framework serious questions need to be addressed and those whowill suffer its health consequences need to be informed and consulted to a far
greater extent than they ever have been. This is a political matter since it isassumed in a democracy the electorate or their representatives have access tothe best information. In the case of radiation risk, the electorate and theirrepresentatives have no access to accurate information on the effects of theseprocesses and the contamination of their bodies or its consequence.
Parliamentary democracy fails under these conditions.
In many instances it is the environmental destruction that appalls
citizens, but that they nevertheless find difficult to reverse. This results fromthe universal intellectual domination of the ethic of capitalism, an economic
system which, to paraphrase Wilde, knows the price of everything and the34

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value of nothing. As Midgley points out, rationality is no longer an adequate
discourse for justifying human activity. Its limitations are made clear by theconclusion implicit in policy-making that while children will inevitably die
from leukemia as a result of radioactive discharges, causality will be denied
and in any case their numbers are ‘absolutely small’ and therefore not worthyof consideration. The moral bankruptcy of such a justification is intuitively
apparent. If we broaden our conception of value beyond that which exists
within the economic growth-driven world system it becomes clear that far frombeing too cheap to meter, civilian nuclear power is in fact too costly to permit.
The question of the systematic increases of medium and very longlived radionuclides in the environment from military-associated activities(weapons tests, Uranium weapons) has never been justified and therefore could
be taken to be beyond the framework of any ethical system, including
utilitarianism. Owing to the cross-border and indiscriminate nature of thecontamination it should be considered to be a universal crime against humanityof the type discussed at Nuremberg following World War II.

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5
The Risk Assessment Black Box
The International Commission on Radiological Protection
5.1 The Black Boxes of Science
The Committee takes the view that the dissonance between model andobservation in the area of radiation risk is now so great that it is necessary to
begin without any assumptions regarding the predictions of accepted scientificmodels and to take a fresh view of the whole system. Having examined thescientific method, we move on to examine the origins of scientific belief.
Although scientists may believe that science moves forward throughthe formal philosophical frameworks outlined in Chapter 3, in reality it is lessrational. In the last twenty years, sociologists have begun to direct their criticalgaze at scientists and their real world. In the fields of sociology and social
anthropology fundamental questions about objectivity led, after the Second
World War, to the examination of the origins of belief and the application ofreflexive methods. We cannot escape from our culture, claimed thephilosophers and anthropologists. What we appear to find when we look atother societies and cultures is largely a reflection of our own subjective view.
And this interpretation is so embedded in the way we ourselves think about or
understand the world that what we find is only our own interpretation of what
we would be doing or thinking if we were the person being studied. Thus what
we find is essentially what we put there ourselves through our interpretative
assumptions.
The early search for objectivity in the late 19th century followed
questions raised by discoveries in the field of relativity. The questions raised
led to the logical positivist view that science was the most objective descriptionof the physical world if the formulations were mathematical. This was because
it was believed that there were somehow ‘scientific facts’ wrested from Natureand elevated to the level of ‘physical laws’, like Newton’s Laws of Motion.
However, recent and closer examination of scientists at work and study and of
how their theories and discoveries eventually come to be accepted in their own
and the wider community shows that science is not as objective as it has been
portrayed. ‘Science studies’, as this sociology has come to be known, finds thatscience is not free from the bias and inaccuracy which permeates all other areasof knowledge, and for the same reasons. Scientists are human beings like nonscientists. And scientific facts are not the unassailable result of forcing Nature
to reveal her Truths, but are assembled from the interplay of many different
items, actors, machines and procedures, all of which may be faulty, biased,inaccurate or uncertain.
In reviewing the evidence available, the Committee found that Latour’smodel of scientific development through the encapsulation of theory in ‘blackboxes’ is very relevant to its enquiry. Latour (1987) finds that scientific truths

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are not unassailable, nor final, nor always without components derived frommuddier sources than Nature herself. His model suggests that what is accepted
at any period of history is a scientific world-view that consists of a system of‘black boxes’. These are encapsulations of earlier theory that are used as
discrete components in the understanding and interpretation of new discoveries.
Most significantly, he finds that as time passes and more knowledge is includedin these black boxes it becomes increasingly difficult for scientists to unravel
the components of their structures or to attack the complex system ofconnections that maintain their status.
The science of radiation risk is exactly such a black box. It wasconstructed during an atmosphere of Cold War secrecy and control largely byphysicists (supported by the military) at a time before the discovery of DNA
and when many of the biological responses of living cells to radiation were
unknown. The body largely responsible for the construction, development andpresent maintenance of the model defining the radiation-risk black box is the
ICRP. The Committee believes that a brief review of the history, structure andcomposition of the ICRP is necessary in order to understand the nature andprovenance of the models which presently underpin statutory radiation-risk
models.
5.2 Historical provenance of the ICRP radiological models for external andinternal exposure
The ICRP claims its origins in the International X-Ray and Radium Protection
Committee of 1928. The truth is that the ICRP developed out of the need, in
1945, to establish a radiation-risk body to advise and reassure those who wereconcerned about the new radiation exposures which followed the development
and testing of nuclear bombs in the US. The immediate forerunner of the ICRP
was the US National Council on Radiation Protection (NCRP). In 1946 the US
Government, having tested the bomb and used it on Japan, clearly recognised
the sensitive nature of nuclear science. It outlawed the private ownership ofnuclear materials and set up the Atomic Energy Commission (AEC) toadminister the area. At the same time, the NCRP was formed by reviving the
US Advisory Committee on X-Ray and Radium Protection. This was a period
when nuclear bomb development, rather than medical X-rays, was the area
where most exposures would occur. The medical profession had originallyestablished the Committee to provide itself with advice on radiation protection.
Now that there was a new source of risk involving the military, government,
and private companies with research contracts it was clearly necessary to
rapidly set up a body with sufficient credibility to claim to be the ultimate
authority on radiation risk. Because recent discoveries had shown that ionisingradiation caused genetic mutations in fruit flies (implying a similar risk topeople), there was a pressing need to revise the existing limits for exposure to37

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X-rays and extend these to the new risks from external gamma rays which
resulted from weapons-development research and nuclear-bomb-test exposures.
There was also need to develop exposure limits to internal radiation from thehost of novel radioisotopes which were being discovered, produced andhandled by workers, and discharged into the environment. There is now ample
evidence that the NCRP was under pressure from the AEC to fix exposure
limits which would not cause blocks to research and development.
The NCRP had eight sub-committees looking at various aspects ofnuclear risk, but the two most important ones were Committee One, on externalradiation limits chaired by G. Failla, and Committee Two, on internal radiation
risks chaired by Karl Z. Morgan, chief health physicist at Oak Ridge.
Following what now appears as negotiation with the AEC over acceptable
exposure limits, the NCRP had decided on its external exposure limits by 1947.
These were 0.3 rem (3mSv) per week, a reduction of the existing standard of
0.7 rem (7mSv) per week. In passing, we note that this value is 8 times higher
than that which is accepted today (e.g. in the Euratom Basic Safety Standards
Directive) for workers and more than 160 times that which is accepted formembers of the public.
Despite the agreement on this value reached by Failla’s (externalradiation) Committee One in 1947, it was not until 1953 that the full reportfrom the NCRP was published. The reason for the delay was that Morgan’sCommittee Two was finding it very difficult to agree on values and methods
which could be easily applied to determining the doses and risks from the manydifferent radioisotopes which could become internal sources of irradiation toorgans and cells within the body. Part of this difficulty had to do with lack ofknowledge at the time of the concentrations and affinities of the radioisotopes
for the various organs and their constituent cells. Part of the difficulty must also
have been the problem of applying the averaging concepts implicit in thedefinition of dose (i.e. the units themselves) to the distribution of energy
density in non-uniform structures. In the event, the NCRP became tired of
waiting for a resolution of these problems and in 1951, its executive committee
summarily ended Committee Two’s deliberations and insisted that its report oninternal emitters be prepared for publication, possibly on the basis that some
guidance on risk was necessary. Nevertheless, the final report was not
published until 1953.
This was the time when the radiation-risk black box was sealed up. Itsinternal workings had been constructed under pressure for the rapid
development of some convenient methodology for defining exposure.
Following the use of ionisation measuring devices like Geiger counters andgas-filled ionisation chambers it was, perhaps, natural that the new system
quantified dose as energy per unit volume, although the first measurements
were of ionisation, not energy (Roentgens). The energy units were the Rad andthe Rem, now translated to the Gray and the Sievert, but it was clear even thenthat these units and the energy per unit volume approach are not applicable

38

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unless the system being irradiated is truly uniform. The model cannot deal withsmall volumes and inhomogeneities of dose, and for this reason, is unsafe toapply to internal irradiation. This point will be elaborated elsewhere. But the
problem today is that this is the black box for radiation risk which represents
the model used by the ICRP. It developed out of the NCRP. The Chair of the
NCRP, Lauriston Taylor, was instrumental in setting up an internationalversion of the NCRP, perhaps to divert attention from the clear evidence that
the NCRP was associated with the development of nuclear technology in the
US and also perhaps to suggest that there was some independent international
agreement over the risk factors for radiation. The new body was named theInternational Commission on Radiological Protection.
Taylor was a member of the ICRP Committee and the NCRP Chairman
at the same time. The NCRP Committees One and Two were duplicated on the
ICRP with the identical chairmen, Failla and Morgan. The interpenetration of
personnel between these two bodies was a precedent to a similar movement of
personnel between the risk agencies of the present day.
Unlike the ECRR, whose members include researchers and which
carries out and commissions fundamental studies, ICRP has always been a desk
organization. It has one permanent paid member, from the late 1980s until
recently its Scientific Secretary Jack Valentin. It is a desktop organization andcarries out no research. ICRP has stated that it relies for its information on thereviews of scientific papers provided by UNSCEAR. But UNSCEAR carries
out no research either: UNSCEAR’s reports choose to cite other research which
its editors choose carefully. These editors are selective in their references as is
the latest ICRP 2007 report.
These radiation risk organisations have personnel in common. For
example, there are overlaps between ICRP and UNSCEAR, the USA BEIR VII
and the International Atomic Energy Agency. In ECRR2003 it was reported
that the then Chair of the ICRP, Roger Clarke, was also the Director of the UK
National Radiological Protection Board (NRPB). Clarke was also a member ofthe 2007 ICRP task group responsible for determining the risk coefficients (andignoring the data that showed they were wrong). The Chair of this task groupwas Dr Roger Cox, Chair of the NRPB (now the HPA) but who was Chairmanof ICRP Committee 1 (2001-2005), is also presently Vice Chair of ICRP andalso contributing author to the 2000 UNSCEAR report. Cox was on the
CERRIE Committee which voted to exclude the evidence that ICRP’s model
was wrong from the majority final report and is also on the USA BEIR VII
Committee for its 2005 report. When these groups refer to each other for
independent support, they don’t have to walk far. There is Dr Abel Gonzalez of
the IAEA, who is also a full member of the ICRP Committee and is listed asdrafting the ICRP 2007 report. Dr Lars Eric Holm of Sweden was the current
Chair of ICRP until very recently and also was also Chair of the Swedish
Radiological Protection organization SSI, was Chair of UNSCEAR in 2001 andis a delegate to UNSCEAR 2006. Holm has famously gone on record as stating

39

ECRR 2010that the total death toll of Chernobyl is limited to 30 seriously irradiated cleanup workers, something that is also stated regularly in public and at conferences
by Abel Gonzalez of the IAEA. The point here is that all the organizations thatgovernments depend upon for a scientific consensus argument ultimatelyinterconnect and rely on one risk model: that of the ICRP. The ICRP is notindependent of the organizations that it depends upon for its evidence, and they
are not independent of it. The system is an internally consistent andepicyclically-maintained fortress of bad science, bias and false conclusions.
What of that other UN organization, which might be reasonable expected tohave a concern about radiation exposures and health, the World HealthOrganisation? In 1959 WHO was constrained into an agreement with IAEA
which left the IAEA in charge of all research into the health effects ofradiation. This agreement is still in force, and covers not only WHO but also
FAO. At the 2001 Kiev Conference on the health effects of the Chernobyl
accident, the Chair of WHO, Prof H Nakajima stated in a public interview: ‘inthe research into the effects of radiation WHO is subservient to IAEA, health issubservient to the atom’. The mandate of IAEA is the development of peacefuluses of the atom, though currently it is more of an international policeman
aimed at limiting the spread of nuclear weapons beyond the USA and othercurrent nuclear states. The lack of research into the health effects of theChernobyl accident has been blamed on the involvement of the IAEA and theemasculation of the WHO (Fernex 2001). The relevant agreement states:. . . it is recognized by the WHO that the IAEA has the primary responsibility
for encouraging, assisting and co-ordinating research on, and development
and practical application of atomic energy for peaceful uses throughout theworld... Whenever either organization proposes to initiate a programme oractivity on a subject in which the other organization has or may have asubstantial interest, the first party shall consult the other with a view toadjusting the matter by mutual agreement. (Article 1, §§ 2-3, ResWHA 12 - 40,
May, 28th, 1959).
This has not prevented the NRPB from telling the UK’s regulator, theEnvironment Agency, that UNSCEAR and ICRP are 'constituted entirely
separately', a statement which the Environment Agency accepted. Thus
credibility for statements on risk is spuriously acquired by organisations citing
other organisations, but it can be seen as a consequence of the fact that they all
have their origins in the same development and the same model: the
NCRP/ICRP post-war process. This black box has never been properly opened
or examined. A full and readable history of the development of radiation-riskstandards is to be found in Caufield (1989). Taylor himself has described thesedevelopments in some detail (Taylor, 1971) and in an interview on thedevelopment of radiation risk in the post-war period Karl Morgan, who left

40

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both the NCRP and ICRP, said of these organisations and their satellites, I feellike a father who is ashamed of his children (Caufield 1989).
In this report the ECRR Committee is not primarily concerned to
criticise the ICRP, but merely to place the development of the contemporary
low-level radiation-risk model into a historical context. The Committee takes
the view that this approach makes it easier to see how such a wide discrepancy
between theory and observation came to exist.
5.3 Criticisms of the ICRP and its methodology made to the STOA unit of theEuropean Parliament in February 1998.
There were four main areas of criticism made at this meeting. However, theproceedings were inadequately reported by the organisers (Assimakopoulos
1998). They are outlined in Table 5.1. The criticisms of the Hiroshima basis ofrisk modelling as discussed by Busby (1995, 1998, 2006) are shown in Table
5.2.
Table 5.1 Criticisms of the ICRP low-dose models made at the European
Parliament meeting in February 1998.
Criticism
1. Hiroshima basis of risk model flawed because the study
and control groups were not representative of a normal
population.
2. ICRP basis of risk assessment is undemocratic andbiased by the membership and historic provenance of theCommittee
3. Hiroshima and all other bases of risk model unable toinform on risk from internal exposure due to averaging andother errors implicit in the units of exposure.
4. Hiroshima base of risk model did not include
contribution from internal exposure from fallout or residual
contamination as controls were exposed to fallout
5. Units of exposure themselves (Sieverts) containinappropriate value judgments and are not physical units.

Author/Presenter
Prof. Alice Stewart

Dr Rosalie Bertell

Dr Chris Busby

SeveralDr David Sumner

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ECRR 2010

Table 5.2 Failures of Hiroshima study to explain or predict consequences of
exposure
Failure mechanism
Inappropriate controls
Extrapolation from high dose to low
dose
Extrapolation from acute to chronic
Extrapolation from external to internal

Assumption of linear no threshold

Extrapolation from Japanese to world
populations
Extrapolation from war survivors
Begun too late and missed early deaths
Excluded illness apart from cancer
Genetic damage modelled on grossabnormality

Notes
Both study group and controls exposed tointernal irradiation from fallout
Cells killed at high dose, mutated at low
dose
Variation in cell sensitivity following
earlier exposure
External gives homogenous doses (single
tracks) whereas internal can give highdoses (multiple or sequential tracks) tocells local to the source.
Patently not true, though the best fit was
linear exponential and linear quadratic forleukemia.
Different susceptibility of different
populations is well establishedWar survivors selected for resistance
Total yield not accurate, lag incorrect
Total health detriment ignored for later
exposures
Ignored cases in first 5 years , ignored sex
ratio effects on birth rates

5.3 More recent arguments about the A-Bomb studies
Since 2003 there have been some further developments in the interpretation of
the A-Bomb Life Span Studies which will be briefly reported here and whichshow that these studies themselves are questionable as a basis for developing
radiation-risk models even for external exposures. The following issues are
relevant:
1. The US-funded Atomic Bomb Casualty Commission ABCC selected
its study groups and began comparing them some seven years after the
exposures. It has been suggested that the total cancer and leukemia
yield is therefore higher than that tabulated by ABCC due to cancers
developing in the early period and missed by ABCC. This is now
known to be true since reports have been discovered which publish thetotal numbers of cases in this period (Kusano 1953).
2. The gap between exposure and clinical expression of cancer andleukemia, the lag period, has been consistently given by current risk
models as greater than 5 years. This has enabled governments and risk
agencies to deny causality in many situations where leukemia and42

ECRR 2010

lymphoma seemed to develop almost immediately after exposures (ABomb Test Veterans, Uranium-exposed veterans of the Gulf War andBalkans). The early Japanese reports show that leukemia cases began
developing in the first year after the bombing (the first case 3 months
after exposure) and also developed in those who were not present at thetime of the bomb but entered later (Kusano 1953).
3. Non-cancer data released by the RERF (e.g. epilation, skin burns) havebeen recently analysed by Sawada to show that there were significant
health effects on populations who were too far from the epicentre tohave received doses from the prompt radiation capable of causing these
conditions. Sawada’s analysis, presented at the 2009 ECRR conference
and also published shows the anomalously great effect of internal
exposure to fallout (Sawada 2007 and ECRR 2009). A similar point
was made in an analysis of this dataset by Stewart and Kneale in 1999.
4. The Indian geneticist, Padmanabhan, has shown that there are genetic
effects on the children of the Japanese A-Bomb survivors if the correct
controls are employed (CERRIE 2004b, Busby 2006). Grossmalformations and observable genetic effects were reported in the
Kusano 1953 and also in anecdotal reports discussed in Busby 2006.
The ABCC geneticists Neel and Schull reported that there were noobservable genetic effects of the A-Bomb, which they must have
known was untrue.

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6
Ionising Radiation: Units and Definitions in the ICRP System

and Extension by ECRR
6.1 Admission by ICRP of inadequacies in the model
Before laying out the system of quantification of dose that is used in its model,
the ICRP admits the possibility of the errors likely to be associated with its use
to which the ECRR report also draws attention. The 1990 recommendations of
the ICRP (ICRP, 1990) stated:(17) Historically, the quantities used to measure the ‘amount’ of ionisingradiation dose have been based on the gross number of ionising events in adefined situation or on the gross amount of energy deposited, usually in adefined mass of material. These approaches omit consideration of the
discontinuous nature of the process of ionisation, but are justified empiricallyby the observation that the gross quantities (with adjustments for different
types of radiation) correlate fairly well with the resulting biological effects.
(18) Future developments may well show that it would be better to use otherquantities based on the statistical distribution of events in a small volume ofmaterial corresponding to the dimensions of biological entities such as thenucleus of the cell or its molecular DNA. Meanwhile, however, the Commission
continues to recommend the use of macroscopic quantities
In passing, the Committee notes that the ICRP’s justification in (17) isbased on external irradiation experiments. But since 2009 Dr Valentin himself
has stated in public that the ICRP model cannot be used to assess risk topopulations following exposures since the uncertainties associated with internal
exposures are too great (greater than two orders of magnitude). Essentially thisstatement by the editor of both the 1990 and 2007 ICRP reports dismisses the
ICRP model totally and makes it valueless.
6.2 Introduction to the basic dosimetric system
Radiation causes damage in living tissue by ionisation of the atoms andmolecules which make up the constituent cells. Fig. 6.1 schematically describes
the interaction of the main three types of ionising radiation with matter.
The process of ionisation is one in which the bonds holding theconstituent atoms of the molecules in tissue together are broken. These broken
ionised fragments may reform but may also react with other molecules to form
new reactive materials which may be harmful to the cell. If cellular damage
does occur and is not adequately repaired it may prevent the cell fromsurviving or reproducing, or it may result in a viable but altered cell.
The energy required to break bonds in biologically important
molecules varies with the bond but is between 6 to 10 electron volts for large
biological molecules like DNA or RNA. Thus the energy available in a single

44

ECRR 2010

650keV decay of the isotope Cs-137 is, in principle, sufficient to cause thebreakage of some 65,000 bonds in such molecules.

Fig 6.1. The interaction of ionising radiation with matter to produce ionised
molecules.
If a large fraction of cells comprising an organ are killed then there will
be an observable overall effect on the function of the organ and the health ofthe organism. The ICRP model distinguishes between such major ‘nonstochastic’ or deterministic damage and the damage which results from theprobabilistic or stochastic development of effects consequent upon theacquisition of harmful but survivable alterations. In this report the Committee
is not primarily concerned with the gross immediate consequences of high-dose
acute irradiation but with stochastic effects following low-dose irradiation. The
probability of cancer resulting from radiation may be expected to increase withincrements in dose to each individual target cell up to a level where the cellcannot sustain the damage and dies.

45

ECRR 2010

For this reason it is important to emphasise that it is the dose to theindividual cell which is the parameter of interest and indeed it is most likely,from Auger substitution experiments, to be the chromosomal DNA andassociated replication apparatus (e.g. membranes) which are the target for
critical damage by ionization effected chemical reactions. For internal or nonisotropically distributed radiation exposure the macroscopically estimated doseto the tissue is unlikely accurately to reflect the doses to individual cells ofthese organelles. In other words, averaging the energy transferred in a given
mass of tissue may suggest a low-dose whilst in reality all the energy may betransferred into a very small part of the tissue. Some cells will then receive avery large dose whilst most will get none. Thus, depending on the severity ofthe dose, the boundary between deterministic and stochastic effects isdependent on the mass of the tissue into which the energy is absorbed
This has implications for, inter alia, the irradiation of the foetus byinternal particulates. In the event that an irradiated cell is altered rather thankilled, the outcome is very different. Despite the existence of cell repair
mechanisms and, in the whole organism, further surveillance systems for theelimination of such cells, the clone of cells which carry the modificationinduced by the radiation will have a higher probability than the original cell of
acquiring the set of genetic changes necessary to cause uncontrolled
replication. This may result in the manifestation of a malignant condition, acancer. It may also result in a detrimental effect on the efficiency of the organor system which the cell is part, with resultant ill-health of the individual. The
severity of the cancer is not affected by the dose. This kind of damage is called‘stochastic’ meaning ‘random or resulting from chance factors’.
In the last fifteen years it has become increasingly clear fromexperimental results that direct damage to the chromosomal DNA and the
production of a clone carrying a fixed mutation is not primarily the source ofradiation-induced changes in exposed organisms. It turns out that radiation(and other types of mutagenic) damage to DNA and associated apparatus cause
the induction of a signalling phenomenon termed genomic instability. This
results in a signal which causes random genetic mutation to occur in the target
cell and its descendants. The signal is also transferred in some way to othercells nearby, a so-called bystander effect. This important discovery, and its
implications are discussed briefly in Chapter 9.
For the ICRP, however, the only late health effects that are expected tooccur in populations following exposure to ionising radiation are increases incancer incidence in those exposed and hereditary disease in their descendants.
It may be, however, that random damage to the genetic material ofmany cells in an organ results in a loss of efficiency of the organ. Such effects
may reveal themselves clinically many years after the original exposure andmay result from changes in the efficiency of descendants of the original
exposed cells. For example, non-cancerous thyroid gland dysfunction may
follow exposure to radioactive Iodine. Such an outcome is not easily classified

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as deterministic or stochastic and is not addressed in the system of risk used by
ICRP. Nor is the significant effect on heart function associated with radiation
exposure. However, the Committee believes that such effects should be
acknowledged and their risk quantified if possible, since they represent
considerable suffering in exposed populations which is presently
unacknowledged. Such general effects may be termed ‘non specific ageing’ but
it should be noted that this concept is not to be identified with the idea of 'life
shortening' utilised by a number of risk agencies to examine the moral
implications of premature cancer death. If damage to the genes of a cell occurs
in cells which function to transmit genetic information to later generations thenthese alterations may become expressed in the progeny of the exposed person.
Such effects are termed ‘hereditary’.
Finally, it must be emphasised that genetic damage entering the humangene pool remains there until it is lost by the death of the carrier prior to
reproduction. Thus heritable damage will always be expressed either in the
exposed individual or a descendant until it is lost through death of theindividual without issue.
6.3 The Committee’s approach to quantifying risk: weighting dose or weightingrisk?
As the ICRP preamble concedes (see para. 6.1), the quantity of interest inradiation risk assessment is the ionisation energy density in the irradiated cell.
ICRP approximates this as an average quantity, the absorbed dose (defined
below). This absorbed energy density (dose) is weighted twice by ICRP toallow for variations in (1) biological effectiveness and (2) organ sensitivity.
The final dose unit employed in radiation protection by the ICRP is a complex
extension of the basic absorbed dose. The units, Sieverts, which are tabulated
against particular types of exposure regime, are a mixture of physical units ofaverage energy density and value judgements about likely health consequences
based upon animal studies, epidemiology, the physical nature of the radiation
types, organ sensitivity and so forth. Originally, the ICRP included thepossibility of extending this system of weighting the fundamental physicalquantity to considerations other than radiation quality and organ sensitivity.
The ICRP noted in 1990:
In previous formulations, provision was made for possible weighting factors
other than the radiation weighting and tissue weighting factors. The product ofthese other unspecified weighting factors was called N.
(ICRP 1990 para 30)
The Committee has learned that one of the main components of N was
the affinity of an internal isotope for DNA; in this system, had it been
implemented, Sr-90, Ba-140 and Uranium would have had their dosecoefficients weighted to increase the effective dose equivalent because of the47

ECRR 2010

locality on the DNA. The idea was quickly abandoned (Jensen 2009). In theevent the ICRP chose to shift the variations in hazard associated with different
exposure types and temporal fractionations away from the calculated doses andonto their published risk factors for fatal cancers—in other words the idea ofmodifying the units of dose was abandoned in favour of modifying the risk
factors per unit dose. This suggested (misleadingly) that the units of equivalentdose had some fundamental or physical significance. In order to account for thequalitatively different exposures at the cell level associated with internal
radionuclide point sources the ECRR was faced with the problem of whether tomodify or wholly restructure the ICRP scheme. The Committee decided that,whilst it would be preferable to begin from first principles and develop a modelin which the deposition of ionisation events at the cell level was accurately
described, in the first instance it is necessary to have a simple system in which
historic exposure calculations based on the ICRP model may be adjusted toprovide more accurate information about health deficits.
The ECRR takes the view that the weighting factors used by the ICRP
to allow for different biological effectiveness of radiations and those allowing
for organ sensitivity are not qualitatively different from weighting factors toallow for different fractionations of radiation dose or for the differing abilities
of various isotopes, particles or contamination types to cause mutation (andwhich it turns out ICRP considered in the 1970s). Consequently, the ECRR
proposes to revive and employ the weighting factor N of the original ICRP
model. This approach has the great advantage that although the new risks of
low-level radiation doses from internal or exotic regimes of exposure may beslightly higher than supposed by the ICRP, there is no great need to alter thepresent legal frameworks in relation to maximum permissible doses. It is thedoses themselves that will be calculated differently. The ECRR has therefore
developed a range of hazard enhancement factors for various exposures which
are incorporated into the Hazard Enhancement Weighting factor N which
will be described further below.
6.4 Absorbed Dose and Equivalent DoseThe fundamental dosimetric quantity in the ICRP radiological model is theAbsorbed Dose, D. This is the energy absorbed per unit mass, and its unit is
now the Joule per kilogram, or Gray (Gy). The early unit which used to be usedis the Rad. One hundred Rad equals one Gray.
D =  





where D is absorbed dose in Grays, M is mass of tissue into which the dose isabsorbed in kilograms and E is energy in Joules. Because there exist in nature
different types of ionising radiation, which have different abilities to ionise
tissue, it was found necessary to allow for this by weighting the absorbed dose48

ECRR 2010

by a factor which accounts for the different ionising power of the radiation. The
ICRP use the term Dose Equivalent for their fundamental unit for radiologicalprotection and define this as the 'absorbed dose averaged over a tissue or organ(rather than at a point) and weighted for the radiation quality that is of interest'.
The weighting factor for this purpose is defined as the radiation weighting
factor w R and is selected for the type and energy of the radiation incident on
the body or, in the case of internal sources, emitted by the source. The final
weighted absorbed dose is termed the Equivalent Dose in a tissue or organ andthe units are Sieverts. 1 Sievert is equivalent to 100 rem, the earlier unit.
The equivalent dose H in tissue T is given by the expression:
HT = R WRDT,R
where DT,R is the absorbed dose averaged over the tissue or organ T, due toradiation R. The unit of equivalent dose is stated by ICRP to be the Joule perkilogram, but the weighting factor values are chosen by the ICRP Committee
and so the equation is not one based in physics but contains human value
judgements about the relative effectiveness of different radiations. For
example, true average absorption of 1 Joule per kilogram may be weighted insuch a way as to be tabulated as 20 Joules per kilogram in the case of alphaparticle exposures. This choice is made by a committee.
The values of the radiation weighting factors wR were chosen by the
ICRP to represent average values of the relative biological effectiveness(RBE) of one radiation type (compared with another. The RBE wastaken to be the inverse ratio of the absorbed doses producing the same degreeof a defined biological end point. The values of wR are roughly equivalent to
the quantity Linear Energy Transfer (LET) a measure of the density ofionisation along the track of the ionising particle or electron track produced
following absorption of a photon. ICRP chose to reference all radiation to theeffects produced by X-rays and Gamma-rays of all energies to which they gave
a weighting factor of unity (1.0).
When the radiation being considered is composed of more than one
type then the absorbed dose must be subdivided in blocks, each with its own
value of wR, and summed to give the total equivalent dose. Radiation weighting
factors chosen by ICRP are given in Table 6.1 below. In general, theseweightings followed the effectiveness of producing cell death in vitro and it
was assumed that the in vivo mutagenic effectiveness would follow a similar
relationship.
It should be noted that these equations on which absorbed doses arecalculated are employed by ICRP and were employed by ECRR2003 in a
modified form as if the mass were a mass of living tissue, essentiallywater. The nature of the absorbing material is not normally a consideration, but
recent work would suggest that if there is contamination with elements of high49

ECRR 2010

atomic number like Uranium, Gold or Platinum. The absorption of gamma andphoton radiation below about 500keV photon energy is proportional to thefourth or fifth power of the atomic number of the atom absorbing the radiation.
Therefore such elements whether as atoms, molecules or particles absorb very
great amounts of energy from the incident photon field and emit the energy as
photoelectrons which are indistinguishable from beta radiation. This is apartfrom any intrinsic radioactivity and is termed the Secondary Photoelectron
Effect or SPE. The matter is important, mainly for Uranium (Z=92) and Iodine(Z=53) and will be discussed below and in Chapter 9.
Table 6.1 ICRP Input Radiation Weighting Factors.
Type of radiation
X-rays and Gamma-rays, all energies
Electrons (beta particles)
Alpha particles
Neutrons and protons

Radiation weighting factor wR
1
1
20
Vary with energy from 5 to 20

The Committee has been made aware that suggestions from within ICRP in the
1980s to adopt weighting factors of 2 for Tritium and 5 for Auger emitters were
not adopted owing to the implication that this would have for the nuclear
industry. The ICRP in fact adopted unity weighting factors for these types of
exposure.
There is added difficulty in assigning a radiation quality factor of unity
to all X-rays and gamma rays. While medical X-rays are usually measured in
Roentgens in air at skin entrance (partial body, site specific), gamma radiationis measured as bone marrow dose to the whole body. The bone-marrow dosefrom a medical X-ray may be significantly lower than the skin dose. For
example, the skin dose for a medical chest X-ray may be 0.5 mSv, with 0.3
mSv soft tissue dose and 0.03 bone-marrow dose. This differential absorptionof the ray corresponds to the sharpness of the image. A high energy gamma
dose is usually taken as being the same for skin, soft-tissue and bone-marrow.
It cannot be used to image internal organs. Therefore if one is using leukemia,
for example, as the biological endpoint of concern, the high energy gamma raydose of 0.5 mSv would have a higher risk than a 0.5 mSv medical chest X-ray
dose (the latter is also a partial body dose).
6.5 ECRR's new system—allowance for biological response in the cell andother factors—the Biological Equivalent Dose.
Earlier it was noted that in the original ICRP formulation, provision was madefor the extension of the weighting factor approach to any number of aspects ofradiation-exposure regimes which might enhance or detract from the efficiency
with which radiation caused cell death, mutation or ill health in the organism.

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The ECRR proposes to use this approach to allow for a number of factors
which have emerged through epidemiological and theoretical discoveries whichhave been made since the ICRP model was developed. The evidence for the
existence of hazard enhancement associated with such exposures is outlined in
Chapters 10 to 13. The ECRR thus defines the quantity biological equivalentdose as the product of the equivalent dose and the new biological hazard
weighting factor N which may be fractional.
The biological equivalent dose B in tissue T resulting from thespecified exposure E of quality R is given by the expression:
BT,E = R NE HT,R
where HT,R is the absorbed dose averaged over the tissue or organ T, due toradiation R, and NE is the hazard enhancement weighting factor for the
specified exposure E.
NE is made up of a number of hazard enhancement factors associatedwith different processes leading to genetic mutation and other relevant
biological damage. For each type of exposure from each internal source S there
will be assumed to be a weighting for the hazard associated with that exposure.
This weighting is made up of biophysical and biochemical factors which are
multiplicative since probabilistically they are deemed to be non-independent
binomial factors which act on the same mechanism (DNA mutation). Thus:
NE =  WJ WK
in the case of J different biophysical aspects of the specified exposure and K
different aspects of the internal exposure which the Committee believes carryenhanced risk of injury.
Components of the overall hazard enhancement weighting factor N are
termed biophysical hazard factors WJ and isotope biochemical hazard
factors WK and these are given for some exposure types and isotopes in Tables
6.2 and 6.3. In the event that the exposure source S involves enhancement
through more than one hazard aspect these are dealt with multiplicatively solong as the source and exposure (binomial probabilistic sequence) leading tomutation is the same. For example, Sr-90 binds to chromosomes but because it
is also a second event decay atom, it carries an enhancement of 30 due to W J
and an enhancement of 10 due to W K (DNA affinity), resulting in an overallenhancement of 300. For Sr-90, Table 6.3 also shows enhancement of hazard
through interfacial adsorption. However, this is considered as a different
exposure and is not included in the calculation for NE but is added in at thestage of calculation of B. If Sr-90 hazard is through barrier transformation to
Y-90 (e.g. Sr-90 enters a system as a divalent ion but transforms to a trivalent
Y-90 and accumulates because of loss of reflexive transport) then only the51

ECRR 2010

hazard factors appropriate to this exposure are used, for example, inestablishing dose to brain tissue.
Table 6.2 Biophysical hazard factors WJ for exposures in the low-dose range.
Type of exposure
Factor WJ
Notes
1. External acute
1.0
2. External protracted (see 1.0
Dose rate sparing is not assumed
3)
3. External: 2-hits in 24
10 to 50
Allows for repair interception
hrs
4. Internal atomic single
1.0
e.g. Potassium-40
decay
5. Internal atomic 2nd
20 to 50
Depends on decay sequences and
Event
dose
6. Internal Auger or
1 to 100
Depends on location and energy
Coster-Kronig
7. Internal insoluble
20 to 1000
Depends on activity, particle size
particulate
and dose*
2 to 2000
Multiply by external gamma dose
8. Internal high atomic
rate factor (see Chapter 6 and 9)
number Z4 factor*Tamplin and Cochran (1974) gave the enhancement of dose for Plutonium oxide hotparticles as high as 115,000

52ECRR 2010

Table 6. 3 Specific internal isotopic biochemical enhancement factors WKIsotope orclass
3-H; Tritium
Ionic
equilibria
cations e.g.
K,Cs, Ba, Sr,Zn
DNA binding
e.g. Sr, Ba, Pu,
Ra, U
14-C
35-S,
132-TeEnzyme andco-enzyme
seekers e.g.
Zn, Mn, Co,Fe
Fat soluble
noble gases
e.g. Ar-41, Kr85
Barriertransmutation
series e.g. Sr90—Y-90

Factor WK

Mechanism of enhanced effect

10 to 30

Transmutation and local dose; Hydrogen bonding;
enzyme amplification
Local concentration by interfacial ionic adsorption:
depends on effect considered

2 to 1010 to 50

DNA primary, secondary and tertiary structure
disruption. Local transmutation ionization

5 to 20
10
10Transmutation and enzyme amplification
Transmutation and enzyme amplification; Hydrogenbonding
Enzyme amplification

2 to 10Depends on effect considered

2 to 1000

Depends on effect considered

53

ECRR 2010

6.6 Allowance for organ sensitivity: Effective DoseThe critical target for ionising radiation is the individual cell. Deterministic andstochastic effects are expressed in the differentiated cells of organs, and themagnitude of both types of effect is dependent both on the identity of cell typeand its location in the cell-cycle (a topic which will be addressed separately). It
has been known since the beginning of the 20th century that rapidly replicatingcell types (e.g. blood cells, epithelial cells of the gut) are more sensitive toionising radiation than cells which rarely divide. Cells which are actively indivision are also much more sensitive. In addition to this, cells of certain
organs (e.g. the eye, the thyroid) are highly sensitive to exposure. The ICRP
system allows only for variations in organ sensitivity and ignores variation incell cycle sensitivity. It does the former by introducing an additional weighting
factor, called the Tissue Weighting Factor WT, which represents the relative
contribution of the organ or tissue to the total detriment due to the effect being
considered resulting from the uniform irradiation of the whole body. The
weighting of the Equivalent Dose (or doubly weighting the absorbed dose)
results in the Effective Dose, E. The unit is the Joule per kilogram, with thespecial name Sievert. However, as with the Equivalent Dose, the unit is not an
objective one and depends on choices made by the ICRP Committee.
The effective dose is the sum of the weighted equivalent doses in all
the tissues and organs of the body:
ET = T WTHT
where HT is the equivalent dose to tissue or organ T and WT is the weighting
factor for tissue T. The effective dose can also be expressed as the sum of the
doubly weighted absorbed dose in all the tissues and organs of the body.
The ICRP system for Effective Dose has also been adopted by thepresent Committee with the replacement of the ICRP’s equivalent dose with
the new biological equivalent dose defined in 6. Thus
ET = T WTBTET is strictly the biological effective dose but the Committee believes that theterm effective dose may be retained without confusion. Its incorporation into
radiological safety and its units will therefore seamlessly follow prior usage.
6.7 Constructing the dose from the organ up or from the body down
It should be apparent that the overall total effective dose to a person built up bysumming the individual effective doses to the different organs (in Sieverts,
derived from double weighting) will not, in general, equal the effective dose
calculated from the uniform equivalent dose derived from the external-

54

ECRR 2010

radiation-field over the whole body. In order to overcome this problem, the
ICRP normalises the sum of the tissue-weighting factors to unity on the
grounds that 'it is desirable that a uniform equivalent dose over the whole bodyshould give an effective dose numerically equal to that uniform equivalentdose.' Thus:
TWT = 1
The tissue weighting factors used by ICRP are given in Table 6.4. In general,
the Committee favours the approach of estimating the doses to each organ oreven organelle but includes the post-ICRP26 weighting factor system sincemuch of the historic data is expressed in these terms.
Further, the weighting factors used by ICRP are based on an assumed
ratio between radiogenic cancer in the tissue organ and radiogenic cancer in thewhole body. This introduces major mathematical problems into such a systemsince a wide variation in the risk factors on an organ basis cannot be subsumed
within the risk factor for overall cancer. In addition, some of the weighting
factors used by ICRP in their partition modelling seem to have been chosen todiminish effects in organs which may carry high tissue loading of man-maderadioactivity. In the ICRP66 lung model the tracheobronchial lymph nodes
where radioactive material is stored, have been given a tissue weighting of
1/1000.
.

