Gulf War Veterans and Depleted Uranium by By Dr. Rosalie Bertell, Ph.D., G.N.S.H

Gulf War Veterans and Depleted Uranium

Prepared for the

Hague Peace Conference, May 1999
By Dr. Rosalie Bertell, Ph.D., G.N.S.H.

Source of Exposure:

Uranium metal is autopyrophoric and can burn spontaneously at room temperature in the presence of air, oxygen and water. At temperatures of 200-400 degrees Centigrade, uranium powder may self-ignite in atmospheres of carbon dioxide and nitrogen. Oxidation of uranium under certain conditions may generate sufficient energy to cause an explosion (Gindler 1973). Friction caused by bullet or missile entry into a tank or armored car, for example, can cause the uranium to ignite, forming a concentrated ceramic aerosol capable of killing most personnel in the vehicle. Depleted uranium was used extensively in place of tungsten for ordnance by the US and UK in the Gulf War.

There is no dispute of the fact that at least 320 tons of depleted uranium (DU) was "lost" in the Gulf war, and that much of that was converted at high temperature into an aerosol, that is, minute insoluble particles of uranium oxide, UO2 or UO3 , in a mist or fog. It would have been impossible for ground troops to identify this exposure if or when it occurred in war, as this would require specialized detection equipment. However, veterans can identify situations in which they were likely to have been exposed to DU. Civilians working at military bases where live ammunition exercises are conducted may also have been exposed.

Uranium oxide and its aerosol form are insoluble in water. The aerosol resists gravity, and is able to travel tens of kilometres in air. Once on the ground, it can be resuspended when the sand is disturbed by motion or wind. Once breathed in, the very small particles of uranium oxide, those which are 2.5 microns [ one micron = one millionth of a meter ] or less in diameter, could reside in the lungs for years, slowly passing through the lung tissue into the blood. Uranium oxide dust has a biological half life in the lungs of about a year. According to British NRPB [ National Radiation Protection Board ] experiments with rats, the ceramic or aerosol form of uranium oxide takes "twice as long" or about a two year biological half life in the lungs, before passing into the blood stream. [Stradling et al 1988]

Because of coughing and other involuntary mechanisms by which the body keeps large particles out of the lungs, the larger particles are excreted through the gastro-intestinal tract in feces. The uranium compounds which enter the body either through the wall of the gastro-intestinal tract or the lungs, can be broken down in the body fluids, and tetravalent uranium is likely to oxidize to the hexavalent form, followed by the formation of uranyl ions. Uranium generally forms complexes with citrate, bicarbonates or protein in plasma, and it can be stored in bone, lymph, liver, kidney or other tissues. Eventually this uranium which is taken internally is excreted through urine. Presence of depleted uranium in urine seven or eight years after exposure is sufficient evidence to substantiate long term internal contamination and tissue storage of this radioactive substance.

Uranium is both a chemical toxic and radioactive hazard: Soluble uranium is regulated because of its chemical toxicity, measured by damage to the kidney and tubules. Uranium is a heavy metal, known to cause uranium nephritis. Insoluble uranium, such as was released in the Gulf War, is regulated by its radiological properties, and not its chemical properties. Because of its slow absorption through the lungs and long retention in body tissues, its primary damage will be due to its radiological damage to internal organs rather than chemical damage to the renal system. Obviously, both types of damage occur simultaneously, therefore it is a matter of judgment which severe damage, radiological or chemical, occurs at the lowest dose level. However, with the lengthening of the time during which the contaminant resides in the body and the low overall dose, the risk of cancer death becomes greater than the risk of significant damage to the renal system.

Uranium decays into other radioactive chemicals with statistical regularity. Therefore, in its natural and undisturbed state, it always occurs together with a variety of other radioactive chemicals, some of the best known being thorium, radium, polonium and lead.

