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    Health consequences of exposures of Britishpersonnel to radioactivity whilst serving in areas

    where atomic bomb tests were conducted

    Supplementary Reportto the composite report for the Royal British Legion, the RAFA

    and Rosenblatts Solicitors in response to Tribunals ServiceDirections Issued 23 July 2010

    Chris Busby PhD

    Castle Cottage, Sea View PlaceAberystwyth SY23 1DZ U.K

    Nov 2010

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    Background

    The earlier composite report on the health effects in the A-Bomb test veterans (Busby2010) was assembled in response to a deadline of 20

    thSeptember 2010. Because of the

    pressure on time I had not been sent details of the Tribunal appeals of three individualswho 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 sometime to follow up some other issues which I touched on in the earlier report and I take theopportunity here to review two of these, which are very relevant to the MoD argumentsabout radiation exposures. These are:

    1. The real wind directions and fallout on Christmas island2. 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 wereprotected 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) Modelaccess via NOAA ARL READY Website (http://ready.arl.noaa.gov/HYSPLIT.php). NOAA

    Air Resources Laboratory, Silver Spring, MD. ;Rolph, G.D. (2010) Real-timeEnvironmental Applications and Display sYstem (READY) Website

    (http://ready.arl.noaa.gov). NOAA Air Resources Laboratory, Silver Spring, MD.) hasmeteorological data from most of the earth back to 1947. In addition, as I pointed out inthe earlier report, the prevailing wind direction for many of the tests was steadily southeast, and since the test position was on the southern tip of the island, which lies southeast/ north west, it would seem likely that the wind never really blows out to sea butblows parallel to the western coast. Furthermore, since the tests involved enormousenergies, local weather conditions will have been perturbed and indeed dominated by thewinds 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 thetests were not at all those implicit in the picture painted by AWRE. For example, incommon with many US tests described by Glasstone, heavy rain fell on the island shortlyafter the test. This rain will have contained components of the weapon (e.g. uranium) andsignificant amounts of Tritium (radioactive tritiated water). There is evidence that at leastone of the tests, Grapple Y, detonated at a much lower altitude than was designed andwould have drawn up significant quantities of ground level material including coral andsea water (Large 1996, Busby and Williams 2010, anecdotal evidence reported below).This will have created significant quantities of fallout. The sea water will haveaccumulated tritium by hydrogen exchange to form tritiated water. This is importantsince Tritium has a very low beta energy and would not indicate any dose on a filmbadge, and Tritiated water will have contaminated the water supplies and causedexposure through ingestion and inhalation. Recent evidence suggests that Tritium (whicheasily enters the body, which is itself made mostly of water) is a radionuclide which isnot correctly modelled by the ICRP risk system.I will therefore lay out this supplementary report as follows:

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    1. The real wind directions at the time of the tests on Christmas Island: a summary of theconclusions of Busby and Williams 2010.2. Tritium and Carbon-143. The cases of Nick Simons, Barry Smith and Herbert Sinfield4. Conclusions

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

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

    1) 4 large Thermonuclear explosions 800kt - 3 Mt, offshore, medium altitude2) 2 smaller Atomic devices 24-25 kt, onshore, low altitude.

    There were two different types of location - onshore low altitude, and offshore/inshore airbursts. Tests were conducted in different seasons: one in April, five between August andNovember. This is relevant since in this area the prevailing winds in the autumn are SElybut 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 differenttests, and in addition air force and naval personnel conducting surveillance roles in theregion. Investigations by Busby and Williams included:

    Re-examination of the weapon test locations: the position, altitude and terrainusing internet sources and eyewitness reports together with geographical plots ofthe 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 andOcean Passages for theWorldHMSO 1974).

    Eyewitness reports of plumes, blast and fallout including rainfall plus short andlong 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 theassertions of MoD and AWRE, there would have been dispersion of fallout and bombmaterial over Christmas Island, at least the western half. This was particularly true ofGrapple X and Grapple Z Burgee and Pennant. But blast effects far exceed prevailingwinds for fallout dispersal in the first hour after detonation. The vacuum resulting fromthe fireball causes air to be sucked into the centre of the explosion. If the fireball touchesthe sea then sea water is sucked in and large amounts of Tritium would have exchangedwith the hydrogen in the sea water to form tritiated water HTO. Further information is

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    needed about the range of dispersal of fallout and other irradiated material within thelocal blast radius - up to 50 km / 30 miles this is not factored into the NOAA modelsbut 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 afterindividual tests. At least one detonation, Grapple Y, occurred at a lower altitude thanintended and will have resulted in significant fallout (Large 1996, anecdotal reports ofbarometric fuzing failure).

