Uranium has the following oxides UO, UO₂, U₄O₉ ,U₃O₈, and UO₃. The normal form is U₃O₈ which is insoluble. Quite how much U₃O₈ is in the environment is, as far as we know, a mystery.

A Parliamentary Question was tabled recently "To ask the Secretary of State for Health what research his department is undertaking or contributing to into the proportions of different forms of uranium oxides resulting from the impact of armour piercing ammunition containing depleted uranium, and associated health effects." (PQ 3793/1998/99)
Answer (about 15th November '99, Yvette Cooper) "The department is not conducting or supporting research into uranium oxides and any possible associated health effects."

At the MEDACT Seminar in London (October 1999) Professor Behar discussed the "Radiological Risks of DU", stating that new experimental evidence is against the hypothesis that "all particles of Uranium smaller than 5micron diameter can become permanently trapped in the lungs." The first research he cited (Henge-Napoli) is of transformation of UO4 by alveolar macrophages. We do not see any relevance in this. UO4 cannot properly be called an oxide - it is a peroxide and is made as a hydrate UO4 2H2O by precipitating a uranyl salt solution with hydrogen peroxide. It is soluble and is a highly reactive oxidising agent. It is entirely unnatural and has nothing to do with the pyrophoric behaviour of Uranium in munitions, as under battlefield conditions (or on the firing range) there is not enough oxygen present in the atmosphere to create it.

Contrary to what Professor Behar suggested, it is not necessary to falsify any hypothesis that all particles of Uranium smaller than 5micron diameter can become permanently trapped in the lungs. It is already known that particles remain in the lungs for considerable periods and that the insoluble oxides are retained longer than soluble forms.

Actinide particles are retained in TBLNs to a far greater extent than in the lung. Below we cite studies which show this. It is also demonstrated by the paper¹ cited by Dr Guthrie at the MEDACT seminar. Proportions of Uranium distributed in various tissues were, for example: Femur 1, Kidney 2, Liver 5, Spleen 32, Lung 580, TBLNs 9064. [NOTE: these are ratios of totalled average values for all monkey tissues analysed throughout the experiment. They are representative of the paper's findings.]

Dr Guthrie said that the study had failed to find evidence of radiation- induced disease. Thus the abstract states:

No evidence of U toxicity was found in body weights or mortality, in the NPN (nonprotein nitrogen) levels of the blood, or in the haematologic picture.

The paper expands on this:

Bimonthly hematologic studies revealed no major change in the peripheral blood picture of dogs and monkeys. Red blood cell counts, hemoglobin values, hematocrit percentages and white blood cell counts were, almost without exception, within normal (control) ranges. Blood NPN levels ... did not vary significantly [from] controls.

The relevance of these relatively crude haematological analyses is questionable. Post mortem, the TBLNs showed gross changes, as might be expected in view of the fact that their Uranium content was up to 14% [by weight, wet tissue]. Other sources of red and white cells would compensate for reductions in the competence of the TBLNs.

TBLN doses in this experiment were very high:
... dose rates ... to lung and TBLNs in all three species exceeded the recommended figure [for maximum permissible organ dose] very early in the experiment.

Some animals died during the experiment. Deaths in the exposed groups were higher:

5% mortality in exposed dogs, vs. none in the controls (5 year study)
8% mortality in exposed monkeys, vs. none in the controls (5 year study)
11% mortality in exposed rats, vs. 3% in the controls (1 year study)
14% mortality in exposed rats, vs. 6% in the controls (second 1 year study)

In view of this imbalance the authors' opinion that None of these deaths could be attributed directly to the inhalation of UO2 dust is questionable. This paper is 30 years old and has been overtaken by techniques capable of detecting subtle genetic changes in human beings as well as in animals.

Other studies cited by Professor Behar are of questionable relevance as far as chronic TBLN doses from insoluble oxides are concerned.

Surprisingly high doses were involved in the in vitro alpha irradiation of alveolar macrophages. This cell killing exercise seems to have nothing to do with in vivo mutation of stem cells which survive irradiation at low dose. The relationship shown between the size of the nucleus and the size of the entire cell suggest that the macrophages were quiescent. Active cells would be far more susceptible to the mutations required to initiate cancers and leukaemias.

