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Health consequences of exposures of British

personnel to radioactivity whilst serving in areas
where atomic bomb tests were conducted

Composite report for the Royal British Legion, the RAFA and
Rosenblatt’s Solicitors in response to Tribunals Service
Directions Issued 23 July 2010
in respect of 16 named appellants

Chris Busby PhD

Castle Cottage, Sea View Place
Aberystwyth SY23 1DZ U.K

Part 1

1.1 Scope

I have been asked by the Royal British Legion, the RAFA and Rosenblatt’s Solicitors
to give my expert opinion on the health consequences of having been exposed to
ionising radiation either through participation in the British atmospheric nuclear tests
1952-1958 or having remained for any length of time in areas where such tests were
carried out e.g. between tests or cleaning up after tests. I have been asked to provide a
generic report on this issue and also to consider individually 16 cases whose exposure
history and diseases are all different. Some of these individuals I have already assisted
with reports in their own cases. I have had little notice to carry out this task but
happily I had already spent a significant time on the issue as an expert retained by
Rosenblatts in the Royal Courts of Justice collective action and the generic report I
present here will be an updated version of the report I produced for that case in 2008.
This is a complex issue involving many different areas of knowledge, all of
which I have made myself familiar with in the last 15 years, and since there is some
question of my expertise in the area of ionising radiation and health, which is the field
of this report, I will address this issue of my filed of expertise at some length
separately in Appendix 2. I shall also respond in this appendix to the report written
about me and my evidence by Mr Ron Brown of the Ministry of Defence.
I will begin by laying out the sequence in which I will address the questions.

Part 1 Introduction; my expertise
I briefly review my expertise which I further address in the Appendix.

Part 2 Ionising radiation and health
The science of radiation and health has developed in the radiation century: the last
100 years. It is an intensely politicised area in science owing to its connection with
the military need to develop weapons and the huge financial civil investments in
nuclear energy. Nevertheless, at every stage, new evidence has continuously brought
about reassessments in the levels of radiation exposure believed to carry significant
harm. This continues to be the case in 2010. Radiation risk is a complex issue which
requires a certain amount of basic scientific knowledge to understand and to follow
the arguments. It is an area which has been characterised by considerable scientific
debate and one where revolutionary new evidence on the mechanisms of radiation
action has emerged in the last fifteen years. I shall therefore begin by outlining the
science underlying radiation risk, its history, and an account of recent discoveries in
this area which are relevant to the issue of the test veterans. I will review the current
debate on the issue of the health effects of low dose exposure to internal radionuclides
and explain how it affects the argument about health in the veterans and their

Part 3 The exposures of the veterans
Next I will turn to the question of whether the level of radiation to which these
personnel were exposed to both (a) during and (b) after or between the tests is likely
to have caused adverse harm to the health of the individual immediately or in the long
term and if such harm may be heritable and show itself in the individuals descendants.
I will explain the mechanisms by which radiation exposures cause harm to health in
those exposed to the gamma rays from the detonations, from the fission-products and
uranium contamination. I will address effects occurring in their descendants.
In order to do this, I begin by looking closely at what preliminary evidence I have
available to determine what the levels of and routes of radionuclide exposure really
were in the test areas where these veterans worked and lived. I will show that some
serious errors were made in the assessment of contamination levels. For example, no
measurements were made, or risks assumed for inhalation or inadvertent ingestion of
the alpha-emitting uranium isotopes, U-238, U-235 and particularly U-234 which
were by far the main component in terms of long lived radiological contamination
hazard and indeed of the composition of the devices in terms of mass. This is also true
of plutonium-239, another massive component of several of these devices. I will
calculate the veterans’ radiation doses from levels of radiation and radionuclide
contamination measured at the various sites, using scientifically acceptable
assumptions based upon standard methodology. I will apply these doses to the
veterans and compare them with natural background radiation in the UK. I will
discuss the likely health outcomes of the exposures which I calculate. I will also
employ the risk model of the European Committee on Radiation Risk.

Part 4 The defence
I will then review the arguments advanced by the military that the veterans could not
have received radiation doses which could have led to any ill health. I will show that
these arguments are false since they are based upon external gamma doses registered
on film badges in only a proportion of the veterans and based upon measurements
made with inadequately sensitive instrumentation often within a regime of
measurement which was demonstrably incapable of determining anything but
enormous levels of radioactive contamination. I will show that the radiation limits at
the time were very high and that no proper precautions were (or could be) taken to
prevent inhalation exposures. I will show that the hazard from uranium and plutonium
was not realised and that uranium and plutonium were not even measured and that
later ad hoc justifications for earlier behaviour were based upon false assumptions.

Part 5 The epidemiology
I will briefly discuss the evidence which exists relating to the issue of whether the
veterans suffered harm. This includes epidemiological case control studies of the
veterans carried out by the National Radiological Protection Board and others in
collaborations with the Ministry of Defence. I will show how they may be considered
to be unsafe as evidence. I will also look at other evidence, the studies of Rabbitt Roff
and Urquhart, and the chromosome test results of Rowlands on the New Zealand
veterans. I will also briefly present the results of my own case control study into the
health of the children and grandchildren of members of the British Nuclear Test
Veterans Association and argue that all these results show the existence of real
genetic damage effects.

Part 6 The Cold War Race
Although strictly unnecessary for the purpose of addressing the issues of causality, I
feel that it would be valuable to the court to put the issue in a historical context, in
order to assist in the interpretation of the sequences of events that lead to the mistakes
which I have argued resulted in the exposures and subsequent illnesses of the veterans
(and others). I will argue that the British operation was thrown together in a hurry,
with every system stretched to the uttermost limit, with inadequate and insufficient
scientific and technical support and instrumentation, operating in a fog of ignorance,
working on the other side of the world, through bravado and guesswork to desperately
impress the USA in an attempt to regain a seat at the high table of international
affairs. I will argue that the dependence of the military on the ICRP safe levels was
unquestioning and occurred and persisted at a time which several books and scientific
papers had been published showing radiation to be far more dangerous in the long
term due to its genetic effects. I will argue that the duty of care required that the
military should have sought to establish independently if this advice were good. I will
argue that the ICRP itself was constrained in its ability to set levels of exposure low
enough protect since it was influenced by the need to develop bombs. I will draw
attention to the bullying tactics of those commanding the test project to marginalise
concerns about health, raised by some individuals and organisations from time to
The test veterans, their children and grandchildren, and countless others on the planet,
exposed to fission-product fallout and uranium were the victims of this stupidity.

Part 7 Individual Cases

Reference ENT Name Represented by
00328/2010 L Abdale RBL
00176/2010 D Battersby RBL
00129/2010 D Beeton RBL
00078/2010 T Butler RBL
00723/2010 D Hatton RBL
00065/2010 Dr NC Hughes/
D Hughes
00279/2010 B Lovatt RBL
00039/2008 Mrs D Pritchard RBL
00658/2008 Mrs L Selby RBL
00054/2010 Denis Shaw RBL
00006/2010 N Simons RBL
00751/2007 H Sinfield Rosenblatts
00680/2008 and
Mr B Smith dec.
Mrs A Smith
00912/2009 D Taylor RAFA
00285/2009 Mrs W Triggs RBL
00768/2008 Mrs M Williams RBL

1.2 My expertise

I have a First Class Honours Special degree in Chemistry from the University of
London and also hold a Doctorate in Chemical Physics from the University of Kent. I
was elected to the Royal Society for Chemistry in 1974 and I am presently a Member
of the International Society for Environmental Epidemiology and the Ukraine
Committee Physicians of Chernobyl. I am a scientific reviewer for The Lancet and
The European Journal of Cancer, The Journal of Paediatric Radiology and the
European Journal of Biology and Bioelectromagnetics and Science and Public Policy
I have studied the health effects of low dose radiation for more than 15 years
and conducted research both at the fundamental cell biology level, theoretically and as
a radiation epidemiologist. I have been a member of two UK government committees
on this issue (Committee Examining Radiation Risks for Internal Emitters, CERRIE,
and the Ministry of Defence Depleted Uranium Oversight Board). I also have
officially advised British Government and other expert or investigative committees
e.g. The Committee on Radioactive Waste Management (CORWM), the US
Congressional Committee on Veterans Affairs and Security, The Royal Society, The
House of Commons Enquiry into the health of A-Bomb veterans and the European
Parliament. I am an official expert witness for the Canadian Parliament on the health
effects of Uranium. I was until 2007 a fellow of the University of Liverpool in the
Faculty of Medicine and I am currently Visiting Professor Department of Molecular
Biosciences in the University of Ulster in Northern Ireland where I am supervising
research on uranium photoelectron enhancement effects. I am also Guest Researcher
at the Julius Kuhn Institute of the German Federal Agricultural Laboratories (FAL) in
Brunswick near Hanover where I am examining the health effects of uranium
exposure. I am Scientific Secretary of the European Committee on Radiation Risk
(ECRR) based in Brussels (Comite Europeen Sur Le Risque de l'Irradiation (CERI) )
and senior editor of its report ECRR2003 Recommendations of the European
Committee on Radiation Risk: The Health Effects of Ionising Radiation Exposure at
Low Doses for Radiation Protection Purposes. This report has now been translated
into French, Russian, Japanese and Spanish and has been used for radiation protection
purpose scoping by many organisations including most recently (2006) the UK
Committee on Radioactive Waste Management (CORWM). I also edited the latest
ECRR report (ECRR2010). I was invited by the nuclear industry in the UK (CIRIA)
to provide advice for best practice in the remediation of contaminated land based on
the ECRR risk model. I was, between 2003 and 2006 Science Policy Interface Group
Leader of the EU Policy Information Network for Child Health and Environment
PINCHE and also the senior rapporteur on both Ionising Radiation and ultraviolet
solar radiation effects on children’s health. My current CV is attached as Appendix 1.
I have acted as an expert witness in over 40 court cases in the UK and the USA on the
issue of radiation and health
My particular area of expertise is the health effects of internally deposited
radionuclides. I have made fundamental contributions to the science of radiation and
health in this area and have published many articles and reports on this issue.
My researches have led me to the conclusion that the health consequences of
exposure to internally deposited radionuclides cannot be either scientifically or
empirically assessed using the averaging methods currently employed by risk
agencies (ICRP, NCRP) based on the Japanese A-Bomb studies and other external
high dose exposures. The radionuclide dose coefficients published by the ICRP and
employed in calculations made by these organisations are unsound since they depend
on inappropriate averaging of energy in tissue, as I shall elaborate. This is actually
common sense; and it is increasingly seen to be so by many official radiation risk
agencies and committees (e.g. IRSN 2005, CERRIE 2004a, CERRIE 2004b), yet the
historic weight of the conventional approach to radiation risk (with whole
organisational and bureaucratic structures committed to the simplistic historic
approaches) has prevented any change in policy in this area. Such an official
acceptance of the scientific illegitimacy of the current radiation risk model for internal
radiation exposures would have far reaching and financially costly policy
implications. Nevertheless, the present radiation risk model can be used as a baseline
for predicting the minimum level of ill health that is likely to result from external
radiation exposures. In my expert opinion, and for reasons which I shall give,
dosimetric analyses and risk calculation based on the current ICRP risk model will
give reasonable correct results for external irradiation, but will significantly
underestimate the additional risks from internal, inhaled or ingested radioactive

Part 2

Ionising radiation and health

2.1 Early history.
I will condense much of the historical evidence from my book Wings of Death 1995.
In 1895 Wilhelm Roentgen discovered X-rays: whilst experimenting with the passage
of electricity through an evacuated glass tube, he noticed that a phosphorescent screen
elsewhere in the laboratory glowed as some invisible energy was created. He later
took X-ray pictures of his wife's hand, which showed the bones and the wedding ring
clearly. This was the first use of X-rays to image bones, and the medical uses of the
discovery expanded from this point to include both investigation and treatment of a
huge range of conditions. It soon emerged that the invisible rays were harmful. By
1900 over 20 cases of X-ray injury had been documented in scientific journals, and in
1904, Edison's assistant, who had been seriously irradiated whilst helping to develop a
new X-ray lamp, died of cancer. Both hands had become malignant and both arms
had been amputated. In 1908, members of the American Roentgen Ray Society were
to hear a presentation describing more than 50 cases of `radiation poisoning'. From
the beginning attempts were made to minimize or dismiss risks. For example, Dr
Mihran Kasabian campaigned against the use of the word `burn' to describe the effects
of over-exposure on the basis of the emotional connotations. He died of cancer in
Shortly after Roentgen's discoveries, Henri Bequerel discovered that uranium
ores also gave off similar invisible radiations and the natural radioactive elements
from which these radiations were originating were separated, identified and
researched in the following twenty years. Researchers who worked with these
substances were to pay the price: the most famous of these, Marie Curie, died of
leukaemia in 1934 with both hands destroyed. But by 1920 deaths from cancers and
leukemias amongst the radiation researchers made protection guidance necessary and
1927 the International Congress of Radiology, a consortium of national groups of
users adopted some guidelines at a meeting in Stockholm. These were, however,
relatively arbitrary, and did not relate to the most important question, both then and
now: how much radiation is dangerous?

2.2 The development of dose limits.
The earliest methods of measuring biological effects were extreme: one indication
was hair falling out as an indication of excessive dose. A more usual objective
indicator was the Erythemal (or skin burn) Dose (ED), the amount of radiation which
caused reddening of the skin. This was a very crude measure and the amount of
radiation needed to have this effect varied over a range of 1000 for different
individuals and different dose regimes: these were primitive concepts of dose
(Eisenbud and Gesell 1997). Although this system of measurement remains in the
present assessment of skin cancer risk following exposure to ultraviolet radiation,
ionising radiation is vastly more energetic and penetrating and causes effects deep
within tissues.
Such crude immediate biological effects as skin inflammation occurred at
radiation levels now known to be enormously greater than those which induce cancer,
yet the safety dose limit suggested in 1924 by X-ray manufacturer Arthur Mutscheller
in a paper to the American Roentgen Ray Society was 1/100th of the ED per month,
or 1/10th per year. The following year Rolf Sievert of Sweden, made the fundamental
move that has influenced the perception of radiation hazard ever since when he
suggested tying the safe dose to Natural Background Radiation (NBR). He had
established that people were exposed externally to an annual dose of about one
thousandth to one ten-thousandth of the ED from naturally occurring ionizing
radiation. He decided arbitrarily that humans could tolerate 1/10th of this erythemal
dose per year without harm, i.e. one hundred to one thousand times the natural
exposure. This figure was close to Mutscheller's. A few years later, two British
physicists, Barclay and Cox, published a study of some individuals who had worked
with radiation for six years without visible effect: they divided the estimated exposure
by a safety factor of 25 to obtain a figure of .08ED per year.
The similarity in these three numbers, though fortuitous, gave some spurious
scientific validity to the choice of the first radiation protection standard; yet at least
these choices were based upon comparison of gross illness in humans with prior
radiation exposure. At this time, the later concept of Absorbed Dose had not been
developed; health risks were described in terms of exposures measured in terms of
ionization of air. And what they did not anticipate, and could not consider, was the
very long development period for the cancers which later became associated with
radiation exposures. The only logical underpinning of the first dose limit was Sievert's
idea to tie exposure to natural radiation. This use of NBR as a measure of exposure
has continued to the present day. Scientifically, of course, it is only valid if the
exposures from natural radiation are the same in type, quality, and magnitude as those
under consideration. Owing to the physical methods which were developed to
measure radiation and the fact that these were devised by physicists, concentrating on
energy and energy transfer, the NBR yardstick approach was not, and is still not,
questioned. Indeed, the Ministry of Defence employ it in arguing that the absorbed
doses to the veterans are too small too cause harm. I will return to this argument.
During the first twenty years of the radiation age physical science developed
many methods for measuring radiation quantity. Until the 1920s radiation was
measured by measuring its ionisation, using an electroscope. It was only in the 1930s
when this crude method was refined by the development of the early Geiger counter, a
device which also measures ionisation but is more sensitive than the electroscope. All
of these devices gave results based on energy transfer. Energy, however, can be
transferred in a multitude of ways, and takes many forms; on its own, energy transfer
is a totally useless measure of quality of biological effect. For example, one cup of
boiling water at 100 degrees centigrade contains the same energy, the same number of
Joules, as a bucket of water at the temperature of twenty degrees. An energy transfer
to a person of one waterthrow unit could encompass either a cupful of boiling water in
the face or a bucket of water at room temperature: more information is needed before
the health consequence can be assessed. Another comparison which I often employ is
that of a person warming themselves by a fire, and then reaching into the fire and
swallowing a red hot coal: the same amount of energy is transferred. As I will show,
this issue is fundamental to the arguments about risk in the test veterans.
The energy transfer unit developed by the physicists was the Roentgen (R)
adopted by the International Congress on Radiology in 1928. The unit was defined as
the amount of radiation needed to produce a given number of ions in dry air in an
ionization chamber, a device for electrically evaluating such a process.
The necessary step was taken: erythemal dose ED was translated into
Roentgens on the basis of common observation in radiation laboratories. Although the
range in different individuals was great, an average of 600R was eventually agreed to
be the threshold ED (Failla 1932). 1/10th of this (the earlier ED defined limit) gave
6R per month as the recommended dose limit. In 1934 the US Committee on X-Ray
and Radium Protection arbitrarily divided this by two and rounded upwards to obtain
the first tolerance level for radiation exposure. This was 0.1R or in modern units
roughly 1mGy per day. One milliGray (mGy) is one thousandth of a Gray. One Gray
replaces the old Rad (Radiation Absorbed Dose). Rads, which were the units
employed at the time of the tests were taken to be approximately equal to 1 Roentgen
although strictly, a Roentgen is an ‘exposure’ and not a ‘dose’ and the conversion of
Roentgen to Rad depends upon the energy of the ionising radiation (which can vary
by a large amount). One Gray is 100 rads. It is the energy of 1 Joule absorbed by
1kilogram of tissue.
The 1934 decision of a limit of 0.1R per day is equivalent to an annual dose of
365mGy. These units have confused many who try to understand these issues, and I
briefly explain them and relate them to one another in Table 2.1. It should be noted
that 365mGy is approximately 180 times the annual natural background dose (about
2mSv, if we include radon) and so the idea that the limits were somehow tied to the
natural background was already questionable.

Table 2.1 The main radiation units explained and compared

Unit Written Definition and usage
Roentgen R Exposure: The quantity of radiation which causes a defined
number of ions in dry air
Rep R Radiation equivalent physical (93ergs/g or 0.0093J/kg) before
and almost equal to the rad below, no longer used but
sometimes encountered in early reports.
Rad R Absorbed dose (0.01J/kg). 1/100
Joule per kilogram
Rem R Absorbed Dose Equivalent. Developed to recognise the
greater biological effect of alpha particles and neutrons (for
alpha absorption e.g. radon gas, 1 rad = 20rem)
Gray Gy Absorbed Dose; Modern (Systeme Internationale SI ) unit. 1
Joule per kilogram = 100rad; natural background gamma
annual doses in UK is about 0.8mGy per year.
Sievert Sv Absorbed Dose Equivalent; Modern (SI) unit. 1 Sv = 100rem;
1 mSv = 100mrem or 0.1rem. Natural background in UK is
about 2mSv per year (200mrem) half of which is from radon
gas exposure for which the alpha multiplier of 20 is used.
Curie Ci Quantity of radioactive material in terms of radium. 1 Ci is a
very large amount of radioactivity. Although it is a mass, a
physical amount, radioactivity is described in terms of its
activity, not its weight, since you can have a large weight of
low activity (e.g. 350 tons of depleted uranium in Iraq) or a
small mass of higher specific activity (e.g. 1.5kg of plutonium
near Sellafield) which have the same radiation i.e. the same
number of decays or ability to cause damage and the same
activity in Curies.
Becquerel Bq Modern unit for quantity of radioactive material; in terms of
its activity 1 Bq is the amount of material giving 1decay per
second, a very small amount of radioactive material.
Milli m 1/1000
. 1 mSv is 1/1000
or 0.001Sievert.
1/millionth or 1 x 10
times the unit quantity

These 1934 standards were presented as being based on a scientifically backed,
reasonably precise understanding of the effects of ionizing radiation. They were, in
reality, guesses based on inadequate research of overt and gross effects and involved
total disregard of the increasing evidence for serious long-term mutation-related
problems like cancer. They were based on inadequate sampling, untested
assumptions, and on physical models for radiation which were, then as now, far too
crude to describe the biological effects of ionizing radiation. Even at the time, the
genetic effects of radiation had been reported in the scientific literature by many
researchers (e.g. Muller, 1929, 1930, Paterson 1932, Hanson 1928, see also Lea 1946
for further references).
Lauriston Taylor, Chairman of the Committee on X-ray and Radiation
Protection in 1933, later said of the work that the standards were based on. This work
was seriously flawed, and yet that is still the basis for our protection standard of
today. It really is. (Caufield, 1989: 21)
With the discovery of the neutron and its ability to penetrate the nucleus and
bring about nuclear transformations and new radioactive substances, new sources of
radiation were slowly appearing. By the late 1930s, with the discoveries by Fermi of
the nuclear transformations and then by Hahn and Meitner that Uranium could be
split, research had begun in earnest on atomic physics and the various transmutations
that would lead to runaway fission. World War 2 was midwife to this principle of
nuclear fission: completely novel substances appeared on earth for the first time in
evolution. These included strontium-90, caesium-137, iodine-131, plutonium-239 all
radioactive substances with chemical affinity for various living organelles.
At this time, the benchmarks for exposures were still 0.1R (1mGy) per day
from whole body external radiation and 0.1µCi (3.7kBq) as the maximum body
burden (MPBB) for Radium-226. This latter concept, MPBB had arisen out of the
discovery made in the late 1920s and forced by media attention and public alarm on
the scientific community, of the extreme dangers of exposures to the internal emitter
Radium-226, used to produce luminous dials. This story is instructive of the ways in
which science is forced by the media and the public to alter its position. For this
reason it is very relevant to this issue of internal radioactive exposures and the current
case of the A-Bomb veterans. I deal with it separately below.
Following the fissioning of uranium in an atomic pile by Fermi in Chicago, it
became clear that an atomic bomb could be made. Factories were enlarged to separate
U-235, the fissile isotope of natural uranium and the Manhattan Project was set up to
use this U-235 and make Plutonium for the bomb. This happened in secret and in near
total ignorance of the effect of plutonium and the other fission products on health.
Plutonium was known to be an alpha emitter so, for expediency, the standards for
Radium were extended to Plutonium, modified by animal experiments comparing the
effects of the two substances. These safety standards were unlikely to reflect the
long-term reality but they did have the huge philosophical advantage of being rooted
in reality; the men and women who drove the inquiry into Radium's effects followed
the essentially scientific principle of looking for a relationship between cause and
effect. Maybe this was because they were medical practitioners, campaigners for
workers' rights and newspapers eager for the human interest angle on any story.
Maybe their investigation enjoyed some liberty because the dial painting industry was
owned privately, rather than by any government, and because at that time the fate of
the free world did not seem to hang on the outcome.
By 1944 everything had changed. Plutonium was being produced in
significant amounts and any potential it might have to kill its own workforce now
affected a top-level policy funded by a bottomless budget with the imperative of
building the bomb before Stalin (or Hitler) could. This was wartime: the aim of
making a bomb took precedence over health and set the stage for the same approach
and the same paramountcy of successful bomb development over health which was to
occur in the 1950s Cold War bomb tests. More crucially for the scientific principles of
radiological safety, physicians were no longer in charge, but physicists, a change
which continued also into the Cold War period. Indeed, in 1959, when evidence must
have been emerging everywhere of the effects of atmospheric dispersion of fission
products, infant mortality and leukaemia, this change was crystallized in the 1959
agreement between the World Health Organization (WHO) and the International
Atomic Energy Agency (IAEA) in which the former UN agency was forced to leave
radiation and health investigations to the latter, whose remit was (and is) the
development of nuclear energy. This conflict of interest agreement is still in force
although calls for its review have been made by the European Parliament following
the extreme lack of research and falsification of data carried out after Chernobyl
(Yablokov et al 2009, Busby and Yablokov 2009).
The main agent of change was a British physicist, Herbert Parker, head of
radiation protection at the Manhattan Project. His earlier career had made him
familiar with X-rays and a kind of therapy that used Radium as an external source,
confining it in tubes and placing it carefully to irradiate cancerous tissues, a medical
application which, for once in those days, did not involve Radium becoming
intimately mingled with the patient's bones. Parker had a physics-based view;
radiation was a single phenomenon, whether it came from an X-ray machine or a
speck of Plutonium. As with light, where the physicist isn't too interested in whether
the source is a candle or a light bulb or the sun, Parker was concerned with how much
energy the radiation delivered to the tissue of interest. The language here was of ergs,
from the Greek for work. It is defined in dynes, the Greek for force; the units are
physical, movement, velocity, grammes of mass, centimetres of length, seconds of
time. In this world there's no call for a doctorly bedside manner; Parker was one of the
first to call himself a Health Physicist.
Using his physicist's approach, Parker shifted the focus from investigating the
effects of specific substances onto a new concept, absorbed dose, which would apply
to radiation from any source and all sources, providing a way to assess workers' total
exposure to all the novel nuclides they were now being generated in the Manhattan
Project. He defined a unit of dose in ergs per gramme of tissue and called it the
Roentgen Equivalent Physical, or rep. Its very name reveals the thinking; Roentgen
was the discoverer of X-rays (for a long time they were called Roentgen rays). The
source of X-rays is always outside the body, so we can see the understanding of dose,
and hence risk, was now to be based on an external paradigm (Cantrill and Parker
The first limit for Plutonium in the body based on Parker's dose model was set
at 0.01 reps per day, making the rep the equivalent of the Roentgen. Now, instead of
the empirical scientific inquiry based on actual tissue damage and instead of the
tentative subjectivity of the 1941 Standards Bureau Committee's decision on a
Radium level, the new model gave an impression of mathematical precision, certainty
and universal applicability.
Any risk model needs two types of data, for exposure and for effect.
Unfortunately, there were no reliable data even for X-rays despite 50 years'
experience. There was too much variability in the machines and the conditions in
which they were used, doses were largely unknowable, and many of the long-term
effects had yet to emerge. But after 1945 the people of Hiroshima and Nagasaki
(those who hadn't been vaporized by the Atom bombs that fell on them on 6
and 9

August) provided the authorities with a fresh opportunity. Funded and controlled by
the USA, data on the survivors' health was gathered (as it still is) in what have
become known as the Life Span Studies or LSS.
There have been many criticisms of the LSS as a method of assessing harm
even from external radiation (ECRR2003, IRSN 2005) and I will return to this topic.
As far as studying internal radioactivity is concerned the flaw is fatal; the control
population providing the base-line of expected rates of disease, to be compared with
disease in the exposed population, was recruited from the bombed cities themselves.
They had either been outside the city when the bomb fell, or in some other way were
shielded from the flash of the explosion. The exposed population consisted of people
who had been in the open and so received a large dose of external gamma rays. Both
groups ingested and inhaled just as much fallout as each other, so the LSS are totally
silent on internal radiation. The only difference was in the external irradiation. LSS
nevertheless is the basis of radiation protection standards all over the world to this day
for both external and internal.
The LSS were not begun until 1952. This was another flaw, since seven years
of epidemiological data would be missing from the study and in addition, those
selected into the study would have been healthy survivors: many of the victims of
radiation would have died in the five years before the study began (Stewart and
Kneale, 2000). It is clear from reports of Japanese scientists that there were many
deaths and leukemias occurring in the irradiated cities in the interim period and
studies of the increases in cancers in the cities using external control data give higher
cancer yields than the LSS yields which effectively employed internal controls
(Kusano 1953, Busby 1995, Busby 2006, Sawada 2009). Long before then America's
Atomic Energy Commission (AEC) urgently needed to regulate the growing nuclear
industry. The AEC pressed the National Council for Radiation Protection (NCRP) to
develop safety standards. An especial concern was the quantity of novel elements
which, being alpha emitters, would present internal radiation hazards. Separate sub-
committees addressed internal and external radiation. The external sub-committee
completed its work quite quickly but the other was slowed down by the many
complexities of internal contamination. The problem is that while physicists can tell
you the ergs from any radioactive decay, they don't have much clue about where
internal radioactivity goes inside the body, how long it stays there or what biological
damage it's doing. Impatient with the delays, NCRP's Executive closed down the
internal committee in 1951, and stretched the report of the external committee to
cover internal radiation.
After the war, American influence revived the international radiation
protection community from its dormancy to be reborn as the International
Commission on Radiological Protection. ICRP's first act was to adopt the NCRP
report. The first formal recommendations in 1951 were for maximum permissible
doses from X-rays and gamma rays of 0.5 R at the surface of the body in any one
week. This represents a dose of 260mSv a year, a reduction on the 1934 limits. The
ICRP took a critical step for science: it adopted the Maximum Permissible Body
Burden (MPBB), defined now as the quantity of radionuclide in the body which
would deliver a radiation absorbed dose equivalent at the radiation limit defined for
external radiation.
The die was cast: this is the source of the error which has been promulgated to
this day, the source of all the discrepancies between predictions of the model and the
many examples of cancer and leukaemia in those exposed to internal radiation,
including the A-Bomb Test veterans. It is here at this point in time that the error
which flowed from Parker’s physically defined rep was crystallized for all time into
the risk model.
In 1953, the ICRP met in Copenhagen and agreed recommendations which
were published in December 1954. The committee agreed no radiation level higher
than the natural background can be regarded as absolutely safe and that the problem
was therefore to choose a practical level that, in the light of present knowledge,
involves negligible risk. For internal radiation, the concept of the critical organ was
introduced: this was a development that conceded that different internal radionuclides
might concentrate in different organs, and so absorbed doses must be calculated on
the organ mass, rather than the whole body mass. This concession shows that the
problem of anisotropy of dose from internal radionuclides (which I will discuss
below) had been conceded. However the ICRP stopped at the organ level: the idea
that such local high dose effects might occur at a more microscopic level, at the
cellular DNA, was not accommodated, and is still not accommodated. (I have recently
been told at a meeting in Sweden that there was pressure on the ICRP to introduce
weighting factors for radionuclides which bound to DNA, but this was not followed
But we should recall that this early attempt was perhaps forgivable: 1953 was
the year when the DNA structure was first described by Watson and Crick. The
location of the radiation effects in the cell nucleus, the critical involvement of the
DNA as target for radiation induced effects would have to wait for twenty years or
more, until the 1980s. Even so, no one made the obvious connection: the point that if
ionisation at the DNA was the critical target, external exposure and internal exposure
could not be described in the same way with the averaging tools of absorbed dose. It
waited until 2003 when the European Committee on Radiation Risk (see below)
published its new risk model for these effects to be considered.
The 1954 report reduced the dose limits to 300mrem (3mSv) per week, or
156mSv per year). In this report, the roentgen equivalent man or rem was introduced:
radiation from external and internal radiation could be summed as if it were the same
exposure. Although seemingly a rational development, as I have made clear, this
decision was to become the basis of the most serious mistake ever made in the area of
radiation risk. Although the report noted: much uncertainty still remains regarding
the behaviour of radioactive materials inside the body it nevertheless went on to
apply the same 300mrem average dose at the organ level when calculating maximum
permissible body burdens of radioisotopes. The Chairman of Committee 2 of the
ICRP, dealing with internal exposure was Karl Z Morgan, who was later was to
become a massive critic of the ICRP and the nuclear industry. He was very concerned
about the lack of knowledge of internal isotopes and their concentration in tissues.
The Ra-226 MPBB at the time was 0.1microCurie (3.7kBq). This was reduced by
Morgan’s Committee a factor of 5 to allow for possible non-uniformity of deposition.
For other radionuclides, the dose limit was set on the basis of the external limit as
applied to the organ where the isotope was likely to be concentrated.
But by 1956, concerns began to be raised in the media about genetic effects.
Muller had written an influential paper on the effects of radiation on Drosophila, the
fruit fly (Muller 1950); other scientists (Ralph Lapp, Linus Pauling) were arguing
from first principles that incorporated radionuclides were going to cause genetic
damage. Pauling, a double Nobel Prize winner (and later the Russian Sakharov) drew
attention to the harmful effects of Carbon-14, produced in abundance in the
atmospheric tests, and Strontium-90, a long lived (28 year half life) bone- and DNA-
seeking isotope from the Calcium Group 2 of the Periodic Table (Busby 1995).
Nevertheless, the requirements of military research for bombs caused pressure on the
regulators. Limits were slightly relaxed, allowing the period of averaging of dose to
be extended to 13 weeks, so long as the total dose to any organ accumulated during a
period of 13 consecutive weeks does not exceed ten times the basic permissible dose.
This introduced the concept of the integrated dose: but note that this new dose limit
permitted an annual dose of up to an enormous 1560mSv. Pressure built up: research
results leaked out. Fallout Strontium began to show up in childrens’ milk. The doses
were again revised in 1958 when ICRP considered the exposure of individuals in a
number of categories. For the highest risk category, ICRP recommended a new
weekly limit of 0.1rem (1mSv) or 52mSv in a year with a proviso that not more than 3
rems (30mSv) were delivered in 13 weeks.
By 1958, books were appearing that argued that radiation was a much more
serious hazard than had been believed: that the health effects were essentially genetic
mutation driven (e.g. Pauling 1958, Alexander 1957, Wallace and Dobzhansky 1959).
The British Medical Research Council were cautiously concerned (MRC 1956). In
1957, in Oxford, Alice Stewart (who was to be the first Chair of the ECRR) looked
for the cause in the sudden increase in a new childhood disease, leukaemia, and found
that a significant cause of the increased levels was obstetric X-raying. She had
identified the sensitivity of the foetus to radiation, finding that a foetal dose of as little
as 10mSv caused a 40% increase in childhood cancer 0-14. Her findings were
attacked by those who had contributed to the MRC reports which had concluded that
the fallout at the level it was at the time could not be a cause of concern (e.g. Richard
Doll) and her career was affected. But she was later conceded to have been correct
(Wakeford and Little 2003). Her conclusions meant that the levels of Strontium
fallout in milk would have significant effects on childhood cancer and this issue
ultimately resulted in the Kennedy /Kruschev Test Ban of 1963. Therefore by 1964,
despite the continued use of such high dose limits, there began to be serious concerns,
particularly about internal irradiation. The British physicist W. Mayneord (an ex-
member of the ICRP) was to write:
my worry about the numerical values of ICRP is the weakness of the
biological and medical foundations coupled with a most impressive numerical façade.
. . we give a false impression of certainty; comforting to administrators but not so
comforting to live with as scientists. (Radiation and Health, Nuffield Hospital Trust
Other members (e.g. Edward Radford, Carl Z Morgan, John Gofman) were to
resign or be sacked and were to attack the ICRP and its dose limits for the rest of their
By 1977 more evidence was coming in from the Japanese A-Bomb Lifespan
Studies (LSS) that the long term effects of external irradiation were significantly
greater than had been believed and so ICRP decided that it had to reduce the
integrated annual doses to members of the public to 5mSv. By 1985, after the
discovery of the Sellafield child leukemia cluster, this was modified to 1mSv. In
1990, more evidence had appeared that radiation was much more dangerous than had
been thought: evidence was appearing from radiation biology, from epidemiology,
from animal studies. The effects were seen to be consequences of genetic damage and
it was decided that there could be no threshold for such effects. The 1990s saw more
and more evidence of the subtle effects of low doses of radiation. However, the 1mSv
level could not be reduced since by then too many industries or other radiation related
operations depended upon this limit. So the limit was held at 1mSv, although the
British NRPB made a limit from a single source of 0.3mSv in a year, and
EURATOM reduced this single source limit to 0.15mSv in 1996/29 Directive, which
became EU law in 2001. The principle of ALARA, as low as reasonably achievable
for exposures was introduced. Even this was tempered in practice by social and
economic considerations. So this is the position that is presently embedded in
legislation. All the major risk agencies now concede that there is no safe dose of
radiation, and that genetic or genomic effects can occur at the lowest possible dose.
It is instructive to see the dose limits plotted over the period of the last
century. It is clear from Table 2.2 and the plots (Figs 2.1 and 2.2) that the exponential
reduction in the perception of hazard shown by the plot has bottomed and cannot be
linearly extrapolated to zero dose only for the reason that the nuclear and other
industries, and the military, cannot operate with radiation discharges at the present
levels if the true hazard from exposure were reflected in legal constraints on
But these dose limit reductions by 2007 still did nothing to address the real
problem with radiation risk, that of internal chronic exposure. The increasing
quantities of novel radionuclides and technologically enhanced natural substances like
Radium and Uranium in the environment has resulted in everyone one earth being
exposed though inhalation and ingestion of contaminated material from an
increasingly contaminated environment. If the understanding of radiation effects from
external acute delivery using X-ray machines was flawed, then this flaw represented
only a minor error, a slight scratch on the surface of the glass, compared with the
shattering inadequacy of the acute physical energy-transfer model used to account for
biological consequences of substances which delivered their energy from within
living tissue. Internal isotope exposure is the overlooked hazard of the nuclear age; it
is necessary here to back-track and return to the discovery and parallel development
during the infant X-ray age of the phenomenon of radioactivity.

Table 2.2 Statutory annual radiation dose limits to members of the public over the
radiation age 1920-present (mSv)

Year Statutory Annual
Limit mSv
1927 1000 Based on erythemal (skin reddening) X-ray dose
1934 365 Following Radium dial painters incident
1951 260 A-Bomb development. Japan Lifespan Study begins
1954 156 Weapons fallout period begins. DNA structure found
1958 52 Weapons fallout peaks 1959-1964. Muller
1966 5 Sr-90 in milk, in bone. Kennedy test ban 1963
1977 5
1985 1 Nuclear site child leukemias; Chernobyl in 1986
1991 1 The 1990s saw discovery of genomic instability
following single alpha tracks in cells
2003 1 ECRR introduces 0.5mSv limit; adjusts internal doses
2007 1 ICRP holds its 1985 1mSv limit despite huge
evidence of harm from internal exposures at lower

Fig 2.1 Statutory (ICRP and predecessors) annual radiation dose limits to members of
the public over the radiation age 1920-present (mSv) (exponential trend fitted to data

Fig 2.2. Logarithmic plot of statutory annual radiation dose limits to members of the
public over the radiation age 1920-present (log(mSv) )with some radiation exposure
events influencing reduction of dose limit. Note that new discoveries in radiobiology
and Chernobyl effects since 1985 cannot reduce the limits further as the industry
cannot take this although the extrapolation is to zero dose by 2005.


2.3 Radioactivity and its Biological Effects
One year after Roentgen's discovery of X-rays, in 1895, Henri Bequerel, in Paris,
found that certain naturally occurring minerals gave off weak, but similar radiation.
The rays that emanated from the Uranium-containing ore, pitchblende, were capable
of fogging sealed photographic plates, in the same way as X-rays. Bequerel showed
that this radiation was capable of passing through thin metal plates. In 1898 Marie
Curie coined the word `radioactivity' to describe the effect. She began to look closely
at the materials which exhibited the effect and identified, in pitchblende, a novel and
highly radioactive element besides Uranium: she called it `Radium'.
Her lifetime work to chemically isolate Radium, processing tonnes of
radioactive ore, resulted in the isolation of one gram. She and her husband Pierre
shared the Nobel Prize but she died in 1934 of leukaemia, her hands terribly scarred
from having handled the radioactive materials. Her daughter Irene who worked with
radiation was also to die of the same disease. Roentgen himself died of bone cancer.
In the period following her discovery, Rutherford, who was laying the
experimental foundations for the understanding of modern atomic theory, was able to
describe accurately the quality of the radiation emitted by radioactive substances and
identify their source in the nuclei of the heavy atoms involved in the phenomenon.
These radiations are the alpha and beta particles and gamma rays.
If their characteristics had reminded Bequerel of X-rays, their biological
effects were equally worrying. In 1901 he borrowed from the Curies a phial
containing a minute quantity of a Radium salt. He carried the tube in his waistcoat
pocket for six hours and noticed that he had burned his skin through several layers of
clothing. The doctor that he consulted pointed out that the lesion was similar to X-ray
In the years that followed this discovery, radioactive materials became used
extensively as a convenient source of radiation in medicine. One of the developing
uses for X-rays was the treatment of cancer: they are still used for this purpose. It had
been discovered that the irradiation of tumours by X-rays or by the radiation from
radioactive substances often caused their regression, although the reason for the effect
remained obscure. We now know that radiation is selective for cancer cells because
radiation kills cells which are dividing more efficiently than cells which are in a
stationary phase of their life cycle. (As a treatment, this is a last ditch strategy, since
all radiation exposure carries risk of mutation and cancer in healthy cells: thus new
cancers can, and do, appear later).
But most of the radiation effects described and understood in this atmosphere
of scientific advance and general euphoria, related to exposure from external sources.
Thus X-rays emitted from a vacuum tube were directed onto the surface of an
individual, who perceived burns. Bequerel's skin-burn was of this type, despite the
source difference. Measurements made by scientists using the detectors developed for
the purpose were measurements of radiation falling on the detector from an external
source. The relation between exposure and background radiation also assumed that
energy was transferred to an individual from an external source.
The discovery of Radium and the existence in Canada of Radium-bearing
uranium mineral ore rapidly resulted in the substance becoming commercially
available. Preparations containing Radium, sold as part of the magical new age, as the
elixir of life, became incorporated into a wide range of nostrums. There were Radium-
containing general tonics, hair restorers, toothpastes and cures for all ills from arthritis
to infertility. A hearing-aid was marketed with the magic ingredient, `hearium'. One
most popular and widely used preparation was `Radium water', often referred to as
`liquid sunshine'. One company in New York claimed to supply 150,000 customers
with radium water. Another brand, `radithor' was so radioactive that several users died
from Radium poisoning. One of these, a Pittsburgh industrialist and amateur golf
champion, Eben Byers, drank a two-ounce bottle daily for several years; he believed it
made him fit, and pressed it on his friends. He died of multiple decay of the jawbone,
anaemia and a brain abscess in 1932.
The first clear evidence that internal irradiation from radioactive substances
like Radium caused serious health problems was the death, between 1920 and 1924 of
nine young girls employed by the US Radium Corporation to paint the dials of
watches and clocks with a luminous, Radium-containing, paint.