    3. Local winds at different altitudes vary up to 180 degrees from prevailing winds. Insome 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 verticalcolumn or stem of rapidly cooling water vapour or ice and explosion debris. Thereforecontamination scenarios need to be assessed for all levels of the nuclear cloud from sea tostratosphere. The whole nuclear cloud including the column is a fallout source.

    Upper winds in the Central Pacific reverse direction in the upper troposphere. In thetransition layer (500-1000 metres) fallout from the nuclear cloud and stem/stalk may staynear 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 islandheats up and air rises over the hot earth drawing air inland from the sea. Thus the plumeswhich NOAA show travelling along the west coast will have been drawn inland at sealevel by sea breezes.

    5. Most important for the exposures of the servicemen, reports of heavy rainfall withdebris 15-45 minutes after each test match Glasstones description of rainout. This isfrom 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 collapsingstem of the nuclear cloud i.e. highly irradiated material which would include largeamounts of Tritiated water. The black rain described by eyewitnesses and which wasalso described at Hiroshima, may be uranium nanoparticles and micron diameter particlessuspended in water and forming condensation nuclei.

    6. These factors may help to explain eyewitness reports and provide a basis for requestingand 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 andusing sophisticated air modelling shows that the assertions of the MoD and AWRE thatservicemen were protected from fallout because the winds were offshore are largelyuntrue.

    7. Finally, no records of any Tritium measurements are available, and it is possible thatthis isotope was entirely overlooked. Nevertheless, it remains a serious hazard since itwill have contaminated food, fish and water on the island and is also inhaled. As a low

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

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

    3.1 TritiumThe 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 energyper unit mass of tissue, the absorbed doses from a Tritium decay (beta energy0.0186MeV) is about 35 times smaller than the decay energy of Caesium-137. But all thismeans is that dose for dose, there are 35 times more ionisation tracks from Tritiumdecays than from Cs-137. These tracks are more highly ionising, that is, their ionisationdensity is greater. Furthermore, Tritium freely exchanges with water and with proteinsand DNA base hydrogens, and a decay in the DNA is a decay into the target for radiationinduced mutation. There are many theoretical arguments that Tritium is anunacknowledged hazard for this reason, and indeed there are studies which show

    remarkable genetic and developmental effects from Tritium exposures at very lowconventional doses, less than natural background (e.g. Jha et al 2006). However, for thepurposes of my current arguments it is sufficient to point out that Tritium as Tritiatedwater HTO will have been major component of the fallout rain and will havecontaminated the water supply on Christmas Island besides contaminating the sea and thelagoons. It will thus constitute an inhalation and absorption hazard. The measurement ofTritium cannot be carried out using conventional radiation measuring equipment and theisotope will not show up on any film badge. It is an internal emitter and the questionsraised about its hazard were discussed in the CERRIE committee and by the ECRR whichgave 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 childleukaemia clusters. If this is so, then the error in the conventional assessment of thisisotope is of the order of 10,000. Whatever its weighting or danger, there is no doubt thatit is produced in prodigious quantities in the thermonuclear explosions on Christmasisland. Miskel (1973) reports that the production of 1Mt of energy by fission produces700Ci of Tritium but that fusion thermonuclear explosions produce about 20MCi (7.4 x10

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

    will have created about 5.1E18 Bq or 5.1 x 1018 Bq of Tritium, much of which wouldhave rained out on the island. To put this in perspective, the entire Chernobyl accidentyield in terms of activity is less: only 2.4 x 10

    18Bq. There is no doubt that the Tritium

    yields from the atmospheric tests were enormous. NCRP 1987 states that the naturalTritium levels in the entire world increased by a factor of 200 due to the tests. Tritium hasa half life of 12 years and so will have remained on the island in the water to exposeanyone who was stationed there whether there was a test or not. It will have contaminatedthe sea and lagoons where the servicemen bathed and the fish that they ate. None of theradiological measuring systems in place, neither film badges nor portable scintillation ofGeiger counters will have detected it.