Table 6. 4. ICRP tissue weighting factors
Tissue or organ
GonadsRed bone marrow
Colon
Lung
StomachBladder
BreastLiver
Oesophagus
Thyroid
Skin
Bone surface
Remainder

Weighting factor WT
0.2
0.12
0.12
0.12
0.12
0.05
0.05
0.05
0.05
0.05
0.01
0.01
0.05

6.8 Dose rate, dose fractionation and protraction of exposure
The ICRP states that the consequences following an absorbed dose depend not
only on the magnitude of the dose, the type and energy of the radiation (dealt

55

ECRR 2010

with by the radiation-weighting factor) and the distribution of the dose within
the body (dealt with by the tissue-weighting factor), but also on the distributionof the dose with time, which they address as dose-rate and protraction of
exposure. In earlier formulations, the ICRP solved this problem by including
further weighting factors which they named N. The system was abandoned infavour of incorporating weighting factors into risk factors. The approach has
been re-introduced by the present Committee (see section 6.5 above). The
ICRP recognises dose-rate effects within the system of risk factors and weightthese according to its beliefs using a term called the Dose and Dose-rate
effectiveness factor DDREF. Thus, giving a dose over a long period of time isbelieved to have a lower effect (called ‘sparing’) compared with the acutedelivery of the same dose. There is some dispute over the magnitude of such
effects. No attempt is made by ICRP to examine the consequences offractionation of doses in the time scale of the induced repair-replication periodof cells.
The ECRR does not accept dose-rate sparing and has subsumed
fractionation enhancement effects within the concept of biological and isotope
weighting factors used to obtain biological equivalent dose. Factors for both are
given in Table 6.2 and 6.3.
One particular regime of fractionation involves split doses over theperiod of the cell cycle: this process, involving a “Second Event’ enhancement
has been addressed elsewhere. The process is of importance in determining risk
from sequentially decaying internal emitters like Sr-90/Y-90 but also occurs inmedical imaging if more than one high-dose CAT scan is delivered within aperiod of 8 to 12 hours.
6.9 Time summed and collective dosimetric quantities
Following the intake to the body of a radioactive material there is a period
during which the material gives rise to equivalent doses in the tissue of the
body at varying rates. The total imparted equivalent dose resulting from this isaffected by the rate of excretion of the material and also its physical decay
characteristics (physical half-life). The time integral of the equivalent dose rateis called the committed equivalent dose, HT() where  is the integration time
following the intake. If  is not specified it is taken to be 50 years for adults andfrom intake to 70 years for children. By extension, the committed effective
dose, ET is similarly defined.
In order to estimate the health detriment (defined by ICRP as cancer
death and heritable damage) to large numbers of people who have beencollectively exposed (e.g. residents exposed near Chernobyl) the ICRP has
extended to such populations the averaging approach for cells which is implicitin the concept of absorbed dose. For such a population the average dose to anindividual is multiplied by the number of individuals exposed. The relevant
quantities are the collective equivalent dose ST and the collective effective

56

ECRR 2010

dose S. If several groups are involved, the total collective quantity is the sum of
the collective quantities of each group. The unit of these collective quantities is
the man-Sievert, sometimes also called the person-Sievert.
The collective quantities can be seen as representing the total
consequences of the exposure of a group. The ICRP provides the caveat that
their use should be limited to situations in which the consequences are truly
proportional to the dosimetric quantity and the number of people exposed andin which an appropriate risk factor is available. The collective effective dose
resulting from the presence of radioactive materials in the environment may be
accumulated over long periods, covering successive generations. The totalcollective effective dose to be expected from a given situation is the integral
over all time of the collective effective dose rate resulting from (i.e. committedby) a single release. If the integral is not infinite then it is described as
truncated at a definite time.
Following the increasing exposure of large (global) populations torelatively low doses from weapons fallout, reprocessing plant releases andaccidents, it has become clear to ICRP that the development of these collective
dose concepts has been a hostage to fortune. This is because the ICRP risk
factors for exposure may be used with such large populations to calculate afinite number of cancer deaths, a situation which many people findunacceptable and which has political consequences both for the nuclear
industry and the military development of nuclear weapons. The result has beena recent move by the ICRP to abandon the concept of collective dose in favourof a concentration on the individuals most exposed. Thus the ICRP would
advise legislators that if the individuals most exposed in any model exposure
were adequately protected at some acceptable level of risk, then all otherexposed persons would be more protected and the overall cancer yield in the
exposed population would be, by extension, also acceptable.
The ECRR takes the view that this is an immoral position to take andtherefore an unacceptable approach, since it is the overall consequence of any
proposed exposure to the whole exposed population which must be assessed.
Any attempt to avoid recognising that a process will result in a finite number ofdeaths by focusing on low probability, high impact risks in individuals, ismorally questionable. In addition, the Committee has pointed out that there is asignificant difference between those who are 'most exposed' and those most 'at
risk' e.g. women, children, the foetus, the radiosensitive.
The dose commitment (Hc,T or Ec) is a calculational tool. It can beassessed for a critical group as well as for a large population. It is defined as
the infinite time integral of the per capita dose rate (dHT/dt or dE/dt) due to a
specified event, such as a year of practice.


Hc,T 

 H (t )dt
T

0

57

ECRR 2010

or


Ec 

 E (t )dt
0

In the case of an indefinite practice at a constant rate, the maximum annual per
capita dose rate (dH/dt or dE/dt) in the future for the specified population will
equal the dose commitment for one year of practice, irrespective of changes in
the population size. If the practice is continued over time then the maximum
future annual per capita dose will be equal to the corresponding truncated dose
commitment defined as:

Hc,T ( )  H (t )dt
T

0

or


Ec ( ) 

 E (t )dt
06.10 Other quantities used in radiological assessments
The activity A of a radionuclide (or radioisotope) or any radioactive material isthe average number of spontaneous decays (or transformations taking place inone second. The units are reciprocal seconds (sec-1) given the name Becquerel.
It is possible to calculate the number of atoms of a pure radioisotope in any
material by multiplying the activity by the half life in seconds using the factor
1.44. Thus:
N = 1.44 x T 1/2
The quantity of the radioisotope in grams can then conveniently be found by
23
dividing by Avogadro’s number (6.02 x 10 ) multiplying by the relative
atomic mass of the isotope.
Activity has also historically been expressed in terms of the isotope
Radium-226 as ‘Curies’. The conversion is 1nCi = 37 Bq (1Ci = 37GBq).
Several other operational quantities are defined and used in radiologicalprotection but will not be addressed in this publication.

58

ECRR 2010

6.11 Secondary Photoelectron Effect
The quantity employed in radiation protection, absorbed dose, is defined in
section 6.4 as D = Hitherto, the mass into which the energy has been
diluted is that of living tissue; ICRU provide tables of absorption coefficientsfor different living tissue, adipose, bone, muscle etc. which can be employed
for calculations involving doses, but generally all these denominator quantities
have the absorption characteristics of water, H 2 O (ICRU35 1984). The
absorption of electromagnetic (photon) radiation is due to a number ofprocesses, the main three being pair-production, Compton scattering andphotoelectron production. For elements of atomic number greater than about
30, and for photon energies of less than about 500keV, the photoelectric effectpredominates. Even for the low atomic number elements that make up living
systems, below 200keV there is fairly quantitative conversion of incident
photon radiation (and induced photon radiation from second order and thirdorder processes) into photoelectrons. These are fast electrons which are
indistinguishable from beta radiation and have the energy of the incident
photon less that of their binding energy (which is generally far less than theincident photon energy and can be ignored). The absorption of photon radiation
by elements is proportional to the fourth or fifth power of the atomic number Z.
Thus the predominant absorber in water is the Oxygen atom Z=8 and it isreasonable to give the effective atomic number of water as 7.5. Of course, there
are elements in tissue with higher atomic numbers than this, but interestingly,
apart from Iodine (Z=53) few elements with Z>26 ( Iron, Fe).The incorporationof high Z elements into living systems would generally be harmful since itwould increase the radiation dose, and therefore such developments have been
lost though evolutionary selection. Iodine is an exception, but it should be
noted that the main sites for radiation damage in terms of sensitivity are themain sites for Iodine concentration, the thyroid gland and the blood. It has beensuggested that the metabolic and cell repair status controls exercised by the
thyroid gland are the reason why Iodine has been incorporated into living
systems and is employed as a kind of radiation-repair control mechanism(Busby and Schnug 2008).
A problem in radiation protection arises when high Z elements areincorporated into living tissue, since the enormously greater absorption ofphoton radiation by such material will result in enhanced doses to tissues
adjacent to the high Z material. The problem was first addressed in 1947 inrelation to X-rays of bone (Speirs 1949) and has been studied in the past in
relation to prostheses. More recently, interest has shifted to the use of high Z
material to enhance photon radiotherapies for tumour destruction where it has
been shown to be effective. Gold nanoparticles have been successfully
employed (and patented) for radiotherapy enhancement (Hainfeld et al 2004).

59

ECRR 2010

Despite this knowledge, the enhancement of photon radiation by highZ contaminants has not been addressed in radiation protection. The situation
may have arisen out of the fact that prosthetic materials are not intrinsicallyradioactive and contamination from high Z elements like Lead (Z=82) areconsidered under the heading of chemical toxicity.
There are two circumstances where the Secondary Photoelectron Effectwould have significant radiological implications. These are for elements thatbind to DNA and for internal particulates. In the latter case, the effect will bemuch greater as the particle size is reduced, since for massive high Z
contamination e.g. prostheses, most of the photoelectrons are lost inside thebulk material. The emergence of the photoelectrons into tissue is a function of
the mean electron path in the material, and the absorbed dose in local tissue is afunction of the electron range and thus its energy.
The radiological implications of the idea emerged in considering theanomalous health effects of Depleted Uranium weapons and were presented to
the CERRIE Committee in 2003 and the UK Ministry of Defence in 2004
although nothing was done. More recently there have been attempts to quantify
the effects for particles through Monte Carlo modelling (Pattison et al 2009)
but these have not generally been very credible treatments, or able to cope withthe small volumes of complex media involved and the answers have been far
removed from the few experimental data published (Regulla et al 1998,
Hainfeld et al 2004).
The particular concern is for the element Uranium, since this has been
employed since 1991 as a weapon; the Depleted Uranium (DU) penetrators
used from the 1991 Persian Gulf War onward produce a fallout comprising
sub-micron Uranium Oxide particles which are environmentally mobile andrespirable. The case of DU is considered in Chapter 12.
Uranium has another quality which makes it of interest in SPE; as theuranyl ion UO 2 ++ it has a very high affinity for DNA phosphate: some 1010 M-1.
(Nielson et al 1992). This affinity has been known since the 1960s when it was
first employed as an electron microscope stain for imaging chromosomes(Huxley and Zubay 1961).
The SPE effect is therefore likely here to cause enhanced photoelectron
ionization at the DNA due to enhanced absorption of natural backgroundradiation (or medical X-rays). A similar process occurs with the Platinum
chemotherapeutic agent cisplatin which binds to the DNA and acts as anantenna for background radiation and radiotherapy beams.
The development of weighting factors to incorporate this development
into the ECRR system of radioprotection is straightforward. The effect is, ofcourse, proportional to the concentration of material in tissue. In the case of themost important element for radiation protection Uranium-238 it is possible toemploy the activity concentration Bq/kg. There is a slight difference fromnormal biophysical weighting since the effect is a multiplier of natural
background radiation. Therefore the photon dose rate has to be incorporated

60

ECRR 2010

into the assessment of effect. This is done by assuming a natural backgroundphoton dose rate D 0 of 100nGy/h (0.876mGy/y) and multiplying theenhancement due to Z4 by this. Thus the dose coefficient from U-238 (due to its
intrinsic radioactivity) as given in the table is divided by 20 (for the alphaweighting) and the resulting number is multiplied by the ratio of Z4 for
Uranium and tissue. The resulting weighting factor is taken to be 1000 for adose rate of 100nGy/h. It is proportionally increased for increased backgroundphoton exposures and for other photon exposures.
For Uranium particulates below 1micron diameter the factors in Table
6.2 apply. Dose conversion factors for Uranium-238 are given in the Annex
Table A1.
For SPE phantom radioactivity in other elements of high atomic
number the tissue doses are enhancements of the incident photon dose at the
point of the atom or particle being considered. Due to the complex interactions
these local doses must be determined by experiment and the Committee iscurrently engaged in preliminary experiments to establish some enhancement
factors in tissue for high Z elements. These experiments are straightforward
and involve X-irradiation of high Z element contaminated tissue at different
doses. In principle, this development suggests that the internalization of any
high Z particle which is biologically long-lived will cause continuous
irradiation of local tissue cell populations, which would represent a
carcinogenic hazard. This has implications for those employing prosthetic
materials and also for the dispersion of high Z particles (Tungsten, Platinum,
Bismuth, lead) in the environment. It also suggests that it may be of interest to
examine tumours for the presence of high Z particles at their centre. Table 6.5
lists a number of potentially hazardous SPE elements.
Finally it should be pointed out that physical modelling through Monte
Carlo codes is unlikely to establish useful data and certainly should not be
employed as an attempt to dismiss the importance of the proposed mechanism.
Nevertheless, a FLUKA Monte Carlo model of the absorption by nanoparticles
of Gold and Uranium carried out by Elsaesser et al 2007 graphically confirmed
the effect. The results for photoelectron track production following absorptionof 100keV photons is shown in Fig 6.2 below.

61

ECRR 2010

Fig 6.2 Photoelectron tracks emerging from (left to right) 10nm particles ofwater (Z=7.5), Gold (Au; Z =79) and Uranium (U;Z=92) after irradiation with
100keV photons. Monte Carlo (FLUKA code) analysis. Track numbers are inproportion to a 4th power Z law (tracks are shown as projections on a flat
plane). Note that the model uses 1000 incident photons for Au and U but
10,000 for water (Elsaessear et al 2007)

Table 6.5 Biologically significant environmental contaminants and materials
exhibiting phantom radioactivity through the Secondary Photoelectron
Enhancement (SPE) of natural background and medical X-rays
Material Z
U
92

Z4/tissue Source
22642
Weapons particles,
nuclear fuel cycle,
atomic andthermonuclear bomb
tests
20736
Incandescent mantles
Contrast media
14999
General contaminant
14289
General contaminant
12945
General contaminant
12310
Prostheses; colloid
used for rheumatism

Th

90

Bi
Pb
Hg
Au

83
82
80
79

Pt

78

11698

W

74

9477

Ta
I

73
53

8975
2493

62

Vehicle catalysers,
general contaminantWeapons; generalparticle contaminant

Capacitors
Thyroid, blood plasma

Note
Binds to DNA; known
to cause cancer inanimals and genomic
damage at very low
concentrations
Highly insoluble
Insoluble
Toxic; SH binding
Toxic; enzyme binding
Friction particles may
travel in body; inert andinsoluble
Inert and insoluble
Associated with childleukemia cluster Fallon
Nevada; known to cause
genomic damage andcancer in animals.
Radiation sensitivity

ECRR 2010

7
Establishing the Health Effects at Low DosePart I: Risk
7.1 Sources of exposure in the low-dose region.
Populations are exposed to ionising radiation from both natural andanthropogenic sources and the estimation of health detriment is often made on
the basis of comparing exposures from human practice with those from natural
sources. Apart from the obvious points made in Chapter 4 about comparing“acts of God” with human activities, the Committee is anxious to establish theprinciple that each exposure should be assessed at the cellular or even the DNA
level and that therefore comparisons across types of exposure are unsafe. In
particular the comparisons in Table 7.1 below are major sources of error in theperception of risk.
Table 7.1 Unsafe comparisons used in radiological protection arguments.
Comparing
Natural

With
Novel

External

Internal

Natural forms of
isotopes

Technically enhanced
natural isotopes

Problem
Unusual or alien radioisotopes forinternal exposure
Exposure of cells is quantitatively
different
Different physico-chemical forms,
concentration

Natural background radiation exposure arguments will be addressed elsewhere,
but a brief review of the sources of radiation exposure will be given here. In
general, the range of exposure from natural radiation is defined by theCommittee as the low-dose region. This is the exposure dose range from 0 toabout 5mSv, as defined by the ICRP system of measurement, though, ofcourse, cell doses or tissue volume doses may be much higher.
7.2 Natural sources of radiation exposure
Sources of natural radiation can be divided into four categories:
 Cosmic radiation.
 External gamma radiation from natural elements in rocks and soil.
 Internal radiation from natural elements in the body.
 Radon and thoron gases from minerals in rocks and soil and their decay
products.
The Committee distinguishes between these exposures and the enhanced
exposure from the same sources due to human activity. In particular, there havebeen increases in exposure to Uranium and Thorium and their decay daughter
products following:

63

ECRR 2010










Burning of coal.
Preparation and use of phosphate fertiliser.
Commercial uses of natural radioactivity e.g. Thorium incandescentmantles, Uranium in ballast weights and shielding.
Oil production pipe scale and process water (radium, Radon daughters)
Natural Gas production (Radon, daughters).
The nuclear fuel cycle (Uranium and daughters).
The military use of Uranium including depleted Uranium (DU)
weapons.
Cosmic ray exposure from high altitude flights.

The ICRP has used its own methodology to quantify exposures to most of thesesources. Examples are given below in Table 7.2.
The predominance of the dose from Radon and its decay products, it
should be noted, is a consequence of the use of the weighting factor of 20 tomultiply the estimated absorbed dose of 60Sv from this source. This matter isreferred to since it shows the extent to which ICRP’s value judgements and its
choice of units of dose may inflate the appearance of hazard. The problem ofRadon gas is reviewed briefly in section 7.3 below.
Table 7.2 Annual effective doses to the UK population from natural sources
according to NRPB. These figures may be taken as a reasonable assessment of
exposure to European populations using ICRP modelling.
SourceAverage (Sv)
Range (Sv)
Cosmic ray secondaries
280
200-300
Cosmic ray neutrons100
50-150External terrestrial
480
100-1000Internal Carbon-14
12
NoneInternal Potassium-40
165
None
Internal Uranium and120*
VariableThorium
Radon and daughters1105*
300-100,000*
Thoron and daughters
90*
50-500*Total
2352*
1000-100000**These numbers include contribution from alpha decays which carry a weighting of 20.
It is this weighting, a value judgment by ICRP, which has made Radon the main
contribution to the total dose.

The Committee is concerned that the definition of natural background radiation
employed by the ICRP and other radiation protection agencies has not been
sufficiently precise to prevent developers unscrupulously using the concept to
subsume man-made radiation exposure from historic discharges within it. Thus
the Committee defines the natural background level of exposure operationally64

ECRR 2010

as that level which would exist in the area of interest before the advent of thenuclear age, which the Committee takes to be 1910. Any sources of exposure
added to the local environment being considered since that date must be
deemed to be anthropogenic and in addition to the basic level and their origin
must be stated, irrespective of any question of liability.
7.3 Radon
The Committee feels that the situation with regard to assessing the effects ofRadon gas should be clarified. It identifies another problem of the ICRP modelin addition to that involving internal vs. external exposure: there is anotherlarge area of discussion involving whole body vs. partial body exposure. The
latter category includes both Radon gas and medical X-rays. Both of these may
have been misrepresented as greater hazards than nuclear pollution in exposure
quantity arguments. Nevertheless, there are a number of open questions
regarding the risk modelling of Radon exposures. For example the absorbed
dose to bronchial epithelium is weighted by a factor of 0.2 by ICRP from
5.5mSv average (derived from the RBE of alphas and the ICRP66 model which
dilutes the energy into surface cells) to an effective dose of around 1mSv. ICRP
considers that contribution to other compartments of the body is negligible andit has been argued that due to this ICRP underestimates Radon dose to the bonemarrow and other critical organs.
Estimates of Radon releases from natural soil vary widely from
0.2mBq/s per square metre, to 52 mBq/s per square metre. It is influenced by
the condition of the soil, its porosity, moisture content and temperature. The
emanation is reduced by snow and ice, heavy rainfall and increasing
atmospheric pressure. There are also diurnal changes, with a maximum
emanation towards the end of the night and a minimum (by half the rate) in theafternoon. Near Uranium mining the rate is several orders of magnitude greater
due to the technologically enhanced releases (TENORM). Surface level
crushed rock will release more Radon gas than radium buried in rock deep
within the earth's crust. Much of the Radon gas problem of today has been
generated by Uranium activities in support of nuclear weapons and nuclear
power since 1950: this includes Radon released from Uranium wastes
discharged to the sea (Hamilton 1989). To summarise, the Committee believes
that the doses from Radon and its daughters may have been overstated and that
this misrepresentation has had the effect of minimising the contributions tohuman exposure from artificial radionuclides. Nevertheless the health effects ofRadon may include development of conditions not currently considered by the
ICRP model which neglects the radiation exposures which lead to cancers otherthan lung cancer. A number of studies of miners and others exposed to Radon
does support such an idea. Radon exposure and health will form the subject ofa separate report.

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ECRR 2010

7.4 Artificial sources of radiation
There are seven main categories of source of radiation from human activity:
 Fallout from nuclear explosions
 Discharges from accidents at nuclear plants Radioactive waste released both without authorisation and underlicence from nuclear plants including resuspension, sea-to-land transfer
and recycling of contaminated material.
 Artificial enhancement of natural radiation, e.g. fertiliser production,
oil production, gas production, Uranium mining, military use ofdepleted Uranium, high altitude flights.
 Medical imaging and treatment
 Occupational exposure including research Electronic measuring devices, e.g. counters, smoke detectors, thickness
gaugesUNSCEAR 2000 lists most of these sources and gives the approximate ICRP
model doses from each source to the most affected group in the northern andsouthern hemisphere. Table 7.3 outlines the range of ICRP annual average dosefrom artificial sources to the UK population. There is a very wide range ofdoses and in general it is not possible to accurately calculate the exposure to
local or distant groups. In this context the Committee is concerned that theassessment of risk from many of these sources has been based on partition
modelling of the movement of radionuclides from the primary source to the
exposed individual(s) followed by the application of the ICRP model outlined
in Chapter 6. The resulting dose is a reductionist and complex combination of
the errors implicit in both routines. However, the result is always a number
which is compared both with average natural background doses and also withthe results of studies of groups exposed to external radiation. This comparison
is made in order to assess the risk to health of the exposed individual. Such risk
to health is implicitly (and often explicitly) based on the idea that variations inlevels of natural background radiation define a range of morbidity which sets a
limit on the size of dose that can cause a measurable increase in some illness,
usually cancer. However, such a comparison is not valid since the individual
cell doses, dose rates or fractionations may be widely different. The biologicaldose-equivalent approach adopted by the Committee is intended to overcome
this problem by making doses from all types of exposure strictly comparable.

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ECRR 2010

Table 7.3. Sources of exposure to artificial radiation and ICRP calculated
doses. Note that the Committee calculates these doses differently (Chapter 6).
SourceFallout from global
weapons tests
Nuclear accidents
affecting Europe

Nuclear plantreleases

Uranium weapons
nanoparticle fallout
Enhanced naturalradiation TENORM
Medical imaging andtreatment
Occupational
including research

Dose range(ICRP model)
Peaked in 1960s with cumulative
dose of 1000 to 2000Sv. Now
about 10Sv per annum.
Windscale 1957 (10-4000Sv)
and Chernobyl 1986 ( 101000Sv )Note

Varies

Dose highest in highrainfall areas by factorof 3:1Highest doses from
Chernobyl were in
Bulgaria, Austria andGreece'Critical group' are fishand shellfish eating;inhalation is a more
important pathway but
not adequately assessedby modelThousands of tons usedin Iraq, Afghanistan,
Balkans,
Not adequately
assessed
Generally elective

Effective dose limit 100mSv in 5
years (average 20mSv/y)Internal exposure notdistinguished

Varies but not more than
5000Sv to critical groups perannum at peak discharges in mid
1970s.
Average dose to public given as<10Sv per annum
Not assessed by ICRP model;
assumed negligible <100Sv to
exposed populations
Varies

7.4 Estimating the exposure
Measuring the impact of nuclear activities begins with measuring the effluence
from the industry into air and water and retained radioactive waste, thedistribution of this debris in the biosphere over space and time; its uptake in theecosystem and food web and its persistence in the biosphere; together withtransfer factors in the environment; human uptake, physiological distribution in
the body and biochemical properties; energy deposits; dose estimates to the
public and workers; and the human and environmental health implications of
this exposure. Some method for quantifying the impact on living systems isnecessary to relate concentration levels to health effects. Historically, and forreasons of simplicity, this impact has been measured in terms of a quantity
involving energy absorbed by unit mass, called absorbed dose. The general
ICRP methodological framework is based on biochemical, physiological andhealth responses to absorbed dose and deciding how many such detriments are
acceptable as a penalty for the benefits of the endeavour (see Chapter 4). The

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ECRR 2010question of the general utility of the physical quantity, 'absorbed dose' will be
explored further below.
7.5 Estimating the risk to health
The health consequences of exposure to ionising radiation follow damage tosomatic cells and germ cells and thus involve almost all illnesses. The ICRP
discourse distinguishes between deterministic and stochastic effects but
assumes that deterministic effects do not exist at low doses and that there are
no stochastic effects except cancer and heritable effects.
Thus, in the stochastic range of effects, ICRP concentrates on cancer asa major outcome of exposure and has established probability factors or risk
factors for cancer based mainly on epidemiological studies of high exposuregroups. In the low and intermediate dose region the ICRP and other risk
agencies have assumed a linear response between dose and cancer yield.
The Committee will not follow the ICRP in assuming that the only
stochastic outcome of radiation exposure is cancer. It will address the generaleffects of radiation on non-cancer outcomes including adult heart disease,infant mortality and foetal death. A comparison of the ICRP's assumptions ofeffect following low-dose exposure and those of the Committee is given in
Table 7.4
Table 7.4 The health effects of low-level radiation to be considered by ECRR
compared with ICRP and other risk agencies.
Possible health effects

ICRP and risk agencies*

ECRR Committee

Fatal cancer

Yes

Yes

Non-fatal cancer

No

Yes

Benign neoplasm

No

Yes

Heritable damage

Yes

Yes

Infant mortality

No

Yes

Birthrate reduction

No

Yes

Low Birthweight

No

Yes

IQ retardation

Yes

Yes

Heart disease

No

Yes

General reduction in
health and non-specificlife shortening

No

Yes

*UNSCEAR, BEIR, NCRP, NRPB and EU member state agencies

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ECRR 2010

The outcome of radiation exposure in the exposed individual follows from theeffects of somatic damage to cells. In the case of cancer as an outcome, there isseen both an immediate effect and a delayed effect. This pattern of risk withtime is a consequence of the multi-stage aetiology of cancer (Busby 1995).
Cancer is now believed to result from the accumulation of genetic damage incells or their descendants. The particular pattern of incidence of cancer withage is most easily explained by assuming that a geometric increase in thenumbers of a damaged cell clone ultimately results in a high enough probability
that one of the cell descendants will acquire a second or subsequent necessary
genetic mutation for cancer to develop in that cell (or group of cells). It follows
that an exposure episode may either cause initial genetic damage in cells whichhave none or add to genetic damage which is already present. For those cells
which have already acquired the initial set of genetic damage, the exposure
may produce the final requirement for cancer. For undamaged cells the episodewill supply the initial damage and start the process.
In addition, the exposure may also promote the cancer process in two
ways. The first is by promotion, i.e. causing a general increase in cell
replication rate (and therefore increasing the likelihood of mutation and also
the development of the numbers of damaged cells). The second is by causing
general immune system stress and thereby inhibiting the normal cancer
surveillance mechanisms based in the immune system.
7.6 Detriment
In order to extend the linear system of dose modelling to risk assessment, the
ICRP has introduced a number of weighting factors under the heading of‘detriment’. Detriment is a measure of the total harm attributable to their
exposure that would be experienced by an exposed group of people. In practice,
this system of weighting factors is employed for a number of purposes. One isto assess the consequence of continued or cumulative exposures. Another is tocompare the results of different distributions of equivalent dose within the bodyand to choose tissue weighting factors. The method, which is a pragmatic
attempt to devise a single set of linear equations that translate every kind of
exposure to every kind of radiation in every kind of population becomes
extraordinarily complex and unwieldy. In addition, many errors and false
assumptions are made invisible by the process which is used to give a final
relationship between effective dose (which contains within it a multitude ofvalue judgements) and cancer yield. Ultimately, the concept of detriment,
though useful qualitatively, cannot be employed accurately in a rational way.
The Committee’s response to this issue is to establish a risk factor for
loss of quality of life of 0.1% per mSv ECRR exposure pertaining to a general
reduction in general health excluding cancer. For loss of quality of life an
exposure to internal fission products conventionally assessed at 0.8mSv by
ICRP calculations may translate approximately to 200mSv ECRR and convey a

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ECRR 2010

20% loss of quality of life; this will involve 20% increased risk from all
illnesses with a genetic or somatic genetic component in the lifetime of those
exposed. In this 2010 report the Committee also includes a specific risk factor
for heart disease of 0.05 per Sv. This is based on the increased risk of heartdisease in exposed individuals from radiotherapists, from those exposed toweapons test fallout and those exposed after Chernobyl. The matter is further
addressed in Chapter13.
Since loss of quality of life also subsumes deaths from causes otherthan cancer, a focus on radiation cancer epidemiology may give incorrect
results due to confounding causes of death. You cannot die of cancer if you
have already died of a heart attack.
7.7 ICRP models for the risk of cancer
For reasons which it does not elaborate, the ICRP assumes that there is always
a latency period between exposure and clinical expression and assumes further
that there is a linear relationship between the cancer yield and exposure. There
are two models available for the expression of cancer following an exposure.
The first assumes that the excess mortality has the same pattern in time as thenatural mortality for the same cancer site. This is called the multiplicative risk
projection model. If this pattern is continued throughout life, there will be asimple proportion between the natural cancer mortality and the excess due tothe radiation exposure. An alternative, the additive risk projection model,
postulates that the excess mortality is broadly independent of the natural
mortality. The rate would rise following exposure and remain constant or fall.
On the basis of epidemiological evidence, mainly from the Hiroshima study,
the ICRP chose to imply a multiplicative risk projection model for all cancers
except leukemia.
Following the assumptions made on linearity of effect and risk
projection, the final estimates of the cancer yield per unit exposure is given by
ICRP as the nominal probability coefficient, also called the risk factor. Thisvalue is a risk factor for representative populations with well-defined exposure
patterns. It applies to low doses at all dose rates. In providing values for thenominal probability coefficient the ICRP makes allowance for the reduction ofthat probability resulting from competing causes of death. This is necessary
following the adoption of a multiplicative model (see above).
In addition, owing to arguments relating to non-linearity of themeasured dose-response curve for external irradiation the ICRP employs acoefficient called the Dose and Dose Rate Effectiveness Factor DDREF which
is chosen to reduce the risk factor for low-level radiation exposure in the belief
that at low doses the effects are less severe than at high doses. The ECRR will
not employ the DDREF approach and has subsumed it within the concept of
biological equivalent dose.

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ECRR 2010

The risk factors expressed by ICRP are given as probabilities and may
be translated in a number of ways, for example:
 The ICRP 2007 absolute risk value for cancer probability in the highdose and high dose rate region is 5.5x 10-2 per Sv (i.e. if this number isused to multiply by the dose and the number of people exposed to that
dose, the result is the number of cancers).
 This may also be expressed as 550 fatal cancers per 10,000 people per
Sievert (i.e. if 10,000 people each receive 1 Sievert, then there will be
550 cancers in this population as a result) Another way of expressing this risk is as a percentage; 5.5% per
Sievert (i.e. if 100 persons received a dose of 1 Sievert each then 5.5
will develop cancer)

7.8 Stochastic effects in progeny: heritable damage
Apart from cancer, which is modelled as a result of somatic cell damage, the
ICRP also recognises that damage to germ cells (mutation and chromosomal
aberrations) may be communicated to offspring. This may manifest itself ashereditary disorders in the descendants of exposed individuals. The 1990
recommendations of the ICRP, which are presently those which underpin
radiation risk models, state that radiation has not been identified as a cause ofsuch effects in man, but experimental studies on plants and animals suggestthat such effects will occur, and that such effects will range from theundetectably trivial, through gross malformations and loss of function, topremature death. Since this statement was made, applications of theminisatellite DNA testing procedure have shown unambiguous evidence ofsuch mutation in the offspring of the Chernobyl ‘liquidators’. The matter isaddressed in Chapter 13.
The nominal hereditary effect probability coefficient for severe
hereditary effects (excluding multi-factorial effects) over all generations andrelated to gonadal dose distributed over the whole exposed population is now
given as 0.2 x 10-2 Sv-1; this is actually a reduction from the ICRP1990 value.
About 80% of the effects are due to dominant and X-chromosome linked
mutations.
ICRP also includes a weighting for years of life lost if the harm occurs:
this is a factor which is part of the system of ‘detriment’ described in 7.5.
7.9 Effects of exposure in utero and other effects
The Oxford Survey data of Alice Stewart showed a 40% increase in cancer inchildren who received a 10mSv X-ray dose in utero. This data has now been
accepted as defining an in utero risk for external photon radiation of 40 per Sv(Wakeford and Little 2003, CERRIE 2004, 2004a). For the internal exposures
to Chernobyl fallout and employing a meta-analysis of 4 countries in Europe

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and addressing infant leukemia this value is at least 160 times too low, though
the effects in the children as they age is not included in this analysis and thedose response is biphasic. Different analyses by foetal dose in the several
countries where data was analysed give error factors of 100 to 600-fold (Busby2009) The Committee use a value of 50 Sv-1 for external X-rays of the fetus;
the internal effects will be subsumed within the method of adjusting doses forinternal isotopes and so the value above may be retained.
7.10 ICRP risk factors for whole body effects
The ICRP risk factors for the different consequences of exposure to radiation in
the low-dose region are given in Table 7.5 These factors include all the various
weightings involved in the concept of detriment but represent values which the
ECRR will use as a basis for its system of risk assessment. A number of studies
have suggested that these risk factors are in error by between 2- and 20-fold i.e.
the cancer risks may slightly greater than suggested but the problem of
distinguishing internal and external exposures has not been addressed in thiscontext until now. The Committee's risk factors are given also in Table 7.5. The
matter is discussed in Chapters 10 to 13.

Table 7.5 ICRP2007 and ECRR modified risk factors for whole population forwhole body effects.
OutcomeFatal cancer
Non-fatal cancer
Benign neoplasm
Heritable disease
Malformation after in utero
exposureHeart disease
Cancer after in utero
exposure
IQ lowering after in utero
exposure
Severe retardation after inutero exposure

ICRP risk factor(per Sievert)
Not specified
0.055
Not considered
0.02
100mSv threshold

ECRR risk
factor(per Sievert ECRR)
0.1
0.2
being assessedb
0.04
No threshold

Not assumed
0.2a

0.05
50

30 IQ points;
100mSv threshold
0.4; 100mSv
threshold

30 IQ points; nothreshold
0.8; no threshold-1

Nominal probability coefficient expressed as SvaThis is the ICRP 1990 value, ICRP2007 avoids giving a value but states that the risk
is the same as for exposure in early childhood and neglects to give that value.
b
For radiogenic benign intracranial tumours see Schmitz Feuerhake et al 200972

ECRR 2010

Note: Values for workers, where applicable, are slightly less than these owing to thedifferent age distribution of workers. Refer to the ICRP publications for details.

7.11 ICRP risk factors for individual organs and tissues.
The tissue weighting factors used by ICRP (described in 5.5) for defining thequantity ‘effective dose’ were chosen by ICRP to ensure that a weighted tissue
equivalent dose would produce broadly the same detriment irrespective of thetissue or organ involved. The weightings applied include: The probability of fatal cancer attributable to the exposure.
 The weighted probability of non-fatal cancer.
 The weighted probability of severe hereditary defects.
 The relative length of life lost.
The model enables the ICRP to partition fatal risk according to tissue
sensitivity and other factors in such a way that fatal cancer risk following
irradiation of individual organs may be assessed. Factors chosen for thispartitioning are given in Table 7.6.
ICRP also gives figures for aggregated detriment and separate sets offigures for workers, which allow for the different age breakdown for the latter.
These are not reproduced in Table 7.6 as the present approach does not require
their use.
Table 7.6 ICRP cancer incidence risk factors for individual tissues and organs
for low-dose exposureaTissue or organ
Risk factor
Bladder
43
Bone marrow
42
Bone surface
7
Breast
112
Colon
65
Liver
30
Lung
114
Oesophagus
15
Ovary
11
Skin
1000
Stomach79
Thyroid33
heritable
20
Remainder
144
Total
1715
a
Nominal probability coefficients per Sv per 10,000 exposed

73

ECRR 20107.12 Calculating the fatal cancer yield in an exposed population
Over the low-dose range to a few mSv ECRR assumes that a linear nothreshold dose response is assumed as an approximation. Thus, to the same
approximation, excess cancer incidence is proportional to radiation dose (thelinear no threshold model LNT); then over this low-dose region the number ofcancer cases that will occur in a population that is exposed to radiation is:Cases = (number exposed x equivalent dose Sv) x Risk factor (per Sv)
If the collective dose is known (in person Sieverts) then the right hand side ofthe equation is simplified to:Collective equivalent dose (PSv) x Risk factor (per Sv)
Because the ECRR has modified the calculation of equivalent dose byincluding weighting factors for the effectiveness of the radiation in causing
mutation at the molecular level, the calculation is the same except that thebiological equivalent dose is substituted. The ECRR calculation of excess
cancer cases would thus take the form:
Cases = (number of people exposed) x (biological equivalent dose, Sv) x Risk
factor (per Sv)
If the collective dose is known (in person Sieverts) then the right hand side ofthe equation is simplified to:Collective biological equivalent dose (PSv) x Risk factor (per Sv)
In Chapter 14 the method is applied to global fallout and other exposures.
Excess cancer mortality may be calculated by applying the incidence-tomortality ratio for the cancer site, population and period as tabulated by cancer
registries for the area.
It will be clear that for the purposes of calculating the cancer yield
above, the Committee have employed the linear no threshold LNT approach of
the ICRP. The true dose-response relation is elsewhere argued to be complex
and generally biphasic, i.e. after a certain dose it falls and then rises again.
However, over the region and type of exposure being considered (fallout andnuclear power station doses, these are less than 1 mSv and it is assumed thatthe dose response is in the rising-from-zero part of the biphasic curve and canbe assumed in that region to be approximately linear. This point is explicitly
made in response to criticism from the French IRSN commentary published in
2005.
The evidence for the need for this approach is presented in thefollowing chapters.

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ECRR 20108
Establishing the Health Effects at Low Dose: Epidemiology
8.1 Evidence and inference: Bradford Hill’s canons.

In Chapter 3 the scientific method was reviewed, and it was established that themethod was essentially one of induction. If we wish to know the answer to thequestion: 'What effect does exposure to ionising radiation have on humanbeings?' then the most accurate answer will come from a study of a group ofhuman beings who have been exposed in a laboratory to a known dosecompared with an exactly similar group who were not exposed. This
experiment cannot, of course, be performed. However, since the beginning of
the last century, there have been a very large number of radiation exposures todifferent groups of people in different parts of the world and the outcome ofmany of these exposures has been studied by epidemiologists in order toconstruct an understanding of the health consequences of different doses andultimately provide some evidence that would enable risk to be quantified.
Before moving on to review the evidence on which the risk factors of
the ICRP and those of the ECRR are based, some account of the procedures
and complications of epidemiology are presented.
Epidemiology is the study of the distribution and determinants of
disease in human populations. A key aspect of epidemiology is that it isobservational rather than experimental and therefore has to operate in an area
where bias or confounding of the inferences drawn from the data may occur. In
chemistry, a blue liquid may be mixed with a green liquid to give a red
precipitate: this will always happen so long as the experiment is exactly
repeated and the results can be used to draw inferences about the nature of theprocesses involved. But it is rare that an epidemiological study has the
specificity of design and sufficient exclusion of uncontrolled variables between
the study and control groups to enable unequivocal conclusions to be drawn.
Therefore this is an area where studies may be electively biased or evendirected to find either a result or no result. In addition, all studies may besubject to considerable criticism by groups who hold opposite views forreasons which may include culture, employment or political pressure. The
Committee has found evidence of all three of these mechanisms of bias inpublished papers and review articles. In drawing inferences from all theepidemiological studies of radiation and health, the Committee has consideredvery carefully the provenance of the study and in particular the likely
directional bias of the study’s funding bodies and researchers.
All epidemiological studies compare a study group or groups, in thiscase those exposed to a known quantity of radiation, with a control group, whoshould be matched in every way except that they are not exposed. Before
examining the real studies that attempt to translate this ideal study and quantify
the risks we will first introduce some aspects of the analytical procedure. The

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most valuable list of procedures which should be followed in order to draw safe
inferences from evidence in epidemiological studies was devised by Sir Austin
Bradford Hill in the 1950s and is termed Bradford Hill’s Canons. They are
sufficiently valuable in assessing the case of radiation and health to give a shortaccount of them so that they may be applied to the radiation studies presented.
8.2 Bradford Hill’s Canons
8.2.1 Statistical significanceA secure foundation for argument in any comparison of an exposed study
group with an unexposed control group is that the difference in health deficit,
cancer mortality for example, is statistically significant and could not haveoccurred by chance. Significance testing is an area of statistics and a number ofbasic tests may be applied to see if a result is statistically significant.
The word ‘significant’ is one that within the scientific community has a
specific, technical meaning, but can also be interpreted generally by those
without a scientific background. When a research finding is said to be‘significant’ this means that it may be considered to be meaningful, in the senseof not being a chance finding. Since statistics is a methodology based on
probability, it accepts a certain level of error as inevitable, meaning that somescientific findings that have passed the ‘significance’ test are still bound to be
wrong.
The level of ‘significance’, which, of course, is directly related to thelevel of error, is chosen by the researcher, and should be set higher if thefindings have more potentially dangerous implications. The level ofsignificance generally adopted in scientific research is 5 per cent. This meansthat researchers are accepting a 5 per cent level of error, or that they will bewrong 1 in 20 times.
The procedure of testing whether results are ‘significant’ is known as‘hypothesis testing’. The scientist tests the ‘null’ hypothesis, which is the
proposition that there is nothing unusual going on, or that the distribution of
results found does not differ from what would be expected by chance.
Statistics defines two types of error that can be made when undertaking
research. The first, known as a Type I error, is the one of most concern toscientists. It involves making a claim to have a research finding when in fact
the results were generated by chance. An example might be a medical trial
which indicated that a certain drug was effective in slowing the progress of
AIDS; follow-up research might fail to find a similar result, suggesting that theoriginal findings fell into the 5 per cent error area. For professional andcredibility reasons, this is the kind of error most feared by a researcher: theerror of claiming a significant result when in fact the finding resulted fromchance.
But there is another type of error which is equally important,particularly in terms of potentially harmful consequences of radiation exposure.