The paper he cited⁵ to show a very low DPUI (dose per unit intake) does not specify the target organ. The LUDEP software ("LUDEP" = lung dose evaluation programme) allows the operator to calculate for specific organs or for whole body doses. We do not have LUDEP (the software costs £300), so we cannot check whether the quoted DPUI of 2.84 x 10^-6 Sv/Bq was dose to the lung or to the whole body. It is of no importance; such calculations are irrelevant to local effects, since they depend on the highly dubious and widely attacked concept of absorbed dose and the averaging of local doses as if they affected tissues outside the range of the radiation tracks concerned.

Flawed basis of radiation protection at low dose:
is "Absorbed dose" relevant? [and see "Absorbed dose" on this site]

The official estimation of radiation hazard at low dose depends on studies of the survivors of the Hiroshima and Nagasaki bombs which ('though NRPB says they are "pivotal") have been widely criticised. Briefly, the group considered to be "exposed" consisted of those who were in the open at the time of the explosion, and so received a single large acute external dose of gamma rays. The control group consisted of people who were elsewhere at the time or were shielded. But both groups lived in the bombed cities, and were therefore exposed to ingesting, inhaling and absorbing fallout. The studies are therefore silent on internal radiation and the very different types of exposure involved - chronic, low dose, low dose rate, internal, alpha and beta emitters.

The official model is essentially physics based. As far as the epidemiology is concerned all that has been done is a straight line extrapolation from the exposed group's high dose data points down to the origin. This is supposed to define risks in the low dose region. The extrapolation has been widely criticised: Goodhead calls it⁶ "a large region of uncertainty"; Wright at MRC⁷ questions the relevance of bomb survivors' data; Sternglass⁸, Busby⁹, Gofman¹⁰, and Alice Stewart¹¹ all attack it on various grounds. Early reports of cancer incidence at Hiroshima were seriously out of line with those later used to set risk factors¹². Other studies which are supposed to inform on risk are mostly of external x-rays. A couple of small internal studies are included, but these are of natural isotopes. They do not include Uranium, and certainly do not include the uniquely anthropogenic exposure involved in making munitions which produce ceramic oxides.

The literature contains a good number of studies which purport to show no correlation between disease and radiation dose, but which do show an effect in populations exposed to radioactive fallout from weapons tests and Chernobyl, and in nuclear workers monitored for internal contamination and in their children. Detailed information can be seen on this website

Recent issues of the European Radiation Protection Research newsletter have carried a discussion on the validity of absorbed dose as a quantifier for the biological effects of ionising radiations. The low dose region is especially dubious:

Arguments against [the validity of absorbed dose] ... have been broached since the early 1970s ... Simulation models intended to describe the mechanisms of radiation damage occur literally by the dozens yet still we have not agreed on how best to predict the actual biological effectiveness of a known radiation field with tolerable accuracy without resorting to empirical techniques even for the simplest of mammalian cells¹³
... scepticism can be observed in our forums and journals regarding its suitability and its meaning for the quantitative assessment of biological effects¹⁴

The phenomenon of radiation induced genomic instability¹⁵ is relevant to internal contamination with Uranium as it is known that it can be induced by single tracks of alpha radiation, causing changes to appear in cells many generations removed from the irradiation. The effect known to researchers as "Bystander killing", whereby genomic instability and cell death are found in unirradiated cells in the same colony as irradiated cells, raises yet more questions.

Recent work by Miller et al¹⁶. shows that two alpha tracks are more likely to cause mutation than single tracks. The Second Event Theory of Dr Chris Busby demonstrates that certain sequentially decaying isotopes such as Strontium-90 have a greatly enhanced risk of causing genetic damage, compared with external radiation.

