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Health consequences of exposures of British personnel to radioactivity whilst serving in areas where atomic bomb tests were conducted

Supplementary Report to the composite report for the Royal British Legion, the RAFA and Rosenblatt’s Solicitors in response to Tribunals Service Directions Issued 23 July 2010

Chris Busby PhD

Service Directions Issued 23 July 2010 Chris Busby PhD Castle Cottage, Sea View Place Aberystwyth SY23

Castle Cottage, Sea View Place Aberystwyth SY23 1DZ U.K Nov 2010

Background The earlier composite report on the health effects in the A-Bomb test veterans (Busby 2010) was assembled in response to a deadline of 20 th September 2010. Because of the pressure on time I had not been sent details of the Tribunal appeals of three individuals who were represented by Rosenblatt Solicitors. This has now been rectified and the present report briefly addresses these three cases. However, in addition, I have had some time to follow up some other issues which I touched on in the earlier report and I take the opportunity here to review two of these, which are very relevant to the MoD arguments about radiation exposures. These are:

1. The real wind directions and fallout on Christmas island

2. Exposures to Tritium and Carbon-14

Since I wrote the earlier report, I have worked with a colleague Dai Willams on re- examining the statements made by MoD that the servicemen on Christmas Island were protected from fallout because the tests were only carried out when the wind was blowing away from the Island. The NOAA-HYSPLIT database (Draxler, R.R. and Rolph, G.D., 2010. HYSPLIT (HYbrid Single-Particle Lagrangian Integrated Trajectory) Model access via NOAA ARL READY Website ( NOAA Air Resources Laboratory, Silver Spring, MD. ; Rolph, G.D. (2010) Real-time Environmental Applications and Display sYstem (READY) Website ( NOAA Air Resources Laboratory, Silver Spring, MD.) has meteorological data from most of the earth back to 1947. In addition, as I pointed out in the earlier report, the prevailing wind direction for many of the tests was steadily south east, and since the test position was on the southern tip of the island, which lies south east/ north west, it would seem likely that the wind never really blows out to sea but blows parallel to the western coast. Furthermore, since the tests involved enormous energies, local weather conditions will have been perturbed and indeed dominated by the winds created by the explosion. This process is well described in Glasstone (1957, 1964). In addition, interviews with many of the surviving veterans show that conditions after the tests were not at all those implicit in the picture painted by AWRE. For example, in common with many US tests described by Glasstone, heavy rain fell on the island shortly after the test. This rain will have contained components of the weapon (e.g. uranium) and significant amounts of Tritium (radioactive tritiated water). There is evidence that at least one of the tests, Grapple Y, detonated at a much lower altitude than was designed and would have drawn up significant quantities of ground level material including coral and sea water (Large 1996, Busby and Williams 2010, anecdotal evidence reported below). This will have created significant quantities of fallout. The sea water will have accumulated tritium by hydrogen exchange to form tritiated water. This is important since Tritium has a very low beta energy and would not indicate any dose on a film badge, and Tritiated water will have contaminated the water supplies and caused exposure through ingestion and inhalation. Recent evidence suggests that Tritium (which easily enters the body, which is itself made mostly of water) is a radionuclide which is not correctly modelled by the ICRP risk system. I will therefore lay out this supplementary report as follows:


The real wind directions at the time of the tests on Christmas Island: a summary of the

conclusions of Busby and Williams 2010.

2. Tritium and Carbon-14

3. The cases of Nick Simons, Barry Smith and Herbert Sinfield

4. Conclusions

1. The Wind Direction and fallout over Christmas Island (see also full report)

Examination of the historical meteorological records and air movement modelling by Busby and Williams 2010 for each of the Christmas Island tests shows quite clearly that the radioactive cloud will have crossed the parts of the island remote from ground zero for a number of the tests. A series of 6 tests were carried out from Nov 57 - Sept 58. There were essentially two different types of tests:

1) 4 large Thermonuclear explosions 800kt - 3 Mt, offshore, medium altitude 2) 2 smaller Atomic devices 24-25 kt, onshore, low altitude. There were two different types of location - onshore low altitude, and offshore/inshore air bursts. Tests were conducted in different seasons: one in April, five between August and November. This is relevant since in this area the prevailing winds in the autumn are SEly but these shift to NWly in the Spring (Trade Winds). All tests were held in the morning. Civilian and military personnel were located in different parts of the island for different tests, and in addition air force and naval personnel conducting surveillance roles in the region. Investigations by Busby and Williams included:

Re-examination of the weapon test locations: the position, altitude and terrain using internet sources and eyewitness reports together with geographical plots of the HYSPLIT particle dispersion results.