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This is the Type II error, defined as the failure to find a significant result when
the hypothesis is in fact correct. It represents the risk of carrying out a study
and, for reasons which may relate to technical issues such as the size of thesample, failing to find a statistically significant result. It may not necessarilymean that the hypothesis is wrong, only that significance was not found thistime. However, it may allow conclusions to be drawn, either to justify use of atechnology or because of extreme caution, that processes are not causing any ill
effects when in fact they are.
Radiation risk studies in the low-level radiation range very often
involve small numbers of people in the exposed study group, those living neara point source such as a nuclear power station for example. Studies with large
populations may have small numbers of cancer cases due to very low naturalrates from the disease in question: an example is childhood leukemia. In eachof these types of situation, statistical methods have been developed to deal withthe mathematical problem, yet finally there may not be sufficient evidence ineach study to draw an inference from measured excess risk from the radiation
exposure because chance could not be ruled out i.e. the result was not
significant at the 5% level. This is usually a consequence of the numbers
involved. When a material difference is apparent between two groups, but, with
the numbers involved, is insufficient to pass the significance test Bradford Hillargues that it is better to take ‘statistically not significant’ as the ‘non-proven’of Scottish law rather than the ‘not guilty’ of English law. It is nevertheless truethat policy decisions in the area of radiation and health have fallen into the trapof assuming that 'there is no evidence that low-level radiation exposure ishazardous' means 'low-level radiation exposure is not hazardous.'
In giving weight to such evidence, the Committee made two decisions.
The first was to take a precautionary approach and avoid making a Type IIerror in such an area of low-probability high-impact risk, for if the evidence
showing excess risk from the exposure were in fact a chance finding, themistaken inclusion of it as evidence of radiation-induced effects would notharm the human race. If on the other hand, the Committee were to take theopposite view and exclude it as evidence when it was, in fact, a true measure ofa real effect but merely formally non-significant, then much harm would follow
its dismissal. Consequently the second decision was to use a Bayesian approachto the refinement of belief in the area of risk assessment and allow each nonsignificant observation (including unpublished results) to weight and modify
the overall probability of belief in the area of radiation risk according to theirdegree of significance. Thus the discovery of a child leukemia cluster in the
1980s near the nuclear reprocessing plant at Sellafield in Cumbria, UK has
been criticised on the basis that the statistical significance of the result for theward (p = .002) enabled no inference to be drawn since there are more wards in
the UK than the 500 wards needed for such a result to be a chance occurrence.
However, since this discovery, child leukemia excesses have been discoverednear two other reprocessing plants and a number of nuclear installations in

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Europe. The most recent example, a very large study of nuclear plants inGermany, found that living within 5 km of the plant doubled the risk ofchildhood leukemia in those aged 0-4 (Spix et al 2008, Kaatsch et al, 2008)).
The Bayesian modification of the probability of the causal relation by each new
example gives the Committee a firm basis of belief in the association andenables robust conclusions to be drawn about the levels of risk from exposure
under these circumstances.
8.2.2 Strength of association
There should be evidence of a strong association between the risk factor andthe disease: in other words, it is necessary to consider the relative incidence ofthe condition under study in the populations contrasted.
8.2.3 Consistency
The association should have been repeatedly observed by different persons indifferent places, different circumstances and times. With much research workin progress many environmental associations may be thrown up. On thecustomary tests of statistical significance, some of them will appear unlikely tobe due to chance. Nevertheless, whether chance is an explanation or whether atrue hazard has been revealed may sometimes only be answered by a repetitionof the circumstances and the observations. Broadly the same answer should begiven by studies using a wide variety of techniques and in different situations.
8.2.4 Specificity and reversibility
The association should be specific. The disease association should be limited,ideally, to exposure to the putative cause and those exposed should not suffer
an excess risk from other kinds of illness or modes of dying. In the area ofradiation risk, where the plausible biological model involves genetic andsomatic damage, disease specificity may be hard to define. One condition
which has become considered as a specific consequence of radiation exposure
is leukemia, particularly in children. However, the specificity should be defined
accurately in terms both of cause and effect. In the case of low-level radiation
exposure, the lack of distinction between external and internal exposure has led
to conclusions being drawn which are incorrect. Associated with specificity isreversibility. Thus removal of the cause should ideally reduce the incidence ofthe disease, although this is a consideration which is difficult to apply in thecase of cancer, where genetic damage is not removed by removing the cause of
the damage.

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8.2.5 Relationship in time.
There should clearly be evidence that the risk factor preceded the onset of thedisease.
8.2.6 Biological gradient
There should be evidence of a dose-response effect. This is usually taken tomean that as the dose increase, the illness rate should also increase in some
proportion. However, some thought will reveal that this may not be true forcertain end-points. Take, for example, birth malformations due to an exposure.
Increasing the stress from zero will cause increasing damage to embryos which
may eventually present as increasing risk of malformation. At some point, theweight of damage will prove too great and the embryos will die: at this dose,
there will be no further congenital malformation, merely a reduction in thebirth rate. It has been shown that women exposed to internal radioactive
isotopes suffer an increase in miscarriages (Fucic et al 2007). Since there aremany possible reasons for reduction in the birth rate, including social ones, thefact that exposure to a large dose of some putative mutagen has not caused any
increase in birth defects ought not be taken as evidence of no effect unless
lower doses are also considered and the dose-response relation adequately
considered. This exact misunderstanding appears to have led to the belief that
exposure to radiation from Chernobyl caused no harmful effect on birth defect,
stillbirth and infant mortality rates in European populations. A number of
papers asserted this on the basis of the data without drawing attention to the
sharp fall in the birth rate that occurred some nine to twelve months after the
exposure. A similar type of error also applies to ecological studies where somegroups of individuals may have greater susceptibility to radiation. The
existence of a dual sensitivity to radiation as a consequence of normal cell
division also results in a dose-response relation which is biphasic, i.e. has twoareas where increased effect follows increased dose, with an intervening area
where increased dose results in reduced effect. The existence of inducible celldamage repair results in a similar biphasic relationship between cause andeffect.
8.2.7 Biological plausibility: mechanism
Bradford Hill stated: ‘It will be helpful if the causation we suspect isbiologically plausible, though this is a feature we cannot demand. What isbiologically plausible depends upon the biological knowledge of the day. It waslack of biological knowledge in the 19th century that led a prize essayist
writing on the value and fallacy of statistics to conclude that among other'absurd associations . . . it could be no more ridiculous for the stranger who
passed the night in the steerage of an emigrant ship to ascribe the typhus, which
he there contracted, to the vermin with which the bodies of the sick might be79

ECRR 2010

infected'. For this reason the Committee is anxious to avoid dismissing
evidence of health detriment following low-level radiation exposure on the
grounds of lack of a plausible biological mechanism. In particular, the ICRP's
assumptions about cell dose at low-level exposures provide a good example of
how mechanistic arguments have been used to argue for a linear relation
between dose and response, a thesis which is only valid for external random
irradiation of large tissue volumes and which, in any case, is being overtaken
by recent research on genomic instability and bystander effects which will be
reviewed below.
8.2.8 Alternative explanation
There should be no convincing alternative explanation or confounding for theobserved association.
8.3 Application to radiation epidemiology
The purpose of this chapter has been to outline the generally accepted methodof assessing causation following questions about environmental causes of
disease. In the following chapters, these methods will be used implicitly or
explicitly to analyse the evidence that low level radiation exposure has harmful
impacts on human health and to approach quantitative assessments of these
impacts. The position of ICRP is that there is no impact whatever: that doses
below 5mSv, as defined by their system, can have no measurable
consequences. Indeed, their risk factors predict that for a dose of 1mSv (asdefined by ICRP) this 'maximum permissable legal dose' gives a fatal cancer-5risk of 5 x 10 . This is one excess cancer death in the 70 year lifespan of
20,000 persons exposed. For those who have increased rates of cancer, andwho live near nuclear installations, and who are exposed to radioactive
pollution at low-dose levels as calculated by the ICRP, causality is clearly
going to be rejected. But apart from the obvious and major criticism that therisk factors are culled from studies of external acute irradiation, strangely there
has been no effort on the part of ICRP to apply Bradford Hill's principles of
causation to their problem. The Committee has attempted such an analysis withresults which are presented in Table 8.1 below.
8.4 Animal Studies
The Committee has reviewed the studies which examine the effects of lowlevel exposures on various animals. They note that the majority of these studies
examine the effects of large external acute doses of various types of ionisingradiation and accept that these may provide useful information. They also notethat a number of studies have examined the health consequences of internal
exposure from a number of radioisotopes. With regard to late effects following
exposure the Committee has three main reservations about the extrapolation of80

ECRR 2010

such results to human beings. First, with studies of short-lived animals, thetime period available for the development of cancer following initial genetic
damage is very restricted and is probably considerably longer than the lifespanof the individual. Second, the need to obtain observable effects results in thedoses used in the study (which for cost reasons must use a limited number ofanimals) being very high and the controls or low-dose groups very often show
anomalously high levels of cancer owing to the assumptions of linear (orcontinuously increasing) dose response. Finally, the use of animals may not bejustified due to inter-species differences in cell repair or cancer surveillancemechanisms.
The Committee notes with interest that a wide range of animal studies
of internal irradiation have revealed profound developmental and offspringmortality effects which have not been addressed by ICRP or other risk
agencies.
Table 8.2 Errors in published epidemiological studies of radiation risk.

Error

Note

Wrong doses

Studies invariably use measured or modelled external dose as thecause covariate and subsume internal dose within it. If the latter ismore hazardous no safe conclusions can be drawn from the results.
1. If the controls were also contaminated the relative risk (deaths
in study group/deaths in controls) will be low, possibly nonsignificant. This mistake has been made consistently, e.g.
Hiroshima LSS, Marshall Islands, Chernobyl fallout.
2. In ecological studies of populations near nuclear sites study
group and controls are generally defined by radii of circles
drawn around the source. This approach makes no allowance forreal movements of radioactive material via wind, water andground topology. Controls may thus be more exposed or equally
exposed. The method has been consistently used in the UK todeny risk.
3. Use of the general population as control group may beinappropriate if the study (exposed) group is not representative,e.g. healthy worker effect (nuclear workers), war survivor effect(Hiroshima LSS cohort).

Wrongcontrols

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Wrong sample

1.

2.

Wrong
assumptions

1.

2.

3.

Wrong
methodology
Wrongmethodology
Wrong end
point
Wrong
conclusions
Wrong data

82

If the sample shows an effect, it may be diluted with those who
were less exposed to reduce the statistical significance of theresult. This is ‘boundary loosening’ e.g. the NRPB study of UK
atomic test veterans.
Many different groups with different genetic susceptibility toradiation and different doses may be aggregated together andstudied through time over a period of radiation exposure
episodes. Lack of any step change is used to argue that there isno effect. e.g. the Nordic leukemia study; ECLIS study ofleukemia after Chernobyl in Europe.
The assumption of a linear no-threshold dose response has
resulted in many clear observations of effect being discounted
because high-dose groups may have lower cancer rates thanintermediate-dose groups. e.g. nuclear workers, Chernobyl
effects in Europe
Inducible radiation resistance has been demonstrated in animalstudies yet no allowance has been made for this whencomparing populations in Natural Background studies.
Cancer as the main outcome of exposure is modelled as aconsequence of a single event. The genetic theory of cancer
causation used as a model omits analysis of later effects on
progression through e.g. immune system stress.

Statistical regression methods using multiple covariates are suspect
because they are easy to design in a way that loses significant
effects.
Ecological studies which ‘lose ‘significant data following Bayesiansmoothing may falsely conclude that there is no effect.
The ICRP has focused heavily on cancer as the end point. Manyother diseases and conditions have been excluded, including infant
and perinatal mortality.
It is common for there to be a study whose conclusion or abstract
claims to show no effect but which, on close examination of theresults in tables and text shows clear evidence of one
The data itself is often suspect. Following Chernobyl, the‘liquidators’ appeared to have lower rates of leukemia than thegeneral population, but reports emerged that Soviet doctors wereforbidden to record the disease (see text). In Wales, cancer cases
have been removed from the database with the result that Sellafield
effects on coastal population have been diminished or erased. After
the Windscale fire, the direction of the fallout plume was changed
and meteorological records were tampered with to minimise theeffects on Ireland and the Isle of Man. In Germany, infant mortality
records were altered to ‘lose' Chernobyl effects.

ECRR 2010

8.5 Ideal epidemiological studies
The Committee believes that epidemiological studies and animal studies should
ideally compare a specific end point and accurate data relating to the irradiatedgroup with similar data from the same source for an exactly matched control
group who were not irradiated. The irradiation pathway and exposure type mustbe specified well and not mixed. Outside the laboratory there are few situations
where this type of study can be made, but the Committee observes that very
often where such studies are possible, they are not undertaken or else the data
are kept confidential. The Committee strongly recommends that morbidity andmortality data for populations of small areas be made freely available forindependent research so that studies may be made which more closely
approximate to the ideal. The Committee believes, moreover, that time series
data on a well-defined population exposed to ionising radiation are likely toprovide the best opportunity for examining its effects since the study groupmay be compared with itself.
8.6 Unequivocal evidence
The Committee draws attention to the unequivocal evidence of low-level
radiation exposure effects demonstrated by the increase in infant leukemia in
six countries following in utero exposure to radioactive material dispersed
following the Chernobyl accident. These results show with no ambiguity that
the ICRP model for low-level radiation exposure is unsound.
Epidemiologically, the observation cannot be faulted since the control group ineach country was the same population, unirradiated, and the lag between
exposure and effect was so short that no other confounding cause existed whichmight explain the leukemia increase. The observation is reviewed in Chapter
10.

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ECRR 20109
Establishing the Health Effects at Low Dose:
Mechanisms and Models.
9.1 The need to consider mechanism'Have the releases from nuclear site X caused the increase in cancer in people
living nearby?' This question, and variations of it, must be addressed within theframework of Sir Austin Bradford Hill’s epidemiological canon outlined in
Chapter 8 and is also one of the principles of scientific method given in
Chapter 3. One of the requirements for causality is that there should be abiologically plausible explanation. However, Bradford Hill himself did notinsist on a mechanism, arguing that the mechanisms for an effect may not yet
be understood. The Committee has considered this area carefully and concludes
that the decisions made by risk agencies like ICRP to dismiss causality in suchcases have been made on the basis of flawed mechanistic reasoning and lack ofknowledge. The ICRP's arguments based on mechanism have led to its belief
that low-level internal irradiation is harmless. Perhaps because of this, there has
been inadequate research in the area with the result that there is a poor state ofknowledge about low-dose effects, particularly from internal irradiation.
The Committee will review the evidence available and also outline
number of mechanisms which predict and explain health detriment associatedwith certain types of internal irradiation.
9.2 Biological damage following exposure to ionising radiation
The damage produced by ionising radiation exposure is a consequence of fourkinds of effect: They are:
 Direct ionisation of critical molecules like DNA with consequent
rearrangement and destruction or alteration
 Indirect destruction or alteration of critical molecules (like DNA) throughfree-radical and mobile-solvent-derived ion formation
 Enhanced absorption of natural background (or medical) photon radiationby contaminants of high atomic number leading to enhanced ionization
though photoelectron production
 Direct destruction or alteration of critical molecules through transmutationof a bonded or Hydrogen-bonded radioisotope.
 Indirect alteration of the cellular genome through epigenetic mechanisms
which result in changes in cellular signalling processes, e.g. genomic
instability, the bystander effect, induced repair efficiency.
Critical molecules are those associated with the viability and integrity of thecell, the most important being chromosomal DNA. In addition to direct attacks
on constituent DNA bases by free radicals, direct hits and transmutation
effects, there are also likely to be secondary causes of damage to DNA

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replication associated with damage to cell membranes, repair/replication
enzymes or cell communication systems. All these systems include substances
which have very high molecular weight and consist of very large numbers of
atoms whose position and identity are critical to their effective functioning
through primary, secondary and tertiary (morphological) structure.
Following the damage to the components of a cell which are necessary
for its genetic integrity and viability, the cell may repair the damage, misrepair
the damage or die. Evidence has emerged recently that the cell may also exhibit
the phenomenon of genomic instability, where the progeny of an irradiated cell
may unexpectedly become highly susceptible to general mutation. This may
also occur in the progeny of cells close to the cell which is traversed by theradiation track but which themselves are not directly hit (Mothershill andSeymour 2001).
9.3 Relationship between absorbed dose and cell dose
Both direct and indirect ionisation is a consequence of the absorption of energy
from the incident ionising radiation beam or track. This causes chemical bondbreakages with the formation of free radicals and reactive species. Because themain constituent of cells is water, the main free radicals and other ‘hot’ species
are those which follow the rupture of the OH bond in water. For every 100
electron volts of energy absorbed, about four water molecules are split into OH'
and H' free radicals. The ' stands for a free electron and these species are
therefore very reactive. They may either react with each other to generate morewater or react with other molecules like DNA to cause alteration or destructionof their chemical identity and biological activity (BEIRV, 1990).
The breakage of a chemical bond may be accompanied by release ofexcess energy in the form of electrons which can cause further bond breakages
and so forth until all the energy is dissipated. Therefore, radiation manifests its
effects in tissue through the formation of structured tracks of charged particles
which cause, in turn, the formation of clusters of highly energetic free radicals
and other electrically charged and reactive chemical species along the track.
From the point of view of biological damage the effects are likely to be
proportional to the concentration of such species and this in turn depends on
the number of tracks in unit tissue volume in unit time and also the density ofionisation within the track. At high free-radical concentrations, however, theproportionality is affected by the increasing number of reverse reactions taking
place.
The track density depends on both the exposure magnitude and type ofradiation. For example, large highly charged alpha particles are relatively slowmoving compared with electrons, and the polarisation effects occurring as they
move through tissue result in high ionisation density. It is largely for thisreason that the ICRP has given them a relative biological effectiveness (RBE)weighting of 20 compared with beta particle irradiation and the secondary
electrons generated following gamma ray absorption. The quality of radiation

85

ECRR 2010that represents its ability to cause ionisation along a track is called Linear
Energy Transfer (LET). Low LET radiation includes gamma rays, X-rays andbeta particles. High LET includes alpha particles, which are slow and highly
ionising. However, this is an approximation since the ionisation density ofelectrons is not uniform and increases at the end of their track as they slow
down.
In the low-dose region, track density is considered to be sparse. The
average track density per unit time for any absorption of radiation energy caneasily be calculated. Table 9.1 gives the results of calculations in which energy
is averaged over tissue to show the number of cell nucleus track traversals per
year at different doses for low and high radiation energy externally incident on
a human body.
9.4 Phantom radioactivity: the Secondary Photoelectron Effect, SPE.
In the above account, it is assumed that absorption and production of electron
tracks is constant across tissues, in other words, it is the variation in thequantity and quality of radiation introduced to the organism as a result of someradioactivity added to the environment, either internally or externally that is thesole determinant of ionization density. This is not the case: the density ofionization tracks is also a function of the molecular and atomic components of
the absorbing tissue. This is an important issue which has been entirely
overlooked for radiation protection purposes, although it has received someattention from medical radiologists. The matter was outlined in Section 6.5 but
will also be briefly discussed here as it is a relevant mechanism for radiation
damage. Since it is universally agreed that it is the ionization density at any
point which is the critical quantity in radiation protection, and since it is also
argued (and shown by countless experiments) that it is the chromosomal DNA
that is a critical target for radiation induced harm, the ability of the DNA toabsorb photon radiation is clearly an important variable. Ionisation on or very
near the chromosomal or other critical DNA is unarguably more likely to cause
more damage than ionization in the bulk liquid in the cell or in interstitialmaterial. Auger substitution experiments have demonstrated this quite clearly(Baverstock and Charlton 1988, CERRIE 2004a). It has been pointed out thatthe absorption of photon radiation, e.g. from natural background radiation is
proportional to the fourth power of the atomic number Z of the element. This
energy is re-emitted as photoelectrons. Internal rearrangements in the atom
may result also in the re-emission of short-range Auger electron showers.
Therefore, high Z elements which are bound to DNA, like Uranium, present a
particular hazard since they act as an antenna for background radiation, reemitting photoelectrons and Auger electrons into the DNA continuously.
The effect also is of significance for micron or nanoparticles of theelement; a situation which exists in the case of Uranium particles from
weapons usage and possibly Platinum particles from catalysers on vehicles, or86

ECRR 2010

Gold particles abraded from prostheses. The effect is not small, and it isentirely independent of the intrinsic radioactivity of the absorbing andphotoelectron re-emitting atom. There is also no doubt of its reality:
radiologists have accepted it for more than 50 years and most recently are
employing it to enhance radiotherapy for cancer. This mechanism is interestingin the Bradford Hill sense since massive epidemiological evidence of harmfrom Uranium exposures has been discounted by governments and the militaryand even the UK Royal Society on the basis that there is no mechanism toaccount for such effects at the low doses involved. The evidence for Uranium
effects on health will be reviewed in Chapter 12.
9.5 The consequences of cell damage following radiation exposure
All life has been exposed to ionising radiation from natural sources overevolutionary time scales. The damage caused by radiation has two main
outcomes. First, it results in finite lifespans for all living creatures bycontribution to the thermal error (Boltzmann) erosion of the genetic material
over the lifetime of the individual and the effects of free radicals formed
through cellular oxidative metabolism. It has been well known since the 1960s
that in mammals the species lifespan is directly proportional to the radiation
resistance (Sacher 1955, Busby 1995,). Second, it adds to the probability ofgenetic mutation of species. Both of these result in health detriment, since theformer is the cause of non-specific ageing and the latter is believed to be amajor element in the causation of cancer and other diseases and conditions ofgenetic origin.
The addition of further and novel sources of radiation exposure as aconsequence of human activity results in increases in exposure but also, in thecase of internal isotopes, exposures which are qualitatively different. Fromconsiderations of radiation action, it is clear that cells in tissue do not suffer
incremental damage as dose increases. A cell is either hit or not hit and evenfor low LET radiation, traversal of the cell nucleus by the primary electron
track results in about 70 ionisations and a dose of 1mSv. The consequence of
this hit depends upon the critical nature of the part of the cell which is affectedby the ionisation, and how sensitive the cell is in that part of its lifespan that isintercepted by the radiation event.
The variation of cell sensitivity over its lifespan is not considered by
the ICRP model, although a very wide variation has been known for 40 years.
Variations in the normal replication rates of cells from one tissue to anothercause the varying radiosensitivity of the tissues. The overall outcome of theradiation hits will also depend on DNA repair and replication systems andfactors affecting their efficiency, a matter which is outlined below. Thus theresult of a hit for the cell may range from 'no measurable effect' through'accurate repair of damage' through 'fixed mutation' to 'cell death', and these are
given in Table 9.2.

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Table 9.1 Typical annual doses and average number of tracks touncontaminated human tissue based on cell diameter of 8 microns, andignoring multiple decays from certain internal isotopes.
Condition

Radiation
LET

Absorbed dose
mGy

Dose
equivalentmSv

Averagepublic whole
body:
Lung:

Low

~0.9

1

Averagenumber of
tracks per cell
nucleus per
year
1

High
(alpha)High(alpha)
Low

0.4

20

0.001

0.005

0.1

0.00001

<50

<50

<50

Medium(neutron)High(alpha)

<5

<50

<0.5

<2.5

<50

0.007

Bone
marrow
Workerwhole body:Workerwhole body:Workerwhole body:

Following increasing radiation exposure the effects in individuals, who aremade up of many cells, will range from no measurable outcome throughmutation effects to loss of viability and ultimately they may die. The samerange of effects may occur in their progeny. Following the discoveries whichhave been made in the area of genomic instability, it now seems that about one
third of all hits result in cell damage to the cell. In addition, nearby cells seemto be affected by some kind of local signalling process which causes genomic
instability in them also. This is known as the 'bystander effect'. These two
effects seem to be very important in the mechanistic understanding of cancer
since they are associated with a general multiplication of genetic damage andthis is detectable as chromosome aberration frequency increase.
As a result of examining the variation of cancer rates with age, cancer
is now believed to be the result of up to six separate genetic changes. These
include acquisition of specific oncogenes and loss of tumour suppressor genes.
Since the normal rate of genetic mutation on replication is about 10-5 per gene,it has been difficult to explain how the acquisition of enough mutations tocause cancer can occur in the lifetime of an individual. Advances in technology
have recently enabled computer control of microbeam radiation sources so thatsingle cells may be hit, and new chromosome staining techniques have enabled
their descendants to be identified and checked for damage. This has shown
important effects. Genomic instability engendered by radiation at very low
doses (i.e. up to 10mSv) results in an increased general level of genetic

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mutation in the progeny of a cell which is hit. In addition, general levels ofmutation increase, through bystander signalling in the progeny of a significant
proportion of cells in the vicinity of the cell which is hit. These effects increase
the general rate of mutation in cell volume elements to a level where enoughmutations are produced to explain the development of cancer (Little 2002, Hall
2002, CERRIE 2004, CERRIE 2004b, Mothershill, 2009 ECRR 2009). Table
9.2 lists the range of outcomes to the individual following increasing dose to
the individual cell.
Table 9.2 The effects of increasing doses on cells and individuals
Increasing
dose range
group
1
2

3

4

5

6

7

Effect on cell

Effect on individual

No measurable effectInduction of genomic
instability/ invisible
damage: cell
descendants prone tomutation
DNA damage withaccurate repair: cell
replicates accurately
DNA damage withirrelevant mutation:
cell replicates with
fixed mutation
DNA damage withcritical mutation: cell
replicates with fixedmutation
DNA damage withlethal mutation: cell
dies on replication

No measurable effect.
Unknown but likely to be finite and include
most health conditions. Effect increases
vertically from 2 to 3 hits, then saturates
rapidly.

Localised DNA
damage to many cells
in a community

No measurable effect.

No measurable effect.

Cancer or leukemia. Genetic malformationor genetic disease if in germ cells.

From no measurable effect through loss of
viability of organ or individual to death ofindividual depending on number and type ofaffected cells.
Field cancerisation though failure of cellcommunication inhibitions

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9.6 The dose- response relationshipThe relationship between radiation dose and response has been studied
extensively. The ICRP risk model assumes that in the low-dose range, therelationship is a linear one with no threshold for onset of effect, known as LNT.
This means first, that there is no safe dose and even the lowest dose has a finite
probability of causing health detriment. Second, doubling the dose causes a
doubling of the effect. There are basically two reasons for this assumption.
The first is that it follows from the considerations of what is known
about radiation action outlined in Section 9.2 above. Clearly if the health deficit
is related to cell DNA damage, which in turn is a consequence of ‘hits’, and if
these hits act independently owing to their distance apart in time and space, theeffect must be linearly proportional to dose. Because a cell is either hit or not
hit there is no condition lower than a single hit. There is no safe dose.
The second reason for believing in linear dose response is that datafrom experimental cell cultures and animals, and people exposed to externalradiation, has been taken to show effects which are linearly proportional todose. However, this has been disputed by those who argue that there is asmaller (or even beneficial) effect at low dose and others who argue that data
show a higher effect at low dose. In the case of external irradiation studies, thesmall populations studied result in wide confidence intervals and a number ofdifferent curves can be drawn through the data.
The Committee has studied this area very carefully, since assumptions
about dose-response are critical to the understanding of epidemiological studiesof radiation exposure. The Committee concludes that there is sufficientevidence to believe that the dose response relationship is unlikely to be linear
in the low-dose region, except as an approximation for external radiation, andhas rejected the LNT approximation in favour of relationships which showmuch higher effects at low dose. The reasons for this are reviewed below.
9.6.1 ICRP linear and linear quadratic response: two-hit kinetics
In experimental results from external exposure studies of cell cultures, animals
and human populations (primarily Hiroshima) over the full range of effect frommedium dose to high dose (but before the death of the individual when therelationship fails altogether), it has been observed in many systems (e.g.
leukemia induction in the LSS group) that the response is best described by alinear quadratic relationship. This is written:
Effect = (dose) + (dose)2

The shape of this curve is shown in Fig 9.1. There are sound theoretical reasonsfor interpreting this as due to independent track action in the linear range with amuch increased effect when the dose is so great that two tracks impinge on acell at the same time. These two tracks (or correlated tracks) are thought by90

ECRR 2010

most to have a high probability of inducing a fixed mutation because they cancause damage to both DNA strands in such a way that there is a ‘double strand
break’, an event which is difficult for the cell to repair. This may not be the true
reason for the increased mutation efficiency but the observation that two hits
have a very much larger chance of causing mutation is now well accepted.
Recent work with alpha particles and cell cultures has confirmed thisempirically.
For a dose of 1mSv of 600eV external irradiation, the probability of
producing two hits within the period of 10 hours which is associated with cell
repair and replication has been calculated to be between 1x10-4 per year
assuming a mathematical model for close packing of mdiameter cells and 5
x 10-6 if an experimentally determined packing fraction is used (Busby 2000,
Cox and Edwards 2000). In other words, the two-hit process is very rare atnormal background levels i.e. in the low-dose range. However, the same is nottrue for a number of situations involving internal irradiation. There arebasically three types of internal exposure which may lead to a high probabilityof two hits in the low-dose range. They are: Immobilised sequential emitters like Strontium-90/Yttrium-90, tellurium132/Iodine-132
 Immobilised, insoluble ‘hot particles’ or aggregates of e.g. Plutonium or
Uranium Oxides; also high Z sources for SPE effects bound to DNA
 The very low energy beta emitter, Tritium which has a high number oftracks per unit dose
Clearly, if the dose-squared region of the accepted risk model, as
defined above, is due to correlated double hits, then it follows that for these
exposures response should be proportional to the square of the dose, andinternal exposures like this cannot be subsumed within the external risk model
without a weighting for this effect. Indeed, it may be that the true doseresponse is a polynomial, in which case, triple-correlated events carry a cubed
hazard weighting and so on. ICRP2007 have discounted the 2nd Event effect onno research basis whatever. But there is another reason why these types of
exposure should be considered separately and this is considered below.

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Fig 9.1 Linear-quadratic dose response relation
9.6.2 Petkau response
A number of independent researchers have drawn attention to the empirical
work of Petkau, who irradiated lipid membranes in water with external X-rays
and also with beta radiation from solvated radioactive sodium ions (Na-23).
Petkau was interested in the effects of ionising radiation on cell membranes,
which he and others came to consider to be critical targets for radiation action.
Petkau showed that the membranes were extremely sensitive to radiation fromions in solution and collapsed at doses in the low-dose range. Using enzymes,
particularly the anti-oxidation stress enzyme superoxide dismutase, he
identified the hydrated peroxide species formed by radiolytic cleavage of watermolecules as the cause of the lipid membrane destruction. He also
demonstrated that the dose response curve for these systems is what is now
called supra-linear. This is a response which rises sharply from zero dose but
flattens out at higher dose. The curve is shown in Fig. 9.2.
The explanation of the curve is straightforward in kinetic theory andfollows from the recombination of radical species at high concentration.
Integration of the rate equation for such a system leads to a dose response of
the form:
2(Response) = Dose
It is possible, however, that Petkau was seeing partly or wholly a Langmuir
type isotherm for the adsorption of radioactive sodium ions on the lipid

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membrane. Nevertheless, Gofman has re-analysed the Hiroshima LSS data toshow that it conforms to the Petkau type of supralinear curve, and many others
have used it to argue against the extrapolation of the Hiroshima data from highdose to the low-dose region.

Fig 9.2 Petkau supralinear dose response curve (genomic instability bystanderyields of damaged chromosomes appear to follow this type of response)
The dose response obtained empirically from microbeam irradiation of cells in
vitro shows such relation when the damage is plotted against the number oftracks traversing a single cell, with saturation of genomic instability effects at 3
tracks. Whether this is a dose effect or track sequence effect is not known.
9.6.3 Burlakova response: inducible repair and/or sensitive elements.
Burlakova has shown in many studies that a number of different cell culture
test systems respond to external low level radiation exposure with a biphasic
response (Burlakova et al 2000). The effect increases from the zero dose point
to a maximum, but then falls back to a minimum as dose is increased. Further
increase in dose past this point causes a second rise in effect. In order toexplain this curious result, Burlakova has suggested that the curve is aconsequence of two separate processes. The first she assumed to be the Petkau
or some other supralinear response to increasing radiation dose. The second is93

ECRR 2010that increasing dose increases repair through a system of inducible repair
efficiency. Such systems have indeed been shown to exist in animals, but theyusually take some time to develop. The biphasic dose response is thus a
consequence of the opposing operation of these two effects. It is shown in Fig
9.3. Burlakova has also been able to show in a meta-analysis of studies ofleukemia and radiation that these studies taken together conform to thisbiphasic pattern. More recently, she has suggested that the effect may be due tothe superposition of response functions from several different classes of system
whose response to radiation damage indirectly affects the end point being
considered. Thus, increased effects at very low dose below 1mSv may reflect
damage to the cell membrane insofar as it is able to support accurate replicationof DNA: at higher dose this mechanism is swamped by a different mechanism,
perhaps direct DNA damage or damage to some other organelle.
9.6.4 Variation in cell population sensitivity
An alternative explanation of the biphasic dose response has been suggested by
Busby, but is also implicit in an idea which Elkind advanced to explain certain
results of experiments showing that split doses of X-rays produced a greater
effect than the same dose given acutely (see Busby 1995 and CERRIE 2004b
for a discussion and references).
It has been known from almost the beginning of the radiation age that
rapidly replicating cells are more sensitive to radiation damage (Bergonie andTribondeau, 1906). Indeed, this is the basis of radiotherapy for cancer where itis the rapidly proliferating cancer cells that are preferentially destroyed. Most
cells in a living organism are in a non-replication mode, sometimes labelled
G0. However, it is clear that, as a consequence for a need to replenish cells thathave died or are senescent, there will always be a proportion of cells actively
engaged in replication, or mitosis. This involves a complex sequence involving
DNA repair and replication, and during these phases, it is well established thatcells are more easily killed. In some cell-culture studies, there is a 600-folddifference in the sensitivity of cells to killing by radiation during this repairreplication period, which lasts about ten hours. Experiments with the Auger
emitter, Iodine-125 bound to uridine, one of the DNA bases, have shown thatcells engaged in repair-replication are also much more susceptible to mutation,and that the target for the effect is either the DNA or some structure that comes
into close proximity to it during this replication phase.
It follows that, if there is a sub-group of any specified cell type which
has high sensitivity to mutation and killing, the dose-response will be biphasic.
These sensitive cells will be mutated at low dose, increasing the magnitude ofthe end point effect, and as the dose in increased more, they will die, thus
decreasing it. At still greater doses, the less sensitive cells will be mutated andthe magnitude of the end-point effect will again rise. The result is shown in Fig
9.3.

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Fig 9.3 Biphasic dose response curve.
Elkind originally made the suggestion in the mid 1990s that there must be a
sub-group of sensitive cells in all tissues, but this idea does not seem to havebeen followed up. This is remarkable, since the idea that cell killing can occur
at high dose has been used to explain dose-response relationships at high dose,particularly for alpha particle effects and 'hot particle' effects. In the latter, it isargued that the high doses in the region of hot particles (highlighted by those
who argue that such doses are omitted from consideration following the
averaging process implicit in the concept of absorbed dose), are less likely toresult in cancer due to cell killing.
The results of animal studies on beagle dogs and mice appear to showthese biphasic effects in the low-dose region (Busby, 1995) as do the results ofrecent mortality studies of radiation workers in the UK.
It has been remarked that for the purposes of radiation-protection
models, ECRR2003 employs a linear no-threshold model despite espousing thebiphasic dose response (IRSN 2005). This is because in the region being
addressed by the ECRR applications the dose response is in the rising part ofthe curve, from zero-dose and this can be approximated as a linear relationship.

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9.6.5 Intra-population and individual sensitivity
There are radiosensitivity group differences both between population
subgroups and between separate populations and also individual variabilities.
There are data about radiosensitivity for:
 races populations (in the strict sense)
 sex
 age
 physiology
All three main racial groups (caucasian, negroid, mongolian) differ inradiosensitivity (see Doll and Peto 1981 for a discussion of cancer incidence
rates by race). Animal and human studies have identified genetic sub-groups
with enhanced sensitivity to radiation, e.g. in the Japanese LSS study and in
women developing early breast cancer. There are data that show that different
strains of laboratory mice differ by an order of magnitude to radiogenic livercancer (Ito, 1999 cited by Yablokov 2002).
In Table 9.3 are listed some examples of the sexual variability ofradiosensitivity in humans and Table 9.4 lists variation in some animals.
There are many studies about age-dependent differences inradiosensitivity in human beings, in vertebrates (fish, amphibians, birds,
mammals) and invertebrates (Majeikite 1978 cited by Yablokov 2002).
Beginning at fertilization each stage of individual development is different in
its radiosensitivity. The radiosensitivity of children, adolescents, adults, elders
and the very old are different. Even adults become more radiosensitive after 45
years.
The foetus is particularly sensitive as has been shown by the work for
Stewart et al 1958 which has been translated into a risk factor for radiogenic
cancer of 50 per Sievert (compared with 0.05 per Sievert for the adult(Wakeford and Little 2003). For effects in children (and possibly also adults,
who are thus selected for survival) increasing dose will eventually result in
decreasing end point in the viable individual due to spontaneous abortions(miscarriages). Fucic et al (2008) showed that there was a 4-fold excess of
miscarriages in women exposed to internal radioactivity in the workplacecompared with those exposed to external X-rays; external radiation is also
associated with an approximate doubling in miscarriage rate (Steele andWilkins 1996, Lindholm and Taskinen 2000) therefore the internal exposures
have an approximately 8-fold effect on miscarriages.

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Table 9.3 Examples of different sexual radiosensitivity (references
op.cit.Yablokov 2002)
Character
Embryo andfoetusradiosensitive

Differences
Male

Reference
Sherb et al.
2001)

Total cancer
mortality
Leukemia
mortality
All cancer
morbidity

Higher for female in Chernobyl
contaminated territories
Twice higher for female

Antipkin,
2001
Wing et al.
1991
Suslin, 2001

Bone andcartilage cancers

Lymphoreticulosarcomas
Monocytic
leucosis
Skin cancer
Cs-90 half-timeof remote frombody
Newborn sex
ratio

More in girl +5 years (compared withsame age boys) on Chernobyl
contaminated territories
More in boys 0- 4 years old (comparewith same age girls) on Chernobyl
contaminated territories
More in girls 0 – 4 years old (comparedwith same age dose) on Chernobyl
contaminated territories
Sixfold more in boys than in girls(average for globe)
Female 7, male - 21 per 100 000 on
Chernobyl contaminated territories
Female 1.77 0.42, male 3.47 0.74 per
100 000 on Chernobyl contaminatedterritories
Female 16.7 (1.1 – 29.0), male 21.6 (3.2
– 36.0) per 100 000 , 19 USSR provinces
Average for female 80 days , for male –110 daysMore newborn girls after intensive X
irradiation; in second generation

Suslin 2001

Healthconsequences…, 1995

Suslin 2001
Mel’nov
2001
Golovachev
1983

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Table 9.4 Differencies in radiosensitivity between female and male in somemammalian species (references op.cit. Yablokov 2002)
SpeciesRat, Rattus
norvegicus
Mice. Mus
musculus
Vole, Microtus
oeconomus
Capra, Meriones
and some otherspecies
Vole,
Clethrionomys
rutilusVole, Microtus
agrestisHare, Lepus
europaeus

Differences
Level of Cs-137 incorporation forfemale three times higher that for maleRadio induced hepatic cancer after
Californium-252 irradiation was ten
times higher in female
Sencitivity of bone marrow andepithelial cells higher in males
Differ between male and female

Reference
Bandashevsky
2001
Ito 1999

Female during breeding season onradioactively contaminated territory
incorporated twice more Cs-137
More Sr-90 incorporated in bones offemalesMore I-131 in bones of females

Il’enko andKrapivko 1989

Zainullin 1998
Majeikite 1978

The level of incorporation of radionuclides in some organs is different for
adults and children (Bandashevsky and Nesterenko 2001). The scale of agedependent variations of radiosensitivity (several times) is usually higher thansex-dependent ones. There are known time-dependent variations ofradiosensitivity (in day, month, seasons) in insects (i.e. Laspereysia
pomonella), rodents, dogs and other mammals (see reviews Majeikite 1978,
Il’enko and Krapivko 1989)
Within any mammal (including Homo) population’s subgroup there arereal individual variations in radiosensitivity. In the extreme cases of thosecarrying the ATM gene for ataxia telangiectasia, there is extreme
radiosensitivity and tendency to leukemia, lymphoma and some solid tumours.
The gene which is defective is associated with a DNA damage sensor protein.
Although the condition is rare and the gene recessive, there is evidence whichsuggests that there is increased risk of cancer from radiation in the larger subgroup which is heterozygous with respect to the ATM gene, about 6% of the
population.
The existence of radiosensitive group variations is in fact seen inradiotherapy patients. From the foregoing it suggests that ethical considerations
demand setting permitted radiation exposures at levels where people who areradiosensitive are protected rather than basing the limits on some standard manconcept. This is another area where the releases of radionuclides to the98

ECRR 2010environment, where there are indiscriminate exposures, demands an ethicalreassessment.