2.4 The Tragedy of the Dial-Painters
The story of the dial-painters and their fight to obtain recognition for the cause of
their cancers and other grave illnesses is similar in every respect to the many attempts
that have been made up to the present day by groups who have tried to argue that their
injuries were caused by radiation, from the Atomic Test veterans to the Sellafield
leukemia victims. For this reason, and as the first example of the assault on the
external versus internal irradiation dose comparison, their history deserves closer
attention. (My account is based on that in Caufield, 1989: 29-43.)
The dial-painters kept their paint-brushes pointed by licking the tips. Although
Radium was known to be highly radioactive, the amounts used in the paint were truly
tiny, and it was assumed that the procedure was safe. The underlying assumption, of
course, was that the energy transfer was very small. It was also believed, on no
evidence, that any Radium ingested would pass straight through the body in a short
Nevertheless, the dial-painters began to suffer serious problems. Death
certificates cited many different causes of death: stomach ulcer, syphilis, trench
mouth, phosphorus poisoning, anaemia, necrosis of the jaw. Many who were still
living were seeing dentists, with severe tooth and jaw problems. In early 1924,
concerned by the emerging illnesses of the dial painters, the local Board of Health
asked the Consumers League of New Jersey, a voluntary group concerned about the
employment of women and children, to investigate working conditions in the US
Radium factory.
Katherine Wiley, the group's secretary, wrote that four of the dead women had
undergone surgery of the jaws, and that many still living former dial-painters were
similarly afflicted. But she found no problems with working conditions at the factory,
nor did the New Jersey State Department of Labor, which also examined the plant.
The US Radium Corporation assured both groups that Radium was not harmful at the
minute levels involved, which were vanishingly small compared to the erythemal dose
from an X-Ray machine. They ascribed the dial-painters troubles to poor dental
hygiene. More recently, in an echo of this, the massive increases in cancer, leukemia
and birth defects in the former Soviet Union following Chernobyl have been blamed
by the risk agencies on hysteria or on malnutrition (see Busby and Yablokov 2006,
In 1924 a consultant dentist, Dr Theo Blum, who had treated one of the dial-
painters, published a paper in the Journal of the American Dental Association. In it he
mentioned that in 1923 he had treated a case of `infection of the jawbone caused by
some radioactive substance used in the manufacture of luminous dials for watches.'
This was the first suggestion that radioactivity from Radium may have been the cause.
The article was noted by Dr Harrison Martland, Medical Examiner of Health for
Essex County, home of the Radium factory. Martland began studying the problem and
decided to perform autopsies on the next US Radium Corporation employees to die.
Meanwhile, Katherine Wiley consulted Florence Kelley, the head of the
National Consumers' League, who, in turn, passed the problem on to Dr Frederick
Hoffman, the Prudential Life Assurance Co.'s chief statistician, to investigate.
Hoffman reported to the American Medical Association in May 1925 (Martland
1925). The epidemiological evidence he presented confirmed that some factor related
to work at the Radium plant was causing death amongst workers from illnesses of the
mouth and jaw. He believed that Radium poisoning was the cause. The company
continued to argue that this was impossible, that the exposure was too low.
But the company itself was well aware of the cause of the illnesses, having
commissioned its own study one year before Martland's report. Cecil Drinker and
colleagues from the Harvard School of Public Health had been asked by US Radium
to investigate and had already reported their findings. They had stated that radiation
was the cause of the employees’ ill health. Examining the girls who worked there, in a
darkened room, they wrote: `their hair, faces, hands, arms, necks, dresses, the
underclothes, even the corsets were luminous.' Tests on twenty-two employees failed
to find a single one whose blood-count was acceptable. That all the workers were
exposed to excessive radiation, both external and internal, was in writing and on the
desk of the director of the US Radium Corporation one year prior to Hoffman's paper.
`It seems necessary therefore, to consider that the cases described, have been due to
Radium' the Report stated. The company blocked external publication with threat of a
lawsuit. When Drinker learned of Hoffman's scheduled address to the AMA on
`Radium Necrosis' he begged US Radium to allow him to publish. They refused,
although they sent an edited version, absolving them of responsibility, to the New
Jersey Department of Labour.
At about the time of the Hoffman Report, Martland was able to do biopsies on
the jaws of two dial-painters who were suffering from `jaw necrosis and severe
anaemia'. Both died shortly after and Martland confirmed high levels of radioactivity
in the women's bones and organs. He tested a number of living dial-painters and
found that their bodies contained so much radioactive material that when they exhaled
on to a fluorescent screen, it glowed (Martland, 1951).
Martland and co-workers became the first to understand that internally
ingested radioisotopes behave in the body quite specifically and in a manner related to
their biochemical nature. Instead of passing through the bodies of the dial-painters,
Radium, an element of the Calcium family, became stored in bone and teeth instead of
Calcium. In addition, as a member of the Calcium family, Radium should bind to
DNA. A build-up of radiation caused damage to the tissue adjacent to the storage site
which had become a radioactive source. Furthermore, and the main reason why
external irradiation studies cannot safely inform internal radiation risk, there was an
enormous dose to adjacent tissues from the intensely ionizing alpha-particle radiation
characteristic of Radium. External dose considerations were wholly inappropriate.
The dose from a single decay was lethally effective against the cells close to the atom.
Such a dose, delivered externally, would have had no effect whatever, since the alpha-
particle would not even penetrate the skin.
Martland continued to investigate Radium: he found that early stages of
internal radiation made victims feel well, as the radiation stimulated excessive red-
blood-cell production. He found that there was a time-lag between radiation ingestion
and the onset of disease, often a considerable time-lag. This time-lag was a death
sentence for many who were part of the Radium Company's operation at the time of
Martland's report. In 1925 Edward Lehman, their chief chemist, was in good health:
he died shortly after of acute anaemia and the autopsy showed radioactivity in his
bones and lungs. Since he had not painted dials it was clear that he had acquired his
dose by inhalation.
The Radium Company refused to accept the radiation poisoning hypothesis.
They commissioned new studies which exonerated them. They blocked reports using
legal pressure. Several families sued them for damages, as did Dr Lehman's widow.
The newspapers took up the case of `The Five Women Doomed to Die' who had filed
for damages. They were so wasted and ill that they had to be carried to the witness-
stand: one was unable to raise her hand to take the oath. The Company maintained
that there was no scientific proof that the dial-painters' injuries were caused by
Radium. Its lawyers, however, chose to fight on a different front, arguing that New
Jersey's statute of limitations required industrial injury pleas to be filed within two
years of the occurrence. The Court accepted this, the women petitioned, and the case
rumbled on. Following huge pressure, the women were granted permission to go to
the Supreme Court. US Radium still denied responsibility for their injuries. The case
seemed set to drag on for years; the women were dying. Eventually the Company
prompted solely by humanitarian considerations settled out of court for half the
amount that the women claimed. They still had not conceded that internal irradiation
from Radium was the cause of the diseases which were killing their employees.

2.5 Development of Dose-Response Relations for internal emitters : the history
With the dial-painters' tragedy came the first recognition that ionizing radiation acted
in ways that were not predictable from simple physical considerations. Internal
irradiation by a specific radioactive element was seen to produce appalling effects,
often long delayed, at levels of energy transfer that seemed vanishingly small. Since
many preparations freely available on the market contained Radium, guidelines were
clearly needed to safeguard the public, and between 1936 and 1938 experiments were
begun on animals to try to establish safe limits. But it was only when the need for
luminous dials increased with the Second World War that, in 1941, the US Bureau of
Standards met to present draft rules for Radium contamination. As in the case of the
early external irradiation limits, the results were hurriedly patched together by
guesswork: a limit of 0.1 Curies in the whole body was given as a reason for changing
personnel to new employment; a limit of 10 picoCuries (pCi) of Radon gas per litre of
air was also set, and the 0.12R per day X-ray limit was extended to ¸-ray exposure.
The establishment of even these high levels of statutory exposure limits probably
saved many lives during the ten years that followed; years that saw, with the US
Manhattan Project, the development of the atomic bomb.
I will comment in passing that the effects of radium on the dial painters were
probably not all due to internal exposures from alpha particles. The external dose
limits of the time (see Fig 3) believed to confer safety, were extremely high, as I have
remarked. I own a prismatic hand bearing compass supplied to the British Army
soldiers as standard issue in WW2. Soldiers wore this on their belt and held it to their
eyes to obtain bearings. A calibrated Geiger Counter shows a gamma dose of 50µSv/h
at 5cm from the small (2mm diameter piece) of Radium compound on the compass
card. This would give an annual dose of 438mSv in a year. This is from a single dab
of paint: the external doses the dial painters received would have been enormously
greater since they would have had a whole paint pot of the stuff in front of them. And
it is not hard to see why the child leukemia rate in WW2 suddenly increased with
planes being shot down, radium paint everywhere and soldiers carrying such
radioactive sources close to their testicles.
Although I have outlined the historical development of the overall dose limits
in the previous section, I will here look more closely at the bodies assessing the risk
from internal radiation. In 1946, to control the development of all things atomic
which, following the Hiroshima bomb were seen to be associated with national
security, in the United States the Atomic Energy Commission (AEC) was formed.
There soon followed the revival of the US Advisory Committee on X-Ray and
Radium Protection, which needed to consider safety levels in view of the new
practices and new isotopic contaminants which followed the development, testing,
and use of atomic weapons. The Committee changed its name to the National
Council on Radiological Protection (NCRP) and expanded.
The NCRP consisted of eight representatives of medical societies, two of X-
ray manufacturers, and nine of government agencies including the armed forces, the
Bureau of Standards, and the Atomic Energy Commission. From the very start, the
AEC put pressure on the NCRP to devise a permissible dose level. Of the eight sub-
committees set up to consider radiation-related practices, those which were attempting
to set dose limits were Sub-Committee One on external dose limits, headed by
Giaocchimo Failla, and Sub-Committee Two on internal radiation limits, headed by
Karl Z. Morgan. External dose limits were set at 0.5R/week (260mSv/year). The
reduction from the previous 1934 limit was partly based on the discovery that
radiation caused genetic damage. Experiments with fruit flies by H Muller had
showed that even tiny doses of radiation resulted in the production of mutated
offspring. This raised the obvious question about similar damage to humans. The
problem was that practices involving doses to workers and members of the public
much higher than those involved in the fruit-fly experiments had already been
sanctioned by the earlier guesstimate dose limits then in use. Since, also, national
security demanded continued research, development, and testing of atom bombs, there
was no way in which NCRP would have been able to set dose limits at zero dose or no
exposure. On the basis that such a move would be unrealistic, the NCRP canvassed
the nuclear industry on what was the lowest value for the dose limit that they could
function with. This figure was the one that was adopted. Owing to arguments
between Failla and Morgan, who felt that more control of exposure was needed, the
dose limits were not published until 1954 when they were reduced again to
0.3rem/week (156mSv/y).
Sub-Committee Two, under Morgan, had the job of assessing the risks from
internal exposure due to ingested radioisotopes. What was required was the
development of an understanding of the effects of ionizing radiation delivered by an
atom incorporated within living material and decaying to deliver its energy into
adjacent tissue. What they proceeded to do instead was to apply the physical model
for external irradiation to internal organs which were assumed to be `target organs' on
the basis of radio-chemical affinity, and to see these organs as neutral volumes of
irradiated water in which a certain amount of energy was dissipated. This is a typical
physics-based reductionist trick. It has great computational utility, but as far as
biological responses are concerned it is entirely inadequate, and as I shall show, gives
the wrong answer.
The primitive erythemal dose threshold arguments together with the
development of the physical-energy-based units-- rad, Gray etc.--gave limits for
external dose based on a model which involved so much energy transfer with a 70 kg.
sack of water called a `reference man'. The modification needed for understanding
internal irradiation was obvious. The organ most likely to concentrate the particular
radioisotope being considered was defined as a `target organ' for that substance. The
dose limit was then set assuming that the organ of mass m was a smaller sack of water
into which so much energy E was transferred. The same ad hoc, and arbitrarily
developed dose limit could then be applied.
These dose limits were translated into maximum permissible concentrations or
body burdens (MPBB) of the particular radioisotope. Morgan clearly recognized the
dubious nature of these arguments and the shakiness of the whole analysis: his
Committee Two proposed that the MPC they calculated be divided by a `safety factor
of ten’ for people who might be exposed for thirty years or more. This represented
official unease about the differences between acute external and chronic internal
exposure: the conflict between the understanding of physics and that of biology.
There was much argument about the adoption of recommendations from
Morgan's group, and the final report did not include the proposals for people likely to
receive prolonged exposure
These radiation protection advisory commissions, and their offspring, the
radiological advisory bodies in most countries like Britain's National Radiological
Protection Board (NRPB, which shares many personnel with ICRP, yet cites the latter
as an 'independent source' of advice), now publish advice on dose limits and
protection which becomes incorporated into law. They control the perception of
hazard from all things nuclear. They are all, however, lineal descendants of the first
NCRP committee, staffed by people who all had interests in the development of the
use of radiation. They remain, to this day, a revolving door through which members
of the nuclear establishment or those with research ties to it, pass in and out.
The first recommendations of the original 1953 committee became US law in
1957, yet those recommendations arose in an atmosphere of haste, error, necessity,
secrecy, and lack of knowledge. In 1962 an AEC scientist, Harold Knapp, studied the
exposure of young children to radioactive iodine in milk. He concluded that standards
were too lax by a factor of ten, and recommended that they be tightened. The
response from the AEC director of the Commission of Operational Safety was that
the present guidelines have, in general, been adequate to permit the continuance of
weapons testing and at the same time been accepted by the public principally because
of an extensive public information programme. To change the guides would raise
questions in the public mind as to the validity of the past guides. (Caufield, 1989: 132)
This continued to be the case with radiological safety, and it continues still.
Present radiation protection laws, based on the cancer yield of acute radiation
exposure events like the Hiroshima bomb, leave much of the actual practice to the
users and producers of radioactivity by asking them to keep doses `as low as
reasonably achievable' (ALARA). Sir Kelvin Spencer, formerly Chief Scientist for
the UK Ministry of Power said:
We must remember that government scientists are in chains. Speaking as a one-time
government scientist I well know that `reasonably achievable' has to be interpreted,
so long as one is in government service, as whatever level of contamination is
compatible with the economic well-being of the industry responsible for the pollution
under scrutiny. (Caufield, 1989: 190)
The 1957 statutory crystallization of the 1954 NCRP recommendations
occurred during the period of intense scientific research which followed the Second
World War. By 1957 enough was known about cell genetics and DNA damage to
understand the cellular origins of radiation effects. It had always been clear that
ionizing radiation did not kill by gross energy transfer: the effects were delayed, the
amounts needed to kill an individual would not heat the body up by more than a
fraction of a degree. With this new knowledge--that it was primarily cellular genetic
changes which were occurring--it must have been apparent by the 1960s that there
could be no safe dose of radiation. Even then it was known that ionizing radiation
caused damage to genetic material in cells under all conditions of irradiation, even for
the smallest doses which can occur. It could be shown that there was no safe dose, or
no threshold below which radiation is safe, and indeed this is now the affirmed
position of both the ICRP, the NCRP, and the Biological Effects Committees of the
US National Academy of Sciences (see BEIR V, BEIR VII).
In the 70s it was belatedly realised that internal exposures, particularly to
plutonium might have much greater harmful effects than were predicted by the
methodology that had been employed until then, there was a great deal of work
funded to justify the approach. The method used was to study the effects of Radium
and Thorotrast, radionuclides which had been used in the 30s and 40s for medical
purposes. These studies were carried out too late, however, as the high doses involved
had killed many of the people exposed. Nevertheless a spurious consistency with the
radiation risk model predictions was cobbled together in an attempt to justify
continued use of the model. The matter briefly will be addressed below.

2.6 External and internal radiation: the science.

In order to help follow the arguments about internal radiation and health I now return
to review some basic principles and examine some of the assumptions at the base of
radiation risk. These issues are key to an understanding of the Test Veterans
exposures. The arguments are elaborated in the CERRIE minority report, the CERRIE
majority report and in the early chapters of the ECRR2003 report. A more accessible
explanation of the basic science is given in my book Wings of Death 1995.
Ionising radiation acts though the damage to cellular genetic materials, the
genes on the DNA, killing some cells but causing fixed genetic mutation in others,
including mutations that signal to descendants a genomic instability message to
increase their rate of incorporated error. These genetic and genomic mutations are
now known to be the main initiation point in the development of cancer and leukemia
and also the origin of heritable damage and increases in many illnesses that were not
originally thought to be radiation related. It is the progression of the cellular mutation
and the acquisition of further mutations over the lifespan of the cell or its descendants
(in the same individual or in the case of germ cells in offspring) that leads eventually
to the clinical expression of the cancer or the development of a wide range of
diseases. The damage to the DNA is caused either by ionisation of DNA materials
themselves directly, or more usually indirectly by the interaction of the radiation track
(which is the track of a charged particle, an electron or a alpha particle) with solvent
water or other molecules to form 'hot' ionic species which are sufficiently reactive to
attack the DNA bases. To a first approximation, it can be argued that over a certain
range of dose, the effect, or likelihood of mutation, is a linear function of the amount
of energy absorbed. That is because this energy goes to break bonds and produce ions,
and twice the energy produces twice the ions and therefore twice the probability of
mutation. But note here that the primary cause of mutation is the reactive ion and so it
is the concentration of reactive ions in the cell which represents the most accurate
measure of mutagenic efficiency (although there are other considerations as we shall
see). The assumptions that underpin the whole of radiation protection are based on the
ideas that the dose and the response are linearly correlated. Thus, if we double the
dose, we double the effect. This is the basis of the present system of radiation risk
assessment, and specifically the basis of the calculation made using the model of the
ICRP. All predictions follow from this assumption, the Linear No Threshold LNT
But whatever the dose response function employed, it is manifestly and
philosophically wrong to employ such a model for internal irradiation. This is because
the quality used to measure radiation, Absorbed Dose (in rads or Grays) represents the
average energy absorbed in unit mass, in the case of Grays, Joules per Kilogram. Such
a quantity assumes at the outset that the energy density is the same in all the cells or
critical parts (e.g. chromosomes, DNA) of the tissue irradiated. Whilst this is a valid
assumption for external irradiation as in the case of the studies used to determine
cancer and leukemia risk (particularly the major study, that of the Japanese A-Bomb
survivors) it is manifestly untrue for modelling risk in individuals who have internal
irradiation. The reason is that in many internal irradiation regimes, averaging is not
appropriate. Radioactive particles which emit short range radiation like alpha and beta
radiation causes high levels of energy density (ionisation) in local tissue (a few
millimetres away) but no irradiation elsewhere. Thus cells near to these particles
receive large either fatal or mutagenic doses. To illustrate this I have shown in Fig 2.3
a photomicrograph of decay tracks from a few radioactive particles in rat lung.
This phenomenon is known as an alpha star: the tracks are alpha particle ionization
tracks such as those produced from uranium and radium dust particles.
Averaging the energy into large tissue masses in whole body or in organs,
dilutes the ionization density and makes it seem as if the whole body doses are very
low, perhaps well below natural background doses. But since cancer always starts in a
single cell (as we know from mosaic studies of tumours) it is the cell dose that is
important, not the tissue dose. As I have argued already, the use of external doses to
calculate cancer risk (as the ICRP do) is like comparing warming oneself by the fire
with eating a hot coal. This argument has now been accepted at the highest level,
although little has been done to incorporate it into risk management. It is a major
plank of the ECRR deliberations and now in the mainstream of argument in the
radiation risk community. Chapters 5 and 6 of ECRR 2003 and pp 48 to 56 of the
CERRIE Minority Report discuss the concept of Dose, used by the ICRP model as a
measure of radiation exposure, in dealing with health effects. In addition, the matter is
reviewed by the CERRIE Majority Report (2004) which agrees that (p13 para 11)
There are important concerns with respect to particle emissions, the extent to which
current models adequately represent such interactions with biological targets, and the
specification of target cells at risk. Indeed the actual concepts of absorbed dose
become questionable and sometimes meaningless when considering interactions at
the cellular and molecular levels.

Fig 2.3 Alpha star photomicrograph showing radiation tracks emanating from hot
particle in rat lung; track length has the distance of about five cells.

This is quoted from an official report of a UK government committee. The point is
made regularly elsewhere in the same report, (e.g. para 60 p27) and the Majority
Report concludes that there is a conceptual uncertainty associated with the use of
absorbed dose of a factor of 10-fold. The Minority CERRIE Report argues that this
figure is more like 100-fold to 1000-fold for very low doses and certain types of
exposure and advances proofs of this (see below). In addition, recently, the French
official radiation risk agency, Institut de Radioprotection et de Surete Nucliare
(IRSN), agree that the ICRP dose averaging approach is insecure. In a report
published in 2005 they point out that the questions raised by the ECRR2003 report
relating to the question of internal doses are valid. The IRSN committee of 15 senior
scientists state that these are fundamental questions with regard to radioprotection
and (p6) that [in the situation of] heterogeneous distribution of radionuclides, the
validity of weighting factors for calculating internal doses, the impact of the
radionuclide speciation on their behaviour and their chemical toxicity make it clear
that the ICRP approach for certain internal radionuclides is strictly invalid. IRSN
state that since the ICRP60 publication, improvements in radiobiology and
radiopathology, or even general biology finally might impair [falsify] the radiation
cell and tissue response model applied to justify radioprotection recommendations.
[IRSN 2005]

ICRP itself was under pressure on this issue by 2005 and conceded in its draft report
on risk:
(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, low-energy 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 quantity for estimating the stochastic damage. The
applicability of the concept of average organ dose and effective dose may, therefore,
need to be examined critically in such cases and sometimes empirical and pragmatic
procedures must be applied.
But ICRP did nothing and still has done nothing in its latest 2008 risk model to
change any of the dose coefficients for isotopes that caused such exposures or to
apply such empirical and pragmatic procedures. And by 2009 the editor of the risk
model presentation and scientific secretary of the ICRP resigned and publicly
conceded that the model was unsafe (see below).

2.7 Dose constraints and risk models after 1980
As I have explained, the history of radiation and health is one in which the cancer and
leukemia risks following exposure have been reassessed continuously upwards over
the whole of the radiation age. The annual dose limits have fallen from around
400mGy in 1934 to 200 mGy (or 200mSv) in the early 1950s and by 1974, ICRP 26
recommended an annual limit of 5mSv to members of the public and 50mSv to
workers. This was modified after the discovery of the Sellafield child leukemias and
the other nuclear site child leukemias. ICRP in 1985 dropped the annual dose limit to
1mSv. NRPB in the UK reduced this further in 1987 to 0.5mSv from a single site
exposure. In the US the single source exposure level, is now 15mRem or 0.15mSv.
Levels are now, in the UK and Europe fixed at 1mSv (100mRem) for members of the
public and 20mSv for workers. I should explain that the mSv is a unit which derives
from the mGy in the same way as the rem is derived from the rad, by the use of a
multiplier of effect based on the type of radiation. Alpha radiation is known to give
very dense ionization over a short track length of about 40 micrometers (three to five
cells). It is assumed to therefore have 20 times more biological effectiveness owing to
its 20-fold greater ionization density and thus, for internal exposure carries a
weighting factor under ICRP of 20. Thus a dose of 1mGy becomes a ‘dose
equivalent’ of 20mSv. This concession to ionization density effects is not extended by
ICRP to other types of internal irradiation (e.g. particles, DNA bound isotopes) where
much higher density of irradiation occurs, because to do so would concede the high
risk effects of such exposures and point to cancer causality in groups who were
contaminated internally. On the other hand, the ECRR model has taken this step and
introduced weighting factors for such regimes (see ECRR2003 Chapter 6), and this
results in significantly higher effective doses from certain types of internal exposure
using the ECRR model than the ICRP model.
As I have already pointed out, it is clear that there can be no safe dose of
radiation. This has been formally conceded since the early 1990s (see e.g NRPB
1995). I repeat that these dose limits have stopped being reduced because of
pragmatic considerations relating to the operation of nuclear facilities only and not
because of a sudden realisation that the health effects are now known and allow us to
make accurate limits which we know will prevent the illness of exposed people. For
example, the dose limit constraints should have been lowered when the most recent
results of the Japanese A-Bomb study data became available in the 1990s and showed
that the cancer risk continued to rise in the survivors study group
By this continuing increase in perceived cancer risk with dose I mean: in
relation to the safety of exposures as measured officially using external radiation
studies, in particular the Hiroshima survivors study. The matter of internal exposure
cannot be informed by these external studies. Indeed, when we look at internal risk
through the lens of epidemiology, we see that the risks are hundreds even perhaps
thousands of times higher than predicted by the external risk models based on
Hiroshima, and enable us to both predict and explain the clusters of childhood cancer
and leukemia near nuclear polluting sites which were discovered in the 1980s.

2.8 The recent revolution in radiation risk perception

2.8.1 Sellafield and the nuclear sites
The first evidence that radiation risk from exposure to internal radionuclides was
significantly greater than that predicted by ICRP was the discovery in 1983 of a
cluster of childhood leukemia cases in children living near the Sellafield nuclear
reprocessing site in the UK. This discovery, made initially by a TV company, was the
subject of a government inquiry which found that the cluster was real but that the
ICRP risk model could not predict the levels of leukemia. The difference between the
prediction of the ICRP model and the excess leukemias was 300-fold. Note that
number. The matter is discussed in the CERRIE minority and majority reports and in
ECRR 2003. The discovery was followed quickly by others so that by the mid 1990s
childhood leukemia clusters had been discovered near all three nuclear reprocessing
sites in northern Europe and a good many other nuclear facilities. These sites had in
common that they released fission product radioisotopes and technologically
enhanced natural isotopes TENORM (e.g. Uranium) to the environment. In all cases,
the relevant authorities discounted causality on the basis of application of the ICRP
external model, even though it was a case of internal exposure. In every case, the
discrepancy between the doses and the measured and predicted effects was between
300-fold and a few thousand -fold. In the case of Sellafield measurements had been
made on autopsy specimens which showed that particulate material released by the
plant (Plutonium, Uranium ) was most concentrated in the lymph nodes draining the
lungs. Thus there was evidence in the mid 1980s that radioactive material from the
nuclear site concentrated in small lymphatic masses weighing about 11gms each. The
Committee on Medical Aspects of Radiation in the Environment COMARE, the main
public body set up after the 1983 inquiry to examine the possibility that the radiation
was the case of the leukemia conceded in its Fourth Report (COMARE 1996) into the
Sellafield leukemia cluster that the lymph nodes were known to be the site of
leukemias in animal studies and yet accepted calculations of the doses to the
lymphatic system from enhanced levels of Uranium from Plutonium that used the
ICRP dilution model, in this case diluting the energy into an assumed body organ
mass of 11kg. Since dose is Energy divided by Mass this dilution reduced the dose by
After the Sellafield discovery, childhood leukemia clusters were reported from
many nuclear sites in the UK and Europe e.g. Dounreay, Aldermaston, Hinkley Point,
La Hague, Kruemmel. A full discussion of the issue and how it illuminates the error
in employing the external risk model is given in ECRR2003.

2.8.2 The German childhood leukemias
Most recently, in 2008, the German Childhood cancer registry (Kinderkrebsregister)
published results of the largest study of childhood leukemia near nuclear power
stations that has yet been carried out. By examining cases and controls by distance
from all the nuclear sites in Germany between 1980 and 2005, the authors have shown
that there is a statistically significant doubling of childhood leukemia risk in the age
group 0-4, thus supporting the various earlier studies of childhood leukemia near
nuclear sites. Scientists from the University of Mainz working for the German
Childhood Cancer registry, founded in 1980, had originally investigated whether there
had been similar excess risks of childhood cancer near nuclear sites by using the
ecological approach employed by COMARE, that is, looking at all children within
some distance of the site, in the German studies 15km. They had also, like
COMARE, examined the age group 0-14, which dilutes any excess by a factor of 3
since the main age group of interest for the disease is 0-4. This may have been
because, like COMARE, at that time, when the Germans were committed to nuclear
power, they didn’t actually want to find anything. And that is what happened: the
examination of the 0-15 year group living within 15km of the sites from 1980-1995
showed no excess risk when compared with the general; national rates (RR = 0.97 CI
0.87<RR<1.08). Nevertheless, examination of subsets revealed that for children living
within 5km of the plant aged 0-4 there was a statistically significant 3-fold excess (RR
3.01 CI 1.25<RR<10.31). In the Kinderkrebsregister case control study published in
January 2008 in the European Journal of Cancer (Spix et al 2008) published results
from 23 years (1980-2003) of data for 6300 children. The authors reported that the
best model to fit the data by distance from the nuclear plants in Germany was an
inverse square root relationship and that in their model, for children aged 0-4, there
was a RR of 1.61 excess risk at 5km for cancer and RR 2.19 (lower one-tailed 95% CI
1.51) for leukemia. This is further evidence of the error in employing the ICRP
external radiation risk model for explaining or predicting risk from internal exposure,
since these children were clearly not exposed directly to radiation from the plant, but
rather inhaled or ingested radionuclides discharged from these plants. We should be
clear that the doses to these children cannot explain their illnesses on the basis of the
ICRP risk model by an error factor of upwards of 1000.

2.8.3 New Science
The last fifteen years have seen a revolution in the scientific understanding radiation
action at the cellular level and of cancer causation by radiation. Much of what I will
briefly say here is elaborated in the CERRIE Majority and Minority reports. I will try
to just make the most important points.

2.8.4 Genomic Instability and the Bystander effect
It was discovered in the mid 1990s that a single track from an alpha particle through a
cell caused an effect called Genomic Instability. What happened was that the cell
survived but the descendants of the cell seemed prone to spontaneous and random
genetic mutations. Prior to this discovery, it was assumed that cancer and leukemia
were caused by a specific genetic mutation which was then passed on to daughter
cells (the clonal expansion theory). However, this latter theory (which is the physical
basis for the present ICRP model) was unable to explain the normal cancer rate in
human populations given the experimentally derived normal mutation rate of 10
Further experiments into the phenomenon showed that it was potentially a
property of all tissues and was induced by the lowest doses of all kinds of ionizing
radiation. It rapidly came to be seen that this was the basis in genetic mutation of most
cancer. In my opinion, this evidence came to be accepted around the end of the 1990s;
that is to say, there was a revolution in the mainstream understanding of radiation risk
which gathered strength from the mid 1990s and would have been largely agreed by
the majority of scientists as representing a need to re-think the basic science by the
year 2000.
But this discovery was followed by second very strange observation. It was
found by several groups that if a cell was hit i.e intercepted by a track of ions, then not
only the cell affected suffered genomic instability, but also cells which were not hit
and which were up to 400 or more cell diameters distant from the target cell. This
phenomenon was termed the bystander effect.
There are three basic implications for radiation protection, and by implication,
the present assessment of the exposures of the Test veterans. The first is that the basis
for assuming that the relationship between cause and effect, dose and cancer yield is a
linear one (i.e double the dose and you double the cancer risk) is shown to be invalid.
The dose response relation of Genomic Instability and Bystander effects is sharply
supralinear. It increases rapidly with the first two tracks, then flattens off. This means
that you cannot, as ICRP have, extrapolate from high dose (Hiroshima survivors) to
low dose. There is a much higher proportionate effect at low dose. Some scientists
have also argued the opposite. There is some data that suggests that low doses of
radiation are protective. This process is termed ‘hormesis’ but it is not conceded by
the official risk agencies. Risk agency models do however apply a factor to their
predictions based upon a lower cancer yield for protracted doses and opposed to acute
doses. In my opinion this is invalid. The application of these Dose Rate Reduction
Factors to low dose radiation arises out of a mistaken interpretation of low dose points
in the experimental results. The same error in interpretation has allowed some to
believe that low doses of radiation are protective i.e. in hormesis.
The second implication of the new scientific discoveries is that two tracks
across a cell or into tissue (since the bystander effect connects all the cells in a small
tissue volume) has a proportionately greater effect than one track and that after three
of four tracks the effect saturates. The outcome is that there is a range of ionization
density that has a much enhanced ability to cause cancer. This range is unlikely to be
reached in external irradiation until the levels of dose to the whole body are high, but
can be reached in the case of tissue exposed to local decays from internal radioactive
particles. The activity of such particles needs to not be too high for if the local
ionization density involves more than three alpha tracks to a cell, the cell is killed.
This leads to the theoretical prediction that in the system as whole, and looking at
cancer or leukemia as an end point, the dose response relationship is likely to be
BIPHASIC (see ECRR2003, Burlakova 2000). That is to say there will be a large
effect at low doses (the doses being conventionally calculated using the ICRP model),
then the effects will fall off as the dose is increased, only to rise again at even higher
doses as tissues of less sensitivity are attacked.
The third consequence of the discovery of genomic instability is that it
predicts that there will be a range of harmful effects from exposure to radiation. There
will not just be cancer and heritable damage, but because of the damage to whole
systems in the body, there would be expected to be effects in a range of diseases. Such
effects have been reported in those exposed to radiation both after the Japanese A-
Bombs and also after Chernobyl (ECRR2003, ECRR2006). For example, Table
2.8.1, copied from ECRR 2003 lists morbidity for those exposed to radiation from the
fallout from the Chernobyl accident and in Table 2.8.2 are listed the increases in ill
health conditions of the Hiroshima survivors published by Dr Dr Katsumi Furitsu.
The current risk model of ICRP only focuses on cancer, so these effects are not
considered. This aspect is relevant to the test veteran cases since many of them are
claiming for non-cancer conditions including coronary heart disease and kidney
diseases which are clearly significantly increased in both the Chernobyl exposed and
the Hiroshima exposed groups. Professor Mikhail Malko, from whose published work
table 2.8.1 is taken is a distinguished scientist, Deputy Director of the Belarus
Ministry of Power and also a member of the ECRR.

Table 2.8.1 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, discussed in ECRR2003).

Non cancer diseases 3 contaminated
5 control

Altogether 62,023 48,479 <.0001
Infections and parasites 3251 2119 <.0001
Endocrine, metabolism,
2340 1506 <.001
Psychic disorders 2936 2604 <.01
Chronic Otitis 250 166 <.01
Circulatory system,
hypertension, ischaemic heart
12060 9300 <.001
Of which (above) stenocardia 1327 594 <.01
Cerebrovascular 1981 1363 <.001
Respiratory 2670 1789 <.001
Digestive organs, e.g. ulcers,
chololelitic, cholecystitis
7074 5108 <.001
Urogenital, nephritis,
nephroses, kidney infections
3415 1995 <.001
Female infertility 84 56 <.01
Skin diseases, dermatitis,
3377 2060 <.001
Osteomuscular, osteoarthritis 5399 4191 <.001

Table 2.8.2 Comparison of morbidity rates (%) of the A-Bomb victims and of the
general Japanese population (Furitsu, 1994)

Non cancer disease A-Bomb victim sample
morbidity rate %
Japanese population
morbidity rate %
Lumbago 29 8
Hypertension 24 15
Ocular disease 18 3
Neuralgia, myalgia 12 2.5
Anaemia, leukopenia 12 1
Dental disease 10 <1
Gastro-duodenal ulcer 9 2
Ischaemic heart disease 9 2
Liver disease 8 1
Diabetes mellitus 7 3
Nephritis, urethral infection 5 1
Skin disease 5 2
Bronchitis, pneumonia 5 0.8
Cardiac arrhythmia 5 <0.1
Cholethiasis, pancreatitis 4 1

Finally, it is valuable to note that the most recent research into genomic instability
finds a very wide range of genetic based radiosensitivity. The range is often quoted at
up to 1000-fold.
This brings me to another theoretical argument which was developed by me in
the late 1980s and is also discussed in the two CERRIE reports. This argument relates
to the Second Event Theory (see Busby 1995, CERRIE 2004 and CERRIE Minority

2.8.5 Doses to local tissue over time.
For external radiation at low dose (1mSv annually), where the track density is low,
cells receive on average 1 hit per year. This damage they have evolved mechanisms
for dealing with. If the damage is great and surveillance enzymes detect a mismatch
between the two halves of the DNA duplex, then the cell may move from quiescent
phase into a repair replication cycle and repair the damage and replicate. The period
of this cycle (which cannot be halted once started) is about twelve hours. The result is
two daughter cells which a have copies of the repaired DNA. However, if a second
track damages the DNA towards the end of this period, there is no possibility of a
repair and the mutation is copied to one of the daughter cells. This is a very efficient
way of introducing a fixed mutation. It is very unlikely to occur with external
radiation tracks (since at low dose, to hit the same cell twice is like discharging a rifle
in the general direction of Texas and expecting to hit the same person twice). But for
internal isotopes bound to DNA or internal particles, this sequence is billions of times
more likely. This represents another reason why internal radiation is not modeled by
the ICRP model (which assumes at low dose that each cell is hit only once in a year
and that all cells in an exposure carry the same probability of a hit).

2.8.6 Uranium: Photoelectron amplification
I will briefly review a recent discovery which is relevant to internal radiation
exposure and which is not incorporated into the current risk model. It is of significant
interest in the case of the A-Bomb Test Veterans since it related to internal exposures
to Uranium. It mainly affects those who are contaminated with high atomic number
elements and also subject to increased external gamma radiation. The most important
elements are uranium and lead: for the Test Veterans, Uranium. It is an interesting and
well known fact that the absorption of gamma rays of energy lower than 1000keV is
proportional to the fourth power of the atomic number Z of the absorbing element.
This means that high Z elements like uranium (92), gold (79) and lead (82) absorb
some 100,000 to 500,000 times more gamma radiation than water, the main
component of the body. The effective atomic number of water is 3.3 or if we take the
oxygen atom as representing the highest atomic number and therefore major absorber,
If the absorbing atoms or particles are bound to DNA or some critical
organelle or protein, this will focus natural background gamma radiation into that
tissue volume through the re-emission of the absorbed energy as photoelectrons. Thus
the absorbed dose to that volume will be significantly higher than that calculated by
the ICRP system. For a full discussion see Busby 2005 and Busby and Schnug, 2008.
The effects will generally occur for any material with a higher atomic number than 8;
indeed it was first pointed out in 1947 by Speirs that there was a 10-fold enhancement
of dose to tissue near bone owing to the presence of the Calcium (Z=20) in the bone.
Inhalation and concentration of uranium in the lymphatic system of the A-Bomb
veterans will increase the doses to their lymphatic system through amplification of the
already enhanced background gamma radiation. Based upon these photoelectron
considerations, the physical enhancement weighting factor w
for the radiation dose
coefficient for U-238 contamination has recently been agreed by the ECRR as 1000
(see below). Since contamination by Uranium was significant on the test sites this
makes a big difference to the equivalent doses received from inhaled and ingested
dust. In 2008-9 I have been co-supervising at the University of Ulster a PhD student
Andreas Elsaessar who has been working on the issue of photoelectron amplification
of natural background radiation by high atomic number nanoparticles. He had carried
out laboratory work on cell cultures and also employed Monte Carlo modelling of
induced electron tracks to show that Uranium nanoparticles (and therefore uranium
atoms0 do indeed cause enhanced absorption of gamma radiation and the production
of photoelectrons, as I predicted. Fig 2.4 shows results of one calculation and
compares the photoelectron emissions from water, gold (Z=79) and uranium
nanoparticles of radius 20nm irradiated with natural background gamma radiation of
energy 100keV.
This work is extremely relevant to the matter of the exposures of the Atomic
test veterans since, as I will argue, the fallout and resides from the bombs contained
large amounts of uranium, probably as nanoparticles and certainly respirable. The
ECRR has a assigned weighting of 1000 to respirable uranium in its 2010 report and
the effects of exposure to uranium particulates from weapons have been found to be
alarming (Busby et al 2010, ECRR2010).

Fig 2.4 Photoelectron tracks emerging from (left to right) 10nm particles of water
(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 in proportion to a
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 (Howard et al 2009)

2.9 Chernobyl Proofs

There are two pieces of information that show unequivocally that the ICRP risk model
is in error by a large amount when applied to internal irradiation. Both result from
examination of populations exposed to the fallout from the Chernobyl accident. They
are both discussed in the two CERRIE reports and also in ECRR2003.
In general, the health effects of the Chernobyl accident have not been
adequately examined by the 'official' radiation risk community, and the very large
body of evidence that the exposed individuals in the ex-Soviet territories have
suffered and continue to suffer serious ill health outcomes has been largely ignored in
the various official reports in the west, though not in Russian language journals. A
compendium of these Russian reports was given as an appendix in the CERRIE
Minority Report, and the situation was flagged up by the eminent Russian
Academicians Yablokov and Burlakova at the Oxford CERRIE workshop b
was done by the CERRIE secretariat. A comprehensive review of the Russian
language literature on the effects of the Chernobyl accident, showing the extrem
serious effect of the radiation exposures form the internal radionuclides, was
published in 2005 (Busby and Yablokov, 2005) and the cover up of the health
has been reviewed in my book Wolves of Water (2006) and W. Tchertkoff’s book Le
Crime de Tchernobyl (2006).
The problem in the cou
ut nothing
rt of scientific opinion (and indeed in a court of law)

nce this proof that the ICRP risk model in wrong by at least a
as the in

l is
able 4A6 where it gives the

with cancer causation is that there is generally a time lag between cause and effect,
and since there are many mutagenic causes, it is difficult to make a connection whic
is unassailable in logic. In the case of the Sellafield childrens’ leukemia (and other
similar clusters) despite the fact that they lived near the most radioactively polluted
site in Europe, and that radiation is the only known cause of childhood leukemia, it
was argued that the ICRP Hiroshima model did not predict the risk and so it must
have been something else. Attacking this logic is easy, but does not result in anyth
approaching proof. It is not like a murder where a knife is thrust into the victim and
the body is found with a knife in its back and the culprit's fingerprints (Busby 2007).
However, after Chernobyl there were two discoveries which show unequivocally that
the ICRP model is, at least in these specific cases, manifestly incorrect by the same
orders of magnitude necessary to explain the Sellafield child leukemias and also many
other observations that had been dismissed on the basis of the ICRP Hiroshima
external risk models.
I will here adva
factor of 100 times. The argument has been published (Busby and Scott Cato 2000,
Busby 2005). This is a simple and brief analysis of the increase in infant leukaemia i
five different countries in Europe in those children who were in the womb at the time
of the fallout. The countries were Wales, Scotland, Greece, Germany and Belarus.
These increases were measured in each country. They were statistically significant
and could not have occurred by chance since the calculation for all the countries
combined makes a probability of 1 in one thousand million that these were
collectively a chance observation. Second, since the group being observed w
utero cohort exposed only to Chernobyl fallout it was an effect of Chernobyl fallout.
They were reported in separate papers in the peer review literature by four separate
groups of researchers so it was not a biased account by one group. The doses (based
on ICRP considerations) had been well described and measured. The only known
cause of child leukaemia is ionising radiation. The differences in the levels of
leukaemia rates in the exposed cohort and the rate predicted by the ICRP mode
greater than 100-fold but varies inversely with the dose.
The CERRIE Majority Report conceded this p88 T
central estimate of error in the ICRP model for Great Britain as 200X, for Greece as
160x and in Germany as 96X. In a paper I published in 2000 with Molly Scott Cato
(Energy and Environment, 2000), I calculated for Wales and Scotland the effects wa
greater than 100X and probably about 300X. This is the exact error in ICRP required
to explain the childhood leukaemia cluster at Sellafield, and also the present cancer
epidemic. These error factors mean that there are 100 to 500 times more leukemias f
a given dose than ICRP calculates. Most recently I reanalysed data supplied by the
Oxford Childhood cancer Research Group and published a meta analysis of the
Chernobyl infant leukaemia data in the International Journal of Environment and
Public Health (Busby 2009) concluding that this provided prima facie evidence of
failure of the ICRP model for internal irradiation, at least in the case of infant

.10 Minisatellite mutations
s the objective scientific measurement by several
d to
.11 Radium and Thorotrast
e ICRP and its adherents base their analysis of internal
n. I

.11 ECRR
lained, the last ten years has seen a revolution in the perception of risk

The further piece of evidence i
groups of significant mutation rates in the minisatellite DNA of children and adu
living in the Chernobyl affected territories but exposed, on average, to ICRP
calculated doses of less that 2mSv a year. Various arguments can be employe
show that this represents an error in the ICRP assessment of genetic damage risk o
the order of 500-2000-fold. In one particularly elegant epidemiological experiment,
children of Chernobyl liquidators who were born after the accident were compared
with siblings born before, to exclude explanations other than the Chernobyl accident
A seven fold increase in minisatellite mutations was found. That these effects are
significant for health is seen by another study which showed that plumage changes
swallows that migrate to the Chernobyl region are also associated with minisatellite
DNA mutations (for references see CERRIE 2004, ECRR 2010).