Weapon information - size, type, features (internet sources plus eyewitnesses)

Initial explosion features and blast effects - (reports and videos of each test)

Potential sources of radiation and fallout - local, medium and long range (Glasstone 1957, Glasstone and Dolan 1977).

Prevailing weather conditions for each test (analysis using NOAA HYSPLIT, historic records and weather maps in Admiralty Pilots and Ocean Passages for the World HMSO 1974).

Eyewitness reports of plumes, blast and fallout including rainfall plus short and long term health consequences.

The conclusions of Busby and Williams 2010 were:

1. First, the NOAA models show that at least for some of the tests, that contrary to the

assertions of MoD and AWRE, there would have been dispersion of fallout and bomb material over Christmas Island, at least the western half. This was particularly true of Grapple X and Grapple Z Burgee and Pennant. But blast effects far exceed prevailing winds for fallout dispersal in the first hour after detonation. The vacuum resulting from the fireball causes air to be sucked into the centre of the explosion. If the fireball touches the sea then sea water is sucked in and large amounts of Tritium would have exchanged with the hydrogen in the sea water to form tritiated water HTO. Further information is

needed about the range of dispersal of fallout and other irradiated material within the local blast radius - up to 50 km / 30 miles – this is not factored into the NOAA models but is described by Glasstone on the basis of studies of US tests.

2. Explosion altitude is important to the type and amount of water and debris sucked into

the explosion vortex and so for differing levels and types of contamination after individual tests. At least one detonation, Grapple Y, occurred at a lower altitude than intended and will have resulted in significant fallout (Large 1996, anecdotal reports of barometric fuzing failure).

3. Local winds at different altitudes vary up to 180 degrees from prevailing winds. In

some cases these may have kept local fallout near or over the island for up to 4 hours. Nuclear fireballs rise rapidly about the test location to 50-80,000 feet, trailing a vertical column or stem of rapidly cooling water vapour or ice and explosion debris. Therefore

contamination scenarios need to be assessed for all levels of the nuclear cloud from sea to stratosphere. The whole nuclear cloud including the column is a fallout source. Upper winds in the Central Pacific reverse direction in the upper troposphere. In the transition layer (500-1000 metres) fallout from the nuclear cloud and stem/stalk may stay near or over the island for 3-4 hours.

4. In the tropics, land and sea breezes are significant. As soon as it is sunrise, the island

heats up and air rises over the hot earth drawing air inland from the sea. Thus the plumes which NOAA show travelling along the west coast will have been drawn inland at sea level by sea breezes.

5. Most important for the exposures of the servicemen, reports of heavy rainfall with

debris 15-45 minutes after each test match Glasstone’s description of rainout. This is

from either or both of two possible sources

(a) condensation clouds within the blast zone condensed by large fluctuations in pressure,

temperature, humidity and precipitation.

(b) delayed rain which may indicate precipitation from melting ice outside the collapsing

stem of the nuclear cloud i.e. highly irradiated material which would include large amounts of Tritiated water. The “black rain” described by eyewitnesses and which was also described at Hiroshima, may be uranium nanoparticles and micron diameter particles suspended in water and forming condensation nuclei.

6. These factors may help to explain eyewitness reports and provide a basis for requesting

and re-assessing radiation and fallout data available from official sources. What is clear, is that the re-examination of the situation at the time of the tests with historical data and using sophisticated air modelling shows that the assertions of the MoD and AWRE that servicemen were protected from fallout because the winds were offshore are largely untrue.

7. Finally, no records of any Tritium measurements are available, and it is possible that

this isotope was entirely overlooked. Nevertheless, it remains a serious hazard since it will have contaminated food, fish and water on the island and is also inhaled. As a low

energy beta emitter Tritium will not register on any film badge nor will it be detectable with any Geiger type instrument or scintillation counter.