Natural uranium in soil is about 1 to 3 parts per million, whereas in uranium ore it is about 1,000 times more concentrated, reaching about 0.05 to 0.2 percent of the total weight. Depleted uranium concentrate is almost 100 percent uranium. More than 99 percent of both natural and depleted uranium consists of the isotope U-238. One gram of pure U-238 has a specific activity of 12.4 kBq, which means there are 12,400 atomic transformations every second, each of which releases an energetic alpha particle. Uranium 238 has a half life of 4.51 E+9 (or 4.51 times 10 to the 9thpower, equivalent to 4,510,000,000 years).

Each atomic transformation produces another radioactive chemical: first, uranium 238 produces thorium 234, (which has a half life of 24.1 days), then the thorium 234 decays to protactinium 234 (which has a half life of 6.75 hours), and then protactinium decays to uranium 234 (which has a half life of 2.47E+5 or 247,000 years). The first two decay radioisotopes together with the U 238 count for almost all of the radioactivity in the depleted uranium. Even after an industrial process which separates out the uranium 238 has taken place, it will continue to produce these other radionuclides. Within 3 to 6 months they will all be present in equilibrium balance. Therefore one must consider the array of radionuclides, not just uranium 238, when trying to understand what happened when veterans inhaled depleted uranium in the Gulf War.

It should be noted that uranium 235, the more fissionable fraction which was partially removed in enrichment, makes up only 0.2 to 0.3 percent of the depleted uranium, whereas it was 0.7 percent of natural uranium. It is this deficit which enables one to use analytical methods to identify the uranium found in veteran's urine as depleted and not natural uranium. The U 235 was extracted for use in nuclear weapons and nuclear reactor fuel. Depleted uranium is considered nuclear waste, a by-product of uranium enrichment.

The difference in radioactivity between natural and depleted uranium is that given equal quantities, depleted uranium has about half the radioactivity of the natural mixture of uranium isotopes. However, because of the concentration of the uranium in the depleted uranium waste, depleted uranium is much more radioactive than uranium in its natural state.

Uranium and all of its decay products, with the exception of radon which is a gas, are heavy metals. Unlike some other heavy metals which are needed in trace quantities by the human body, there is no known benefit to having uranium in the body. It is always a contaminant. Ingesting and inhaling some uranium, usually from food, is inescapable however, in the normal Earth environment, and we humans basically take in, on average, 5 Bq per year of uranium 238 in equilibrium with its decay products. This gives an effective radiation dose equivalent to the whole body of 0.005 mSv. Using a quantitative measure, we normally ingest about 0.000436 g a year.[UNSCEAR 1988, 58-59] This is a mixture of soluble and insoluble compounds, absorbed mostly through the gut.

Regulatory limits recommended by the International Commission on Radiological Protection [ICRP] assume that the maximum permissible dose for members of the public will be the one which gives the individual 1 mSv dose per year. This is in addition to the natural exposure dose from uranium in the food web. Assuming that this dose comes entirely from an insoluble inhaled uranium oxide, and using the ICRP dose conversion factor for uranium 238 in equilibrium with its decay products, one can obtain a factor of 0.84 mSv per mg, or a limit of intake of 1.2 mg (0.0012 g) per year for the general public. This would give an added radiation dose of 1.0 mSv from uranium, and an increase of almost 2.75 times the natural uranium intake level. Nuclear workers would be allowed by the ICRP maximum permissible level, to reach an annual dose of 20 mSv, comparable to an intake of 24 mg of uranium, 55 times the normal yearly intake.

The US has not yet conformed to the 1990 international recommendations which were used for this calculation, and it is still permitting the general public to receive five times the above general public amount, and the worker to receive 2.5 times the above occupational amount. The US may have used its domestic "nuclear worker" limits during the Gulf War, if it used any protective regulations at all. The military manual discusses the hazards of depleted uranium as less than other hazardous conditions on an active battle field!