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    3.2 Carbon-14

    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 fornatural carbon-12. The exposures will have been principally initially to radioactive CO2and then to food which contained C-14. The yield is 1.3PBq per Mt (Eisenbud and Gesell1997) so the Christmas Island yield is about 8.8PBq. Like Tritium, C-14 is a low energyBeta emitter and will not be detected by any of the Geiger or scintillation equipmentemployed at the island, nor will either of these nuclides give any indication on a filmbadge.

    3.3 Drinking water, eating food, swimming in the sea

    The veterans who were stationed on Christmas Island could have received enormousdoses 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 thesenuclides were produced in prodigious quantities in the tests, to measure them or ensurethat the water and food were free of them. Swimming in the sea or in lagoonscontaminated with Tritiated water will cause severe radiation exposures of the skin (dueto absorption by the skin of the Tritium contaminated seawater) and epithelial surfaces ofthe nasophanyx. Many veterans have described rashes and unusual boils which had to belanced. Many have described suffering from nosebleeds. I have drawn attention in themain report to the exposures to Uranium and alpha emitters like Plutonium. These twoweak beta emitters, because of their association with living systems, should also beconsidered 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 veteranscase are not as exhaustive as they would be if I were to have considered them separatelyas I have in the past for the separate tribunals. I will reproduce the table I used in theearlier report to give the level of probability I associate with each of the followingindividuals.

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

    Probability

    level

    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

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    0 Possible Heart disease, atherosclerosis, check age onset

    - Aging related Various conditions, check age onset

    -- Unlikely Various conditions

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

    Ref Name Condition Prob Notes

    ZY055568D Simons DiabetesAtherosclerosisOsteoarthritisSpondylosisSleep ApnoeaGoutIncontinence

    -O-------

    These are age related conditions.Most were increased in theChernobyl and Hiroshimaexposed relative to controls (seetext) The sleep apnoea andincontinence are secondary to theother conditions

    ZS 230667B Smith. d Cancer ofpancreas

    +++ (ICD 157) Accepted byNIOSH-IREP as radiation related

    ZS765640B Sinfield. d Non Hodgkinlymphoma

    +++

    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) Gout Atherosclerosis Sleep Apnoeia Urinary incontinence.

    He was a Royal Engineer stationed at Maralinga from Feb 1964 to March 1965 and willhave been exposed in the forward (controlled) area (231) to residual radioactive materialby 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 toconsider, mainly because these are age-related conditions, and so I will devote somespace to it. Mr Simons developed these conditions in his early 60s but then so do manymen who never attended any test site. The assessment of contributory causation shouldtake into consideration the background rate of the conditions being considered but shouldnot rule out contributory causation since rates of ageing and onset of disease processesare genetically determined: some people age at different rates from others in the absenceof any stress, and indeed there may be lifestyle stresses to include in any assessment. In

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    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 numberof studies of those exposed to radiation, and heart diseased is now recognised to beassociated with radiation prior radiation exposures. The MoD concede this (240). Iconsidered this matter in my 1995 bookWings of Death where I pointed out that the

    atherosclerotic plaques were monoclonal mosaics and thus benign tumours, that theywere produced in animals by exposure to carcinogens; I also analysed in that book thecohort effects of the increases in heart disease in England following the weapons testexposures 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 resultsfrom Chernobyl and Hiroshima survivors have shown strong evidence that ischaemicheart disease and atherosclerosis are associated with exposure to radiation, particularlythe 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 Chernobyleffects ( Burlakova, 1996, Busby and Yablokov 2006, 2009, Yablokov et al 2009. Sincethe 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 ofdifference contamination level in the Chernobyl affected territories. These results areparticularly relevant to Mr Simons.

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

    Disease Novozybkov

    N=3892

    Vyshkov

    N= 1074

    Russia

    control

    Ukraine

    Mean Cs-137 Ci/sq.km 18 30

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    2009, p 62) relative to the national population.