3. More missing radionuclides: exposures to Tritium and Carbon-14

3.1 Tritium The hydrogen isotope Tritium H-3 is a very low energy beta emitter which decays to He- 3. Since the ICRP risk model assesses exposures for health purposes in terms of energy per unit mass of tissue, the absorbed doses from a Tritium decay (beta energy 0.0186MeV) is about 35 times smaller than the decay energy of Caesium-137. But all this means is that dose for dose, there are 35 times more ionisation tracks from Tritium decays than from Cs-137. These tracks are more highly ionising, that is, their ionisation density is greater. Furthermore, Tritium freely exchanges with water and with proteins and DNA base hydrogens, and a decay in the DNA is a decay into the target for radiation induced mutation. There are many theoretical arguments that Tritium is an unacknowledged hazard for this reason, and indeed there are studies which show remarkable genetic and developmental effects from Tritium exposures at very low conventional doses, less than natural background (e.g. Jha et al 2006). However, for the purposes of my current arguments it is sufficient to point out that Tritium as Tritiated water HTO will have been major component of the fallout rain and will have contaminated the water supply on Christmas Island besides contaminating the sea and the lagoons. It will thus constitute an inhalation and absorption hazard. The measurement of Tritium cannot be carried out using conventional radiation measuring equipment and the isotope will not show up on any film badge. It is an internal emitter and the questions raised about its hazard were discussed in the CERRIE committee and by the ECRR which gave it a provisional weighting of 20 since it is a pseudo Second Event nuclide (ECRR2010). But the factor may be much greater and at least one independent scientist, Ian Fairlie, has suggested that Tritium exposure is the origin of the nuclear site child

leukaemia clusters. If this is so, then the error in the conventional assessment of this isotope is of the order of 10,000. Whatever its weighting or danger, there is no doubt that

it is produced in prodigious quantities in the thermonuclear explosions on Christmas

island. Miskel (1973) reports that the production of 1Mt of energy by fission produces

700Ci of Tritium but that fusion thermonuclear explosions produce about 20MCi (7.4 x

10 17 or 750PBq) per Mt. Therefore the 6.85Mt of the combined Christmas Island tests

will have created about 5.1E18 Bq or 5.1 x 10 18 Bq of Tritium, much of which would have rained out on the island. To put this in perspective, the entire Chernobyl accident yield in terms of activity is less: only 2.4 x 10 18 Bq. There is no doubt that the Tritium

yields from the atmospheric tests were enormous. NCRP 1987 states that the natural

Tritium levels in the entire world increased by a factor of 200 due to the tests. Tritium has

a half life of 12 years and so will have remained on the island in the water to expose

anyone who was stationed there whether there was a test or not. It will have contaminated the sea and lagoons where the servicemen bathed and the fish that they ate. None of the radiological measuring systems in place, neither film badges nor portable scintillation of Geiger counters will have detected it.



Another “measurement invisible” radionuclide produced in large quantities is Carbon-14, half life 5730 years. Like Tritium (radioactive hydrogen, radioactive water) C-14 easily enters the food chain and the human body and becomes incorporated as a substitute for natural carbon-12. The exposures will have been principally initially to radioactive CO2 and then to food which contained C-14. The yield is 1.3PBq per Mt (Eisenbud and Gesell 1997) so the Christmas Island yield is about 8.8PBq. Like Tritium, C-14 is a low energy Beta emitter and will not be detected by any of the Geiger or scintillation equipment employed at the island, nor will either of these nuclides give any indication on a film badge.

3.3 Drinking water, eating food, swimming in the sea

The veterans who were stationed on Christmas Island could have received enormous doses from Tritium and Carbon-14 without anyone knowing. They probably did. No attempt seems to have been made, despite it being well known at the time that these nuclides were produced in prodigious quantities in the tests, to measure them or ensure that the water and food were free of them. Swimming in the sea or in lagoons contaminated with Tritiated water will cause severe radiation exposures of the skin (due to absorption by the skin of the Tritium contaminated seawater) and epithelial surfaces of the nasophanyx. Many veterans have described rashes and unusual boils which had to be lanced. Many have described suffering from nosebleeds. I have drawn attention in the main report to the exposures to Uranium and alpha emitters like Plutonium. These two weak beta emitters, because of their association with living systems, should also be considered as a significant overlooked hazard.

3. The three outstanding veteran appeals

First, I should make clear that as with the earlier report, the reviews of each veteran’s case are not as exhaustive as they would be if I were to have considered them separately as I have in the past for the separate tribunals. I will reproduce the table I used in the earlier report to give the level of probability I associate with each of the following individuals.

Table 3.1Scale of levels of probabilistic basis of causality for conditions for which pensions are claimed.






Highly Likely

High radiation risk related cancers: Leukemia (including CLL), lymphoma, Malignant myeloma, thyroid etc



All other cancers



Radiation related, Uranium related e.g. kidney disease, thyroid disease



Heart disease, atherosclerosis, check age onset


Aging related

Various conditions, check age onset



Various conditions

Table 3.2 The individual cases and levels of probability of causation or contribution










These are age related conditions.