9.6.6 Hormesis response
A number of animal and in vitro studies have been cited as evidence that small
doses of radiation have a protective effect named ‘hormesis’(from the Greek
hormein, ‘to excite’). In this dose response, the curve dips as the radiation dose
is first increased. The lowest dose controls thus exhibit a greater health deficit
than those who are given slightly greater though still low doses, although as thedose is increased the curve rises again and the effect increases. The curve isshown in Fig. 9.4

Fig 9.4 Hormesis dose response curve
The explanation given for this effect is that at the lowest doses, increased
efficiency of cell repair is induced by the radiation exposure. Thus, as dose
increases, the radiation first has a protective effect, with a reduction of cancer
yield. The Committee has considered hormesis and its supporting evidence
carefully and concludes that such a process is possible. Effects appear to occur
at intermediate dose ranges (i.e. above 20mSv) and may have a number of
explanations:
1. Sensitive sub-groups of cells are being killed rather than mutated.
2. Immune system surveillance is being potentiated in the short term (withpossible long term detriment).

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3. In the case of high background effects, foetal and infant death of sensitive
individuals results in selection for radiation resistance. This is a population
version of the cellular effect in (1) above.
It may be that inducible repair efficiency exists, comparable with otherinducible systems, like Haemoglobin-Oxygen dissociation at altitude or
suntanning in tropical climates. This may be one explanation (among others)
for the lack of variation in cancer rates between regions of different natural
background. However, the existence of radiation-inducible repair means thatthe repair systems themselves may be open to attack, also by radiation (seebelow). In addition, the existence of such a process may have othercomplications. The question needs to be asked why, if repair replication were
inducible in this way, would any species not automatically evolve to thehighest state of repair efficiency and remain permanently in that state? The
answer may be that if cells were induced into a state of high sensitivity forrepair replication, then the cell line would undergo a greater rate of replication
throughout the period of stress, and since it is now well established that nonspecific ageing is a function of the total number of cell replications, theconsequence of the short-term advantage conferred by hormesis is probably along-term loss of viability due to accumulated DNA damage caused by highnumbers of replication-copying processes.
It may be, however, that some of the hormesis evidence results from an
artifact. If the dose response in the low range follows a biphasic curve, all thatis needed to show an apparent hormetic effect is to leave out the zerodose/zero-effect point. It may be that because deductive conclusions from highdose experiments could not be squared with the possibility of such variation inthis low-dose region, either the points were interpreted as scatter or they wereforced into a hormesis dip by leaving out the lowest dose responses as outliers.
The Committee provisionally concludes that hormesis may exist, but if
it does exist its long-term effects are likely to be harmful for the reasonsdetailed above. The Committee recommends that no consideration should bemade of hormesis in respect of radiation protection.
9.6.7 The Committee’s conclusions on dose-response relationships
The Committee has agreed that the ICRP's linear no threshold assumption isinvalid except as an approximation which may hold over a small range, andindeed the Committee employ such a relation in the low-dose region as amatter of pragmatism. There is not sufficient evidence to show that there is auniversal dose-response relation for all types of exposure and all end points,
and to assume such a function is an example of a fatal reductionism. However,there are good reasons for assuming that effects in the low-dose range fromzero dose to about 10mSv (ICRP) are likely to follow some kind of supralinear
or fractional exponent function. Since there is good theoretical and empiricalevidence for the existence of biphasic dose-response relationships, the100

ECRR 2010

Committee strongly recommends that no epidemiological finding should bedismissed on the basis that it does not conform to a continuously increasing
dose-response relation of any form.
9.7 Factors affecting the biological efficiency of radiation action
The damage caused by radiation exposure has been shown to be a function ofionisation energy density. However, the cell is not a passive target in thisprocess, nor is the organism. Since the discovery in the 1960s that cells
repaired radiation damage the emphasis of research has been to examine how,
and what factors augment or inhibit such repair. For the overall scheme ofradiation damage, outlined in Table 9.1, there is a set of damage-inhibition
systems based on cellular and systemic responses. Thus, for stochastic end
points like cancer, there are a number of processes involved, shown in Table
9.3. Discussion of all the factors listed in Table 9.3 is beyond the scope of thiswork. The factors are listed in order to show that the emphasis on initialradiation-damage processes implicit in the ICRP system is only valid for highdoses delivered externally. In the low-dose range, other factors are of major
importance in deciding the outcome of any exposure. The response of the cell
to low-level non-lethal radiation exposure is a critical system in thisprogression. The discovery of the system of cellular responses to sub-lethal
exposure has an important consequence which was pointed out by Busby in1995. If cells in the repair-replication cycle are significantly more susceptible
to radiation exposure than cells which are not replicating then this phase of thecell lifespan therefore represents a window of opportunity for mutation. If
circumstances could be arranged to irradiate in this window, a hazard
enhancement would occur as we shall discuss below.
9.8 The Second Event Theory
It was pointed out that most cells in a living organism are in a non-replicationmode, sometimes labelled G0. These cells are contributing to the organism as
part of the normal living process and do not need to replicate unless there issome signal requiring it, perhaps because of tissue growth, damage orsenescence. Throughout the growth and lifespan of individual organisms there
is a constant need for cellular replication, and therefore there is always somesmall proportion of cells which will be replicating: the magnitude will naturally
depend upon the type of cell. When cells receive the signal to move out ofstasis or G0, they undertake a fixed sequence of DNA repair and replication,labelled G0-G1-S-G2-M, with various identifiable check points through thesequence which ends in replication M or Mitosis. The period of the repair
replication sequence is about 10 to 15 hours and the sensitivity of replicating
cells to damage including fixed mutation is extremely high at some points
during this sequence. In the case of Chinese Hamster Ovary cells, for external

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low LET radiation there is a 600-fold variation in the sensitivity for cell killingover the whole cycle though the sensitivity for mutation has not been studied.
If there is large variation in sensitivity for mutation over the cell
lifespan, what follows? Although naturally dividing cells may accidentallyreceive a radiation ‘hit’, this process can be modelled by averaging over large
masses of tissue, even if the dose response curve is not linear. However,
unplanned cell division, preceded by DNA repair can be forced by a sub-lethal
damaging radiation track: this is one of the signals which push the cell out of
G0 into the repair-replication sequence. It follows that two hits separated byabout ten hours can firstly generate a high sensitivity cell and then hit this same
cell a second time in its sensitive phase. This idea, the ‘Second Event Theory’,is described, and supporting evidence for it advanced in Busby 1995 and its
mathematical description has been approached slightly differently in Busby
2000. It has been the subject of some dispute by the UK's NRPB and has been
discounted by ICRP 2007 on the basis of some questionable reasoning
presented to the CERRIE Committee by Roger Cox, ICRP’s Deputy Chair.
Developments in micro techniques have allowed the emergence someevidence that supports the two hit idea. Miller et al, (1999) in a considerationof Radon exposure risks, have been able to show that the measured
oncogenicity from exactly one alpha particle hit per cell is significantly lower
than for a Poisson-distributed mean of one alpha particle hit per cell. The
authors argue that this implies that cells traversed by two alpha particles ormore contribute most of the risk of mutation, i.e. single hits are not the cause ofcancer. However, as yet, the differences in effect between two hits delivered
within the space of a few minutes and within the cell cycle repair period of
about 12 hours have not been compared.
There are three types of internal exposure which would be expected toresult in an enhancement of risk from any Second Event source. The first is due
to sequentially decaying radioisotopes like Strontium-90. Following an initial
decay from a Sr-90 atom bound to a chromosome, the second decay from thedaughter, Yttrium-90, whose half-life is 64hrs can hit the same cell within thetime period of the induced replication sequence with a probability that is simple
to calculate. The same dose from external radiation has a vanishingly small
chance of effecting the same process since, in this case, the target DNA iswithin a few tens of nanometres of the source. The second type of Second
Event exposure is from micron or sub-micron sized ‘hot particles’. If lodged intissue, these will decay again and again increasing the probability of multiple
hits to the same cell inside the ten hour repair-replication period. Finally, highZ elements bound to DNA will catalytically increase the ionization rate at the
DNA through the secondary photoelectron effect.
The Committee is aware of the speculative nature of these proposedmechanisms, but in view of their plausibility assumes that this kind of effectcannot be ruled out, and recommends further research in this area.

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Table 9.3 Factors affecting the progression of radiation damage to cancer
Contributions to
final cancer
Increasing densityof ionization

Increasing track
density in space

Increasing track
density in time

Increased
replication rate ofcell

Position in cell
cycle
Decreased repair
efficiency

Decreased immune
surveillance
Decreased
replication
inhibitory field

Factors

Radiation quality; 
Auger emitters, weak decays e.g. Tritium
Electromagnetic field interactions.
Increasing doseInternal exposure from point source
Internal exposure from hot particle
Internal exposure from immobilised sequential decay
Concentration of ionic radionuclides at interfacial layers
by adsorption
6. Concentration of radionuclides in organelles bybiochemical affinity
1. Internal exposure from point source
2. Internal exposure from hot particle
3. Internal exposure from immobilised sequential decay
4. Concentration of ionic radionuclides at interfacial layers
by adsorption
5. Concentration of radionuclides in organelles bybiochemical affinity
1. Cell type
2. Prior exposure/prior damage
3. Electromagnetic field
4. Growth rate of individual (e.g. children)
5. Concentration of replication promoters including
radiation
1. Prior exposure/prior damage
2. Electromagnetic field
1. Genetic identity
2. Prior exposure/prior damage
3. Antioxidant status/repair enzyme status
4. Concentration of repair system poisons
Various, including prior exposure

1.
2.
3.
1.
2.
3.
4.
5.

1.
2.

High local doses
Hot particles

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9.9 Other factors affecting cancer expression
9.9.1 Immune surveillance
Although it is now generally accepted that cancer has its origin in a single
mutation event, there are a number of factors involved in the progression fromthis event to clinical expression. The most obvious of these is the system of
immune surveillance, which prevents tumours from progressing. The
suppression of immune response by organ transplant drugs or cytostatic drugs
is associated with enhanced risk of cancer. Irradiation of the organism is a welldocumented cause of immune-system suppression, not only from high-energy
ionising radiation but also ultraviolet radiation. This aspect of radiation
exposure has not been addressed by ICRP but is believed by Sternglass andothers to provide a mechanism for low-level radiation effects. Thus lowefficiency immune-system response would augment the probability ofdeveloping cancer following an exposure, suggesting a mechanism which
would cause enhancement of hazard if an individual who had been exposed
were also to be chronically exposed over the period following the initial
exposure.
9.9.2 Cell proliferation fields
Recent theories of cancer expression (Sonnenschein and Soto, 1999) address
the finding that transplanted cancer cells do not grow in non-cancerous tissue
whilst normal cells transplanted into cancerous tissue become cancerous. These
researchers propose the existence of a cell-communication-field effect which
requires a certain threshold number of genetically damaged cells to occur
before cancer can develop. The arguments are based on the theory that thedefault state for cells in metazoa is, like metaphyta, proliferation: it follows that
there has to be a permanent inhibitory signal. Sonnenschein and Soto assume
that this involves various components of cell-cell communication collectively
termed a ‘field’. If this is found to be generally so then the effects of high local
doses, as occur in the region near hot particles, may be particularly effective incausing cancer, since the damaged cells are all close to one another. That suchfields exist has been shown recently by the discovery of the ‘bystander effect’in which genomic instability is found to occur in cells which are close to thecell which is traversed by a radiation track but which do not themselves receive
any direct track traversals. Furthermore, the phenomenon of ‘fieldcancerization’ whereby certain cancers seem to start from independent loci inthe same site (e.g. larynx cancer) supports the idea that cell communication
within a community of cells is a critical component of cancer expression(Boudewijn et al 2003).

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ECRR 20109.10 Biochemical and biophysical effects
The concentration of certain radioisotopes in organs through biochemicalaffinity is incorporated into the ICRP scheme only through the organ
weightings. Thus it is accepted that Iodine concentrates in the thyroid and that
this represents a hazard in terms of thyroid cancer and other thyroid conditions.
However, arguments from chemical considerations should also be applied to all
isotopes, and extended to concentration effects at the molecular level, as wellas the organ level. For example, Strontium has a particular affinity for the DNA
phosphate backbone: indeed, Strontium Phosphate co-precipitation is a methodof choice in genetic research for removing DNA from solution. Thus exposure
to the isotopes Strontium-90 and Strontium-89 should result in decays within
the DNA itself. This effect should extend to isotopes of Barium also, which arealso common environmental contaminants from nuclear processes.
There is also the ‘Trojan Horse’ exposure to a sequentially decaying
isotope whereby the isotope enters a system with one chemical identity and on
decay changes to a different chemical species which is also radioactive. An
example here is the series Sr-90/Y-90. The radioactive decay product of thedipositive ion Sr-90 decay is a tripositive Y-90 ion. The Committee isconcerned that such a sequence might result in accumulation of Y-90 in partsof the organism (e.g. the brain) where there are biological filters based on ionicstrength or valency and that this might result in enhanced local doses.
A similar enhancement of local dose would occur as a result ofadsorption of radioactive ions (e.g. Cs-137) at an interface. The positive ionsinvolved in nervous system signalling collect at synaptic junctions and thesimilar concentration of radioactive species with the same chemical groupaffinity would increase the local dose.
9.11 Transmutation
One mechanism which is entirely absent from ICRP's deliberations results fromthe effect of the radioactive decay process changing one atom into another.
There are three common radioisotopic pollutants where this effect is likely tohave serious consequences: Carbon-14, Tritium and Sulphur-35. All three aremajor components of enzyme systems and critical to the processes which are
fundamental to living systems. The macromolecules which are the operators ofliving systems—proteins, enzymes, DNA and RNA—depend upon theirtertiary structure, or shape, for their activity and biological integrity. Alterationof this shape results in inactivity of the macromolecule. This inactivation couldin principle be effected by the sudden transmutation or alteration of one atomin the macromolecule. Since the molecular weight of these macromolecules isusually greater than 100,000 it is clear that incorporation of one atom (of e.g.
C-14 which decays to Nitrogen) may result in an enhancement of effect ofmany thousand-fold. The isotope Tritium is a form of Hydrogen and thebiochemical processes in living systems depend on the weak bonds called

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Hydrogen Bonds which bridge and support all enzyme systems and holdtogether the DNA helix. The sudden decay of such a Tritium atom to Helium(which is inert and does not support chemical bonds) may have a catastrophic
effect on the activity and normal processing of such macromolecules.
Hydrogen bonded in these systems is easily exchangeable and will exchange
under equilibrium conditions with Tritium Oxide, or tritiated water, the normal
form of this isotope in the environment. There is also some evidence that
Tritium may be preferentially taken up in some systems. This needs to be
confirmed by further research. Sulphur is also an important component inmacromolecular proteins, forming disulphide bridges which support tertiary
structures.
The Committee feels that this area has received insufficient attention
and that more research is required to establish the risks to biological systems
from transmutation effects. Although this sentiment was implicit in the review
of internal radioactivity effects by Gracheva and Korolev published in 1980
nothing has followed.
9.12 Increase of dose due to particle in placenta and genomic signal transfer tofoetus.
The size of particle which may be transferred across the placenta has not been
determined. Recent unpublished research suggests that particles as large as
100nm (0.1) pass across the placenta into the foetus. For early developing
foetuses, the local doses from particles of Plutonium Oxide or other actinidealpha emitters will be massively high and may result in a range of effects from
foetal death and early miscarriage to effects in childhood. This is a case where
the biological end-point may result from a very low-probability, high risk
event. Plutonium particles are common contaminants in the atmosphere near
the Irish sea and other areas close to nuclear plants.
Even if the particle may not transfer across the placenta, it is known
that there are genomic instability signal molecules which are quite small inprotein terms and are one origin of the bystander effect whereby cells remotefrom those receiving the radiation damage are caused to increase their rate of
mutation. Thus genomic and bystander effects are in principle mechanisticallylikely to transfer from the placenta to the foetus, and indeed thetransgenerational genomic instability effects have now been seen in Chernobylaffected populations and in laboratory animals (ECRR2009).

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Risk of Cancer following Exposure Part 1: Early Evidence
10.1 Basis of the ECRR risk model
Following the publication of ECRR2003, the French IRSN (and others)
criticized the model for having failed to explain its basis in scientific evidence.
The evidence which the Committee used as a basis for its new model of riskarises first from human epidemiology, next from a number of human, animal
and cell studies and finally on knowledge of the physico-chemical andbiological nature of the interactions between radiation and molecules at the celllevel. It is not primarily physics-based (and this is the essential difference from
ICRP) but instead begins inductively with the epidemiological evidence andthen explains these in terms of the interactions between radiation and tissue atthe molecular level as dilute solution biophenomena.
Primarily, the model is based on empirical data on internal exposures
to fission-product radionuclides and Uranium in the fallout from atmosphericweapons tests. These tests, which peaked in 1959-63 were the first experimenton the effects of human exposure to internal radionuclides, since theradioactivity was globally dispersed. It was an experiment with an outcome thatno-one examined. There was never any systematic study at the time, possibly
because the World Health Organisation was rapidly constrained from any such
effort in 1959, when the early health effects began to appear. WHO, as we
previously noted, were made to sign an agreement with the International
Atomic Energy Agency, which left research to IAEA, an agreement which isstill in place. But behind the scenes, away from the public, it was clear toauthorities that the fallout was beginning to kill people. Early suggestions that
this might be so were quickly denied by reference to the Japanese A-Bombstudies; there were cover-ups at the highest level (Medical Research Council
1957). Nevertheless a Test Ban was signed in 1963.
Although weapons fallout was globally dispersed, it was not uniformly
dispersed, and was greater in the northern hemisphere than the southern. It wasalso greater in regions of high rainfall than in regions of low rainfall, often bysignificant amounts. The overall doses, as assessed using the ICRP model, were
calculated however, and tabulated by UNSCEAR. The contamination wasmeasured in a number of countries and results were published. One country
where excellent contamination data was available from the 1950s continuously
to the present day was the United Kingdom. This included data on
contamination by individual radionuclides in England and separately in Wales.
These are also two countries in the UK which have functional cancer registries
which collected incidence data from 1974, although separate mortality registers
are available for causes of death back to the 1930s in the UK. Wales is on the
Atlantic coast of the UK and the fallout in Wales and therefore (because ofhigher rainfall) the measured contamination, and thus doses (dominated by the107

ECRR 2010

isotope Strontium-90) were twice to three times greater than those from thefallout in England.
It was a straightforward matter to compare the trends in the age
standardized incidence of cancer in Wales and England, countries with similar
genetic populations and similar lifestyles, to see what effect the higher level of
exposure from weapons fallout produced. The effect was startling (Busby 1994,
1995, 2006). The age standardized cancer incidence trend in the two countries
was similar. The trend was parallel and flat from 1974-1979 when the Wales
rates began to climb relative to the England rates. By 1984, the rates in England
began to rise, but by then the Wales rates had increase by about 30%. The
peculiar shape of the trend in Wales exactly followed the earlier fallout
exposures, even to the discontinuity which occurred in 1959 from the partial
test ban treaty which resulted in a sharp fall in radioactive precipitation. The
temporal correlation of the cancer trend on the earlier trend in fallout exposure,modeled as Sr-90, was highly statistically significant. Comparison of the doses
and the predictions of cancer excess at those doses by the ICRP model gave anerror of 300-fold in the application of the ICRP predictions (Busby 1994, 1995,
2002, 2006). This level of error (2 to 3 orders of magnitude) was to appear
again and again in studies of internal fission product exposures. Recent
powerful confirmation comes from the study by Tondel et al (2004) of cancer
in northern Sweden after the Chernobyl accident where it can be shown that theerror involved is upwards of 600-fold. This will be discussed in the following
Chapter. Support also comes from the increased cancer rates in Belarus
reported by Okeanov in 2004.
It is one thing to establish that there is an error in the application of the
ICRP model to internal exposures; it is quite another to partition the error
among the various isotopes that make up the fallout. Are they all equally
mishandled mechanistically? Are some more dangerous than others? The doses
from fallout as tabulated arise from the ICRP model in which Sr-90 confers thegreatest dose, because of its relatively long half life (29 years) and its ability tostore in bone as a Calcium substitute. It thus provides ‘energy per unit mass’
for longer. But on the basis of the Committee’s approach, Uranium might also
represent a significant hazard. Yet Uranium levels were not measured nor were
the doses from Uranium assessed. At this stage, it is necessary to bring inevidence on individual radionuclide risks from other sources, and this has been
the Committee’s approach. If the main fallout exposures were to Cs-137, Sr-90
and Uranium, then it seems plausible that Cs-137 doses may be discounted for
two reasons: that the element has a short biological half life and that, from its
chemical nature, it is uniformly dispersed in the body. It can thus be modeled
as an external radiation hazard for reasons given in Chapter 6. In animal
experiments Cs-137 has far lower effect than Sr-90 on genetic damage (Luning
and Frolen 1963). The same considerations apply to Carbon-14 (uniformly
dispersed), Tritium (short biological half life) and many short half life
radionuclides.

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In the following two chapters, which review the main evidence, the Committee
briefly presents the studies and results which inform the position that it has
adopted. This chapter deals with the situation up to and including the effects ofglobal weapons fallout in the period which ended with the Atmospheric Test
Ban Treaty in 1963. Chapter 11 begins with evidence from the nuclear plantleukemia and cancer clusters to the present day. For reasons of space, thesechapters are not a comprehensive review of all the evidence.
10.2 Specificity
The Committee has decided to address the risks of internal and external
irradiation separately, for reasons which have been discussed. However, it isclear that the evidence upon which the risk factors depend are from real-world
situations in which it is rare that exposure is entirely external or entirelyinternal but is usually a mixture of both. If internal irradiation carries asignificantly higher risk than external, then it is easy to see that the external
irradiation risk factors, deduced from a study of populations who had received
a large external dose compared with internal dose to the same populations,would show higher yield than those obtained from the same dose delivered
purely externally and that this discrepancy would increase as the overall
proportion changed to include greater internal dose. For the Hiroshima LSS
study, for example, at the lowest doses, such an effect would show itself as asupra-linear dose response or some other form of high response at low dose,
although other factors will contribute to the empirical result. It is of interest that
the US-directed studies of the Hiroshima survivors consistently denied that
there was any internal component to the exposures received by the study group
because the bombs were exploded in the air. However, measurements madesince then have showed presence of Plutonium and Caesium in soil near
Hiroshima and recently fallout isotopes from the Hiroshima bomb have been
identified in ice cores from the Arctic. These findings may explain the puzzlingincrease in leukemia in the control group relative to all Japan recorded in thefirst studies. Evidence has now emerged that the ABCC failed to include earlyleukemia’s in the bombed towns in the LSS and failed also to report theexistence of fallout in the towns and also rates of general illnesses which would
have falsified their ultimate conclusions: this is particularly true of non-cancer
illnesses and heritable damage (Kusano 1953, Sawada 2007). It should berecalled that non-cancer illness affects cancer statistics and radiation cancer
epidemiology since an individual that dies of any disease but cancer below theage of about 50 is not available to die of cancer above that age when cancer
rates begin to increase exponentially.
The Committee has nevertheless decided to treat studies of mainly
external irradiation, where the external dose, conventionally modelled, is morethan 100 times the internal dose (as the ICRP expresses these) as external risk
studies and to accept that some of the discrepancies and anomalies revealed

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may have their basis in internal exposures. This approach has the advantagethat it results in values for external irradiation risk factors, which may be used
for radiation protection purposes in those pure external irradiation scenarios
where advice is necessary.
10.3 Base studies of radiation risk.
The studies given in Table 10.1 are the main ones which underpin the risk
factors used in the models of the ICRP and which define the present radiation
protection regime. It is clear that these are almost exclusively studies ofexternal irradiation risk, and with the exception of the Hiroshima study, are allcomparisons of purely externally irradiated subjects with controls who were notirradiated. The risk factors for cancer which were obtained from these studies
are largely in agreement one with the other, and the Committee believes
therefore that for external acute irradiation and cancer as an end point, theserisk factors are not likely to be wildly inaccurate.
The most recent data on late cancer effects in the Hiroshima LSS showthat the yield of cancer continues to exceed that predicted by previous risk
factors. The independent analysis by Gofman of the LSS data, Stewart's
findings relating to the homogeneity of the LSS study populations and the workof Padmanabhan on the choice of control group suggest that the risk factors forcancer given by the LSS study may be in error by as much as 20-fold. The
Committee is aware, however, that the LSS is based on an anomalous
population exposed to both external and internal radiation and is not an ideal
basis for obtaining pure external risk factors. The lifetime absolute risk of fatal
cancer of 0.2 per Sievert, chosen by the Committee, represents a decision basedon a review of all external irradiation studies.

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Table 10.1 Summary of studies used to determine risk factors from ionisingradiation by ICRP and others but used by ECRR to determine external
exposure risk factors for cancer and leukemia.
Study

Persons

1. Hiroshima
Lifespan study(LSS)

91,0002. UK
Ankylosing
spondylitis
3. Cervicalcancer patients
4. Canadianfluoroscopy
5. Post partum
mastitis
6.
Massachusetts
fluoroscopy

14,000

Doses
(Gy)
0-5
high

RegimeControls

Comments

Singleacute

In city‘unexposed’

3-4
high

Acute

Averagepopulation

Abnormalpopulation;
bias in controls;late effects stilldeveloping
X-rays150,000

high

Chronic

31,7000.5-1.2

601

0.6-1.4

1,700

high

Severalacute
Severalacute
Severalacute

Averagepopulation
Unwellcontrol
Untreated
mastitis
Averagepopulation

Radium capsule
Unwell group, Xrays
Small study, Xrays
Highlyfractionated, Xrays, small study

10.4 Natural Background Radiation
The Committee has examined the evidence regarding human health indicators
including cancer and congenital illness with variation in natural backgroundradiation exposure. The main studies which contribute to the understanding of
the health consequences of living in high background radiation areas are given
in Table 10.2

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Table 10.2 Variation in cancer and other effects in areas of high Natural
Background radiation
Cancerincrease?

Chromosome
defects?

predicted

Yes

notinvestigated+24% bone
cancer.
No

Yes

Yes

DisputedYes

3-4mSv/yr.

Apparently not

Yes

16000

-backgroundnot examined

8. Iowa

28 towns

Ra-226

9. Japan

All areas background

10. Scotland

All areas background+0.15mGy+43% (+132%
stomachcancer)+68% morelung cancer+stomach andliver cancer+ 60% higher
leukemia

Area ofstudy

Numberstudied

1. Austria

122

2. Finland27

3. Iowa

111 towns

4. Brazil

12,0005. Kerala,India
6. China
Yanjiang
7. Brittany

70,000Ra-226 4pCi/l;controlled
Monazite:
6.4mSv/yr.
4 mGy/yr.

70,000

Exposure

1-4mGy ().0116mGy ()Radon in water

Yes

Yes
Not investigated
Not measured

For a number of reasons, it is uncertain how the results of these studies caninform discussion about risk from radiation exposure. First, for many of thesestudies, the populations suffer stresses associated with living in the Third
World where cancer is not a major cause of death owing to earlier competing
causes and the generally shorter lifespan. In addition, natural selection forradiation resistance over a long period may be expected to confound any
attempt to find a suitable control group: thus the repair efficiency for cancerinducing lesions in genes might be expected to be higher in the exposed
populations than the controls. In addition, the considerable amount of evidence
which shows that different populations have different genetic susceptibility tocancer of different sites makes it impossible to draw any universally applicableconclusions from background radiation studies. There are also confounding
geographical factors relating to the levels of man-made radioactive
contaminants in high background regions. In Table 10.3 are listed possible
confounding components of health indicators in areas of high natural radiation.

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Table 10.3 Difficulties with interpretation of natural background studies
Problems with comparisons of health indicators across areas with high and low
background

1. Competing causes of death in disadvantaged populations
2. Difficulty in establishing rates due to lack of health data
3. Difficulty in finding genetically comparable controls
4. Development of induced responses in study group in their lifetime
5. Natural selection for radiation resistance in populations over generations
6. Variation in fallout contamination due to rainfall effects
7. Lack of epidemiological strength for the range of external dose

Despite these difficulties, it is clear from all the studies that chromosome
aberrations and breakages are present in populations exposed to high natural
background radiation. This is often associated with other flags for genetic
damage, like Down's syndrome frequency. Since cancer is a consequence ofgenetic damage, evidence of increases in chromosome damage would suggestthat the cause of such damage would also be a cause of cancer increases if thegroup lifespan was greater. Increased cancer risk does not seem to be a generalobservation, although a number of studies have demonstrated increases incancer rates for some cancers in high background areas. However, it may bethat populations who had developed in conditions where such damage had
occurred might enjoy increased evolutionary resistance to cancer as aconsequence of the death before birth of sensitive individuals or even increases
in resistance to cancer at the metabolic level bought at some expense to theoverall lifespan.
There is also the problem of epidemiological strength over the rangesof dose found within the studies themselves. If this range is between 1 and 5mGy delivered annually from natural radiation (mainly external gamma) thenaccording to the ICRP risk model for fatal cancer (which ECRR largely accepts
for external irradiation) the radiation component of the cancers after a 50 year
accumulated dose would increase from 0.6% to 3%, which would be difficult toshow.
The Committee concludes that evidence from this area of research is
not useful for radiation protection purposes. In particular, arguments which are
based on comparisons of cancer incidence across areas of high background andextrapolated to populations living in low background areas are inadmissible asevidence of low risk from low level exposure to fission-products or TENORM.
10.5 Cancer and Global Weapons Fallout
Overall, the dominating source for radioactive contamination from humanactivity is the global fallout of debris from the atmospheric nuclear bomb tests
conducted in different parts of the world between 1945 and 1980. In total, 520

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nuclear explosions were carried out, with periods of the most intensive testingin the years 1952-4, 1957-8 and 1961-2. 78 percent of the activity released bythese tests has been spread over the earth, contributing the major component of
the exposure to fission products and transuranics suffered by living creatures.
These substances are now universal environmental contaminants and also
universal in the cells of living systems, yet very little research has been aimed
at investigating their possible health effects. Many of the isotopes are periodictable-group mimics of elements which are utilised by living systems; they
therefore become incorporated into cells and organs.
The period of major atmospheric weapons testing and fallout exposure
which ended in 1963 with the Kennedy-Kruschev test ban was the firstoccasion that the health effects of such internal exposure could be assessed.
However, very little research was undertaken and very few studies were
published either drawing attention to or discounting the existence of any
consequences. Suggestions by Sternglass and others that the fallout had caused
increases in infant mortality were ridiculed and attacked. This climate of denial
was probably due to the secrecy and control associated with Cold-War politics
and, as has been pointed out above, this was institutionalised in 1959 in anagreement between the World Health Organisation (WHO) and theInternational Atomic Energy Agency (IAEA) which had the effect of giving the
IAEA a power of veto over WHO research into radiation effects.
Thus, although during the weapons test period there was enormous
activity in the fields both of cancer research and radiobiology, there is only asmall number of reports and studies which throw useful light on theconsequences of exposure to weapons fallout. Those that do exist aresummarised in Table 10.4.
According to UNSCEAR, using ICRP models, the cumulative northernhemisphere internal fallout dose over the period 1955-65 varied between about
0.5 mSv to doses of between 1 and 3mSv in parts of Europe where high levelsof rainfall caused increased deposition. The trend in dose showed a sharp
increase between 1958 and 1963 due to increasing testing of megaton
thermonuclear bombs. For internal isotopes the cumulative trend showed thesame sharp increase and reached a plateau in 1965, after which the trend fell
slowly (through biological loss and physical decay) by about 20% to the value
in 1999. The internal dose was dominated by two isotopes: Caesium-137 with ahalf-life of 30 years and Strontium-90 with a half-life of 28 years, althoughother more active isotopes gave high doses at the time. Contamination by
Uranium does not seem to have been reported. Details of the isotopes and doses
calculated on the IRCP basis are summarised in UNSCEAR 1993 andUNSCEAR 2000 and the main components of exposure are given in Table 10.5

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Table 10.4 Fallout cancer studies considered by the ECRR
Study Group
1. MarshallIslanders

Exposure doses
External +Internal: 1-10Gy

Finding
Thyroid cancer,
leukemia, still birth,miscarriage.
+ Thyroid+ Leukemia
Leukemia (4x) Thyroid(7x), breast (1.7x) bone(11x) etc.
Leukemia correlation
with Strontium-90
levels in US

Notes
Only 200 persons
Controls also
contaminatedDose unknown /Arizona controls
Dose unknown

2. U.S. Utah test
contamination
3. Utah test:
Mormons(C.Johnson)
4. U.S.
Leukemia vs.
global fallout.
(V.E.Archer)
5. Scandinavia:
Leukemia vs.
global fallout.
( Darby et.al)External Internal 1Gy
As above

Internal < NBRFound little correlation
with childhood
leukemia in
Scandinavia .

Unconvincing
analysis;questionable
protocol6. UK leukemia
and rainfall.
(Bentham
1995)

Internal <NBR

Found a significant
correlation withchildhood leukemia andrainfall in UK.

Disagrees with
Study No 5

7. US fallout
cohorts(RPHP: Gould
and Sternglass
1995 -)
8. US NAS
cancer study
9. UK and Wales
female breast
cancer (Busby
1995, 1997)
10. UK andWales allcancerincidence
1974-90(Busby 19952002, 2006)

Internal <NBR
Strontium-90
cited

Various cancer excess
risks in fallout exposed
birth cohort in USA

Present cancer
epidemic
predicated on thefallout

Iodine fromNevada tests
Strontium-90
1mSv
cumulative dose+thyroid
Cohort effect in breast
cancerBreast cancer
epidemic predicted
and explainedInternal
Strontium-90
1mSv
cumulative dose

Significant correlationin time lag study; allmalignancy

Regression analysis
gives error in risk
factor of 300-foldInternal <NBR

Highlights error in
ICRP risk factors

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Table 10.5 UNSCEAR 1993 calculations of fallout average committed
effective doses in person Sv to world populations. Doses were calculated using
ICRP models and would be much larger using the ECRR model where internal
doses carry various weightings
PeriodExternal
1945 – 2,160,000
infinity. [UNSCEAR 1993 Table 11]

Ingestion
27,200,000

Inhalation
440,000

Total
29,800,000

The Committee interprets the evidence from the studies it has considered tosuggest that the exposure to global weapons fallout has had a significant impact
on human health. This impact has been both immediate, causing infantmortality at the time (a subject which is reviewed in the next chapter), andprotracted, resulting in increases in cancer, leukemia and other diseases ofgenetic origin (including coronary heart disease) with a delay between
exposure and the clinical expression of disease. In reaching this conclusion, theCommittee has been impressed by the lack of evidence as to the origin of the
global cancer epidemic which began in the period 1975-85. Cancer is now
widely seen, in the medical community, as a genetic disease expressed at thecellular level, and both early and recent research have supported the idea thatthe origin of the disease is essentially environmental exposure to a mutagen. Ifcancer rates began to increase sharply in the period 1975-1985, and sinceresearch has shown that the disease is known to lag the exposure by 15-20
years, clearly, the origin of the epidemic must be the introduction of somecancer-producing mutagen quite suddenly into the environment in the period
1955 to 1965. The identification of this mutagen with radionuclide pollution
from weapons fallout is persuasive. In addition, the variation in cancer
incidence rates across regions of high and low rainfall and deposition points toradiation as the main cause of the cancer epidemic.
Only two groups appear to have studied this possibility: the Radiation
and Public Health Project (RPHP) of Gould, Mangano and Sternglass in the US
and the Green Audit group of Busby et al. in the UK. The latter has used cancer
incidence in England and Wales to examine variation across similar
populations with cumulative exposures to the isotope Strontium-90 of between
0.2 and 1 mSv and has been able to show that variations in the fallout exposure
are highly correlated with later cancer incidence (R = 0.96). Green Audit
researchers have shown that this demonstrates a 300-fold error in the ICRP risk
model. Both groups are engaged in examining geophysical factors likeestuaries and river valleys, where fallout becomes concentrated, and haveshown that these areas consistently show excess risk for cancer and leukemia.
The RPHP researchers have provided evidence that breast cancer is caused byStrontium-90 in fallout and downwind of nuclear sites, and are presently
examining cancer rates in relation to Strontium-90 in measurements they have116

ECRR 2010

made on deciduous teeth. Preliminary unpublished results of this study show asignificant correlation between levels of Sr-90 in the teeth and cancer incidence
later in life (Mangano 2009).
In addition to the increases in all cancers which have occurred since thepeaks in fallout, there have also been some specific cancer sites which haveshown notable increases. Significant and unexplained increases have occurredin female breast cancer and male prostate cancer. Both these diseases arecaused by radiation. The Committee has noted the evidence which links breast
cancer to Strontium-90 published by Sternglass et al. and the cohort studies ofbreast cancer mortality reported by Busby 1997, both of which provide
persuasive evidence about the origin of recent increases in the disease. Prostatecancer has also been shown to have displayed its highest incidence in Wales
following the fallout trend by about 15 years. The excess prostate cancer risk
found by Roman et al. in nuclear workers who were monitored for internal
contamination suggests an error of up to 1000-fold in the risk model used by
the ICRP (Atkinson et al. 1994).
Table 11 of the 1993 report to the United Nations (given above as
Table 10.5) shows that the committed effective dose to world populations as aconsequence of the weapons testing is just under 30,000,000 person Sieverts.
From this dose the ICRP 2007 cancer risk factor of 0.05 per Sievert predicts a
total yield of 1,500,000 cancers in the world population. UNSCEAR 2000
gives similar calculations for the committed effective doses from weapons
fallout but the results differ significantly (are smaller) than those given in the1993 volume.
Table 10.6 (from UNSCEAR 1993) shows committed effective doses
to northern temperate latitudes (40-50 deg. N) from each of the main isotopes
involved. For comparison the table also shows the total doses calculated using
the proposed model of ECRR, which recognises excess risk from internal
emitters. Use of the ECRR adjustment for internal risk using the ratios ofexternal to internal isotopes given in Table 10.6 would increase the cancer
yield from the 1990 ICRP value given above to more than 60,000,000 persons.
The greater part of this yield would be in the 50 years following the exposure,and these cancer increases predicted are, of course, only too visible. This
calculation is revisited in Chapter 13.