The Second Event Theory: a brief summary and a new development

The Second Event Theory was reviewed by Dr Douglas Holdstock for MEDACT in 1996. He wrote: The two-event hypothesis is of potential importance. Other reviews can be seen on this site. MEDACT and LLRC organised a Symposium on this topic in the House of Commons in April 1996, the Proceedings of which are published.¹⁷

The theory predicts that where body tissue incorporates a localised source of multiple radiation tracks any given dose of energy transfer carries an enhanced probability of damage, (i.e. enhanced relative to the conventional yardstick of natural background) as the tracks will have a higher likelihood of affecting the same microscopic target more than once. More particularly, the first track may sublethally damage a cell and thus induce it to begin repairing itself; a subsequent track (the "second event") has a high chance of damaging the cell again at a critical phase of the repair process, thus increasing the chance that a mutation will be transmitted to the cell's daughters and all its descendants. Dr Ryle outlined this idea at the MEDACT seminar.

Sources of second event hazards are thought to be a) single atoms of isotopes which have sequential decay pathways (e.g. Strontium-90 and Tellurium-132) and b) insoluble hot particles containing many millions of atoms, particularly of alpha emitting isotopes like Plutonium (e.g. from bombs and reprocessing, and Uranium, e.g. from armour-piercing weapons).

For several years the theory was excluded from publication in the scientific literature on demonstrably erroneous grounds.¹⁸ This allowed the establishment to dismiss it in the same way as Professor Richard Lacey's warnings on BSE were at first dismissed. However, the high profile of the theory and its inherent simplicity and plausibility have forced the National Radiological Protection Board to address it, and Drs. Edwards and Cox of NRPB have now submitted their own version of Busby's calculations to the International Journal of Radiation Biology. It is published¹⁹, and it shows that from an initial position of denying that the theory had any validity at all, Dr Cox now admits that the effect does exist and that for the example of Strontium-90 the hazard is greater than from Natural Background Radiation. Dr Busby's reply^19a is also published; while not accepting NRPB's calculations, he points out that there are other sources of local dose which present even greater hazard than Sr-90. The debate has shifted to disagreement only about the degree of additional hazard from the man-made isotopes and anthropogenic Uranium.

Table of doses to sphere of tissue 30 micron radius
by single particles of U₃O₈ of various diameters

Particle diameter microns	Particle volume cm3	Mass U308(g)	Mass U238(g)	Activity of particle (Bq)	Hits /day(dose mSv)	Hits/year(annual dose mSv)
0.2	4.2 x 10-15	3.6 x 10-14	3.06 x 10-14	3.8 x 10-10	3.3 x 10-5 (3.96 x 10-3mSv)	0.012 (1.44mSv)
0.5	6.5 x 10-14	5.6 x 10-13	4.8 x 10-13	5.9 x 10-9	5.1 x 10-4 (0.06mSv)	0.186 (21.9mSv)
1	5.2 x 10-13	4.3 x 10-12	3.7 x 10-12	8.8 x 10-8	7.6 x 10-3 (0.91mSv)	2.77 (332mSv)
2	4 x 10-12	3.5 x 10-11	2.9 x 10-11	3.6 x 10-7	0.031 (3.72mSv)	11.32 (1358mSv)
5	6.5 x 10-11	5.6 x 10-10	4.75 x 10-10	5.9 x 10-6	0.51 (60mSv)	186 (21900mSv)

The table shows that for particles as small as 0.2 microns diameter, average annual alpha dose to the lymphatic tissue surrounding the particles is about the same as the total average natural background dose of 2mSv. (It is, of course, additional to NBR) For larger particles the local dose rapidly increases.

Particle sizes from 0.1 to 5 microns are frequent in the environment. The dangerous size range for genetic mutation is between 0.5 and 5 microns since "Second Event" processes will occur for particles of this size.

Officially accepted estimates of exposure and doses from incorporated actinides.

This field seems to have been the subject of a cover-up, especially as far as TBLNs are concerned.