Most were increased in the



Chernobyl and Hiroshima



exposed relative to controls (see

Sleep Apnoea


text) The sleep apnoea and



incontinence are secondary to the



other conditions

ZS 230667B

Smith. d

Cancer of


(ICD 157) Accepted by NIOSH-IREP as radiation related



Sinfield. d

Non Hodgkin




3.1 Nicholas Simons

Nicholas Simons, born 01/1943 was 65 when he claimed for a range of conditions, namely:

Osteoarthritis of the hips and knees

Thoraco-lumbar spondylitis

Cervical spondilitis

Diabetes (maturity onset)



Sleep Apnoeia

Urinary incontinence.

He was a Royal Engineer stationed at Maralinga from Feb 1964 to March 1965 and will have been exposed in the forward (controlled) area (231) to residual radioactive material by inhalation and ingestion, mainly uranium and plutonium but also other fallout isotopes present in the soil and resuspended by dust creation. This is an interesting case to consider, mainly because these are age-related conditions, and so I will devote some space to it. Mr Simons developed these conditions in his early 60s but then so do many men who never attended any test site. The assessment of contributory causation should take into consideration the background rate of the conditions being considered but should not rule out contributory causation since rates of ageing and onset of disease processes are genetically determined: some people age at different rates from others in the absence of any stress, and indeed there may be lifestyle stresses to include in any assessment. In

the case of Mr Simons, he was a smoker, and this certainly contributes to atherosclerosis. On the other hand, atherosclerosis rates were found to be significantly higher in a number of studies of those exposed to radiation, and heart diseased is now recognised to be associated with radiation prior radiation exposures. The MoD concede this (240). I considered this matter in my 1995 book Wings of Death where I pointed out that the atherosclerotic plaques were monoclonal mosaics and thus benign tumours, that they were produced in animals by exposure to carcinogens; I also analysed in that book the cohort effects of the increases in heart disease in England following the weapons test exposures and concluded that the epidemic of heart disease was due to the fallout, principally Sr-90. Heart disease was found to be raised in Radiologists. Since then results from Chernobyl and Hiroshima survivors have shown strong evidence that ischaemic heart disease and atherosclerosis are associated with exposure to radiation, particularly the internal exposures like those received by Mr Simons, i.e. largely the same isotopes. Examples are to be found in ECRR2010 and in collections of reviews of Chernobyl effects ( Burlakova, 1996, Busby and Yablokov 2006, 2009, Yablokov et al 2009. Since the Burlakova book is difficult to obtain I reproduce some of the data from Table 3 of Oradovskaya (Burlakova 1996) which compares certain conditions in four areas of difference contamination level in the Chernobyl affected territories. These results are particularly relevant to Mr Simons.

Table 3.1 Frequency of diseases in the Bryansk regions differently affected by radiation contamination from the Chernobyl accident. (Oradovskaya I.V, Institute of Immunology, Russian Federation, in Burlakova EB 1996)







N= 1074


Mean Cs-137 Ci/





Ischaemic heart disease





Atherosclerosis without IHD





Arthritis, spondylitis





Chronic pharyngitis, nasopharyngitis, laryngitis





Chronic bronchitis





Chronic pyelonephritis





The same paper compares various conditions between the two contaminated regions of the Bryansk oblast. The prevalence of various clinical symptoms of immune system deficiency are compared and shown to correlate with the radioactive contamination. Other evidence of the increased prevalence of non cancer illnesses and conditions in those exposed to radiation is presented in ECRR 2010, particularly for both Chernobyl and Hiroshima victims. These are condensed into Table 3.2 and 3.3 below

Additional reports of non cancer effects related to radiation and radionuclide exposure after Chernobyl are to be found cited and reviewed in Yablokov et al 2009. There are many examples but relevant to the current case in the report of a 3-fold increase in Type II diabetes in Belarus liquidators and evacuees (Yablokov et al 2009 p 79) and a significant excess risk of heart disease in male and female liquidators (Yablokov et al

2009, p 62) relative to the national population.