The maximum dose per year from anthropogenic sources can be converted to the maximum concentration permissible in air using the fact that the adult male breathes in about 23 cubic metres of air in a day [ICRP 1977]. The maximum permissible concentration in air for the general public would be: 0.14 microgram per cu metre, and for workers: 2.9 micrograms per cu m assuming the Gulf War situation of continuous occupancy rather than a 40 hour work week, and an 8 hour day. It is common in the US and Canada to refer to 2000 pounds as a "ton", whereas the British "ton" is 2240 pounds. Both are roughly 1000 kg. Just in order to understand the scale of the ceramic uranium released in Desert Storm, at least 300 million grams were "lost", and breathing in only 0.023 g would be equivalent to the maximum permissible inhalation dose for a nuclear worker to receive in a year under the 1990 recommendations of ICRP.

Medical Testing for
Depleted Uranium Contamination:

Potential testing includes:

* chemical analysis of uranium in urine, feces, blood and hair;

* tests of damage to kidneys, including analysis for protein, glucose and non-protein nitrogen in urine;

* radioactivity counting; or

* more invasive tests such as surgical biopsy of lung or bone marrow.

Experience with Gulf War veterans indicates that a 24 hour urine collection analysis shows the most promise of detecting depleted uranium contamination seven or eight years after exposure. However, since this test only measures the amount of depleted uranium which has been circulating in the blood or kidneys within one or two weeks prior to the testing time, rather than testing the true body burden, it cannot be directly used to reconstruct the veteran's dose received during the Gulf War. However, this seems to be the best diagnostic tool at this time, eight years after the exposure.

Feces tests for uranium are used for rapid detection of intake in an emergency situation, and in order to be useful for dose reconstruction, must be undertaken within hours or days of the exposure. Blood and fecal analysis are not advised except immediately after a known large intake of uranium.

Whole body counting for uranium, using the sodium iodide or hyper pure germanium detectors, is designed to detect the isotope uranium 235, the isotope of uranium partially removed from depleted uranium. For lung counting, again it is the uranium 235 which is detected, and the minimum detection limit is about 7.4 Bq or 200 pCi. Since normally humans take in only 5 Bq per year, this is not a very sensitive measure. Seven or eight years after the Gulf War exposure, this method of detection is most likely useless for veterans.

Routine blood counts shortly after exposure, or during a chelating process for decontamination of the body are useful. This is not a search for uranium in blood, but rather a complete blood count with differential. This is done to discover potentially abnormal blood counts, since the stem cells which produce the circulating lymphocytes and erythrocytes are in the bone marrow, near to where uranium is normally stored in the body. The monocyte stem cells in bone marrow are known to be among the most radiosensitive cells. Their depletion can lead to both iron deficient anemia, since they recycle heme from discarded red blood cells, and to depressed cellular immune system, since monocytes activate the lymphocyte immune system after they detect foreign bodies.

Hair tests need to be done very carefully since they tend to reflect the hair products used: shampoos, conditioners, hair coloring or permanent waves. Pubic hair would likely be the best material for analysis. I am not aware of good standards against which to test the Uranium content of hair, or how the analysis would differentiate between the various uranium isotopes.

Testing of lymph nodes or bone on autopsy would be helpful. However, invasive biopsies on live patients carry no benefit for the patient and are usually not recommended because of ethical considerations about experimentation on humans. If a veteran is recommended for bronchoscopy for medical reasons, it would be advisable to also take tissue samples for analysis for depleted uranium.

When chelation processes have been initiated the rate of excretion of uranium in urine will be increased and there is a risk of damage to kidney tubules. Therefore careful urine analysis for protein, glucose and non-protein nitrogen in important. Some researchers have also reported specifically finding B-2-microglobulinuria and aminoaciduria in urine due to uranium damage.