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Table 10.6 The major isotopes contributing to human exposure from different
routes after weapons fallout together with average committed effective doses tothe population of northern temperate latitudes (40-50 deg.) from each isotope
calculated by UNSCEAR using ICRP models. * denotes an isotope and routethat ECRR consider hazardous and would weight. The final two rows compare
doses based on ICRP and ECRR models (see 6.9 above). Uranium is notincluded in this calculation as exposures are not known
External

Dose
Ingestion(Sv)
Cs-137
510
Cs-137
Sb-125
47*C-14
Ru,Rh-106
70
*H-3
Mn-54
93
*Sr-90Zr,Nb-95
207
I-131
Ru-10320
Ba,La-140
25
Ce-14423
Total ICRP
995
Total ECRR 995(based on UNSCEAR 1993 Table 9)

Dose
(Sv)
280
2600 (26000)
48 (1440)
170 (51000)
79

Inhalation*Pu, Am*Sr-90*Ru-106*Ce-144

3177
78440

Dose
(Sv)
81 (24300)
15 (4500)
110 (5500)
86 (4300)

292
38600

10.6 Childhood cancer, leukemia and global weapons fallout
One of the most alarming developments in the period following the use andtesting of nuclear weapons was the sharp increase in leukemia and brain
tumours in children, which together make up the main types of childhood
cancer. The early increases in childhood cancer in the 1950s were so
remarkable that governments began to ask if they were caused by fallout, andattention focused on the isotope Strontium-90, which was becoming asignificant contaminant of milk. In the UK, the Medical Research Council was
asked to study the hypothesis and, advised by Sir Richard Doll, reported thatthe Hiroshima findings ruled it out on the basis that the doses were too low.
Despite this, uncertainty fuelled by the contemporary discoveries of Alice
Stewart that low-dose obstetric X-rays caused increases in leukemia in thechildren resulted in the banning of atmospheric tests in 1963.
A 1993 study by Darby, Doll et al. of childhood leukemia and fallout
in Nordic countries has often been cited as support for the contention that lowdose internal radiation is safe. This study spliced together (in a time series)
cancer registry data on childhood leukemia from Denmark, Norway, Sweden,
Finland and Iceland—countries with very different sized populations anddifferent exposures to fallout. The trend in leukemia rates in the 0-4 year olds
over the period of the study, 1948-88 apparently showed a modest increase
from 6 to 6.5 per 100,000 between the periods 1948-58 and 1965-85, whichbracket the peak testing period of 1958-63 when the dose to children was about

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0.5mSv, conventionally modelled. However, close examination of the study
revealed that the early period is represented by data from the Danish cancer
registry alone. After 1958 all registry data was pooled from the five countries.
Thus the study was flawed (CERRIE2004b, Busby 2006). Close examinationof the pooled data from 1958 suggests the increase in leukemia in the 0-4 year
olds is from about 5 per 100,000 to 6.5 per 100,000, an increase of about 30%.
This is in fair agreement with a study of childhood leukemia mortality in
England and Wales published by Bentham.
The leukemia incidence increase of 30% in the children exposed overthe 5-year period followed a cumulative dose of between the 0.15mSv bonemarrow dose received in utero and the 0.8mSv received between ages 0 and 4.
This suggests an error in the ICRP risk factor of between 3 and 15-fold if nofurther excess leukemia occurred in this cohort and an error of between 40 and
200-fold if this excess risk continued throughout their lives. In the US, Archer
examined leukemia increases following fallout from Sr-90 and showed a fairly
consistent increase of about 11% across all age groups following his estimateddose of 1.3mSv to adults and 4mSv to children. If these doses are accurate,then this suggests a higher rate at lower doses in the European studies. As with
Bentham and Haynes, Archer was able to demonstrate a clear variation inleukemia related to high, medium and low rainfall areas.
The Committee notes that the childhood leukemia rate in the UK has
risen steadily following the development of routine X-ray examinations, theextensive use of radium in the dials of wristwatches in the period 1930-40 andthe first releases of fission isotopes to the world environment, with a sharp risein 1945. Childhood leukemia mortality trends in the period 1916-1950 inEngland and Wales correlate with data for world radium and therefore Uranium
production. The doses from radium dial sources have never been established.
Attempts by the Committee to examine another possible source of leukemia
increases by obtaining data on the mobile X-ray systems which were
universally used in the period 1950-1960 to screen for tuberculosis have so far
been proved fruitless.
10.7 Echoes of the fallout effects in the following generation
The Nordic leukemia trends published by Darby et al. show a rise in rates
across the period of maximum weapons fallout 1958-63. However, they also
show a marked increase in the rates from 6.5 to 7.5 per 100,000 beginning in
1983. This step-like increase began prior to the Chernobyl accident and isremarkable. It may be seen clearly in most datasets and shows itself in datafrom Wales and also Scotland as two close peaks centred on the two years 1984
and 1988. It is possible that these are trans-generational echoes of the genetic
damage caused to parents born in or around the years 1959 and 1963, some 25
years earlier.

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The Committee has investigated this hypothesis further by examining asmall dataset obtained from a leukemia charity. This records the year of birth ofthe parents of children in England diagnosed with leukemia. Analysis showsthat the highest risks are in those children whose parents were born around1960, suggesting that their exposure to weapons test fallout may be asignificant factor. The UK government's medical statistics department has
refused to release additional data on the birth years of parents whose children
were born after 1981. A study examining childhood leukemia by cohort year ofbirth of parent was commissioned as part of the CERRIE process but it wascancelled when the Minister who set up CERRIE was sacked.
Also supportive of this hypothesis is some evidence from animal
experiments. In 1963, Luning and Frolen showed that the offspring of malemice exposed to Strontium-90 suffered significant genetic damage whichshowed itself as foetal death due to development defects. The genetic damage
was passed on to the next generation, two generations away from the exposure.
A similar effect on leukemia was found by Setsuda et al. in 1962 afteradministering Sr-90 to albino rats and examining leukemia in the offspring.
Such an effect may be expected in human disease also and is further discussed
in Chapter 13.
10.8 Other fallout studies: the overall effectStudies which have been used to assess the risk of exposure to weapons fallout
in global populations and in downwinders are listed in Table 10.4. These sufferfrom various problems which are noted in the table, but mainly from the sameproblem experienced by the Hiroshima study—the difficulty of finding
unexposed controls. This is significant if the dose-response relationship is not
linear, since low exposure controls may show a higher yield of cancer thanhigher exposure groups, where cells (or the foetus) may be killed rather thanmutated. Nevertheless, the overall picture which emerges from theconsideration of all these studies is not a reassuring one in view of thequantities of material released in the fallout. Even on the basis of
UNSCEAR/ICRP calculated doses and risk factors the predicted cancer yield is
between 1.6 and 3 million extra cancers world-wide—hardly a trivial figure.
The ECRR model predicts between 60 and 130 million extra cancers or an
approximate 20-30% increase in cancer incidence rates in those populations
exposed over the period 1958-63 in Europe. This rise is apparent in the data.
ECRR also predicts a cohort effect increase in cancer in those born between
1958 and 1966 and is concerned about evidence (e.g. the leukemia dataconsidered above) which suggests an increase in risk in their children also.

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11
Risk of cancer following exposure Part II: recent evidence
11.1 Nuclear sites and their proximity
In 1983, a TV company discovered the first of the nuclear site childhood cancer
and leukemia clusters at Seascale near the nuclear fuel reprocessing plant
Sellafield (earlier ‘Windscale’) in West Cumbria. Following the confirmationof this by epidemiologists and after a government enquiry, the UK government
set up two new Committees to (a) develop epidemiological surveillancemethods for small areas and (b) investigate the origin of the leukemia excesses
near nuclear sites. In the 15 years following the Sellafield leukemia cluster,similar clusters were established near the other two reprocessing plants in
Europe, Dounreay in Scotland and La Hague in northern France. In addition,
childhood leukemia clusters were reported for other nuclear sites which
released radioisotopes to the environment, Aldermaston, Burghfield, Harwelland Hinkley Point and Chepstow in the UK, Kruemmel in Germany andBarsebeck in Sweden. Recently, a study of childhood cancer and leukemia by
distance from all the nuclear sites in Germany from 1984 to 2004
unequivocally demonstrated the effect; in children aged 0-4 the risk was morethan doubled. The authors of the study argue that the ICRP risk model has to bein error by at least 1000-fold to explain this finding (Kaatsch et al 2007, Spix et
al 2008). The sites which have been studied are given in Table 11.1.
The Committee has examined the considerable weight of evidence
relating to the existence of childhood cancer clusters near nuclear sites,
including evidence from aggregations of nuclear sites in the UK and Germany
and has concluded that it is exposure to internal radiation from discharges fromthe sites which is the cause of the illness. The arguments against this position
are well summarised in reports from the UK National Radiological Protection
Board, the various reports of COMARE, and the three French government
Nord-Cotentin missions. The response to the KiKK study has been more
muted, nevertheless, despite this clear example of a finding which should force
a re-appraisal of the risk model, nothing has been done.
For Sellafield (Seascale) these arguments were rehearsed in a courtcase in 1993 in which the Judge found, on the scientific evidence presented,
that the leukemia cases could not have been caused by the radiation. However,the court in this instance was presented with the hypothesis that the cases werecaused by the father's pre-conception irradiation, and little independent
evidence to support this hypothesis was presented, owing to the unfortunate
unexpected death of the chief witness, Prof Martin Gardner. No examination
was made by the court of the alternative hypothesis, which was that the risk
factor calculations presented were based on external acute irradiation and were
therefore unsafe.
This is a general concern of the Committee. All the analyses of
causality in the case of nuclear site clusters rely exclusively on the ICRP risk

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model to show that the calculated doses to the children or their parents wereinsufficient to have been the cause of the disease since the linear ICRP model
did not predict the leukaemias or cancers. The approximate discrepancy
between the doses and the observed cases of leukemia in the various studies isgiven in Table 11.1.
Table 11.1 Studies establishing excess leukemia and cancer risk in children
living near nuclear sites.
Nuclear SiteYeara
Sellafield/
Windscale,UKaDounreay,
UK

1983

Defined ICRP
risk
multiplier100-300

1986

100-1000a
La Hague,France1993

100-1000c
Aldermaston/
Burghfield,UKb
Hinkley
Point, UKdHarwellb
Kruemmel,GermanydJulich,GermanybBarsebaeck,
Swedenb
Chepstow,

1987

200-10001988

200-1000

Discharges to offshore mud bank1997

200-1000

Discharges to atmosphere and river1997

200-1000

Discharges to atmosphere and river1996

200-1000

Discharges to atmosphere and river1998

200-1000

Discharges to atmosphere and sea

2001

200-1000

Discharges to offshore mud banks

2007

1000

Various types aggregatedNotes

Well studied by COMARE: highlevel of discharge to atmosphereand sea
Well studied by COMARE:
particle discharges to atmosphereand sea.
Particle discharges to atmosphereand sea: ecological and casecontrol studies
Well studied by COMARE:
particle discharges to atmosphereand rivers

UK
Germany all;
KiKK
a

b
Reprocessing plants discharging to sea; Nuclear power station discharging to sea orcdriver; Atomic weapon and nuclear material fabrication plants; Atomic research with
discharges to local rivers

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The scientific basis for this approach has already been discussed in Chapter 3.
The Committee concludes that these nuclear site cancer clusters together
provide evidence for errors in the ICRP risk model resulting from the use of
external irradiation studies to inform internal radiation risk. The explanation forthe high level of risk associated with the discharges is that the exposurescausing the leukemia and cancer are to novel radioisotopes like Strontium-90
and also to inhaled sub-micron diameter particles, including Uranium. These
are translocated from the lung to the lymphatic system and thence in principle
to any part of the body where they cause high doses to local tissue. The
geophysical processes involved are well described and in the case of Plutonium
and Sellafield, measurements have been made which show the presence of
Plutonium and other radioactive particles in marine intertidal sediment, in the
air near the coast, in sheep faeces, children’s teeth and autopsy specimens takenfrom parts of the UK. The concentration of Plutonium with distance from thesea follows a trend with a sharp increase in levels within 1km of the sea falling
rapidly and flattening out to a finite but reducing level up to 300km or morefrom the sea. The evidence is reviewed in the discussion of cancer near the
Irish Sea below. However, the ICRP model used by COMARE and NRPB in
their analyses of the Sellafield leukemia cluster averages the inhaled Plutonium
doses over a very large mass of tissue and consequently the reports entirely failto make the case that these exposures are a likely cause of the observed illness.
All of the other nuclear site clusters studied involve exposures either tothe novel man-made isotopes which carry hazard weightings under theCommittee’s model or to airborne particle exposures. All the nuclear sites inTable 11.1 have in common that they contaminate local sea coasts or rivers
which flood and are thus near areas where there are significant deposits ofradioactive particles in intertidal, estuarial or river bank sediments. Pooled
studies of leukemia and cancer near nuclear sites have shown that apart fromsome specific nuclear sites (those discussed), the existence of leukemia orcancer clusters is not a significant feature. These studies of aggregates ofnuclear sites have various faults. The Committee believes that epidemiologicalstudies of nuclear sites must establish which populations are most likely to be
at risk on the basis of measurements of the dispersion of radioactive material in
the environment near the source. Studies are usually made in which populations
within a certain radius of the plant are compared with populations living at agreater radial distance, without consideration of the flow of radioactive
material from the site, via rivers, sea-to-land transfer, land slopes andprevailing weather and wind directions. Good examples are afforded by recent
studies of small area populations near two nuclear sites in the UK. In thevicinity of Bradwell in Essex, the UK Small Area Health Statistics Unit,
SAHSU (one of the two Committees referred to in para. 1 of this chapter) drew
radii of of 4, 10 and 17 km on the grounds that proximity to the plant wasconsidered to be a proxy for radiation exposure. In a similar study of
populations near the Nycomed Amersham plant in Cardiff SAHSU chose rings

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ECRR 2010of 2.5 and 7.5 km. Ward level studies by Green Audit established that the
specific choice of radii enabled biased conclusions to be drawn (Busby 2006).
The nuclear sites listed in Table 11.1 have common factors; first, thatthey discharge novel radioactive materials in a way that results in theiringestion and inhalation, and second, that local cancer and leukemia clusters
have been identified. This may be used to invite the application of the Bradford
Hill canons for environmental causation. A Bayesian calculation to refine theassessment of the statistical probability of childhood cancer occurring near
nuclear sites has never been applied to all the plants together although the
NRPB and SAHSU epidemiologists in the UK have played down each cluster
alone on the basis of the individual p-values.
In most of the cases in Table 11.1 the doses are not known but may be
assumed to be small, on the basis of knowledge of the quantities released.
However, for the most studied of these cases, Sellafield, the discrepancy
between the modelled dose and the predicted number of leukemia cases basedon the ICRP risk factors defines a discrepancy between the two of 300-fold and
it is this value, and its similarity to the discrepancies found in other studies ofinternal radiation, that the Committee has used to develop the hazard adjusting
coefficients employed in their model.
The confirmation of cancer and leukemia clusters in children living
near nuclear sites has put considerable pressure on the scientific model of the
ICRP. The confirmed observations of excess childhood cancer near the sites
demonstrate a dissonance that cannot be accommodated within the scientificbasis of ICRP paradigm. The only serious attempt to address this has been thework of Kinlen et al., whose suggestion is based on studies of population
mixing. Their idea is that the nuclear site leukemia clusters are caused by a rare
response to a viral infection which is more likely in situations where there are
new people mixing with rural groups whose immunity to the infection is poor.
The Committee has carefully considered this theory and feels that it is unable
to explain the Sellafield cluster, which has persisted long after any population
mixing occurred, is more closely associated with the commencement of nuclear
operations on the site than with its construction, and which involves asignificant excess risk of cancer as well as leukemia. In addition, the magnitudeof the effect found by Kinlen et al. for locations other than Sellafield iscomparatively modest and could easily be explained by a number of less exotic
mechanisms than the one they propose. In any case, there is no aetiologicalbasis for it since no virus associated with childhood leukemia has ever been
discovered; it is more likely that the modest increases in leukemia have a moreprosaic explanation and that the effect of population mixing can be relegated toa second order phenomenon. Thus the Committee agrees that the existence of
nuclear site leukemia and cancer clusters represents a response to exposure to
the radioactive substances discharged and therefore is a ‘Popperian
Falsification’ of the ICRP models.

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ECRR 201011.2 Recent research on the Irish Sea and other contaminated coastal sites
The Committee has had access to unpublished results of a three-year study ofcancer and radiation on the shores of the Irish Sea. Busby et al. examinedcancer incidence from 1974-90 in Wales and 1994-96 in Ireland. They usedsmall area data which were adjusted for socioeconomic disadvantagement, sex
and age to look at the effect of living near the sea and made several discoveries.
For Wales they found: Risk of developing most cancers increases sharply near the coast.
 The increase is greatest in the 800 metre strip nearest to the sea.
 The increase is greatest near areas of low tidal energy where highest levelsof radioactive material from Sellafield have been measured.
 The effect increased over the period and followed the peak releases from
Sellafield in the mid 1970s by about five years.
By the end of the period, risks of childhood brain tumours or leukemia insome towns in north Wales near radioactive offshore mud banks were morethan 5 times the national average.
For Ireland, using data only for all cancers, they found: The effect existed on the east coast but not on the south or west coast The effect existed in women but was weak or non-existent for men
 There was a strong cohort effect in both men and women born around thetime of the Windscale reactor fire in 1957.
In addition, the group examined closely a part of Ireland, Carlingford, on
the east coast. Using data from a local GP they were able to identify leukemia
and brain tumour excesses in the period 1960-1986. They also conducted aquestionnaire study in the area which revealed that the sea coast effect existed
as close as 100 metres from the sea. People living within 100 metres of the sea
had almost four times the probability of developing cancer than those living
more than 1000 metres away.
The researchers believe the cause of the effect to be sea to land transferof radioactive material trapped in intertidal sediment. This process was
discovered in the mid 1980s and is well described. The trend of Plutonium with
distance from the sea is similar to the trend in sodium chloride penetration, andshows a sharply rising concentration in air in the first kilometre. In the UK,
Plutonium has been measured in sheep droppings across the whole country andthe concentration in grassland, measured in the 1980s, shows a significant trendwith distance from Sellafield. Plutonium has been measured also in children’s
teeth with the same trend, and has been found in autopsy specimens from allover the UK. Levels are highest in the tracheobronchial lymph nodes (TBN)
which drain the lungs. Particles of about 1 micron diameter entering the lungs
are transposed to the lymph nodes and lymphatic system where they can, in
principle, reach any part of the body. Very recent work shows that in rarecases, particles of about 0.1 micron diameter can pass into the placenta and125

ECRR 2010

possibly into the foetus. Such alpha emitting particles cause very high doses tolocal cells in the 40micron range of their disintegration tracks. In addition, cells
will be hit again and again since the particle will continue to emit radiation.
Thus the Second Event process considered in Chapter 8 is possible andrepresents a low probability/ high risk consideration. Beta emitting hot particles
can irradiate the foetus from within the placenta. This is an area where there isinsufficient evidence, and where more research is required.
Following the Irish Sea work, Busby et al. examined other nuclear sites
which discharge to the sea, using cancer mortality data from 1995-1999. They
discovered the same sea-coast effect on cancer near the Hinkley Point nuclear
power station in Somerset and near the east coast nuclear power station at
Bradwell in Essex which discharges to a muddy estuary. There was a high rateof cancer in those living near the sediment compared with those living inland.
In the case of Bradwell, there was a good control town based on a similar
estuary which had no nuclear power station, and which showed no increase incancer above the national average.
The findings of these studies, which were supported by other recent
work by the Radiation and Public Health Project in the US, may be seen as
confirmation of the high degree of risk associated with internal exposure to
micron sized radioactive particles.
The Committee is aware that these researches are based on ecologicalepidemiology and may suffer from all the problems of confounding associatedwith such studies but in view of the relevance of the results to human health areconcerned to encourage further research in this area as a matter of urgency.
11.3 Nuclear accidents
The nuclear accidents which have contributed to significant releases to theglobal environment are listed in Table 11.2.
Table 11.2 Major nuclear accidents and their overall releases.
Accident

Kyshtym,
USSR,
1957
WindscaleUK, 1957
3-MileIsland,US, 1979
Chernobyl
USSR,
1986

126

Total
(PBq)
74

Particles

Notes

High

High particulate yield from Ce-144: no adequate
follow-up of health effects published

0.83

Moderate

Attempts to cover up the direction of fallout;

566

No

Almost completely gaseous: no adequate followup

2088

High

Cover-up of early data. High and anomalous
thyroid cancer admitted. Other effects disputed
and an area of considerable argument (see text).

ECRR 2010

The Committee is concerned that the health consequences of the three nuclear
accidents which occurred prior to the Chernobyl explosion in 1986 have notbeen studied by epidemiology. Evidence has been obtained that the Windscale
accident may have caused increases in Down’s Syndrome births in eastern
Ireland, and there is recent evidence from the Irish Sea studies that there is asignificant cancer cohort effect in those who were born around 1957. In
addition the Isle of Man, a small island in the Irish Sea some 70km to the westof Windscale, has provided some evidence for a sharp increase in mortality
from all causes beginning shortly after the accident. This is seen in data
supplied by the government of the Isle of Man. The Committee has also seen
evidence that the official meteorological wind direction records from this event
have been tampered with, with the apparent motive of concealing the likely
location of any effects.
The most recent nuclear accident, the Chernobyl explosion in 1986,
was the largest accidental release of radioactive material to the environmentand caused contamination in most countries in the northern hemisphere. A
number of studies of health in the affected countries have been published orhave been presented at conferences. The overall picture which emerged in theWest by the time of the ECRR2003 report was one of confusing and mutually
exclusive reports of increases in cancer, leukemia and genetic illnesses on the
one hand, and of denial of any adverse health effect associated with theexposures on the other.
It now is clear that this was due to falsification or concealment of thebasic data by the Soviet authorities. A number of official regulatory orders
have been discovered and are reproduced in Yablokov et al 2009. For example,
an order from the USSRs First Deputy Minister of Public Health, O.Shchepin
on May 21st 1986 wrote:. . . for specified persons hospitalized after exposure to ionizing radiation andhaving no signs or symptoms of acute radiation sickness at the time of release,the diagnosis shall be vegetovascular dystonia.
Another example is given in an explanatory note of the Central Military
Medical Commission of the USSR Ministry of Defence:(1) for remote consequences caused by ionizing radiation and a cause-andeffect-relationship, it is necessary to consider: leukemia or leucosis 5-10 years
after radiation in doses exceeding 50 rad. . . . the presence of acute somatic
illness and activation of chronic disease in [liquidators who] do not have acuteradiation sickness, the effect of ionizing radiation should not be included as a
causal relationship.
Assessment of the true health effects of the accident has been
dominated by heavy handed cover-ups and suppression of data by UNSCEAR
and IAEA. The WHO have been excluded from any real involvement in theissue, as the WHO President H Nakajima stated on camera at the conference inKiev in 2001. At this conference, the UNSCEAR representative, Dr N Gentner
wrote the conclusions of the conference himself, producing a statement which

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denied the existence of any measurable effects of the radiation, and although
the conference refused this version and voted strongly for an highly amended
statement calling for research, the final statement was adjusted back to theoriginal one (Busby 2006).
The Committee believes that a significant proportion of conclusions
regarding increases in radiogenic illness are misguidedly based on a presupposed linear response between dose and effect. Such an assumption isinvalid because of the confusion between external and internal doses and also
because of the considerations relating to cell doses and cell sensitivities
discussed Chapter 8. In addition, epidemiological studies have been influenced
by or countered with the predictions of the ICRP risk models for populations
exposed to the discharges. These predict very modest effects which would
generally be difficult to establish against the large background cancer rates
experienced by the study populations and therefore, when increases in cancer
are seen in such populations, they are ignored or at least not ascribed to
exposures from Chernobyl. The main reports examined by the Committee arelisted in Table 11.3. With regard to cancer, the first evidence of late effects may
be divided into evidence for increases in thyroid cancer, leukemia and solid
tumours.
Since the 2003 report the situation with regard to Chernobyl healtheffects has markedly changed. This is largely because the Russian language
peer reviewed reports of ill health and of animal and genetic studies whichwere ignored by UNSCEAR and ICRP have now been translated and reviewed(Yablokov and Busby 2006, Yablokov et al. 2009). Profs Yablokov andBurlakova attended the CERRIE conference in Oxford in 2003 and told the
CERRIE secretariat that the evidence from Russian language publications wasquite different from that being reported by IAEA and UNSCEAR. Many ofthese papers were then translated and were abstracted into English by
Yablokov and Busby. However, the CERRIE report omitted them and any
reference to them: they were included in the CERRIE Minority report(CERRIEa, CERRIEb). ECRR set up a sub-Committee on Chernobyl in 2003,
chaired by Prof Yablokov: this resulted in the publication of ECRR2006Chernobyl 20 Years on which can be downloaded free from the euradcom
website. This monograph has contributions by several eminent scientists fromthe Russian Federation, Ukraine and Belarus and the reader is referred to thebook for details. Briefly, it reported serious health effects of the accident,
including genetic and genomic effects in humans and in animal and plant
populations. Thus the total exclusion of Chernobyl epidemiology andChernobyl effects from UNSCEAR 2000, UNSCEAR 2006 and ICRP 2007 isastonishing. In UNSCEAR 2006, a volume apparently devoted to radiation
epidemiology, there is little mention in to Chernobyl and not one of the papers
in any of the above are cited or discussed.

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The evidence of the situation in these countries and in Europe is more
recently reviewed by Yablokov et al. 2009, a publication of the prestigious
New York Academy of Sciences.
Chernobyl effects were also a major topic of discussion and the subjectof several papers given at the 2009 ECRR conference in Lesvos Greece; theproceedings of this conference are in preparation. The concluding statementfrom the conference calls for governments and researchers to see the Chernobyl
accident as an opportunity to properly assess the health effects of radiation
exposure. This statement, the Lesvos Declaration is in Appendix C.
ECRR is also currently assembling a report by Bandashevsky on his findings in
the contaminated territories on Belarus.
In summary, the effects of the Chernobyl accident have been
downplayed or dismissed by the ICRP, UNSCEAR and IAEA. It is quite clearthat this was necessary in order to continue to support the ICRP model; theChernobyl effects reported in the Russian language papers falsify that model.
There are two cancer studies which have been published using data fromwestern sources: the infant leukemia analyses and the analysis of cancer
incidence in northern Sweden. Both falsify the ICRP model and the error in therisk model is approximately the same in both cases and the same as thatpredicted by ECRR on the basis of the earlier considerations. These will be
discussed below.

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Table 11.3 Chernobyl studies and reviews used as basis for the Committee’s
examination of the effects of the accident.
Reports/
assessments

Note

IAEA, 1994

Official Atomic Energy Agency Conference in Vienna
characterised by reports showing either massive healthdeficit or little significant effect apart from thyroid
cancer. Arguments from the floor. Proceedings still not
published.
Independent conference held in Vienna at the time of the
IAEA conference where scientists reported significant
adverse health effects.
UNESCO book by Belarus academician Savchenko
reports thyroid cancer solid tumours, leukemia andcongenital disease increases.
Edited by Russian academician Burlakova, reports
various cancer, leukemia and ill health related
biochemical and immune system indicator changes andalso novel dose response to radiation.
Book published by BELRAD organisation in Minsk
reporting increases in thyroid cancer, leukemia and solid
tumours; in children from Belarus.
Draws together selection of published studies with acommentary suggesting the only significant increase inill health from radiation is due to thyroid cancer.
Clumsy attempt to show results follow ICRP predictions
even for thyroid cancer.
Conference in Kiev characterised by reports showing
either massive health deficit or little significant effectapart from thyroid cancer. Conference resolution to ask
for a re-assessment of risk models.
International collaborative work reports including
accounts of dissonance between the ‘official reports ofradiation effects’ and the real results in the affected
territories.
Book showing increase in cardiac pathologies associatedwith measured internal contamination in children from
Belarus.
Various reports from Poland and Bulgaria show sharp
increases in cancer and ill health effects in infants andanomalous birth outcomes immediately following
Chernobyl.

IPPNW, 1994

Savchenko
1995
Burlakova,
1996

Nesterenko,
1998
UNSCEAR,
2000

WHO, 2001

Kyoto, 1998

Bandashevsky,
2000
Poland,Bulgaria,
various130

ECRR 2010

Busby, 2001

Infantleukaemias
Minisatellite
mutations

IARC, various

Belarus andUkraine reports
in Russian

CERRIE 2004b

Okeanov et al
2004
Tondel et al
2004
ECRR2006
ECRR2009

Bandashevsky
2008
ECRR 2009
Yablokov et al
2009

Report to Belarus Embassy with review of data andpredictions of new risk model from cancer yield in
BelarusInfant leukemia reported in six countries in cohort
exposed in utero defines error in ICRP risk factor of
100-fold or more (see text).
Various papers report increase in minisatellite mutation
rate in children from high exposure region and in
offspring of liquidators: implied error of up to 2000-foldin ICRP model.
‘Official’ examination of leukemia increases in Europe
using pooled database suggests no increase that is
ascribable to Chernobyl: flawed approach.
Many reports from Belarus, Ukraine and RussianFederation contain evidence of increases in leukemia,
solid tumours, thyroid cancers, congenital
malformations and general massive health deficit
following and ascribable to the exposure. Reports nottranslated or included in official reviews.
Contains section with abstracts of 40 major peer
reviewed papers in Russian n the health effects of theChernobyl accident
Report in Geneva of levels of cancer increase registeredby the Belarus Cancer Registries (see text Chapter 14).
Study of cancer in northern Sweden associated withChernobyl fallout (see text Chapter 14).
Chernobyl 20 Years On Eds. AV Yablokov, CC Busby.
Compilation and review of peer reviewed studies on thehealth effects of the Chernobyl accident published in
Russian; 2nd edition 2009
Update of Yuri Bandashevsky’s work published in
Lithuania.
3rd International Conference of the ECRR Lesvos
Greece May 5/7th 2009
Chernobyl. Consequences of the Catastrophe for People
and the Environment131

ECRR 2010

11.4 Dispersion of Chernobyl fallout and doses
Owing to prevailing weather conditions, the dispersion of the material fromthe Chernobyl explosion and subsequent fire was very variable, but was wellcharacterized due to measurements which were made in many countries of theworld. It was global, with detection of radionuclides as far away as the USA,south-east Asia and Japan. It is therefore predicted by the ECRR risk modelthat health effects will be detectable in many countries, but very little seems tohave been done to look for such evidence, possibly because the doses werevery low and at such low doses the ICRP model predicts no measurable effects.
But when researchers did look, they found results. The increase in infantleukemia in Europe in the in utero cohort has been mentioned; this increase
was also reported for the USA by Mangano (Mangano 1997). Cancer increases
in Sweden were reported by Tondel et al. 2004. There was a sharp increase incancer incidence in the UK registries for Wales and Scotland (Busby 2006).The
average first year committed effective (ICRP) doses reported by Savchenko
1995 by country for these various contaminations ranged from about 2mSv in
Belarus through 1mSv in Ukraine, between 0.5 and 0.7mSv in Bulgaria,
Austria, Greece, Romania, Finland and the Russian Federation, to 0.08mSv inthe UK and China. Of course, the ECRR weightings would increase these doses
significantly but without an analytical breakdown of the isotopes involved only
an approximation can be made. The radionuclides involved in the dispersion
were very high levels of initial Tellurium-132/Iodine 132, a gaseous Second
Event pair, Caesium-137, Plutonium 239, Strontium-90 and Uranium fuelparticles containing various fission-product beta-emitters. The amount of
uranium in the fallout was not measured, although these particles contaminatedthe air and crops (Hohenemser et al, 1986). The ECRR weightings for such
exposures are very high, some 3 orders of magnitude. On the basis of theincreases in cancer in the intervening period, the doses calculated byapplication of the ECRR weightings to the mainly Cs-137 gamma doses which
represent the basis of the Savchenko estimates seem to predict the increases
fairly well.
11.5 Reported effects of the exposures
On the basis of the ECRR effective doses which are certainly greater than
600mSv in Belarus it would be expected that there would be clear healtheffects in that country and indeed such are reported in the Belarussian
literature: cancer, birth defects, a sick population, loss of lifespan (Yablokov etal 2009, Okeanov 2004, Bandashevsky 2000, 2000a -2000c, Bandashevskaya
2003, Busby and Yablokov 2006, Busby and Yablokov 2009, Yablokov et al2009). What is most apparent in the data is the enormous range of healtheffects and conditions which correlate with exposure to radionuclides from thecontamination. This wide range makes it difficult to assess health outcomes in132

ECRR 2010

terms of a simple indicator of cancer rates. As pointed out above, increased
death rates in children and young adults from any disease or condition will
lower the incidence rates from cancer since this is a disease of old age. In thispublication, the Committee has no space to review the full spectrum of disease
which has followed the Chernobyl fallout exposures and refers those who wish
to follow up this issue to its own publication Busby and Yablokov 2006 (2nd
Edition 2009) and to Yablokov et al 2009. Effects of the Chernobyl accident
exposures also appeared in many other countries in Europe, where researchers
were prepared to look, for example Trisomy 21 Downs births in Germany,
Sweden and the UK, changes in minisatellite DNA and thyroid diseases.
11.6 Thyroid cancer after Chernobyl
The remarkable and aggressive increases in thyroid cancer in territories mostaffected by the disaster were initially denied by the radiation risk establishment
but later, owing to the fact that the disease is normally very rare, wereconceded. Although no formal calculation was published, the increases
appeared to show that there were two significant errors in the risk models of the
ICRP, apart from the fact that the effect was orders of magnitude larger thanthat predicted by the ICRP risk factors. The first error concerned the belief thatinternal irradiation of the thyroid by radio-Iodine was less effective than
external irradiation in causing cancer. The second was in the belief that there
would be a time lag of more than ten years in the onset of the clinicalsymptoms. In the event, thyroid cancer increases began a few years after thedoses were delivered.
The risk agency community, having had to concede the facts of theincrease, promptly responded by adjusting the doses to as high a level as
possible to try and fit the data to the model. The idea was to assume that thechildren who were affected had been Iodine-deficient and therefore their
thyroid glands would take up more Iodine. This was unsuccessful since doses
large enough to fit the cancer data would be so high that the children would
have died of radiation sickness. Early data was presented in ECRR2003 but
Table 11.4 shows the situation in Belarus up to 2004 (Malko 2009). In the mostcontaminated region, Gomel, the difference between the expected numbers ofcases and those observed is 126. Other data from 1986 to 2007 presented by
Malko 2009 shows that the effect peaked in Belarus in 1995 and by 2001 had
fallen back to just around the baseline pre 1986 levels. It should be noted thatthe thyroid gland is very radiation sensitive due to its iodine content sinceiodine has a high atomic number Z = 53 and therefore living in an areas of highgamma radiation or being internally exposed to gamma emitters apart from I131 will significantly add to the exposures through the secondary photoelectron
effect. In parts of northern Finland where inhabitants were also exposed tointernal uranium (though local geology) the Iodine exposure from Chernobyl
had a much greater thyroid cancer producing effect than in areas where there

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was no uranium (Slama 2009). The ICRP and UNSCEAR have been unable torespond credibly to the increase in thyroid cancer and its dissonance with theirradiation models.
Table 11.4 Thyroid cancer incidence and Relative Risk (based on ICRP model)
in children in Belarussian regions from 1986 to 2004 (Malko 2009)
Regions
Brest
Vitebsk
Gomel
GrodnoCity Minsk
Region Minsk
Mogilev
All

Observed
165
11
378
43
62
42
43
744

Expected
3
2
3
2
3
3
2
18

O-E
162
9
375
41
59
39
41
726

RR
55
5.5
126
21.5
20.7
14
21.5
41.3

The error in both the absolute magnitude of the effect and also the rapid onset
may be a consequence of the fact that the extremely active Tellurium132/Iodine-132 Second Event couple was a major exposure hazard in the earlydays. In addition, the basis of the radio-Iodine risk model is a series of studies
by Holm on hospital thyroid patients in which any cancers which developed
within the first five years of exposure were discarded from the study as being
due to pre-existing lesions on the basis that the Hiroshima LSS had shown asignificant time lag for thyroid cancer. Lars Erik Holm has been mentioned
earlier in connection with the ICRP.
11.5 Leukemia after Chernobyl
Since Hiroshima, observations of high leukemia yields following the A-bomb,
leukemia and especially childhood leukemia has become the first symptom to
be investigated in any irradiated population. For this reason, leukemia
incidence is likely to be the first data that would be addressed byestablishments wishing to control the perception of harm following a nuclear
accident. Recalling that the accident occurred during a period when state
control of data by the former USSR was significant, the Committee interprets
the confusion over increases in leukemia rates in Chernobyl affected territories
as due partly to this factor. The problems in interpreting leukemia data andstudies of leukemia following Chernobyl are listed in Table 11.5.

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Table 11.5 Problems interpreting data on leukemia after Chernobyl
Problems in interpreting data on leukemia after Chernobyl
1. Soviet cover-up at the diagnosis stage, so no leukemia appears on medical forms.
2. Soviet cover-up at the registry/report stage so figures are adjusted to fit controls.
3. Later researchers use database containing incorrect totals.
4. Assumption of linear response means that controls may have higher rate than
exposed.
5. Regression method assume linear response: coefficients will include Type II error.
6. Small numbers make result critically dependent on removal or exclusion of few
cases.
7. Pooled data will give confused results owing to dose response variation.

There have been reports of leukemia increases in the main Chernobyl-affected
territories of the ex-Soviet Union (listed in Table 11.3); reviews assert that noincreases are predicted and that any increases found are due to better
ascertainment or cannot be caused by radiation owing to lack of a positive dose
response coefficient (also listed). The Committee takes the view that leukemia
data from the Chernobyl affected territories are difficult to analyse in such a
way as to develop useful models owing to lack of accurate data for internal andexternal doses, the insecurity of the databases and other problems listed inTable 11.5
There have been two main sets of studies which inform on leukemia
risk in Europe, the series of studies undertaken by IARC in Lyon and the infantleukemia reports. In the IARC series, childhood leukemia incidence data werepooled from most of the cancer registries in Europe and the ex-Soviet
territories, and analysed as a time series and using regression methods toexamine the hypothesis that the exposure period was followed by a significant
step in childhood leukemia. Although an increase was observed, it did not show
as a step change and in addition, the highest doses did not correlate with thehighest incidence. This resulted in the authors concluding that the accident had
no significant effect. The Committee views this study as essentially flawed
owing to variation in dose and in genetic susceptibility across the pooled
dataset and considers that examination of individual time series from eachcountry might reveal an effect, as it did in data from Scotland and Wales.
The second set of studies involved examining the increase in infantleukemia 0-1 in the cohort who were in utero over the period of maximum
exposure to internal irradiation from Caesium-137 or other isotopes.
Examination of this phenomenon, which was reported from six separate
countries, forms part of an analysis which the Committee accepts as
unequivocal evidence for a significant error of 100-fold or greater in the ICRP
risk factors for internal irradiation. This will be considered separately.

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ECRR 201011.6 Cancer in Northern Sweden after Chernobyl
Weapons fallout studies of Wales and England followed differential exposuresof populations in two countries. Tondel et al 2004 published a sophisticatedepidemiological analysis of differential Chernobyl fallout effects in small areasof one country, northern Sweden. They correlated Cs-137 precipitation insmall areas (communities) with cancer incidence from 1984 to 1996 in order toexamine the effects of exposure. Cs-137 data were obtained from the Swedish
Radiological Protection agency SSI and cancer incidence from the Swedish
Cancer Registry. The study found a statistically significant 11% increased risk
per 100kBq/m2. Using external exposure data only this translates to a 650-folderror in the ICRP model, but if internal exposure is added in, one the basis of
Cs-137 alone, this number will probably reduce to a 400-fold error. It should be
noted that the real dose is unknown; the radiation covariate was Cs-137 area
contamination. The Chernobyl fallout was not the same as the weapons fallout
in terms of the spectrum of radionuclides. There will have been other isotopes
and the material will have included Uranium fuel particles. However, in termsof ICRP analyses, it is the external Cs-137 dose that would be the quantity
employed for radiation protection. Nevertheless we see good agreement withthe earlier study of Wales and England which gave a 300-fold error.
11.7 Nuclear workers and their children
Nuclear workers and their children are an obvious category for the analysis ofradiation induced disease and the Committee has examined the main studies
which have looked at cancer and leukemia rates in this group. Most studies
have shown that the group (with some exceptions) has a lower rate of incidenceof these diseases than controls from the general population. This is concededby the authors of these studies as due to the fact that nuclear workers have in
general better health than the general population owing to their higher
socioeconomic status, the ‘healthy worker effect’. The magnitude of this effecthas been hard to assess from published data. However, a very large recent
study gave information which enabled the Committee to reanalyse the data andto show a trend in cancer risk with length of employment in the nuclear
industry. The results are given in Table 11.6

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Table 11.6 making allowance for the healthy worker effect in data from the‘Second Analysis of the National Registry of (UK) Radiation Workers’
Years inindustry

All deaths

SMR
allcausesAll cancers

SMR allcancers

SMR allcancercorrected
a

0-1
281
64
67
64
112
2-4
623
72
159
73
128
5-9
1466
79
443
89
156
10-14
1863
81
508
80
140
15-19
2162
87
589
85
149
20-25
4194
85
1186
82
143
30+
2176
83
646
80
140
a
Based on extrapolation of trend in cancer SMR to zero time to give SMR = 57

The method used to obtain a value for the ‘healthy worker effect’ is based on
the extrapolation of the trend in standardised mortality ratio to the moment theworker enters the nuclear industry. Using the resultant zero dose, zero time
SMR as a control, it is clear that although nuclear workers may have lower age
specific mortality than the general population, they die at a greater rate thanthey would if they worked not in the nuclear industry but in some other
employment which conferred the same economic and social benefits. The
results in Table 11.6 show that this effect occurs within the first five years of
employment and by 5-9 years working in the industry their risk of death fromcancer is more than 50% higher than it would be if they had not been employedin this way.
A problem with the nuclear industry workers’ studies is that the doses
are measured by film badges and therefore are external. No real data exist forinternal doses although there is considerable indicative evidence that it is the
low internal doses that are responsible for the slightly increased rates of cancer
and leukemia that are found among nuclear workers and their children. These
increases are usually discounted on the basis that the dose-response relationshipis not linear, and that the groups with highest cancer risk are not the high dosegroup, but are usually the intermediate dose group. This effect, the Burlakova
type response, was found in recent studies of UK workers as Table 11.7 shows.