Table 3.2 Non cancer illnesses per 100,000 adults of three contaminated and 5 control regions of the Brest region in Belarus in 1990 (from Malko 1990 cited in ECRR2003,



3 contaminated

5 control








Circulatory system, hypertension, IHD




Osteomuscular, osteoarthritis




Urogenital, nephritis, nephroses, kidney infections




Endocrine, metabolism, immune system




Table 3.3 Comparison of morbidity rates (%) in Japanese A-Bomb survivors and the general Japanese population (Furitsu 1994 in ECRR2003, 2010)


A-Bomb sample

All Japan

Ischaemic Heart Disease



Anemia, leukopenia



Dental disease






Nephritis, urethral infection



Cholethiasis, pancreatitis



Bronchitis, pneumonia






It should be clear from these tables that exposure to radiation, particularly internal exposures to fission products and uranium causes a wide range of health problems most easily seen as premature ageing. Indeed, in extreme cases like the contaminated areas of Belarus, children are found to have conditions (arrythmias, gastric conditions) which are clearly seen on biopsy to be due to cellular ageing effects (Bandashevsky in Yablokov et al 2009, ECRR2003, 2010). It follows that the range of conditions for which Mr Simons has claimed can be subsumed within this heading. The only question is the extent to which his lifestyle and his exposures at Maralinga contributed. For this we need to look at the prevalence rates in an unexposed (to Maralinga) background population. I have used the very large sample in the 1997 Welsh Health survey (which I have studied and employed elsewhere) as a control. For ischaemic heart disease in the age group 55-64 35.6% of the sample had been “ever treated” for heart disease i.e. this is quite prevalent. So we can say that, on average, Mr Simons might have had a 35% chance of developing heart disease at age 64 without having visited Maralinga. In the same sample age group, 40.9% had arthritis, and 7.6% diabetes. I note from the records that Simons presented

with bad teeth (46) in 1962 and pharyngitis (45), kidney problems in 1968 (47) and 69 (50) all conditions reported in the Chernobyl groups. He has a daughter with congenital malformation and a grandchild also with congenital disease (225) and in my opinion this in itself is evidence that he has been affected by the exposures at Maralinga. I am however somewhat cautious about ascribing Mr Simon’s somatic problems entirely to his exposures. Nevertheless, I have no doubt that his exposures will have had some finite contribution to his spectrum of conditions, and indeed the particular spectrum is one which is seen in the two irradiated populations I have considered. The interesting aspect of this case is that it indicates clearly that a concentration on cancer and leukaemia as end points (as is the case with the various NRPB studies of the veterans) may have lost a number of individuals who died of other causes. This is seen clearly in the many studies of internal Radium and Thorotrast exposures where the cancer yield is not a true representation of the effects of these internal irradiations since many individuals died of other causes, and you cannot die of cancer if you have already died of a heart attack. I will be addressing these Radium/Thorotrast studies elsewhere. The tribunal will have to make up its mind on the case of Mr Simons. It is not as straightforward as the others and I would hesitate to use this as a test case in any major litigation.

3.2 Anna Smith/Barry John Smith

Barry Smith, born 05/1939 served in the RAF at Christmas Island from 10/1959 to 11/1960. He claimed 01/08 for a pension in respect of pancreatic cancer and was refused. At the time of his diagnosis with pancreatic cancer he was 68 and had been suffering from ischaemic heart disease for 5 years. He has since died and the case is being carried on by his widow, Anna Smith. The AWE report is the common one for Christmas Island servicemen. AWE contend that Mr Smith was not exposed to radiation at Christmas Island (207) and indeed that there was no residual radioactivity there. This is wrong and I have dealt with this issue in my earlier report and the new one, Busby and Williams 2010. The bundle does contain a copy of a paper by Prof Shoji Sawada which questions the results of the A-Bomb studies on the basis that the exposures of the controls to residual radiation was overlooked. This is a point I raised in my 1995 book Wings of Death. Sawada is a member of the ECRR and one of the signatories of the Lesvos Declaration (see my earlier report). Sawada himself was present at the time of the bomb as a 12 year old and buried in rubble in Hiroshima; he had to leave his to mother die.

I have no doubt that Smiths pancreatic cancer and death was caused by his exposures at

Christmas Island as his is a standard case described in the earlier report and his illness is

a radiation induced disease. I have already in the earlier report written about another case of pancreatic cancer in a veteran, that of the late Alun Williams, also a Christmas Island RAF veteran, also dead. These two cases on their own might suggest that there was a causal link with their earlier history.

3.3 Herbert George Sinfield

Sinfield was born 11/1938 and served as a driver in the army (RASC) at Christmas Island from 06/1958 to 06/1959 during the four Z Grapple tests (47). He was diagnosed with Non Hodgkin Lymphoma NHL in 2005 at age 67 died of lymphoma in 2007 having claimed for Non Hodgkin Lymphoma and Large cell lymphoma. A posthumous appeal was lodged 05/2007. Large cell or large T-cell lymphoma is a rare sub class of NHL and so we are concerned with examining the possible causes of this disease.