Relating Depleted Uranium Contamination
with Observed Health Effects in Veterans:

There are two ways of documenting the radiological health effects of a veteran's exposure to depleted uranium. The first, and the one usually attempted in a compensation argument, would be to reconstruct the original dose and then appeal to regulatory limits or dose-response estimates available in the scientific literature. This methodology is not recommended for the Gulf War veterans, because the uranium excretion rate seven or eight years after exposure cannot be used to estimate the original lung and body burden of depleted uranium. Moreover, no dose-response estimates for the chronic health effects of such exposure are available from the literature, as will be seen later in this paper. Recognized dose-response estimates for radioactive materials are unique to fatal cancers (and even these are disputed). It is not clear whether regulatory limits for exposure to ionizing radiation apply in a war situation, or, if they do, whether the veteran should be considered to have been "general public" or a "nuclear worker". Beyond this, the question of whether international or US standards should be used for a multinational situation needs to be addressed.

The second methodology would require ranking veterans on an ordinal scale for their original exposure, based on their current excretion rate of depleted uranium. This involves the reasonable assumption that the original contamination, although not precisely measurable, was proportional to the current excretion rate. The analysis of a 24 hour urine sample, for example, could be rated on a specific research scale as having "high", "medium" or "low" quantities of the contaminate. By collecting detailed health and exposure data on each veteran, one can use biostatistical methods to determine firstly, whether any medical problems show an increase with the ordinal scale increase in exposure, determined through urine analysis; and secondly, whether there is a correlation between the descriptive accounts of potential depleted uranium exposure and the assigned ordinal scale determined on the basis of the urine analysis.

Using Non-Parametric Statistics one could determine the statistical significance of various medical problems being depleted uranium exposure related. This would undoubtedly eliminate some medical problems from consideration and highlight others. It could point to future research questions. It could also provide a fair method of dealing with the current suffering of the veterans using the best scientific methodology available at this time. Risk estimates based on radiation related cancer death are obviously unable to provide a reasonable response to current veteran medical problems.

Known Occupational Health Problems
Related to Uranium Exposure:

In Volume 2 of the Encyclopaedia of Occupational Health, under uranium alloys and compounds, page 2238, it reads:

"Uranium poisoning is characterized by generalized health impairment. The element and its compounds produce changes in the kidneys, liver, lungs and cardiovascular, nervous and haemopoietic systems, and cause disorders of protein and carbohydrate metabolism.......

Chronic poisoning results from prolonged exposure to low concentrations of insoluble compounds and presents a clinical picture different from that of acute poisoning. The outstanding signs and symptoms are pulmonary fibrosis, pneumoconiosis, and blood changes with a fall in red blood count; haemoglobin, erythrocyte and reticulocyte levels in the peripheral blood are reduced. Leucopenia may be observed with leucocyte disorders (cytolysis, pyknosis, and hypersegmentosis).

There may be damage to the nervous system. Morphological changes in the lungs, liver, spleen, intestines and other organs and tissues may be found, and it is reported that uranium exposure inhibits reproductive activity and affects uterine and extra-uterine development in experimental animals. Insoluble compounds tend to be retained in tissues and organs for long periods."

Human and Animal Studies on Uranium Exposure:

In a study of uranium toxicity by the US Agency for Toxic Substances and Disease Registry [ATSDR 1998], released for public review and comments by 17 February 1998, exposure times were divided into three categories: acute, less than 15 days; intermediate, 15 to 365 days; and chronic more than a year. Most of the Gulf War Veterans would have had chronic duration exposure from the point of view of the length of time the material remained in the body. However, this ATSDR division was based of the duration of the presence of the external source of contamination, not its residence time in the body, therefore it would, in most cases be considered intermediate duration exposure. There is very little human research available to clarify the effects of intermediate duration exposure to humans.

It should not be assumed that lack of research implies lack of effect on that particular system. It should also be noted that although one or more papers may exist for acute and chronic duration exposures, these do not necessarily cover the questions which one might like to raise. No comments on the quality or extent of the research is implied by this table.