As I have mentioned above, th
radiation exposures on studies of patients exposed to high doses of Radium and
Thorotrast mainly before the 2
world war when it was not net realized how
dangerous internal radiation exposures were. These substances have been em
as surrogates for all internal exposures, particularly plutonium, in an attempt to show
that the application of the averaging external dose model gives the correct cancer
yield for all internal exposures without consideration of any of the biophysical or
biochemical issues highlighted by the ECRR. The ECRR has been studying the
evidence from studies of Radium- and Thorotrast-exposed patients, and animal
studies using Radium and Thorotrast. A report on the issue will be published soo
can say that the report will largely discount all such studies on the basis that they wer
carried out too late after the exposures and examined populations which had already
lost significant numbers of cases as a result of competing causes of death. It is quite
clear from the evidence available that non-cancer deaths in both groups were
extremely high and this fatally flaws the outcome of the studies in both Radium
Thorotrast groups which were studies of cancer as end point. Therefore deaths from
other diseases do not figure in the risk model. Further points which will be made in
the final report are that the linear no threshold model is not appropriate for these high
dose studies and indeed for radiation studies generally (for reasons given in
ECRR2010). In addition, the different exposures, to Ra-224, Ra-226 and Tho
are to very different materials in terms of anisotropic doses to target DNA. ECRR
(and indeed common sense) holds that each isotope has to be considered as a separ
chemical and physical entity in terms of ionization at the target.

As I have exp
from ionising radiation and from radioactive substances existing inside the body
following inhalation or ingestion. This debate was the subject matter of the three y
deliberations of the UK CERRIE committee and also of the considerations leading to
the risk model of the European Committee on Radiation Risk ECRR.
The European Committee on Radiation Risk arose out of a deep concern
among many distinguished scientists and experts that the risk models for radiation
exposure currently employed by national governments to set legal limits for exposure
were incorrect by a large amount when applied to internal irradiation. Its committee
was begun in 1997 and its origins and remit are outlined in the 2003 and 2010 reports
and also on the website In the ECRR reports, the ICRP models
are shown to be scientifically incorrect for internal irradiation since their basis is
external irradiation (from outside the body). Such a model is philosophically
irrelevant when applied to internal irradiation from a point source (such as a particle
or an atom bound chemically to DNA) as I have explained. I refer to chapters 1, 2, 3
and 6 of ECRR2010. The ECRR deals with the enhancement of hazard from internal
radionuclides by extending the method used by the ICRP for radiobiological
effectiveness of alpha, neutron etc to situations where the chemical affinity of an
internal radionuclide, or its physical decay characteristics makes it more effective at
delivering ionisation to the DNA. The dose coefficients developed by the ICRP are
used but with weighting multipliers w
and w
to represent physical and chemical
enhancement mechanisms. Therefore a dose of 1mSv from an isotope that binds to
DNA strongly, like Sr-90, is multiplied by a w
of 50 and so the dose becomes 50mSv
in the same way that ICRP multiply the absorbed doses from alpha emitters by 20 to
obtain their equivalent dose.

2.12 ECRR in Lesvos
In May 2009 there was an International Conference of the ECRR in Lesvos, Greece,
hosted by the University of the Aegean. Research papers and evidence falsifying the
ICRP risk model were presented at this conference by eminent radiation scientists
from Japan, Canada, UK, Germany, France, Russia, Ireland, India, Ukraine and
Belarus. The proceedings are currently being prepared. However the radiation risk
situation and the level of error involved was considered to be so important the
conference culminated in a agreed declaration signed by all the scientists present, the
Lesvos Declaration (see This is attached with the names of the
signatories. It demonstrates that a large body of eminent expert opinion exists that the
ICRP model is unsafe and should no longer be used to calculate the effects of internal
radiation exposure. This ICRP model is essentially the same as that of the US BEIR
committee. In its stead, political and courtroom decisions should be made on the basis
of the ECRR risk model.
The new 2010 updated risk model was published in May 2010 and is appended as
evidence in this case (ECRR2010).

2.13 IRSN
Independent support for the arguments that internal radiation effects are not properly
modelled by the current ICRP risk model comes from a report commissioned by the
French government and published in 2005 (IRSN 2005). A team of scientists from the
official French Institute for Radiological Protection examined the 2003 report of the
ECRR (above). They concluded that the criticisms made by ECRR of the current
ICRP risk model were important and were valid, though the IRSN report did not agree
with the way in which ECRR modified the risk model to account for the resulting
errors (IRSN 2005).

2.14 Recent proofs of the failure of ICRP from Sweden and Belarus
Cancer in Northern Sweden after Chernobyl was studied by Martin Tondel who
published results in 2004 (Tondel et al 2004, 2006). By comparing cancer rates
before and for 10 years after the Chernobyl fallout in Sweden by Caesium-137
contamination of communities in Northern Sweden, Tondel was able to determine a
risk of 11% excess cancer incidence per 100kBq/m
. This translates to an error factor
of a minimum of 600-fold in the application of the ICRP cancer risk model to the
external gamma dose associated with this contamination integrated over one year
(ECRR2010). In 2004 also Okeanov reported significant increases in cancer in
Belarus following the Chernobyl accident: these increases also were not predicted by
the ICRP model since the mean dose to the Belarus population from Chernobyl was
about 2mSv, approximately equal to the annual background radiation dose, yet the
cancer incidence rates had increased by about 40% (ECRR2010).
These pieces of evidence support the assertion that the ICRP model is in error
by two or three orders of magnitude when applied to internal exposures.
The ECRR2003 model accurately predicted the findings of Tondel and
Okeanov and the matter is discussed in ECRR2010.

2.15 Admission of the error following the resignation of the ICRP secretary
In April 2010 I personally carried out a public interview with the ex-Scientific
Secretary of the ICRP Dr Jack Valentin in Stockholm, Sweden. The interview was
recorded on video and is available to the court. It will shortly be put on the internet.
And a transcript is available of the critical part on the website of the Low level
Radiation Campaign It should be noted that Valentin was the editor
and author of both of the 1990 and 2007 ICRP risk model reports (ICRP2007). In the
interview, Valentin made two statements which are relevant to the present case. First,
he said that since he was no longer Scientific Secretary, having resigned a few weeks
earlier, that ICRP and UNSCEAR (the United Nations Scientific Committee on the
Effects of Atomic Radiation), he could say that both organizations were wrong in not
addressing the evidence that falsified their model evidence form Busby, from
Chernobyl and from the nuclear site child leukemia clusters. Second he said that the
ICRP risk model could not be employed to asses the risk of radiation in human
populations because the uncertainties in internal radiation exposure modeling could be
two orders of magnitude. This statement is in broad agreement with the ECRR thesis
and model and agrees with what I have written in my earlier report on this case.
I provide the video of the interview as evidence in this case and a transcript of part of
the interview in the Appendix.

Summary of Part 2

The history of radiation risk models shows that the exposure levels permitted by
policymakers have continuously been readjusted throughout the last 80 years as every
new discovery both in science and in epidemiology has shown that radiation exposure
is more dangerous than previously thought. This process of discovery continues today
although the dose limits are stuck at their 1990 levels. This is because the current
official radiation risk models have not incorporated the most recent discoveries since
to do so would force a complete reappraisal of the current use of nuclear power and
the historic harm done by releases of radioactivity in the past. Contemporary radiation
risk models are so inaccurate for internal exposures that even some official risk
agencies (IRSN) have pointed this out: yet they continue to be employed by
governments and used by polluters to justify their past and present behaviour. There is
now sufficient scientific proof of this in peer reviewed published literature. These
discussions are of relevance to those who were exposed at the test sites.
It is now clear, with hindsight, that the risk models in operation at the time of the tests
were wrong. They failed to recognise the dangerous nature of internal exposure and
did not even measure it. They concentrated on external exposure, and as I will show,
even then applied limits which were too high and which they just accepted, limits
which were clearly cobbled together in order to permit the development of nuclear
weapons. When these limits were questioned by many independent scientists, by the
media and in several books, those responsible for the safety of the personnel
dismissed or ignored the claims.
My reason for discussing the history and development of risk models is to
show that all the scientific evidence is that even current statutory dose limits do not
adequately safeguard human health. It has become clear that the dangers of low dose
radiation should have been apparent to all who worked with radioactivity or employed
those who worked with radioactivity at least from the early 1980s when the nuclear
site child leukemias were widely reported and when the dose limits were reduced to
the point that they could not be reduced further without seriously affecting industry
and the military. It should have been clear to the military by the 1957, certainly to
those who were responsible for the health of the personnel, that what was being done
was likely to cause long term ill health to the people who worked at the test sites, and
indeed those who lived on the planet.
The weight of scientific belief about the dangers from internal radiation began
to change in the mid 1990s with interest on the increasing evidence from nuclear site
clusters and Chernobyl effects which clearly showed that the contemporary risk
models were somehow false by a very large amount. Between about 1996 and 2000,
evidence began to emerge from the laboratory for genomic and bystander effects.
Since the then current ICRP model was based on genetic damage and a linear relation,
it was implicit by 2000 that this basis was completely incorrect. This, and various
other epidemiological evidence (which had now to be re-assessed) led to the
Committee Examining Radiation Risks from Internal Emitters and the ‘Radiation
Science Wars’ of the early 2000s. The critical impact of the 2003 report of the
European Committee on Radiation Risk, and the clear demonstrations in
epidemiological evidence from the Chernobyl; affected territories (infant leukema,
minisatellite mutations, cancer in Sweden, Belarus and Ukraine) that the ECRR
predictions were close to what was seen was a turning point in a paradigm shift that
continues today.
It is so clear to a rational audience that I have persuaded all of the courts or
juries that I have given presentations to. It is only the biased scientists of the nuclear
military project and the economic and military vested interests that continue to
support the conventional model. Part of the problem is that the area of radiation risk is
not one area but many. Each expert or employee sees only part of the picture. The
physicist sees the world as energy transfer and mathematics. The epidemiologist sees
the effects but doesn’t understand the physics and assumes absorbed dose is a real
parameter, a given. This was the problem with the late Sir Richard Doll, who I spoke
with about this. Doll based everything on absorbed dose and died believing that the
Sellafield leukaemia cluster was not of radiological origin. The biochemist also
assumes absorbed dose is meaningful but here we are approaching reality if we are
prepared to think through the ionisations and their position on the target DNA. I have
met very few experts in this field who see the whole picture; yet it is the whole picture
that is necessary if one wishes to understand the issue. Each expert is an expert in one
filed, and can pass the buck: the epidemiologist says that the cancers are there but
they cant be due to radiation because the physicists say the dose is too low. The late
Martin Gardner, the Sellafield epidemiologist, tried to get round the dose problem by
assuming it was dose to the fathers sperm that was the trouble: he never questioned
the paradigm, he never questioned is dose was a real thing. The physicists in their turn
use dose: they invented it. They say that the Hiroshima studies show the cancers are
only there when the dose is high, but they don’t see the chemistry, they don’t know
the stuff gets inside you and binds to the DNA they aren’t interested in such messy
stuff, you cant use mathematics there. No one asks the chemists because why would
they? The chemists do chemistry? What do they know about dose? But if dose isn’t
appropriate or real (and it isn’t) the whole house of cards collapses.
Before 2000, the military could just about argue that the science backed their
denials of harm for the veterans, and also for the depleted uranium effects in other
veterans of the Gulf War. After 2003 their defences became increasingly shrill, as the
juggernaut of empirical evidence became heavier and slowly rolled toward them.
Thus any argument about limitation, that the veterans should have taken action closer
to the time of their exposures would have to deal with the fact that before the mid
1990s, there was not sufficient scientific basis in belief to explain or predict their ill
health. After 2000, this situation changed. And HH J Foskett agreed.

Part 3

Real Exposures of the Test Veterans

3.1 Routes of exposure
There are a number of sources for data needed to examine the issue of the exposures
of those who visited the test areas either between or when detonations occurred. In
this report I have still not yet seen all the documents I wish to and therefore reserve
the right to add to or change anything I will state below. I am also short of time for
this report for the Appeal Tribunals.
The test sites were at Maralinga and Emu Field in Australia, the Monte Bello
Islands and at Malden and Christmas Island. Personnel were exposed to external and
internal radiation through a number of routes. I outline the most important in Table
3.1 and identify the information that could be used to assess the doses in each case.

Table 3.1 Exposure routes of test veteran ionising radiation and sources of data

Radiation exposure Type of radiation Data and criticisms
Acute, from
Gamma, neutrons Personal Film badges, dosimeters; poor
sensitivity, not issued to all, mislaid etc.
Ground shine Gamma, beta Personal Film badges, dosimeters; not
issued to all; ground surveys with
Geiger and scintillation detectors;
results sparse or not available or too
instruments insensitive; beta not
registered by film badges; badges worn
high. Limits too high.
Internal fallout and uranium
Inhalation of
contaminated dust
Alpha, beta,
gamma, uranium
Highly significant route, not addressed
by MoD now or adequately protected
against at time; uranium not addressed;
alpha not measured; limits too high for
redlined contaminated areas. Sparse
deployment of high volume air
samplers and useless screening of filters
employing inadequately sensitive
Inadvertent ingestion
of soil and dust
Alpha, beta,
gamma, uranium,
Highly significant route, not addressed
by MoD now or adequately protected
against at time; uranium not addressed;
alpha not measured; clothing
contaminated; redlining of clothing too
Ingestion of food Alpha, beta,
gamma, uranium,
Possible route; limited by diet; fish
radiation measurements ridiculous.
Ingestion of water Alpha, beta,
gamma, uranium,
Possible route, especially by sea
bathing, drinking water.

The personnel who lived and worked at the test sites were subject to all of the routes
of exposure shown in Table 3.1, but at the time, from the documents available, it is
clear that the emphasis was on what would now be seen as large gamma doses. In the
first tests, in Australia, the instruments available to those who were recording
radiation levels were very insensitive by today’s standards; even by the time of the
Christmas Island tests, the instruments employed for general surveys, or often the
method itself laid down for surveys of fallout were not well thought out and the
results generally worthless for the purposes of health safety. Those military men who
operated the systems of measurement and control of exposure seemed not to
understand what they were doing, or how the instruments worked. They seemed to
use the instruments more as a Transylvanian technician might routinely use garlic
flowers than in the way scientists would use an instrument of which the utility,
purpose and shortcomings were familiar.
The focus was on the gamma radiation from the blasts; following that, the
initial ‘hot’ fallout: material with neutron activation products and short half life decay
products from the immediate fission of U-235. It was assumed that after about three
weeks from detonation there was no further real radiological hazard from the fallout.
As an example, in one report for Operation Buffalo it is written [Jones, 1957]:

Radioactivity decays at a steady logarithmic rate. Because of this, complete
decontamination of very low level activity is not necessary

The gamma radiation from the fallout had fallen by a large fraction of its original
value. There was no concern about, or significant attempt to measure, contamination
by uranium, despite the fact that uranium was the main component of the bombs and
almost all the trials. Huge amounts of uranium were used for these weapons. U-238 as
tampers, U-235 as fissile material and, completely overlooked, the alpha emitter U-
234 which came in in huge quantities with the U235. In one bomb there was almost a
ton of uranium. Since the actual proportion of the uranium that fissioned was quite
small, a few percent, the rest of the uranium was atomised, converted into micron and
nanometer particles of oxides, and dispersed at the site of the bombs. The instruments
employed were mainly gamma detectors, unable to measure betas except in certain
types of instrument. Those instruments with thin windows that could measure betas
did not detect alphas, which in any case have a range in air of a few centimetres and
are stopped by thin films of water. I have discovered and examined a small amount of
data collected at the time and some data from many years later which show that the
contamination of the areas where the veterans lived and worked was very high. In this
preliminary report, because I am constrained by the reports I have seen, I will
examine two areas and analyse the fallout levels in these areas on the basis of the
small amount of data I have. As far as I can judge, the measurement of fallout at the
test sites was not made at a sufficient number of positions, and when the levels were
measured, they seem to have been discounted in terms of hazard. I draw conclusions
about the levels of fallout in two areas and apply conventional methods to calculate
the doses received by the men who worked and lived at these sites.

3.2 Christmas Island; Overall exposure of personnel.

The Ministry of Defence state in their own defence to the class action, and also in all
veteran tribunal defences that I have been involved in, and also in letters to the
Pensions Offices that I have seen, that the radiation doses received by those who
remained at Christmas Island during or after tests was considerable less than the same
personnel would have received in the UK. This is demonstrable false, and is a result
of considering only the gamma ray component of external irradiation. The
background at Christmas Island is given as 610 µSv and this is compared by the
military with the annual natural background of about 2500µSv (2.5mSv) in the UK.
This is a false comparison since the mean gamma background in the UK is about
700µSv, about 80nSv/h. The remainder of the dose in the UK is made from internal
alpha exposure to radon gas, which is exalted by the weighting factor of 20 applied to
its absorbed dose due to the ICRP alpha weighting factor. The Christmas Island dose
employed by the military in this argument has no component from radon gas, or any
other internal alpha emitter; no attempt (that I have seen) was made to assess internal
alpha radiation. There would have been a great deal of this since massive amounts of
uranium contamination will have occurred and uranium is an alpha emitter. In
addition, significant activities of plutonium were also present. These were not
measured nor assessed for dose calculations. The argument that doses were lower than
would have been received in the UK is therefore incorrect. I will attempt to use the
data I have seen to remedy this deficit and calculate the doses to the personnel using
conventional methodology.

3.3 Christmas Island and the Grapple operation. Measurements of fallout at the
time: 1. sticky papers

My source for the data which I assess here is stated to be review of all the records
available. These included airborne activity from pumped air filter samplers, water
activity, and sticky papers. Results are displayed on graphs which show a timeline
including the various tests that took place and the activity (concentrations) of fallout
measured as beta and gamma measured using various different devices. The report
was published in October 1993 by the AWE and entitled Environmental Monitoring
at Christmas Island 1957-58. I will concentrate first on the measurements of sticky
papers which appear to have been deployed rather sporadically at various points on
the Island at various times. It is not clear from the text how many of these were
deployed and how often they were examined: there does not seem to have been any
systematic measurements, or at least I have not seen tables of continuous
measurements at specific sites. I show the location of various sampling sites on the
map of Christmas Island in Fig 3.1
I will begin by assuming that the measurements were accurate and were
accurately reported. It is clear that the island was fairly well bracketed by
measurement points for sticky papers. These were sheets of ‘sellotape’ which were
exposed to the air and fallout collected on the surfaces and was subsequently
measured in the UK at AWRE. Results were collected together from the various
reports and reported by Clare et al in the form of a timeline graph. I show one in Fig
3.2 . On this diagram, the activity of the fallout on a specific day is shown for a
specific site. For example, we see that on 22nd August 1958, the sticky paper at the
camp about 3µCim
. On the top of the diagram we see that this was on the day of the
Grapple Z1 test. Other diagrams examine other sites. Where there is no cross on the
diagram, we are to assume that the sticky paper activity was below 5 x 10-4 µCim
the limit of detection. First, 3µCim
translates to modern units of 111,000Bqm
is quite a significant level of radioactivity. For example, the UN definition of
contaminated land is 37,000Bqm
. The authors of Clare et al, and others, have
discounted the sticky paper measurements on the basis that the papers often showed
levels below detection. They summarise their findings:

The summary is believed to include all the surviving data gathered at the time. The
measurements usually gave results below the level of detection. On the few occasions
when radioactivity above this limit was detected, the levels were low, decayed or
dispersed rapidly, and did not constitute a hazard . . .

They failed to take account of the fact that each measurement that was positive on the
sticky papers represented a fallout episode on the island at that point and that each
fallout deposition was in addition to a previous one. Thus the island was gradually
acquiring a cumulative deposition of fission products. I can calculate this cumulative
deposition by averaging the various sites and adding up each fallout episode. I show
results of this approach in the graph Fig 3.3. We must note that the activity here is
gamma activity and does not include beta and certainly alpha activity. Since, as I will
show, the beta activity exceeds the gamma activity by a factor of from 3 to 20, the
combined beta gamma cumulative activity will be between 3 and 20 times the
cumulative activity I calculate from the Clare et al sticky paper results for inhabited
areas, that is Port, Sites A and C, Airfield, Main Camp and JOC.
Radioactivity on the sticky paper on the west side of the island were
significantly higher. I show some results in Table 3.1 . By the end of September 1958,
the mean cumulated gamma activity of the fission product deposition (based on the
value at H+1) was 67µCim
. This is in stark contrast with the values for the
‘inhabited areas’ which were considerable lower, perhaps by a factor of about ten by
the same time. Looking at the map of the sample sites in Fig 3.1, it is hard to see how
there could be such a great discrepancy. I conclude that there was some selectivity in
collecting sticky papers or in reporting embarrassing results. To put these levels in
context, the mean cumulative deposition of 67µCim
for the uninhabited areas
represents four times the level of activity in the 30km Chernobyl Exclusion Zone, the
area evacuated by the Soviet Authorities, and still empty today. In modern units it is
Of course, these activities reported by Clare et al shown in Table3.2 and Fig
3.2 have been extrapolated to H+1, and therefore include the ‘hot’ isotopes with short
half lives. But on the other hand, the figures do not include the pure beta emitters
(Strontium-90, Strontium-89, Barium-140, Protoactinium-234, Thorium-234) and
dangerous alpha emitters (Uranium 238, Uranium-235, Uranium-234 and Plutonium-
239) which have half lives in millions of year. I will show below in Section 3.4
evidence that these substances were in the fallout, were overlooked, and remained on
Christmas Island.
Where I have calculated the cumulative deposition for the inhabited areas (Fig 3.2) I
have used the results as measured i.e. not extrapolated to H+1 hrs.
In addition to the Radiation Monitoring Group (RMG) results which I have
used, there were also local surveys. Until I know more about the methods used, and in
view of the varying quantities of fallout reported, and the lack of correlation with the
RMG results I will ignore these limited data. Results show highest levels of fallout
deposition for Grapple Z1 and Grapple Z4, but measurements for Main Camp were
only reported for Grapple Z1 at 2.8µCim
. Strangely, for the RMG and Local
surveys, there are few measurements for the Main Camp.


Fig 3.1 Christmas Island with locations of personnel and test position. I have inserted
sticky paper fallout measurement points. (from: Clare et al. AWE: 1993)


Fig 3.2 Graph of sticky paper measurements at various sites on Christmas Island
1958. Radiation Monitoring Group (RMG) AWE measured 10 to 20 days after
collection and extrapolated to H+1hour. (Copied from Clare et al 1993.)

Fig 3.3 Cumulative build up of mean activity of predominantly gamma emitting
fission products on inhabited areas (Port, Sites A and C, Airfield, Main Camp and
JOC) of Christmas Island, 1957-58.

Cumulative Deposition of fallout Christmas Island
Month 1957-58


Table 3.2 Mean significant activities at various uninhabited sites Christmas Island
1958; µCim
extrapolated to H+1hours. Radiation Monitoring Group (RMG) results
See map Fig 3.1 for sites. (Clare et al 1993)

Site Grap Y
28 April
Grap Z
22 Aug
Grap Z2
2 Sept
Grap Z3
11 Sept
Grap Z4
22 Sept
200 200
D site 0.005 0.005
100 0.05 0.01 100.06
Target 50 50
RMF 20 0.8 20
B site 0.3 0.001 0.01 0.311
A site 0.1 0.1
Trig point 0.5 0.5
RM17 2 2
RM2 300 300
Mean 20.005 17.03 0.015 0.001 30.33 67.3
20.005 37.035 37.05 37.051 67.3 67.3

From the sticky paper measurements there are a number of conclusions that can be
initially drawn:
- There was significant fallout on the island.
- The main fallout events were associated with Grapple Y, Grapple Z1 and
Grapple Z4
- It appears that much more fallout was reported the sites designated
‘uninhabited’ than those designated ‘inhabited’. This is hard to believe given
the relatively short distances (a few kilometres) between these areas. This
suggests bias in reporting.
- A significant fallout event was reported at the Main Camp following Grapple
- Cumulative fallout resulted in mean levels on the island at the time of the
fallout and shortly after, which were well in excess of the UN definition of
contaminated land associated with the Chernobyl Accident.
- No measurements were made of uranium isotopes and plutonium, nor of the
pure beta emitters, resulting in a considerable under-assessment of the total
I have not seen (but would like to) results of systematic beta gamma surveys of the
ground at any part of Christmas Island at the time. I feel these would shed further
light on the existence and activity of fallout. I cannot believe that such surveys were
not conducted.

The consequences of this inadequate monitoring is that we can be fairly certain that
there was considerable contamination of Christmas Island with alpha and beta
emitters which went unnoticed, and as I will show, the consequences were significant
for health.

3.3.2 Christmas Island and the Grapple operation. Measurements of fallout at the
time: Air filters, water and fish

I have concentrated on the sticky filters, since results for these were obtained from
laboratory measurements made in the UK. Measurements were also made by
measuring radioactivity of air filters, through which air had been pumped, on
rainwater samples and on fish.
The measurements of radioactivity in rain water samples appears to have
involved evaporating 1 litre to dryness and holding a Geiger Counter to the residue.
Fish measurements involved catching a fish and holding the Geiger counter to the
surface of the fish. Most measurements were reported to show no radioactivity. This
is unsurprising. I do not want to dwell on the absurdity of the methods here: they
were primitive, and with the equipment available in the field will not have detected
anything in either the water or the fish unless the samples were extraordinarily
radioactive. For example, reporting radioactivity in fish was based on an elevated
radiation detector reading that was one and a half times the natural background level
(McLean, 1959). A radiation detector of the most sensitive type will have a surface
area of about 16 square inches. The instrument was the AERE Type 1257C used (for
some unaccountable reason) with the beta window shut. It will be looking at about 4
square inches of the surface of a fish. It will be receiving gamma radiation from a
sphere of 2tsolid angle, a background radiation exposure of about 100nSv/hour,
which would register as B counts per second. Therefore the fish would have to
contribute 0.5B in the direction of the detector and 0.5 B away from the detector, and
roughly 2B in the directions parallel to the detector. Thus the radioactivity of the fish
would have to provide 300nSv/h just to hit the devised limit. This is 3 x 10-5 rad/hr
from a 6sq cm surface. From graphs in the Handbook of Radiological Protection, for a
700keV gamma radiation (about correct for fallout) the specific activity of a fish 5cm
thick for this to occur is about 11,000Bq/kg of gamma emitter. This level is 10 times
higher than the current cut off under the UK Radioactive Substances Act. Beta and
alpha radiation from the fish would not be measurable: indeed the beta window is kept
shut. If the beta component is added in at a ratio (fresh fallout) of 20, then the critical
activity of the fish to trigger concern would be 220,000Bq/kg!
Another really silly method of examining radioactive contamination was the
method of examining surfaces by smear test. This involved gently rubbing a 10cm
diameter filter paper on the surface being considered and then placing the filter in
front of a Geiger Counter. I have carried out some pilot experiments here to see how
much material adheres to a filter paper of this size. The answer is between 1 and 4mg.
For an increase in background counts of 50% (the threshold for assuming the
existence of radioactivity in this scheme) the specific activity of the tiny 1-4 mg
amount of dust would have to be dangerously high whatever instrument was
The emphasis seems to have been on external radioactivity. The idea that
internal radioactive contamination might be hazardous was not one that was ever
properly addressed. Sea water was also monitored in a similar way. I will address
these results more closely elsewhere when more data becomes available

3.4 Christmas Island; measurements of radiation in 1983: the beta gamma ratio
and its interpretation.

3.4.1 Oldbury’s report
What I am going to do, is to show that the fallout contamination contained massive
quantities of uranium isotopes which were entirely overlooked in the calculations
carried out by those assessing the exposures of the veterans and health effects. I am
going to do this by examining the ratio of beta to gamma radiation measured at the
same points using different instruments or the same instrument with and without a
beta absorbing window in position.
The contemporary measurements of fallout at Christmas Island, discussed in
3.1, suggested that there was accumulation of fallout. This is an important question
since it will have contributed to the doses. Another important question is how much
contamination was there from alpha emitters, particularly the uranium used in large
quantities in the bomb as fissile material and as tamper (to reflect neutrons). Uranium
is an invisible or overlooked element in all the reports I have seen of test veteran
exposures. Very large amounts of uranium were employed: it was, after all, the main
component of the bombs. I will return to uranium and its radiological properties
below. However, the question of the long lived fallout at Christmas Island can be
examined from data obtained in a study of the Island carried out some time after the
tests. I will first take a look at fallout and list ( Table 3.3) the main radioisotopes that
remain in bomb fallout after 2 years since it will later become clear that measurements
made at Christmas Island in 1964 by A.E Oldbury when the base was being closed
down demonstrate the existence of large quantities of a predominantly beta emitting
series of isotopes which I believe can only be Uranium 238 and its daughters. Note
that the ratio of beta to gamma emitters in the fallout is 12: 3.38 or 3.55:1.


Table 3.3 Main isotopes remaining after 2 years from debris of megaton weapons,
their beta gamma decay characteristics and their proportions in fallout (Eisenbud and
Gesell, 1997; Carter et al 2006; L’Annunciata 1997) Uranium isotopes and plutonium
not included
Isotope 2 years beta gamma E (Mev) Energy contribution
Sr-89 0
Sr-90 0.015 1 0 0 0
Y-90 0.015 1 0 0 0
Y-91 0.001 1 0.003 1.21 0.0036
Zr-95 0.002 1 0.49 0.76 0.3704
Nb-95m 0 0 0 0
Nb-95 0.004 1 1 0.77 0.766
Mo-99 0 0.16 0.75 0.12
Tc-99m 0 0
Ru-103 0 0
Rh-103m 0 0
Ru-106 0.235 1 0 0
Rh-106 0 0
Te-129m 0 0
I-131 0 0
Te-132 0 0
I-132 0 0
Xe-133 0 0
Cs-137 0.044 1 0.85 0.66 0.561
Ba-137m 0.042 0 0 0
Ba-140 0 1 0.26 0.54 0.1404
La-140 0 0
Ce-141 0 0
Pr-143 0 0
Ce-144 0.14 1 0.11 0.13 0.0143
Pr-144 0.14 1 0.01 0.7 0.007
Nd-147 0 0
Pm-147 0.094 1 0 0 0
Eu-155 0.013 1 0.5 0.1 0.05
U-237 0 0
Np-239 0 0
Pu-239 6.90E-03 0 0 0

Sum 0.7519 12 3.38

In general so far it has been impossible to obtain measurements of radiation made at
Christmas Island at the time of and shortly after the tests. Despite the many statements
that radiation levels were low, there seems to be no data to back this up. What would
be necessary would be contemporary gamma and beta gamma radiation surveys of
grids, particularly of areas where personnel were stationed or worked. Nor have I seen
any measurements of radionuclide concentrations. However, in 1964, the paper by AE
Oldbury gave the results of some surveys made in 1963 prior to closing the base. By
1963, the island had not been subject to tests for some years and so any material
present should have contained only longer lived isotopes. In addition, it is important
to know that by the time Oldbury’s survey was carried out, the island had already
been decontaminated by the US Radsafe organisation. The purpose of Oldbury’s visit
was to follow this US decontamination and reduce all residual surface contamination
to below tolerance level. In order to do this, Oldbury carried out some grid surveys
using beta gamma and pure gamma measuring equipment and reported the results.
This report is a valuable resource since it has enabled me to discover that the beta
gamma ratio is anomalous and can only be due to the existence of large amounts of
uranium. This uranium will not contribute to any film badge doses, but as an alpha
emitter and as a photoelectron amplification element will have contributed significant
harm to personnel through inhalation and ingestion. The existence of the uranium is
also supported by environmental samples collected by Oldbury and analysed.
I start with the raw data, copied in Fig 3.4 which shows Oldbury’s beta +
gamma grid of the aircraft washdown pad, about 200ft x 100 ft area. The instrument
employed was a 1320C detector and readings are shown in counts per second above
background: background was given as 1-2 cps. In Fig 3.4 is also shown my own
gridding from which I reduced the data to a form that enable me to produce a contour
map of the mean beta+gamma contamination which I show in Fig 3.5


Fig 3.4 Beta + gamma counts per second over the aircraft washdown pad Christmas
Island, 1963 (Oldbury 1964)

Fig 3.5 Contour plot of mean beta + gamma levels over the washdown pad shown in
Fig 3.4. Note that the height is approximately the amount of times above natural
background that the exposure level was. (Data from Oldbury 1964).Mean beta +
gamma 16cps; SD 22cps

Oldbury also surveyed the same area with a pure gamma detector, the 1413. I have
converted his grid into a surface plot and show the result in Fig 3.6. Note the
variability between the beta + gamma and the pure gamma. The mean levels of
gamma are 0.032mR/h but the main gamma emitters are at the periphery of the pad.
For most of the pad, excluding these outliers, the exposure means were 0.02mR/h. or
200nGy/h. The background measured and recorded at the land away from the
washdown strip we can take to be the general background for the area. The lowest
recorded gamma exposure was 0.004mR/h which is 40nGy/h, about the same level
found in England and Wales. This would give an annual dose from gamma of
0.35mSv. Note that this is not comparable with the average natural background dose
in the UK as the internal radon exposures have not been added in.

Fig 3.6 Contour of gamma exposure rates over the washdown pad on Christmas
Island; mR/h on the 1413 gamma instrument in 1963 (AE Oldbury, 1964) Mean
gamma 0.032mR/h SD 0.04

The purpose of the present exercise is to compare these gamma levels with the beta
counts from the 1320 instrument. If the mean gamma level is 0.032mR/h we can
convert this into counts per second on the 1320 since we know (Oldbury p2) that 2-3
cps with the beta window shut is a gamma exposure of 0.5mR/h. On this basis, if this
is true, then 0.032mR/h should give 0.032/0.5 * 3cps at maximum i.e. 0.1cps. From
my own knowledge of instruments like the 1320, I think that the reported equivalence
of 0.5mR/h and 3cps is a misprint, or is wrong. I believe that the gamma response of
such an instrument at a background of 0.032mR/h is about 1cps, but this is unlikely to
be in error by more than a factor of 50% either way. I can refine the calculation when
the gamma response of the 1320 in cps is found. The point is, that the results show
that the majority of the signal from the beta gamma 1320 probe is from beta radiation.
Indeed, Oldbury states as much. In Table 1 the sludge pit gave 40cps with the beta
window shut and 400cps with it open. If we take the background radiation exposure
away from the washdown area (1-2cps) as being entirely due to gamma, then from the
beta + Gamma readings on the washdown area, the beta/ gamma ratio is enormously
high. In Section 4.2.4 Oldbury examined the Ultrasonic cleaning centre. Here he
reported 40cps beta + gamma and 1-2 cps gamma over a small area. This is a beta
gamma ratio of between 40 and 20 to 1.
Oldbury gave values for the beta and gamma level at the washdown pad, using the
same beta gamma probe with the beta window in or out. I show his results in Table
3.4 and I gather some of these beta gamma ratios together in Table 3.5.
In Table 3.4 I have also included a column in which I have subtracted the expected
beta levels, calculated from the normal ratio of beta to gamma emitters in fallout from
megaton weapons, obtained from the fissioning of the material and shown in Table
3.3. It is clear from all these considerations and these analyses, that there are far too
many betas, that is to say, there is a large amount of material which is a beta emitter
but not a gamma emitter. It is not a fission product, since I have included all these.
What can it be? In terms of activity, it is in large excess. Indeed where there is high
activity, it is most of the material. In the sludge pit we see 400cps beta and only 40cps
gamma. Since the normal ratio in fallout is 3.55, we should expect 40* 3.55 = 142 cps
of beta. We find 400 cps, an excess of 258cps. What is the material, the unknown and
unrecorded isotope responsible?

Table 3.4 Contamination survey results of aircraft washdown pad showing beta and
gamma and ratio from the same 1320 instrument (from Fig 4 of Oldbury 1964) Cps
above background. The excess beta column is based on the normal beta gamma ratio
expected in 2-year decayed fallout from megaton weapons of 3.55 (see Table 3.3)

Position | + ¸ cps ¸ cps Ratio |/¸ Excess beta
A 50 8 5.25 14
B 150 15 9 82.5
C 20 6 2.3 -7
D 50 30 0.7 -85
E 100 10 9 55
F 20 3 5.7 6.5
G 30 3 9 16.5
H 20 5 3 -2.5
J 70 9 6.8 29.5
K 350 35 9 192.5
L 55 7 6.9 23.5
M 70 5 13 47.5
N 22 1 21 17.5
P 20 2 9 11
R 60 10 5 15
S 70 9 6.8 29.5
T 50 4 11.5 32
U 7 1 6 2.5
V 40 2 19 31
W 55 3 17 41.5
X 9 1 8 4.5
Y 8 1 7 3.5

Table 3.5 Beta gamma ratios at various locations on Christmas Island as reported by
A.E.Oldbury in 1964 compared with 2-year old fallout.

Location Beta/Gamma Note
2-year old fallout 3.5 From literature
Washdown pad mean 8.64 Directly from 1320
Washdown pad SD >20 Deduced from 1320 and 1413 response
Sludge pit 10 Direct from 1320 with window off/on
Ultrasonic centre 20-40 Direct from 1320 with window off/on

3.4.2 The Missing Isotope

The missing isotope can only be uranium. U-238, the parent, was used in the bombs
as tamper. U-235, the fissile component, was used in the bombs as fissile fuel. Only
5% of it fissioned, leaving the rest as U-235. In addition, when U-235 is removed
from the natural uranium by separation, it carried with it the lighter and much more
radioactive U-234. The activity of the U-234 is about 23 times greater than the
activity of the U-235. These uranium isotopes have in common that they decay by
alpha emission to short half life decay products which are beta emitters. I list the
decays in Table 3.6.

Table 3.6 Uranium isotopes, decay process, half lives

U238 o, 4.5 x 10
y U235 o, 7.0 x 10
y U234 o, 244500y
Th-234, |, 24d Th-231, |, 25.5h Th-230 o, 7.7 x 10
, |, 1.17m Pa-231, o, 2.3 x 10
U-234, o, 244500y

We can now choose which if the uranium isotopes is the most likely contaminant and
responsible for the extra betas. The most conservative assumption is U-238, since
each decay of U-238 produces two betas (from the Thorium and Protoactinium
isotopes. To calculate the contamination by U238 we just therefore divide the excess
beta cps by 2 and this gives us the cps from the U-238 and therefore the activity of U-
238 in the mix. If we assume that any of it is U-235, then immediately the level of
contamination is doubled (since U-235 has only one beta daughter), and in addition
there is immediately 23 times the level of U-234, a dangerous alpha emitter. In fact, at
a meeting in 1951 between senior members of the UK bomb development team and
some US scientists, Karl Morgan, the US chief of internal radiation and health warned
the British that at the Nevada site there was 100 times the beta radiation relative to the
gamma radiation and that they should take care to recognise the serious effects of the
overlooked isotope U-234. Clearly this warning was not heeded or passed on.
I can use these results now to calculate the level of contamination from U-238.
At point K we see 350cps beta and 35cps gamma. If the expected beta on the basis of
the fallout composition is 3.55 * 35 = 125cps, there is an excess beta activity at K of
225cps. Oldbury tells us that 4cps is equivalent to 1 µCim
and therefore the activity
at K due to the U-238 daughters is 125/4 µCim
= 31µCim
of beta daughters and
half of this level, i.e. 15µCim
of U-238 and U-234 (which is in stochastic
equilibrium with its parent). This is 110,000Bqm
of the two alpha-emitting long
lived uranium isotopes. Similar calculations can be carried out for any point on the
washdown pad. The same approach can be carried out for the readings at the sludge
pit or at the ultrasonic area. The mean levels on the washdown area were an excess of
beta and therefore a surface contamination by U-238 of 12µCim
of addition to the 3.5µCim
of mixed fission products.
My conclusion is simple. The results show that the beta levels are
(a) very high and
(b) indicate the presence of large amounts of uranium contamination.

Of course, plutonium was also used in the bombs and will no doubt be present but
invisible due to the fact that it is a pure alpha emitter and undetectable with the
measuring instruments used by Oldbury (and others before him). It is only because we
can see the betas, that we can infer the presence of uranium.
There is some equivocal supporting evidence in Oldbury’s report for the existence of
the uranium-238 contamination of Christmas Island.
Table 1 of Oldbury’s report shows some measurements of environmental samples. It
lists K-40, Cs-137 and U-238. It is not clear how these results were obtained since K-
40 and Cs-137 can easily be determined by gamma spectrometry. But U-238 cannot.
Attempts to measure U-238 using gamma analysis of the daughter weak gamma
emitters always fail due to variation in solubility between Thorium and Uranium. U-
238 levels are listed at X-site in the soil at 0.84pCi/g (31Bq/kg). For soil this seems
not excessive. However, measurements in coconuts and in fish seem higher than in
soil with goatfish viscera having 1.67 pCi/g (61Bq/kg). Levels in fish were generally
high, above 30Bq/kg. These are unusually high levels of uranium contamination in
biological material and they were found some 2-4 years after the bomb. Green grass
had 13Bq/kg U-238. Coconut milk had 6.3Bq/litre U-238, a high level of uranium for
a liquid.

3.5 The health effects of exposure: the internal doses
I can now look at internal doses at Christmas Island on the basis that the surface
contamination in inhabited areas was between 1.6 and 15µCim
. The sticky paper
exposures are gamma exposures of 0.2µCim
. These translate into beta and alpha
exposures of an average of 8 times this level i.e. 1.6 µCim

These two limits
originate in the measurements made by AE Oldbury and the sticky paper
measurements I analysed in 3.2. For health purposes I will examine only the internal
exposures and will assume a mean surface contamination of 6µCim
of U238 and
U234 (222000Bqm
) plus 1.8µCim
( 66000 Bqm
) of mixed fission products which
I will model as half each of Cs-137 and Sr-90. I will ignore plutonium at this stage
until I have more information. I will employ the dose coefficients of the ICRP and
will model:
Inhalation for 1 year
Inadvertent ingestion for 1 year

3.5.1 Inhalation
The resuspension factor for dusty areas which are consistently being disturbed is
between 10
and 10
as measured by AWE and others (Stewart, 1960). I will employ
a range of values from 1 x 10
to 1 x 10
, but assume that the level will be at the
lower end of this range. The air concentration over the fallout and uranium dust was
between 2.22 and 222Bqm
of uranium isotopes plus 33 to 0.33Bqm
of Cs-137 and
the same of Sr-90. Standard man breathes 839 m
in a year (ICRP23, 1975) and so
will inhale between 1862 and 186258 Bq of uranium and between 27687 and 277Bq
of Cs-137 and Sr-90.

These inhalation exposures, the ICRP dose coefficients and resulting 10 month
committed dose equivalents are given in Table 3.7

Table 3.7 Range of Inhalation exposures to uranium isotopes and fission products,
ICRP dose coefficients (Sv/Bq) and committed dose equivalents for 12 month
exposures at Christmas Island. Plutonium not included.

U-238 U-234 Cs-137 Sr-90/Y-90 total
2-222 2-222 0.3-33 0.3-33
ICRP coeff 8.0E-6 9.4E-6 3.9E-8 3.2E-7
Dose 0.018-
negligible negligible 0.04 to

3.5 2 Inadvertent ingestion
Simon (1998) examined the matter of inadvertent ingestion and referred to
measurements of fallout etc in fecal matter in aboriginals who inhabited or travelled
in the test sites in Australia. He concluded that in dusty conditions as much a 2gm of
material could be ingested per day by this route. I will use 1g per day, which is 365 g
in a year. I will take the contaminated dust to contain, as before, 222000Bqm
uranium isotopes and 66,000Bqm
of Cs-137 and Sr-90. I will assume the layer
containing the activity on the surface is 2mm thick. Assuming a density of 1.5 for
sandy dust this gives the specific activity in the dust as about 37,000Bq kg
for each
of the uranium isotopes and 11,000Bqkg
for each of the fission products.
The dose calculation is given in Table 3.8.