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Table 11.7 Trends with increasing external doses for mortality risks from allcancers and from leukemia derived from the Second Analysis of Nuclear
Industry Workers (UK) and adjusted for healthy worker effect.
Film badge
dose (mSv)

SMR Allcancers

Corrected SMRaall cancers

SMR
leukemia

Corrected
SMRaleukemia
1.00
1.86
1.22
1.4
2.2
2.1

0 (zero time)
0.57
1.00
0.57
<10
0.97
1.7
1.06
101.011.8
0.7
200.971.7
0.77
501.10
1.9
1.24
b
1.01
1.8
1.19
>100
a
Corrected on the basis of a healthy worker cancer mortality risk of 0.57 relative to thegeneral publicb
Averaged over the dose groups 100-200, 200-300 and 300+ due to small numbers inthese groups

No real attempt has been made by the authors of the various studies of nuclear
workers and their families to establish the magnitude of the healthy worker
effect and the Committee feels that this is an important issue which must be
addressed. The use of internal comparisons using groups within different
external radiation dose ranges is not helpful since the dose–response linearity
assumptions are built in to the interpretation of the results. In addition, it is notclear with pooled studies that such a stratification is epidemiologicallyhomogeneous, and may compare individuals from different sites or withdifferent internal doses from internal isotopes. The main nuclear industry
studies considered by the Committee are given in Table 11.8.

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Table 11.8 Main studies of nuclear workers considered by the Committee
Study
1. Hanford, USA

2. UKAEA
3. UKAEA Prostate

4. Sellafield, UK

5. AWE, UK
6. All workers UK

7. Oak Ridge US
8. Nuclear Industry
Family Study UK

9. Offspring Record
Linkage Study UK

Notes
External: 10-fold error in the external risk factor found;
doubling dose for all cancers 340mSv; leukemia excess
not dose related.
External: increased mortality from various kinds ofcancer. Clear excess from prostate cancer.
Case control study: prostate cancer associated with
monitoring for internal exposure with relative risk up to
20-fold. Defined error in ICRP model from internal
isotope exposure risk at about 1000-times.
External: excess cancer risk found with wide confidence
intervals. Central estimate about 0.1 per Sv in 10mSv
region.
Average external dose 8mSv. Evidence of increased risk
with period of employment.
Analysis of pooled data; Burlakova type response; excess
risk from all cancers based on healthy worker effect (seetext).
Increased risk in older workers reported.

Leukemia in <25-year-old offspring of nuclear workers in
UK found significant excess risk of leukemia withrelative incidence risk in offspring of fathers with
>100mSv of 5.8. Biphasic dose response; doubling risk
from internal monitoring.
After exclusion of Sellafield fathers, there was asignificant excess risk of leukemia or non Hodgkin
lymphoma in the offspring of radiation workers (fathers
RR=1.77, mothers RR = 5) with evidence for Burlakova
response and highest risk if monitored for internal
isotopes (RR = 2.91 vs. 1.61 not monitored). Authors use
non-linear response as evidence that radiation was not thecause.

11.8 Unequivocal evidence
All the evidence which associates low level internal exposure with cancer andleukemia suffers from the problem that other causes for the effects may be
advanced, however implausible they may be. Kinlen et al.’s population mixing(discussed above) is a good example of this. There is also the problem that withlow level radiation, cause and effect are separated by the lag period between
initial genetic damage and final clinical expression of a cancer which can be
confirmed by histopathology, and during such a period other possible causes

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may be found. However, in the last few years, advances in technology and theexistence of well defined populations who were exposed after the Chernobyl
accident, together with a slight easing of the situation with regard to access tosmall cancer incidence and mortality data have made possible two study
situations where there is now unequivocal evidence of error in the ICRP model
as it relates to internal exposure. The two sets of such studies providing
unequivocal evidence of risk factor error are listed in Table 11.9
Table 11.9 Recent studies which the Committee takes to show unequivocal
evidence of error in the ICRP models.
Study
1. Minisatellite DNA mutation
after Chernobyl

2. Infant leukemia in fivecountries

Shows
Objective scientific indicator in children bornafter Chernobyl accident shows 7-fold increasein mutation relative to siblings born before.
Error in ICRP 700- to 2000- fold for this endpoint.
Increases in infant leukemia in children who
were in utero over the exposure period forinternal radiation define error in ICRP risk
factor from 100- to 2000-fold for this end-point.

11.9 Studies representing unequivocal evidence of errors in ICRP model
11.9.1 Minisatellite DNA
The ICRP model of genetic mutation after irradiation is based, like ICRP'scancer risk model, on the Hiroshima LSS yield of gross genetic effects andstudies of radiation effects in mice.
Although subtle genetic effects on sex ratio were apparent in the LSS
offspring, the RERF researchers excluded them from the study because they
did not accord with their notions of the expected direction of such an effect[Padmanabhan, 1997, Busby 2006]. Neels’s exclusion of the sex ratio effects
resulted in the belief that the genetic effects of 10mSv in the first generation
would be unmeasurable. Thus BEIR V gives the incidence of total genetic
effects including chromosomal effects (unbalanced translocations andtrisomies) at 6 per million offspring compared with the natural rate of 4,200. It
predicts a 10mSv excess risk of 10 cases of congenital malformation in anatural rate of 25,000 per million offspring and similar vanishingly small
increases are given for autosomal dominant, X-linked and recessive disorders.
Using a combination of mouse studies and the epidemiology of the LSS, thedoubling dose for spontaneous genetic burden has been estimated to be 1
Sievert. [e.g.BEIR V, 1990 p 70]
However, the development of molecular techniques has enabled
objective measurements of the consequences of irradiation to be investigated in140

ECRR 2010human populations. There have been several studies of minisatellite DNA
mutation in children living in parts of the ex-Soviet Union and exposed toradiation from Chernobyl. Using the technological development of ‘DNA
testing’ in which minisatellite DNA is separated into bands which arecharacteristic of its genetic identity, it has been possible to show that children
living in Belarus and exposed to radiation from fission-product isotopes whichcontaminated their environment suffered a doubling in genetic mutation.
[Dubrova, 1996, 1997]. Similar work with barn swallows exposed in Belarus
showed that these genetic changes were also present and were associated withphenotypic changes in plumage patterns as well as reduced survival, therefore
underlining the potential importance of such mutations. [Ellegren et al. 1997].
Most recently, the minisatellite DNA tests have been applied to thechildren of Chernobyl liquidators who were born after the accident comparedwith siblings born before the accident. [Weinberg et al. 2001] There was aseven-fold increase in genetic damage found in the post-exposure children. By
comparison with mutation rates for the loci measured, this finding defined anerror of between 700-fold and 2000-fold in the ICRP model for heritable
genetic damage. In addition, the research results could be stratified by dose
range and this resulted in a biphasic or Burlakova type response. It isremarkable that studies of the children of those exposed to external radiation at
Hiroshima show little or no such effect, suggesting a fundamental difference inmechanism between the exposures. [Satoh and Kodaira, 1996]. The most likely
difference is that it was the internal exposure to the Chernobyl liquidators thatcaused the effects.
This evidence of a substantial error in the ICRP model may have been
accepted by the Chairman of the UK Committee on Medical Aspects ofRadiation in the Environment, Professor B. A. Bridges, who conceded that thetime may have come for a paradigm shift. In his outline of concerns, Bridges
focused on the bystander effect whereby intercellular communication between
cells traversed by an ionising track causes nearby cells to exhibit genomic
instability resulting in genetic mutation in a large number of cells which were
not subject to the initial ionisation injury [Azzam et al. 1998, Hei 2001]. It
remains to determine a model in which external and internal irradiation may
result in significant differences in such an end point since, in principle,
genomic instability and bystander effects are applicable to internal and external
irradiation and to natural and novel sources equally.
11.9.2 Chernobyl infants
Following the Chernobyl accident in 1986, the cohort of children who were
exposed in their mother’s womb to radioisotopes from the releases suffered an
excess risk of developing leukemia in their first year of life. This ‘infantleukemia’ cohort effect was observed in six different countries. It was firstreported in Scotland [Gibson et al., 1988], and then in Greece [Petridou et al.,141

ECRR 2010

1996], in the United States [Mangano, 1997] and in Germany [Michaelis, et al.
1997].
Busby and Scott Cato examined the relationship between the observed
numbers of cases and those predicted by the ICRP model. For the first time, thespecificity of the cohort enabled them to argue that the effect could only be aconsequence of exposure to the Chernobyl fallout. There could be noalternative explanation.
Because the National Radiological Protection Board had measured andassessed the doses to the populations of Wales and Scotland and because they
themselves had also published risk factors for radiogenic leukemia based on
ICRP models it was a simple matter to compare their predictions with theobservations and test the contemporary risk model. The method simply
assumed that infants born in the periods 1980-85 and 1990-92 were unexposedand defined the Poisson expectation of numbers of infant leukemia cases in thechildren who were in utero over the 18 month period following the Chernobyl
fallout. This 18 month period was chosen because it was shown that the inutero dose was due to radioactive isotopes which were ingested or inhaled by
the mothers. Whole-body monitoring had shown that this material remained in
the bodies of the mothers until Spring 1987 because silage cut in the Summerof 1986 had been fed to cattle in the following winter. The result showed astatistically significant 3.8-fold excess of infant leukemia in the combined
Wales and Scotland cohort (p = 0.0002). The leukemia yield in the exposed inutero cohort was about 100 times the yield predicted by the ICRP model. Table
11.10 compares the effect in the three main studies. In this table, the B cohort
were those children exposed to the internal exposure from Chernobyl in utero
in the 18 month period following the event and born between June 1987 andJanuary 1988. These exposure periods were defined by the whole bodymonitoring results. The control periods A and C were the ten years before(1975-85) and the four years after 1988 for which data was available.
Since the World Health Organisation has given approximate exposurelevels in Greece, Germany and the United States, it was also possible toexamine the leukemia yield in the infant ‘exposed cohort’ reported by theseveral other studies and establish a dose response relationship. It was foundthat a biphasic or Burlakova type relationship existed for the data from theseparate countries.
The importance of this study as evidence of falsification of ICRP
caused it to be included in the CERRIE Committee agenda. Members of theCommittee from both sides of the argument analysed a new dataset which wasprovided by the Oxford based Childhood Cancer Research Group. This gave
infant leukemia numbers in the same exposure cohorts employed by the study
carried out in Greece and that in Germany. This was a cohort of those who
were in utero over the period of the fallout as defined by Petridou et al. 1996.
Analysis by Muirhead of NRPB and by Wakeford of British Nuclear Fuels
showed an excess of infant leukemia in the various countries with errors

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ranging from about 100 to about 1000. Nevertheless, the final CERRIE reportmarginalised these results and ignored their significance, despite displaying theactual numbers and confidence intervals in a table in an Appendix. Later the
UK data was aggregated with that from Germany and Greece to show that there
was a highly statistically significant 43% excess infant leukemia risk in the
combined cohort in the UK, Germany and Greece (Busby 2009).
The Committee accepts that the infant leukemia results represent
unequivocal evidence that the ICRP risk model is in error by a factor of
between 100-fold and 1000-fold for the type of exposure and dose, the latter
figure allowing for a continued excess risk in the cohort being studied. The
Committee notes that it will be necessary to follow the cohort as it ages. The
Scottish Cancer registry has refused to release data to allow this to be done.
Table 11.10 Unequivocal evidence of ICRP risk factor errors: comparison
between infant leukemia rates after Chernobyl in Wales and Scotland andsimilar data from Greece and from the former Federal Republic of Germany
Group
Exposed cohort B
Cohort size
Number of cases
Rate
Unexposed cohort
A+C
Cohort size
Number of cases
Rate
Risk Ratio
Cumulative Poisson
ProbabilityaWales and Scotlandb

GreececGermany

156,600
12
7.67

163,33712
7.34

928,64935
3.77

835,200
18
2.15
3.6

1,112,566
31
2.79
2.6

5,630,789
143
2.54
1.5

0.00020.0025

0.02

a

b
c
See text for A B and C periods Petridou et al.(1996) Michaelis etal.(1997)

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ECRR 201012
Uranium
Depleted Uranium Weapons
For there is nothing hid that shall not be manifested;neither was anything kept secret, but that it should come abroad
Mark 4,22

12.1 Introduction
The element Uranium is the basis of and parent of almost all releases ofradioactivity to the environment, yet curiously, until it began to be employed asa weapon, it had been quite neglected as a hazardous component. It is notmeasured routinely near nuclear power stations or reprocessing sites. It istreated as if it were natural which of course it is, but its concentration in theseplaces, and the form it is released in is not.
The intense and increasing interest in the health of the troops who
participated in the first Persian Gulf War in Iraq, and later those who served in
the Balkans, where Uranium weapons were also used, and of course the civilian
populations of those areas have resulted in evidence that the genotoxicity of
Uranium is far greater than the military who used it, and the states whichsanctioned this, believed. Despite the increasing evidence of its anomalous
propensity for harm, from epidemiology and from laboratory and theory, the
ICRP risk model, here as in everywhere else in radiation protection, is used todeny the evidence and to sanction its continued use as a weapon of war. As
with the fallout from bomb tests, Chernobyl and the child leukemias near
power stations, clear evidence of harm from exposure to Uranium is denied on
the basis of deductive logic, that the absorbed doses are too low to cause any
measurable effect. By 2006, when massive population-based evidence that the
exposures to so-called Depleted Uranium, DU were causing harm, andevidence from laboratory studies and theoretical research had also emerged,
UNSCEAR, in their 2006 report allowed 11 lines on one page in their 400 page
report to the consideration of DU effects. UNSCEAR based its dismissal of any
problem with Uranium exposures on three citations, desktop reviews, the
RAND corporation 1999 report (Harley et al 1999), the US Institute ofMedicine 2001 report and that of the Royal Society in 2001. None of thesereports were peer-reviewed, and the RAND corporation is believed to beclosely associated with the US Pentagon. All were selective in their references.
And all were out of date. None of these could deal with the particulate
nanoparticle inhaled Uranium from weapons fallout, since no-one had studied
it. Yet all three (and also countless reports from agencies like WHO) employed
the ICRP model to show that the doses were too low.

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Despite the many studies which will be reviewed below and which wereaccessible to UNSCEAR, its 2006 report (which appeared in 2008) states(p53):
There appear to be several possible reasons why Uranium is not. . . considereda human carcinogen (by the Institute of Health): Uranium is not very
radioactive ( having such a long half life of billions of years, 238U decays very
slowly) and its chemical properties are often such that any inhaled or ingested
Uranium is excreted rather quickly from the body.
By 2004, the way that official agency reports ignored the increasing peer
reviewed evidence that Uranium was much more genotoxic than its
radioactivity suggested became so embarrassing that the senior radiation healthadvisor to the WHO, Keith Baverstock wrote a paper with Carmel Mothershillon the issue to the Director General. He was sacked but the paper was later
published (Baverstock 2005).
The scientific investigation of DU gives a curious condensed echo of theearlier investigations into the nuclear site child leukemias. This is not
surprising given the political consequences of having to concede that the low
doses of DU, conventionally assessed, were capable of causing such graphic
and appalling genetic effects on populations exposed to the dust. For if this
could happen with Uranium, it means that all of the basic equations andassumptions of the risk model are wrong. The matter has been painstakingly
researched and reviewed recently by an American academic, Paul Zimmerman
whose conclusions, independently gained by an academic, closely agree with
the ECRR thesis developed in 2003 and in the present 2010 report(Zimmerman 2008).
It is an interesting fact that the military and the nuclear industry
internally take Uranium exposure very seriously as far as handling the material
is concerned. Spills, even small ones have to be dealt with, with all the rigours
associated with contamination by radioactive material. The same is true for the
military, who publish internal documents warning of the health effects.
However, as soon as the Uranium is shot from the gun and has contaminatedthe theatre of war, it suddenly becomes benign, in all the reports of the issue,
and in the denials of the military and its risk agencies and those of thegovernments involved.
The effects of exposure to Uranium are not, of course, restricted to DU
and passive weapons fallout. Uranium is increasingly contaminating theenvironment, near nuclear sites, near isotope separation plants, near fuelmanufactories, near Uranium mines and in atomic and thermonuclear weapons
fission fallout, near and remote from the test sites. Uranium is increasingly
found in food and drinking water as it is a significant component of agricultural
fertilizer. It is therefore also found near fertilizer factories and phosphate mines
and in the transportation of phosphate ore and its agricultural products

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(Eisenbud and Gesell 2000, Busby and Schnug 2008). The mining of Uranium
began at the beginning of the last century. Also beginning at the same time wasa new disease: childhood leukemia, which is believed to result from a mutationin utero. The temporal correlation between the incidence of this disease and the
production of Uranium (modeled as Radium) is startling, and is shown in Fig
12.1 below. Despite this, Uranium seems to have been forgotten in
investigations into contamination near nuclear sites, diseases associated withweapons fallout, Chernobyl effects. It is the invisible substance. Measurements
made new nuclear sites will show concentrations of exotic isotopes, vanishingconcentrations of Plutonium in fish, but few measurements are made of the
Uranium emerging from the nuclear sites. In the COMARE analysis into the
Sellafield child leukemias, it was concluded that although the doses from
Plutonium to the tracheobronchial lymph nodes of the children were high, thedoses from natural radionuclides were higher, and so the nuclear site could not
be responsible, even if these were the source of the disease. After Chernobyl,large amounts of Uranium were released as fuel particles, but no measurementof Uranium is to be found in any of the reports on Chernobyl fallout.
ECRR set up a sub-Committee in 2001 to examine the issue of Uranium
weapons. This chapter will present a brief account of the findings, will review
the evidence for DU and Uranium effects and will make recommendations.
ECRR set up a sub Committee to examine the issue of Uranium weapons. This
chapter will present a brief account of the findings, will review the evidence for
DU and Uranium effects and will make recommendations.
Fig 12.1 Trend in child leukemia mortality (line) and world Radium production(g) (Source: Busby 2002 acknowledging Bramhall R)

146

ECRR 201012.2 Depleted Uranium: Uranium weapons.
Depleted Uranium is a by product of the nuclear industry where the fissile
isotope U-235 in natural Uranium ore is concentrated to produce reactor fuelconsisting of ‘enriched Uranium’. The isotope discarded by this process is
Uranium 238 which is generally classed by the risk agencies as a low radiation
hazard material owing to its long half life (4.5 x 109 y) and its weak gamma
emission of 48keV. However, it is an alpha emitter and thus poses an ingestionrisk owing to the high ionization density of alpha tracks and their highbiological effectiveness in inducing mutation. In addition, there is a risk fromthe beta-emitting daughter isotopes Thorium 234 ( 0.26MeV, half life 24days) and Protoactinium-234m (; 0.23MeV, half life 6.75 hours) which decay
through one another to Uranium-234, also an alpha emitter with a half life of
2.47 x 105 years. The overall activity of Uranium 238 therefore increases assoon as it is produced due to ingrowth of the beta daughters and by 30 weeks
these are in total secular equilibrium. The activities per kilogram are given in
Table 12.1 below. Uranium-238, because of its long half life, has a low specificactivity, 12MBqkg-1 which means that, unlike most radionuclides which areconsidered in risk analyses, at environmental concentrations which represent a
radiological exposure, the chemical concentration is significant. 1Bq is 83gand 1Bqg-1 in tissue represents a concentration of 3.5 x 10-4 M which is asignificant physiological concentration.
Over centuries, the specific activity of U-234 should be the same as theparent U-238, and thus the environmental concentrations of these isotopes are
generally the same if the source is natural. The specific total activity is thus
about 37MBq/Kg. It should be pointed out that DU material recently found inbattlefields in Europe contains small quantities of isotopes of Plutonium,
Neptunium and other fission products: thus the source of this DU is refinementof nuclear reactor waste. However, the quantities are very small and are notconsidered by the Committee to be of serious radiological significance. Morecurious are reports of weapons which have isotopic signatures showing
enriched Uranium, first reported in Lebanon, then Gaza, and most recently inanalysis of biological materials from a veteran of the Bosnia theatre in 1996
(Busby and Williams 2006, 2008, Ballardie et al 2008). Indeed, tables ofisotope ratios in environmental post conflict samples published by the United
Nations Environment program UNEP show clear evidence of enriched
Uranium usage in Bosnia (UNEP Bosnia report 2002). (UNEP haveconsistently denied finding enriched Uranium, and this mistake was quickly
covered up when pointed out: the table has been taken off the UNEP website).
For this reason, the ECRR prefers the term Weapons Derived Uranium (WDU)
to describe the issue.

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ECRR 2010

Table 12.1 Specific Activity (MBq/kg) in decay of U-238 in Depleted Uranium
to U-234 and ingrowth of daughters
Weeks
0
5
10
20
30

U-238 (
12.43
12.43
12.43
12.43
12.43

Th-234 (
0
7.89
10.77
12.21
12.4

Pa-234 (
0
7.84
10.75
12.21
12.4

U-234 (
0
0.001
0.004
0.01
0.017

Owing to the high density of Uranium, (19 g.cm-3 metal and 10.96 g. cm-3 forthe dioxide) and the fact that the metal is pyrophoric (burns in air) the
substance is used in the manufacture of armour piercing shells, missile nose
cones and penetrators. It is also employed in certain ballast materials in someaircraft (e.g. helicopter rotors, commercial aircraft counterweights). As aweapon, on impact, the DU burns to a fine aerosol of ceramic Uranium oxide
particles of mean diameters from about 1000nm (down to below 100nm
depending on different study results and distances from targets. These particles
are long lived in the environment (and in tissue), and can travel significant
distances from the point of impact up to thousands of miles (Busby andMorgan 2005). They become resuspended in air, are found in air filters in cars
at some distance from the attacks, and are respirable. Because their diameters
are so small, below 1000nm, they are able to pass through the lung into thelymphatic system and in principle can lodge anywhere in the body. Here they
may remain for several years in the same place. The biological half life of suchparticulate Uranium is unknown but is very long. According to research withanimals it can be greater than 13 years (Royal Society 2001).
A single Abrams 120mm tank shell contains about 3kg of DU(111MBq of radioactivity) and there is 275g in a 30mm GAU3A A-10
Thunderbolt Gatling Gun round. These munitions were used in Gulf War 1.
More recently evidence has emerged that hard target warheads have been
deployed on cruise missiles and bunker busting bombs, each containing up to
one tonne of Uranium. Estimates of the quantity of Uranium used in Gulf War
2 in 2003 are as high as 1700 tonnes (Al Ani and Baker 2009).
Military penetrators explode on impact with hard targets with about
80% conversion to micron diameter Uranium Oxide particles of a ‘ceramic’nature. These particles are highly mobile and extremely long lived in theenvironment, owing to the very high degree of insolubility of Uranium Oxides
UO2 and U3O8. They can be inhaled and the sub-micron diameter particles aretranslocated from the lung to the lymphatic system, building up in the
tracheobronchial lymph nodes and potentially able to circulate everywhere in
the body since they incapacitate macrophages (Kalinich et al. 2002). They canpass through the skin and through most gas-mask filters. Alpha and beta

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disintegrations from these particles cause very high and repetitive doses to cells
local to the range of the disintegration i.e. about 30 microns for the alpha and
450 microns for the beta tracks. The instantaneous (t = 0) dispersion (spectrum)of particle size from DU impacts was obtained using special cascade impactor
collectors at the US Aberdeen proving grounds by Glissmeyer et al. (1979).
The mean geometric diameter for collected behind the target were found to be
0.8ore recently, the EU SHER (2010) report states that 31% of theparticles have mean diameters below 0.18 Particles of this size are effectively
gaseous and can pass through the skin and penetrate to any part of the body.
They are therefore not comparable to historic studies of Uranium exposuressince such concentrated forms have never existed and have never been studied:they are completely new exposures that have to be assessed de novo.
The reason that DU is employed is that the weapons are astoundingly
successful and have revolutionised warfare, rendering the tank and its armour
useless. In addition, its use represents a route for the nuclear industry to rid
itself of a waste product which would otherwise be expensive to dispose of. But
the downside is that the material clearly represents a radiation hazard which isindiscriminate: battlefields are going to be contaminated and civilian
populations are going to be exposed.
Apart from the evidence that Uranium is far more genotoxic than ismodeled, which will be reviewed below, there is an immediate argument fromquantity of radioactivity. The average Natural Uranium content of soil is about
10-20 Becquerels per kilogram, including all the Uranium isotopes. The
average excretion of Uranium in urine is less than 10nBq l-1 (in the UK) as aresult of absorption of natural Uranium in food and water. Pure Depleted
Uranium contains about 12.4MBq of U-238 per kilogram and in Kosovo, some
soil samples analysed by the United Nations Environment Program (UNEP)
contained 250,000Bq/kg (UNEP 2001, Annex). The 350 tonnes of DU used in
the first Gulf War represent 4.3 TBq (4.3 x 1012 Bq) of Uranium alpha activity(13.0 x 1012 if the radioactive beta emitting daughter isotopes are included).
The 1700 tonnes that were used in the 2003 war, represents 63 TBq of activity
dispersed mainly into a populated area of perhaps 100km2. This gives a meandensity of deposition of radioactivity of 630,000Bq/m2. These sums are
instructive and are collected together in Table 12.2.
It is possible to find a comparison to illustrate the overall radiologicalsituation. As an alpha emitter and long-lived environmental particle Uranium
can be compared with Plutonium-239 a radionuclide released by Sellafield anda major contaminant of the Irish Sea. Plutonium in the environment is also in
the form of sub-micron sized oxide particles. The comparison is made in Table
12.3.
Like DU, these Plutonium Oxide particles are also long lived andmobile. Plutonium from Sellafield has been measured in autopsy specimens
across the UK, in sheep droppings on the east coast of England 100 km from
Sellafield at the same latitude and even in the teeth of children up to 200 km

149ECRR 2010

from the site in south east England. U-238 has a very long half life, 4500
million years, so owing to its much shorter half life of 24,100 years, thespecific activity of Pu-239 is far greater. It is 2.3TBq/kg. But this means that
350 tons of DU (or 4.30TBq of U-238) is equivalent in activity (quantity ofradiation) to about 2 kg of Plutonium-239. The ethical dimensions of theintentional scattering of 2kg of Plutonium-239 over a populated area are easy to
imagine.
Table 12.2 Mean density of deposition of radioactivity from DU in the two
Gulf Wars and Kosovo including decays from U-238 and beta daughters Pa234m and Th-234 compared with other radioactive contamination.
Event

Activity released or
estimated deposited

10 tons of DU in Kosovo
350 tons of DU in Iraq 1
1700 tons of DU in Iraq 2
Global weapons fallout
Strontium-90 (Sr-90)
Northern Hemisphere lat.
50-60deg (UNSCEAR,
2000)
Chernobyl 30km Exclusion
Zone measured Sr-90(IAEA)UK North WalesRadioactive Sheep
restrictions measured
Caesium-137 (Cs-137)
UNSCEAR definition ofcontaminated area. (Cs-137)
Irish Sea cumulative
Plutonium from Sellafield
1952-1996 [Busby, 1995]

0.37TBq
13 TBq
63TBq
73.9PBq

150

Mean activity density
Bq per square metre(area)
3700
130,000 ( into 100 km2)
630,000 ( into 100 km2)
460

37,000 to
more than 111,000
15,000 to 30,000> 37,000
1350TBq

20,000ECRR 2010

Table 12.3 Comparing Plutonium-239 and Uranium-238 in the environment

Environmental form
Density of material g.cm-3
Solubility
Environmental Longevity
Main radioactive emissions
Alpha particle energy
Half life
Specific activity
Main present
contamination source
Mass for equal activity

Uranium-238
0.2-2 oxide particles(UO 2 ) 10.9;(U 3 O 8 )8.3
Insoluble
Long lived
Alpha + beta + beta
4.19MeV
4.51 billion y
37.2MBq/kg (+
DU
175 tons

Plutonium-239
0.2-2 oxide particles(PuO 2 ) 11.46
Insoluble
Long lived
Alpha
5.15MeV
24400y2.3TBq/kg ()Fuel reprocessing e.g.
Sellafield
1kg

12.3 The evidence of harm from Uranium exposures
Uranium oxide nanoparticle exposure from weapons does not represent thesame kind of hazard as Uranium exposures in people living in high background
Uranium areas, nor those who work as Uranium miners and machinists. The
exposures are quite different in quality and type. Comparisons of miners
exposed to Uranium ore dusts will compare those who inhale particles whichhave very low concentrations of Uranium and which are fairly large. In Gulf
war veterans and civilian populations the Uranium is almost pure. The local
doses to and concentrations in tissue will be thousand of times greater in thecase of the weapons exposures and the much smaller particle sizes will ensure
the rapid internalisation of the uranium, through completely evolutionarily
novel routes, though the lungs or directly through the nose to the mid brain oreven through the skin. The nanoparticles will penetrate individual cells. Thus
the highest concentrations will begin in the cells, where the DNA is, andconcentration will fall towards the blood supply reservoir, the opposite of what
happens with those who ingest uranium contaminated solutions of food.
Comparing Uranium urine excretions or blood concentrations to get an idea ofsimilar levels of exposure and making calculation on the basis of average doseconversion coefficients will also be invalid for this reason. It is an averaging
problem, like all the others associated with comparing external and internal
irradiation. Nevertheless, because there are overlaps, the effects of exposure to
Weapons Derived Uranium will be discussed in parallel with other Uranium
exposures. We should expect many of the effects found but at much lower
apparent doses in the case of WDU. The above caveat should be borne in mind.

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ECRR 201012.3.1 Health effects: epidemiology
Uranium is primarily genotoxic. Exposure to Uranium causes genetic andgenomic changes and therefore impacts most organs in mammals. Particularly
targeted are the kidney, the brain and the reproductive system. A list ofreported conditions associated with Uranium exposure is given in Abu Quareand Abou-Donia 2002 and Craft et al 2004. Bertell 2005 has reviewed the areaand drawn attention to significant gaps in knowledge and recently a number ofauthors have discussed the problem in a UN report (UNIDIR 2008).
The teratogenicity of exposure to Uranium weapons aerosols isreviewed by Hindin et al (2005). Many reports of congenital defects in children
born in Iraq following the first and 2nd Gulf wars (e.g. Hamburg 2003) have notbeen followed up by any studies by WHO or any responsible authorities. The
main reported illnesses and conditions associated with exposure to Uranium arelisted in Table 12.4
It will be apparent that Uranium exposure will have a profound effecton the health of any population, and that the range of effects covers the entire
spectrum of disease.
Table 12.4 Illnesses and conditions reported in the literature to be associatedwith exposure to Uranium.
Mutagen: Reproduction: teratogenic and genotoxic; causes lower fertility,
miscarriages, heritable defects in children, stillbirths, childhood cancer
and leukemia. Oestrogenic mimic with responses in humans and animals.
Mutagen: Cancer and leukemia increases in those exposed and theiroffspring in humans and animals.
Kidney disease generally, problems below 100ng/g contamination,
glomerular and tubular lesions, tumorigenic changes, creatinine levels
alter with dose, glomerular structures altered, IgE and IgG nephropathy,
persistent structural and functional and functional damage.
Blood; cytotoxic and leukemogenic; reduction in red blood cells.
Brain; targets the brain and causes wide range of effects associated withdamage to deep brain and brainstem fuction, effects shown by objective
tests. Basis of the Gulf War syndrome. Weapons Uranium particles enter
the mid brain directly from the nose.
Concentration: circulates as uranyl ion which has the same affinity as
Calcium, therefore binds to and targets DNA, nervous tissue, bone,
sperm. For this reason most organs will be affected (mitochondrial DNA
affecting energy conversions in cells).
Chromosome aberrations found in those exposed to Uranium; the effect isout of proportion to the ICRP calculated dose for external radiation.
Mutagen: retinoblastoma rates highest in Navajo tribes living on Uranium

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ECRR 2010

tailings; rates also high in offspring of Sellafield workers and near
Rocketdyne site near Los Angeles contaminated with Uranium.
Mutagen: Sex ratio effects in offspring of male Uranium miners
Inflammation: associated with oxidative stress at site of Uranium
Carcinogen: cancer increases in BNFL Uranium fuel-element workers
Despite this, there have been virtually no epidemiological studies carried out of
populations exposed to weapons Uranium. The one exception is a study carriedout at the request of the Italian military into cancer in the Balkans
peacekeepers. The first report showed a significant excess of lymphoma(equivalent to 8-fold) in peacekeepers stationed in Bosnia and Kosovo (Italianreport 2001). More recent investigation of the data shows that the cancers weremainly from those who served in Bosnia, making the relative risk more like 14fold. A recent update on the situation seems to have been kept confidential;
reports are that levels of cancer in this cohort are startlingly high and checks
are being carried out. No credible study of cancer or birth defects in UK or US
veterans has been published although parliamentary questions have elicited
data which show an increase in lymphoma in UK veterans of the 1st Gulf War.
Recently, a coroner’s jury in the UK found that a British Gulf war veteran,
Stuart Dyson, died of colon cancer because of exposure to Depleted Uranium
in Iraq (Dyson 2009) and the Minister was informed under Section 43 of the
UK Coroners Act. Evidence was taken from ECRR and from scientists fromthe UK Ministry of Defence but clearly the jury believed that the cancer wascaused by the exposure.
Cancer data from Sarajevo in Bosnia has been reported, and show
remarkable increases (up to 20-fold) in the incidence at many sites (Hamburg
2003). A cohort study of cervical cancer in Greece concluded that exposure to
Uranium aerosols was the cause of a statistically significant increase in the
disease those exposed as shown by cervical smear screening results(Papathanasiuo et al 2005). There have also been many reported of high levelsof cancer in Iraq following the bombing both in 1991 and later in 2003, but nosystematic study has been published. An early study by McDiarmid et al(2002) found no evidence of increased risk of cancer in US veterans of the first
Gulf war, though ill health from many conditions (generally, Gulf War
syndrome) was reported.
Gulf war syndrome itself was examined in a sophisticated Factor
Analysis by Haley et al (2000) in the USA, funded by Ross Perot. The
syndrome encompasses many conditions, problems which the military and theiradvisors in the UK blamed on stress, but which Haley identified as having incommon that they resulted from damage to the brainstem and lower brain
housekeeping functions. Haley went on to show that this was the case bycarrying out a magnetic resonance imaging case control study of US veterans.
The P32 and H1 studies identified significant loss of viability in cells in thebrain associated with the housekeeping functions of the brain which were153

ECRR 2010

manifesting themselves as Gulf War syndrome. Haley was not aware of thetargeting of the brain and lower brain by Uranium and blamed the effects hefound on exposures to organophosphates. However, research which was carriedout some years after Haley’s work showed the profound targeting of this areaof the brain by Uranium, and the fact that inhaled Uranium has a direct accessto these parts of the brain through the olfactory lobe (see below).
The situation in Iraq has become serious: genotoxicity of Uranium
exposures has resulted in a catastrophic increase in cancer and congenital
disease. This was reported at the September 1998 General Conference of the
IAEA and has been comprehensively reviewed by Al Ani and Baker (2009).
In the same volume, these authors review other evidence of increases in genetic
and genomic based disease in those parts of Iraq contaminated with Uranium
and cite the many studies that report the levels of contamination and also thehealth indicators. However, none of these reports have been considered by therisk agencies and in addition no western based study has been carried out on
the populations of Iraq in order to investigate the concerns. The Committee iscurrently engaged in a study of cancer and congenital birth defects in Iraq.
Statistically significant Uranium effects have been reported at the
Springfields fuel fabrication plant in the UK (McGeoghegan and Binks 2000).
A strong association, related to Uranium exposure, was reported for Hodgkin’s
lymphoma and Non Hodgkin lymphoma, though the authors did not believe therelation was a causal one since the absorbed doses were too low.
12.3.2 Genetic damage: chromosome aberrations
Chromosome aberration analysis can be used as a flag for earlier exposure toionizing radiation. Indeed, it is possible to reconstruct the doses and make someassumptions (on the basis of the types of chromosome damage, dicentrics andcentric rings) on the type of exposure, whether low or high LET (Hoffman andSchmitz Feuerhake 1999).
Unexpectedly high levels of chromosome aberrations in Uranium
miners in Namibia were reported by Zaire et al 1997. Studies of chromosome
aberrations in a set of Gulf War veterans suffering from Gulf War syndrome
were also examined by Schroeder et al, 1999. Results showed levels ofdamage consistent with earlier exposures of about 150mSv although clearlythese veterans could not have been exposed to more depleted Uranium thanwould account for a committed dose of 100Sv. Both these studies identify anerror in the calculation of dose from the Uranium exposures of approximately
1000-fold. It should be noted that chromosome damage leaves the body with ahalf life of about 2 years, yet these Gulf veterans were showing this damage
some ten years after the exposures, suggesting some depot of Uranium which
was long lived. The Royal Society (2001) cite references to support the viewthat the half life of some types of Uranium in the body is longer than 10 years
and may be considered to be perhaps indefinite. Chromosome aberrations have154

ECRR 2010

been found in a case control study of New Zealand Atomic test veterans (also
exposed to Uranium at the test sites) some 40 years after the exposures.
Chromosome aberration analysis in Bosnia has shown significant
Uranium exposure effects in an ecological study by Ibrulj et al (2007). The
study evaluated peripheral lymphocytes from 84 individuals split between
inhabitants of Hadzici where NATO strikes involved Uranium (and UNEP
measurements showed presence of Uranium in 2002) and a control area where
there was little exposure. Results showed a statistically significant increase inchromosome aberration frequencies in the exposed group in 2007, some ten
years after the attacks. Micronuclei were also increased in peripheral
lymphocytes in the same populations exposed to Uranium (Ibrulj et al 2004).
Hadzici in Bosnia was also studied by Krunic et al (2005) to evaluate
the genetic damage to those who were exposed to Uranium weapons. The
authors were able to show excess micronuclei in peripheral lymphocytes
compared with controls from west Herzegovina.
In cell culture experiments, Miller et al 2002 were able to induce
dicentric chromosome changes and neoplastic transformation in human cells
exposed to depleted Uranium at 50M (i.e.200ng/l) for 24hrs. This is a very
low concentration and the presence of alpha emissions per cell is stochasticallyabsent. Using different Uranium isotopes the study showed that there was aspecific activity related effect and the conclusion was that radioactivity canplay a role in the neoplastic transformation frequency. Nevertheless, theexposure was so low that this result supports the argument for secondary
photoelectron enhancement outlined in Chapter 6 and reviewed below.
From these studies it can be concluded that Uranium exposure causes
chromosome damage and micronuclei formation in human populations at levelsof radiation exposure (conventionally assessed) which are more than 1000
times too low to explain these effects. Similar results have been reported fromlaboratory research on cell cultures (Darolles et al 2010). The authors finddifferences between enriched and depleted Uranium in cell culture studies atquite low concentration levels. Reduced to basics, depleted Uranium causes
aneuploidy and micronuclei formation whereas the enriched Uranium causes
chromosome aberrations. This would, of course, be an expectation of the two
types of action implicit in the discussions of mechanism above. Owing to thehigher activity of U-235 the main chemical species in solution is uranyl U-238
in both the enriched and the depleted Uranium experiments. Therefore there
will be significant binding of the U-238 uranyl to the chromosomes resulting in
destruction of whole chromosomes through the photoelectrons emitted
throughout their length at the binding sites of the U-238 atoms along thephosphate backbone. The U-235 effects are then the normal alpha track highionisation effect where a chromosome is cut (double strand break) andrecombines anomalously to give the aberrations which are found. The authors(who are associated with the French IRSN) point out that the aneuploidy

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ECRR 2010

produced by U-238 is associated in other reports with cancer induction andthey call for a reassessment of the carcinogenicity of Uranium.
12.3.3. Reproductive and transgenerational genetic effects
The teratogenic effects of Uranium exposures have been reviewed by Hindin
et al (2005) who concluded from the evidence that Uranium represented a
teratogenic hazard. Certainly many reports have emerged from areas where
Uranium weapons have been employed showing that there follow major
increases in stillbirth, and congenital malformations of a particularly alarming
and unusual kind. Despite these, no credible western studies have beencommissioned or carried out. A case control study of UK Atomic Test Veteranschildren and grandchildren identified a 9-fold excess of congenital conditionsin the children and an 8-fold excess in the grandchildren relative to national
controls (Busby and de Messieres 2007). These veterans were exposed mainly
to Uranium since their gamma film badge doses were in general known andanalysis showed the existence of significant quantities of Uranium on the testsites.
A review of the reproductive toxicity of natural and depleted Uranium
by Domingo (2001) concluded that Uranium was a development toxicant when
given orally or subcutaneously to mice. Decreased fertility, embryo toxicity,
teratogenicity and reduced growth were shown to occur. Paternain et al (1989)
had already showed developmental and birth outcome effects in mice at doses
as low as 5mg/kg with no zero effect dose. A study of the effects of Uranium
on the hatching success, development and survival in early stages of zebrafish(danio rerio) was reported by Bourrachot et al (2008). The authors used levelsof depleted Uranium in the water of 200-500g/l (about 3Bql-1) but also
employed a higher specific activity Uranium isotope U-233 to examine theeffects of what they believed to be chemical rather than radiological stress.
Both regimes showed significant developmental effects at the lowest
exposures. 250gl-1 showed a 43% reduction in median hatching times relative
to a control. A 15 day exposure to this concentration of depleted Uranium gave
a 100% mortality at the pro-larval stage. The more radioactive U-233 was more
effective, but both isotopes showed the effects at this very low concentration.
The radiation doses at which this was occurring are vanishingly small andwould not be considered harmful on the basis of current risk models.
Raymond-Whish et al (2007) found that drinking water below the US
EPA standard caused estrogen receptor dependent responses in female mice.
The authors exposed pregnant female mice to drinking water containing from
0.5 gl-1 to 28mgl-1 and found estrogen receptor effects including selective
reduction of primary follicles, increased uterine weight, greater uterine luminal
epithelial cell height and other conditions. Mouse dams that drank the Uranium
containing water had morphologically normal pups but these had fewer primaryfollicles than pups from dams that drank normal water.