Health Effects which have been
associated with inhalation of uranium:

The more soluble compounds of uranium, namely, uranium hexafluoride, uranyl fluoride, uranium tetrachloride, uranyl nitrate hexahydrate, are likely to be absorbed into the blood from the alveolar pockets in the lungs within days of exposure. Although inhalation products also are transported through coughing and mucocilliary action to the gastro-intestinal tract only about 2 percent of this fraction is actually absorbed into the body fluids through the intestinal wall. Therefore all of the research papers on acute effects of uranium refer to these soluble uranium compounds via inhalation. The main acute effect of inhalation of soluble uranium compounds is damage to the renal system, and the main long term storage place of these compounds in the body is bone.

These research findings do not apply easily to the insoluble uranium compounds to which the Gulf Veterans were exposed when the depleted uranium ordnance was used in battle.

The uranium compound used for ordnance was uranium 238 and limited amounts of its decay products. Particles of these compounds smaller than 2.5 microns are usually deposited deep in the lungs and pulmonary lymph nodes where they can remain for years. According to research done in the UK by the NRPB, ceramic uranium is formed when uranium ignites through friction, as happened in the Gulf War. In this form, it is twice as slow to move from the lungs to the blood than would be the non-ceramic uranium. Of the portion of inhaled uranium which passes through the gastro-intestinal tract, only 0.2 percent is normally absorbed through the intestinal wall. This may be an even smaller portion for ceramic uranium. This fraction of the inhaled compound can, of course, do damage to the GI tract as it passes through because it emits damaging alpha particles with statistical regularity. The residence time of the insoluble uranium compounds in the GI tract (the biological half life) is estimated in years. [ibid.]

The chemical action of all isotopic mixtures of uranium (depleted, natural and enriched) is identical. Current evidence from animal studies suggests that the chemical toxicity is largely due to its chemical damage to kidney tubular cells, leading to nephritis.

The differences in toxicity based on the solubility of the Uranium compound (regardless of which uranium isotope is incorporated in the compound) are more striking: water soluble salts are primarily renal and systemic chemical toxicants; insoluble chemical compounds are primarily lung chemical toxicants and systemic radiological hazards. Once uranium dioxide enters the blood, hexavalent uranium is formed, which is also a systemic chemical toxicant.

It is important to note that there is no scientific evidence which supports the US Veteran Administration claim that the insoluble uranium to which the Gulf War Veterans were exposed will be primarily a renal chemical toxicant. Yet this is the criteria which the VA proposes for attributing any health problems of the Veteran to depleted uranium. Intermediate and chronic exposure duration to insoluble uranium is regulated in the US by its radiological property. The slow excretion rate of the uranium oxide allows for some kidney and tubule repair and regeneration. Moreover, because of the long biological half life, much of the uranium is still being stored in the body and has not yet passed through the kidneys. The direct damage to lungs and kidneys by uranium compounds is thought to be the result of the combined radiation and chemical properties, and it is difficult to attribute a portion of the damage to these separate factors which cannot be separated in life.

There is human research indicating that inhalation of insoluble uranium dioxide is associated with general damage to pulmonary structure, usually non-cancerous damage to alveolar epithelium. With acute duration exposure this can lead to emphysema or pulmonary fibrosis (Cooper et al, 1982; Dungworth, 1989; Saccomanno et al, 1982; Stokinger 1981; Wedeen 1992). Animal studies demonstrate uranium compounds can cause adverse hematological disturbances (Cross et al. 1981 b; Dygert 1949; Spiegel 1949; Stokinger et al 1953).

Important information from a chart developed by ATSDR [referenced earlier] is reproduced here, the reader will find all of this information and the references in the original document.

Availability of Human or Animal Data
for the Presence of a Particular Health Effect
after Exposure via Inhalation to Insoluble Uranium

Effect on body system studied: Effects of acute duration exposure (less than 15 days) Effects of intermediate duration exposure (15 days to 1 year) Effects of chronic duration exposure (more than 1 year)
Respiratory Human Studies:
rales, slight degeneration in lung epithelium; hemorrhagic lungs [1]