3.3.1 Non-Hodgkin lymphoma

Non Hodgkin lymphoma comprises a group of diseases which consist of certain malignant cell expansions within the lymphatic system, and which are distinct from Hodgkin’s Disease, which is a proliferation of a specific type of cell that can be detected by microscopic analysis. The non-Hodgkin lymphomas are essentially cancers of the immune system: they are subdivided through consisting of proliferations of many different types of cell. There are two main types of lymphocytes involved: B- lymphocytes (B-cells) and T-lymphocytes (T-cells). It is malignant cancerous growth of

B or T-cells that is the main basis of NHL. B-lymphomas are more common, accounting

for 85% of all cases, compared with 15% of cases from the T-cell origin (American Cancer Society). Normal B-cells produce antibodies that guide the immune responses to harmful elements e.g. bacteria. T-cells are involved in the recognition of virus-infected or cancer

cells; in organ transplantation it is the T-cell suppression that is necessary to prevent rejection. This immune system suppression, through drugs that kill the T-cells (and the other cells also) results in significant increased risk of NHL in later years. Thus NHL incidence is associated with prior immune suppression, or with substances or exposures

that cause or contribute to immune system suppression.

increase in the incidence rate of NHL in the last twenty years which has puzzled the international scientific community, resulted in considerable epidemiological and other investigation, and led to many suggestions about its cause. What remains is a general agreement that the origin of this increase is unknown, and that there are many risk factors for NHL, one of which has been conceded to be ionising radiation exposure, although there have also been studies suggesting that ionising radiation is not a major cause. Nevertheless, NHL has been designated as a specified cancer under the Energy Employees Occupational Illness Compensation Plan and is included in the NIOSH-IREP causality system for ionising radiation exposures. My own belief is that the increase, like the increases in most cancer rates unaffected by changes in lifestyle (e.g. smoking) is due

to the feed through of the global weapons fallout exposures, a position which I staked out

in 1994 (Busby 1994) and in Wings of Death (Busby 1995).

There has been a significant

Causes of non-Hodgkin lymphoma Since the condition begins, like all cancers and leukemias, with a fixed genetic mutation

or collection of mutations in a single cell, it is clear that any agent which confers an

increased risk of mutation must be a risk factor for the disease. Bende et al (2007) discuss molecular pathways in the development of B-cell lymphoma and conclude that the

initiating event for more than 90% of cases of the most common form is a mutation (a chromosome translocation) which leads to expression of an anti-apoptotic protein BCL-2. Ionising radiation is the largest single class of mutagen, and therefore exposure to ionising radiation must contribute excess risk. In children, the association with leukaemia and non-Hodgkin lymphoma has been highlighted in a number of studies of nuclear sites, the most famous being the Sellafield reprocessing site in the UK, but excess risk was also found near other nuclear sites which release uranium and other radioactivity e.g. the

Atomic Weapons Establishment Aldermaston (Beral et al 1990). Nevertheless, the literature is confusing on this issue especially with regard to the disease in adults. BEIR

V (p329) cite Anderson and Ishida 1964 who found an increased incidence of NHL in the

Japanese A-Bomb Lifespan Study (LSS) cohort although later studies by Shimizu et al 1987 (now the RERF group) no longer showed an excess of the disease. I interpret this as a time lag problem with exposure and controls in the Hiroshima LSS cohorts. The lag period for these cancers (lymphomas and leukemias) is believed to be shorter than for the

solid tumours (BEIRV 1990) and so these findings are in agreement with the earlier increases of NHL found by Anderson and Ishida and reported in 1964. By 1987, all those who were going to develop the disease will have done so. Therefore, the implicit conclusions of the BEIRV committee are misleading and perhaps disingenuous. BEIRV

do, however, draw

treated with radiation for Ankylosing Spondylitis (Darby et al, 1987); O/E = 2.24. Wagoner, 1984, reported an excess of NHL in women who were treated with ionising

radiation for benign gynaecological disorders. More recently Inskip et al, 1992 have reported that NHL risk was not elevated in a study of women treated for benign disorders. On the other hand, excess risk was found in women treated with radiation for cervical cancer, RR = 2.5 (90% CI 0.8, 7.6) (Boice et al. 1988). BEIRV, 1990 also draw attention

to increased mortality (RR = 2.73) from lymphosarcoma (strictly, lymphoma) in US

radiologists who entered practice in the 1920s to 1930s , though apparently this excess

risk does not exist in more recent radiologist cohorts.