    Table 3.2 Non cancer illnesses per 100,000 adults of three contaminated and 5 controlregions of the Brest region in Belarus in 1990 (from Malko 1990 cited in ECRR2003,2010)

    Diseases 3 contaminated

    districts

    5 control

    districts

    p-value

    Altogether 62,023 48,479

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    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 congenitalmalformation and a grandchild also with congenital disease (225) and in my opinion thisin itself is evidence that he has been affected by the exposures at Maralinga. I amhowever somewhat cautious about ascribing Mr Simons somatic problems entirely to his

    exposures. Nevertheless, I have no doubt that his exposures will have had some finitecontribution to his spectrum of conditions, and indeed the particular spectrum is onewhich is seen in the two irradiated populations I have considered. The interesting aspectof this case is that it indicates clearly that a concentration on cancer and leukaemia as endpoints (as is the case with the various NRPB studies of the veterans) may have lost anumber of individuals who died of other causes. This is seen clearly in the many studiesof internal Radium and Thorotrast exposures where the cancer yield is not a truerepresentation of the effects of these internal irradiations since many individuals died ofother causes, and you cannot die of cancer if you have already died of a heart attack. Iwill be addressing these Radium/Thorotrast studies elsewhere. The tribunal will have tomake 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 to11/1960. 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 sufferingfrom ischaemic heart disease for 5 years. He has since died and the case is being carriedon by his widow, Anna Smith. The AWE report is the common one for Christmas Islandservicemen. AWE contend that Mr Smith was not exposed to radiation at ChristmasIsland (207) and indeed that there was no residual radioactivity there. This is wrong and Ihave 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 theresults of the A-Bomb studies on the basis that the exposures of the controls to residualradiation was overlooked. This is a point I raised in my 1995 bookWings 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 yearold 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 atChristmas Island as his is a standard case described in the earlier report and his illness isa radiation induced disease. I have already in the earlier report written about another caseof pancreatic cancer in a veteran, that of the late Alun Williams, also a Christmas IslandRAF veteran, also dead. These two cases on their own might suggest that there was acausal link with their earlier history.

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    3.3 Herbert George Sinfield

    Sinfield was born 11/1938 and served as a driver in the army (RASC) at Christmas Islandfrom 06/1958 to 06/1959 during the four Z Grapple tests (47). He was diagnosed withNon 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 appealwas lodged 05/2007. Large cell or large T-cell lymphoma is a rare sub class of NHL andso 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 certainmalignant cell expansions within the lymphatic system, and which are distinct fromHodgkins Disease, which is a proliferation of a specific type of cell that can be detectedby microscopic analysis. The non-Hodgkin lymphomas are essentially cancers of theimmune 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 ofB or T-cells that is the main basis of NHL. B-lymphomas are more common, accountingfor 85% of all cases, compared with 15% of cases from the T-cell origin (AmericanCancer Society).

    Normal B-cells produce antibodies that guide the immune responses to harmfulelements e.g. bacteria. T-cells are involved in the recognition of virus-infected or cancercells; in organ transplantation it is the T-cell suppression that is necessary to preventrejection. This immune system suppression, through drugs that kill the T-cells (and theother cells also) results in significant increased risk of NHL in later years. Thus NHLincidence is associated with prior immune suppression, or with substances or exposuresthat cause or contribute to immune system suppression. There has been a significantincrease in the incidence rate of NHL in the last twenty years which has puzzled theinternational scientific community, resulted in considerable epidemiological and otherinvestigation, and led to many suggestions about its cause. What remains is a generalagreement that the origin of this increase is unknown, and that there are many risk factorsfor NHL, one of which has been conceded to be ionising radiation exposure, althoughthere have also been studies suggesting that ionising radiation is not a major cause.Nevertheless, NHL has been designated as a specified cancer under the EnergyEmployees Occupational Illness Compensation Plan and is included in the NIOSH-IREPcausality system for ionising radiation exposures. My own belief is that the increase, likethe increases in most cancer rates unaffected by changes in lifestyle (e.g. smoking) is dueto the feed through of the global weapons fallout exposures, a position which I staked outin 1994 (Busby 1994) and in Wings of Death (Busby 1995).