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ECRR 201012.3.4 Kidney
The kidney has been identified as a target for Uranium toxicity by manystudies; the early research is reviewed in the Royal Society reports (RS2001,
2002). More recently interest has followed concerns relating to weapons
exposures and research has focused on the levels needed to produce
nephrotoxic effects. A number of relevant studies are listed in Table 12.5.
A most relevant and interesting report by Ballardie et al 2008 presents
the results of a comprehensive medical and physical analysis of a veteran of theBalkans who presented with a range of kidney conditions and many Gulf war
syndrome conditions. Rather than assuming that this man’s spectrum ofconditions was a result of stress, a team of doctors and scientists at the
Manchester Royal Infirmary and the University of Sheffield set about
analyzing everything they could in order to try and discover the cause. By
biopsy analysis they discovered that his kidney was contaminated withenriched Uranium, which was uniformly disseminated throughout the
mitochondrial tissue. Treatment with heavy metal chelating agents effected acure. This is a major piece of evidence in the arguments which the Gulf War
and Balkans veterans have regarding the origin of their ill health and wassignificant in persuading the jury about causality in the above-mentioned
coroner’s inquest on Stuart Dyson who also suffered from Gulf War syndrome
before dying prematurely from colon cancer.
Table 12.5 Recent studies of relevance to the effects of Uranium on kidney
structure and function
Study
Prat et al 2005

Berradi et al 2008

Goldman et al
2006
McClain et al
2002

Results
Identified a set of 18 genes which were deregulated
following exposure to Uranium; the Calcium pathway isheavily implicated; nephroblastoma genes implicatedRats exposed to 40mg/l DU in water for 9 months.
Kidney deterioration and lower red blood cell counts(renal anemia).
Investigated effects of DU on rat kidney brush bordervesicles. Uranyl at 140g /mg protein reduced ability totransport glucose.
Effects of embedded fragments of DU (shrapnel) in
rodents. Uranium from implanted fragments found inbone, kidney, muscle and liver distant from the site of
implant.
Alters neurophysiological parameters in rat hippocampus,
crosses the placental barrier, enters foetal tissue.
Decreased rodent litter size when animals bred 6 months

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ECRR 2010

Fukuda et al 2006

Zhu et al 2008
Zimmerman et al
2007

after implantation. No kidney effects found suggesting
adaptation.
Toxicity and biochemical markers in rats exposed to
Uranium at 0.2, 1 or 2g/g animal. Measurable changes
in many markers in bone and kidney at the lowest doses.
Renal dysfunction after long term chronic exposure to
Uranium pieces surgically implanted in rats.
Clinical chemistry and microscopic renal effects in rats
exposed to single injection IM of 0.1, 0.3 and 1.0 2g/g
animal. Nephrotoxocity seen at all doses.

12.3.5 Brain
The effects of Uranium on the brain have only recently emerged. As alreadyoutlined above, the studies by Haley demonstrated a link between lower brain
function and the spectrum of conditions which make up Gulf War syndrome.
Inhalation of Uranium nanoparticles from the weaponised aerosols provides a
direct route to the lower brain through the physiological connections with thenasal passages and olfactory bulb. The French (IRSN and other) studies wereperhaps the first to show the accumulation of Uranium in nervous tissue, towhich it seems to have an affinity, probably because of the similarity of theuranyl ion to Ca++. Monleau et al (2005) of the IRSN laboratory in France
showed that Uranium concentrations in the brains of rats exposed by inhalation
were as follows: olfactory bulb> hippocampus> frontal cortex> cerebellum.
Uranium is normally excluded from the overall system by a low gut transfer
factor. Evolutionarily there will never have been a period when aerosols ofpure Uranium existed in the environment and even Uranium miners will not be
exposed to the same extent since the dusts in the mines have very low Uranium
content. A list of recent studies is given in Table 12.6.
It is clear from the results of Lestaeval et al 2005 that at levels where
there is no nephrotoxicity, there are measurable changes in behaviour in rats
exposed to 144g/kg. by injection. Taken together, these studies strongly
suggest that Gulf War syndrome is an effect of inhalation of micrograms of
Uranium and draw attention to the extraordinary neurotoxicity of the material.
Table 12.6 Recent studies of neurological effects of Uranium
Study
Monleau et al
2005
IRSN, France
Barillet et al
2007

158

Results
Inhalation of Uranium by rats. Uranium concentration inbrain: Olfactory bulb> hippocampus> frontal cortex>
cerebellum. Behavioural changes shown
Oxidative stress and neurotoxicity in adult male zebrafish
exposed to U-238 and U-233 in water. Oxidative stress andECRR 2010

IRSN, France
Pellmar et al
1999
McDiarmid et al
1999
Briner andMurray 2005
Lestaeval et al
2005
IRSN France

Barber et al2005

neurophysiological changes (increase in ACh) in exposures
to both isotopes
Depleted Uranium fragments implanted in rats and caused
electrophysiological changes in hippocampal slices
Gulf war veterans studied found subtle effects on
reproductive and central nervous system function
Rats exposed to drinking water containing 75 or 150mg/l
DU. Behavioural changes after 2 weeks; increased lipidoxidation
The brain is a target organ after depleted Uranium
exposure. 144g/kg injection in rats caused at kidney levelsof 2.6g/g. This level would be normally seen as a sub
toxic dose to the kidney. However, this was associated withdecrease in food intake and sleep wake cycle disturbance.
Short term kinetics of Uranium in rat brain after
intraperitoneal injection 1g/g animal. Uranium entered thebrain rapidly and was initially concentrated in the
hippocampus and striatum. Clearance was slow; contents ofhippocampus, cerebellum and cortex was still high after 7
days

12.4 Animal studies, cell cultures and mechanisms
The ICRP-based desk analyses (Royal Society, WHO, SHER, RAND, ATSDRetc.) which employ absorbed dose and use risk factors for cancer culled fromthe Japanese A-Bomb cohorts do not predict the observations and must now beabandoned. Clearly Uranium exposure is much more hazardous. Cell culture
and animal experiments have provided useful information for developing andunderstanding of the mechanism involved. What all these studies seem toshow, is that internal Uranium exposure, to particles but also to ionic forms,
seems to be acting as if it were considerably more radioactive than it is on thebasis of its intrinsic radioactivity. Thus U-238 exposure causes oxidative stress,
genomic instability, chromosome damage, micronuclei formation, allconsequences of ionizing radiation exposure, yet in some experiments theconcentration is so low that there is stochastically no radiation exposure
because there are too few decays. This finding has been variously interpreted assuggesting a chemical mutagenic effect, a heavy metal effect, or a synergy
between radiation and chemistry. Of course, one re-discovery is the affinity of
Uranium for DNA phosphate. The affinity of the uranyl ion, UO 2 ++ for
Calcium Ca++ sites was known in the 1960s when the substance began to be
employed as an electron microscope stain. The affinity constant was measured
in an elegant flow experiment by Nielsen et al in 1992 and was of the order of
1010M-1. This would suggest, in mass-action equilibrium terms, that at quite159

ECRR 2010

low concentrations (100ng/l) there is a significant amount of Uranium bound to
the phosphate backbone of the DNA. This seems to agree with theexperimental observations of biological effects reviewed here. The ECRR
model is particularly concerned with radionuclides which bind to DNA(Strontium-90, Barium-140) since these beta emitters decay into the DNA andalso change their charge and transmute into a radioactive daughter producing
an ion and perhaps Auger electrons. The charge change alone will cause an
ionization on the DNA. It seems that Uranium is therefore in this category,
which would result in a weighting (see Chapter 6).
But there is also the fact that Uranium has a high atomic number andwould therefore amplify natural background gamma radiation (and also thephoton radiation which it, itself, produces, in addition to any photon radiationfrom other Uranium isotopes present in any mixture. The conclusion of theCommittee is that such a mechanism is capable on its own of explaining themany anomalous findings reviewed in this chapter and in this section. The
extent of the enhancement must await experimental investigation, but theseexperiments are straightforward, involving simultaneous exposure to Uranium
and to X-rays of various energies. The use of dilute uranyl salts as anenhancing agent for X-ray targeted radiotherapy for cancer was suggested in a
British Patent Application in 2007 (Busby 2008). It is clear from the studies
that significant binding in vitro occurs at 200M or 84ng/l. This concentration
is not currently considered toxic but is in the same range as that found in many
drinking waters and in the urine of Gulf veterans.
A list of some studies which bear on the issue of the mechanism for the
anomalous enhancement of Uranium both as ionic and as particulate is given in
Table 12.7.
Table 12.7. Studies of Uranium effects in cell culture and in animals which
reveal information on possible mechanisms for its anomalous hazard.
Study
Gueguen et al 2007
Miller et al 2005
Miller et al 1998

Miller et al 2002

Yang et al 2002

160

ResultDrug metabolism is altered following exposure of DU
to rats; induces expression of CYP enzymes
Leukemic transformation of haematopoietic cells inmice internally exposed to DU pellets.
Transformation of human osteoblast cells totumorigenic type after exposure to DU; 0.0014% cells
were hit by alpha particles. Suggests no radiation effect.
Showed both Uranium and tungsten capable of causing
micronuclei in human osteoblast system andtumorigenic transformations.
Malignant transformation of human bronchial epithelial
cell by exposure to Uranium; DU shows carcinogenesis
in vitroECRR 2010

Kalinich et al 2002
Gueguen et al 2006
Pariyakaruppan et al
2006
Grignard et al 2008
Tissandie et al 2006
Yazzie et al 2003

Busby 2005a

Busby 2005b
Stearns et al 2005
Busby and Schnug
2008
Elsaesser et al 2007

Wan et al 2006

Pattison et al 2008

Hahn et al 2002
Darolles et al 2010

Depleted Uranium induces apoptosis in mouse
macrophages
Hepatic effects of Uranium on liver metabolism
enzymes
Uranium causes oxidative stress in lung epithelial cells
Contamination with depleted or enriched Uranium
differently affects steroid metabolism in rats
Short term DU exposure affects vitamin D metabolism
in rats
Uranyl acetate causes DNA single strand breaks in vitro
in the presence of ascorbate. Suggests that affinity for
DNA is greater than affinity for ascorbate.
Suggests and attempts to quantify secondary
photoelectron effect for Uranium bound to DNA
phosphate. Draws attention to affinity of Uranyl forDNA.
As above for Uranium particles
Induction of hprt mutations and DNA adducts in
Chinese Hamster ovary cells at 200M (80ng/l).
Discusses SPE for Uranium in ionic form as
explanation for observed effects
Monte Carlo simulations of Uranium, Gold and water
nanoparticles of different sizes confirm theenhancements due to SPE
In vitro immune toxicity of depleted Uranium: effects
on mouse macrophages. At 50 and 100M.
Macrophage activity altered at 200M for 2 h.
Monte Carlo simulation of Uranium particles in tissue
confirm SPE effect is ‘significant’ but lower thansuggested by Busby.
Implanted DU fragments cause soft tissue sarcomas in
the muscles of rats.
Different toxicological profiles of depleted andenriched uranium: U235 causes chromosome
aberrations (alpha) U238 causes aneuploidy(photoelectron toxicity explains this spectrum)12.5 Conclusions
It is necessary to conclude that Uranium represents a perfect example of the
problem resulting from the physics-based approach to radiation risk which161

ECRR 2010

ECRR2003 drew attention to. When doses are calculated in terms of absorbed
dose following ICRP, the quantities of Uranium usually found in theenvironment confer very small doses compared with natural backgroundgamma radiation, and even smaller when compared with the levels of dose
which correlated with cancer in the A-Bomb groups. But it is clear that thisapproach is massively in error, since it has avoided or, more accurately, knows
nothing about, chemistry, biology, physiology and pharmacology. Thesesciences were historically considered of less importance than physics andmathematics, in some deeply felt (by the physicists anyway) philosophical andemotional way. This is the flaw in rational analysis: it is only as good as its
data, and if, in order to solve a problem, it has to be reduced to the level wherea solution can be claimed, the answer is often wrong.
The Committee has had to deal with this very real problem bypresenting a real solution; in this case the solution is to weight Uranium
exposures by a factor of 1000 at normal background gamma photon levels(100nGy/h). This will be modified when experimental results of Secondary
Photoelectron effects become available. It is clear that the effects of Uranium
are wide ranging, and so to consider only genetic effects from Uranium
exposure would be quite wrong. In addition, different types of exposure willcause different spectra of conditions.
In the case of conventional estimates of risk from internal Uranium,
which essentially compare it with external doses, the errors are arguably
greater than for any other material. There is now sufficient evidence to treat
Uranium aerosols as if they had infinite biological effectiveness. The
Committee therefore believes that using a risk factor to assess causality in
Uranium-exposed populations or individuals should be done with extreme
caution, even if that risk factor has been modified by application of a weightingthat approximates observation.. If a disease or condition or genetic heritableeffect of any kind is seen to increase after exposure to Uranium, causality
should not be ruled out whatever the dose differential between a population
before and after the exposure, or between exposed populations relative to
unexposed controls.

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13
Risk of Exposure: Non-Cancer Risks
13.1 General health detriment
The Committee considers that the ICRP’s concentration on cancer as the main
outcome of radiation exposure is inadequate for the purposes of public
protection. This is clear from all the data and is particularly true for Uranium
exposures. The fundamental biological mechanisms of radiation action are now
well established, and these clearly predict general harm to the organism at all
doses. DNA damage to cells, which occurs at the lowest doses and which may
become enhanced through a number of mechanisms not addressed by ICRP,
must cause general and specific health detriment to the organism, even if this is
not measurable epidemiologically. Thus the Committee notes the reports whichargue both for and against non-cancer effects in human populations but feelthat arguments from the cellular level demand that the general harm of
exposure to ionising radiation be broadly assessed.
Arguments relating to natural background exposures have been shown
to be quantitatively in error for cancer and there is evidence that they are also inerror for other more general health indicators. However, general healthdetriment suffered throughout a lifetime is difficult to quantify within a system
where other factors are confounding the analysis. For example it is very likelythat weapons fallout exposures will be the cause or a main cause of general illhealth and non-specific life shortening in the cohort who were exposed at or
around birth, although little work has been done on this problem and as far as
mortality rates are concerned it is too soon to say if the early elevated age
specific mortality rates will continue. This problem has already been addressed
for cancer, and indeed the contemporary breast cancer epidemic has beencorrelated with this exposure by Sternglass in 1994 and Busby in 1997.
However, it may be difficult to resolve the issue since data informing nonspecific ageing and more general health detriment are confounded by advancesin health care and improvements in social conditions and therefore the effectsof radiation are very difficult to establish. This does not mean that there arenone. Therefore, the approach taken by the Committee is to decide on risk
factors for those categories of harm which can be measured and, in the absenceof any hard data, to extrapolate the data on infant mortality and other indicators
to a mean life quality reduction factor which would operate on a broad
spectrum of morbidity and would feed through to premature death in a system
where other factors remained constant. One change that has taken place since
the ECRR2003 report is to advise on a specific risk factor of 0.05Sv-1 for heartdisease.

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ECRR 201013.2 Foetal development and infant mortality
Global weapons fallout caused infant mortality, largely through the operationof foetal development defects of the heart and circulatory system. It may be
assumed also that there was an increase in early foetal death, although figures
for this effect are not available.
The ground-breaking work of Luning et al. in 1963 on foetal
development in the offspring of Strontium-90 injured male mice has never beenadequately or credibly followed up. The Committee finds it unacceptable thatthese critical findings have been ignored despite their applicability to humanpopulations. In a very large study Luning et al. injected small quantities ofStrontium-90, a major component of fallout, into male mice and mated themwithin an hour to females. The pregnant females were killed just before term toestablish the extent of foetal death in the offspring in utero. Controls were
injected with sodium chloride or the other fallout isotope Caesium-137. Results
showed a significant increase in foetal death in the Strontium-90 group but noeffect in either control. In a further series of experiments Luning went on tomate surviving males with untreated females to show that there was also asignificant foetal death rate in the second generation. There are only two otherpublished works which examine the genetic effects of Strontium-90 inmammals. The first, a Russian study by Smirnova et al., employed rats in thesame system and confirmed the effect; pathology of the dead foetuses showedthat the deaths were caused by heart development defects. The second study, bySatsuda, showed increases in leukemia in live survivors. This is less relevant to
the present chapter, but pointed to a transgenerational effect.
Increased infant mortality over the period of the peak period of global
weapons fallout (1959-63) was first reported by Sternglass, using time-series
analysis, for the USA and then for England and Wales. Since then the effecthas been confirmed by Whyte, Busby and most recently by Koerblein, who
examined the effect in Germany. In a separate study Busby was able to show avery high degree of correlation of infant mortality from heart and circulatory
system defects with Strontium-90 contamination. The effects were mainly inearly neonatal and stillbirth mortality and in the UK they were sufficiently
alarming for the government to order a confidential inquiry by the Medical
Research Council in 1966. This was finally published in the mid 1980s and was
unable to find a cause for the effect although no attempt was made to connect itwith radiation exposure.
The level of the effect in England and Wales, together with the known
doses to the parents, enables the Committee to establish a risk factor for infantmortality following exposure to Strontium-90. The risk factor for foetal death is
not easy to establish since 1959-63 was a period when the birthrate wasfluctuating rapidly due to the effects of the large population peak from theSecond World War baby boom. However, the Chernobyl accident exposurescaused sharp depression in the birthrate in many countries and this was164

ECRR 2010

established by Bentham for Wales and Cumbria, parts of the United Kingdom
where doses were well established (though the doses of Strontium-90 werequite low). The Committee has therefore used this data to decide on a risk
factor for early foetal death which is presented as an approximation in theabsence of better data.
The risk factors chosen by the Committee for infant mortality andfoetal death effects are given in Table 13.1 The Committee recognises that
infant and foetal mortality effects are unlikely to follow a linear dose response,
owing to the death of the foetus at many stages in its development and its
probable response to different biochemical and biophysical (particulate) aspectsof the exposures (see Fucic et al 2007). Thus the risk factors are based on
percentage excess rates per mSv (ECRR) annual exposure to parents and are
for the exposure range 0-5mSv. The exercise is intended to make clear the costof radiation exposure of the foetus and parent and to add this into the general
health cost of exposed populations.
In support of the risk factors adopted by the Committee, recent
correspondence from Yablokov has revealed data which are relevant to theassessment of the infant mortality yield following exposure to fission isotopes.
These support the estimate of 20-40% per mSv (ICRP). Two nuclear cities in
the Soviet Union, Snezhinsk and Ozersk, are of the Mayak nuclear site in theSouth Urals. They have exactly the same population types, weather patterns
and natural background radiation but suffer exposure to different doses oflargely the same fission isotopes.
Table 13.1 Risk factors for infant, neonatal, stillbirth and birth rate depression
Birth effectInfant (0-1year)
mortality
Neonatal (0-28adays) mortalityaStillbirth
Birth rateb
depression

Percentage increase inbaseline rate per mSvc(ECRR) parental exposurein year of conception
0.05 %

Observed excess number
per thousand live birthsd1963 per mSv (ICRP)
parental exposure
21 increase to 24 = 3

0.07%

13 increase to 16 = 3

0.04%

13 increased to 17 = 4

0.05%

-

a

b
Based on Sr-90 exposure to parents in 1963 in England and Wales; Based on fall incbirth rate in Finland and parts of the UK after Chernobyl; Dose calculated accordingdto ECRR model and including new weighting factors Wj and Wk ; Dose calculated at
the time using ICRP model

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Infant mortality was reported by Petrushinka et al.. (1999) for the period 19741995. Table 13.2 shows the rates which suggest an infant mortality increase ofabout 45% per mSv (ICRP) dose to the foetus.
Table 13.2 Infant mortality and stillbirth at the two Soviet Mayak cities Ozersk
and Snezhinsk (1974-1995)
Average effective dosemSv
Infant mortality/1000
Stillbirth/1000

Ozersk (n=20983)
1.6 (0.05-3.36)

Snezhinsk (n=11994)
0.98 (0.04-2.04)

14.9
7.0

11.7
5.8

13.3 Heritable Genetic Effects
Although infant mortality effects reviewed in 13.2 probably represent heritable
genetic effects the ICRP only considers heritable effects which are measurable
in phenotype after birth e.g. congenital defects and perhaps increases inclinically diagnosed heritable genetic diseases. Thus foetal death and infantmortality are not addressed as radiation exposure outcomes by ICRP. The ICRP
risk factor for heritable genetic effects is based on the Hiroshima LSS and theCommittee therefore concludes that this risk factor is deficient for theconsequences of internal exposure. It is also deficient since it fails to include
effects which were reported for the interim period between 1945 and 1953 by
the Japanese (Kusano 1953). This Committee decision is supported by recent
work in which minisatellite DNA examination of genetic damage has been
applied to the offspring of those who were exposed at Hiroshima, with theresult that no significant excess DNA mutation was found. Although this waspresented as an opposition to the findings of minisatellite DNA damage in thechildren of Chernobyl, the Committee takes the contrary view that the
Chernobyl findings were a consequence of internal exposure whilst theHiroshima findings were from external exposure. Padmanabhan has shown that
there were significant genetic effects following Hiroshima, but these weremanifested as sex ratio changes in the study group and were discarded by the
US led team because they could not explain them (see Busby 2006).
The ICRP risk factor for total Mendelian, chromosomal andmultifactorial heritable genetic damage is now 2.4% per Gy in the reproducing
population. This falls to 0.38% per Gy in the first generation. The Committeechooses the same value for the exposed reproductive generation but owing to
the effects of transgenerational genomic instability considers the value of
0.38% too low for effects in the first generation. It notes that the calculation ofdose for internal exposures will generally result in an adjustment of the dose toa value that will accurately reflect the increased risk of genetic damage foundin the Chernobyl minisatellite studies. Thus a dose of 1mSv calculated by the
ICRP models from Strontium-90 will be increased by the Committee's hazard

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weighting factors to 300mSv by applying the values for W k and Wj from
Tables 6.2 and 6.3. This would effectively increase the numbers affected by a
1mSv exposure to Sr-90 from 0.01 per 1000 births to 5, a figure which roughlyreflects both the predicted and observed infant effects and also the 7-foldincrease in minisatellite mutation rates in the offspring of the Chernobyl
liquidators.
13.4 Broad spectrum health detriment following low-level radiation exposure
The Committee has examined data relating to populations exposed to low levelinternal radiation from fission products released from Chernobyl, following
Hiroshima, and also following exposures to Uranium weapons particles in the
war zones of Iraq and the Balkans. It is clear that the general health detrimentpredicted by the cell-damage models is found in such populations. The
Committee has chosen to model such general health deficit as a percentage
decline in mean life quality, although in reality the effects are seen as both areduction of lifespan and also throughout the life of the exposed individuals.
They may be expressed probabilistically as well defined clinical or
physiologically measurable effects in individuals who have been examined andas ill defined conditions which result in reduced quality of life. A list of
conditions which are found in populations exposed after Chernobyl and in
Hiroshima inhabitants following the A-bombing was provided Malko in 1997.
The conditions are very similar in spectrum to those presented by Ammash in2000 for populations exposed to Depleted Uranium particles in Iraq. Malko's
findings for adults and adolescents are given in Table 13.3, for children in 13.4.
Bandashevsky has reported significant associations between measured
Caesium-137 contamination in children as measured by whole bodymonitoring, and cardiac arrythmias in contaminated regions of Belarus near
Gomel. The non-specific effects of radiation reported for populations living in
the regions of Hiroshima and Nagasaki are also of interest here; for example, ina study of morbidity in victims of the A-Bombing that has not been cited orconsidered by ICRP, Furitsu reports non cancer somatic effects very similar to
those found in the Chernobyl affected territories. Results are shown in Table
13.5. Morbidity rates for 1232 victims of the A-Bombing were examined in
the Hannan Chuo Hospital, Osaka between 1985 and 1990. Results are shownin Table 13.5.
Global weapons fallout effects on IQ and attainment scores have beenstudied by Oftedal for Scandinavian countries and by Sternglass for the USA.
Both show a significant reduction in performance scores in children born
during the peaks in weapons fallout.
The Committee has chosen a value of 0.1% per mSv exposure
calculated according to ECRR models to express the reduction in general
health due to exposures. This represents a 0.1% excess probability of any
person suffering loss of life quality due to developing one or more somatic167

ECRR 2010

illness or life-quality affecting condition during their lifetime as a consequenceof exposure to 1mSv. The Committee has chosen to make the approximationthat the effect will be linear with dose in the range 0-500mSv and have based
this on Eyring and Stover's considerations of equilibrium harm but believe that
this may be a conservative estimate and recommend research to establish amore accurate figure.
Table 13.3 Indices of somatic illness per 100,000 in adults and adolescents of 3
contaminated and 5 control regions of the Brest region in Belarus in 1990
(from Malko 1997).
Non cancer diseases

Altogether
Infections and parasites
Endocrine, metabolism, immunity
Psychic disorders
Chronic Otitis
Circulatory system, hypertension,ischaemic heart disease
Of which (above) stenocardia
Cerebrovascular
Respiratory
Digestive organs, e.g. ulcers,
chololelitic, cholecystitis
Urogenital, nephritis, nephroses,
kidney infections
Female infertility
Skin diseases, dermatitis, eczema
Osteomuscular, osteoarthritis

3
contaminateddistricts
62,023
3251
2340
2936
250
12060

48,479
2119
1506
2604
166
9300

<.0001<.0001
<.001
<.01
<.01
<.001

1327
1981
2670
7074

594
1363
1789
5108

<.01
<.001
<.001
<.001

3415

1995

<.001

84
3377
5399

56
2060
4191

<.01
<.001
<.001

5 control
districts

P-value

13.5 Accelerated ageing
The non-specific effects discussed in the previous section may be seen as a
general accelerated ageing effect. Indeed, the accumulation of somatic genetic
damage which is the inevitable consequence of exposure would beindistinguishable from the similar accumulation of somatic genetic damage
associated with natural ageing. Both are associated with evidence of somatic
genetic damage, e.g. chromosome aberrations. The focus of research into theeffects of ionising radiation has historically been cancer incidence andmortality. However, it has been known for many years that the trend inincidence of most cancers and the incidence of age-related processes including
death are both best modelled as a logarithmic survival function. For ageing thisfunction is named after Gompertz. A mathematical description of radiation
damage given by Eyring and Stover for beagle dogs exposed to Plutonium

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ECRR 2010

involved opposing rate processes where damage and repair are balanced until
the repair systems are overwhelmed over time by accumulated damage. The
functions are equally applicable, with different coefficients, to natural ageing
processes and the Committee believes that this effect of radiation exposuremust be included in any discussions of policy.
Table 13.4 Indices of somatic illness per 100,000 in children of 3 contaminatedand 5 control regions of the Brest region in Belarus in 1990 (from Malko
1997).
3-contaminateddistricts

5-control
districts

p-value

Non cancer diseases

Altogether
Infectious and parasitic
Endocrine, metabolism
Psychic
Nervous system and sense organs
Chronic rheumatism
Chronic pharyngitis, sinusitis
Digestive organs
Includes chronic gastritis
And cholelitic, cholecyctitis
Atopic dermatitis
Osteomuscular and connective
Congenital malformations
Includes heart and circulation

68725
7096
1752
2219
4783
126
117
3350
129
208
1011
737
679
306

59974
4010
1389
1109
3173
87
83
2355
40
61
672
492
482
242

<.01
<.01
<.01
<.01
<.01
<.01
<.01
<.01
<.01
<.01
<.01
<.01
<.01
<.01

Bertell has addressed the issue of accelerated ageing epidemiologically. She
studied the effects of low-dose, high dose-rate medical X-rays compared with
the natural background component of ageing, and found, among other things,
that there is no acceptable dose rate factor reduction for low-dose rate. She
suggested that the effect was due to breakdown of intercellular communication
through small mutations accrued over time due to background radiation, or
quickly through medical X-rays. The mutations are not perceived by theindividual until they accumulate. As a yardstick, Bertell used the natural rate ofincrease of non-lymphatic leukemia in a large population (3 million followed
over three years in the US Tri-State leukemia survey), which followed acompound interest type increase from age 15 years, at about 3% per year, as ayardstick. Her question was: how much medical X-ray exposure would
increase the non-lymphatic leukemia rate by the same amount as one year of
natural ageing does? The two turned out to be equal, although the dose ratefrom background is very much slower.
The concept of accelerated ageing is supported by the discovery of theepigenetic phenomena associated with genomic instability.

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Table 12.5 Comparison of morbidity rates (%) of the A-Bomb victims and of
the general Japanese population (Furitsu, 1994)
Non cancer disease

LumbagoHypertension
Ocular disease
Neuralgia, myalgia
Anaemia, leukopenia
Dental disease
Gastro-duodenal ulcer
Ischaemic heart disease
Liver disease
Diabetes mellitus
Nephritis, urethral infection
Skin disease
Bronchitis, pneumonia
Cardiac arrhythmia
Cholethiasis, pancreatitis

A-Bomb victim sample
morbidity rate %
29
24
18
12
12
10
9
9
8
7
5
5
5
5
4

Japanese population
morbidity rate %
8
15
3
2.5
1
<1
2
2
1
3
1
2
0.8
<0.1
1

13.6 Effects of radiation on the general environment
The Committee emphasises that even from the most anthropocentric viewpoint(as discussed in the chapter on ethics) people cannot be considered to be
independent of the environment that supports them. Harmful effects of
exposures on living creatures, plants and ecosystems must be prevented if only
through human selfishness. Environmental discharges from nuclear processes
result in much higher doses to creatures which are in contact with them: thus
discharges to the sea result in very large doses to marine creatures many ofwhich concentrate radionuclides and thus receive very high doses. If such doses
are known to cause health detriment in people and in animal and cell studies,marine organisms must suffer similar effects since they are composed ofsimilar cells which operate their living processes in very similar ways (see e.g.
Jha 2006)
At the gross level there are reports of increases in skin and othercancers in fish caught in the Irish Sea where they are exposed to discharges
from the Sellafield plant. Because these reports have become widely known the
Irish Sea fishing industry has suffered enormous economic damage - an effectknown in Ireland as ‘Sellafield Blight’. In County Louth, the nearest part of
Ireland to the Sellafield plant, ‘Sellafield Blight’ affects the ability of farmers
to sell produce and the use of beaches for recreational purposes. Beaches in170

ECRR 2010

Cumbria are now no longer used by people for recreation and indeed on
occasion have been ‘red flagged’ by the nuclear industry.
In addition to such obvious and socially significant effects, theCommittee is aware of research which indicates major effects of exposure
which have been largely ignored. Some examples will be given. For example,
the sharp decline in fish stocks in the northern hemisphere in the late 1960s has
been conventionally ascribed to over-fishing. Sternglass has suggested thatsome if not all of it may be a consequence of radiation exposures from weapons
fallout. If even part of this suggestion is true, the resulting consequences of thetesting and by implication, of discharging materials to the sea, are notaccounted for in the cost-benefit analyses supporting nuclear projects. They
may be massive. The post-war period also saw a very large reduction in bird
populations, an effect which was seen also after the Chernobyl accident. One of
the most startling examples of this has been the entire loss of the black-headedgull population from the Ravenglass estuary near Sellafield. Researchsuggested that the egg shells were affected by the discharges from Sellafield
but experimental work showed that the effect was not due to external radiation
but must be some consequence of one of the internal nuclides, perhaps Sr-90 or
Ba-140 exposure in the shell. Lobster carapaces in the Irish sea have been
recently shown to concentrate the isotope Technetium-99 to a very large extent.
Some lobsters with over 100,000Bq/kg of this isotope have been tested. The
isotope Strontium-90 has been shown to cause genetic effects in many animaland plant systems. For example, Ehrenberg showed genetic mutations in wheat
at very low doses of Sr-90.
Results of research into contamination of the Irish Sea carried out inthe late 1990s showed significant affects on coastal communities of theradionuclides which contaminated that shallow and constrained water body.
Nevertheless, Caesium does flow out of the northern and southern channels andcoastal levels are now falling, and are less than 20Bq/kg in sediment at thehighest points. The situation is much worse in the Baltic Sea where there isvirtually no exit and radioactive material from weapons and Chernobyl fallout
combines with radionuclides from the various nuclear plants in Sweden,
Finland and Russia to aggregate in the sediment and biota. The HELCOM
reports show levels of Cs-137 in sediment at 1000Bq/kg, more than ten times
higher than levels found in the Irish sea at the peak of Sellafield discharges.
ECRR has opened an office in Sweden to begin researching the effects of theselevels of contamination.
There are meteorological implications of radioactive discharges also.
An interesting suggestion has been that the large quantities of the radioactive
gas Krypton-85 released following fission may be a contributing factor in thethinning of the ozone layer, since its ionisations will result in more rapid
breakdown of molecules in the stratosphere which absorb the far ultraviolet
solar radiation. Krypton-85 has also been cited as an agent which will alter the171

ECRR 2010

normal conductivity of the atmosphere and thus alter the processes which affectweather patterns.
These examples, involving social, psychological and physical damage,suggest that discharges may have effects which must be included in any
assessment of the consequences of any release. However, such research as has
been done to establish the health consequences in non-human species suffers,
as Pentreath has pointed out (Pentreath 2002), from lack of scientific credibility
and of common terminology at even the most basic level.
The Committee believes that arriving at an understanding of the impact
of environmental discharges is a massive project which is beyond the scope of
the present recommendations. However, two general points must be made:1) People are part of the environment, and human mortality and morbidity at
low dose has been studied more closely and more consistently than any otherspecies. The existing evidence described in these recommendations indicatesthat releases currently thought to be trivial do in fact confer unacceptable risks.
It follows that, as far as regulation is concerned, it may be unnecessary to
determine the effects on non-human species. The exception to this is practices
which cannot be avoided, such as dealing with waste and contaminated land.
The types of exposure associated with such practices should determine theemphasis and direction of research.
2) Present indications are (ICRP 2002) that research on non-human impact will
be dominated by the assumption of a linear dose response and mathematicalmodelling. The alternative is to look in the real world using ecological studies
comparing populations in contaminated areas with those less contaminated. If
the mistakes of the past are to be avoided these studies will have to beundertaken using protocols which will render their results scientificallycredible. Since there is no dispute about the similarity of effects in human andnon-human species the responsible agencies should come to a more coherent
position on the ability of epidemiological studies to inform on low doses than
ICRP currently has (see ICRP 1999) and resolve their problems withecological/ correlation studies, in which, according to the UK NRPB’s Colin
Muirhead (NRPB 2001) it is not possible to tell from the data available
whether the infants who developed leukemia received higher radiation doses
than healthy infants in the same areas.