Studies of radon exposure and NHL have given various results. The analysis of non-lung cancer mortality in miners by Darby et al 1995 did not identify excess risk from lymphoma, but the number of cases was only 36 in 1179 cancers, other than lung. However a number of ecological studies of radon and cancer have found excess risk from lymphoma. A discussion in BEIR VI focuses on epidemiology and the biological arguments of Henshaw et al 1990 that the fat solubility of radon will result in increased exposure to cells in the bone marrow and hence increases in leukaemia and lymphomas, which they pointed out could be seen in an ecological analysis of radon exposure by country. I have spoken with Denis Henshaw about this issue and he is sure that radon doses to the bone marrow are significant. Chromosome aberration analysis by Bauchinger et al (1994) of the peripheral lymphocytes of people living in houses where the radon levels were higher than 50Bq m -3 did in fact show significant 3-fold excess chromosome damage even at these low exposures, thus supporting Henshaw’s arguments. Despite various criticisms, the weight of evidence reported in BEIR VI does seem to support an association between radon exposure and NHL. Supporting the causal link, in the USA, an ecological study by Cohen (1993) using radon concentrations and cancers in 1600 counties also found association between radon and NHL. BEIR VI cites a number

of studies which do not, however, find any association with radon exposure and conclude,

attention to significant excess mortality rates of NHL in patients

incorrectly in my opinion given the clear association with chromosome damage, that radon need not be considered as a cause of non-lung cancer illnesses. A recent study by

Karunanayake et al 64 found a significant increased risk of NHL with exposure to ionizing radiation (radium) in a case-control study of Canadian men diagnosed with NHL between 1991 and 1994 (adjusted OR: 3.26, 95% CI: 1.38-7.73). This finding is clearly relevant to the present case. Radium and Uranium were present on Christmas Island according to the New Zealand NRL 1981 though unfortunately the report fails to report the measurements (McEwan et al 1981).

I will now review some of the general epidemiology relating to causation of non- Hodgkin lymphoma and then draw some general conclusions. McNally and Parker (2006) review environmental factors in the causation of childhood NHL and identify a range of exposures including magnetic fields, pesticides, benzene, maternal alcohol consumption, contaminated drinking water, infections and high birth weight. For NHL they highlight ionising radiation, pesticides and in utero exposure to cigarette smoke, benzene and nitrogen dioxide. Gurney and Cartwright 2002 studied NHL in England and Wales from 1986-1993 confirming the real increases in the disease, proportionally greater for middle aged men; they suggested that environmental factors such as sunlight may be responsible. Sunlight was also suggested as a factor by Bentham (1996) who made geographical analyses across areas with different ultraviolet light indices. UV light is, of course both mutagenic and causes immune system suppression. Immune system suppression is certainly a strong cause of NHL: the increase in the disease in people who have been treated with immune suppression drugs for bone marrow or organ transplants and those with inherited immunodeficiencies, has been reported to be as high as 30% (Filipovich et al 1992). This is also true of those who have HIV/AIDS related immunodeficiency who have high rates of NHL, as do those who have been treated with radiation or chemotherapy for an earlier cancer. Patients treated with chemotherapy or radiation for Hodgkin’s disease have a 5% excess risk of developing NHL over a ten year period. Linos et al 1991 found elevated risks of NHL in those living near industrial facilities in Iowa and Minnesota particularly associated with residing near stone, clay or glass industry facilities. Scherr et al (1992) examined occupational risk using a case control study and concluded that excess risks for NHL was associated with working in agriculture, forestry and fishing (RR = 3.0), the construction industry (RR = 2.1), and the leather industry (RR = 2.1). Particular jobs that carried high risk were farmers (RR = unbounded), painters and plasterers (RR = 6.0) and carpenters, brick and stone masons (RR = 12). Johnson et al (2003) studied proximity to industrial plants in Canada and found a significant association with residence near copper smelters and sulphite paper mills. Others have found associations with organic solvents (Rego et al 2002) although a meta-analysis (Lamm et al (2005) concluded that a reported association with benzene (Blair et al 1992) was not supported. Viral exposures, particularly to the Epstein Barr virus also represents a significant causal association but whether the infection is a result of (due to immune system inadequacy) or a cause of the NHL is not established. Weisenburger (1994) regarded the cause of the NHL ‘epidemic’ as being a result of many different environmental factors each of low risk acting on large segments of the population, and this seems plausible. However, the largest single exposure element affecting the immune system has been to ionising radiation, from the weapons test fallout components in the food chain which peaked in the environment in the late 1960s early