The COMARE 4th Report 1996 on the undisputed Seascale leukaemia cluster acknowledges that the lymphatic system is a critical organ in leukaemogenesis, but cites NRPB paper R276 to show that the dose from Sellafield is too low to account for the excess. However, R276 models the human lymph system as the sum of virtually every internal organ - a large volume of tissue into which to dilute the radiation dose which is actually being delivered within the lymph nodes. COMARE has recently told us that they were misinformed about this reference; the correct reference is COMARE 95/40: Thoracic Lymph Doses due to Sellafield Discharges and Natural Background Radiation by J. R. Simmonds et al. This has not been published nor even internally reviewed, but we have obtained a copy. It is based not on measurement but on questionable assumptions which include extrapolating doses to people aged 2 - 25 from the lung capacity and air intake of a baby from birth to 1 year of age, although the capacity and intake of the older people are far greater. Even so, Simmonds et al found that inhaled Plutonium in the worst year (1955) conferred on the TBLNs of its model infant a dose seven times "natural" background. This 7-fold risk should have been increased by doses from additional Plutonium inhaled in subsequent years, while the dose from "natural" sources was inflated by the inclusion of Uranium (the substantial amounts of U emanating from Sellafield are not a natural exposure). We are discussing these anomalies with NRPB’s Director of Dose Assessments and will publish a further report.

The UK Government relies on COMARE 4 to this day (see Answer to Parliamentary Question 37911/1998/1999)

Speculation based on inhalation and injection experiments using human volunteers, such as have received widespread press coverage this year20, should be regarded with caution. These experiments exclusively use Nitrates and Citrates of Plutonium which are soluble. It is known that Plutonium concentrates in human Tracheobronchial lymph nodes²¹,²². This is typically the behaviour of insoluble particles.

A recent paper²³ suggests that urinalysis makes estimating the systemic plutonium burden problematic. It also states that insoluble particles not exhaled or removed by clearance processes will become trapped in the lungs or will be ingested by macrophages, eventually passing to the respiratory lymph nodes. Likewise, those entering via a wound will either become isolated in fibrotic material or, again, be moved by macrophages to the local lymph nodes. Insoluble plutonium can remain in the lymph nodes for many years.

Similarly, studies of Uranium in rat lungs²⁴,²⁵,²⁶ conducted to inform radiation protection agencies about risks to occupationally exposed workers show that insoluble forms (especially U₃O₈) are poorly transportable to blood and are retained in the lung to a far greater extent than soluble forms. They acknowledge that Uranium accumulates in the lymph nodes.

Plutonium has recently been shown to have far higher effects than would be expected on the basis of the NRPB's primitive physics-based modelling. Lord et al have shown unexpected transgenerational effects in mice²⁷, as well as quantifying the additional hazard from alpha particles from Plutonium²⁸ ascribing to them a Relative Biological Effectiveness factor 240 times that of gamma rays. Busby et al have shown²⁹ that there was a clearly defined increase in the incidence of infant leukaemia after Chernobyl (i.e. in an age group for whom there are very few confounding factors) which coincided with an increase in environmental levels of Plutonium in grassland³⁰ and the Irish Sea³¹. The sharp peak in infant leukaemia at that time was observed also in Greece³² and the USA³³. It has been proposed³⁵,³⁶ that the known Actinide pollution in the neighbourhood of the AWEs³⁴ is at least a contributory factor in the observed high mortality from childhood leukaemia in the area.

Vietnam

Dr Guthrie suggested that DU was used in Vietnam with none of the spectrum of symptoms now associated with its use in Iraq. It was used, he said, in the form of flechettes. From what we see on the WWWeb these are also known as beehive bombs - essentially anti personnel weapons, a sophisticated kind of nail bomb. The name "beehive" comes from the noise the little arrows (flechettes) make as they fly through the air.

We feel that it is extremely unlikely that flechettes travel nearly as fast as armour piercing rounds, and that the low velocity would decrease the chance of impact creating enough heat to ignite the uranium and create ceramic particles. [It occurs to us, on the intuitive level, that the nick-name "beehive" would not have attached itself to these weapons if they did not have relatively low velocity]. The pulverisation required to help the Uranium burn would also be less likely at low velocity, and another relevant factor would be the fact that flechettes would be used against soft targets, not armour. One of the websites we have seen says that they are useless against armour, though they do damage unarmoured vehicles.