Table 3.8 Inadvertent ingestion of contaminated soil/ dust etc and consequent dose
U-238 U-234 Cs-137 Sr-90/Y-90 Total
13505 13505 4015 4015
ICRP coeff 4.5E-8 4.9E-8 1.3E-8 3.0E-8
Dose 0.6mSv 0.66mSv 0.05mSv 0.12mSv 1.43mSv

3.5.3 Total doses from ingestion and inhalation
The calculations I have run through show the effect that including uranium has on the
overall doses received by the personnel. Uranium carries a major equivalent dose
because of its long biokinetic half life (its similarity in ionic form to Calcium, hence
its targeting of DNA and bones) and the fact that although it is weakly radioactive, it
is an alpha emitter. On the basis of the inferred existence of uranium in the surface of
Christmas Island, and the level I have calculated based on the measurements I have
seen, the total doses to personnel living for one year on the island were between
1.47mSv and 5.2mSv. This is in addition to external gamma doses which are
probably about 0.6mSv. Nor have I included in these calculations other sources of
exposure to uranium, drinking coconut milk and water, eating fish. The methods
employed to screen fish for radioactivity (like the methods generally) could not detect
uranium, nor could they detect plutonium. It is likely that the plutonium doses were
about equal to the uranium doses, but I have no way of assessing plutonium at
present. What does emerge here is the significant role played by these alpha emitters
in contributing to internal doses, as conventionally modelled.
We should also bear in mind that the contamination measured by Oldbury
dated from 1958 and much had already been removed by the US Radsafe team. In the
5 years since 1958 much of the uranium will have been washed off the
decontamination area into the surrounding soil. Originally the levels will have been
far greater. I can assess roughly how far greater by using the measurements made on
the sludge pit.
There is another way of looking at this problem. Oldbury found 400cps beta
and 40cps gamma on the surface of mud in the sludge pit. This was a mass of
material, perhaps several feet deep. The ratio of beta to gamma is 10. But the
significant point is that beta radiation cannot penetrate more than 0.5mm of solid
material at most, whilst gamma is capable of penetrating metres of such material. If
we assume that the material was 1 metre deep (it was probably more) then assuming a
400cps beta originated in a mass defined by the surface of the probe and 5mm deep,
this mass would be not more than 100gm. Assuming 30% counting efficiency, the
specific beta activity of this sludge would then be 2400/0.1 = 24000Bqkg
. However,
the gamma signal was from a depth of at least 50cm i.e. a hemisphere of radium 50cm
(HRP 1972). The mass in that case would be about 700kg, yet the gamma signal was
only 40cps. The gamma specific activity was thus 0.03Bqkg
. Assuming a 30%
counting efficiency for gamma this gives a beta/gamma ratio of 800,000. The material
contributing to the radiation signal is therefore almost a pure beta emitter and is
therefore either U-238 + daughters (Th-234 and Pa-234m) or U-235 and daughter or
Sr-90. Sr-90 would be present with Cs-137 and so would have a larger gamma signal.
In view of the fact that the bombs were made from U-238 and U-235 (See Table 3.9)
it is certain that it is U-238 in the sludge. It is of interest that Oldbury reported mean
value for Cs-137 of 100Bqkg
and a maximum of about 1000Bqkg
on leaves at the
airfield (Table 2 of Oldbury 1963 ).

Table 3.9 Uranium composition of some Grapple devices used on Christmas Island

Green Bamboo
June) Z2
5700lbs weight U238 tamper 170kg, U-235 70kg +
core U-235 17kg
Orange Herald Small 2200lbs; 7.5kg U-235 core + 110kg U-238
Orange Herald Large
June) Z3
As above, large supercharger
Green Granite Large
July) Z4
4400lbs 12kg U-235 + 3kg plutonium + + 20kg U-
235+ 260kg U-238+ lead + bismuth
Green Granite Small
May) Z1
As above, same fissile material
Total uranium alphas in
the above
430kg U-238; 386kg U-235

3.5.4 ECRR doses from uranium and strontium
The internal doses from uranium and strontium which I have calculated were based on
the latest effective equivalent dose coefficients published by the ICRP. This is the
conventional approach, and led to doses of about 5mSv. However, these dose
coefficients are certainly incorrect for these two isotopes. The European Committee
on Radiation Risk examined internal exposures and in 2003 published weighting
factors to be applied to specific types of exposures from internal radioisotopes. The
most recent weighting factors for Sr-90 exposures amount to a multiplier of 300 due
to DNA binding and Second Event considerations. Sr-90 binds to DNA, decays to a
daughter element Y-90 which may then damage the DNA a second time after all
repair has taken place and so introduce a genetic lesion which is unrepairable before
replication. There is also currently a multiplier of 1000 on U-238 due to its high
atomic number causing it to be a photoelectron amplification element and one which
binds strongly to DNA. Applying these weighting factors to the doses calculated
using the ICRP models give results which I show in Table 3.10. For further
explanation of the specific hazards from and approaches to uranium and strontium see
Busby 1995, Busby 2005, Busby and Schnug 2007 and ECRR2003, ECRR2010 and
the Uranium report of ECRr2010 which is a free download on
The inhalation doses may be at the lower limit of the range; even so and allowing for
this, the committed effective dose equivalents from internal uranium contamination
are significant. Note also that I have employed a figure of 1g per day for inadvertent
ingestion, whereas Simon (1998) found empirically that under dusty conditions, the
value was twice this.

Table 3.10 Committed effective dose equivalents (mSv) to personnel stationed at
Christmas Island for one year according to methodology of the ICRP and ECRR;
major dose sources only

Route ICRP dose (mSv) ECRR dose (mSv)
External 0.6 0.6
Internal U-238 0.62-2.36 620-2360
Internal U-234 0.68-2.73 6.8-27.3
Internal U-235 No information No information
Internal Pu-239 No information No information
Internal Sr-90/Y-90 0.12 36
Total 2.02-5.81 663-2424mSv

3.5 Maralinga and the Australian Tests, the Naval support vessels, the RAF support

I have concentrated in Section 3 on Christmas Island in order to see if the MoD were
correct in their arguments (which occur in the defence to this action, and in many
individual appeal tribunals) that the doses at Christmas Island were far lower than
those the veterans would have received had they remained in the UK. To make this
analysis I have had to rely on fairly sparse data, often measurements made with
inadequate equipment using techniques that were unlikely to show anything. I have
also left out a number of routes of contamination because I do not have the data, and
maybe it is not in existence. There are many reports I have asked to see but which
have not yet appeared. I am sure there must be results which exist which I could in
principle examine which would enable me to refine the analysis. My Freedom of
information request to the MoD in January 2009 has been blocked, avoided, and
treated dismally. Few results of any import have emerged even after a judge ordered
the documents I did find to be released. The MoD did not even list in their FoI
response the Oldbury Dominic reports. These I originally had obtained by a different
route and therefore knew of their existence. What other reports are missing?
What has clearly emerged is that internal exposure to uranium and plutonium has not
been assessed. The existence of uranium is clear from the beta gamma ratios
measured in 1963 and in the few environmental samples examined and reported. The
build up of fallout, including uranium is shown by the sticky filter measurements.
Levels on the uninhabited parts of the island were strangely orders of magnitude
greater than those reported for the inhabited part, even though the distances involved
were trivial. I conclude that there was significant biased reporting involved. But what
of the earlier tests in Australia? I have examined some data for Maralinga which
suggests that the situation there was probably far worse. The tests were mostly at or
near ground level and employed large amounts of uranium and plutonium. Again, the
contamination by uranium (and plutonium) is overlooked and reliance is placed on
film badges. It is of interest that some considerable effort later was expended to try
and cover up the residual contamination (Operation Brumby, 1967). In all the tests,
the reliance on external film badge doses is generally also true in the case of the RN
and RAF veterans. If the individual’s film badge dose was low, there could be no
adverse health effect. In order to deal with this argument on a position by position, or
person by person basis, I would rather wait until I have obtained more quantitative
information, if such information exists, or more important, if it becomes available.
However, as an indicator of the hazards, based on contamination measurements made
in Australia, inhalation doses to aboriginals reoccupying areas around Maralinga
have been assessed as high as 300mSv per years doses for plutonium alone (Johnston
et al 1992, Haywood and Smith 1992, ARL Maralinga Contamination ). These studies
concentrated on plutonium since they could measure plutonium through the gamma
energy spectral line of the daughter Americium-241. No real effect seems to have
been made to look at Uranium contamination, probably because the substance cannot
easily be measured. The uranium contamination can be assessed approximately
through a knowledge of the relative quantities involved in the tests. At Kuli, in the
minor trials, 7000kg of uranium was explosively dispersed. At TM50 both uranium
and beryllium were dispersed. This also occurred at Wiweak. . At TM 100 and
TM101 explosive dispersals of plutonium and uranium took place. Nevertheless, if
these levels of plutonium existed in 1992 after the ploughing in and remediation
carried out in 1967 by the British in Operation Brumby, just imagine the situation at
the time.

Table 3.11 Tests at Maralinga and Emu fields in Australia

Major tests Minor tests Notes on major tests
EMU (Totem1) 1953 EMU 1953 31m tower
EMU (Totem2) 1953 TM100/101 1957, 1958
1959, 1960, 1961, 1962,
31m tower
One Tree 1956 Dobo 1958, 1959, 1960 Buffalo; 31m tower
Marcoo 1956 Wewak 1959, 1969, 1961 Buffalo; ground level
Kite 1956 Rats 1956-60 Buffalo; airdrop 150m
Breakaway 1956 TIMS 1955-1961, 1963 Buffalo; 31m tower
Tadge 1957 Taranaki 1960, 1961, 1962 Antler; 31m tower
Biak 1957 Vixen B 1960-1963 Antler; 31m tower
Taranaki 1957 Rats 1956-60 Antler; balloon 300m
Kittens 1953; 1955-7,

Vixen A 1959-61
Major clean ups 1964, 1967

As a consequence of having represented the widow of one Test Veteran, Gerald
Adshead I do have a certain amount of information on the exposure conditions at
Maralinga. In this case, Gerald was stationed at Maralinga and died of a brain tumour
in his late forties. His widow, Eva, was refused a war pension on the usual grounds,
that his dose was given in a letter to the Pensions Agency by AWE as zero. I have all
the paperwork, and have written about the issue in Wolves of Water (Busby 2006).
Adshead spoke of dusty conditions. I was also involved in another Maralinga veteran
who had been refused a war pension on the same grounds: that his dose was
effectively ZERO. Brian Gay, stationed and camped in a tent at Roadside, Maralinga ,
some 5 miles from the test sites, developed a kidney tumour in his 40s which
metastasized to the lungs. In order to make more real the conditions in the field, will
copy here some extracts from a letter written by a friend in June 1989, a letter which
was part of the Tribunal Appeal:

I was posted to Maralinga, S. Australia on 2
May 1957 and ended my tour abroad
on 10
February 1958. When I arrived I was situated at a tented area that was called
‘Roadside’ which was the forward group of servicemen. . . We were to work alongside
two AWRE Aldermaston electricians to wire three towers of an aluminium structure
on all of them and a passenger lift on Gona. . . The towers, in the main, were to be
used to detonate the bombs on.
Because of the nature of the work it was practice to supply a mid day meal,
but the brewing of tea and coffee meant we had to build a fire so we used to clean a
shovel from the land rover and have a fry up with food supplied by the cooks as a
thank you for an early morning call with a cup of coffee or tea. . . .The only drawback
was when in the middle of cooking, a dust storm blew up; these didn’t take notice of
clean areas or sites of previous explosions and , not knowing anything of radiation, if
we had a bit of sand in our food, it was a bit of hard luck.
The first explosion was called Tadje a 120ft aluminium tower which I
positioned along with others as near to the explosion as most. I was positioned on the
range boundary near ‘Roadside’ next to the checkpoint. When the countdown
completed, we had to stand with our backs to the blast, with hands over our eyes. The
countdown went 3-2-1 turn after 1. I felt a terrific heat on my back as I was wearing
my KD shorts and when I turned I swear I could see my bones through my fingers. It
really was frightening. Then, it seems ages after, although it was only seconds, the
scrub began to shake, coming towards us, and an almighty bang hit me that left our
ears ringing. That was a warhead for rocket. I swear everyone about us was
frightened for the future.
After Tadje we had to go back to the various sites and shut down the
generators and then clean, service and return them to the MoT pool at the village.
This kept us fully occupied until the time drew near for the second test.
In the meantime, I had been suffering several heavy nose bleeds and the MO decided I
would be flown down to Adelaide to a private clinic.

The letter continues with descriptions of Mr Gay’s further adventures at the test sites
and then the diagnosis of kidney cancer in 1972. The reason I present this extract is to
show that the personnel were living, eating and drinking in dusty conditions. Gay also
cleaned out and serviced generators which will have concentrated radioactive material
in the air filters. They will have inhaled radioactive dust, uranium and plutonium dust.
Gay (and others who responded to the survey carried out by Green Audit in 2007)
suffered nose bleeds. This is almost certainly a consequence of the trapping of highly
radioactive particles in the nasal passages with the subsequent formation of burns or
polyps. I gave expert evidence in the Brian Gay Pensions appeals tribunal and the
veterans appeal was allowed. Since then I have been retained as expert witness on
other cases which have also been successful.

3.6 The effects on the exposed personnel and their offspring

In Part 2, I discussed the historical development of science in the area of radiation
risk. Although it is not part of the current Pensions Appeals the genetic effects on the
veterans children do have a bearing on the exposures so I will address the question
Radiation is genotoxic: it alters genes at the somatic level and also in the germ
cells, the sperm. In this regard, internal radiation is far more dangerous than external,
for the reasons given in Part 2. Clearly elements like Strontium and Uranium which
bind chemically to DNA are more likely to damage the DNA then elements that do
not, that are more uniformly distributed. And this non-uniformity (anisotropy) of dose
will result in far greater damage to the DNA than the same dose applied externally.
This is why the results of the Hiroshima bomb survivors cannot be used to assess risk
in those internally contaminated, like the veterans. Indeed, the Japanese A-Bomb
survivors studies are faulted since the controls received internal radiation from the
fallout there (Sawada 2007).It is why there are child leukemia clusters near nuclear
plants and so forth. This is the error in the conventional model that the ECRR risk
model addresses.
Those who were exposed to uranium, plutonium and strontium during or
between or after the tests will have received genetic damage to somatic and germ
cells. They will have had genomic instability induced in the somatic and germ cells.
The DNA that controls the cell behaviour will have been altered, and the cell
behaviour will also have been altered in such a way as to increase the chances of
random mutations. This process will be passed to the children and to the
grandchildren, and probably their children and so on. After Chernobyl, the
transgenerational genomic instability signal persisted in Bank Voles for 22
generations (Busby and Yablokov 2006). This is probably why there was an increased
risk of genetic heritable conditions in both the children and the grandchildren of the
British Nuclear Test Veterans Association (BNTVA). Risks of heritable conditions
have been shown to be increased by about 8-fold in a recent case control study of the
BNTVA (Busby et al 2007). In the same study, there was shown to be a statistically
significant excess risk on miscarriage in the wives of the veterans. The increased risk
of miscarriage in wives of nuclear workers has been shown to occur (Fucic et al
2007). These effects are early effects of genetic damage to the sperm.
The increased level of somatic genetic damage will show itself as cancer and
leukaemia/ lymphoma, but also as a general increased risk of all diseases, a kind of
accelerated aging. Thus there will be also increased risks for diseases like diabetes,
arthritis, heart disease, etc. The interesting epidemiological consequence of this fact is
that cancer excess risk may not be fully indicative of the health damage received since
the rates of cancer incidence are more sharply associated with age than the rates of
some other induced diseases (.e. coronary disease). Therefore the exposed will die of
non-cancer illness before the cancer develops. A very wide spectrum of illnesses,
including cancer, have been reported in those exposed to uranium(Craft et al 2004,
Busby 2007). There is further and more objective evidence. Chromosome aberrations
were found in Gulf war veterans exposed to uranium (Schroeder et al 1999) and
chromosomal aberrations have also been found in uranium miners (Zaire et al 1992).
Chromosome aberration analysis is now generally accepted as evidence for prior
radiation exposure (Hoffmann and Schmitz Feuerhake 1997). Rowlands et al recently
found significant excess chromosomal aberration frequency in a sample of New
Zealand test veterans (Rowlands et al 2008).

3.7 Conclusion of Part 3

The argument that the veterans received lower doses than they would have received in
England is falsely constructed and specious. For Christmas Island the comparison is
beween external doses at the sites based on film badge and gamma measurements
(some 600µSv annually) with the annual background in the UK which is about
2000µSv. But the UK background is made up mainly of internal Radon exposures and
the internal components of the annual doses are not included in the Christmas Island
case which is built on film badge or external gamma doses.
I examine some data from Christmas Island and employ the sticky filter
measurements, which appeared sporadic and suspect, to determine cumulative fallout
deposition of gamma emitters. For example, levels of fallout detected in uninhabited
areas were recorded at much higher levels than inhabited areas even though these
areas were a few kilometres apart. Results show that there were significant exposures
to fallout at Christmas Island but apparently no attempt was made to assess the
cumulative deposition or to characterise the fallout except in terms of gamma
exposure. This left out consideration of the alpha emitters uranium and plutonium,
large proportions of the bombs themselves by mass. Since there was only 5% fission,
this left most of the uranium and plutonium to be distributed near the site. That this
was indeed the case for uranium is clear from a forensic examination of the beta to
gamma ratio if material examined in grid surveys carried out in 1963. These analyses
show that there were large amounts of U-238 and U-234 and probably U-235 also in
the surface contamination. The hazard of uranium contamination was communicated
to the government by the US scientists in 1953, but nothing seems to have been done
to assess risk and measure levels. The following is a record of the minutes of a
meeting held in 1953 at Harwell:

Other subjects were touched upon and Dr (Karl Z) Morgan (Oak Ridge Tennessee)
promised to send details of some of their analytical methods for estimating
radioactive substances in the urine. In reply to a question from Dr Butterworth he
said that the hazard from enriched uranium would be a radioactive hazard rather
than a toxic one and related to the presence of U-234.
Minutes of meeting held AERE Harwell, 8
July 1953

The main routes of exposure were inhalation and inadvertent ingestion. Calculation of
the annual dose including this uranium source and Caesium 137 and Strontium-90 and
using conventional ICRP methods gave doses of between 2 and 6 mSv i.e. more than
in the UK. The main doses were from the uranium. Plutonium will have added to this
dose but was not included by me since levels were not known. Application of the
dosimetric model of the European Committee on Radiation Risk increases these doses
to between 663and 2424mSv. This is largely a consequence of the photoelectron
hazards of U-238.
In general, I have concluded from the reports I have seen that the methodology
for assessing radiation content of water and fish samples was useless.
I have briefly addressed the Maralinga exposures but have not seen any results
which enable me to calculate doses. From what I have seen, however, it would seem
that the doses at Maralinga were far greater than at Christmas Island because the tests
were at or near ground levels and much larger quantities of uranium and plutonium
were dispersed. Levels of Plutonium seem to have been assessed for the purposes of
restoration of the land to the local tribes: these give calculated annual doses as high as
300mSv per year even now. Plutonium can be measured now by gamma spectrometry
through its daughter Americium-241. Uranium has not been assessed as far as I can
The safety case of the military is based on external gamma radiation. At the
time, they were aware, and had been told, that the beta radiation was much higher
than the alpha radiation and significant effects could follow from uranium exposure. I
conclude that the exposures to internal alpha emitters, particularly Uranium, were
significantly high and will have caused significant genetic damage to personnel who
lived and worked at the test sites with a result that cancer rates will have increased
and heritable genetic damage caused to germ cells and therefore the offspring of these
men. I conclude that the MoD and AWRE personnel in charge of the operations did
not take adequate care of ensuring that the men were safe. Radiation measurements
were badly carried out, too few on number, instruments were often too insensitive to
detect hazardous levels of radioactivity (particularly in the early period), and no
measurements were made of alpha emitters as far as I am aware. The staff will have
known of the quantity and likely exposures to uranium since they constructed the
bombs out of the stuff. At no time have I seen that they considered its effect after
I reserve the right to add to or alter these conclusions when and if I receive
further data.

Part 4
The defence

You already know of my anxieties on the subject [of tests fallout] in general and I
confess I am somewhat hesitant to mention them again since one usually gathers from
physicists that they have little foundation. I did however have a word on the subject
with Mayneord the other day and I don’t think I am misinterpreting him when I say he
is not entirely free from misgivings. . . . in any event one is entitled to ask certain
questions, e.g. if slight contamination occurs 2500 miles away, what is the situation
say 100 miles around the test explosion?
. . . One thing does frankly terrify me, namely the appearance of morale committees
and stooges whose only job seems to be to provide the”right” answers and avoid
anything in the nature of unpleasantness.

1951 letter from Prof. Alex Haddow, Chester Beatty Research Institute, Royal Cancer
Hospital, London to Sir John Cockroft AERE Harwell 12
Nov 1951

4.1 The defence to the Class Action (also the defence in the PATs).

I have read the summary defence submitted to the Class action. I have also seen a
letter from the Defence Minister Derek Twigg to Linda McAvan MEP on 21 Feb
2008 and which disputes some of my arguments and which I will subsequently
address. I will in due course also address the report of Ron Brown of the Ministry of
The Summary Defence to the master Particulars of Claim Order Dated 12 Dec
2007 (hereafter SDC) relies on a number of points which I will now address.

4.1.1 Radiological safety standards at the time
#18 p5: those radiological safety standards [of the time] were and are no less
rigorous than contemporary standards of radiation protection

This statement is incorrect and it is hard to see how anyone with any knowledge could
have written it. As I have shown in Part 2, the radiation safety standards applied by
the military at the test sites were enormously less rigorous than they are at present.
The currently accepted exposure limits as incorporated into UK law, which follows
the EURATOM 96/29 Directive and which became EU member state law in May
2000 give an annual limit of 1mSv. In #27 of SDC it is stated that the lower working
level of exposure as 1mSv per day , subsequently increased to 3mSv a week in 1956.
The maximum dose allowed per test was 30mSv, 30 times the current annual dose
limit. A dose of 30mSv in one week is a continuous dose rate of least
1786microSieverts per hour. The normal natural background dose rate in the UK is
about 80nanoSieverts per hour. Thus this limit is 22,300 times higher than natural
background. In addition, under certain circumstances, these limits were relaxed to
higher integrated dose limits of 100mSv or even 250mSv.
In addition, the dose limits were based upon external radiation. Internal
radiation doses were not assessed or measured. Internal contamination was not
assessed or measured and so this source of risk is entirely overlooked. Current
radiological practice (e.g. in the nuclear industry, in the Depleted Uranium Gulf War
Veterans) involves screening personnel who may have been exposed to internal
radioactivity. This was not done in the case of the test veterans. Personnel who did
not experience a detonation were assumed to be free from risk even though they were
living and working in conditions of extreme contamination. Current radiation
regulations would ensure that such personnel were routinely monitored through urine,
blood testing and perhaps whole body monitoring.

4.1.2 Internal radiation risks

#29-33 Further stringent safety precautions were taken to minimise exposure. . . In
relation to internal exposure, the Defendant took steps to avoid or minimise such by
monitoring the external environment in order to ensure that levels of radiation were
not beyond certain levels. . . in the event of there being considered a risk of water
being contaminated with radioactive fallout . . . prohibited from swimming . . .
radiation levels of water and fish regularly monitored. . . relevant international
standards set out in Appendix 2.

#33It is denied that each and every Claimant Participant was exposed to ionising
radiation, radiation contamination, radioactivity, radioactive fallout and/or
biological residue during the programme of atomic weapons testing conducted by the
defendant as alleged or at all.

I will take the second point first. It seems to be based upon the 2003 analysis of the
NRPB and the follow up, of 19,672 attendances by British test veterans of the sites. In
this study, at least in the part relied upon in the above defence, there are listed only
1562 persons recorded as having a non zero dose of radiation and only 870 with
recorded doses greater than 0.99mSv.
I have criticised the epidemiology of the NRPB studies during the CERRIE
process and more recently in Busby 2006. I do not accept that NRPB are unbiased and
independent. I have found several major flaws in a number of their studies and have
shown in Busby 2006 and in reports to the CERRIE committee that principal
researchers (Darby, Doll) on these studies were also associated with one other study
of radiation and health where their approach was demonstrably dishonest (see Busby
2006 for details). In addition to these criticisms, I do not accept that the information
given to the NRPB by the MoD regarding the doses was unbiased, nor do I believe
that the choice of the personnel to be included in the study was unbiased. Since the
number of cancer cases in such a study required to prove an excess risk in cases
relative to controls is very small, it would be very easy to remove awkward cases, and
there is some evidence that this occurred between the first and second NRPB studies
when a “re-examination” of the cases in the first study resulted is the “discovery” that
a number of cases could be excluded. This excluded group included a high proportion
of the leukaemia cases that drove an excess risk in the initial study (Busby 2006). In
addition, many servicemen have come forward with evidence that the choice of cases,
or exclusion of cases from the study group, was a biased process. I would like to see
details of all the film badge data that was supplied to the NRPB and copies of the
calculations and spreadsheets that enabled the NRPB statement to be made.
However, even if we assume that the film badge data was indeed accurate, the
statement #33 is ridiculous. At the time of the atmospheric tests, measurements were
made of global fallout and published e.g. in the various UNSCEAR reports (see
Eisenbud and Gesell 2000). The tests were banned in 1963 precisely because ordinary
people were receiving fallout doses through inhalation and ingestion routes. The MRC
report in 1956 and the later MRC reports conceded these exposures. How much more
must the men who lived and worked at the Test sites have been exposed to? This is
Haddow’s point to Cockroft in the quotation at the beginning of this section. Of
course, the doses referred to in the NRPB reports on which the defence depends were
film badge doses. Film badges are worn on the chest and do not register even beta
radiation, let alone alpha radiation. This is because apart from the insensitivity of the
film, the beta range is not great and at the chest height distance the beta electrons
from ground contamination will have been largely stopped by the intervening air. The
internal contamination of the personnel was entirely invisible to the NRPB study.
The only defence presented to this assertion is that of the first two statements
#29-32. In other words, the men cannot have been exposed to internal radiation if they
walked about in areas where the external radiation was lower than some ‘redlined’
limit that defined a high dose area (and this would have been a high dose by today’s
standards). But dust is blown about by the wind and fallout is always in the air. The
particles of uranium and plutonium were certainly not constrained by a piece of red
ribbon and a sign saying “high dose area: keep out”.
This is a key issue. In #38 the defence states that they believe that they are so
Whilst film badges and dosemeters did not measure internal dose directly, to receive
a significant internal dose an individual would have to enter an area with high levels
of resuspendable fallout, which was also a source of photon and beta radiation. It is
therefore unlikely that an individual could have done this without at the same time
receiving a significant external dose which would have been indicated on the film
There is a simple example which falsifies this argument. It is universally conceded
that the doses to individuals living in the UK over the period of weapons tests was
between 1mSv and 3mSv (ICRP) depending largely on the level of rainfall.
Calculations have been made by UNSCEAR and other authorities (see
UNSCEAR2000). I first pointed out in the British Medical Journal (Busby 1994) and
later in my book (Busby, 1995) that this global exposure is the origin of the current
cancer epidemic which began some 20 years after the fallout in areas of high rainfall
and (and high measured fallout). The dose trend in Sr-90 correlates well with the
increase in cancer and enables an estimate to be made of the cancer yield per mSv.
This is the origin of the weighting factors developed by the ECRR. However, the
simple point is that it is inconceivable that the veterans, who worked in the test site
and on top of the immediate fallout can have received a lower exposure to these
substances than people living several thousand miles from the test sites. Yet these
people, in the UK would not have registered measurable external doses above
background on film badges had they worn such devices.
In the case of plutonium and uranium internal exposures from inhaled dust,
these materials need not have been associated with high activity fission products.
Indeed, in parts of the Maralinga test site large amounts of plutonium and uranium
were dispersed by high explosive with no fission whatsoever. This alpha emitting
contamination would be completely undetectable and would not register on any film
badge or dosimeter available even today. The only reason the plutonium was
discovered in the 1990s by the Australian researchers was because by then enough of
the plutonium had decayed through to Americium-241 which can be detected though
its low energy gamma peak at 50 keV or so. Uranium has been almost entirely
ignored, and in my opinion, the levels of the isotope U-234 are likely to be significant.

4.3 Natural Background radiation

#36 of the SDC states that actual dose exposure should be considered against the
context that all humans are continually exposed to small amounts of ionising
radiation as a result of exposure to radon in the natural environment and cosmic
radiation. . .
The statement omits mention of gamma background from uranium and thorium in
rocks. The argument is misleading since the concept of dose itself is not one which
can be applied to all exposures as if it had the same relation with health outcome. This
is a matter which I have dealt with in Section 2.

4.4 Use of protective equipment; HMS Diana and Buffalo Indoctrinee Force
#41-#60 of SDC
The use of respirators (i.e. filter gas masks) on e.g. HMS Diana would have been of
little value in the case of uranium oxide particles which have diameters of less than
0.1µ. There is some doubt about their efficacy in the case of radioactive gases like
Iodine and Krypton. Even if they held up radioactivity in the filters, these themselves
will have become highly radioactive delivering gamma radiation to the head. The
levels of radioactivity in the fallout on deck of HMS Diana (4R/h) can be shown, on
the basis of the infinite plane relationship given in HRP1972 and assuming mean
gamma energy of 0.7Mev to be in excess of 0.26 Curies per square metre or 260, 000
Curies per square kilometre. For comparison , the levels in the 30km Chernobyl
Exclusion Zone were defined by 40 Curies per square kilometre (Savchenko 1995).
The Soviets kept people out.

4.5 Monitoring
# 65 -71
Monitoring was only as good as the monitoring instruments. In general these were not
very sensitive and in particular would not have detected plutonium, and perhaps
uranium also except though beta daughters. In #67 we learn that in the early period it
was discovered that most film badges were not registering radiation exposures. The
extraordinary response was to reduce the number of film badges issued and give them
only to people who were believed to be entering areas where there was radiation. I
have asked for but nor seen critical documents showing monitoring results at the test

4.6 Redlining
#25 Survey Teams of the Radiological Measurements Group moved forward in Land
Rovers towards ground zero to confirm that the site previously chosen for Health
Control was clear of fallout and to erect warning notices at the 2Roentgen per Hour
From HRP 1972 I can calculate that an exposure redline of 2R/h at 1metre from the
ground represents a contamination on a flat plane of 0.13Cim
. This is 130,000Cikm

and can be compared with the Chernobyl exclusion zone level of 40Cikm
What would the inhalation be and what would the dose be? Using a resuspension
range as before of 10
to 10
for dusty conditions with Landrovers driving about etc,
the air concentration would have been between 1.3 x 10
and 1.3 x 10
Standard man inhales 24m
a day the inhalation activity per day at the redline border
would be between 0.13 x 10
and 0.13 x 10
Curies or between 4800 and 48
Becquerel. 4800 Becquerel of Sr-90 conveys a committed dose of 1.44mSv in one
day. If one tenth of the measured activity was equivalent to alpha activity from
plutonium or uranium, this would give a further dose of about 4mSv( twice UK
natural background) in one day of exposure. We do not assume that these redlined
districts were like walls of glass where there was a step jump to a exposure of 2R/h.
And therefore those who were in areas near to but not inside these areas will have
been exposed to the responded fallout which would, of course, blow all over the
place. One week exposure in such an area would lead to a fairly hefty ICRP dose
(30mSv) and a really seriously dangerous level of exposure as assessed by the ECRR

4.7 Epidemiology
The defence discusses epidemiological evidence from NRPB and Australian studies. I
have briefly mentioned the NRPB studies with regard to the dose data in 4.1.2. This
is an important issue which I will consider in Section 5.

4.8 The Minister’s 2008 letter on these issues; the key question.

I will complete this section by responding point by point to the arguments contained
in the letter from the Armed Forces Minister Derek Twigg to Linda McAvan MEP in
so far as it deals with the arguments I have advanced here and in earlier papers I have

On page 3 of his letters he states: it is well known that doses of ionising radiation
could arise from intake of radioactive material into the body. Although alpha emitting
substances would be the most hazardous in this respect, they are an insignificant
component of the fallout from a nuclear detonation compared with beta and photon
emitting materials.
The Minister was incorrectly advised. This is true for gamma doses from fission
products. It is not true for beta doses, which are between 3 and 100 times higher than
the gamma doses, as I have shown. The reason why film badges do not detect beta
doses is that they are worn at chest level and beta ranges from fallout in air are from
10 to 30 cm.
But the statement misses the most important point, which is that the bombs
were made up of massive amounts of natural and also enriched uranium and
plutonium. Only 5% of this was converted to fission products. The 95% remained and
was turned into oxide particles. The uranium and plutonium, alpha emitters were
undetectable. And since very large amounts of U-235 were employed, hundreds of
kilograms, and since the enrichment also removes U-234 from the natural mix, and
since the activity of U-234 in enriched uranium is some 23 times the activity of U-
235, this will have contributed a significant dose.
Because they were very dense (density of between 10 and 20gcm
) uranium
and plutonium would have come to earth more quickly than the lighter elements and
would have remained closer to the test site. Their distribution would not have
followed the distribution of the fallout. This was found to be the case when the
Chernobyl reactor exploded. The uranium and plutonium stayed near the site: the
lighter elements and gases, Caesium, Iodine ended up as far away as Wales. They are
environmentally long lived, insoluble, particulate, unreactive and resuspendable. I
measured uranium in Iraq in 2000, 9 years after it was used, and in Kosovo 11 months
after it was used and reported my findings to the Royal Society and the US
Congressional Committee on Veterans Affairs. The genetic effects of uranium
particulates can be seen vividly in Iraq (Busby et al 2010).
This answers the Ministers later assertion on the same page of his letter
Although a film badge did not measure internal dose directly, in order to receive a
significant internal dose, an individual would have to enter an area with high levels of
resuspendable fallout that was also a source of photon and beta radiation.
The Minister continues:
We have made clear that comprehensive programmes of environmental measurements
were made at all the UK nuclear test sites.
I have not seen the results of these and await them with interest. What I have seen so
far I have considered earlier and these show the presence of significant hazard.

4.9 Summary of Section 4

The essence of the defence case seems to be that stringent precautions were taken at
the time based upon the risk models that were in existence then. Their argument that
those risk models, and the dose limits that were implicit in them were as rigorous as
they are today is laughable and easily shown to be untrue. The defence argues that the
doses received by the personnel at the sites was less than they would have received in
the UK is incorrect. It is based upon film badge doses. There is no independent
verification of this statement, and I have not seen records which convince me that
these doses were the true ones and that there was no bias or dishonesty in the
reporting or reducing the dose records. In a criminal court case, the prosecution would
not accept a general statement like this from the defence without asking to see original
records and subjecting them to forensic analysis. After all, it is the accused in this
case who are also providing the evidence that they are innocent, and no original
evidence of how they reduced their own records into the statements which they have
made and which are reported by the NRPB. The NRPB researchers have themselves
been shown to be biased in cases involving radiation and health and so we should
have no blind faith in their assertions or their studies. In any case, the film badges
used recorded only external gamma radiation and not beta (despite what they state) or
certainly alpha. The major contributor to radiation risk has been, in my opinion,
exposure to uranium and plutonium. The argument that exposure to resuspended alpha
emitters assumes that their concentration will accurately follow the lighter fission
products, but this is not true. The arguments entirely fail to address exposures from
uranium, and particularly U-234. Finally, as I point out in sections 2 and 3, the
hazards from internal emitters, particularly from U-238, have been massively
underestimated by the risk model of the ICRP which is currently in use.


Section 5

5.1 Introduction

If service at the test sites resulted in hazardous exposures to radiation, the veterans
will have become ill from a range of diseases but particularly genetic based ones.
They will have increased cancer rates. Their children will show genetic heritable
damage effects. If unbiased epidemiological studies found that they were not more ill
than matched people, a control group, who did not visit the test sites, then whatever
doses they received, whatever internal radiation they inhaled or ingested, whatever
models predict, there is no case to answer. It is important to stop right here and take a
step back. The hypothesis is that the veterans suffered increased genetic damage due
to exposures to external radiation, weapons fallout and the components of the bombs,
uranium and plutonium. How can we prove this? By epidemiology and perhaps by
biomarker studies like chromosome aberration analysis. By examining the health of
the offspring. But in all such epidemiological studies we come up against a problem:
one that has not yet been mentioned. It is that everyone on the planet was exposed to
radioactive fallout from bomb testing. This is particularly true of people living in
areas of high rainfall in the UK as I have shown in Busby 1994 and 1995 and many
other studies. It is less true of those living in the southern hemisphere. The major
fallout episodes were due to Northern Hemisphere bombs: the various US test sites in
Nevada, Los Alamos and the Russian site in Kazakhstan. Then also there have been
exposures in the northern hemisphere to radioactivity from the Kyshtym accident in
1957, the Windscale fire also in 1957 and, of course recently, Chernobyl. So any
controls for the epidemiological studies of the UK veterans will have been exposed to
fission products at roughly the same time as, and also after the exposures to the
personnel at the Test sites. The difference will be exposure to uranium.
For Australian and New Zealand veterans this is far less true. Whilst mean
fallout doses in the UK from the tests was about 1-3mSv, in Australia the population
fallout doses were a few microSieverts (UNSCEAR reports). The Chernobyl radiation
further levelled up the exposures to the test veterans and controls so that by the time
of the second NRPB study in 1993 the controls have been exposed to the Chernobyl
fallout in England. The predictions of this argument are clear. Epidemiological studies
of the Australian or New Zealand veterans will give a better indication of risk than
those of the UK veterans and should show higher levels of cancer in the veterans
relative to controls. The global fallout caused a significant increase in cancer rates as I
have argued in many publications (Busby 1995, Busby 2002, CERRIE 2004, Busby
2006). The ECRR model predicts and explains the current cancer epidemic (about
30% increase in all malignancies in the UK since 1984 with higher cancer in high
rainfall areas). It is within the context of this that we need to interpret the studies of
veterans’ ill health.

5.2 Two NRPB studies

5.2.1 The first study, 1988

First, as I have stated, I do not accept that NRPB are unbiased and independent. I have
found several major flaws in a number of their studies and have shown in Busby 2006
and in reports to the CERRIE committee that principal researchers (Darby, Doll) on
these studies were also associated with one other study of radiation and health where
their approach was demonstrably dishonest (see Busby 2006 for details). In addition
to these criticisms, I do not accept that the information given to the NRPB by the
MoD regarding the doses was unbiased, nor do I believe that the choice of the
personnel to be included in the study was unbiased. It is an interesting fact that for
some reason the accused (the MoD) has been allowed to provide its own defence and
argue it innocence of the crime that it has been accused of. It is not as if the military is
an organisation renowned for its truthfullness: in time of war (and this is a war as far
as the miltary is concerned, one which it may very well lose) anything goes. Consider
all the spy stories, the psychological operations etc that were associated with the Cold
War, when all these bombs were being developed. In no criminal or civil action
would the alibi of the accused be accepted if it were not independent; in this case, the
military supplied the dose and personnel information and, as we shall see from other
studies, this information is suspect.
The NRPB initial study was published in the British Medical Journal and
examined death from 38 causes in 22347 men who participated in the UK
atmospheric tests between 1952 and 1967 in Australia and the Pacific Ocean
according to MoD archives. Their mortality and cancer incidence was compared with
22,326 matched controls. The period of the study was up till 1984 just before
Chernobyl. Note the numbers. The standardised mortality ratio from all causes was
1.01 and for cancers was 0.96: this just means that they were very fit men being
compared with a general population, another favourite trick of biased epidemiologists.
But even so, comparing with the controls for leukemia and multiple myeloma there
was a significant excess risk (RR, leukemia = 3.45, 22 deaths observed, 6 in controls)
(RR myeloma = infinite; 6 deaths observed, 0 in controls). For incidence, the risk
from leukemia was also high RR = 2.43 with 28 reported developing the disease
compared with 11 controls and for multiple myeloma, 10 in the participants and none
in the controls On the basis of these findings, the military were forced to concede that
at least leukemia and multiple myeloma were caused by the exposures and give war
widows pensions. Clearly this cost the military relatively little; however it had serious
implications for radiation risk models since the participants should not have been
developing leukemia at the film badge doses involved which were generally below 1
mSv. So something had to be done. And it was. Remember that this was the time of
the Sellafield child leukemia studies when there was new interest in low dose

5.2.2 The second study, 1993

This was apparently an update to the first study with seven extra years of data to
1991. It was published by NRPB (R-266-1993) and also in the BMJ. Its conclusions
were different and it allowed the MoD to do a U turn on the leukemia and the
pensions. The argument was that the intervening seven years of data showed a very
low rate of leukemia in the irradiated group relative to the controls, and so therefore
the initial study must have been a chance result.. This second study involved largely
the same though a reduced number of 21,358 vets and 22,333 controls. But here is the
problem: there was a crucial difference in the study group and a questionable analysis.
First, 1503 men had been taken out of the veterans group on the basis that these men
‘had no more potential for radiation exposure than the general public’. The second
change was that any leukemias or cancer occurring in the first two years were
assumed not to be caused by the tests and were discounted when analysing the extra
period of 7 years. 6 leukemia deaths had occurred in the extra five years according to
the report. and 3 additional deaths from multiple myeloma. The abstract of R-266

The suggestion from a previous study that participants may have experienced small
hazards of leukemia and multiple myeloma is not supported by the additional data
and the excesses observed now appear likely to be a chance finding although the
possibility that test participation may have caused a small risk of leukaemia in the
early years after the tests cannot be ruled out.