Animal Studies:
severe nasal congestion, hemorrhage; gasping in 100 percent [2]
Animal Studies:
slight degenerative changes in lung;[3] pulmonary edema; hemorrhage; emphysema; inflamation of the brochi; bronchial pneumonia; alveoli and alveolar interstices; edematous alveoli; hyperemia and atelectasis.; lung lesions; minimal pulmonary hyaline fibrosis and pulmonary fibrosis. [2] Animal Studies:
minimal pulmonary fibrosis [3] Lung cancer in dog [3]
Hepatic

Animal Studies:
moderate fatty livers in 5 of 8 animals that died; focal necrosis of liver.[3] Animal Studies:
increased bromo-sulfalein retention [2]
Hematological Animal Studies:
increased macrophage activity; increased plasma prothrombin and fibrinogen.[3] A (increased percentage myeloblasts and lymphoid cells in bone marrow; decreased RBC; increased plasma prothrombin and fibrinogen; increased neutrophils ; decreased lymphocytes) Animal Studies:
lengthened blood clotting time, decreased blood fibinogen [2]
Gastro-intestinal Human Studies:
anorexia, abdominal pain, diarrhea, tenesmus or ineffective straining, and pus and blood in stool [1] Animal Studies:
anorexia; vomited blood; ulceration of caecum.[1],[6]
Renal Human Studies:
proteinuria, elevated levels of NPN, aminoacid nitrogen/creatinine, abnormal phenol-sulfonphthalein excretion. Increased urinary catalase; diuresis.[1]

Animal Studies:
Proteinuria, glucosuria and polyuria; severe degeneration of renal cortical tubules 5-8 days post exposure. [2]
Animal Studies:
diuresis, mild degeneration in glomerulus and tubules. [3] proteinuria, increased NPN.[3] minimal microscopic lesions in tubular epithelium [1] Animal Studies:
slight azotemia [4] slight degenerative changes [3] minimal microscopic lesions [1], [5],[6] tubular necrosis and regeneration [6]
Cardiovascular
Musculo-skeletal Animal Studies:
severe muscle weakness; lassitude [3 with F].
Endocrine
Metabolic
Dermal
Ocular Animal Studies:
conjunctivitis [2] Animal Studies:
eye irritation [2]
Body Weight Animal Studies:
26 percent decrease inMetabolicght; 14 percent decrease at 22 mg / cu m air; [1], [3] 12 percent decrease at 2.1 mg/cu m air.[2] 2.9 to 27.9 percent decreased body weight guinea pig [6]
Other Systemic Animal Studies:
weakness and unsteady gate, [1] minimal lymph node fibrosis.[3] rhinitis [1] Animal Studies:
minimal lymph node fibrosis [3] lung cancer (dog) [3]
Mortality Animal Studies:
20 percent for dogs at 2 mg per cu. m air [2] Animal Studies:
10 percent rat and guinea pig [4] 17 percent dog [4] 60 percent rabbits [3] 67 percent rabbits [4] Animal Studies:
4.5 percent mortality dog [3]

1. Uranium tetrafluoride, UF4 , insoluble in water.

2. Uranium hexafluoride, UF6 , soluble in water, highly chemically toxic.

3. Uranium dioxide, UO2 , insoluble in water, highly toxic and spontaneously flammable, used in ordnance in place of lead in the Gulf War. (Also called uranium oxide.)

4. Uranium trioxide, UO3 , insoluble in water, poisonous, decomposes when heated. (Also called uranium oxide.)

5. Uranyl Chloride, UO2Cl2 , uranium oxide salt.

6. Uranium Nitrate, UO2(NO3)2.2H2O , soluble in water, toxic and explosive.

With respect to ORAL exposure, there is no human data but a great deal of animal data. This was not as likely a pathway in the Gulf War as was inhalation, but possible contamination of food and water can not be totally ignored.

DERMAL exposure was researched in humans only in the acute duration of exposure case. Animal studies on dermal exposure include acute, intermediate and chronic duration of exposure, and immunologic/lymphoreticular and neurologic effects.