    Causes of non-Hodgkin lymphoma

    Since the condition begins, like all cancers and leukemias, with a fixed genetic mutationor collection of mutations in a single cell, it is clear that any agent which confers anincreased risk of mutation must be a risk factor for the disease. Bende et al (2007) discussmolecular pathways in the development of B-cell lymphoma and conclude that the

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    initiating event for more than 90% of cases of the most common form is a mutation (achromosome translocation) which leads to expression of an anti-apoptotic protein BCL-2.Ionising radiation is the largest single class of mutagen, and therefore exposure toionising radiation must contribute excess risk. In children, the association with leukaemiaand 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 alsofound near other nuclear sites which release uranium and other radioactivity e.g. theAtomic Weapons Establishment Aldermaston (Beral et al 1990). Nevertheless, theliterature is confusing on this issue especially with regard to the disease in adults. BEIRV (p329) cite Anderson and Ishida 1964 who found an increased incidence of NHL in theJapanese A-Bomb Lifespan Study (LSS) cohort although later studies by Shimizu et al1987 (now the RERF group) no longer showed an excess of the disease. I interpret this asa time lag problem with exposure and controls in the Hiroshima LSS cohorts. The lagperiod for these cancers (lymphomas and leukemias) is believed to be shorter than for thesolid tumours (BEIRV 1990) and so these findings are in agreement with the earlierincreases 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 implicitconclusions of the BEIRV committee are misleading and perhaps disingenuous. BEIRVdo, however, draw attention to significant excess mortality rates of NHL in patientstreated 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 ionisingradiation for benign gynaecological disorders. More recently Inskip et al, 1992 havereported that NHL risk was notelevated in a study of women treated for benign disorders.On the other hand, excess risk was found in women treated with radiation for cervicalcancer, RR = 2.5 (90% CI 0.8, 7.6) (Boice et al. 1988). BEIRV, 1990 also draw attentionto increased mortality (RR = 2.73) from lymphosarcoma (strictly, lymphoma) in USradiologists who entered practice in the 1920s to 1930s , though apparently this excessrisk does not exist in more recent radiologist cohorts.

    Studies of radon exposure and NHL have given various results. The analysis ofnon-lung cancer mortality in miners by Darby et al 1995 did not identify excess risk fromlymphoma, 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 fromlymphoma. A discussion in BEIR VI focuses on epidemiology and the biologicalarguments of Henshaw et al 1990 that the fat solubility of radon will result in increasedexposure 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 bycountry. I have spoken with Denis Henshaw about this issue and he is sure that radondoses to the bone marrow are significant. Chromosome aberration analysis byBauchinger et al (1994) of the peripheral lymphocytes of people living in houses wherethe radon levels were higher than 50Bq m-3 did in fact show significant 3-fold excesschromosome damage even at these low exposures, thus supporting Henshaws arguments.Despite various criticisms, the weight of evidence reported in BEIR VI does seem tosupport an association between radon exposure and NHL. Supporting the causal link, inthe USA, an ecological study by Cohen (1993) using radon concentrations and cancers in1600 counties also found association between radon and NHL. BEIR VI cites a numberof studies which do not, however, find any association with radon exposure and conclude,

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

    Karunanayake et al64

    found a significant increased risk of NHL with exposure to ionizingradiation (radium) in a case-control study of Canadian men diagnosed with NHL between1991 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 NewZealand 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 childhoodNHL and identify a range of exposures including magnetic fields, pesticides, benzene,maternal alcohol consumption, contaminated drinking water, infections and high birthweight. For NHL they highlight ionising radiation, pesticides andin utero exposure tocigarette smoke, benzene and nitrogen dioxide. Gurney and Cartwright 2002 studiedNHL in England and Wales from 1986-1993 confirming the real increases in the disease,proportionally greater for middle aged men; they suggested that environmental factorssuch as sunlight may be responsible. Sunlight was also suggested as a factor by Bentham(1996) who made geographical analyses across areas with different ultraviolet lightindices. 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 thedisease in people who have been treated with immune suppression drugs for bonemarrow or organ transplants and those with inherited immunodeficiencies, has beenreported to be as high as 30% (Filipovich et al 1992). This is also true of those who haveHIV/AIDS related immunodeficiency who have high rates of NHL, as do those who havebeen treated with radiation or chemotherapy for an earlier cancer. Patients treated withchemotherapy or radiation for Hodgkins disease have a 5% excess risk of developingNHL over a ten year period.