It is now time to look at the numbers of leukemia deaths. The second study lost 1503
men that were in the first study. The first study found 22 leukemia deaths in the 22347
participants in the entire period of follow up to 1983 with 6 deaths in the 22326
controls (RR = 3.45; p = 0.0000). The second study (1984-91) found an extra 6 deaths
in the participants (after the three deaths in the excluded group had been removed) in
the extra seven years and an extra one death in the earlier period which brings the
total deaths in the participants for the whole period to 29. In the control group, in this
extra 7 years there were 11 deaths. It is bad practice and suspect behaviour to remove
participants from the study after it had begun, especially since there were three deaths
in only 1503 persons, a crude rate of 200 per 100,000 compared with the rate in the
controls of about 67 ( RR = 3.02). It looked like they were trying to get rid of cases.
Why? Well one possibility was that these cases were in the extra 7 year period. If we
assume this, then this period gives a RR about equal to unity. But the main problem
with the conclusions of the second study was one that is so enormous that it is
Men are irradiated during their tour of duty, either from internal radioactivity
or from an external dose. This is mainly in the period 1955-60. If this was Hiroshima,
then the results of the study of the survivors show increases in leukemia peaking ten
years after the exposure and decaying away relative to the controls after about twenty
years. The first study examined the differences between the veterans and the controls
up to 1984, i.e. about 25 years of follow up. By then, all the differences in leukemia
will have emerged between the irradiated and the controls. And they have: we see a
three-fold excess in the 1988 paper, highly sigificant, not related to dose, indeed most
of the recorded doses were below 1mSv. This is very bad news for the nuclear
industry. In 1988 they were in the full throes of the Sellafield arguments. Leukemia
clusters were popping up near nuclear sites all over. Even if all the doses were 1mSv,
a three-fold excess of leukemia represents a jolly big error in the ICRP model.
Now here is the truly extraordinary development. The NRPB using the miltary
data examined a small period following the end of the earlier period, the seven years
from 1984 to 1990. After removing some cases (I don’t know when these removed
deaths occurred, but we would like to) found that the rate in the participants was now
less than that in the controls. There were 6 deaths in the participants and 11 in the
controls in this period. On this late 7-year basis they argued that the earlier 27 year
span result finding was chance. But not only was the earlier period much longer with
more deaths, it included the ten year lag peak when all the leukemias would have
presented themselves. The second study looked at a period from 27 years after the
irradiation to 34 years after the irradiation. On this basis we could take a look at the
difference in the leukemia rates in the Hiroshima controls and irradiated group 30
years after the bomb and conclude that any large excess found ten years after the
bomb was a chance finding. In addition, with a variation in the susceptibility in a
fixed population, removal of a person by dying of leukemia will make the survivors
more resistant. Furthermore, by 1963, the controls were receiving large doses from
northern hemisphere weapons fallout.
To reinforce what was done by NRPB I will give an example of the trend in
risk from leukemia in the irradiated. Boice et al (1985) show that acute leukemia
increased in those patients treated with radiation for cervical cancer in the 10 years
after the treatment. But after this increase, between 10 and 24 years after the
treatment, the rate was actually about 50% lower than the control group. If Boice et al
used the logic of NRPB, they could have argued that the decrease in risk in the second
period showed that the increase in the firrst period was a chance effect.
There were other major problems with both studies which I will just briefly
(1) Army men who were discharged on medical grounds were excluded from both
studies. The Army represented about 42% of the total. This introduced a serious bias
at the outset.
(2) A further and admitted bias has to do with Social Security (DHSS) claimants. This
would be concentrated in the early period. The authors claimed to have controlled for
this bias by leaving out the Army men, but most of the Army were Royal Engineers,
and a final quality control check involved only a 1% sample of RE records, turning up
one further participant who had been missed. This indicated a further 100 DHSS
claimants axiomatically likely to be sick, missing from the participants group.
(3) 40% of known participants could not be included as their service records were
missing: these were known to be at dirty Maralinga, like Gerald Adshead, the veteran
who I represented in the Tribunal, who was one of them: not actually included in the
study but who would have contributed a cancer death had he been included. Another
47% were at Christmas Island.
(4) The studies made much of the fact that the soldiers had the same mortality as the
general public. This is another trick. As with studies of nuclear workers, the
comparison with the general public is irrelevant since the participants were chosen as
healthy. I have drawn attention to the exposure of the controls. The control group
served in the 'tropics' but where they were serving is not noted. In view of the wide
ranges of fallout contamination (like the serious contamination that occurred in the
case of the Japanese fishing boat 'Lucky Dragon', hundreds of miles from the
Marshall Is nuclear tests in the Pacific) the use of such people as controls was itself
questionable unless we can be sure they were not exposed to fallout from the tests.
So to summarise all this, I can say that the initial study (which may or may not
have looked at all the people involved) nevertheless found that there was an excess of
leukemia and multiple myeloma in men whose external dose was too low, on the
ICRP predictions to have been the cause. Therefore a subsequent study removed cases
and focused on a short period more than twenty five years after the initial exposure,
when all the leukemia rates had fallen back to normal, to argue that the initial fiinding
was due to chance.
NRPB have revisited these studies in 2004 but I see no useful purpose in addressing
the updated studies since they are flawed for all the reasons I have pointed out. More
interesting is to look at the Australian studies, which as I mentioned, have the
advantage that the controls were relatively unaffected by global fallout.

5.3 The Australian Studies

In 2006 Carter et al published reports of their assessment of radiation exposures to
Australian Veterans of the nuclear tests in Australia. The first report, Vol1 examined
contamination and calculated doses. The report concluded that the doses were small,
79% receiving less than 1mSv. The mean cumulative doses found were 2.8mSv but
my criticisms of the various reports produced by the UK Ministry of defence in their
own defence also apply to the calculations carried out by the Australians, particularly
with regard to (a) Uranium and (b) the ICRP dosimetry.
In this section I concentrate on the epidemiological study. As I stated in 5.1 we should
expect to find higher levels of cancer in the Australian veterans simply because their
controls will not have been exposed to global fallout which mainly occurred in the N
The Australian study (Carter et al 2006 Vol 2) examined the health of 10,983
males. Subjects were followed to 31
Dec 2001. The study differed from the UK
NRPB studies in that the disease incidence and mortality were compared to the
National Population rather than to a control group chosen by the MoD. Since the
veterans were much more healthy to begin with than the national population we can
begin by assuming that their illness rates would be approximately 20% lower. I obtain
this figure from various studies of the healthy worker effect, particularly studies of
nuclear workers where the figure is 30%. We should thus expect their rates to be
substantially lower than those of the national population. In cancer epidemiology,
because rates increase rapidly with age, it is normal to employ age standardisation and
to calculate Standardised Incidence Ratio (SIR) and Standardised Mortality Ratio
(SMR). What is done is to multiply each 5-year age group by the age specific national
rate for the cancer and thus calculate the total expected number of cases. This is then
compared with the observed number and the ratio expressed as a percentage.
Therefore, if the veterans were more healthy than the national population by 20% (due
to their having been those who were chosen for these arduous military duties in the
first place) then if there had been no effect of the exposures, their SIRs and SMRs
would be 80. Table 5.1 gives the results for SMR of main causes of deaths and 5.2 the
results for cancer. In Table 5.2 I have corrected for the healthy worker effect for SIRs.

Table 5.1 Standardised Mortality Ratios (SMR) for main cause of death in Australian
Veterans of the nuclear tests. * represents statistically significant at the p<0.05 level.

Cause of Death SMR
All causes 1.02
All cancer 1.18*
Heart disease 0.9*
Stroke 0.86*
Respiratory disease 1.05
External (accidents, poison) 0.88*
Suicide 0.35


Table 5.2 Standardised Incidence Ratios (SIR) and Standardised Mortality Ratios
(SMR) for cancer in Australian Veterans of the nuclear tests. * p-value < 0.05; ** p-

Cancer SMR SIR SIR corrected for healthy worker
All cancers 1.18* 1.23* 1.5**
Lip, oral cavity,
1.5* 1.41* 1.7*
Oesophagus 1.15 1.48* 1.8*
Lung 1.2* 1.28* 1.54*
Mesothelioma NA 1.46 1.75
Colorectal 1.24* 1.16* 1.4*
Melanoma 1.22 1.40* 1.7*
Prostate 1.26* 1.22* 1.5*
All leukemia 1.18 1.43* 1.72*
All leukaemia except
1.25 1.61* 1.93*

The results show statistically significant increased risk of cancer of about 50%
relative to the national population after conservative adjustment for the healthy
worker effect. This is what would be predicted in Australia where the national
population were less exposed to the fallout (but note, not unexposed). These excess
risks are fairly well in line with predictions of the ECRR risk model but such a
calculation would need to be carried out on a case by case basis. The authors
examined risk by exposure category and found that there was no relation between
dose and risk. However, since as we have seen, their dose is not a surrogate covariate
for internal dose, such an exercise is meaningless. In addition, the most recent
evidence is that the dose response relation is not linear, but is biphasic (see
ECRR2003, ECRR2010). This would be another reason why an attempt to correlate
dose with response would fail to be evidence of a link between the exposures and the
outcome. Therefore the studies conclusions that the cancer excess, and particularly the
leukaemia excess found was not causal, was at fault since the covariate modelled was
dose as recorded by film badge.
I was unimpressed by this report although its data were interesting and support
my thesis. I found it extraordinary that the authors dismissed what were clear findings
of risk on any basis they seemed to pluck out of the air that seemed convincing. For
example, we were told that head and neck cancers occurred in significant excess. We
were then told that these cancers are strongly smoking related and also related to
alcohol intake. We are also told that the lack of excess liver cancer suggests that
alcohol was not excessive. There was no data to support these explanations. What no
one thought to do was to see if the study group actually did smoke and drink more
than the general population, an elementary piece of epidemiology. It is more likely in
my opinion that wearing respirators and inhaling radioactive fallout would have
delivered large radiation doses to the head and neck. Inhaling radioactive particles
would have given large local doses to the pharynx. Indeed in my studies a significant
number of veterans have told of nose bleeds at the time they were stationed at the

5.4 The Rabbit Roff Study of the BNTVA
This questionnaire study, mainly of the members of the British Nuclear test Veterans
Association (Rabbitt Roff 1999) adds evidence to the issue of the veterans’ health and
that of their children. Data was received from 2500 UK, 238 New Zealand and 62
Fijian men. Two approaches were described in the report. A hypothesis generating
retrospective cohort study was carried out on 608 notifications of death received by
the BNTVA between 1983 and 1997. Membership of the BNTVA is about 10% of the
total number of UK test Veterans. Nearly 66% of the sample had died before their 60

birthday. Nearly 665 died inside 30 years of the attendance at the tests. There was a
highly statistically significant excess of deaths from multiple myeloma (N=21) and
brain tumours (N=17). Mean age of death was 56 (compared with 74 for men
nationally). These findings are in agreement with the premature ageing effect of
radiation and the mean loss of lifespan in men in the contaminated ex-Soviet
territories found after Chernobyl (Yablokov and Busby 2006). The younger the
individual was at the time of exposure, the lower the lifespan. Thus for those 10
individuals in the study who were in their teens at the test site, the average age of
deaths was found to be 44.5 This is in line with the predictions of the amplifying
effects of genomic damage, younger individuals having greater replication rate in
cells. There were 311 cancer deaths in 450 veterans: for over a quarter of the cancers,
the primary site could not be identified. 18 men died of leukaemia in this sample of
450 men, an extraordinary high number give the rate of death reported by the NRPB
study, 22 deaths in 22,000. Death from oesophageal cancer were also very high with
12 men dying between the ages of 51 and 69 years. I refer to the original report for
further details. It is clear that these results call into question the results of the NRPB
study since for certain causes of death (multiple myeloma), there were more cases in
the 450 sample than in the entire NRPB study group.
In addition Rabbitt Roff examined morbidity in a questionnaire analysis of
2087 then (1997) current members of the BNTVA. 1041 questionnaires had been
returned. Analysis seemed aimed at psychological health and common age related
conditions, but since there was no control, and national rates are not available for such
a group for the conditions reviewed, it is difficult to draw firm conclusions, especially
also since this study would suffer from selection bias. The author reported that cancer
rates were not elevated above the expected level but unfortunately gave no data on
which to base this conclusion. Attempts to obtain the data in 2007 to further analyse it
have been refused, which is unfortunate. From the evidence that was given in the
report, and using a proportional incidence and age rate approach, it seems very
unlikely that the conclusion was correct. It seems to me that the cancer rate was
significantly elevated in this group, and certainly for specific and rather low incidence
cancer (myeloma, leukaemia and lymphoma). These haematological malignancies are
associated with radiation exposure.
Rabbitt Roff also looked at hereditary conditions in the children and
grandchildren, using the questionnaire data. She reported on effects in 2261 live born
children and 2342 grandchildren. Health problems were reported for almost 40% of
the children and 21% of the grandchildren 2% of the children having died in infancy.
Cancer numbers were recorded for the children and grandchildren. Generally, levels
of congenital illness seemed to be significantly both in both children and
grandchildren although no statistical analysis was carried out.
Rabbitt Roff then strongly criticize the NRPB studies for incompleteness and
continues to. Her findings are necessarily subject to selection bias but do show
unequivocally for certain cancers that she is correct to point out the serious problems
with the NRPB/ MoD studies. It would be valuable to re-analyse Rabbitt Roff’s data
if this became possible.

5.5 The Green Audit study of the children and grandchildren of the BNTVA

In 2007 Busby and de Messieres conducted a questionnaire case control study of the
BNTVA members in order to examine the health of their children and grandchildren.
This study differed from the Rabbitt Roff 1999 study in that each veteran selected a
non-veteran colleague or relative of roughly from a defined list and these controls also
filled out a questionnaire. The authors were able to examine miscarriages, stillbirth,
infant mortality, congenital illnesses and cancer for 605 children of veterans and 311
children of controls, a total of 916 children. They also obtained basic data on 1157
grandchildren made up of 749 veteran and 408 control grandchildren. Comparisons
were made between cases and control groups but also analysed where possible against
national rates for cancer and congenital anomalies on the basis of data from national
cancer registries and five UK contributors to the EUROCAT registry on genetic
anomalies (North Thames, Northern, Oxford, Trent and Wessex Regions). They
obtained data on father’s exposure history and also data on mother’s smoking. Results
showed high levels of miscarriages, stillbirths, infant mortality and congenital
illnesses in the veterans’ children relative both to control children and expected
numbers. There were 105 miscarriages reported in the veteran mothers compared with
18 in controls OR = 2.75 (1.56, 4.91; p = .00016). There were 16 stillbirths compared
with 3 in the controls (OR= 2.70 (0.73, 11.72; p = 0.13). There were 57 veteran
children with congenital conditions compared with 3 controls (OR = 9.77 (2.92, 39.3);
p = 0.000003) these rates being also about 8 times those expected on the basis of UK
EUROCAT data for 1980-2000 suggesting that the control children had not been
selected for healthiness. In the grandchildren, these high levels of congenital illness
also occurred with 46 veteran grandchildren recorded with congenital conditions
compared with 3 controls OR = 8.35 (2.48, 33.8) p = 0.000025. There was higher
infant and perinatal mortality in the veteran children than control children. There was
a slightly higher cancer rate with 16 cancers reported in the veteran children and 5 in
the control children. They calculated the expected numbers using national rates and
summing the 5-year expected numbers to show that the cancer levels in the veteran
children were only 25% more than expected. The birth years of the children with
congenital conditions was not clustered near the period of the test suggesting that the
effects were unlikely to be associated with the acute external exposures. Indeed, most
of the fathers had not been issued with film badges and many had only been at the
sites between tests. The authors suggest that these results support the idea that the
effects are caused by contamination of the veteran’s bodies by radioactive fallout and
uranium. Many veterans reported suffering flu like illnesses, diarrhoea, skin burns and
rashes which would support the idea of such contamination. The authors discussed the
findings of this study in relation to earlier ones. They also discussed the problems
associated with self selection bias but argue that the astonishingly high levels of
congenital ill health in the children and also grandchildren make it extremely unlikely
that the results we see are more than partly associated with such an effect. The
unusually relatively high levels of congenital anomaly in the grandchildren were
suggested as being due to genomic instability effects like those being found in the
Chernobyl affected territories. It is clear that the veterans received significant genetic
damage as a result of their period near the test sites. The veterans were asked to recall
any health effects at the time they were at the test site and shortly afterwards. Many
reported strange flu-like illnesses, diarrhoea, extreme sunburn and nosebleeds. There
was no correlation between recalled issue of a film badge and any of the conditions
reported at the time or in the children or wives. Smoking in veterans and wives and in
controls was reported but not associated with any of the effects in the children or
grandchildren. I refer the reader to the report for the full details. The report was
presented during the 2007 hearings of the Parliamentary Committee of John Barron
MP and Ian Gibson MP.

5.6 Urquhart’s study of Down’s syndrome in the veteran offspring
The epidemiologist John Urquhart conducted a study in 1992 of Down’s syndrome,
known to be associated with radiation exposure in the fathers (Urquhart 1992)
Cleverly, Urquhart compared rates in children born to fathers both before and after
their attendance at the tests, thus removing any genetic or selection bias. He found a
modest but statistically significant excess risk in the children born after the exposures
to the fathers after allowing for the age related incidence of the condition.

5.7 Cancers of the head and neck
It is notable that in the Rabbitt Roff and also the Australian studies, the rates of
cancers of the head and neck were anomalously high. Indeed, the proportional rates
for unusual cancers in the veterans in both of these studies were high. A proportional
rate analysis I carried out shows that the spectrum of cancers in the BNTVA veterans
reported by Rabbitt Roff is unusual and does not conform to the spectrum of cancer
from the national population. This shows that her the results were not due to selection
bias. If veterans selected themselves into the BNTVA on account of being sick, the
spectrum of cancer would be the same as the national population, there would just be
higher rates. This is an important point. In addition, since film badges do not respond
to inhaled radioactive particles, there would be no relation between recorded dose and
cancer rates, which is what was found by the Australian study which foolishly
concluded that this meant no causal relationship.

5.8 Chromosome aberration analysis
Recently, a chromosome aberration analysis of New Zealand test veterans has shown
a significant excess of chromosome aberrations in peripheral lymphocytes. The
method used was fluorescence in situ hybridisation (FISH) and the study was carried
out by Rowlands et al. Chromosome aberration analysis has been used since the 1990s
as a method for biological dosimetry and was employed after Chernobyl to examine
various groups to ascertain exposures and make some estimate of dose levels
(Hoffmann and Schmitz Feuerhake, 1999). A group of Gulf War veterans exposed to
uranium were examined by Heike Schroeder in the late 1990s and shown to have
significant peripheral lymphocyte excess of centric rings and dicentrics (Schroeder et
al 2003. Uranium miners in Namibia have also been examined and they also show
significant chromosome damage (Zaire et al 1997). Interestingly, those exposed to
uranium seem to have an anomalously high level of chromosome damage, suggesting
much higher radiation damage that is found on the basis of any conceivable dose. My
conclusion, which I have given elsewhere, is that uranium exhibits anomalous
phantom radioactivity though photoelectron amplification. The DU exposed veterans
of gulf War 1 had chromosome damage levels equivalent on the basis of external
exposures to about 150mSv of external radiation. Their uranium exposure was such
that their doses, as calculated by the conventional model, could not be more than a
few microSieverts.

5.8 Conclusion of Section 5
Epidemiology of test veterans themselves has been carried out by three groups. As
evidence, the UK studies have suffered from the problem that they are not
independent of the military and also from the fact that the controls were not free from
exposure. There is also a question of bias raised by the way in which these studies
were carried out. The Australian study used Australian national rates as a control and
because Australia did not suffer exposure to global weapons fallout to the same extent
as the UK, the study did find an excess of cancer. However, the authors dismissed
their own findings as evidence of causality because the excess was not correlated with
film badge doses. This was an error since it was internal exposure that was driving the
excess, as shown by the high level of cancer of the head and neck, which would be the
sites expected on the basis of inhalation and contaminated respirator exposure.
The study of Rabbitt Roff also found high levels of cancers of the head and neck. This
study found sufficient evidence to be able to argue that the NRPB studies were not
reliable. Rabbitt Roff also looked at children and grandchildren, as did the recent
Busby et al. case control study. Both studies, and a smaller study by Urquhart, showed
statistically significant and alarmingly high levels of heritable effects in children and
grandchildren. The Busby et al study also revealed miscarriage effects in veterans’
wives. Evidence of genetic damage in New Zealand veterans has recently been found
by chromosome aberration analysis.


Part 6
The Cold War Race

CONFL. . .
Telegram found in the Public Records Office relating to interpretation of MRC advice
on Test fallout.

In this section, which will be short, I will outline what I believe to be the reason why
the personnel were exposed to dangerous levels of ionising radiation. I believe that the
principal reason was that those whose job it was to drive the development of the
Atomic and Hydrogen Bomb were physicists and engineers. They were not biologists
nor were they medical doctors. They were under tremendous pressure of time: the
increasing complaints from the public and even from medical research fraternity, who
by then knew pretty well what radiation could be doing, were putting pressure on the
governments of the nuclear powers, to stop atmospheric testing. The British needed
the bomb for political reasons. Thus we have a classic tension between health and
industrial or military progress. This is the same tension axis that presently exists in
Depleted Uranium use and many other areas. Physicists see the world as mass, space,
time, energy, and they carry out calculations using these quantities. Biologists see the
world of living things, at the cell level, and the genetic level: a very different world.
This is a world where chemistry rules. In physics, a ball will roll downhill: in
chemistry an atom will move towards another atom it is attracted to by chemical
affinity. In the body, the complexity is enormous: we now know that cells usually
repair themselves after receiving genetic damage. They do so by virtue of the fact that
DNA has a copy. But DNA was not discovered until 1953! The responses to radiation
at the cell levels had begun to be described in books as early as 1949 (Lea, 1949), but
I doubt if the physicists were concerned: their job was to make hydrodynamic
calculations on neutron flux. And in those far off days, biologists were looked down
on by physicists as people who couldn’t do mathematics and therefore had to do
biology! I can remember that even in the 1960s. In the 1950s the nuclear physicist
was the hero. Professor Calculus.
So the question arises, how much did the people who organised the safety of
the personnel know about the health effects of the exposures the men received? We
see in the MoD defence that they believe that the ICRP knew. Sir William Penney, the
head man in this affair, states in his evidence to an earlier enquiry: the ICRP was our
Bible. But others were writing about the effects of radiation. In 1956 the MRC began
to be nervous. In 1957 Rotblat wrote an article in Science magazine suggesting that
the internal doses would cause significant genetic effects. Penney wrote to Cockroft,
to complain and dropped on Rotblat like a ton of bricks accusing him of
scaremongering. I have referred earlier to the letter from the Director of the Chester
Beatty Cancer institute to Cockroft which raises the issue. In 1957 a Pelican
paperback appeared which made alarming reading: Radiation and Health. Written by
Peter Alexander, a radiobiologist and researcher, it laid out the scientific evidence
which existed at that time that radiation was a very dangerous genotoxic agent. As I
have mentioned in Section 2, the genetic damage from radiation was known
throughout the period of testing: it is inconceivable that those who organised the
program were ignorant. Hermann Muller had been publishing evidence of the genetic
effects of radiation in fruit flies since the 1940s. In 1959 Wallace and Dobzhansky
published Radiation Genes and Man. So really the only excuse that the military have
is that they were obeying the rules of the ICRP. But the ICRP rules were written by
physicists. The ICRP was (and still is) a self selected body with no democratic
accountability. Did the military know this? Were they all in it together in a conspiracy
to cover up the health effects? Maybe. They certainly forced the World Health
Organisation into an agreement with the international Atomic Energy Agency by
1959 and as a consequence WHO did not look research radiation and health, leaving it
to the IAEA. And this is still the case: radiation effects on children at nuclear sites are
routinely denied. Chernobyl effects are ignored or dismissed (by IAEA) as
I would say that there was enough information in existence at the time,
certainly by 1956, for the government and the military to have known that what they
were doing was going to cause ill health in those exposed. The precise mechanisms
would not have been known, but I believe they knew that they were causing health
damage to the men who worked for them. They had other priorities.
There is another point. The program was put together in a hurry. There was a
shortage of equipment and trained personnel. In particular, the instruments used to
detect radiation were primitive and insensitive. Alpha activity could not be measured.
Some of the procedures used to measure radiation (e.g. in fish) were absurd. It is
desperately sad to imagine, in my mind’s eye, the antics of the poor servicemen like
those on the cover (the picture is taken from the military Geiger manual, I was given
Gerald Adshead’s device by his wife) waving around these massive primitive Geiger
counters over the fish they had caught from the contaminated lagoons and believing
that they were safe.
Reports I have had from the BNTVA veterans show that there the immediate
effects of radiation were apparent: many soldiers were hospitalised for short periods.
There were odd symptoms which should have been seen as effects of radiation but
were not. Nose bleeds, nasal polyps, skin rashes, diarrhoea, flu like illnesses etc. I
believe that after 10 or 15 years following the tests it must have been apparent to the
military that there were serious health problems. At that point, I believe that it became
necessary to cover up these effects, and I believe that the NRPB reports were an
apparent attempt to airbrush history. This is because by then, these evidences of
effects could be directly translated into evidence that affected the nuclear industry and
would have resulted in litigation on an unheard of scale. It would have raised
questions about the then (and now) current cancer epidemic. To me, having seen these
cover-ups in other areas where radiation is involved (Busby 2006) it is inconceivable
that Rabbitt Roff and also the Australian studies could find such significant and
alarming effects whilst the NRPB and their epidemiologists find effectively nothing.
Professor Darby and Doll, associated with the NRPB studies are, remember,
epidemiologists which I have reported to the British Medical Journal and the Danish
Committee for Scientific Dishonesty and also the CERRIE committee for bias in
another study of radiation and health the Nordic Leukemia Study. And one of these
two, the late Sir Richard Doll, left posthumous evidence and an admission of his own
bias in epidemiology and his secret connections with industry.
Although the military knew that it was dangerous, perhaps they did not know
specifically why. The answer had to wait until the scientific developments of the late
1990s on genomic instability and the differences between internal and external
radiation, which had been flagged up earlier but ignored. Relevant new science has
also developed in the area of the health effects of uranium in the period 2000-2010.
As I have pointed out, for some reason, the bomb projects made little attempt to
assess or even measure uranium contamination even though it was by far the main
component of the bombs they were testing.
In conclusion, as with BSE/CJD, but in orders of magnitude greater, this affair
is a science-driven collision with reality. It arose from the clash between two
scientific world views, the physical and the biological, in a peculiar historic period.
Those responsible are culpable: though this might possibly be their only defence, the
extenuating circumstances. Their legacy is beyond measure and goes far beyond the
health effects in the Test Veterans. As I have written in Busby 1995, the imprint of the
global weapons fallout is to be found in the human genome, and the effects will be
there for generations. Kennedy’s Test Ban Treaty is there to see, in the cancer rate
trend in Wales 20 years after the exposures.


Part 7
Individual Cases

7.1 Introduction
Table 7.1 lists the individual cases. The question of causality in these cases is difficult
to address because each case is different. They suffered different illnesses and were
exposed at different test sites in different periods.

Table 7.1 The individual cases, their reference and the representatives

Reference ENT Name Represented by
00328/2010 L Abdale RBL
00176/2010 D Battersby RBL
00129/2010 D Beeton RBL
00078/2010 T Butler RBL
00723/2010 D Hatton RBL
00065/2010 Dr NC Hughes/
D Hughes
00279/2010 B Lovatt RBL
00039/2008 Mrs D Pritchard RBL
00658/2008 Mrs L Selby RBL
00054/2010 Denis Shaw RBL
00006/2010 N Simons RBL
00751/2007 H Sinfield Rosenblatts
00680/2008 and
Mr B Smith dec.
Mrs A Smith
00912/2009 D Taylor RAFA
00285/2009 Mrs W Triggs RBL
00768/2008 Mrs M Williams RBL

Ionising radiation exposure from external acute high doses is shown to confer an
increased risk of cancer from the A-Bomb and other external dose studies. The risk
factors, i.e. the probability of cancer following a given dose is the area of so-called
Health Physics”, and radioecological tables, based on the radiation risk models of
ICRP have been set up by a number of organisations. A useful example is the
radioecological computer program NIOSH IREP, from the US Department of Labour
used for adjudicating worker claims which is available on the internet. The program
calculates the probability of cancer for a range of sites following exposures (see ). In the USA courts, where I have been retained as
an expert, proof of causation is based on a greater than 50% probability as calculated
by such a program. However, I have gone to some length to show that calculations
using doses from internal radionuclide exposures are unsafe, and so the Health
Physics approach which is the basis of NIOSH is of little use. In its stead, we could
use the risk coefficients published by the ECRR which have built in weightings for
different isotopes. However, without knowing the internal doses to each of the
veterans, and the isotopes involved, we cannot do this. And in addition , certain
cancer sites e.g. Chronic Lymphatic Leukemia are not considered to be radiation
related by NIOSH since the rates were not increased in the external acute A-Bomb
exposures. Nevertheless, there is evidence that CLL is increased in those who have
been exposed to internal radionuclides as I will show. There is another problem. A
number of the veterans who I have been asked to consider have not developed cancer
but have suffered from other diseases, e.g. kidney disease or coronary heart disease,
atherosclerosis. There is no doubt that radiation exposure increases the risk of these
diseases (evidence is available from Chernobyl, for example), but how are we to
partition attributed risk in such cases when the individuals are in their 60s and 70s
where the prevalence of such conditions is significant. Yet both laboratory work and
epidemiology show that ionising radiation causes premature aging: the process is a
result of genomic instability, so I can argue that all the veterans who were exposed to
internal radionuclides and uranium will have inevitable suffered in some way in this
regard, and this will have increased their risk of age related conditions. How are we to
deal with these problems?
My approach is foremost to state that the defence argument that these
individuals cannot have developed their conditions because the doses were too low/
lower than background etc is fundamentally false for all the reasons I have laid out.
This immediately opens the possibility that the various diseases and conditions were
radiation related. There is now reasonable doubt that the Pensions refusal was unjust.
I then look at the type of disease being claimed for. Is it cancer, leukaemia or
lymphoma: diseases associated with prior radiation exposure. If so, this increases the
likelihood that the radiation exposure caused or materially contributed to the
condition. But I have to be careful: cancer is now believed to be a multistage process:
several genetic lesions are involved. For example, in the case of colon cancer it is
thought to be about 5 different genetic damage events in the same cell or in a
community of cells. Now it seems clear that the contamination and subsequent doses
received at the test sites are unlikely, in the case of cancers being expressed some 40
years later, to have provided all these necessary lesions. If they had, the cancer would
have been expressed earlier (as many were in other veterans). And it follows that the
injury received at the time of the exposure can only have either been the first or
second necessary injury. Can we say that the veteran’s radiation exposure caused his
cancer? I think probably not: but it certainly contributed to his cancer.
And then there are the non-cancer illnesses. How should we deal with those? I
think that my position is that all these veterans who I am representing were injured by
exposure to the fallout and uranium when they were at the test sites. This injury will
have contributed in some way to the development of the disease for which they are
claiming a pension. The extent of the contribution I will assess on the basis of a scale
which I lay out in Table 7.2. The reasons for the attributions will be based on my
interpretation of the medical history of the individual, the type of condition, its normal
prevalence or rate in the greater population and the statement made by the individual
of their recollection of the events at the test site. An important aspect will be any post-
test site medical data, though I have to be careful since not everyone consults doctors
for mild radiation related effects, and the absence of medical records may have more
to do with individual behaviour and personality than real exposure effects.


Table 7.2 Scale of levels of probabilistic basis of causality for conditions for which
pensions are claimed.

Description Examples
+++ Highly Likely High radiation risk related cancers: Leukemia
(including CLL), lymphoma, Malignant myeloma,
thyroid etc
++ Likely All other cancers
+ Probable Radiation related, Uranium related e.g. kidney disease,
thyroid disease
0 Possible Heart disease, atherosclerosis
- Aging related Various conditions
-- Unlikely Various conditions

I should point out that in the time I have available I have done my best to consider
each case individually. However, this report is not intended to be a full analysis of
each case. If these cases were being taken one by one in separate pensions Appeals
Tribunals I would address causality at greater depth. Table 7.3 lists each case and
gives the condition for which they have claimed a pension, the levels of probability I
ascribe to their conditions and the briefly notes my reasons. I also address the
individuals separately.

Table 7.1 The individual cases and level of probability of causation

Reference Name (age 2010) Condition(s) prob* Notes
00328/2010 L Abdale 1. Bladder cancer 2006
2. Skin cancer 2004
3. Cataracts
Both conditions radiation related. Was present at 6 Grapple
tests. Essential personnel. Issued a badge but no record of
00176/2010 D Battersby Chronic Lymphatic Leukemia XXX Dusty Maralinga Buffalo, cleaned radioactive aircraft
00129/2010 D Beeton Atherosclerosis O Plaques are of monoclonal origin
00078/2010 T Butler Immune system/ kidney X Film badge dose/ uranium?
00723/2010 D Hatton d 5/7/09 Polycythemia rubra vera XXX Associated with fallout at test sites in the literature.
00065/2010 Dr NC Hughes d.
D Hughes
transferred ?
00279/2010 B Lovatt Atherosclerosis, CHD O
00039/2008 Mrs D Pritchard
Gwilym d.
Kidney disease, diabetes X Associated with uranium; also in Balkans uranium exposed
veterans; conditions followed close on exposure
00658/2008 Mrs L Selby Idiopathic Fibrosing Alveolitis
Diabetes Mellitis
Biologically plausible/ distinguish from radiation alveolitis?
Diabetes increased in Chernobyl/ Hiroshima exposures
00054/2010 Denis Shaw Sub capsular Cataract X Suffered skin rashes and warts shortly after tests
00006/2010 N Simons transferred ?
00751/2007 H Sinfield Not provided ?
Mr B Smith d.
Mrs A Smith
Not provided ?
00912/2009 D Taylor Not provided ?
00285/2009 Mrs W Triggs XXX
00768/2008 Mrs M Williams
Alun d.
Pancreatic Cancer XXX Radiation related/ exposure to uranium

* see Table 7.2

7.2 Individual cases
7.2.1 Leonard Coulson Abdale ENT 00328 2010

Abdale was born in 1935 and was in the RAF from 1953-1976. He claimed for
bladder cancer (2006, aged 70) cataracts in both eyes and had earlier claimed for skin
cancer (basal cell, 2004, aged 68). He never smoked and stated that he had been
present near the epicentre of 6 Grapple tests at Christmas Island as an RAF essential
personnel individual. He had been issued a film badge but apparently this had been
thrown away in a cardboard box i.e. it was not developed because “experience had
demonstrated” that the badge would not have evidenced any exposure. He claims to
have experienced blast and heat. MoD accepts that Abdale was present at Christmas
Island for the tests he claimed but relies on the dose argument. Also MoD states that
there is no proven relationship between cataract and exposure to sunlight. This is
irrelevant. The relation between cataract and exposure to ionising radiation is well
known. Bladder cancer is also a radiation related illness according to NIOSH IREP as
is skin cancer. The 9 tumours in his bladder could be caused by internal exposure to
uranium or other fallout particles lodged in the bladder. MoDs synopsis of causation
includes ionising radiation as a cause of cataracts (bundle p117, p122). MoDs
argument that “published work does not suggest a specific risk for bladder cancer” is
hard to understand especially since they refer to ionising radiation as a cause (Bundle
140). For “abnormally high levels of radiation” cells local to the radioactive or
uranium particles will receive local high doses. I conclude that the bladder cancer has
a high probability of contributory causation by exposure to radioactive particles
inhaled and translocated. Both other conditions claimed may have been contributed to
by his exposures.

7.2.2 Donald Battersby ENT 00176/2010

Battersby was born in 1936 and served at Maralinga Australia with the RAF from
1954-56. He was involved in the Buffalo trials and developed Chronic lymphatic
leukaemia CLL in 2005 at the age of 69. He states that he was involved in cleaning
aircraft that had flown though the dust clouds but wore no protective clothing. These
aircraft were seriously contaminated with fission products and uranium as is shown by
the readings tabulated in the operation DOMINIC reports which I have obtained under
the Freedom of Information requests I made in 2010. Beta gamma measurements
made on the aircraft gave higher than 20,000 cps at a background of 2cps (DOMINIC
report 1963). He also states that he “wore a Geiger counter” clipped to his shorts but
that his was lost (I assume a film badge or quartz dosimeter). Battersby’s pension
application was rejected for the reason that CLL is not a radiation related disease. This
is untrue. Whilst it is true that CLL was not found in excess in the Japanese A-Bomb
studies, these studies are silent on internal exposures of the kind Battersby will have
received at Maralinga. There is now considerable evidence that CLL is increased in
those individuals who are exposed to internal radioactive particles. This is conceded
in the supplementary report for this case (Bundle 59) although that report still assumes
for some extraordinary reason that CLL does not relate causally to ionising radiation
(Bundle 59 para 9). I conclude that Battersby’s CLL was caused or contributed to by
his exposure to radioactive particles inhaled when he was stationed at Maralinga.
I have elsewhere examined the relation between CLL and radiation for a case in the
USA and so copy my conclusions here.

7.2.2A Chronic Lymphatic Leukemia CLL and radiation
1. Present understanding is that Chronic Lymphocytic Leukemia (CLL) results from
an acquired injury to the DNA of a single cell, a lymphocyte, in the bone marrow.
This injury is not apparently present at birth. It is thought that the change in the cell's
DNA gives the CLL cell a growth and survival advantage. This results in the
uncontrolled growth of CLL cells in the marrow, leading to an increased
concentration in the blood. The DNA injury is the result of a mutation, and since
ionizing radiation causes mutations, in principle at least we would expect exposure to
ionizing radiation to increase the risk of CLL.
2. CLL is an abnormal neoplastic proliferation of B cells. The cells accumulate in
bone marrow and blood. CLL is related to a type of non-Hodgkin's lymphoma which
presents primarily in the lymph nodes.
3 The association between ionising radiation exposure and leukaemia is a long
established one. However, it is commonly stated that this association does not extend
to the particular form of leukaemia, CLL. The Oxford Textbook of Pathology states
that: CLL has the unusual characteristics that it is one of the few hematological
malignancies in which the incidence does not rise following exposure to radiation.
BEIRV 1990 (p243-245) refers to Darby et al 1987 and the results of the studies of
patients irradiated for ankylosing spondilitis which showed no excess risk for CLL at
mean external X-ray doses of 3.2Gy to the bone marrow. In addition BEIRV notes no
increase in CLL in the A-Bomb survivors, nor in the irradiated cervical cancer patient
studies (BEIRV 1990). However, these were all studies of large external doses and it
is not scientific to employ these findings to dismiss causality in the case of chronic
internal irradiation. This use of the external acute high dose A-Bomb data to inform
effects of chronic internal irradiation has been criticised by ECRR2003, ECRR2010
by the CERRIE committee (2004a and 2004b) and by IRSN 2006 and in the main text
of the present report.
3. On the basis of these external radiation studies and the statement by risk
committees like BEIR that CLL is not a radiation related disease (though this is not
what the data show) it has become common to dismiss findings of excess CLL in
individuals exposed to internal chronic radiation. A good example of this was the
finding of elevated CLL in the workers at the Rocketdyne nuclear plant in Los
Angeles (Boice et al 2006). Researchers found an increased risk of CLL but did not
include this in their analysis of leukaemia cases. They stated: The nonsignificant
increase in leukemia (excluding CLL) was in accord with expectation from other
radiation studies, but a similar nonsignificant increase in CLL (a malignancy not
found to be associated with radiation) tempers a causal interpretation.
4. It is biologically plausible that a disease which follows genetic mutation to cells in
the lymphatic system should be caused by the incorporation of radioactive particles
into the lymphatic system through inhalation and transfer across the lung to the
tracheobronchial drainage system. The local doses (ionisation density) in cells in the
lymphatic system are not adequately described or modelled by the averaging external
models of the ICRP, which are routinely employed in studies of people exposed to
internal radiation (ECRR2003, CERRIE2004, CERRIE 2004a, IRSN 2006). If CLL
were cause by chronic internal irradiation, it might be expected to be raised in miners,
or those exposed to radioactive dusts.

5. The argument over biological plausibility has been made recently by Richardson et
al 2005 in an extensive review of the evidence that CLL is not associated with
radiation exposure. These authors argue that there is not persuasive evidence that CLL
is not a radiogenic cancer and maintain that recent US Government rules on
compensation to individuals with cancer which excludes CLL as a radiogenic cancer
are unsafe. They discuss molecular, clinical and epidemiological evidence that
pertains to the issue. In particular they make the point that due to the low fatality rate
for the disease, interpretation of the epidemiology is not straightforward. They draw
attention to the fact that chromosome abnormalities are detectable in 80% of CLL
cells, and that the deletion or alteration of certain tumour suppressor genes are also
associated with the disease. They argue that since the types of mutations observed
commonly require double strand breaks to occur in chromosomes, and that radiation is
a known cause of such lesions, the implication of radiation in the aetiology of the
disease is reasonable.

6. Miners studies have been reviewed in BEIRV and BEIR VI. The large meta study
by Darby et al (1995) of miners found no substantial evidence of cancer mortality
other than lung cancer. There was however a non-significant excess of leukaemia
excluding CLL. In other words, CLL was not included in the study as it had already
been excluded on the basis of the idea that it was not a radiogenic cancer. My point is
that such an exclusion was not scientific as the exposures were different.

7. In any case, the mortality studies, like those included in the Darby et al (1995)
analysis are not good at examining CLL since this disease has a much lower fatality
rate than other leukemias.

8. Supporting this idea is a recent incidence study by Rericha et al (2006) who
examined 177 cases of leukaemia in 23043 uranium miners in Czechoslovakia. They
found a significant increased risk of CLL, RR 1.98 (95% CI 1.1 to 3.6; p = 0.016).
They stated in the abstract that: CLL, not previously believed to be radiogenic, was
linked to radon exposure. The authors could not distinguish between radon exposure
and uranium dust exposure.

9 Increased CLL appears to have been found in a study of populations living near the
Techa River nuclear complex in the Soviet Union and who were exposed to internal
radioactive contamination. In the 1950s many thousands of people living in rural
villages on the Techa River received protracted internal and external exposures to
ionizing radiation from the release of radioactive material from the Mayak plutonium
production complex. The Extended Techa River Cohort includes 29,873 people born
before 1950 who lived near the river sometime between 1950 and 1960.The excess
relative risk per gray for solid cancer is 0.92 (95% CI 0.2; 1.7), while those for
leukemia, including and excluding chronic lymphocytic leukemia, are 4.2 (CI 95%
1.2; 13) and 6.5 (CI 95% 1.8; 24), respectively. I have not been able to obtain this
paper in order to see if it is possible to examine CLL separately.

10. I have already argued that to compare cancer in the X workers exposed to
radioactive dust with A-Bomb survivors is poor science, and that a more inductive
comparison would be with other workers exposed to radioactive dusts, like uranium
miners, and following this I suggest that that Working Level Months (WLM) would
be a better exposure quantity than Absorbed Dose. If we do this for the CLL, we see
that there is indeed evidence linking the disease to working in a uranium mine
(Rericha et al 2006).

11. In conclusion, in my opinion, there is sufficient evidence to link CLL with chronic
internal exposure to radioactive particles. The evidence for CLL not being a
radiogenic disease is based entirely on external radiation exposure at high doses, and
this argument is not scientific as it is deductive and does not compare like with like.
This belief has historically skewed research in this area. Other evidence from miners
and studies of individuals exposed to internal irradiation supports the position that the
risk of developing CLL is increased by exposure to inhaled radioactive particles.

Boice,J.D.; Cohen,S.S.; Mumma,M.T.; Dupree,Ellis E.; Eckerman,K.F.; Leggett,R.W.;
Boecker,B.B.; Brill,A.B.; Henderson,B.E. (2006) Mortality among radiation workers at
Rocketdyne (Atomics International), 1948-1999
Radiat.Res. 1661 (1) 98-115

CERRIE (2004a) Report of the Committee Examining Radiation Risk from Internal Emitters

CERRIE (2004b) Minority Report of the Committee Examining Radiation Risk from Internal
Emitters (CERRIE). Bramhall R, Busby C and Dorfman P. Aberystwyth: Sosiumi Press.