Mortality Within 30 Days of Exposure:

The lowest acute duration lethal dose observed, with exposure to the soluble uranium hexafluoride, was 637 mg per cu metre of air. No acute dose deaths were found using insoluble compounds. Since there were acute deaths in the Iraqi tanks in persons not directly hit, one can assume concentrations of uranium aerosol were greater than this amount. It should also be noted that it was the radiation protection units of the military which designated these contaminated tanks off bounds. They were acting because of radiological (not chemical) properties of the aerosol.

The intermediate duration exposure, 15 to 365 days, dose level for mortality with insoluble uranium oxide, was 15.8 mg per cu metre of air. With soluble uranium hexachloride it was much lower, 2 mg per cu metre air.

The dose resulting in lung cancer in the dog study, with chronic duration inhalation of the insoluble uranium oxide, was 5.1 mg per cu metre air, for 1 to 5 years, 5 day a week and 5.4 hours a day.

Systemic Damage:

Damage to body organs occurred with intermediate or chronic exposure at doses as low as 0.05 mg per cu metre air. A generally sensitive indicator of exposure seems to be loss of body weight. However this finding is somtimes attributed to the unpleasant taste of the uranium laced food given to animals. There is also damage to the entrance portals: respiratory and gastro-intestinal systems; and the exit portals: intestinal and renal systems. Uranium oxide was associated with fibrosis and other degenerative changes in the lung. It was also associated with proteinuria, and increased NPN (non-protein nitrogen) and slight degenerative changes in the tubules. The more severe renal damage was associated with the soluble compounds uranium tetrafluoride and uranium hexafluoride (not thought to have been used in the Gulf War ordnance).

Focal necrosis of the liver was only associated with uranium oxide. This may be a clue to one of its storage places in body tissue. Uranium oxide is also associated with hematological changes, lymph node fibrosis, severe muscle weakness and lassitude at intermediate or chronic dose rates in 0.2 to 16 mg per cu metre air. None of the uranium research dealt with the synergistic, additive or antagonistic effects potentially present in the Gulf War mixture of iatrogenic, pathological, toxic chemical and electromagnetic exposures.

Potential US Government administration of
radio-protective substances to combat military:

It is obvious that the US had some expectation of the health effects related to using depleted uranium ordnance in the Gulf War. This is evident based on military research and manuals. They would also have had access to information on chemical and biological agents which could protect against some of the harmful side effects. These agents might also "confuse" the toxicology of this exposure. Some potential radio-protective agents are thiols (also called mercaptans, these are organosulfur compounds that are derivatives of hydrogen sulfide), nitroxides (used as a food aerosol and an anesthetic), cytokines (non-antibody proteins released by one cell population, e.g T-lymphocytes, generating an immune response), eicosanoids (biologically active substances derived from arachidonic acid, including the prostaglandins and leukotrienes), antioxidants and modifiers of apoptosis (fragmentation of a cell into small membrane bound particle which are then eliminates by phagocytes).

Just in case this is the reality and not merely a suspicion, it would be good to examine the after effects of exposure to ceramic depleted uranium in Iraqi veterans and in the survivors of the El Al crash at Shipol Airport, Amsterdam. It is unlikely that these two populations were given any protective agents.

Proposal for assisting the Gulf War veterans:

In keeping with the above findings, it is proposed to undertake an analysis of both questionnaire and clinical data for a sample of each of the following populations: US, Canadian and British Gulf War veterans or civilian base workers exposed to DU; US, Canadian and British military personnel not exposed to DU; Iraqi Veterans exposed to DU; Iraqi Veterans not exposed to DU; and firemen and civilians exposed to the El Al crash.

Sampling strategy and sample size to be determined:

Each participant should complete a questionnaire [See draft questionnaire in Appendix A] covering general background variables, exposure profile and medical problems and symptoms. Each participant will agree to collect a 24 hour urine sample for analysis, and to take 500 mg blue-green algae (Spirulina) 48 hours before beginning the collection. This is a mild chelating agent. Each participant will agree to the analysis of this data for the benefit of all exposed persons, and to the release of the results of the analysis without identifying characteristics for individuals.