1970s, and which were supplemented in the USA by releases from the many nuclear sites and by the large amounts of technologically enhanced natural materials (TENORM) increasingly released to the environment with industrial expansion, particularly in the USA where the increase in NHL has been greatest. Occupations which have been particularly associated with NHL are those where there is significant exposure to dusts and respirable particles e.g farmers, carpenters, stonemasons. The association with farming has also been ascribed to the agricultural use of toxic chemicals. In my opinion, and from consideration of the epidemiology and the likely aetiology, it is both the assault on the lymphatic system by inhaled particulate matter, and the suppression of the immune system, which represent the major causal hazards for NHL.

3.3.2 Mr Sinfields exposure

The radiation exposures received by Mr Sinfield at Christmas Island though inhalation of radioactive particulates, though ingestion of radioactive materials including alpha emitters, tritium and C-14 were, in my expert opinion, the cause or a substantial factor in his developing the disease. This was also the conclusion of the haematologist who treated him (43, 44, 63). AWE state as usual that he could not have been exposed; I have deal with this defence in the earlier report. Sinfield writes (51) that we were gathered at the port area and that the cloud [from the test] hung around for most of the day. On one occasion it rained, as I remember wearing a poncho. The NOAA plots shown for Grapple Z tests that for some of them the cloud passed over the port. In addition, Sinfield’s work will have placed him in contact with dust, and resuspended material since he delivered material to the South East corner of the island in connection with the extension of roads to that area.

4. Conclusions

In my continued examination of the circumstances of illness in veterans of Christmas Island Tests and in reviewing everything I have discovered, I cannot fail to be concerned about the arguments advanced by AWE in this case. Many of the statements made by the MoD and AWE are clearly incorrect or misleading. The defence states that the natural background radiation on Christmas Island is 30nSv/h leading to an annual dose of 0.26mSv and this is very much lower than in the UK where it is 2mSv. But a map in the defence bundle for one veteran (Butler 432) has scrawled on it in pen background is 29 Micro Roentgens per hour. This is 2.5mSv per year and that does not include Radon; the equivalent annual gamma dose in the UK is less than 0.5mSv. AWE states that there is no Radon on Christmas Island (it is the radon dose in the UK that pushes up the figure to 2mSv). But the New Zealand 1981 report (McEwen et al, 1981) clearly states that there was Radium-226 measured in soil at 230Bqkg -1 . This is a high level of Ra-226. This would produce radon which is the decay product of Ra-226. But no one measured radon on Christmas Island, or at least there are no data. And unfortunately, McEwen et al 1981 did not report the gamma dose rates they found, nor the levels of Uranium and Radium they measured and reported on. They stated that they were naturally occurring

radionuclides and

are not tabulated nor discussed in this report. It is likely that they

were present in large amounts and that is why they were not reported since it would have been clear that they were from the bomb, contained U-235 in large amounts, and were not natural. This is what I concluded from the Oldbury 1964 report. This is the principal problem. The defence statement that there was no fallout exposure on land as the tests were only carried out when the wind was offshore seems to be questionable; many of the NOAA calculations made by Busby and Willams 2010 based on historic meteorological data show the plumes travelling over the western part of the island and over where the personnel were stationed. After most of the tests, rain reportedly fell on the unprotected personnel, rain which was black and which arguably contained uranium, tritium and


AWE do not mention Tritium and C-14; the contemporary reports do not mention them. None of the documents mention them. Yet it was known at the time that these nuclides were created in prodigious quantities. Reasons are given for refusing pensions which incorrectly state that a specific cancer is not associated with prior radiation exposure when a cursory literature search reveals many papers which show that it is. I have been able to show without any doubt that these veterans have all been exposed to significant levels of internal radionuclide exposure which would not have been detected by the film badges or survey instruments used at the test sites; from Uranium, Plutonium, Tritium and Carbon-14 and Strontium-90. It is not surprising they have suffered health effects; nor is it surprising that their children and grandchildren have a 9-fold excess of congenital diseases and conditions (Busby and de Messieres 2007), evidence on its own of the earlier genetic damage to the veterans as a result of their exposures to radioactivity at the test site areas where they were stationed.

I reserve the right to add to this report or amend it in the light of further information which may emerge following the order made to the MoD to release relevant documents.

Chris Busby 11 th Nov 2010


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