Darby SC et al (1995) Radon exposure and cancers other than lung cancer in underground
miners: a collaborative analysis of 11 studies J.Natl.Cancer.Inst. 87 378-384

ECRR2003 (2003) 2003 recommendations of the European Committee on Radiation Risk.
The health effects of ionising radiation exposure at low doses for radiation protection
purposes. Regulators Edition ed-Chris Busby, Rosalie Bertell, Inge Schmitz-Feuerhake,
Alexey Yablokov (Brussels: ECRR)

Krestinina,L.Y.; Preston,D.L.; Ostroumova,E.V.; Degteva,M.O.; Ron,E.; Vyushkova,O.V.;
Startsev,N.V.; Kossenko,M.M.; Akleyev,A.V.
2005 Protracted radiation exposure and cancer mortality in the Techa River Cohort
Radiat.Res. 164(5) 602-611

IRSN (2006) Health consequences of chronic internal contamination by radionuclides.
Comments on the ECRR 2003 Report DRPH 2005-20 Fontenay-aux-Roses: Institut de
Radioprotection et de Sortie Nucliare
Rericha V et al (2006) Incidence of leukemia, lymphoma and multiple myeloma in Czech
uranium miners: a case cohort study. Environ. Health Perspect. 114 (6) 818-122

Richardson DB, Wing S, Schroeder J and Schmitz-Feuerhake I (2005) Ionising radiation and
Chronic Lymphocytic leukemia Envir Health Perspect. 113 (1) 1-5

7.2.3 Darryl Beeton ENT 00129/2010

Beeton was born in 1937 and served on Christmas Island as a cook with the RAF at
times from 1956,57 and 1958 where he would have been present during the Grapple X
and Y tests. He was apparently not issued with a film badge. He claims for the
condition atherosclerosis and subsequent heart conditions for which he has had bypass
surgery in 2001 when he was 64. He is a non smoker and states that there is no history
of bad health in his family.
Despite the aetiology report of the MoD (Bundle 97) there is no doubt that heart
disease risk is increased after exposure to ionizing radiation (ECRR2003, 2010). It
was found to be increased in Radiologists and in those exposed to the fallout from the
Chernobyl accident. I have linked atherosclerotic heart disease with radiation from
weapons fallout in Busby 1995. The fact is that atherosclerotic plaques are
monoclonal mosaics in origin and therefore can be considered benign as tumours.
Experiments with animals have shown that they are produced by exposures to known
mutagens (see Busby 1995, Benditt and Benditt 1978). There is a good ecological
argument that the increases in coronary diseases in the northern hemisphere were due
to exposure to atmospheric test fallout, specifically to Sr-90. The first onset of this
epidemic (which was blamed on saturated fat intake) was in countries of high fallout
exposure like Finland, Wales and Scotland. The increases in saturated fats which were
blamed for the increases in CHD were, on closer inspection, increases in dairy
products which had high levels of Sr-90 and Uranium.
However, having stated this, it is not possible to attribute Beeton’s atherosclerosis to
his radiation exposure at Christmas Island since the condition is so widespread in the
population at the age he developed it. I therefore conclude that it is possible that his
CHD was contributed to by his exposure to fallout on Christmas Island.

7.2.4 T Butler ENT 00078/2010
Trevor Butler, born 1938, served at Christmas Island from 12/57 to 12/58 and
claimed for a number of conditions in 2006 and was refused a pension. The conditions
Staphylococcal lumbar discitis
Streptococcal viridans infection
Klebsiella urinary tract infection
Immune system dysfunction

He apparently appealed this decision but lost the appeal in 2008. He then appealed to
the upper tribunal and this was allowed for various reasons. Butler argued that he was
often at B site which is very close to the ground zero of the balloon Grapple Z rounds.

His array of conditions points to kidney and immune system problems.
Refusal was based on the standard response that he could not have been exposed to
any radiation. Immune system suppression was found in the Hiroshima A-Bomb
survivors (Bundle 9) and also in the Chernobyl fallout groups (Yablokov et al 2009
p87, Yarilin, 1996). The kidney conditions claimed by Butler are known
consequences of exposure to Uranium (ECRR2010, Ballardie et al 2009). Two
research publications advanced in his case (Bundle 306, 305) are questionable. Other
conditions claimed by Butler are associated with the immune system and kidney
problems. He also developed a unilateral cataract followed by retinal detachment
shortly after his tour at Christmas Island which might be seen as supporting evidence
of exposure to radiation and clearly interested Prof Lindop the radiation expert at St
Barts.(Bundle 39, 51).
AWE concede that Butler was issued a film badge and this registered 30mR (0.3mSv).
AWE state that he may have received 0.18mSv external dose. Point (2) on Bundle 69
relates to Butler’s cataract and states that servicemen were told to look away from the
flash. This would have no effect on the radiation dose since the gamma radiation will
have passed through the individuals head unaffected by any sensible shielding by the
skull. However, there is evidence in the Bundle that his cataract developed before his
tour of Christmas Island (Bundle 84) and so it seems that the radiation may not be a
primary cause. I have to smile at Butler’s letter about this cataract where he writes
(Bundle 86) Why was there such a panic when Chernobyl blew up and the fallout
travelled to this country-farmers were compensated when their animals were affected-
I was 7 miles from the hydrogen bombs and 31 miles from the atom bombs
There was a PAT decision on Butler in 2008 which found against his appeal.
Butler was a field engineer and it was conceded (Bundle 260) that he participated in
rebuilding towers after the balloon tests of Grapple Z were detonated. It is
inconceivable that he was not exposed to fallout and uranium. The AWE report is
confusing (Bundle 261). For example it describes a “blue area” where Butler worked
as an area where there was risk of penetrating radiation but no risk of inhalation. I find
it hard to imagine such a possibility. Butler lived in north of island in tented
accommodation, suffered boils to neck after the tests (Bundle 274) and skin rash
(Bundle 275).

7.2.4A New evidence in the Butler bundle
In the new appeal papers AWE state (Bundle 412) that the fallout at B site in
beta/gamma was not more than 1 microCurie per square metre on the basis of the
radiological measurements group report (Operation Grapple Z Interim Report Part 12
Radiological Measurements Group. This is 1Ci per sq km which is the UN definition
for radioactively contaminated land. But the fallout report (Bundle 425) gives the final
decay radiation dose rate as 2mR/h 7 days after the test. (In passing this dose rate
translates to an annual dose of 24.8 rem or 248mSv about 124 times the background
annual dose in the UK). This is an important new piece of information as it enables
me to calculate the level of contamination of gamma emitters at these positions. It is
far greater than the 1 microCurie level given by AWE in Bundle 412 and so (as usual)
they are creative or are incompetent. Using the relationship published in the HMSO
Handbook of Radiological Protection (HMSO1971) and assuming that the gamma
energy was 660keV ( Cs-137) I can find that 2mR/h is the exposure rate over an
infinite plane source of activity133microCuries per square metre which is significant
contamination, 133Ci/sqkm, or about ten times higher than the inner Chernobyl
exclusion zone. This does not include any alpha or uranium components. The very
important map on Bundle 431 shows that a plume of radioactivity existed over the
western coast of the island the outer limit of which 18microRoentgens (180nSv) per
hour more than 8 hours after the detonation. This is about 6 times the normal gamma
background and represents significant fallout over the limits of the survey. It is
unfortunate that the aircraft did not fly across and sample the background over the
northern part of the island, though it does appear that 17microRoentgens was obtained
over the middle of the island. The map on Bundle 432 is astonishing since it has
handwritten: “background 29microRoentgens per hour”. Elsewhere in AWE
arguments about the background gamma levels at Christmas Island they state that the
backgrounds are about 3 microRoentgens per hour (30nSv/h). The map on Bundle 433
shows huge levels of radioactive contamination producing about 150mR/h at T+36
hours. This is the first time that I have seen these data in any of the tribunal bundles or
the huge amount of data I waded through for Rosenblatts or any of the FoI request
responses I had from MoD.

I conclude that Mr Butler’s conditions could have been caused or contributed
to by his exposures. I note that one of the books mentioned by HH Judge Williams in
allowing the appeal is my book Wolves of Water which I am happy to provide for the

Yarilin AA (1996) Immunological disturbances in victims of the Chernobyl accident.
P 62 in EB Burlakova Ed. Consequences of the Chernobyl Accident Moscow: Centre
for Russian Environmental Policy
Yablokov AV , Nesterenko VB amd Nesterenko AV (2009) Chernobyl:
Consequences of the Catastrophe for people and the environment. Annals of the New
York Academy of Sciences vol 1181

7.2.5 Derek Hatton ENT 00723/2008
Hatton was RAOC personnel stationed at Christmas Island in 1958 and experienced
the four Grapple Z tests (Bundle 356). He was born in 1938 and claimed for the
condition polycythemia rubra vera in 2007, which claim was refused. His condition
was recorded in 1997 when he was 59 but may have been pre-existent (Bundle 39,
41). His doctor believed that the condition was caused by his exposures to radiation at
Christmas Island (Bundle 41), and I concur. I have already made a report in 2009 for
Mr Hatton but sadly it seems the gentleman has since passed away. The report I made
for this case is in the bundle (Bundle 290 et seq). MoD state that he would not have
been exposed to fallout (Bundle 356) but provide no evidence of this. MoD deploy the
usual dose argument which I have addressed.
AWE have provided further information (Bundle 331 et seq.) The report on aetiology
(Bundle 346) now concedes that the condition follows somatic mutation and is
associated with radiation exposure. It is also stated that exposure to Strontium 90 (a
component of fallout) causes the conditions in laboratory animals.
I concluded that his polycythemia rubra vera was caused by his exposure to internal
radionuclides at Christmas Island.

7.2.6 Mr E Hughes/ Dr NC Hughes d. ENT 00065/2010
Case transferred

7.2.7 Brian Lovatt ENT 00279/2010
Lovatt was born in 1937 and served in the RAF from 1955-59 and on Christmas
Island from 9/57 to 9/58. He claimed for atherosclerosis and coronary heart disease
and was refused in Jan 2010. He is an ex smoker and suffered from high blood
pressure and ischaemic heart disease. He was not issued with a film badge.
My position on Mr Lovell is similar to the position I take on Mr Beeton, Section 7.3
above, that his condition could have been contributed to by exposure to radioactivity.
It is conceded that his lifestyle will also have contributed.

7.2.8 Mrs D Pritchard (Gwilym Pritchard d.) ENT 00039/2008

Gwilym Pritchard served in the RAF at Christmas Island. He claimed, and his wife
claims that his illness and death from kidney disease were caused by or contributed to
by exposure to radiation at the test site. I have argued that his kidney disease could
have been caused by or contributed to exposure to uranium in the fallout.
My report on Mrs Pritchards’s case is in the bundle. I say in passing that I have
consulted with and helped Mrs Dawn Pritchard for the best part of a year, with the
PATs continually being adjourned and moved around the country. I was very sorry to
hear that Mrs Pritchard, who is a delightful person, recently suffered a stroke and was
hospitalised. I do hope she will make a full recovery.

7.2.9 Mrs Laura Selby ENT 00658/2008

Mrs Selby has claimed for a widow’s pension on the basis of her husband’s death
from Idiopathic fibrosing alveolitis and Type II diabetes was due to or substantially
hastened by his service. Selby served at in the Royal Engineers at Christmas Island
during Grapple X and Grapple Y. In my opinion these conditions may have been
contributed to be exposure to internal radionuclides at the test sites. IFA is caused by
scarring and/ or multiple inflammation of lung tissue, so its development in Mr Selby
is biologically plausible in an individual who will have inhaled radioactive particles
and uranium. Indeed, radiation is known to cause alveolar fibrosis and fibrosing
alveolitis is distinguished from external radiation alveolitis by the distinct loci.(Haston
et al 2007) However, inhaled particulates will, of course, mimic radiation exposure at
high dose to distinct loci. In addition, Uranium (as particles) has been shown to cause
inflammation in the lungs in animal inhalation studies (ECRR2010, ENVIRHOM
2005 report). Diabetes was found to be increased in Chernobyl and Hiroshima
exposed individuals (ECRR2010). In general these conditions may be subsumed
under the catch-all category associated with genomic damage to cells and consequent
premature aging. However their prevalence in human populations makes it difficult to
identify Mr Selby’s exposures at the test site as anything more than a possible
contributory agent.

7.2.10 Denis Shaw ENT 00054/2010

Shaw was born in 1937 served at Christmas Island from 12/58 to 12/59 with the
Royal Engineers. His claim for basal cell skin cancer and solar keratosis was 30%
allowed in 2000. His claim for a unilateral (left) cataract and was refused and
appealed in 2009. In a letter relating to this case (Bundle 7) reference is made to three
documents as follows:
1. July 1975 radiological Survey by University of Washington conclude that
radioactivity from nuclear trials was far less than that due to naturally
occurring radionuclides
2. New Zealand National Radiation laboratory NRL was commissioned by the
UK Overseas Development Administration to carry out a radiological survey.
3. A further survey was carried out by the Ministry of Defence in 1998

The letter in which this information is laid out is AWE/DHEG/C/LET/(A/RE/DS)/001
from Dr KG Harrison, copied to Sc(Nuc)2 MoD MB.
I would very much like to have COPIES of the abovementioned reports which
Harrison relies upon for his 2 July 1999 letter about Denis Shaw. The references on
the internet direct you to some kind of travel brochure for Christmas Island which is
rather suspicious. Very odd.
My position on causation is that cataracts are a well established result of radiation
(Bundle 76) exposure and therefore Mr Shaw’s cataract could have been caused by or
contributed to by his exposure at the test site.

7.2.11 Mrs M Williams ENT/00768/2008

Mrs Euronwy Williams claimed for a widow’s pension in respect of her husband
Alun, who was 66 when he died in 2005 of pancreatic cancer. Williams served with
the RAF at Christmas Island from 07/58 to 07/59. He developed cancer of the
pancreas in 2005. Mrs Williams states that Alun witnessed 2 atomic bombs and 2
hydrogen bombs. Pancreatic cancer [ICD9 157] is known to be associated with
exposure to ionising radiation and is accepted by the US NIOSH IREP as a radiation
related disease. Mrs Williams asked me to provide a report in this case and my 2009
report is in the bundle. With regard to the statements by AWE and MoD that Mr
Williams will not have been exposed to fallout I note that Mr Williams wrote (Bundle
4 massive doses of radiation as gygercounter of [off] scale when first tested after
showers returned to green and that reading on my records not the ones before the
I have not seen the reading on my records as it is not in the evidence, but would
suggest that Mr Williams was describing a decontamination procedure following his
working with cameras which recorded the detonations (Bundle 197). In the additional
report (Bundle 197) it is now conceded that Williams was issued a badge which
recorded an external dose of 0.5mSv. Williams statement has the ring of truth and the
shower part is not something he would have made up. This is evidence, in my
opinion, that he was at some time exposed to radioactive fallout which had to be
showered off him.

7.2.12 Mrs W Triggs SD/00285/2009

Mrs Wendy Triggs claimed on behalf of he father, Mr David Thomas who died aged
70 in 2008 from lung cancer. His lung cancer was diagnosed in 1994 when he was 56
and he had one lung removed. Thomas served at the clean-up operation at Maralinga
in 1963-64 well after the tests there and the refusal was based on the standard denial
by MoD that Mr Thomas had been exposed to radiation. Mr Thomas had smoked until
1999. Radiation is a known cause of lung cancer and has been found in excess in
miners exposed to radon and to radioactive dusts.
Medical records show (Bundle 22) that Thomas suffered some kidney troubles in
1963 whilst working at Maralinga. This may be relevant since uranium exposure will
cause kidney inflammation. Part of the claim refusal was based on the type of lung
cancer involved. It was stated that ‘oat cell’ lung cancer and not the squamous cell
variety would be the consequence of radiation exposure (Bundle 28). This is not true.
Squamous cell lung cancer has been reported in uranium miners exposed to uranium
dust and radon gas (Molloy KB, James DS, Mohr K and Kornfeld M (2001) Lung
cancer in a non smoking uranium miner Env.Health.Perspect. 109(3) 305-309).
It seems that the consultant who treated Thomas also had treated another Maralinga
serviceman who had died of lung cancer (Bundle 162). This Dr Fairfax attempted to
discover if there was any radioactive material in Mr Thomas’s lung (Bundle 161) and
wrote to the pathologist, Dr Gibbs at Llandough Hospital. He writes, “thank you for
agreeing to look for residual radioactivity in the lung tissue taken from my patient. . .
.” Unfortunately the material was unsuitable for analysis. The tracheobronchial
lymph nodes would have retained significant quantities of inhaled radioactive
particles; these were found in Sellafield workers and members of the public from
Cumbria and who lived near the Irish Sea.
Apparently the coroner found that Thomas’s deaths was due to “Industrial Disease” in
other words his exposures At Maralinga, though for some reason the coroner report is
not in the Bundle. (Bundle 329)


Since discovering the new data in the Butler bundle I have begun to re-examine the
statements made by MoD regarding the fallout dispersion from the bombs. I have
begun looking at the metereology of the area. I use the NOAA-HYSPLIT computer
system which is available on the web and which I have used in several other court
cases. HYSPLIT is a free resource and enables the computation of dust trajectories
and fallout dispersion from historical events and any location on earth. What I
discover is that the prevailing winds for most of the tests were south east, and would
have dispersed the fallout or post-fallout radioactive dust from ground zero, which
was on the southern tip of the island, towards the north where the camps were. I have
begun programming each test, but this is a tedious process and I have only begun. I
have examine two tests, Grapple X on November 1957 and Grapple Z Flagpole in
September 1958.

Grapple Z: On the basis of the historic metereological data the HYSPLIT sea level
plots show the direction of the plume moving to the north west along the coast.
Therefore, it is relevant to question the MoD about their assertion that the tests were
only carried out when the wind was blowing offshore. The plot is shown in Fig 7.3.1
These calculations made by HYSPLIT do not take into consideration sea breezes and
indeed these would have been extremely intense due to the location of the fireball at a
high altitude. The sea breezes are generated by the temperature differential between
land and sea in these sunny areas. This would have drawn sea level contamination on
to the land.

Grapple X: I show the dispersion plots at T+1 hr and T+3hrs for the material
generated by Grapple X. It is clear that the radioactive fallout moves north west along
and over the coast. Results are shown in Figs 7.3.2, 7.3.3. and 7.3.4 . Note that these
calculations do not take into consideration airflow perturbations due to the explosions


Fig 7.3.1 Grapple Z Flagpole 1 2 Sept 1958 1724 GMT NOAA-HYSPLIT 120H
trajectories. Note that the tracks move along the west coast of the island. Sea breezes
will probably have drawn in the material at sea level on to the island.

Forward trajectories starting at 1700 UTC 02 Sep 58
CDC1 Meteorological Data
Meters AGL Source H at 1.67 N 157.23 W
J ob ID: 301870 J ob Start: Sun Sep 5 12:42:31 UTC 2010
Source 1 lat.: 1.66881 lon.: -157.234242 height: 500 m AGL
Trajectory Direction: Forward Duration: 120 hrs
Vertical Motion Calculation Method: Model Vertical Velocity


Fig 7.3.2 HYSPLIT plumes at different heights 3hrs after the Grapple X test in
November 1957

Fig 7.3.3 HYSPLIT Fallout dispersion calculation for Grapple X 1 hour after


Fig 7.3.4 HYSPLIT fallout dispersion 3 hrs after Grapple X detonation in November

7.4 Questions from Rosenblatts

Here I will collect together brief answers to a number of questions which have been
asked by Rosenblatts in relation to this issue.

1. Were the levels of radiation to which the test participants exposed (a) during and
(b) after the blasts likely on the balance of probabilities to have caused adverse harm
to health

The answer to (a) is probably that they were not significantly harmed if the film
badges are to be believed. For external radiation (including the immediate acute
effects) I believe that the MoD case stands. The answer to (b) is that there was
significant harm to their health as a result of exposure to internal fallout, uranium and
plutonium and subsequent genetic and genomic damage. The levels of harm will
depend on individual cases and individual tests. The mechanisms of such harm are
damage to DNA by internal exposure with subsequent genetic and genomic alterations
leading to cancer, general accelerated aging and heritable alterations to germ cells.

2. What steps should the MoD have taken to avoid any risk to the participant’s

The MoD relied on the dose limits of the ICRP. Were they right to do so, given that
the ICRP had no special status and its recommendations were not peer reviewed?
Should the MoD have set up a radiation effects research unit, given the amount of
work they were carrying out with radionuclides? I believe they should have assumed
independent responsibility for examining the issue. The MoD could have measured
radiation more carefully than it did, even with the instruments available at the time.
The senior personnel should have listened to the concerns of the medical people: they
did not. They marginalised these concerns and occasionally covered them up. They
made no apparent attempt to measure uranium and plutonium although methods at the
time existed for making such measurements. If they had simply realised that given
that the bombs were actually made from uranium and plutonium there would be
contamination from these substances (and it seems amazing that they did not) they
should have assessed the inhalation of these substances. It, however, is quite hard to
see that anything they did would have prevented such exposures. The whole test
project was inevitably going to cause harm to those who were involved, whatever
precautions were taken. It is just a question of how far such harm could be minimised.

3. What were the levels of radiation fallout to which the veterans were exposed to in
the hours, days, weeks and months they remained in the area within 250 miles of the
detonation? Was that level unsafe?

I cannot answer this question in this form without more information. I would ideally
like to see gamma and beta measurements on the ground in the areas of the tests. I
could then make calculations. I have examined the data I have available and this
shows (see this report) that the levels on Christmas Island were high enough to have
caused ill health, as were some levels at Maralinga.

4. Is there a safe dose of radiation, what is that dose?

There is no safe dose of radiation: this is now conceded by all the risk agencies. The
natural background dose, which is commonly advanced as a baseline safe dose,
cannot be used as a comparison with internal exposures to fallout and uranium etc.

5. How long would the fallout remain at unsafe levels on land.

The hot fallout (short lived isotopes) have high gamma and beta activity and decay
within a few weeks. The long lived Caesium-137 and Strontium-90 have half lives of
about 30 years and so remain dangerous in the area for perhaps about the same time.
Upland areas of Wales contaminated with Cs-137 from Chernobyl are still under
sheep restriction 25 years after the deposition. The half lives of Uranium and
Plutonium are very long, thousands and millions of years, and under dry conditions
these dangerous alpha emitters remain. Any person or animal living on that land will
become contaminated through inhalation and ingestion.

6. If the fallout fell on the sea or fresh water, how would it be absorbed by the water
and any fish or organism. How safe would it have been to eat fish or any animals
after the detonation? How safe would it be to swim in the sea or fresh water.

The highly radioactive immediate fallout would mostly be dispersed in sea water but
less so in fresh water depending on the quantity of water. To swim in the water which
had been so contaminated immediately after the test would be dangerous. In the long
term (weeks) the radiation in the sea would become fairly dispersed and swimming in
the sea would probably not be harmful. The concentration of uranium, plutonium and
strontium isotopes by fish and shellfish would make these potentially a serious source
of internal exposures. This contamination would not be in any way detectable by a
Geiger counter or any of the instruments employed by the MoD at the time to screen
the fish for consumption.
The contamination of the seabed or river sediment with uranium and plutonium would
result in contaminated fish and shellfish for a very long time tens of years or more.
No attempt has been made by MoD (or by me) to address the contamination by
Tritium, which was probably significant.

7 What steps should have been taken to remove all fallout that fell on land and onto
fresh water and to the sea to make these areas safe to occupy.

The massive general dispersion of fallout and uranium and plutonium on the land and
sea would be generally impossible to remediate totally. What could have been done
might have been to mechanically overturn the topsoil, thus diluting and burying the
surface fallout and uranium and plutonium. This would have had to have been done
very carefully as the disturbance would have caused large amounts of radioactive
dust. There is no way of remediating seabed or freshwater sediment. Given the huge
areas involved, the size of such a project would have been impossibly costly at the
time and even now, although I see that in Operation Brumby, plutonium
contamination was plowed into the topsoil in areas where it was significantly high.

8. What about the claim that illnesses to which men claim to have suffered by reason
of exposure to low levels radiation (including cancer, skin condition and teeth loss)
would have been suffered by the participants anyway as part of normal ageing?

Radiation has long been known to cause accelerated ageing and the onset at an earlier
age than usual of normal conditions associated with age. References to observations
of increased levels of these conditions in (a) Hiroshima survivors and (b) Chernobyl
exposed individuals are given in ECRR2003. The mechanism is now known to be
genomic instability, discovered in the mid-1990s. As far as cancer is concerned, the
excess rates seen in the veterans are already age standardised and so the question is

9. What have been the effects of exposure on the male reproductive system?

I have reviewed this issue in the main report. The effects of fallout isotopes which
bind to DNA, strontium-90, are known to cause genetic effects in mice and rats.
Luning and Frolen in 1963 investigated the genetic effects of Sr-90 and found that it
was profound. I have reviewed this issue in the bulk of the report and refer also to
Busby 1995 which deals at some length with the Strontium effects. Uranium and
plutonium are also known to bind to DNA and have serious transgenerational effect
on sperm. This would mean that we should expect increases in heritable damage in
children and increased rate of foetal loss for the same reason.


BEIR VI (Committee on Biological Effects of Ionizing Radiation) (1999) The Health
Effects of Exposure to Radon. National Academy of Sciences, National Research
Council. Washington, DC, National Academy Press

BEIR VII (2005) Health Risks from Exposure to Low Levels of Ionising Radiation
Washington: National Academy Press

Boice JD, Day NE and Andersen A (1985)-Second cancers following radiation
treatment for cervical cancer. J Nat Canc Inst 74, 955-975)

Bond VP (1981) The cancer risk attributable to radiation exposure: some practical
problems. Health Phys. 40 108-111

Busby C (1995) Wings of Death: Nuclear Pollution and Human Health Aberystwyth:
Green Audit

Busby C (2006) Wolves of Water Aberystwyth: Green Audit

Busby C and Schnug E (2007) Advanced biochemical and biophysical aspects of
uranium contamination. In- LJ de Kok and E Schnug Loads and fate of fertiliser
derived uranium Leiden: Backhuys

Busby C and Yablokov AV (2006) ECRR 2006. Chernobyl 20 years on. The health
Effects of the Chernobyl Accident. Brussels: ECRR/ Aberystwyth: Green Audit

Busby C C, Scott Cato M, (2000) ‘Increases in leukaemia in infants in Wales and
Scotland following Chernobyl: evidence for errors in risk estimates’ Energy and
Environment 11(2) 127-139.

Busby, Chris; Hamdan, Malak; Ariabi, Entesar. (2010) Cancer, Infant Mortality and
Birth Sex-Ratio in Fallujah, Iraq 2005–2009. Int. J. Environ. Res. Public Health 7, no.
7: 2828-2837.

Busby C.C. (2009) Very Low Dose Fetal Exposure to Chernobyl Contamination
Resulted in Increases in Infant Leukemia in Europe and Raises Questions about
Current Radiation Risk Models. International Journal of Environmental Research and
Public Health.; 6(12):3105-3114.

Busby C.C (2002). ‘High Risks at low doses.’ Proceedings of 4th International
Conference on the Health Effects of Low-level Radiation: Oxford Sept 24 2002.
(London: British Nuclear Energy Society).

Busby Chris (2007) New nuclear risk models, real health effects and court cases. Pp
35-46 in- Updating International Nuclear Law Eds—Stockinger H, van Dyke JM et
al. Vienna: Neuer Wissenschaftlicher Verlag
Busby, C. (1994), `Increase in Cancer in Wales Unexplained', British Medical
Journal, 308: 268.

Cantrill ST and Parker HM (1945) The Tolerance Dose. MDDC-110 Washington: US
Atomic Energy Commission

Carter M, Robotham F, Wise K, Williams G and Crouch P (2006) Australian
participants in British nuclear tests in Australia. Vol1 and Vo2

Caufield K (1989) Multiple exposures: chronicles of the radiation age. London:
CERRIE (2004a) Report of the Committee Examining Radiation Risks from Internal
Emitters Chilton UK: National Radiological Protection Board

CERRIE (2004b) Minority Report of the Committee Examining Radiation Risk from
Internal Emitters (CERRIE). Bramhall R, Busby C and Dorfman P. Aberystwyth:
Sosiumi Press.

Clare PM, Woods SJ, Woodville AC and Harrison KG (1993) Environmental
monitoring at Christmas Island 1957-58. AWE. Safety Division Technical Note 16/93

Committee on the Medical Aspects of Radiation in the Environment (COMARE)
(1996) Fourth Report. The incidence of cancer and leukaemia in young people in the
vicinity of the Sellafield site, West Cumbria: further studies and an update of the
situation since the publication of the Black Advisory Group in 1984. Department of
Health, London.

Doll R and Peto R (1980) The causes of cancer. Oxford: University Press

Dorfman P, Bramhall R and Busby C (2004) CERRIE (Committee Examining
Radiation Risks from Internal Emitters) Minority Report 2004 Aberystwyth: Sosiumi

ECRR2003 (2003) 2003 recommendations of the European Committee on Radiation
Risk. The health effects of ionising radiation exposure at low doses for radiation
protection purposes. Regulators Edition ed-Chris Busby, Rosalie Bertell, Inge

Schmitz-Feuerhake, Alexey Yablokov (Brussels: ECRR)
Eisenbud M and Gesell T (1997) Environmental Radioactivity IVth Edition San
Diego: Academic Press

Eisenbud M and Gesell T (1997) Environmental Radioactivity San Diego: Academic

Failla HP (1932) Radium Protection Radiology 19 12-21

Fucic A, Franco Merlo D, Ceppi M and Lucas JN (2008) Spontaneous abortions in
female populations occupationally exposued to ionising radiation. Int Arch Environ
Health 81 873-879

Hanson FB (1928) Effects of X-rays on productivity and sex ratio in Drosophila
Amer. Nat. 62 352

Haston CK, Begin M, Dorion G and Cory SM (2007) Distinct loce influence
Radiation-Induced alveolitis from Fibrosing alveolitis in the mouse. Cancer res. 67

Haywood SM and Smith JG (1992) Assessment of potential doses at Maralinga and
Emu test sites. Health Phys. 63 (6) 624-630

Health consequences of chronic internal contamination by radionuclides. Comments
on ECRR2003: The health effects of ionizing radiation exposure for radiation
protection purposes. Fontenay aux Roses: IRSN

Hoffmann W and Schmitz-Feuerhake I (1999) 'How radiation specific is the discentric
assay?' Journal of exposure analysis and Environmental Epidemiology 2, 113-133

Elsaesser A, Busby C, McKerr G and Howard CV (2007) Nanoparticles and
radiation. EMBO Conference: Nanoparticles. October 2007 Madrid

C. V. Howard, A. Elsaesser & C. Busby (2009) The biological implications of
radiation induced photoelectron production, as a function of particle size and
composition. International Conference; Royal Society for Chemistry NanoParticles

HRP (1971) Handbook of Radiological Protection. London HMSO

ICRP (1990) Recommendations of the International Commission on Radiological
Protection ICRP60 Oxford: Pergamon

ICRP (2005) Consultative Draft of ICRP 2005 (ICRP website, 2004)

ICRP (2008) Publication 103: Recommendations of the ICRP: Annals of the ICRP
Volume 37/2-4: Annals of the ICRP v. 37/2-4 (International Commission on
Radiological Protection) by ICRP ed- J Valentin Amsterdam: Elsevier

ICRP 23 (1974) Report of the task Group on Reference Man. Oxford: Pergamon

ICRP(1996) ICRP72 Age dependent doses to members of the public from intake of
radionuclides: Part 5. Compilation of Ingestion and Inhalation Dose Coefficients

IRSN (2005) Institut de Radioprotection et de Surete Nucliare Report DRPH 2005-20

Ivanov E, Tolochko GV, Shuvaeva, LP et al. Infant leukemia in Belarus after the
Chernobyl accident. Radiat Environ Biophys, 37, 53-5 (1998).

Johnston PN, Lokan KH and Williams GA (1992) Inhalation doses for aboriginal
people reoccupying former weapons testing ranges in South Australia Health Physics
63 6 631-640

Jones EJB (1957) A report on a visit to Maralinga to study aircraft decontamination

Kendall GM and Phipps AW (2007) Effective and organ doses from thoron decay
products at different ages. J.Rad. Prot. 27 427-435

Krestinina,L.Y.; Preston,D.L.; Ostroumova,E.V.; Degteva,M.O.; Ron,E.;
Vyushkova,O.V.; Startsev,N.V.; Kossenko,M.M.; Akleyev,A.V. 2005 Protracted
radiation exposure and cancer mortality in the Techa River Cohort Radiat.Res. 164(5)

Kusano N, (1953) Atomic Bomb Injuries; Japanese Preparatory Committee for Le Congrès
Mondial des Médicins pour lÉtude des conditions Actuelles de Vie Tokyo: Tsukiji Shokan

Lea DE (1946) The action of radiation on living cells. 1
Edition. Cambridge:
University Press

Mangano JJ (1997) Childhood leukaemia in US may have risen due to fallout from
Chernobyl. Brit Med J, 314, 1200.

Maralinga Contamination:
Martland (1951) Collection of reprints on radium poisoning 1925-39. USAEC Oak
Ridge Tennessee

Martland HS (1925) Some unrecognized dangers in the use and handling of
radioactive substances. Proc. N.Y.Pathological Soc. 26 6-8

Mayneord WM (1964) Radiation and Health. The Rock Carling Lectures. Oxford
:Nuffield Provincial Hospitals Trust

McLean JT (?1959) Operation Grapple Z. Sampling of radioactivity at outlying
stations in the pacific during the period July-November 1958

Muller HJ (1929) Gene as basis of life Proc Int Congr Plant Sci 1. 897

Muller HJ (1930) Radiation and genetics Amer. Nat. 64 220

Muller HJ (1938) Biological effects of radiation with special reference to mutation
Act. Sci. Ind. No 725 477

Muller HJ (1940) Analysis of process of structural changes in chromosomes of
drosophila J.Genet. 40, 1.

Muller HJ (1941) Induced mutations in Drosophila. Cold Spring Hr Symposium 9
Muller HJ (1950) Our load of mutations. Amer. J. Human. Genet. 2 111-176


NRPB (2000) Generalised Derived Limits for Radioisotopes of Polonium, Lead,
Radium and Uranium. Documents of the NRPB Vol 11 No 2 Chilton: NRPB

Oldbury AE (1964) Report on final radiological survey and decontamination
operations at Christmas Island prior to the closing down of the base on June 30
Aldermaston: AWE

Paterson JT (1932) Lethal mutations and deficiencies produced by X-rays in the X-
chromosome of Drosophila. Amer. Nat. 66.193

Petridou E, Trichopoulos D, Dessypris N et al (1996) Infant leukaemia after in utero
exposure to radiation from Chernobyl. Nature, 382, 352-3.

Rabbitt Roff S (1999) Mortality and Morbidity of members of the British Nuclear
tests Veterans association and the New Zealand Nuclear Tests Veterans associations
and their families. Med.Conf.Surv. 15 S1 1-52

Aldermaston: UKAEA: AWE
Reading: Atomic Weapons Establishment (self published, not peer reviewed).

Richardson DB, Wing S, Schroeder J, Schmitz Feuerhake I and Hoffmann W (2005)
Ionizing radiation and chronic lymphocytic leukemia. Environmental Health
Perspectives 113 (1-5)
Sawada S (2007) Cover up of the effects of internal exposure by residual radiation
from the atomic bombing of Hiroshima and Nagasaki Medicine, Conflict, Survival 23
(1) 58-74

Schroder H, Heimers A, Frenzel Beyme R, Schott A and Hoffmann W (2003)
'Chromosome aberration analysis in peripheral lymphocytes of Gulf War and Balkan
War veterans.' Rad. Prot.Dosim. 103(3) 211-219

Simon SL (1998) Soil ingestion by humans: a review of history, data and etiology
with application to risk assessment of radioactively contaminated soil. Health Physics.
74(6) 647-72

Spix Claudia, Schmiedel S, Kaatsch P, Schulze-Rath R and Blettner M (2007) Case
control study on childhood cancer in the vicinity of nuclear plants in Germany 1980-
2003. Eur. J.Cancer doi: 10.1016/j.ejca 2007.10.024 In Press

Steiner M, Burkart W, Grosche B, Kaletsch U, Michaelis J (1998) Trends in infant
leukemia in West Germany in relation to in utero exposure from the Chernobyl
accident Radiat. Environ. Biophys. 37 87-93

Stewart A/M and Kneale GW (2000) A-Bomb Survivors: factors that may lead to a
reassessment of the radiation hazard. Int.J.Epidemiol. 29 (4) 708-714

Stewart K(1960) On the resuspension in the atmosphere of of fallout or other fine
particulate matter deposited. AWE Report T 10/60

Taylor LS (1971) Radiation protection Standards CRC Critical Reviews in
environmental control. 81-124Boca Raton Fla: CRC Press

Thompson, DE, Mabuchi K, Ron E et al (1994) Cancer incidence in atomic bomb
survivors Part II Solid Tumours 1958-87. Radiat.Res. 137 S17-S67.

Tondel Martin, Lindgren Peter, Hjalmarsson Peter, Hardell Lennart and Persson
Bodil, (2006) Increased incidence of malignancies in Sweden after the
Chernobyl accident, American Journal of Industrial Medicine, (49), 3, 159-

Tondel M, Hjalmarsson P, Hardell L, Carisson G and Axelson A (2004) Increase in
regional total cancer indidence in Northern Sweden. J Epidemiol. Community
Health. 58 1011-10
UNSCEAR (2000) Sources and effects of ionizing radiation. United Nations
Committee on the Effects of Ionizing Radiation. UNSCEAR 2000. Report to the
General Assembly. Vol 1 Sources (New York: United Nations)

UNSCEAR 2000 United Nations Scientific Committee on the Effects of Atomic
Radiation, 2000 report to the General Assembly. Volume II Effects (New York:
United Nations).

Urquhart J (1992) Radiation exposure and subsequent health history of veterans and
their children. In Neue Bewertung des Strahlenrisikos; Internationale Konferenz der
Gesellschaft fur Strahlenschutz e.V. Kiel 1992.

Zaire R, Notter M and Thiel E (1997) Unexpected rates of chromosome instabilities
and alteration of hormone levels in Namibian Uranium Miners. Radiation Research
147 (5) 579-584


Appendix A
The Lesvos Declaration

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 and standards 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 and indispensable
opportunity to discover the yields of serious ill health following exposure to fission products
and has demonstrated the inadequacy of the current 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 be applied 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 chemical affinities for DNA, so that the
concept of absorbed dose as used by ICRP cannot account for the effects of exposure to these

F. Whereas, the ICRP has not taken into consideration new discoveries of non-targeted effects
such as genomic instability and bystander or secondary effects with regard to understanding
radiation risk and particularly the spectrum of consequent illnesses,

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 these coefficients leads
to radiation risks being significantly underestimated,

2. assert that employing the ICRP risk model to predict the health effects of radiation leads to
errors which are at minimum 10 fold while we are aware of studies relating to certain types of
exposure that suggest that the error is even greater,

3. assert that the yield of non-cancer illnesses from radiation exposure, in particular damage to
the cardio-vascular, immune, central nervous and reproductive systems, is significant but as
yet unquantified,

4. urge the responsible authorities, as well as all of those responsible for causing radiation
exposures, to rely no longer upon the existing ICRP model in determining 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 of another 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 epidemiological studies of exposed populations,
including re-examination of the data from Japanese A-bomb survivors, Chernobyl and other
affected territories and independent 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

8. are concerned by the escalating use of radiation for medical investigation and other general

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 not meant 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, Greec

Appendix B
My expertise

B1 My expertise
The Treasury solicitor provided an application for the PAT Directions Hearing on 19

July 2010. In this there was a section (Paras 33-38) relating to question of my
expertise, and following this HH Judge Stubbs made a Direction that I should provide
the details sought by the Secretary of State.

I will begin by stating that I am an expert in the area described by the phrase:
The health effects of low doses of ionising radiation.
This is an area which includes many specific areas of knowledge and expertise listed
in Table B1. I have been engaged in a considerable number of legal cases as an expert
in this area in the UK and the USA and have advised many organisations on these
issues. A list of my activities in this area is to be found in my current CV which is
attached. I also attach letters from 4 separate USA law firms which have retained my
services as expert witness and which testify to my expertise. Two separate attempts to
have me excluded from providing testimony in radiation cases under the Rules of
Daubert vs Merrell Dow Pharmaceuticals 1993 have failed to persuade the court of
my lack of expertise.
Unlike most of my critics from the military and the nuclear industry (e.g. Ron
Brown) I have published a significant number of peer reviewed and non peer
reviewed papers and articles which report my own original research in the area of
radiation and health, including theoretical aspects of radiation and health at the cell
level and also radiation epidemiology. I am an internationally consulted expert on the
health effects of exposure to uranium and on the basis of this both a visiting Professor
at the University of Ulster and a Guest Researcher at the German Agricultural
Research laboratories in Braunschweig. I currently co-supervise a PhD student at
Ulster. I was Science Policy Group leader of the EU Policy Information Network on
Child Health and Environment and was senior rapporteur of the ionising radiation and
radon groups being responsible for the final report in this area (van den Hazel et al
2006, Busby and Fucic 2006).
I was a fellow of the University of Liverpool where I co-supervised a PhD student
John Newby who employed a novel epidemiological method which I invented to
examine the risks of cancer with age. The PhD was awarded and the method
published. I was for 10 years the National Speaker on Science and Technology for the
Green Party of England and Wales. I have written two books on the issue of radiation
and health, Wolves of Water and Wings of Death both funded by the Joseph Rowntree
Charitable Trust whose trustees were convinced that I was sufficiently expert to fund
me for 6 years to write these books. I am Scientific Secretary of the European
Committee on Radiation Risk whose membership includes some very eminent
radiation research scientists (see the signatories on the Lesvos Declaration, Appendix
A). I was senior editor of three of its publications, ECRR2003, ECRR2010 and
ECRR2006. I was a member of two UK government committees examining the health
effects of low doses of ionising radiation, CERRIE and DUOB.

Table B1 List of some areas of expertise necessary to advise or testify on cases
involving radiation and health

Radiation epidemiology Have published papers, CERRIE,
supervise a successful PhD student
(Newby) (Liverpool) legal cases
Statistical inference Have published papers, CERRIE, legal
History and philosophy of Science Books and articles
History of radiation and health research Books and articles
Politics and Science Books and Chapters, PINCHE
Radiation biology of humans Books, Developed original ideas and
published (Elsaessar, Schnug). PINCHE
Radiation measurements Have my own lab and equipment,
employed to do this is legal cases
Exposure dose calculations For legal cases, see testimonies
Dispersion modelling For legal cases, see testimonies
Chemical Physics Degree and experience, published
papers, Lab experiments, supervise a
PhD student (Ulster)
Physical Chemistry at the molecular level
in the cell
Degree and experience, published
papers, lab experiments
Cancer induction and development Books, legal cases, see testimonies
Analytical methods, spectroscopy, Wellcome, original research
radiation transfer
Human physiology Studied at Wellcome
Aetiology of disease processes Studied at Wellcome, books
Cell biology Studied at Wellcome, books

There is no doubt that the nuclear industry and military take my expertise very
seriously. They have tried extremely hard to have me excluded from testifying in
court cases and have attacked me at every opportunity. Their friends and supporters
have written to my University, to the editor of the journals in which I publish, on
internet blogs with lies about me and my work in a desperate attempt to have my ideas
discounted or marginalised. There is even an internet site called chrisbusbyexposed or
some such thing where I am attacked by anonymous hack calling himself Richard D.
The report by Mr Ron Brown, which I will address below, is another example. At
least I know who Brown is. Brown also wrote to HM coroner in the West Midlands
with a similar report on me and my method including the same ad hominem approach
that he has employed in the PAT statement which is common to all the MoD
responses for the cases I address. The coroner and the jury were apparently not
convinced and discounted his report in that case.
I might also point out that I have already acted as an expert witness in several PATs
since 2005, all of which were successful
My response to the question of my expertise is the same one I use for the USA

I am sufficiently expert in the area of the health effects of low dose radiation to be
able to assist the court in understanding the science in this area and to assist it in
coming to an unbiased decision regarding the cases it is considering.

This is the level of expertise required by Daubert.

My qualifications and publications are given in my latest CV which is attached as an

I have been retained in legal cases as an expert witness on radiation and health in the
UK and the USA. I list these below.