We have initiated inquiries about the velocity of flechettes but have received no replies yet. If the Uranium used in Vietnam did not burn, then the case is not parallel with later use in Iraq and Kosova. This issue remains unresolved.

Is DU illegal?

Dr Guthrie made much of alleged confusion over the legality of weapons of mass destruction and weapons whose effects are indiscriminate. We are not sure that we have quite understood his point but the UN CONVENTION ON PROHIBITIONS OR RESTRICTIONS ON THE USE OF CERTAIN CONVENTIONAL WEAPONS WHICH MAY BE DEEMED TO BE EXCESSIVELY INJURIOUS OR TO HAVE INDISCRIMINATE EFFECTS AND PROTOCOLS (1980) appears relevant, and makes clear that a weapon does not have to be a weapon of mass destruction to contravene the Convention. The Convention is based on the principle of international law that the right of the parties to an armed conflict to choose methods or means of warfare is not unlimited, and on the principle that prohibits the employment in armed conflicts of weapons, projectiles and material and methods of warfare of a nature to cause superfluous injury or unnecessary suffering, and that it is prohibited to employ methods or means of warfare which are intended, or may be expected, to cause widespread, long-term and severe damage to the natural environment [our emphases].

Under Article 3 the indiscriminate use of weapons to which this Article applies is prohibited. Indiscriminate use is any placement of such weapons: (a) ... (b) ... (c) which may be expected to cause incidental loss of civilian life, injury to civilians, damage to civilian objects, or a combination thereof, which would be excessive in relation to the concrete and direct military advantage anticipated.

The fact that ceramic particles of Uranium in the range 0.1 micron - 10 micron can be transported very large distances in air means that there is a route by which large numbers of civilians are exposed.

We suggest that if research identifies specific mechanisms of health detriment from such particles, this would establish Uranium as contrary to the Convention. It is worth repeating here that the UK Government "is not conducting or supporting research into uranium oxides and any possible associated health effects" (recent answer to PQ 7393/1998/99 see above).

Conclusions and research proposals

We feel that the DU exposure of a large number of people from NATO nations provides an opportunity to remedy at least part of the weakness of the official model of radiation hazard outlined above. The infrastructure available would make the results of study far more reliable than studies of people in the war zones. Failure to conduct such research is irresponsible - a wasted opportunity which mocks the suffering of the victims.

The MoD's failure even to attempt to find out whether Gulf War veterans are carrying Uranium contamination is unacceptable. The situation is reminiscent of the long delay in establishing ABCC (the Atomic Bomb Casualty Commission) in Japan after WW2 - a 5 year delay during which information about many of the victims was lost, as they had died in the interim. We draw attention to recent press revelations37 about the inadequacy of MAP (the Medical Assessment Programme) -- i.e. that it lacked the means to detect Uranium even in the few men in whom they did look for it. We had been told about this inadequacy long before the Daily Express reported it. Seen in this light, Professor Lee's failure to attend the MEDACT seminar is a serious matter.

1.    We propose that MoD should immediately establish a lifetime follow-up study of the health of Gulf War veterans and their children conceived after 1991, controlled against servicemen who did not serve in the Gulf. The history of the ABCC, which was dominated and controlled by the American military, indicates that it would be wise for the study to be subject to independent scrutiny. MEDACT might consider adopting such a role.

2.    MAP should establish the body burdens of both soluble and insoluble forms of Uranium in all surviving veterans. It should seek to obtain post mortem tissues which should be analysed and archived. Analysis results should be fed into the lifetime study.

3.    MAP should use genetic fingerprinting techniques to identify mutations, especially those of the haematopoetic system.

4.    NATO should be urged to reveal the sites where Uranium munitions were used in Kosova; MAP should be extended to UK nationals who have worked in the places so revealed.

5.    The WHO / UN should be urged to monitor the environment in and near combat zones for DU and to set up a programme similar to MAP for civilians where DU is detected. [This should be done as a matter of urgency, despite the 1959 agreement³⁸ between WHO and the International Atomic Energy Agency which gives IAEA a right of veto over research on nuclear issues]

6.    COMARE's 4th Report should be reconsidered in the light of the complete inadequacy of the Simmonds et al. calculation of TBLN doses.