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14
Examples of Application
14.1 Introduction
The ECRR model partitions internal and external doses. For internal doses, it
discriminates between specific isotopes and between distributions of those
doses depending on whether they arise from atomic (molecular) forms of theisotopes as against sub-micron and micron sized particles.
In Table 10.6, asterisks denote isotopes where the route of exposure or
exposure type will carry excess weightings under Wj and Wk due to theirability to cause mutation through mechanisms not considered by ICRP. Someof these isotopes and their weightings are given in Table 14.1
Table 14.1 ECRR weightings for weapons fallout internal exposure isotopes
IsotopeH-3

Weighting
10

C-14

5

Sr-90

300

Pu, Am
Ce-144
Ru-106
U-238

300
50
50
1000

Note
Transmutation/ Hydrogen bonding
amplification
Transmutation and enzyme
amplification
DNA binding (10) and Atomic
Second Event (30)
Insoluble particles
Insoluble particles
Insoluble particles
Secondary Photoelectrons/ DNA

The purpose of this chapter is to give an idea of the process by which the
ECRR's new risk model may be used to assess the human health impact of any
given exposure. Disease yields from three different exposure episodes arecalculated approximately using both the ICRP and ECRR models. These
episodes are:
 Mortality from global weapons fallout, mortality, morbidity and loss oflife quality from the entire nuclear project up to 2000
 Chernobyl and increases in cancer in Belarus Chernobyl effects in Northern Sweden studied by Tondel et al 2004
Internal doses from specific isotopes to the various exposed populations
discussed here may be unknown. Some approximations have therefore beennecessary.
14.2 Global mortality yield of atmospheric weapons testing
The difference between the ECRR and ICRP mortality predictions for world
populations is shown in Table 14.2. The dose figures for global fallout given by
UNSCEAR were averaged over the whole planet. The true distribution of173

ECRR 2010

fallout was not uniform: the northern hemisphere in general received more
fallout, and levels in parts of Europe were higher still, owing to the effect ofrainfall. An understanding of the real effect in Europe may be approached bytaking England and Wales as an example. The measurements made by the UK
authorities allowed quite accurate assessments of the fallout isotope doses.
Cumulative Sr-90 doses over the period 1950-63 to England and Wales(population 46,000,000) were about 0.6mSv as estimated by the Agricultural
Research Council using ICRP models.
Table 14.2 mortality and morbidity yield of weapons fallout using figures fromUNSCEAR 1993 and comparing the models of the ICRP and the ECRR.

a
b
c
d

EffectICRP dose mSv

1

ICRP yield
Deathsa
1,116,000
0Cancer deaths

4.464

c

Infant deaths
Life quality loss
Early foetal
death + stillbirth

ECRR dose
mSv
104

24

4.464

0

104

1

0

24

ECRR yield
Deathsb
52,000,000
857,000d
10%
1,660,000

Using the risk factor 0.05/Sv due to inclusion of a DDREF of 2
Using the risk factor 0.1 /Sv and avoidance of DDREF
In the cohort exposed in the five years 1959-1963 assuming a 5-yr dose of 1mSv
Averaged over the world population of 5 Bn in the lifetime of the peak 5-year exposed cohort

Using the ECRR weightings, this global fallout figure becomes equivalent to
180mSv internal dose. In the 46 million population this translates into
46,000,000 x 0.1 x 0.18 = 828,000 extra cancer deaths over the lifetime of the
exposed individuals, say 70 years. This is roughly 11,800 extra cancer deaths
per year. In 1958, before the fallout exposure could have fed through to cancer
mortality, there were 96,342 deaths from all cancers in England and Wales. In
1990, the figure was 144,577, a 50% increase in a population of roughly
unaltered size. Thus, despite advances in cancer therapy, an extra 48,235 cancer
deaths occurred. Many of these will have been a result of the increased averageage of the population, however, standardisation for this shows that there has
been at least a 20% increase in cancer incidence in England and Wales
combined. This increase began in the 1980s in England and in the mid 1970s in
Wales (where it was greater, about 35%, see chapter 10). Thus in the UK there
has been an increase of about 18,000 cancer deaths per year over the 1958
number; it has a temporal spectrum consistent with the fallout trend, which ishigher in Wales where the fallout was higher, and is ascribable to some cause
apart from ageing of the population. That this cause is environmental was
implicit in WHO statements in the 1960s relating to cancer causes and is174

ECRR 2010

confirmed by the recent 2001 statement of the ASPIS conference on Kos
Island. The predictions of the ECRR risk model of just under 12,000 extra
deaths per year suggest that the fallout was the cause of this cancer epidemic.
The higher cumulative dose for the population in Wales similarly accounts forthe proportionately larger effect in that country. As pointed out earlier, thisstudy is the basis for the ECRR approach to obtaining weighting factors forinternal exposures. Its results are spectacularly confirmed by the intracommunity Chernobyl exposure study of Tondel et al 2004 which is discussed
below.
14.3 Total yield of mortality, morbidity and loss of life quality from the nuclear
project up to 2000 from ICRP and ECRR.
Figures from UNSCEAR 1993 give total estimated ICRP collective dose
equivalents to the world population up to 1989. Assuming that these doses,
which are based on ICRP models, are accurate, this table gives a baseline forcalculating the total fatal cancer yield. The sources are given in Table 14.3 andthe calculation, based on ICRP and ECRR models in Table 14.4
Table 14.3 ICRP-based global effective dose commitment from nuclear project
up to 1993 and approximate ECRR model effective dose commitment.
(Source UNSCEAR 1993 Table 58)

Source of exposure

Global nuclear tests
Weapons fabrication
Nuclear power production
Radioisotope production
Accidents
Local and regional doses
Total

ICRP based collective
effective dose
commitment(person Sieverts)

22,300,000
10,000100,000
80,000602120380000b
23,472,120 ( 4.7mSv)

a

ECRR based
collective effective dose
commitment(person Sieverts)
579,800,000
260,000
2,600,000
8,000,000
15,655,120
9,880,000b
616,195,120 ( 123mSv)

a

ECRR figures assume the same proportion of isotopes and internal radiation as
calculated by UNSCEAR for fallout except for allowance for higher internal doses
from radioisotope production.
b
9. based on world population of 5 x 10 assumed by UNSCEAR

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ECRR 2010

Table 14.4 Global consequences of exposures from nuclear project based on
UNSCEAR figures up to 1989.
EffectCancer death
Cancer total
Infant death
Foetal death

ICRP yield
1,173,606
2,350,000
00

ECRR yield
61,619,512
123,239,024
1,600,000
1,880,000

Loss of life quality

010%

14.4 Predicted mortality yield of Chernobyl accident: caveats over linear
modelsUNSCEAR 1993 gave (Table 58) the total committed effective dose from the
Chernobyl accident to the world population as 600,000 person Sieverts. The
ICRP60 risk factor of 0.05/Sv would predict 30,000 fatal cancers in the worldfrom this; as UNSCEAR 2000 points out, such an increase would bestatistically invisible.
Gofman has used the area deposition of Cs-137 to calculate theexternal committed dose to the major countries of the world with significant
exposure and has applied his own risk factor of 0.37 per Sievert (derived fromhis approach to the Hiroshima LSS data) to calculate the fatal cancer yield of
970,500 but in this calculation, no internal doses were used whatever. In any
case, Gofman did not distinguish between external and internal doses (Gofman
2000).
In a report commissioned by the Belarus Ambassador to the UK,
Busby (2002) has used the fallout yield of cancer in Wales to approximate anultimate increase in fatal cancer rate in Belarus of 50%, or 25,000 extra fatal
cancers a year in the population of 9,800,000 due to exposures in the first five
years following the accident. In ECRR2003, for Belarus, the Committee
partitioned the dose given by UNSCEAR 1993 amongst individual radioisotope
exposures and applied the weightings for internal excess risk given in Chapter
6. The Committee made an approximate calculation as follows. The first year
average committed effective dose to Belarus was given by Savchenko as 2mSv.
If this is extrapolated to five years and one third of the dose is weighted as Sr90 or hazardous particulates, the ECRR calculation results in an ECRR model
cumulative dose of about 900mSv and a fatal cancer yield of 882,000 which theCommittee assumes will express over 50 years which is 17,640 extra fatal
cancers per year, roughly in line with Busby’s calculation. The 70 year overall
yield is 1,200,000 in Belarus alone. The same approach to the global figures
estimated by UNSCEAR suggests that the overall 70 year global cancer
mortality yield following Chernobyl is in excess of 6 million.
The predictions made by Busby in 2002 using the ECRR risk model,
and followed by ECRR2003 were borne out by results presented by Okeanov et176

ECRR 2010

al in Geneva in 2004. In November 2004 the Swiss Medical Weekly publishedfindings by workers at the Clinical Institute of Radiation Medicine andEndocrinology Research in Minsk, Belarus. They showed that between 1990
and 2000 cancer rates had risen by 40% overall, compared with rates before thecatastrophe in April 1986. Belarus has had a national Cancer Registry as longas anywhere in Britain, keeping a computer database of all new cases ofmalignant tumours. The Okeanov paper presented an overall comparison ofchanges in the incidence of cancer morbidity in Belarus. Increases in thevarious oblasts (regions) were:









Brest 33%
Vitebsk 38%
Gomel 52%
Grodno 44%
Minsk 49%
Mogilev 32%
Minsk city 18%
all Belarus 40%

The view of conventional radiation protection community however was
predictable. On the basis of the ICRP model, based on absorbed dose, very
little if any cancer had resulted or would result from the fallout. This was
expressed, for example, in UNSCEAR 2000:
Apart from the substantial increase in thyroid cancer after childhood exposure
observed in Belarus, the Russian Federation and Ukraine there is no evidenceof a major public health impact related to ionising radiation 14 years after the
Chernobyl accident. No increases in overall cancer incidence or mortality that
could be associated with radiation exposure have been observed. The risk ofleukemia, one of the most sensitive indicators of radiation exposure, has notbeen found to be elevated even in the accident recovery operation workers orin children. There is no scientific proof of an increase in non-malignant
disorders related to ionising radiation. … For the most part [the public] were
exposed to radiation levels comparable to or a few times higher than thenatural background levels. Lives have been disrupted by the Chernobyl
accident but from the radiological point of view, based on the assessment of
this Annex, generally positive prospects for the future health of mostindividuals should prevail.
The increases in ill health reported from the Chernobyl-affected territories ofthe ex-Soviet Union were regularly ascribed by IAEA and WHO to‘radiophobia’. However, publications began to emerge which showedmeasurable objective indicators of genetic harm in animals and in plants. The
ECRR Chernobyl sub-Committee addressed the issue of lack of translation

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(and consideration) of Russian language peer review publications and produced
a report Chernobyl-20 Years After in 2006 where this evidence was presented(Busby and Yablokov 2006). This was reprinted and revised in 2009. Also inlate 2009 Yablokov et al edited a book on the issue which was published by the
US New York Academy of Sciences (Yablokov et al 2009). This presents avery large array of data showing increases in cancer, congenital disease andgeneral health effects caused by the Chernobyl exposures. There is now nocredible support for the assertions of the risk agencies that the Chernobyl
fallout had no measurable effect. Interested researchers are referred to thesevolumes which present data which are largely in line with the predictions in
ECRR2003.
The wide difference between the predictions of the Committee's modeland those based on the ICRP approach shows the extent to which internalradiation with the enhanced ability to give high doses to individual cells canalter the expected health detriment. As in the case of global fallout, the two
approaches should be easily testable by examining the observed increases incancer in the exposed groups. However, it must be borne in mind that implicitin the modelling assumptions of the ICRP based method with weightings forthe radionuclides is that there is a linear response. The Committee has madeclear that this is unlikely to be the case, and therefore emphasise that the model
which they apply to calculate the health detriments is only an approximate one
and will be roughly linear over the narrow range it is applied. It is intended to
be used to obtain a more rational and accurate assessment of risk in a
population to which the collective dose model of ICRP has already been
applied or where such doses are available. It is intended to represent the best
rational correction currently available to historical ICRP collective dosemodels. Within these populations, the high dose group will haveproportionately lower levels of cancer as a consequence of the biphasic orsupralinear dose response relationships reviewed by the Committee. Studies ofthe effects of Chernobyl should therefore compare health data from before theaccident with data from after the accident rather than using control groups andarguing from linear risk assumptions.
This success of the ECRR approach in Belarus was followed in thesame year by a second piece of supporting evidence. A study in 2004 of cancer
in northern Sweden also gave results which are largely predicted by the ECRR
model.
14.5 Cancer in northern Sweden after Chernobyl.
In 2004 a report was published of work carried out by Martin Tondel as part ofa PhD thesis. The report examined cancer rates small communities in northern
Sweden for the period 1988-1996 in relation to measured levels of Caesium137 area contamination from the Chernobyl fallout (Tondel et al 2004). The
study used cancer incidence rates supplied for community areas by the Swedish

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Cancer Registry and carried out various regression analyses allowing forconfounding variables. The conclusion was that there was an effect of theradiation on cancer rates which was monotonic and approximately linear over
the ten year period following the accident. The increase in cancer was 11% per
100kBqm-2 of Cs-137 contamination. Tables in HRP 1972 show that 100kBqm2
of Caesium-137 (photon energy 660keV) delivers a dose at 1m of 0.39Gyh-1.
Thus the first year annual dose from the gamma shine from this level would be
3.4mSv. Thus the 11% increase in cancer per 100kBqm-2 is equivalent to a
32.5-fold increase in cancer per Gy which is some 640 times greater than the
lifetime risk factor of 0.05Sv-1 published by ICRP. It should be noted that thisstudy does not include cancers in the exposed populations in their lifetime, butjust in the 10 years after the exposures.
At first this is certainly strong support for the ECRR approach:
ECRR2003 predicts such a finding. However there are two aspects which areinteresting. The weapons fallout comparison based its own dose reconstruction
on the UNSCEAR data which gave a dose dominated by the isotope Sr-90
which carried a weighting of 300. The fallout from the Chernobyl accident had
a different spectrum of fission products. Both contained the easily measured
Cs-137 as the major component, but in the case of Chernobyl, Sr-90 was not amajor component at some distances from the site of the reactor. However
Chernobyl fallout contained (1) Te-132/I-132 and (2) a high proportion of
Uranium fuel particles although the amount that precipitated in Sweden does
not seem to have been reported. It seems that the exposures in Sweden weremore hazardous than the weapons fallout exposures in Wales. This would
suggest that the increases reported by Tondel are already greater per dose than
the weapons fallout exposures. The main increases were in the 5-year period
following the exposures. They were therefore the first spike in the temporal
spectrum of cancer increases following exposure (discussed earlier in thisreport) and it can be expected that there will be a large increase in cancer in
Sweden beginning in about 2006 or earlier.
This is a prediction of the ECRR model which will be easy to follow
up. This increase will probably not have the same area relation to the originalcontamination as rainfall mainly disperses these materials to the sea. As
reported above, the Baltic Sea is extremely contaminated with radioactivity.
Levels of Cs-137 in sediment are as high as 1000Bq/kg according tomeasurements reported by the Helsinki Commission (HELCOM). This can becompared with 100Bq/kg Cs-137 in Irish Sea intertidal coastal sediment inareas when cancer studies showed a 30% increased risk relative to inland
populations between 1974 and 1990 (Busby 2002, 2004b, 2006). The Baltic
Sea regional offices of ECRR in Stockholm Sweden and Riga Latvia are
currently discussing a joint study to examine this issue.

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ECRR 201015
Summary of risk assessment method, principles and recommendations
15.1 Risk assessment method
The model for establishing the health consequences of an exposure to ionisingradiation broadly follows that of the ICRP except that the ECRR has
recognised both theoretical and epidemiological grounds for introducing asystem of enhanced hazard weighting for certain kinds of internal exposure.
Therefore the basic units of dose developed and used by the ICRP for exposure
are adjusted for those isotopes and exposures which carry the ECRR
enhancement weighting factors. Following these adjustments, it is possible toobtain an approximate value for health detriment from fatal cancer if a linear
dose response relationship is assumed for a restricted dose range approximating
to the range 0-10mSv externally averaged.
The Committee emphasises that this model has been developed entirely inorder to provide a convenient approximation and wishes to make clearthat the dose response relationship is unlikely to be linear in most cases.
The basic method follows the following procedure:
1. Partition the doses into external and internal doses.
2. Use the biokinetic models of the ICRP to establish committed doses for thevarious organs and the whole body.
3. Weight the doses using the Quality Factor weightings (relative biologicaleffectiveness) to obtain committed effective dose.
4. Partition these internal doses between the various isotopes and types of
exposure (hot particle or by radionuclide).
5. Weight the doses using the ECRR weighting factors.
6. Add all the doses together, external, internal and weighted internal.
7. Multiply the result by the appropriate risk factor (e.g. for fatal cancer this is0.1 per Sievert).
8. This gives the approximate absolute value for the risk considered over the
lifetime of the exposed individual.
In many cases, the early parts of this exercise will have been carried out by oneof the risk agencies and the resulting tables of doses from the various isotopes
and exposures can then be adjusted according to 4-8 above. In the event that
only the overall dose has been published, some approximation of the
proportions of external and internal doses must be made. For the major isotopic
exposures of interest, the Committee lists dose coefficients for adults, children(1-14) and infants (0-1) in Table A1.

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ECRR 201015.2 Principles and Recommendations
1. The Committee has developed its modelling to allow assessment of theeffects of radiation exposure for the purposes of policy and regulation.
2. The method involves the calculation of collective doses from different
types of exposure and different sources to exposed groups and thecalculation, by simple rules and coefficients, of the collective averaged
health detriment.
3. The Committee believes that the model may also be used toapproximate the effects of natural background radiation and forTechnologically Enhanced Naturally Occurring Radioactive Materials.
4. The Committee recommends that the total maximum permissible
annual dose limit to members of the public involving releases ofanthropogenic isotopes or natural isotopes delivered in a novel fashion
should be kept below 0.1mSv as calculated using the ECRR model.
5. The Committee thus argues for a level of exposure much lower thanthe level recommended by ICRP and recognises that mostundertakings associated with releases of radioactivity to theenvironment would be severely curtailed by the adoption of such a
recommendation. However, the Committee feels that this is an area
where political decisions must be made based on accurate knowledgeof the consequences of those decisions.
6. The Committee recommends that annual exposure limits for nuclear
workers should be 2mSv. Nuclear workers must be made fully awareof the likely harm to them and their offspring.
7. The Committee endorses the principle of justification contained inradiation safety legislation but does not believe that such justification
can be made on a utilitarian basis where the costs may be borne bysome whilst the benefits accrue to others: rather the rights of all
individuals must be respected equally.
8. The Committee recommends that radiation exposures be kept as low
as reasonably possible using best available technology.
9. The Committee recommends that all health deficits associated with
exposure be included in any assessment of the policy implications of
exposure and holds that the unborn should in this regard beconsidered as having equivalent rights to living people.

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10. The Committee holds that environmental consequences of radioactive
discharges including effects on all life forms be considered in assessing
the overall deficit of any practice involving radiation exposure.
11. The Committee will continue to examine research on radiation
exposure and health detriment and will adjust the models it hasdeveloped to reflect both radiobiological theory and observational
epidemiology.
12. The Committee calls on all governments of the world to abandon thecurrent ICRP based risk model as a matter of urgency and to
substitute for it the ECRR2010 risk model.

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ECRR 201016
Members of the European Committee on Radiation Risk and Individuals
whose Research and Advice contributed to the Present Report
At 1st January 2010 the following individuals are or had been members,
advisers or consultees of the ECRR. Their inclusion in this list may not meanthat they endorse all the contents of the report but does imply that they areconvinced that the ICRP system of modelling seriously underestimates the risk
from low level ionising radiation exposure from anthropogenic sources. It will
be noted that many of the new members and supporters of the ECRR and its
analytical model are scientists for the former Soviet Union. This is unsurprisingsince it is these individuals who have been in a position to see first-hand and to
study the effects of low-dose exposure to internal radionuclides.
Dr. Kaisha Atakhanova, Russia
biologist (Karaganda State University, Kazakhstan)
Prof. Yuri Bandashevsky, Belarus and Ukraine
M.D., PhD, physician, radiation reseacher
Dr. Rosalie Bertell, Canada
PhD, GNSH, epidemiologist and radiation researcher (International Institute forConcern on Public Health)
Dr Peter Bein, Canada
PhD, P.Eng, engineer and media analyst
Ms Edel Havin Beukes, Norway
BSc, MSc, radiobiologist, teacher (WILPF Norway).
Mr Richard Bramhall, UK
NGO, Low Level Radiation Campaign
Prof., Dr. Elena Bourlakova, Russsia
Chemist, radiobiologist (Director, Institute for Biochemical Physics, Russian
Academy of Science, Moscow)
Dr Araceli Busby, UK
BSc, MSc (Ecol), PhD, public health epidemiologist (National Health Service,
London School of Hygiene and Tropical Medicine,)
Prof Chris Busby, UK(Green Audit, University of Ulster)
PhD, Chemical Physics, radiation researcher

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Dr Cecilia Busby UK
MA.(Cantab) PhD, social anthropologist, radiation researcher
Mr Otto Carlsen Denmark
BSc, (Physics), NGO
Dr Molly Scott Cato, UK
MA (Oxon), MSc., PhD, statistician and economist
Mr Hugo Charlton, UK
BA, LLB, barrister
Mrs Mary Curtis, UK
MA (Oxon), MSc, physicist
Dr Paul Dorfman, UK
PhD, sociologist, risk studies, University of Warwick
Dr Michel Fernex, Switzerland
MD, PhD, physician
Mrs Solange Fernex, Switzerland
NGO, radiation researcher (Dec)
Mrs Eva Fidjestol, Norway
Assistant professor of physics
Prof Daniil Gluzman, Ukraine
Medical doctor, radiation researcher, childhood leukemia epidemiology
Prof Roza Goncharova, Belarus
Dr Sci. radiation genetics and cytology (National Academy of Sciences,
Belarus).
Prof. Dr. Dmitry Grodzinsky, Ukraine
radiobiologist, botanist (National Academy of Sciences of Ukraine, Kiev)
Dr Jay Gould , US
PhD epidemiologist and mathematician (*Dec)
Mr Grattan Healy, Ireland
BSc (Physics), energy researcher

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Mr Per Hegelund, Denmark
NGO
Prof Malcolm Hooper, UK
PhD medicinal chemist, Depleted Uranium effects researcher
Prof Vyvyan Howard , UK
MD, PhD, MRCPath, foetal toxicologist
Prof Wolfgang Hoffman Ger
Dr. Med, MD, MPH, epidemiologist
Ms Charly Hulten, SweNGOProf Wolfgang Koehnlein, Ger
Prof. Dr. rer, nat, radiation biologist
Dr Alfred Koerblein, Ger
Dr. rer.nat, physicist, epidemiologist
Dr. Ludmila Komogortseva, Russia
ecologist (Member of Kaluga’ province parliament, Russia)
Prof. Sergey Korenblit Russia
theoretical physicist (Irkutsk State University, Irkutsk, Russia)
Prof Horst Kuni Ger
Prof. Dr. Med, physicist and radiation scientist
Mr J-Y Landrac, Fra
BSc , NGO
Prof Mikhail Malko (Belarus)
Physicist, Deputy Director Ministry of Power, epidemiologist
Mr Joseph Mangano, US
MPH, MBA, epidemiologist
Dr. Nataly Mironova, Russia
sociologist (Movement for Nuclear Safety, Chelyabinsk, Russia)

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Prof Carmel Mothershill, Canada
PhD radiation biologist, authority on epigenetic effects, Mc Master University
Mrs W McLeod-Gilford UK (*dec)
NGO and radiation researcher
Mr Mick Gilford, UK
MA, PhD (Cantab), mathematician
Dr. Valery Naidich, Russsia
radiobiologist (Institute for Biochemical Physics, Russian Academy of
Science, Moscow)
Prof W Nesterenko, Belarus
Physicist, radiation scientist, contamination measurements (*Dec)
Prof Alexey Nesterenko, Belarus
Physicist, radiation researcher, contamination measurements
Captain Alexander Nikitin, Russia
radiologist (“Bellona”, St Petersburg, Russia)
Mr VT Padmanabhan, India
BSc, MSc, geneticist, radiation epidemiologist
Dr Sebastian Pflugbeil , Ger
PhD, physicist, radiation scientist (Society for Radiation Protection, Berlin).
Mr Alasdair Phillips, UK
BSc, Non ionising radiation scientist, cancer epidemiologist
Dr Marvin Resnikoff, USA
Health physicist, radiation researcher
Ms Ditta Rietuma, Sweden
MSc, BA, gender economist
Prof Shoji Sawada, Japan
DSc, particle physicist, radiation researcher, Nagoya University
Prof Hagen Scherb, Germany
Physicist, radiation researcher, epidemiologist
Prof Inge Schmitz-Feuerhake, Germany

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ECRR 2010

Prof Dr rer nat, physicist, radiation scientist, University of Bremen
Prof Albrecht Schott, Germany
Prof, Dr., chemist, radiation researcher
Dr Klaus Seelig, Germany
Dr MD, physician, radiation researcher,
Dr. Galina Sergeeva, Russia
cytogenetics (Russian Scientific Centre for Radiology, Moscow)
Prof. Janette Sherman-Navinger, USA
Physician, toxicologist (Environmental Research Center at Western Michigan
University,)
Ms G Soderstrom G, Fin
BA, NGOProf Ernest Sternglass, USA
Emeritus Prof., PhD, radiation researcher
Prof Alice Stewart, UK
Prof., MD, PhD , epidemiologist (*Dec)
Dr. Andrey Talevlin, Russia
environmental lawyer (Chelyabinsk State University)
Dr. Alexey Toropov, Russia
ecologist (Siberian Ecological Agency, Tomsk)
Mr E Weigelt, Ger.
Dip. Sci, radiation and health researcher
Dr Ian Welsh UK
PhD, risk sociologist
Mr Dai Williams UK
MA psychologist and Uranium weapons researcher
Prof Alexey K Yablokov, Russia
PhD, zoologist ecologist and radiation researcher (Russian Academy of
Sciences)187

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ECRR
2010 Recommendations of the European Committee on Radiation Risk
The Health Effects of Ionising Radiation Exposure at Low Doses for
Radiation Protection Purposes. Regulators' Edition.
Executive Summary
This report updates the model presented by the Committee in 2003. It outlines
the Committee’s findings regarding the effects on human health of exposure toionising radiation and presents a new model for assessing these risks. It is
intended for decision-makers and others who are interested in this area andaims to provide a concise description of the model developed by the Committee
and the evidence on which it depends. The development of the model begins
with an analysis of the present risk model of the International Commission on
Radiological Protection (ICRP) which is the basis of and dominates all present
radiation risk legislation. The Committee regards this ICRP model as
essentially flawed as regards its application to exposure to internal
radioisotopes but for pragmatic reasons to do with the existence of historicalexposure data has agreed to adjust for the errors in the ICRP model by defining
isotope and exposure specific weighting factors for internal exposures so thatthe calculation of effective dose (in Sieverts) remains. Thus, with the new
system, the overall risk factors for fatal cancer published by ICRP and otherrisk agencies may be used largely unchanged and legislation based upon these
may also be used unchanged. It is the calculation of the dose which is alteredby the Committee's model.
1. The European Committee on Radiation Risk arose out of criticisms of therisk models of the ICRP which were explicitly identified at the European
Parliament STOA workshop in February 1998; subsequently it was agreed
that an alternative view should be sought regarding the health effects oflow level radiation. The Committee consists of scientists and risk
specialists from within Europe but takes evidence and advice fromscientists and experts based in other countries.
2. The report begins by identifying the existence of a dissonance between therisk models of the ICRP and epidemiological evidence of increased risk of
illness, particularly cancer and leukaemia, in populations exposed tointernal radioactive isotopes from anthropogenic sources. The Committee
addresses the basis in scientific philosophy of the ICRP risk model asapplied to such risks and concludes that ICRP models have not arisen outof accepted scientific method. Specifically, ICRP has applied the results ofexternal acute radiation exposure to internal chronic exposures from point
sources and has relied mainly on physical models for radiation action to
support this. However, these are averaging models and cannot apply to the239

ECRR 2010probabilistic exposures which occur at the cell level. A cell is either hit or
not hit; minimum impact is that of a hit and impact increases in multiplesof this minimum impact, spread over time. Thus the Committee concludes
that the epidemiological evidence of internal exposures must takeprecedence over mechanistic theory-based models in assessing radiation
risk from internal sources.
3. The Committee examines the ethical basis of principles implicit in the
ICRP models and hence in legislation based on them. The Committee
concludes that the ICRP justifications are based on outmoded philosophicalreasoning, specifically the averaging cost-benefit calculations ofutilitarianism. Utilitarianism has long been discarded as a foundation forethical justification of practice owing to its inability to distinguish between
just and unjust societies and conditions. It may, for example, be used tounderpin a slave society, since it is only overall benefit which is calculated,and not individual benefit. The Committee suggests that rights-based
philosophies such as Rawls's Theory of Justice or considerations based on
the UN Declaration of Human Rights should be applied to the question of
avoidable radiation exposures to members of the public resulting frompractice. The Committee concludes that releases of radioactivity without
consent can not be justified ethically since the smallest dose has a finite, if
small, probability of fatal harm. In the event that such exposures are
permitted, the Committee emphasises that the calculation of ‘collective
dose’ should be employed for all practices and time scales of interest sothat overall harm may be integrated over the populations.
4. The Committee believes that it is not possible accurately to determine‘radiation dose to populations’ owing to the problems of averaging over
exposure types, cells and individuals and that each exposure should be
addressed in terms of its effects at the cell or molecular level. However, inpractice this is not possible and so the Committee has developed a model
which extends that of the ICRP by the inclusion of two new weighting
factors in the calculation of effective dose. These are biological andbiophysical weighting factors and they address the problem of ionisation
density or fractionation in time and space at the cell level arising frominternal point sources. In effect, they are extensions of the ICRP’s radiation
weighting factors employed to adjust for differences in ionisation density
resulting from different quality radiations (e.g. alpha-, beta and gamma).
5. The Committee reviews sources of radiation exposure and recommends
caution in attempting to gauge the effects of novel exposures bycomparison with exposures to natural radiation. Novel exposures include
internal exposures to artificial isotopes like Strontium-90 and Plutonium239 but also include micrometer range aggregates of isotopes (hot240

ECRR 2010

particles) which may consist of entirely man-made isotopes (e.g.
Plutonium) or altered forms of natural isotopes (e.g. depleted Uranium).
Such comparisons are presently made on the basis of the ICRP concept of‘absorbed dose’ which does not accurately assess the consequence for harmat the cell level. Comparisons between external and internal radiation
exposures may also result in underestimates of risk since the effects at thecell level may be quantitatively very different.
6. The Committee argues that recent discoveries in biology, genetics andcancer research suggest that the ICRP target model of cellular DNA is not agood basis for the analysis of risk and that such physical models ofradiation action cannot take precedence over epidemiological studies of
exposed populations. Recent results suggest that very little is known about
the mechanisms leading from cell impact to clinical disease. The
Committee reviews the basis of epidemiological studies of exposure andpoints out that many examples of clear evidence of harm following
exposure have been discounted by ICRP on the basis of invalid physicalmodels of radiation action. The Committee reinstates such studies as abasis for its estimates of radiation risk. Thus the 300-fold discrepancy
between the ICRP model's predictions and the observed cases in the
Sellafield childhood leukemia cluster becomes an estimator of risk forchildhood leukemia following such exposure. The factor is thus
incorporated by the Committee into the calculation of harm from internal
exposure of specific types through its inclusion in the weighting factors
used to calculate the ‘effective dose’ to the children in Sieverts.
7. The Committee reviews the models of radiation action at the cell level andconclude that the ‘linear no threshold’ model of the ICRP is unlikely torepresent the response of the organism to increasing exposure except forexternal irradiation and for certain end points in the moderately high dose
region. Extrapolations from the Hiroshima lifespan studies can only reflectrisk for similar exposures i.e. high dose acute exposures. For low-dose
exposures the Committee concludes, from a review of published work, that
health effects relative to the radiation dose are proportionately higher at
low doses and that there may be a biphasic dose response from many ofthese exposures owing to inducible cell repair and the existence of highsensitivity phase (replicating) cells. Such dose-response relationships may
confound the assessment of epidemiological data and the Committee points
out that the lack of a linear response in the results of epidemiologicalstudies should not be used as an argument against causation.
8. In further considering mechanisms of harm, the Committee concludes that
the ICRP model of radiation risk and its averaging methods exclude effects
which result from anisotropy of dose both in space and in time. Thus the241

ECRR 2010

ICRP model ignores both high doses to local tissue caused by internal hot
particles, and sequential hits to cells causing replication induction andinterception (second event), and merely averages all these high risk
situations over large tissue mass. For these reasons, the Committee
concludes that the unadjusted ‘absorbed dose’ used by ICRP as a basis ofrisk calculations is flawed, and has replaced it with an adjusted ‘absorbed
dose’ which uses enhancement weightings based on the biophysical andbiological aspects of the specific exposure. In addition, the Committee
draws attention to risks from transmutation from certain elements, notably
Carbon-14 and Tritium, and has weighted such exposures accordingly.
Weightings are also given to radioactive versions of elements which have aparticular biochemical affinity for DNA e.g. Strontium and Barium andcertain Auger emitters.
9. The Committee reviews the evidence which links radiation exposure toillness on the basis that similar exposures define the risks of such
exposures. Thus the Committee considers all the reports of associations
between exposure and ill health, from the A-bomb studies to weapons
fallout exposures, through nuclear site downwinders, nuclear workers,
reprocessing plants, natural background studies and nuclear accidents. The
Committee draw particular attention to two recent sets of exposure studies
which show unequivocal evidence of harm from internal irradiation at low
dose. These are the studies of infant leukemia following Chernobyl, and theobservation of increased minisatellite DNA mutations following
Chernobyl. Both of these sets of studies falsify the ICRP risk models byfactors of between 100 and 1000. The Committee uses evidence of risk
from exposures to internal and external radiation to set the weightings forthe calculation of dose in a model which may be applied across all
exposure types to estimate health outcomes. Unlike the ICRP theCommittee extends the analysis from fatal cancer to infant mortality andother causes of ill health including non-specific general health detriment.
10. The Committee concludes that the present cancer epidemic is aconsequence of exposures to global atmospheric weapons fallout in the
period 1959-63 and that more recent releases of radioisotopes to theenvironment from the operation of the nuclear fuel cycle will result insignificant increases in cancer and other types of ill health.
11. Using both the ECRR's new model and that of the ICRP the Committee
calculates the total number of deaths resulting from the nuclear projectsince 1945. The ICRP calculation, based on figures for doses topopulations up to 1989 given by the United Nations, results in 1,173,600
deaths from cancer. The ECRR model predicts 61,600,000 deaths fromcancer, 1,600,000 infant deaths and 1,900,000 foetal deaths. In addition,

242

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the ECRR predicts a 10% loss of life quality integrated over all diseases
and conditions in those who were exposed over the period of global
weapons fallout.
12. The Committee refers to new research which demonstrates enhanced
radiation hazards from internalized elements of high atomic number
through enhanced absorption of natural background electromagnetic
radiation and its conversion into photoelectrons. The Committee identifies
this effect as a major cause of the health effects of exposure to the element
Uranium and creates a weighting factor for such exposures. The Committee
discusses the effects of Uranium weapons on populations exposed to
Uranium fallout and asserts that the anomalous health effects observed
following Uranium exposures are mechanistically explained by suchprocesses.
13. The Committee notes that since the publication of its 2003 model there
have been epidemiological observations that support the model’s
predictions, namely Chernobyl effects in Belarus reported by Okeanov
2004 and Chernobyl effects in Sweden reported by Tondel et al 2004.
14. The Committee lists its recommendations. The total maximum permissible
dose to members of the public arising from all human practices should not
be more than 0.1mSv, with a value of 2mSv for nuclear workers. This
would severely curtail the operation of nuclear power stations andreprocessing plants, and this reflects the Committee’s belief that nuclear
power is a costly way of producing energy when human health deficits areincluded in the overall assessment. All new practices must be justified insuch a way that the rights of all individuals are considered. Radiation
exposures must be kept as low as reasonably achievable using best
available technology. Finally, the environmental consequences ofradioactive discharges must be assessed in relation to the total
environment, including both direct and indirect effects on all living
systems.

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Annex A
Dose coefficients for the main isotopes of radiological interest
The rules for calculating effective doses have been described in Chapter 6. For
the main isotopes of radiological interest, dose coefficients have been
calculated by the Committee using these rules and assumptions. Table A1 gives
dose coefficients for low-dose exposure through ingestion and inhalation. In
general, for these isotopes, the effective dose E to an individual in age group a
may be calculated according to the equation:
E total = E external +  I k(a) I, ingest I I,ingest +  I k(a) I, inhale I I, inhale. . . . . . .(1)

Table A1 Dose coefficients of various isotopes for low-dose exposure
following ingestion and inhalation.

aIsotope (form)

Half lifeaH-3 (HTO)
H-3 (CHT)
C-14
S-35 (inorganic)
S-35 (NS, CS etc)
Co-60
Sr-89
Sr-90/Y-90
Zr-95/Nb-95
Mo-99
Tc-99m
Tc-99
Ru-106
Ru-106 particle
Te-132/ I-132
I-131
Cs-134
Cs-137
Ba-140/La-140
Pb-210Bi-210Po-210Ra-226 ingestion
U-238 inhalation
U-238 particle
U-238 ingestion
Pu-239Pu-239 particle
Am-241

12.3y
12.3y
5.7 E+3y
87.4d
87.4d
5.27y
50.5d
29.1y/2.67d
64.0d/35.0d
2.75d
6.02h
2.13 E+5y
1.01y
1.01y
3.26d/2.3h
8.04d
2.06y
30.0y
12.7d/40h
22.3y
5.01d
138d
1.6 E+3y
4.5 E+9
4.5 E+9
4.5 E+92.41 E+4
2.41 E+4
4.32 E+2

1.0 E-9
5.0 E-9
1.5 E-8
5.0 E-10
5.0 E-9
1.75 E-7
1.3 E-7
4.5 E-5
2.4 E-7
1.5 E-8
5.5 E-10
1.6 E-8
3.5 E-9
1.7 E-6
5.5 E-6
5.5 E-7
1.0 E-7
3.2 E-7
3.9 E-6
3.5 E-6
6.5 E-9
6.0 E-6
1.4 E-5
2.5 E-3
2.5 E-2
2.5E-4
1.0 E-5
3.0 E-4
1.0 E-6

coefficients to foetus multiply by 10244

k(0-1) Sv/Bqk(1-14)Sv/Bq
4.0 E-10
2.0 E-9
5.8 E-9
2.0 E-10
2.0 E-9
7.0 E-8
5.2 E-8
1.8 E-5
9.5 E-8
6.0 E-9
2.2 E-10
6.4 E-9
1.4 E-8
7.0 E-7
2.2 E-6
2.2 E-7
4.0 E-8
1.3 E-7
1.6 E-6
1.4 E-6
2.6 E-9
2.4 E-6
5.6 E-6
1.2 E-3
1.2 E-2
1.2E-4
5.0 E-6
1.5 E-4
4.0 E-7k(adult) Sv/Bq
2.0 E-10
1.0 E-9
2.9 E-9
1.0 E-10
1.0 E-9
3.5 E-8
2.6 E-8
9.0 E-6
4.7 E-8
3.0 E-9
1.1 E-10
3.2 E-9
7.0 E-9
3.5 E-7
1.1 E-6
1.1 E-7
2.0 E-8
6.5 E-8
7.8 E-7
7.0 E-7
1.3 E-9
1.2 E-6
2.8 E-6
8.4 E-4
8.4 E-3
8.4E-5
2.5 E-6
7.5 E-5
2.0 E-7

ECRR 2010

In the expression for total dose, E external is the external dose, calculated
according to the rules in Chapter 6. Internal doses are obtained by summationof the isotopic contributions from inhalation and ingestion using dosecoefficients k(a) I, ingest and k(a) I, inhale given in Table A1 for different age groups(a).
The Committee will publish a complete list of dose coefficients for all
isotopes of radiological interest.

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ECRR 2010

Appendix

ECRR - CERI
European Committee on Radiation Risk
Comité Européenne sur le Risque de l'Irradiation
The Lesvos Declaration
6th May 2009
A. Whereas, the International Commission on Radiological Protection (ICRP)
has promulgated certain risk coefficients for ionizing radiation exposure,
B. Whereas, the ICRP radiation risk coefficients are used worldwide by federal
and state governmental bodies to promulgate radiation protection laws andstandards for exposure to workers and the general public from waste disposal,
nuclear weapons, management of contaminated land and materials, naturally
occurring and technologically enhanced radioactive materials (NORM and
TENORM), nuclear power plant and all stages of the nuclear fuel cycle,
compensation and rehabilitation schemes, etc,
C. Whereas, the Chernobyl accident has provided the most important andindispensable opportunity to discover the yields of serious ill health following
exposure to fission products and has demonstrated the inadequacy of thecurrent ICRP risk model, especially as applied to foetal and early childhood
exposures to radiation,
D. Whereas, by common consent the ICRP risk model cannot validly beapplied to post-accident exposures, nor to incorporated radioactive material
resulting in internal exposure,
E. Whereas, the ICRP risk model was developed before the discovery of the
DNA structure and the discovery that certain radionuclides have chemicalaffinities for DNA, so that the concept of absorbed dose as used by ICRP
cannot account for the effects of exposure to these radionuclides,
F. Whereas, the ICRP has not taken into consideration new discoveries of nontargeted effects such as genomic instability and bystander or secondary effects
with regard to understanding radiation risk and particularly the spectrum ofconsequent illnesses,

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ECRR 2010

G. Whereas, the non-cancer effects of radiation exposure may make it
impossible to accurately determine the levels of cancer consequent upon
exposure, because of confounding causes of death,
H. Whereas, the ICRP considers the status of its reports to be purely advisory,
I. Whereas, there is an immediate, urgent and continuing requirement for
appropriate regulation of existing situations involving radioactivity, to protect
the human population and the biosphere,
We the undersigned, acting in our individual capacities
1. assert that the ICRP risk coefficients are out of date and that use of thesecoefficients leads to radiation risks being significantly underestimated,
2. assert that employing the ICRP risk model to predict the health effects ofradiation leads to errors which are at minimum 10 fold while we are aware ofstudies relating to certain types of exposure that suggest that the error is evengreater,
3. assert that the yield of non-cancer illnesses from radiation exposure, inparticular damage to the cardio-vascular, immune, central nervous andreproductive systems, is significant but as yet unquantified,
4. urge the responsible authorities, as well as all of those responsible forcausing radiation exposures, to rely no longer upon the existing ICRP model indetermining radiation protection standards and managing risks,
5. urge the responsible authorities and all those responsible for causing
exposures, to adopt a generally precautionary approach, and in the absence ofanother workable and sufficiently precautionary risk model, to apply without
undue delay the provisional ECRR 2003 risk model, which more accurately
bounds the risks reflected by current observations,
6. demand immediate research into the health effects of incorporated
radionuclides, particularly by revisiting the many historical epidemiologicalstudies of exposed populations, including re-examination of the data fromJapanese A-bomb survivors, Chernobyl and other affected territories andindependent monitoring of incorporated radioactive substances in exposed
populations,
7. consider it to be a human right for individuals to know the level of radiation
to which they are exposed, and also to be correctly informed as to the potential
consequences of that exposure,247

ECRR 2010

8. are concerned by the escalating use of radiation for medical investigationand other general applications,9. urge significant publicly funded research into medical techniques which do
not involve radiation exposures to patients.
Statements contained herein reflect the opinions of the undersigned and are notmeant to reflect the positions of any institution to which we are affiliated.
Professor Yuri Bandazhevski (Belarus)
Professor Carmel Mothersill (Canada)
Dr Christos Matsoukas (Greece)
Professor Chris Busby (UK)
Professor Roza Goncharova (Belarus)
Professor Alexey Yablokov (Russian Federation)
Professor Mikhail Malko (Belarus)
Professor Shoji Sawada (Japan)
Professor Daniil Gluzman (Ukraine)
Professor Angelina Nyagu (Ukraine)
Professor Hagen Scherb (Germany)
Professor Alexey Nesterenko (Belarus)
Dr Sebastian Pflugbeil (Germany)
Professor Michel Fernex (France)
Dr Alfred Koerblein (Germany)
Professor Inge Schmitz Feuerhake (Germany)
Molyvos, Lesvos, Greece

248

The first report of the European Committee on Radiation Risk was
published in 2003. It presented a rational model for calculating thehealth risks of exposure to ionizing radiation. Unlike the then-current
framework of modelling radiation-risk, based on the effects of theexternal acute exposures of the US Atomic Bombs on the Japanese, the
ECRR model employed evidence from those exposed to internal
radioactivity. The publication made a significant impact on the radiation
risk assessment landscape, has been reprinted three times and translated
into Japanese, French, Spanish and Russian.
Since then a large amount of new data has emerged in thisimportant area both from epidemiology and from radiobiology. A verylarge number of peer-reviewed reports and published studies, from
Chernobyl effects in Sweden to cancer and Uranium related congenital
disease in Iraq, confirm the accuracy of the Committee’s 2003 radiation
risk model for explaining and predicting the health effects of human
exposure to internal radionuclides. As well as confirming the broad
accuracy of the ECRR approach, the new evidence has required somemodification to the model, in particular the inclusion of discoveries in
the area of Uranium and high-Z element secondary photoelectron risks.
The developments since 2003 have been incorporated into an expanded
and largely re-written presentation of the ECRR’s radiation risk model.
There is increasing concern over the embarrassing dissonancebetween the conventional modelling of health outcomes of radioactive
releases to the environment and the observations. In this volume, theCommittee explains how the current physics-based risk model came tobe universally used, and points out its scientific and politicalshortcomings. In addition, the Committee addresses the ethical basis ofreleasing radioactive materials to the environment.
The volume is essential reading for anyone involved inlegislation in this area and should also be of interest to members of the
public who need to estimate the effects of nuclear discharges.
Price: £75.00
MELODI WORKSHOP PARIS OCT 2010
DIGITAL COMPLIMENTARY EDITION

Donated through the generosity of the International Foundation for
Research on Radioactivity Risk, Stockholm, Sweden.

ISBN: 978-1-897761-16-8