Dr Chris Busby
Court cases as expert witness

Case and
lawyer/ team
Court Year Details (expertise) Result
1. R vs
Hipperson et al
Crown Court
1998 Criminal Damage Atomic
Weapons Establishment
Aldermaston (radiation
health effects)
2. R vs Helen

Crown Court
1999 Criminal Damage House of
Commons London
(uranium health effects)
3. Sellafield Irish Dublin High 1999- Case against Sellafield Case
(McGuill, Herr,
Irish State)
Court 2001 THORP reprocessing plant
(epidemiology, radiation
effects, Irish Sea)
in 2008
4. Millstone
Reactor Public

State Court
2001 Opposition to relicensing
of Millstone Reactor
(Radiation health effects
and sea dispersion)
5. Fatmir Mata
(Wilson , Berry)
Appeal Court
Human Rights immigration
appeals Kosovo (uranium
health effects)
6. Lela Pelumb
(Wilson & Co,
appeal court
2001 Depleted Uranium Kosovo
(uranium health effects)
7. Ladrim Spata
(Clore and Co,
appeal court
HX 06027
2001 Depleted Uranium Kosovo
(uranium health effects)
8. Shaquiri,
Zogu, Malo,
Deda and Hidri
vs. Secretary of
State Home
appeal court
2002 Depleted Uranium Kosovo
(uranium health effects)
9. Hadjarmata vs
Sec.State Home
Office (Wesley,
Gryk, Amador)
appeal court
2002 Depleted Uranium Kosovo
(uranium health effects)
10. Mr and Mrs
Ardian Kuci vs
Sec.State Home
appeal court
2002 Depleted Uranium Kosovo
(uranium health effects)
11. Gerald
Adshead vs
Ministry of
appeals court
2002 A-Bomb Test Veteran
cancer (epidemiology,
radiation health effects)
12. R.vs
Margaret Jones
and Erika
Wilson (Alan
Crown Court
2002 Criminal Damage Nuclear
Submarine base Plymouth
(radiation and health)
13. Lee Dell
Craft Snr vs
Tubular ITCO
(Stuart Smith)
New Orleans 2005- Cancer following exposure
(Epidemiology, radiation
and health)
Settled by
14 Barbara
Castell vs
Tubular ITCO
CDC No 2002-
New Orleans 2005- Cancer following exposure
to NORM (Epidemiology,
radiation and health)

12334 Dv A
section 5.
(Stuart Smith)
15 Ursula Bulot
et al vs Exxon
Mobil Corp and
(Stuart Smith)
New Orleans 2005- Cancer following exposure
(Epidemiology, radiation
16 James Bailey
vs Exxon Mobil
Corp and others
(Stuart Smith)
New Orleans 2005- Cancer following exposure
(Epidemiology, radiation
17 Zachary
Finestone, Lowe
et al vs St Lucie
Power and Light
( Lytal Reiter,
Palm Beach Fla).
Florida USA
Case 03-
2005 Case of children with
cancer near St Lucie
Nuclear Power Station.
(Epidemiology, radiation
dispersion modelling and
health effects)
18 R.vs Pritchard
and Olditch
(Bindmann and

Crown Court
2005-6 Criminal Damage US
bombers 2003 (uranium
and health)
(famous case)
19 R vs RV
Jones and
Crown Court
2005-6 Criminal Damage US
bombers (uranium
(famous case)
appeal to
20 Brian Gay vs
Ministry of
2007 A-Bomb Test veteran
Maralinga ; was his kidney
cancer caused by radiation?
(Epidemiology, radiation
and health)
21 Richard
David vs
Royal Courts
of Justice,
Bench Divn.
2007-8 Uranium contamination
and health; contaminated
via aero engines filters
from high altitude
(Epidemiology, radiation
and health)
litigant in
22 Cindy Mays
and others vs
(Suzelle Smith)
Los Angeles
2007 Did radiation releases from
the Rocketdyne SSFL
cause retinoblastoma in 9
Los Angeles children?
Epidemiology, radiation
dispersion modelling and
health effects).
Settled by
23 Bonnie
Anderson et al vs
Ashland Oil
(K. Mathis et al)
Circuit Court
2008 Contamination of property
by oilfield NORM
(Epidemiology, radiation
and health)
but being
24. A-Bomb Test
veterans vs UK
Ministry of
Royal Courts
of Justice,
Cancer and illness in A-
Bomb Test veterans
(Epidemiology, radiation
and health)
won, but
on appeal
25 Various vs
Exxon Mobil
Houston TX 2009-
Measuring gamma and
advising on NORM
contamination for potential
26 Derek Hatton
Vs Ministry of
(Derek Heaps)
2009 Cancer and polycythemia
rubra vera
See below
27 Etienne
Pellegal vs
Lincoln Electric
New Orleans
No 2006-
003684 Sec 6
Div L
NORM radiation and
laryngeal cancer
Settled by

28 Stuart Dyson
dec. vs MoD
Court Black
2009 Cause of Death; did
depleted Uranium cause
cancer. Big case, reported
29 Colin Duncan
Vs. Ministry of
appeal Court
2010 Exposure to fallout in A-
Bomb Tests caused cancer
30 Lowell
Ryman vs
Regents of
University of
Los Alamos
2010 Exposure to radioactivity
from Los Alamos and
Malignant Myeloma
31 Michael Nase
vs Teco Energy
(Stuart Smith)
New Orleans
2009 Exposure to radon and
radiation and lymphoma
32 Dawn
Pritchard vs
Ministry of
2010 A-Bomb Test veteran
widow. (Radiation and
33 L Abdale vs
Ministry of
(Royal British
ENT 00328
2010 A-Bomb Test veteran
appeal (Radiation and

34 D Battersby
vs Ministry of
(Royal British
ENT 00176
2010 A-Bomb Test veteran
appeal (Radiation and

35 D Beeton vs
Ministry of
(Royal British
ENT 00129
2010 A-Bomb Test veteran
appeal (Radiation and

36 T VButler vs
Ministry of
(Royal British
ENT 00078
2010 A-Bomb Test veteran
appeal (Radiation and

37 D Hatton vs
Ministry of
(Royal British
2010 A-Bomb Test veteran
appeal (Radiation and

38 NC Hughes
dec vs Ministry
of Defence
(Royal British
2010 A-Bomb Test veteran
appeal (Radiation and

39 B Lovatt vs
Ministry of
(Royal British
ENT 00279
2010 A-Bomb Test veteran
appeal (Radiation and

40 D Pritchard
vs Ministry of
(Royal British
ENT 00039
2010 A-Bomb Test veteran
appeal (Radiation and

41 L Selby vs
Ministry of
(Royal British
ENT 00658
2010 A-Bomb Test veteran
appeal (Radiation and

42 Denis Shaw
vs Ministry of
(Royal British
ENT 00054
2010 A-Bomb Test veteran
appeal (Radiation and

43 N Simons vs
Ministry of
(Royal British
ENT 00006
2010 A-Bomb Test veteran
appeal (Radiation and

44 H Sinfield vs
Ministry of
ENT 00751
2010 A-Bomb Test veteran
appeal (Radiation and

45 B Smith dec.
vs Ministry of
ENT 00680
2010 A-Bomb Test veteran

46 Mrs A Smith
vs Ministry of
2010 A-Bomb Test veteran
appeal (Radiation and

47 D Taylor vs
Ministry of
(Chris Francis
ENT 00912
2010 A-Bomb Test veteran
appeal (Radiation and

48 Mrs W Triggs
vs Ministry of
(Royal British
ENT 00285
2010 A-Bomb Test veteran
appeal (Radiation and

49 Mrs M
Williams vs
Ministry of
(Royal British
ENT 00768
2010 A-Bomb Test veteran
appeal (Radiation and

50 Kingscliffe
Waste Watchers
vs Augean Ltd
2010 Effects of radioactive
waste on health (radiation
and radioactivity
dispersion, exposure and

In two of the above cases I was deposed by defence attorneys with a view to having
my status as an expert witness disallowed by the trial judges under the rules of
Daubert vs Merrel Dow Pharmaceuticals whereby the judges have conferred on them
the power to decide whether an expert witness is expert in the area of expertise being
claimed and to disallow his or her testimony if not. In both cases, in the State of
Florida and in State of Kentucky the Daubert motions were unsuccessful.

I have asked two the attorneys I have worked for in the USA to provide references
and I submit these separately.

I worked for the Howarth and Smith firm in Los Angeles on a major case against the
Boeing Corporation involving my employing epidemiology, statistical inference,
exposure modelling and environmental dispersion. The case was settled for a
significant sum. I submit a .pdf of this and another testimony of this kind to this report
but this one best summarises the position with expertise in this complex area, so I feel
it is useful to add it here.

From Howarth and Smith, Los Angeles

We have been i nf or med t hat cer t ai n adver se l i t i gant s i n a UK
cour t have r ai sed an i ssue concer ni ng t he exper t i se of Dr . Chr i s
Busby i n t he ar ea of i oni si ng r adi at i on and i t s heal t h ef f ect s and
have done so i n an at t empt t o pr ecl ude or l i mi t hi s sci ent i f i c
t est i mony. Dr . D. Howar t h and Dr . S. Smi t h ar e t he f oundi ng member s
and pr i nci pal s of Howar t h & Smi t h. Dr . Howar t h has a B. A. , M. P. P.
and J . D. al l f r omHar var d Uni ver si t y. Dr . Smi t h has a B. A. f r om
Bost on Uni ver si t y, an M. Phi l f r omOxf or d Uni ver si t y and a J . D. f r om
t he Uni ver si t y of Vi r gi ni a. Dr . Howar t h i s an el ect ed f el l ow of t he
Amer i can Col l ege of Tr i al Lawyer s and of t he I nt er nat i onal Academy of
Tr i al Lawyer s. Dr . Smi t h i s an el ect ed f el l ow of t he I nt er nat i onal
Academy of Tr i al Lawyer s ( Boar d Member ) , t he I nt er nat i onal Soci et y of
Bar r i st er s, and t he Amer i can Boar d of Tr i al Advocat es. Dr . Smi t h i s
a member of t he Boar d of Tr ust ees of t he Uni ver si t y of Vi r gi ni a Law
School . Bot h Dr . Howar t h and Dr . Smi t h ar e Vi si t i ng Fel l ows i n l aw
at Lady Mar gar et Hal l , Oxf or d Uni ver si t y.

The f i r mof Howar t h & Smi t h has been i nvol ved i n cases
addr essi ng t he heal t h ef f ect s of i oni zi ng r adi at i on f or over t went y
f i ve year s. The pr i nci pal s have l ect ur ed on t he l aw and i oni zi ng
r adi at i on at numer ous l egal and sci ent i f i c conf er ences, i ncl udi ng t he
Def ense Resear ch I nst i t ut e, t he Annual Cal i f or ni a St at e Bar
Conf er ence, and The Royal Soci et y. Dur i ng t he cour se of i t s l egal
wor k, t he f i r mhas r et ai ned and wor ked wi t h many exper t s on t he
heal t h ef f ect s of i oni zi ng r adi at i on, i ncl udi ng t he l at e Si r Ri char d
Dol l , Dr . Ar t hur Upt on, chai r man of t he BEI R I I I Commi t t ee, and t he
l at e Dr . Edwar d Radf or d, chai r men of t he BEI R V Commi t t ee. We ar e
t her ef or e ver y f ami l i ar wi t h t he pr ocess of qual i f yi ng exper t s t o
gi ve cour t t est i mony and t he pol i t i cal i ssues whi ch can i nf ect and
sabot age t he l egal pr ocess. I nevi t abl y i n t hese cases, l ar ge sums
ar e at st ake and power f ul economi c ent i t i es may have pr i or i t i es whi ch
come i nt o conf l i ct wi t h t he goal of pr ot ect i ng l ong t er mpubl i c
heal t h and compensat i ng vi ct i ms of i ndust r i al or mi l i t ar y exposur e.

The pr i nci pal s have consul t ed wi t h and r et ai ned Dr . Chr i s Busby
as an exper t advi sor and exper t wi t ness i n l i t i gat i on t hat we have
managed. We r ecogni ze t hat Dr . Busby may have sci ent i f i c vi ews whi ch
di f f er f r omcer t ai n ot her sci ent i st s, i ndeed t hat he i s somet i mes a
mi nor i t y publ i c voi ce, at l east f or some per i od of t i me. Ever y
exper t we have ever wor ked wi t h, i ncl udi ng Si r Ri char d Dol l ,
exper i enced per i ods of di sbel i ef f r omcol l eagues, and pr of essi onal
cr i t i ci sm. Cont r over sy does not and cannot mean t hat voi ces of
l egi t i mat e sci ent i st s shoul d be si l enced. I ndeed, i t i s t he
di scussi on and debat e i n t he ver y i mpor t ant f or umof t he cour t r oom,
whi ch may l ead and has l ead t o publ i c awar eness and changes i n l aws
whi ch pr ot ect t he publ i c heal t h. I t i s al so t he pl ace wher e on t he
i ndi vi dual or gr oup l evel , ci t i zens can pet i t i on f or r edr ess when
t hey have been i nj ur ed, and compet ent sci ent i st s gi ve t hei r opi ni ons
as t o causat i on. Dr . Busby has al ways used sci ent i f i cal l y r i gor ous
and val i d pr ocedur es i n t he wor k he has done wi t h our f i r mand i n t he
publ i c r esear ch we ar e awar e of . Sci ence does not r equi r e
i nf al l i bi l i t y, and no sci ence coul d ever be pr esent ed i n cour t i f t he
st andar d was per f ect i on. However , Dr . Busby st r i ves f or t he hi ghest
l evel of excel l ence i n hi s wor k, whi ch i s why i t has become so not ed
i n t he sci ent i f i c and l egal wor l ds. Dr . Busby has been i nval uabl e t o
us i n t he ar ea of t he heal t h ef f ect s of i oni zi ng r adi at i on. He has
an encycl opaedi c knowl edge of t he ar ea, and has per sonal l y car r i ed
out si gni f i cant r el evant r esear ch st udi es. Hi s assi st ance t o us and
t o t he cour t s i ncl ude advi ce on r adi at i on epi demi ol ogy, st at i st i cal
i nf er ence, t he hi st or y of r adi at i on and heal t h, r adi at i on bi ol ogy of
humans, genet i c ef f ect s, l abor at or y cel l cul t ur e and ani mal st udi es,
exposur e cal cul at i ons, di sper si on model l i ng of r adi oact i vi t y and
gener al l y al l t he ar eas wher e an under st andi ng of t he heal t h ef f ect s
of exposur e t o r adi oact i vi t y and r adi at i on ar e r equi r ed. We have no
hesi t at i on i n r ecommendi ng Dr . Busby as an over al l exper t i n t hi s
compl i cat ed and di f f i cul t ar ea, f ul l y capabl e of def endi ng hi s
met hods and opi ni ons on pr oper cr oss exami nat i on. Dr . Busby has been
qual i f i ed as an exper t i n t hese f i el ds of exper t i se i n cour t s i n t he
Uni t ed St at es despi t e det er mi ned chal l enges t o di squal i f y hi m, whi ch
at t empt s f ai l ed.

Si gned

Don Howar t h Suzel l e M. Smi t h

B2. The report by Mr Ron Brown

This report is titled: Comment on Dr Busby’s research note 2008/8 entitled: Do
gamma doses from film badges give information about internal doses to atmospheric
atomic test participants from beat and alpha emitters.

This report is difficult to assess as it seems to consist of a confused stream of
consciousness which is peppered with ad hominem asides and builds up to a personal
attack on me. But I will try.

1. Mr Brown begins (p1 para 2) by stating that the film badges do give information on
internal doses. This is quite untrue. They do not, and the fact that he states this
destroys at the outset any credibility that his report may have had.

2. On page 1 para 4 he then disagrees with his previous assertion by stating that the
film badges and quartz fibre dosimeters give immediate indication of deposited
gamma dose (which they do not, they are cumulative dose devices) and then in para
(6) he again disagrees with his earlier statement in para (1) and states that the film
badges do not detect beta gamma signals from uranic materials. It must follow
therefore that for internal exposures (or indeed external exposures) to uranic materials
and plutonium, the film badges are no good. Which is my point. This is most
confusing. Indeed, later on p2 para (3) point 2 he disagrees again with his para (6)
statement stating that Dr Busby does not appear to be aware that film badges respond
to beta as well as gamma radiation. I am aware that the film badges react to beta
radiation but the point is that at the height above the ground that they are worn, there
is little or no beta radiation.

3. para (3) Paucity of literature. I read the Australian government report on dosimetry
(Carter et al 2006) Brown refers to long ago when I was writing my report for the
Class Action. It adds nothing to the arguments I gave in that report which is largely
the same one I present here except that it does show evidence of higher cancer rates.
Brown, of course, to be fair, never saw my report. However it is an interesting insight
into his biased selection of data that he fails to mention that the introduction to Carter
et al 2006 majors on the epidemiology of the Australian veterans and reveals the
significantly higher levels of cancer they had than the general population, a matter
that I draw attention to in my main report. Since it is of interest, I copy the relevant
part of the introduction to Carter et al 2006.

The overall death rate in test participants was similar to that of the general population.
There were 4233 deaths observed in participants, compared with 4150 expected from the
general population.
The most common cause of death in test participants was cancer, and death from cancer
was 18% greater in test participants than would be expected in the general population.
Deaths from causes other than cancer were generally fewer than expected in test
participants compared with the general population, with the number of deaths from heart
disease, cerebrovascular disease (mostly strokes), and external causes (suicide,
accidents, poisonings, etc) fewer than expected. The number of deaths from respiratory
diseases in test participants was about the same as expected from the general population.
The cancer incidence study showed an overall increase in the number of cancers in test
participants, similar to that found in the mortality study. The number of cancer cases
found among participants was 2456, which was 23% higher than expected. A significant
increase in both the number of deaths and the number of cases was found for (figures in
brackets show increase in mortality and incidence):
• all cancers (18% and 23%)
• cancers of the lip, oral cavity and pharynx (50% and 41%)
• lung cancer (20% and 28%)
• colorectal cancer (24% and 16%)
• prostate cancer (26% and 22%).

The number of cancer cases (but not the number of deaths) was also significantly greater
in test participants for the following cancers (figures in brackets show increase in
• oesophageal cancer (48%)
• melanoma (40%)
• all leukaemias (43%)
all leukaemias except chronic lymphatic leukaemia (61%).

Other findings included:
• of the 26 mesothelioma cases in test participants, 16 occurred in RAN personnel,
which was nearly three times the number expected
in RAAF personnel, there was nearly double the expected number of deaths from
melanoma, and cases of melanoma were increased by two–thirds.

The increases in cancer rates do not appear to have been caused by exposure to
No relationship could be found between overall cancer incidence or mortality and
exposure to radiation. None of the above cancers occurring in excess showed any
association with radiation exposure in this study. In particular, there was no link
between radiation exposure and leukaemia, excluding chronic lymphatic leukaemia (non-
CLLleukaemia), which is commonly found to be increased in groups exposed to radiation.
These findings are consistent with the low levels of radiation exposure found in this
study. Only 4% of the study population had an estimated radiation exposure greater
than 20 millisieverts (mSv) from test participation, and 79% had an estimated exposure
of less than 1 mSv. The estimated mean radiation exposure of the study population due
to participation in the tests was 2.8 mSv, only slightly greater than the background
exposure received by every Australian every year.
In the absence of a correlation with radiation exposure, the excess of non-CLL
leukaemia is unexplained. Other than radiation, the best established cause of leukaemia
is exposure to benzene, but there . . .

The point I make is that, like the MoD, Carter et al are using absorbed dose when they
write about exposure to radiation (highlighted sentences). No relation could be found
because there is none, since it was the internal doses that caused the cancers. This was
clearly higher on the RAN personnel and the cancers were higher in the head, neck
and respiratory system which in itself should have alerted any epidemiologist to
exposures by inhalation and on the surfaces of the head and neck open to the air.
Something that this group had in common was a carcinogen which had a highest
concentration on the surfaces of the head and neck and the airways and throat and the
lymphatic drainage of the lung (leukaemia). On the surfaces of the skin (melanoma).
Mmmm, what could that be? Obviously not radiation, since the film badge doses were
lower than natural background. Mmmmm.

4. In para 5 Brown makes the point that the MoD have used in all their defence
statements and which I have dealt with in the body of my report. He states that the
beta gamma signal can be used as an indicator of the presence of all radioactive
material from the detonation. But the film badges do not measure the beta gamma
signal, they measure the gamma signal, and as my analysis of the Oldbury report
shows, the beta emitters are predominant and do not have the same dispersion as the
gamma emitters suggesting that neither do the alpha emitters, specifically Uranium.
That was the point of my analysis, and Brown seems to have missed this altogether.

5. Page 2 para (1) contrary to Dr Busby’s assertions. . . This again misses the point I
make. Let me make it again with a thought experiment so it is quite clear. Let us
imagine that there are only two exposures, to external Caesium 137 gamma and
internal Uranium-238 alpha and its photoelectrons. The energy from these two defines
the doses received from them according to ICRP and the badges. Let is say that at 200
days the ICRP dose that Brown refers to (energy per unit mass) from external Cs-137
is 100microGray and from U-238 the internal ICRP dose is 1 microGray. Then his
statement would be correct. But the ICRP already weight the biological effectiveness
of internal Uranium at 20, so the equivalent doses then become 100 microSieverts and
20 microSieverts. Now less clear: this is because alpha emitters like Uranium cause
much more havoc in cells than beta emitters like Caesium-137. One step further:
ECRR add a weighting of 1000 because U-238 is a photoelectron amplification
nuclide. So now the dose from Uranium is 20,000 microSieverts whilst the dose from
Cs-137 is still 100 microSieverts. The situation is reversed. But these doses are not
discoverable from the film badge since the U-238 does not give any indication of its

6. Page 2 para 2 Resuspension of contamination
I can think of no reason why resuspension would vary with anything but weather
conditions. Brown must have misunderstood something.

7. para 3 various points as follows:

(1) aim of safety regime? Don’t understand. I’m aware of its aim: I point out that it

(2) film badges respond to beta. Yes I know this but there is no beta as by the time the
electrons get to the badge; if they do, there is no energy left to interact with the
emulsion. Brown should be aware of the ranges of beta electrons in air. He can find
them on the internet or from ICRU 35 Electron Beams with energies between 1 and
50MeV (Bethesda: ICRU 1984).

(3)The incomprehensible data Only to Mr Brown

(4) Does not provide complete discrimination between beta and gamma. . . aware of
or corrected for this. No need as the beta is so much greater than the gamma and in
any case the instruments had beta windows so the beta could be totally excluded, as
Oldbury stated and even recorded for some cases. I am perfectly aware of the limits of
these instruments as I measure beta and gamma regularly in the field myself and with
similar instruments.

(5) Australian government same as MoD Yes they are similarly invalid for the reasons
I have given

8. Page 2 para 4. Distances travelled. Fair point. It is possible to model these
resuspensions etc. but I haven’t done this yet and nor, it seems has anyone else.

9. Is he saying that because there was still some radioactivity on the ground, it had not
been inhaled by the veterans. I can’t believe that. What an argument. But what is he

10. No benefit in a more detailed critique OK by me.

11 Page 3 Dr Chris Busby
I do not feel it should be appropriate for me to respond to this section in detail. Others
will have to make up their own mind on these issues in an open and unbiased manner.
However, it should be noted that this DSTL report and the section on me is the
work of one man, Ron Brown, a person with a Chemistry degree from St Andrews
and a diploma in Radiological Protection, an individual with little or no research
experience and no scientific publication record in the peer review literature as far as I
can determine. I was on the Depleted Uranium Oversight Board where it was clear
that his understanding of the issues was not impressive though he had plenty of
enthusiasm for conflict and regularly had to be reined in by Prof Coggon. Mr Brown’s
job, has been to work for the Ministry of Defence behind a desk as a civil servant and
to apply there the principles and formulae of the International Commission on
Radiological Protection (ICRP), whose risk model is universally employed by
national governments and agencies.
It is not my purpose here to belittle Mr Brown, who may genuinely believe
what he says, just to make it clear that he is not a hands-on researcher, merely an
analyst, interpreter and presenter of other people’s work. As someone who has been
trained in the system of the ICRP he is (and was on the DUOB) hostile to any
suggestion or any evidence that the model he has applied all his working life, is
flawed. ICRP, as Mr Brown admits, represent the cornerstone of the ‘scientific
consensus’ on which his arguments depend. If it is seen to fail, then all his arguments
and those of the bodies he cites, also fail.
Brown makes the point that I am in a minority, that my view is a minority
view as if there were some scientific consensus majority view and this is how science
works by weighing research papers or people on scale pans. It does not: Galileo,
Newton, Einstein, Phlogiston, bacteria and antisepsis, are many examples and there
are less well known ones. It is worth exploring this idea of consensus. Mr Brown
relies on the ICRP model. Apart from a great deal of evidence showing ICRP models
to be faulty, the cornerstone of his argument has recently been removed, as I have
stated earlier, by the resignation in April 2009 from the ICRP of Dr Jack Valentin the
Editor of the 2008 ICRP report that Brown depends on for his position here and also
in the similar 2009 DSTL attack Brown made on me in the paper he wrote for the
Coroners case on Stuart Dyson. That Gulf War veteran died of colon cancer which,
after hearing my evidence and Browns, the jury attributed to depleted uranium
exposure. As I have written in my main report, following his resignation, Valentin
stated to me in a public meeting in Stockholm that the ICRP risk model ‘could not be
employed’ to predict the health outcomes of exposures to ionizing radiation because
for certain internal exposures the uncertainties were as high as two orders of
magnitude i.e.100 to 900 times. This means that there could be between 100 and 900
times the cancer yield per unit dose than is predicted by the ICRP model. Thus the
nuclear site child leukemia clusters, the Chernobyl cancer effects and the effects of
uranium are explained. Valentin also stated that since he was no longer the Scientific
Secretary of the ICRP he could now say that he believed that ICRP and the United
Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) had
been wrong in not addressing the many examples of evidence from Chernobyl and
from nuclear site leukemias and also other evidence that the ICRP model was unsafe
(Valentin 2009).
The meeting in Stockholm where Dr Valentin and I were discussing the validity of the
ICRP model was audio and videotape recorded and I have the tapes which can be
shown in Court if required. I have added the relevant transcript to this report.
Now to the point about scientific consensus. ICRP is a desk organization with
one permanent paid member: its Scientific Secretary Jack Valentin. Like Brown, it
carries out no research. It depends for its position on the reviews of scientific papers
provided by UNSCEAR but they are not independent of each other. Nor does
UNSCEAR carry out its own research. It trawls the literature cherry-picking papers
that support its own position i.e. UNSCEARs reports are selective. UNSCEAR
ignores any reports (and there are many) that falsify this position. In addition, the two
committees have members in common, and also members who have been or are
members of the International Atomic Energy Agency (IAEA) whose remit is the
development of nuclear energy. One example is Dr Roger Cox, Chair of the UK
National Radiological Protection Board (now the HPA) who is also Vice Chair of
ICRP and also contributing author to the 2000 UNSCEAR report. Another is Dr Abel
Gonzalez of the IAEA, who is also a full member of the ICRP committee and drafted
the ICRP 2008 report. Dr Lars Eric Holm of Sweden was until recently the Chair of
ICRP and also was Chair of the Swedish Radiological Protection organization SSI
and also Chair of UNSCEAR in 2001. Holm has famously gone on record as stating
that the total death toll of Chernobyl is limited to 30 seriously irradiated clean up
workers, something that is also stated regularly in public and at conferences by Abel
Gonzalez. Worryingly, Holm is now Medical Officer for Health for all Sweden and
there he shut down the research by Martin Tondel that showed increases in cancer in
Sweden after Chernobyl, not cited or referred to by UNSCEAR or ICRP. The point
here is that all the organizations that Brown and DSTL depend upon for scientific
consensus arguments and minority/majority arguments about radiation ultimately
interconnect and come back to one risk model and rather a small number of people.
The ICRP is not independent of the organizations that it depends upon for its
evidence, and they are not independent of it. The system is an internally consistent
and epicyclically-maintained fortress of bad science, bias and false conclusions. All
the points made by Brown to support his arguments ultimately dependent upon the
methodology and modelling of the ICRP. Brown in his report to the coroner attacked
my own group, the ECRR. He stated that the new independent radiation risk
committee, the ECRR, has been criticized for being a ‘self-styled organization with no
links to official bodies’ (Brown DSTL 2009 para 16). This should, in this context, be
a valuable asset.

12. The photoelectric effect Despite considerable sabre rattling and promises of a
paper in the peer review literature HPA have still not (Aug 2010) addressed this idea
which was reported in the New Scientist and in the peer review literature in 2008. This
is clearly because they cannot. It is almost certainly the reason Valentin resigned.

13. Various criticisms from various people including Dr Richard Wakeford. Brown
fails to mention that Wakeford is not unbiased: the senior research scientist for British
Nuclear Fuels Sellafield and whom I also believe to be the anonymous blogger
Richard D since the blogger quotes Wakeford too accurately. Wakeford’s attacks on
me in the Journal of Radiological Protection referred to by Brown (and Richard D)
were a serious abuse of his position as the editor of that journal: he would not have
succeeded in writing such libellous nonsense in any other journal since his articles
would not have made it past any referees (or lawyers).

14 COMARE 2003. Of course, this is a Press Release by COMARE and not peer
reviewed. COMARE were forced to retract their 2003 statement about my
epidemiology in 2006 following an analysis by Prof Griffiths, the President of the
Royal College of Public Health Medicine which showed the Wales Cancer
Intelligence Unit analysis to be false and based on erroneous population data. The true
picture is given in my peer-reviewed paper, Busby and Howard 2006 (Busby C C and
Howard C V (2006) ‘Fundamental errors in official epidemiological studies of
environmental pollution in Wales’ Journal of Public Health March 22
) which
naturally Brown failed to cite. I asked Griffiths to chuck John Steward (author of the
Wales cancer papers that COMARE and Wakeford relied on) out of the College of
Public Health Medicine but Griffiths said he couldn’t legally do that. However instead
Griffiths gave me a free run at WCISU in that journal to attack Steward but I couldn’t
be bothered.

12. My expertise. I have addressed this elsewhere for the PAT July 19




Name: Prof. Dr Christopher Busby

Home Address: Castle Cottage, Sea View Place, Aberystwyth SY23 1DZ UK
Tel: ## 44 (0) 1970 630215
Mob: 07989 428833

Professional Address:
Green Audit
Castle Cottage
Sea View Place
Wales SY23 1DZ
Tel. & fax: +44 (0) 1970 630215


Date/Place of Birth: 01/09/45, Paignton, Devon UK
Nationality: British


Education: 1966-69 Chemistry, University of London

BSc, PhD, C.Chem, MRSC

Qualifications: 1969 University of London First Class Honours Special Degree
in Chemistry
1970-71 SRC research studentship for PhD Physical Chemistry
(nmr spectroscopy), Queen Mary College, London
1974 Elected Member of Royal Society of Chemistry
1974 Chartered Chemist
1981 PhD Chemical Physics (Raman
spectroscopy/electrochemistry) University of Kent, Canterbury

Learned Societies:

Member: Royal Society of Chemistry
Member: Royal Society of Medicine
Member: International Society for Environmental Epidemiology
Member: Ukraine Committee: Physicians of Chernobyl

UK Government Committees
Member: (Department of Health and DEFRA) CERRIE
Committee Examining Radiation Risk from Internal
Emitters 2001-2004

Member: Ministry of Defence DUOB
Depleted Uranium Oversight Board

Other Committees
Scientific Secretary: European Committee on Radiation Risk

Science Policy group Leader: Policy Information Network on Child
Health and Environment PINCHE


1969 – 1975 Research physical chemist, Wellcome Foundation, Beckenham
1975 - 1978 Self employed scientific consultant and science writer
1979 - 1981 PhD student University of Kent
1981- 1982 SERC Research Fellow University of Kent
1983- 1992 Self employed scientific consultant and science writer
1992- present Science Director, Green Audit, commissioned to
research the health effects of ionizing radiation and funded by a
number of charities and independent bodies.
1995 Funded by the Joseph Rowntree Charitable Trust to write and
produce 'Wings of Death- The health effects of low level
1997-2000 Directed research at Green Audit Funded by Irish State to
research health effects of Sellafield
1997 Appointed UK Representative of European Committee on
Radiation Risk (ECRR)
1997 Foundation for children with leukaemia; research on non-
ionising radiation
2001 Appointed Scientific Secretary of ECRR and commissioned to
prepare the report ECRR 2003- The Health effects of low doses
of Ionizing Radiation (Published 2003)
2001 Appointed to UK Government Committee Evaluating Radiation
Risk from Internal Emitters (CERRIE)
2001 Appointed to the UK Ministry of Defence Oversight Committee
on Depleted Uranium (DUOB)
2002 Funded by the Joseph Rowntree Charitable Trust to write a new
book on the epidemiological evidence of health consequences
of exposure to ionizing radiation: 'Wolves of Water'
2003 Appointed Honorary Fellow, University of Liverpool, Faculty
of Medicine, Department of Human Anatomy and Cell Biology
1992-2008 Science Director, Green Audit
2003 Funded by Joseph Rowntree Charitable Trust to write Book
Wolves of Water Cancer and the Environment
2004 Leader of Science Policy for( EU) Policy Information Network
for Child Health and Environment PINCHE based in Arnhem,
The Netherlands
2005 3 year research funding by Joseph Rowntree Charitable Trust;
Corporate Responsibility in Science and Policy
2008 3-year research funding from The Joseph Rowntree Charitable
Trust; Corporative Responsibility in Science
2008 Appointed Guest Researcher, German Federal Research
Laboratories, Julius Kuhn Institute, Braunschweig, Germany
2008 Appointed Visiting Professor, School of Molecular Bioscience,
Faculty of Life and Health Sciences, University of Ulster,
Coleraine, Northern Ireland


1970 Taught O-level Chemistry part time, Inner London
Education Authority
1980-1981 Gave tutorials in quantum mechanics at the Dept. of
Chemistry. University of Kent
1995-1997 Invited lecturer at the University of Sussex Dept. of
1995-1997 Invited lecturer in the University of Wales,
`Aberystwyth, Physics Department and Geography
2000 – 2005 Invited lecturer in the University of Liverpool Faculty of
Medicine SSM5 ‘Environment and Health’ addressing
internal radiation risk and cancer epidemiology of small
2005 Invited lecturer University of West of England;
Radiation Risk and epidemiology
2006 Invited lecturer: Dept. of Law, University of Wales,
2006 Invited lecturer: Dept. of Environment, University of
West of England
2007 Invited lecturer: Centre for Molecular Bioscience,
University of Ulster (annually)


Professional Administration:
Senior Scientist
Dept of Physical Chemistry, Wellcome Research Laboratory, Langley Park,
Science Director, Green Audit
2004-2006 Leader: Workpackage 6 Science and Policy; PINCHE (EU)

Editorial boards (Current):
European Journal of Biology and Bioelectromagnetics

Invited Reviewer
European Journal of Biology and Bioelectromagnetics
European Journal of Cancer
Journal of Public Health (Royal College of Physicians, School of Public Health)
Science and Public Policy
The Lancet
Occupational and Environmental Medicine (BMJ)


Since 1997 Chris Busby has been engaged as an expert witness in several cases that
relate to the effects of radioactive pollution on health, in several refugee appeals
(Kosovo) based on Depleted Uranium risks, several trials of activists accused of
criminal damage at weapons establishment and one at the House of Commons
(evidence on Depleted Uranium and other radioactive substances), MoD pension
appeals tribunals for the widow of a A-Bomb test veteran and once in the
Connecticut State Court for an appeal against licensing releases of radioactivity from
the Millstone reactor on Long Island Sound. He is currently acting or has recently
acted as expert witness on two cases in the UK involving the health effects of
internal irradiation from Depleted Uranium. One of these is in the Royal Courts of
Justice and also in three cases in the USA. Two of these (against Exxon) have
recently been settled. The third, a landmark case involving childhood cancer near a
nuclear plant in Florida is currently being appealed in the US Supreme Court. He
also advised on the case of Rocketdyne (Boeing) and the Santa Susana Field
Laboratory childhood retinoblastoma cluster in Western Los Angeles which was
settled in January 2008 and a TENORM radiation case involving Ashland Oil in
Martha Kentucky, also other TENORM cases in Louisiana. He is currently also
expert witness and advisor on the UK Atomic Test veteran litigation in the Royal
Courts of Justice. He has been active in several test veterans pensions appeals
tribunals gaining reversal in every case of MoD refusals to pay war service pensions
in respect of diseases linked to radiation exposure at the test sites. He testified in
2009 before a coroners jury in the case of the death of Stuart Dyson arguing that
Dyson probably died of cancer due to his exposure to depleted uranium in the
Persian Gulf. Despite opposition from the MoD the jury unanimously agreed that the
uranium exposure was the probable cause of death. A full list and brief description
of the court cases in which Dr Busby has been retained as an expert witness is given
Dr Chris Busby
Court cases as expert witness

Case and
lawyer/ team
Court Year Details (expertise) Result
1. R vs
Hipperson et al
Crown Court
1998 Criminal Damage Atomic
Weapons Establishment
Aldermaston (radiation
health effects)
2. R vs Helen

Crown Court
1999 Criminal Damage House of
Commons London
(uranium health effects)
3. Sellafield Irish
(McGuill, Herr,
Irish State)
Dublin High
Case against Sellafield
THORP reprocessing plant
(epidemiology, radiation
effects, Irish Sea)
in 2008
4. Millstone
Reactor Public

State Court
2001 Opposition to relicensing
of Millstone Reactor
(Radiation health effects
and sea dispersion)
5. Fatmir Mata
(Wilson , Berry)
Appeal Court
Human Rights immigration
appeals Kosovo (uranium
health effects)
6. Lela Pelumb Immigration 2001 Depleted Uranium Kosovo Failed
(Wilson & Co,
appeal court (uranium health effects)
7. Ladrim Spata
(Clore and Co,
appeal court
HX 06027
2001 Depleted Uranium Kosovo
(uranium health effects)
8. Shaquiri,
Zogu, Malo,
Deda and Hidri
vs. Secretary of
State Home
appeal court
2002 Depleted Uranium Kosovo
(uranium health effects)
9. Hadjarmata vs
Sec.State Home
Office (Wesley,
Gryk, Amador)
appeal court
2002 Depleted Uranium Kosovo
(uranium health effects)
10. Mr and Mrs
Ardian Kuci vs
Sec.State Home
appeal court
2002 Depleted Uranium Kosovo
(uranium health effects)
11. Gerald
Adshead vs
Ministry of
appeals court
2002 A-Bomb Test Veteran
cancer (epidemiology,
radiation health effects)
12. R.vs
Margaret Jones
and Erika
Wilson (Alan
Crown Court
2002 Criminal Damage Nuclear
Submarine base Plymouth
(radiation and health)
13. Lee Dell
Craft Snr vs
Tubular ITCO
(Stuart Smith)
New Orleans 2005- Cancer following exposure
(Epidemiology, radiation
and health)
Settled by
14 Barbara
Castell vs
Tubular ITCO
CDC No 2002-
12334 Dv A
section 5.
(Stuart Smith)
New Orleans 2005- Cancer following exposure
to NORM (Epidemiology,
radiation and health)

15 Ursula Bulot
et al vs Exxon
Mobil Corp and
(Stuart Smith)
New Orleans 2005- Cancer following exposure
(Epidemiology, radiation
16 James Bailey
vs Exxon Mobil
Corp and others
New Orleans 2005- Cancer following exposure
(Epidemiology, radiation
(Stuart Smith) effects)
17 Zachary
Finestone, Lowe
et al vs St Lucie
Power and Light
( Lytal Reiter,
Palm Beach Fla).
Florida USA
Case 03-
2005 Case of children with
cancer near St Lucie
Nuclear Power Station.
(Epidemiology, radiation
dispersion modelling and
health effects)
18 R.vs Pritchard
and Olditch
(Bindmann and

Crown Court
2005-6 Criminal Damage US
bombers 2003 (uranium
and health)
(famous case)
19 R vs RV
Jones and
Crown Court
2005-6 Criminal Damage US
bombers (uranium
(famous case)
appeal to
20 Brian Gay vs
Ministry of
2007 A-Bomb Test veteran
Maralinga ; was his kidney
cancer caused by radiation?
(Epidemiology, radiation
and health)
21 Richard
David vs
Royal Courts
of Justice,
Bench Divn.
2007-8 Uranium contamination
and health; contaminated
via aero engines filters
from high altitude
(Epidemiology, radiation
and health)
litigant in
22 Cindy Mays
and others vs
(Suzelle Smith)
Los Angeles
2007 Did radiation releases from
the Rocketdyne SSFL
cause retinoblastoma in 9
Los Angeles children?
Epidemiology, radiation
dispersion modelling and
health effects).
Settled by
23 Bonnie
Anderson et al vs
Ashland Oil
(K. Mathis et al)
Circuit Court
2008 Contamination of property
by oilfield NORM
(Epidemiology, radiation
and health)
but being
24. A-Bomb Test
veterans vs UK
Ministry of
Royal Courts
of Justice,
Cancer and illness in A-
Bomb Test veterans
(Epidemiology, radiation
and health)
won, but
on appeal
25 Various vs
Exxon Mobil
Houston TX 2009-
Measuring gamma and
advising on NORM
contamination for potential
(Gordon) case
26 Derek Hatton
Vs Ministry of
(Derek Heaps)
2009 Cancer and polycythemia
rubra vera
See below
27 Etienne
Pellegal vs
Lincoln Electric
New Orleans
No 2006-
003684 Sec 6
Div L
NORM radiation and
laryngeal cancer
Settled by

28 Stuart Dyson
dec. vs MoD
Court Black
2009 Cause of Death; did
depleted Uranium cause
cancer. Big case, reported
29 Colin Duncan
Vs. Ministry of
appeal Court
2010 Exposure to fallout in A-
Bomb Tests caused cancer
30 Lowell
Ryman vs
Regents of
University of
Los Alamos
2010 Exposure to radioactivity
from Los Alamos and
Malignant Myeloma
31 Michael Nase
vs Teco Energy
(Stuart Smith)
New Orleans
2009 Exposure to radon and
radiation and lymphoma
32 Dawn
Pritchard vs
Ministry of
2010 A-Bomb Test veteran
widow. (Radiation and
33 L Abdale vs
Ministry of
(Royal British
ENT 00328
2010 A-Bomb Test veteran
appeal (Radiation and

34 D Battersby
vs Ministry of
(Royal British
ENT 00176
2010 A-Bomb Test veteran
appeal (Radiation and

35 D Beeton vs
Ministry of
(Royal British
ENT 00129
2010 A-Bomb Test veteran
appeal (Radiation and

36 T VButler vs
Ministry of
(Royal British
ENT 00078
2010 A-Bomb Test veteran
appeal (Radiation and

37 D Hatton vs
Ministry of
(Royal British
2010 A-Bomb Test veteran
appeal (Radiation and

38 NC Hughes
dec vs Ministry
of Defence
(Royal British
2010 A-Bomb Test veteran
appeal (Radiation and

39 B Lovatt vs
Ministry of
(Royal British
ENT 00279
2010 A-Bomb Test veteran
appeal (Radiation and

40 D Pritchard
vs Ministry of
(Royal British
ENT 00039
2010 A-Bomb Test veteran
appeal (Radiation and

41 L Selby vs
Ministry of
(Royal British
ENT 00658
2010 A-Bomb Test veteran
appeal (Radiation and

42 Denis Shaw
vs Ministry of
(Royal British
ENT 00054
2010 A-Bomb Test veteran
appeal (Radiation and

43 N Simons vs
Ministry of
(Royal British
ENT 00006
2010 A-Bomb Test veteran
appeal (Radiation and

44 H Sinfield vs
Ministry of
ENT 00751
2010 A-Bomb Test veteran
appeal (Radiation and

45 B Smith dec.
vs Ministry of
ENT 00680
2010 A-Bomb Test veteran

46 Mrs A Smith
vs Ministry of
2010 A-Bomb Test veteran
appeal (Radiation and

47 D Taylor vs
Ministry of
2010 A-Bomb Test veteran
appeal (Radiation and
(Chris Francis
ENT 00912
48 Mrs W Triggs
vs Ministry of
(Royal British
ENT 00285
2010 A-Bomb Test veteran
appeal (Radiation and

49 Mrs M
Williams vs
Ministry of
(Royal British
ENT 00768
2010 A-Bomb Test veteran
appeal (Radiation and

50 Kingscliffe
Waste Watchers
vs Augean Ltd
2010 Effects of radioactive
waste on health (radiation
and radioactivity
dispersion, exposure and

In two of the above cases, Dr Busby was deposed by defence attorneys with a view to
having his status as an expert witness disallowed by the trial judges under the rules of
Daubert vs Merrel Dow Pharmaceuticals whereby the judges have conferred on them
the power to decide whether an expert witness is expert in the area of expertise being
claimed and to disallow his or her testimony if not. In both cases, in the State of
Florida and in State of Kentucky the Daubert motions was unsuccessful.