We are still looking into the question of the solubility of Uranium in body fluids and the consequent translocation to tissues other than lung and TBLN.

We have confined our attention to the TBLN issue and to evidence that it is greatly underestimated. We do not mean to suggest that this is the only radiological mechanism of concern, nor that one can rule out other factors such as vaccines, pesticides, chemical and biological weapons, and natural hazards. The possibility of synergistic interactions must also be considered.

We agree with Professor Behar's recommendation that sanctions against Iraq should be lifted. We do not agree that ending sanctions is an alternative to open minded research on the health effects of Uranium munitions.

Further observations

---

References

1 Leach LJ Elliott AM et al A five year inhalation study with natural uranium dioxide dust. 1: retention and biological effect in the monkey dog and rat. Health Physics 1970 18 599-612

2 e.g. Dubrova, Y. E. Nesterov, V. N. Jeffreys, A. J. et al. 1996 Human minisatellite mutation rate after the Chernobyl accident. Nature 380 no. 6576 25 April 1996
and Dubrova, Y. E. Nesterov, V. N. Jeffreys, A. J. 1997 Further evidence for elevated human minisatellite mutation rate in Belarus eight years after the Chernobyl accident. Mutation Research 381 pp 267 - 278 (1997)

3 for example Ellegren, H. Moller, A. P. et al. Fitness loss and germline mutations in barn swallows breeding in Chernobyl.Nature 389, 9th Sept. 1997 593 - 6

4 Lizon C, Bailey L, Le Foll L, Jouanny F, Poncy J-L, Fritsch P, Mesure de la survie des macrophages alveolaires aprés irradiation alpha pour l'evaluation de la toxicité des oxydes d'actinides inhalés Radioprotection 1997 5, 637-644.

5 Ansoborlo E, Chazel V, Houpert P, Hengé-Napoli M H, Paquet F, Interprétation des données physico-chimiqes et biocinétiques pour le calcul de dose: exemple d'un composé industriel UO2 appauvri fabriqué pour le combustible MOX Radioprotection 1997 32 no. 5 603-615

6 "The Health Effects of Low Level Radiation: Proceedings of a Symposium held at the House of Commons, London 24th April 1996" R. Bramhall (Ed): Green Audit ISBN 1 897761 14 7 page 45

7 Radiation Roulette: New Scientist 11th October 1997

8 Sternglass 1981 "Secret Fallout" New York, McGraw Hill

9 Busby C. C. 1995, Wings of Death Green Audit ISBN 1-897761-03-1

10 Gofman, J 1990 Radiation induced cancer from low dose exposure: an independent analysis, San Francisco, Committee for Nuclear Responsibility.

11 Stewart, A. M. 1982 Delayed effects of A-bomb radiation: a review of recent mortality rates and risk estimates for five-year survivors. J. Epidemiology and Community Health 26/2: 80-6

12 ICRP 1965 The Evaluation of Risks from Radiation. ICRP publication 8, Pergamon Press Oxford 6see Westminster Proceedings op. cit. page 45

13 David E.Watt School of Physics and Astronomy University of St. Andrews, writing in European Radiation Protection Research newsletter issue No. 4 Jan 1999.

14 Pascal Pihet and Hans Menzel, writing in European Radiation Protection Research newsletter issue No 3, July 1998. Further correspondence on this topic.

15 subject of several current projects; see e.g. European Radiation Protection Research newsletter no. 3 July 1998.

16 Miller R.C, Randers-Pehrson G, Geard C. R, Hall E. J, Brenner D. J, 1999: The oncogenic transforming potential of the passage of single alpha particles through mammalian cell nuclei" Proceedings of National Academy of Sciences USA 96, 19-22 1999

17 see Westminster Proceedings op. cit.

18 see "Wings of Death: Nuclear Pollution and Human Health" Chris Busby Green Audit, Aberystwyth 1995 ISBN: 1-897761-03-1 pp. 200 et seq.and p. 317

19 see IJRB January 2000 issue

19a see Busby in IJRB January 2000 issue

20 e.g. "Plutonium harmless" say Scientists who inhaled it: Guardian 9th Aug '99 and many other newspapers.