All questionnaire data will be entered into computer using Epi Info Software (WHO) and transferred on disc to the Biostatistical Support Unit of the University of Toronto for analysis.

Research Hypotheses to be tested:
(to be written as a null hypothesis)

There will be a high correlation between the questionnaire exposure estimates and the level of depleted uranium found in urine. Medical problems related to damage of the blood and/or hepatic systems will show an association with exposure data and urine sample analysis for depleted uranium.

Preliminary work to be accomplished:

* Identification of principal investigators for each identified study group.

* Development of a Grant Proposal, including the null hypotheses and protocols.

* Development of a budget for each population study group.

* Agreement of the Research team to undertake the study.

* Raising of funds or assignment of costs for the study.

* Identification and training of data entry processors for each group.

Benefits for Participants:

In addition to the general benefits to be obtained by clarifying the health effects of exposure to this toxic material, especially in the ceramic form experienced in the Gulf War, each participant testing positive for DU in a urine analysis will be assisted to enter a chelating process to remove as much as possible of the contaminant from the body.

References:

ATSDR 1998: "Toxicological Profile for Uranium" Draft for Public Comment, US Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Ragistry, September 1997.

Cooper JR, Stradling GN, Smith H, et al 1982. "The behaviour of uranium 233 oxide and uranyl 233 nitrate in rats. International Journal of Radiation Biology and Related Studies in Physics, Chemistry and Medicine. Vol 41(4): 421-433.

Cross FT, Palmer RF, Busch RH et al, 1981. "Development of lesions in Syrian golden hamsters following exposure to radon daughters and uranium dust". Health Physics Vol 41:1135-153.

Dungworth DL. 1989 "Non-carcinogenic responses of the respiratory tract to inhaled toxicants." In: Concepts in Inhalation Toxicology. Editors: McClellan RO, and Henderson RF. Hemisphere Publ. Corp. New York NY.

Dygert HP 1949. Pharmacology and Toxicology of Uranium Compounds. Pages: 647-652, 666-672, and 673-675. McGraw Hill Books Inc.

Encyclopaedia of Occupational Health and Safety, Third (Revised) Edition. Technical Editor: Dr. Luigi Parmeggiani, published by the International Labour Organization in 1983 (ISBN: 92-2--103289-2) Geneva, Switzerland.

Gindler JE, 1973. "Physical and Chemical Properties of Uranium." In: Uranium, Plutonium and Transplutonic Elements" Editors: Hodge et al. New York NY: Springer Verlag; 69-164.

ICRP 1991: Recommendations of the International Commission on Radiological Protection. Publication, accepted in 1990 and reported in Publication 60. Pergamon Press, UK.

Saccamanno G, Thun MJ, Baker DB, et al 1982. "The contribution of uranium miners to lung cancer histogenesis renal toxicity in uranium mill workers". Cancer Research Vol. 82 43-52.

Spiegel CJ, 1949. Pharmacology and Toxicology of Uranium Compounds. McGraw Hill Book Co.Inc.

Stokinger HE, Baxter RC, Dygent HP, et al 1953. In: Toxicity Following Inhalation for 1 and 2 Years. Editors: Voegtlin C and Hodge HC.

Stokinger HE, 1981. Uranium. In: Industrial Hygiene and Toxicology. Vol 2A, 3rd Edition. Editors:Clayton CD and Clayton FE. John Wiley and Sons, New York NY, 1995-2013.

Stradling GN, Stather JW, Gray SA, et al. "The metabolism of Ceramic Uranium and Non-ceramic Uranium Dioxide after Deposition in the Rat Lung." Human Toxicology 1988 Mar 7; Vol 7 (2): 133-139.

UNSCEAR: United Nations Scientific Committee on the Effects of Atomic Radiation reports to the UN General Assembly.

Wedeen RP, 1992. "Renal diseases of Occupational Origin". Occupational Medicine Vol 7 (3):449.