    Linos et al 1991 found elevated risks of NHL in those living near industrialfacilities in Iowa and Minnesota particularly associated with residing near stone, clay orglass industry facilities. Scherr et al (1992) examined occupational risk using a casecontrol study and concluded that excess risks for NHL was associated with working inagriculture, forestry and fishing (RR = 3.0), the construction industry (RR = 2.1), and theleather 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 andfound a significant association with residence near copper smelters and sulphite papermills. Others have found associations with organic solvents (Rego et al 2002) although ameta-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 Barrvirus also represents a significant causal association but whether the infection is a resultof (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 resultof many different environmental factors each of low risk acting on large segments of thepopulation, and this seems plausible. However, the largest single exposure elementaffecting the immune system has been to ionising radiation, from the weapons test falloutcomponents in the food chain which peaked in the environment in the late 1960s early

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    1970s, and which were supplemented in the USA by releases from the many nuclear sitesand by the large amounts of technologically enhanced natural materials (TENORM)increasingly released to the environment with industrial expansion, particularly in theUSA where the increase in NHL has been greatest. Occupations which have beenparticularly associated with NHL are those where there is significant exposure to dusts

    and respirable particles e.g farmers, carpenters, stonemasons. The association withfarming 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 assaulton the lymphatic system by inhaled particulate matter, and the suppression of the immunesystem, 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 ofradioactive particulates, though ingestion of radioactive materials including alphaemitters, 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 treatedhim (43, 44, 63). AWE state as usual that he could not have been exposed; I have dealwith this defence in the earlier report. Sinfield writes (51) that we were gathered at theport area and that the cloud [from the test] hung around for most of the day. On oneoccasion it rained, as I remember wearing a poncho. The NOAA plots shown forGrapple Z tests that for some of them the cloud passed over the port. In addition,Sinfields work will have placed him in contact with dust, and resuspended material sincehe delivered material to the South East corner of the island in connection with theextension of roads to that area.

    4. Conclusions

    In my continued examination of the circumstances of illness in veterans of ChristmasIsland Tests and in reviewing everything I have discovered, I cannot fail to be concernedabout the arguments advanced by AWE in this case. Many of the statements made by theMoD and AWE are clearly incorrect or misleading. The defence states that the naturalbackground radiation on Christmas Island is 30nSv/h leading to an annual dose of0.26mSv and this is very much lower than in the UK where it is 2mSv. But a map in thedefence bundle for one veteran (Butler 432) has scrawled on it in pen background is 29Micro Roentgens per hour. This is 2.5mSv per year and that does not include Radon; theequivalent annual gamma dose in the UK is less than 0.5mSv. AWE states that there is noRadon on Christmas Island (it is the radon dose in the UK that pushes up the figure to2mSv). But the New Zealand 1981 report (McEwen et al, 1981) clearly states that therewas 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 radonon Christmas Island, or at least there are no data. And unfortunately, McEwen et al 1981did not report the gamma dose rates they found, nor the levels of Uranium and Radiumthey measured and reported on. They stated that they werenaturally occurringradionuclides and . . . are not tabulated nor discussed in this report. It is likely that they

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    were present in large amounts and that is why they were not reported since it would havebeen clear that they were from the bomb, contained U-235 in large amounts, and were notnatural. This is what I concluded from the Oldbury 1964 report. This is the principalproblem.

    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 theNOAA calculations made by Busby and Willams 2010 based on historic meteorologicaldata show the plumes travelling over the western part of the island and over where thepersonnel were stationed. After most of the tests, rain reportedly fell on the unprotectedpersonnel, rain which was black and which arguably contained uranium, tritium andcarbon-14.

    AWE do not mention Tritium and C-14; the contemporary reports do not mentionthem. None of the documents mention them. Yet it was known at the time that thesenuclides were created in prodigious quantities.

    Reasons are given for refusing pensions which incorrectly state that a specificcancer 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 beenexposed to significant levels of internal radionuclide exposure which would not havebeen detected by the film badges or survey instruments used at the test sites; fromUranium, Plutonium, Tritium and Carbon-14 and Strontium-90. It is not surprising theyhave suffered health effects; nor is it surprising that their children and grandchildren havea 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 theirexposures 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 furtherinformation which may emerge following the order made to the MoD to release relevantdocuments.

    Chris Busby 11th

    Nov 2010

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