In addition to the above Dr Busby has been invited or commissioned to provide expert
evidence on the health effects of low doses of ionising radiation, or exposure to
uranium for and to, amongst others :

The UK Royal Society Committee on Depleted Uranium
The UK Committee Examining Radiation Risk from Internal Emitters
The UK Committee on Radioactive Waste Management
The US Congressional Committee on Veterans Affairs and Security in the UK House
of Lords (Depleted Uranium)
The Canadian Parliament
The Greens in the European Parliament
The UK Environment Minister Michael Meacher MP
The Federal German Agricultural Laboratory, Brauschweig
The EU Policy Information Network on Child Health and Environment, Arnhem,
The British Nuclear Test Veterans Association
The UK House of Commons Cross Party Committee on A-Bomb Test Veterans (John
Barron MP, Neil Gibson MP)
The United Nations (UNIDIR) Geneva
The World Health Organisation/ Physicians of Chernobyl (Kiev)
The Government of Belarus
The Green Party of England and Wales
SAFEGROUNDS (Nuclear Industry Organisation for waste disposal discussions)
The British Nuclear Energy Society
The British Nuclear Test Veterans Association
The Royal British Legion
The New Zealand Royal Society


Various national and supra-national groups have sought advice from or appointed Dr
Busby as an advisor on various issues e.g.
Green Group European Parliament; Radiation and Health (Caroline Lucas MEP)
Canadian Government: Uranium and Health (appointed by Alex Atamenenko MCP,
British Columbia)
UK Committee on Radioactive Waste Management (invited by Prof Gordon
Royal Society Committee on Health Effects of Depleted Uranium Weapons (invited
by Prof. Brian Spratt)
US Congressional Committee on Veterans Affairs and Security (Uranium weapons)
(invited by Senator Christopher Shays)
UNIDIR Geneva (United Nations Institute for Disarmament Research) (Kirstin


Overview of major lines of investigation

Chris Busby spent seven years at the Wellcome Foundation, where he conducted
research into the physical chemistry and pharmacology of molecular drug receptor
interactions. He subsequently moved to the University of Kent at Canterbury where
he studied Laser Raman Spectro-electrochemistry in collaboration with Shell
Research and later as SRC Research Fellow, a project which resulted in a PhD in
Chemical Physics. He developed and published theoretical and experimental details
of silver and gold electrodes with surface array properties which enable acquisition
of laser Raman spectra of adsorbed molecules in dilute solution.

In the late 1980s he became interested in the mechanisms of low dose internal
irradiation and developed the Second Event Theory, which distinguishes between
the hazards of external and internal radiation exposure. In 1995 he was funded by
the Joseph Rowntree Charitable Trust to develop his arguments and write ‘Wings of
Death: Nuclear Pollution and Human Health’, an account of the results of his
research into radiation and cancer and also into cancer increases in Wales, which he
argued were a result of global weapons fallout exposure. In 1997 he became the UK
representative of the European Committee on Radiation Risk.

From 1997-2000 he was funded by the Irish Government to carry out research into
cancer incidence and proximity to the coast. In June 2000 he was invited to present
evidence to the Royal Society committee on Depleted Uranium and health, and
shortly after this was invited to Iraq to measure DU in the country and relate exposure
to health effects which followed the Gulf War. In 2001 he was asked to visit Kosovo
to investigate the dispersion of DU using field monitoring equipment. He discovered
DU in many areas from analytical measurements made on samples he collected (paid
for by the BBC) he showed that there was atmospheric resuspension of DU particles.
His work and expertise in the field of environmental health and radioactivity was
recognised by his appointment to CERRIE a Government committee reporting on the
effects of low level radiation on health. Following his evidence to the Royal Society
on the effects of Depleted Uranium, he was appointed to the UK Ministry of Defence
committee on Depleted Uranium in 2001. He was invited to address the US
Congressional Committee on Veterans Affairs of the Health effects of Depleted
Uranium in 2002. He is presently also the Scientific Secretary of the European
Committee on Radiation Risk and was commissioned to organise the preparation of
the new risk model on radiation exposure and to organise the publication of ECRR
2003: The Health Effects of Exposure to low Doses of Ionizing Radiation, published
in January 2003 and now translated into and published in French, Russian, Japanese
and Spanish. This work he updated with a chapter on Uranium and evidence of the
success of the 2003 model in explaining increases in cancer near nuclear sites and also
the reports of increases in cancer in Sweden after Chernobyl reported by Tondel et al.
in 2010. In 2004, he (jointly with two other colleagues) published the Minority Report
of the CERRIE committee (Sosiumi Press) which was supported and introduced by
Environment Minister the Rt Hon. Michael Meacher MP. In 2006 he produced and
jointly edited with Prof. Alexey Yablokov of the Russian Academy of Sciences
ECRR2006 Chernobyl 20 Years On. A second edition was produced in 2009.

Between 2004 and 2006 he was leader of the Science and Policy Interface Group of
the EU funded Policy Information Network for Child Health and Environment
(PINCHE) and organised the discussions and collation of information leading to their
final report on the issue which he wrote large parts of. The culmination of this project
which involved over 40 scientists and physicians from all major EU countries was the
recommendation that as a result of bias in scientific advice to policymakers, all advice
committees involving areas of dispute and possible harm to the public should be
oppositional committees with reports including all sides of any argument.

Since 2006 Dr Busby has been conducting laboratory experiments researching
photoelectron emission from Uranium and elements of high atomic number. He is
currently co-supervising a researcher at the Centre of Molecular Biosciences in the
University of Ulster on this matter.

He is also currently engaged in experimental and theoretical development of a novel
theory of living systems and their origin.


Dr Busby's early research was in the Physical Chemistry aspects of molecular
pharmacology at the Wellcome Research Labs. This involved the use of
spectroscopic and thermodynamic methods for examining cell drug interactions at
the molecular level. For a year he began a research degree in NMR on molecular
conformational changes on protonation but left to return to Wellcome and resume
his drug interaction research. From there he moved to developing descriptions of
intercellular and intracellular communication mechanisms, a subject which he is still
engaged in researching in the laboratory. Later he moved to examining molecular
behaviour at charged interfaces and developed a Surface Raman
spectroelectrochemical method as a Science Research Council Fellow at the
University of Kent.
Between 1992 and 2004 Dr Busby was engaged in research in three areas
associated with ionising radiation and health and also was funded for a year (1997)
by the Foundation for Children with Leukemia to research the interaction between
non ionising radiation and ionising radiation. His research in the area of ionising
radiation has been split between the development of theoretical descriptions of
radiation action on living cells and the epidemiology of cancer and leukaemia in
small areas. After 1994 he conducted survey epidemiology of Wales and England
and was the first to point out (in a letter to the British Medical Journal) that increases
in cancer in Wales might be related to weapons fallout. Later he examined childhood
leukaemia mortality near the Harwell and Aldermaston nuclear sites and suggested
that the excess risk might be related to inhalation of radioactive particles. These
results were also carried in a research letter in the BMJ which attracted considerable
criticism. His description of the mode of radiation action from sequential emitters
(his Second Event Theory was developed originally in 1987) has attracted a great
deal of interest and also criticism. Between 1997 and 2000 he was funded by the
Irish State to carry out epidemiological studies of cancer rates and distance from the
Irish Sea using data from Wales Cancer Registry and through a collaboration with
the Irish National Cancer Registry. Following this he and his team in Green Audit
developed novel small area questionnaire epidemiological methods and applied them
to a number of areas in different studies which included Carlingford Ireland,
Burnham on Sea in Somerset and Plymouth, Devon and Trawsfynydd, Gwynedd,
Wales, which resulted in a TV documentary in 2004. In addition he carried out
cancer mortality small area studies in Somerset and later in Essex. He extended
these to wards in Scotland in 2002. He has supervised a PhD student, who has
subsequently graduated, at the University of Liverpool in the Faculty of Medicine in
an epidemiological study of cancer mortality in Scotland with regard to proximity to
putative sources of cancer risk. In all the small area studies he carried out it was
possible to show a significant effect of living near radioactively contaminated
intertidal sediment. The papers and reports were all published by Green Audit and
most have been presented by invitation at learned conferences in Europe including
through invitations by the Nuclear Industry itself.
In addition to this, in 1998 Busby set up a radiation measurement laboratory
and equipped it with portable alpha beta and gamma measuring systems including a
portable gamma spectrometer made in Dresden which uses a 2" NaI detector. He
used these to show the presence of Depleted Uranium in Southern Iraq in 2000 when
he was invited by the Al Jazeera TV channel to visit the country as a consultant and
examine the link between leukaemia in children and levels of Depleted Uranium.
Since then he has measured radiation spectra in the filed in many countries and now
employs a 7” detector manufactured in Kharkov to obtain rapid analysis of field
gamma radiation. In 2001 he visited Kosovo with Nippon TV and was the first to
show that DU was present in dust in towns in Western Kosovo and through isotope
measurements funded by the BBC was able to report to the Royal Society in 2001
and the EU Parliament in Strasbourg that DU became resuspended in dry weather
and was rained out, and that it remained in the environment for a considerable time.
This subsequently led to UNEP deploying atmospheric particle measuring
equipment in areas where DU had been used. More recently, from 2006, Dr Busby
has been developing laboratory methods for measuring radiation conversion and
amplification by high atomic number micron diameter metal and metal oxide
particles (Uranium, Gold). It is his recent contention that such particles amplify
background radiation effectiveness by photoelectron conversion and he is the author
of a provisional patent application for the use of photoelectrons in cancer therapy to
destroy tumours.
In 2005 he was invited by various organisations in New Zealand (NZ Royal
Society) to give evidence on the health effects of Depleted Uranium. In 2005 and
2006 he worked with Prof Alexey Yablokov on the ECRR2006 report on Chernobyl
which was published on the 20
anniversary of the accident. In 2004 he conducted a
study of the health of people living in the vicinity of the Trawsfynydd Nuclear plant
in Wales for HTV and later also a study of the veterans of the Porton Down human
experiments in the 50s. The results of the Porton Down veterans study led to a
settlement and an apology by the government to the veterans in 2008. In 2007 he
began epidemiological studies of the children of A-Bomb Test veterans and also of
people living near mobile phone base stations. The A-Bomb veterans epidemiology
study highlighted high rates of miscarriage and congenital illness in their children
and grandchildren. The results were presented to the House of Commons committee
investigating this issue in November 2007 and have led to a recent agreement by the
UK government to fund further epidemiological research on this issue, research
which Dr Busby will oversee on behalf of the Test Veterans. In 2005, with Saoirse
Morgan he analysed data from the filters of the Atomic Weapons site in
Aldermaston and employed NOAA geophysical modelling to show that uranium
from Gulf War 2 weapons use had migrated to the UK. He has become interested in
the use of Uranium Weapons and has recently been involved in obtaining samples
from the Israeli actions in The Lebanon and Gaza and analysing vehicle filters for
uranium. His discovery of enriched uranium in such samples has received significant
media coverage and resulted in an invitation to write a 12-page article for the
United Nations Disarmament Forum Journal published in Geneva in 2009. His 2010
study with Malak Hamdan and Entear Ariabi of the cancer increases and sex ratio
changes in Fallujah Iraq following the US led attacks on the city has achieved
considerable prominence.

He is currently an expert advisor on the Test Veterans' litigation and expert
witness on their litigation against the British Government where the initial issue of
limitation was recently won in a landmark case in the Royal Courts of Justice. He is
official scientific advisor to the British Nuclear Test Veterans' Association and has
appeared for them in many legal tribunals for Pension Appeal cases. He was
appointed Visiting Professor in the School of Molecular Biosciences in the
University of Ulster in 2008 where he is co-supervising research on the health
effects of uranium. His uranium photoelectron theory was the top 2- page news story
in the New Scientist of 6
September 2008 and is receiving considerable attention
from the international nuclear risk agencies. Also in 2008 he was appointed Guest
Researcher at the German Federal Government Julius Kuhn Institute in
Braunschweig where he is co-supervising research on Uranium uptake in plants. He
is also currently working on the health effects of radioactive contamination of the
Baltic Sea with colleagues in Sweden, Finland and Latvia and has set up offices to
organise such research in Riga Latvia and in Stockholm Sweden.
In May 2009, in his capacity as Scientific Secretary of the European
Committee on Radiation Risk (ECRR) he organised an International Conference on
the Greek Island of Lesvos attended by eminent radiation scientists from all over the
world. The final statement from this conference The Lesvos Declaration called for
the abandonment of the current (ICRP) radiation risk models which all the delegates
agreed was insecure for its purpose of protecting human health from radiation


Year Place, Subject etc.
1995 House of Commons. Symposium on Low Dose Radiation
1995 Jersey, Channel Islands: International conference on nuclear shipments; Health
effects of low dose radiation
1995 Oxford Town Hall: Low dose radiation effects
1995 Drogheda, Ireland: Sellafield effects
1997 Strasbourg EU Parliament: Euratom Directive
1997 Brussels, EU Parliament STOA workshop on criticisms of ICRP risk models
1997 Kingston Ontario: World Conference on Breast Cancer: paper on cohort effects
and weapons fallout
1998 Muenster, Germany, International Conference on Radiation: Second Event
1998 Manchester Town Hall, Ethics and Euratom
1999 Copenhagen: Danish Parliament: Euratom Directive and low dose effects
1999 Carlingford, Ireland: Sellafield effects
2000 Kos Island: ASPIS (EC) meeting on 'Is cancer an environmental effect'; low
dose radiation and cancer
2000 London: Royal Society: low dose effects and Depleted Uranium
2001 Strasbourg: Green Group; Health effects of Depleted Uranium
2001 Bergen: International Sellafield conference, Sellafield effects on health
2001 Oslo: Nobel Institute: Health effects of low dose radiation and DU
2001 London: Royal Society: Health effects of Depleted Uranium (again)
2001 Kiev: WHO conference on Chernobyl: paper on infant leukaemia
2001 Prague: Res Publica International Conference on Depleted Uranium
2001 Strasbourg: EU Parliament, with UNEP; Health effects of Depleted Uranium
2002 Bergen: Conference on Sellafield
2002 Helsinki: Health effects of low dose radiation
2002 London: US Congressional Committee on National Security: Gulf war
syndrome and Depleted Uranium
2002 London Greenpeace: Small area statistics and radiation effects
2002 Chilton: Health effects of radioactive waste
2002 Oxford, British Nuclear Energy Society: Effects of low doses of radiation
2002 Royal Society of Physicians: Small area health statistics and radiation
2003 Birmingham: Non ionising radiation. Chaired
2003 Liverpool University: Depleted Uranium and Health
2003 Oxford University: Health Effects of Radiation from Internal Emitters
2003 Munich: Whistleblowers
2003 Copenhagen: Radiation and the foetus
2003 Hamburg: Depleted Uranium
2004 Berlin: Low level radiation
2004 London: PINCHE, child health and environment
2004 London, Westminster: Children with leukaemia
2004 Chicago: Radiation studies
2005 New Zealand Royal Society, Wellington
2005 New Zealand, Auckland University
2005 Chicago: Small area epidemiology by citizen groups
2005 Salzburg, Austria. PLAGE; International Nuclear Law and Human Rights
2005 Stockholm, Swedish Parliament; Low Dose Radiation and Depleted Uranium
2006 ECRR, Charite Hospital, Berlin, Health effects of the Chernobyl Accident
2006 Hiroshima Japan, Depleted Uranium
2007 Kuala Lumpur, Depleted Uranium: War Crimes Tribunal
2007 London, House of Commons: Chernobyl and health; anniversary lecture.
2007 London: Safegrounds Nuclear Industry CIRIA conference; low dose effects
2007 Blackpool: A-Bomb Veterans and low dose radiation effects
2007 University of Ulster: Childhood leukaemia in Ireland and Sellafield
2007 Hanover: Federal Agricultural Laboratories; Uranium chemistry and physics
2007 Geneva: United Nations. Health effects of Uranium weapons
2007 Geneva: United Nations. Chernobyl: WHO and the IAEA
2007 London, House of Commons Select Committee: Nuclear Test Veterans
Children Epidemiology study
2007 London, Royal Society: Science Policy Advice and Scientific Dishonesty
2008 Ljubljana Slovenia: Parliament; Nuclear Energy and Human Health
2008 Malmo Sweden; Uranium and health- new discoveries
2008 Helsinki; Chernobyl effects
2008 Moscow, Russian Academy of Sciences; A new theory of living systems.
2009 Malmo Sweden, Uranium weapons and health
2009 Stockholm Sweden, ICRP, SRM, Errors in radiation risk model
2009 Lesvos Island Greece; Requirements of a Adequate Radiation Risk Model
2009 Academy of Sciences, Riga, Latvia: the ECRR and ICRP radiation risk models
2009 Arusha Tanzania: Health effects of Uranium mining
2009 Dar es Salaam, Tanzania: Health effects of Uranium Mining
2010 Riga Latvia; Environment Ministry; Baltic Sea Radioactivity and Health
2010 Stockholm Sweden; Finlandhuset; Cancer and Birth Defects in Fallujah Iraq



Busby, Chris; Hamdan, Malak; Ariabi, Entesar. (2010) Cancer, Infant Mortality and Birth
Sex-Ratio in Fallujah, Iraq 2005–2009. Int. J. Environ. Res. Public Health 7, no. 7: 2828-

Busby C.C. (2009) Very Low Dose Fetal Exposure to Chernobyl Contamination Resulted in
Increases in Infant Leukemia in Europe and Raises Questions about Current Radiation Risk
Models. International Journal of Environmental Research and Public Health.; 6(12):3105-

Busby Chris (2009) Depleted Uranium, Why all the fuss? Disarmament Forum 3 25-33
Geneva: United Nations

Busby Chris, Lengfelder Edmund, Pflugbeil Sebastian, Schmitz Feuerhake, Inge (2009) The
evidence of radiation effects in embryos and fetuses exposed by Chernobyl fallout and the
question of dose response. Medicine, Conflict, Survival 25(1) 18-39

Busby Chris (2008) Is there a sea coast effect on childhood leukaemia in Dumfries and
Galloway, Scotland, 1975-2002 ? Occupational and Environmental Medicine 65, 4, 286-287

Busby Chris and Schnug Ewald (2008) Advanced biochemical and biophysical aspects of
uranium contamination. In: (Eds) De Kok, L.J. and Schnug, E. Loads and Fate of Fertilizer
Derived Uranium. Backhuys Publishers, Leiden, The Netherlands, ISBN/EAN 978-90-5782-

Busby C C and Howard CV (2006) ‘Fundamental errors in official epidemiological studies of
environmental pollution in Wales’ Journal of Public Health March 22

Busby C and Fucic A (2006) Ionizing Radiation and children’s health: PINCHE conclusions
Acta Paediatrica S 453 81-86

Newby JA, Busby CC, Howard CV and Platt MJ (2007) The cancer incidence temporality
index: An index to show temporal changes in the age of onset of overall and specific cancer
(England and Wales, 1971-1999) Biomedicine & Pharmacotherapy 61 623-630

Van den Hazel P, Zuurbier M, Bistrup M L, Busby C, Fucic A, Koppe JG et al (2006) Policy
and science in children’s health and environment: Recommendations from the PINCHE
project. Acta Paediatrica S 453 114-119

Koppe JG, Bartonova A, Bolte G, Bistrup ML, Busby C, Butter M et al (2006) Exposure to
multiple environmental agents and their effects. Acta Paediatrica S 453 106-114

Van den Hazel P, Zuurbier M, Babisch W, Bartonova A, Bistrup M-L, Bolte G, Busby C et al,
(2006) ‘Today’s epidemics in children: possible relations to environmental pollution’ Acta
Paediatrica S 453 18-26

Elsaesser A, Busby C, McKerr G and Howard CV (2007) Nanoparticles and
radiation. EMBO Conference: Nanoparticles. October 2007 Madrid

C. V. Howard, A. Elsaesser & C. Busby (2009) The biological implications of
radiation induced photoelectron production, as a function of particle size and
composition. International Conference; Royal Society for Chemistry NanoParticles

Busby CC (2005) Does uranium contamination amplify natural background radiation
dose to the DNA? European J. Biology and Bioelectromagnetics. 1 (2) 120-131

Busby CC (2005) Depleted Uranium Weapons, metal particles and radiation dose. European
J. Biology and Bioelectromagnetics. 1(1) 82-93

Busby CC and Coghill R (2005) Are there enhanced radioactivity levels near high
voltage powerlines? European J. Biology and Bioelectromagnetics. 1(2) Ch 7.

Busby Chris and Bramhall Richard (2005) Is there an excess of childhood cancer in North
Wales on the Menai Strait, Gwynedd? Concerns about the accuracy of analyses carried out by
the Wales Cancer Intelligence Unit and those using its data. European J. Biology and
Bioelectromagnetics. 1(3) 504-526

Busby Chris and Morgan Saoirse (2005) Routine monitoring of air filters at the Atomic
Weapons Establishment Aldermaston, UK show increases in Uranium from Gulf War 2
operations. European J. Biology and Bioelectromagnetics 1(4) 650-668

Busby C.C (2002). ‘High Risks at low doses.’ Proceedings of 4th International Conference
on the Health Effects of Low-level Radiation: Oxford Sept 24 2002. (London: British
Nuclear Energy Society).
Busby, C. C. and Cato, M. S. (2000), ‘Increases in leukemia in infants in Wales and Scotland
following Chernobyl: evidence for errors in risk estimates’ Energy and Environment 11(2)
Busby C.,(2000), ‘Response to Commentary on the Second Event Theory by Busby’
International Journal of Radiation Biology 76 (1) 123-125
Busby C.C. and Cato M.S. (2001) ‘Increases in leukemia in infants in Wales and Scotland
following Chernobyl: Evidence for errors in statutory risk estimates and dose response
assumptions’. International Journal of Radiation Medicine 3 (1) 23
Busby Chris and Cato, Molly Scott (1998), ‘Cancer in the offspring of radiation workers:
exposure to internal radioisotopes may be responsible.’ British Medical Journal 316 1672
Busby C, and M. Scott Cato, (1997)`Death Rates from Leukemia are Higher than Expected in
Areas around Nuclear Sites in Berkshire and Oxfordshire’, British Medical Journal, 315
(1997): 309.
Busby, C. (1994), `Increase in Cancer in Wales Unexplained', British Medical Journal, 308:

Busby C and Creighton JA (1982)' Factors influencing the enhancement of Raman spectral
intensity from a roughened silver surface'. J.Electroanal. Chem. 133 183-193

Busby CC and Creighton JA (1982)' Efficient silver and gold electrodes for surface
enhanced Raman spectral studies' J. Electroanal Chem 140 379-390

Busby CC (1984) J.Electroanal Chem 162 251-262

Busby CC (1984) 'Voltage Induced intensity changes in surface Raman bands from silver
electrodes and their variation with excitation frequency'. Surface Science 140 294-306

Busby, C. C. (1992), Low level radiation from the nuclear industry: the biological
consequences. (Aberystwyth: Green Audit)

Busby C.C (1992) Peledriad isaf o'er diwydiant niwcliar: yr canleniadau biolegol.
(Aberystwyth: Green Audit)

Busby, C. C. (1994), Radiation and Cancer in Wales (Aberystwyth: Green Audit).

Busby, C. C. (1995), Wings of Death: Nuclear Pollution and Human Health (Aberystwyth:
Green Audit)

Busby C.C (2003) ed with Bertell R, Yablokov A, Schmitz Feuerhake I and Scott Cato M.
ECRR2003: 2003 recommendations of the European Committee on Radiation Risk- The
health effects of ionizing radiation at low dose--Regulator's edition. (Brussels: ECRR-2003)
2004 Translations of the above into French Japanese Russian and Spanish (see for details)

Busby CC, with Bramhall R and Scott Cato MS (2000) I don’t know Much about Science:
political decision making in scientific and technical areas. Aberystwyth: Green Audit (this
book influenced the structure and formation of the CERRIE committee and advocates an
oppositional structure to science advisory committees in order to allow for cultural bias in
science advice. It has now been carried forward by PINCHE in Europe.).

Busby CC, Bramhall R and Dorfman P (2004) CERRIE Minority Report 2004: Minority
Report of the UK Department of Health/ Department of Environment (DEFRA) Committee
Examining Radiation Risk from Internal Emitters (CERRIE) Aberystwyth: Sosiumi Press

Busby CC and others (2004) Report of the Committee Examining Radiation Risk from
Internal Emitters (CERRIE) Chilton, UK: National Radiological Protection Board

Busby C and Yablokov AV (2006) ECRR 2006. Chernobyl 20 year On. The Health Effects
of the Chernobyl Accident. Brussels: ECRR/ Aberystwyth: Green Audit

Busby Chris (2006) Wolves of Water. A Study Constructed from Atomic Radiation,
Morality, Epidemiology, Science, Bias, Philosophy and Death. Aberystwyth: Green Audit

Busby Christo (2009) Our Mother who art in Everything. Poems 2004-8 Llandrinddod
Wells, Wales: Sosiumi Press

Busby C and Yablokov AV (2009) ECRR 2006. Chernobyl 20 year On. The Health Effects
of the Chernobyl Accident. 2
Edition Brussels: ECRR/ Aberystwyth: Green Audit

Busby C, Yablolov AV, Schmitz Feuerhake I, Bertell R and Scott Cato M (2010)
ECRR2010 The 2010 Recommendations of the European Committee on Radiation Risk.
The Health Effects of Ionizing Radiation at Low Doses and Low Dose Rates. Brussels:
ECRR; Aberystwyth Green Audit

Busby C (2010) The health effects of exposure to uranium and uranium weapons.
Documents of the ECRR 2010 No 2. Brussels: ECRR download free from

Busby C (2004) Nuclear Cover-Ups Video DVD Aberystwyth: Green Audit Films
Busby Christo (2009) Songs from a Cold Climate (CD) Aberystwyth: Green Audit
See also

Busby, C. C. (1996a), ‘ in Bramhall, R. (ed.), The Health Effects of Low Level Radiation:
Proceedings of a Symposium held at the House of Commons, 24 April 1996 (Aberystwyth:
Green Audit).

Busby, C. C. (1998), ‘Enhanced mutagenicity from internal sequentially decaying beta
emitters from second event effects.’ In ‘Die Wirkung niedriger Strahlendosen- im kindes-
und Jugendalter, in der Medizin, Umwelt ind technik, am Arbeitsplatz’. Proceedings of
International Congress of the German Society for Radiation Protection. Eds: Koehnlein W
and Nussbaum R. Muenster, 28 March 1998 (Bremen: Gesellschaft fur Strahlenschutz)

Busby C.C and Scott Cato M (1999) 'A Planetary Impact index' in Molly Scott Cato and
Miriam Kennett eds. Green Economics- beyond supply and demand to meeting peoples
needs. Aberystwyth: Green Audit

Busby C (2004) Depleted Science: the health consequences and mechanisms of exposure to
fallout from Depleted Uranium weapons. In The Trojan Horses of Nuclear War Kuepker M
and Kraft D eds. Hamburg: GAAA

Busby Chris (2007) New nuclear risk models, real health effects and court cases. Pp 35-46
in- Updating International Nuclear Law Eds—Stockinger H, van Dyke JM et al. Vienna:
Neuer Wissenschaftlicher Verlag

Busby C (2008) Depleted Uranium. Why all the fuss? United Nations Disarmament Forum
Journal UNIDIR, Nov 2008

Numerous articles for 'The Ecologist' on low dose radiation effects have been
translated into most languages and reprinted.
Numerous articles and reports in Radioactive Times: the Journal of the Low level
Radiation Campaign

Main Green Audit published papers
Busby C and Scott Cato M (2001) Increases in leukemia in infants in Wales and
Scotland following Chernobyl: Evidence for errors in statutory risk estimates
and dose response assumptions. Kiev WHO conference paper. Occasional
Paper 2001/7. Aberystwyth: Green Audit
Busby C C, Bramhall R and Dorfman P (2001) Environmental risk methodology and
Breast cancer mortality near Bradwell nuclear power station in Essex 1995-
1999. Occasional Paper 2001/8 Aberystwyth: Green Audit
Busby C C, Kaleta R and Rowe H (2000), The effects of Sellafield on cancer
incidence in Ireland from 1994 to 1996. Analysis of national Cancer Registry
small areas data., Report 2000/12 (Aberystwyth: Green Audit)
Busby C, (1994), 'Investigation of the Incidence of Cancer around Wylfa and
Trawsfynydd Nuclear Installations, 1974-86- Welsh Office Report A-EMJ28.
An appraisal for Wales Green Party', Aberystwyth: Green Audit
Busby C, Dorfman P, Rowe H (2000) Cancer Mortality and Proximity to Hinkley
Point Nuclear Power Station in Somerset: Part I Breast Cancer. Occasional
Paper 2000/2 Aberystwyth: Green Audit
Busby C, Dorfman P, Rowe H (2000) Cancer Mortality and Proximity to Hinkley
Point Nuclear Power Station in Somerset: Part II Prostate Cancer. Occasional
Paper 2000/3 Aberystwyth: Green Audit
Busby C, Dorfman P, Rowe H (2000) Cancer Mortality and Proximity to Hinkley
Point Nuclear Power Station in Somerset: Part III All malignancies, lung and
stomach cancer. Summary Occasional Paper 2000/4 Aberystwyth: Green
Busby C, Rowe H (2000) Cancer Incidence in Carlingford and Greenore, County
Louth: Results of the STAD/ Green Audit Questionnaire Report 2000/06
Aberystwyth: Green Audit
Busby C.C (2000), Science on Trial: On the Biological Effects and Health Risks
following exposure to aerosols produced by the use of Depleted Uranium
weapons. Invited presentation to the Royal Society, London July 19
2000 and
also given at the International Conference against Depleted Uranium,
Manchester 4
November 2000.Occasional Paper 2000/10
Busby C.C (2001) ' Depleted Uranium in Kosovo: Review of UNEP Report of 13

March 2001' Occasional Paper 2001/3 Aberystwyth: Green Audit
Busby C.C (2001) Health Risks following exposure to aerosols produced by the use of
Depleted Uranium Weapons. Presentation to Res Publica International
Conference Prague 24
Nov 2001. Occasional Paper 2001/12 (Aberystwyth
Green Audit)
Busby C.C (2002) 'Review of the Home Office statement on the health Consequences
of exposure to Depleted Uranium in Kosovo' Report 2002/2 Aberystwyth:
Green Audit
Busby C.C, (2000) Radiation from Sellafield and Cancer near the Irish Sea. The
Second Annual progress report from the Irish Sea Group in support of the
litigation Short and Others vs BNFL and Others Aberystwyth: Green Audit
Busby C.C, Dorfman P, Rowe H and Kocjan B (2001), Cancer mortality and
proximity to Oldbury Nuclear Power Station in Gloucestershire 1995-1999.
Including all malignancies, female breast, prostate and lung cancer mortality.
With an analysis of childhood leukemia incidence in ages 0-4 between 1974 to
1990 in Welsh Areas of Residence. Occasional paper 2001/6 (Aberystwyth:
Green Audit)
Busby C.C. (2002) 'Lymphoma Incidence in Italian Military personnel involved in
Operations in Bosnia and Kosovo' Occasional Paper 2002/3 Aberystwyth:
Green Audit
Busby CC (2000) From Sellafield to Chernobyl and Beyond: Exposure to man-made
ionizing radiation as the primary environmental cause of recent cancer
increases. ASPIS ( European Commission DG XVI) Conference: Is cancer
predominantly an environmental disease? Kos Island September 2000.
Occasional Paper 07/00 Aberystwyth: Green Audit
Busby C C (2001) On internal irradiation and the health consequences of the
Chernobyl accident; Presented at the 6
Conference of the British and Irish
Charity Organisations ‘Mitigating the consequences in Belarus of the
Chernobyl Catastrophe’, London April 6
2001/ Occasional Paper 2001/5
Aberystwyth: Green Audit
Busby, C (1996) `Childhood Leukemia and Radiation new Newbury’, Occasional
Paper 96/5 (Aberystwyth: Green Audit).
Busby, C. C. (1996), ‘Nuclear waste reprocessing at Sellafield and cancer near the
Irish Sea: arguments for an independent collaborative study’ Occasional
Paper 96/1 (Aberystwyth: Green Audit).
Busby, C. C. (1996), ‘Cancer and Leukemia in Children born in Wales and Scotland
after Chernobyl: Preliminary Note’, Occasional Paper 96/2 (Aberystwyth:
Green Audit).
Busby, C. C. (1997), ‘Breast cancer in England and Wales and Strontium-90 in
atmospheric weapons fallout’, Proceedings of the World Conference on
Breast Cancer (Kingston, Ont.: ).
Busby, C. C. (1998), ‘Childhood leukemia and radioactive pollution from the Atomic
Weapons facilities at Aldermaston and Burghfield in West Berkshire:
causation and mechanisms’, Occasional Paper 98/1 (Aberystwyth: Green
Busby, C. C. and Cato, M. S. (1998), ‘Increases in leukemia in infants in Wales and
Scotland following Chernobyl: evidence for errors in risk estimates’,
Occasional Paper 98/2 (Aberystwyth: Green Audit).
Busby, C. C., (1998), ‘Averaging Errors in the perception of Health Risks from
Internal radioisotopes with specific emphasis on mutagenic enhancement due
to 2nd Event effects from sequentially decaying man-made fission-product
beta emitters’, Proceedings of the European Parliament STOA workshop,
February 1998. (Aberystwyth: Green Audit)
Busby, C. C., Cato, M. S., Kocjan, B., and Mannion, E. (1998), ‘Proximity to the
Irish Sea and leukemia incidence at ages 0-4 in Wales from 1974-89’
Occasional Paper 98/4 (Aberystwyth: Green Audit).
This resulted in a 30 minute BBC TV Wales documentary)
Busby C.C (2002) 'The health effects of Depleted Uranium weapons: Invited
Written evidence to the US Congressional Subcommittee on National
Security, Veterans' Affairs and International Relations Hearing. London 18

June 2002; Occasional Paper 2002/3 Aberystwyth: Green Audit
Busby C.C (2002) 'Lymphoma Incidence in Italian Military Personnel Involved in
Operations in Bosnia and in Kosovo' Occasional Paper 2002/2 Aberystwyth:
Green Audit.
Busby C. Glyn E, Griffiths A, de Messieres M. Morgan S (2006) A Survey of
Cancer in the Vicinity of Trawsfynydd Nuclear Power Station. 2006/3
Aberystwyth: Green Audit.
(this was the basis for a 40 minute TV documentary by ITV Wales)
Busby C, de Messieres M and Morgan S (2006) Did Chemical Exposures of
Servicemen at Porton Down Result in Subsequent Effects on their Health?
The 2005 Porton Down Veterans Support Group Case Control Study. First
Report. Paper 2006/2 Aberystwyth, Green Audit.
(Shortly after this study was reported in the media the government
apologised to the Porton Veterans and gave them £3M compensation)
Busby Chris, de Messieres Mireille (2007) British Nuclear Test Veterans
Association/ Green Audit Children’s Health Study 2007 Report 2007/5
Aberystwyth: Green Audit
(This was presented to the House of Commons Committee on Test Veterans and is
the basis for an ongoing discussion with the MoD about further studies of the
veterans children and grandchildren)
Busby Chris, de Messieres Mireille, Morgan Saoirse (2007) Infant and Perinatal
Mortality and Stillbirths near Hinkley Point Nuclear Power Station in
Somerset,1993-2005. Occasional Paper 2007/6 Aberystwyth: Green Audit
(This was peer reviewed by Derek Pheby of the University of the West of England for
the BBC and covered in a short TV documentary by BBC Points West)

'Chernobyl: the definitive history', by RF Mould (Bristol: Institute of Physics):
reviewed for 'The Ecologist' in 2001
‘Animal Pharm’ by Mark Purdey (Clairview Books) reviewed for Caduceus in 2008


Dr Busby has 7 children and 11 grandchildren and lives in Aberystwyth Wales,
close to the sea. His interests include music and writing and performing songs (he
plays guitar, banjo, diatonic accordion, bandoneon, violin, viola, and Hardanger
fiddle: see ) writing poetry and sailing his 5-ton
1953 wooden yacht Carefree which is moored in Pembrokeshire (and belonged to
William Penney) and his 65 ton 1903 Dutch Barge Marius (which belonged to Susan
Ross of New York) based in France in which he is creeping south.

Partial transcript of conversation between Professor Chris Busby,
Scientific Secretary of the European Committee on Radiation Risk,
Dr J ack Valentin, Scientific Secretary Emeritus International
Commission on Radiological Protection.
Part of a public meeting in Stockholm, 22 April 2009 marking the 23rd
anniversary of Chernobyl (Video available)
CB: As scientists we ought to look at all sources of information, but ICRP has
never cited any one of the many articles that falsify [ICRP] or which show your
levels of risk are in error. Why?
JV: This puts me in a slightly difficult position, of course, because I tend to
agree with you — we should have quoted some of your stuff because since
we don’t agree with what you are saying we should then have said why we
don't. […] If you’ve got the Scientific Secretary of ICRP you press a button on
its back and it says what it's supposed to say but I'm retired so I can say what
I like But not many people are greatly impressed by the evidence that you
bring. It would have been much wiser in that situation to state more clearly
why we are not impressed, thus giving you a chance to come back again.
[Then we could have a debate and understand why we don't agree with each
CB: [cited as an example the 2006 ECRR publication Chernobyl 20 Years On
and a "Russian studies" section of the 2004 Minority report of the UK
Government Committee Examining Radiation Risks of Internal Emitters,
CERRIE] … hundreds of references from the Russian language literature
showing extraordinary effects from radioactivity - on genomic instability,
genetic effects in plants and fish which cannot suffer from radiophobia — an
enormous document which has been entirely ignored, suggesting bias.
JV: I have already agreed [ICRP, UNSCEAR, BEIR should not ignore these
findings] But we're not talking here about individual results but on most of
them I believe my colleagues would make technical comments [on individual
CB: Don't the leukaemia clusters near nuclear sites falsify ICRP?
JV: but there are other clusters around sites which were proposed for nuclear
power stations but the reactors were not built.
CB: That study is confounded by the unused sites being on previously
contaminated sea coasts and in areas of high rainfall [and high weapons
JV: We're now talking about confounders — that's the problem we have with
all of your [epidemiological] studies. You have insufficient controls. ICRP has
no official position on this but in principle people don’t agree and will point to
[epidemiological] studies where you get quite contradictory results, for
example lowered cancer. Bernie Cohen and radon is the most famous, falsely
showing a health benefit of radiation.
CB: These arguments about confounding disappear in the case of infant
leukaemia after Chernobyl. The babies were in the womb. The same results
from 5 groups in 5 countries published in different journals with doses
calculated in microSieverts but statistically significant excesses. How do you
explain that?
JV: I can't, but I don’t think you have enough explanations either. I honestly
don’t think you can convince me that you are right. There are technical
arguments. We should have emailed reports and gone them slowly and
thoroughly. That would be a clever way of continuing a discussion between
CB: Yes and no, but to get here we have had to be robust, chaining ourselves
to nuclear power stations, writing in the literature and using every possible
method of publicising that your risk model is bankrupt. Otherwise we wouldn't
be here.
JV: Are you sure you wouldn't have had more success if you just came up
friendly like and talked to the people at the Health Protection Agency? [UK
radiation protection advisers]
CB: [refers to long and well known experience of bad faith in various
dialogues including by the Chairman and secretariat of CERRIE and the UK
government departments involved.]
JV: Yes and I have heard many stories not very favourable to you. It's a
mistake to look back and argue about who did things wrong. Can't we look
forward and be more constructive?
CB: Yes, I agree. I have a question here that I was asked to put to you. It is
"Can the ICRP model be used by Governments to predict the consequences
of a nuclear accident, in terms of cancer yield?"
JV: Basically no, because the uncertainties we are talking about would be too
large; one order of magnitude. You are talking about two orders, but even at
the one order I am talking about it's not useful for that sort of prognosis.
CB: What's the point of it then?
JV: We're talking of the upper limit of course. Your most likely number of
cases would be X but ten times X cannot be excluded.
CB: Ok, ok, ok, and that means it is useful. So would the Government be
formally reasonable, using ICRP risk models to calculate the risks — the
cancer yield — from some hypothetical explosion at Barsebeck for example,
even if they'd have to say it might possibly be ten times that predicted figure?
JV: It would automatically be misused by both camps and that therefore is
why it is not … you don't do it like that. You look at individual doses — the
highest individual doses and calculate which is the sort of area where people
should not live — which is the sort of area where they should have special
needs — quick evacuation in case of emergency so this number exercise. I
think it's just silly. It serves no good purpose whether you're in your camp or a
pro-nuclear camp or an ICRP camp.
CB: Well in this case I'm in a political camp […] there are questions that
politicians need to know the answer to. When you build new nuclear power
stations, or [consider] any nuclear policy, you need to know what would
happen if something went wrong. You need some kind of model, and at the
moment they are using your ICRP model. Are you saying they should be or
they shouldn't be? You seem to be saying they should use no model at all. Is
it guesswork, or what?
JV: Well I certainly wouldn't say they should use your model because …
CB: ECRR gives the right answer
JV: … no it's the wrong answer, leading to large expenditure that would not
be sensible and could be used to save lives in other [ways]
CB: The draft ICRP Recommendations said that for many internal exposures
the concept of absorbed dose was not valid. We would agree with that of
course, but it disappeared from the final report. Why?
JV: In fact there is a whole section of the Biological annex which talks about
the difficulties. I don't know exactly why the specific statement disappeared
but a person reading those paragraphs in the annex will be able to see there's
huge uncertainty.
CB: We're not talking about uncertainty but about the impossibility of using
absorbed dose for internal nuclides.
JV: ICRP's position is that it's possible to use it albeit with large uncertainties.
CB: How large is large?
JV: Two orders is a very large uncertainty.
CB: So it could be in error by two orders for some internal exposures — so we
JV: (laughing) I'd hate for you to go home and say "J ack agreed with me"
CB: but I need an answer
JV: Then the answer is I don't agree with you. (laughing)
CB: but you just said Two orders of magnitude …
JV: Yes but you can find, I'm sure you can find, an exceptional case, a
specific case, where there would be that sort of uncertainty but remember it
can go in another direction, and I'm sure that you can find in most cases there
are uncertainties which are less than one order of magnitude, which you
would find normally. If we look at the existing evidence I don’t think you have
enough evidence to prove your case.
CB: The existing evidence is three orders of magnitude, if we take the
childhood leukaemia clusters around nuclear sites; three orders.
JV: That's what you are claiming on the basis of a handful of cases.
CB: I'm claiming it on the basis of the German study, Aldermaston, Sellafield,
Harwell and many others […]
End of extract.