21 for example Popplewell DS Ham GJ Johnson TE Barry SF 1985 "Plutonium in autopsy tissue in Great Britain" Health Physics 49 304 shows TBLN concentrations up to 40 times higher than in the lung itself. NOTE: versions of this work published later had the TBLN data cut out.

22 McKinroy, J. F. Kathren, R.L. Voelz, G.L. Swint, M. J. 1991 U. S Transuranium Registry Report on the 239 Pu distribution in a human body Health Physics, Vol. 60 No. 3 307-333 March 1991 almost exactly reproduces Popplewell's 40:1 ratio of TBLN to lung

23 Chromosome Aberrations in Radiation Workers with Internal Deposits of Plutonium, Caroline A Whitehouse et al, Radiation Research 150, pp 459-468 (1998).

24 Stradling G N, Stather J W, Ellender M, Sumner S A, Moody J C, Towndrow C G, Hodgson A, Sedgwick D, Cooke N; Metabolism of an Industrial Uranium Trioxide Dust after Deposition in the Rat Lung Human Toxicol. (1985) 4, 563-572

25 Stradling G N, Stather J W, Gray S A, Moody J C, Ellender M, Hodgson A, Cooke N; The Metabolism of Ceramic and Non-ceramic Forms of Uranium Dioxide after Deposition in the Rat Lung Human Toxicol. (1988) 7, 133-139

26 Stradling G N, Stather J W, Gray S A, Moody J C, Ellender M et al; Metabolism of Uranium in the Rat after Inhalation of Two Industrial Forms of Ore Concentrate: the Implications for Occupational Exposure Human Toxicol. (1987) 6, 385-393

27 Lord B I, Woolford LB, Wang L, Stones V A, McDonald D, Lorrimore S A, Papworth D, Wright E G, Scorr D, 1998 Tumour induction by Methylnitroso Urea following preconceptional paternal contamination with Pu239: Brit, J. Cancer MSS. 974914 (since published)

28 Lord B I, Jiang T N, Hendry J H, 1994 Alpha particles are extremely damaging to developing haemopoesis compared with gamma irradiation. Radiation Research 137 380-384

29 Busby, C. Scott Cato, M. 1998 Increases in Leukaemia in Infants in Wales and Scotland Following Chernobyl: Evidence for Errors in Statutory Risk Estimates. Green Audit Aberystwyth Occasional Papers No 98/2; June 1998

30 Survey of radioactivity 1984 - 1986, Welsh Office Cardiff March 1988

31 Kershaw P J, Denoon D C, Woodhead D S, Observations on redistribution of Plutonium and Americium in Irish Sea sediments 1978 - 1996: Concentrations and Inventory J. of Environmental Radioactivity 44 191-221 1991

32 Petridou, E. Trichopoulos, D. . Dessypris, N. et al. (1996) 'Infant leukemia after in utero exposure to radiation from Chernobyl,' Nature, 382: 352-353.

33 J.Mangano(1997) Childhood leukemia in US may have risen due to fallout from Chernobyl' BMJ 314 1200

34 Croudace I, et al An assessment of radioactive contamination in the environment as a result of operations at the AWE sites in Berkshire Report No. 1 August 1999 University of Southampton Oceanography Centre

35 Busby, C. Scott-Cato, M 1997 Death rates from leukaemia are higher than expected in areas around nuclear sites in Berkshire and Oxfordshire: B.M.J 2nd August 1997 p 309

36 Dickinson H. O. et al. Numbers of observed deaths were closer to those expected .. BMJ 315 8th Nov 1997 p 1232 , confirming Busby and Scott-Cato 1997 above. It should be noted that these data are only for mortality, which is not to be confused with the far larger incidence, much of which is cured. The Oxford Cancer Intelligence Unit has refused to release incidence data even when ordered to do so by a Court.

37 "Gulf War veterans: We were betrayed" Daily Express 3rd November 1999

38 Res WHA 12-40, 28.5.59