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 Celsius, uranium powder may self-ignite in atmospheres of carbon dioxide and nitrogen. And, oxidation of uranium under certain conditions may generate sufficient energy to cause an explosion (Gindler 1973). For example, friction caused by bullet or missile entry into a tank or armored car can cause the uranium to ignite, forming a concentrated ceramic aerosol capable of killing people 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 facts that at least 320 tons (about 320.000 Kg) of depleted uranium (DU) were “lost” in the Gulf War, and that much of it was converted at high temperature into an aerosol – that is, a mist or fog of minute airborne particles of uranium oxide, UO₂ or UO₃. 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 were conducted may also have been exposed.

Uranium oxide and its aerosol form are insoluble in water. The aerosol is able to travel tens of kilometers in the air. Once on the ground, it can be resuspended when disturbed by motion or wind. When inhaled, very small particles of uranium oxide, those that are 2.5 microns or less in diameter, can reside in the lungs for years and slowly pass through the lung tissue into the blood. Uranium oxide dust has a biological half-life in the lungs of about a year, but, according to British NRPB 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 of uranium oxide are excreted through the gastro-intestinal tract in feces. The uranium compounds that enter the body either through the wall of the gastro-intestinal tract or through the lungs can be broken down in the body fluids. 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 can be stored in bone, lymph, liver, kidney or other tissues. This uranium which is taken internally is eventually excreted through urine.

The presence of depleted uranium in urine is sufficient evidence to substantiate tissue storage and long-term internal contamination of this radioactive substance, seven or eight years after exposure.

URANIUM IS BOTH A CHEMICAL TOXIN AND A RADIOACTIVE HAZARD:

Uranium is a heavy metal, known to cause uranium nephritis. Soluble uranium is regulated because of its chemical toxicity, which is measured by damage to the kidney and tubules. Insoluble uranium, such as was released in the Gulf War, is regulated through 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 judgement which of the 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 substances, each decay having its characteristic half-life. Therefore, in its natural and undisturbed state, it always occurs together with a variety of other radioactive elements, some of the best known being thorium, radium, polonium and lead.

Natural uranium in soil occurs at about 1 to 3 parts per million, whereas in uranium ore it is many times as concentrated, reaching about 0.05 to 0.2% of the total weight. Natural uranium contains 99.3% of the isotope uranium-238 and 0.7% of uranium-235. In depleted uranium, the percentage of uranium-235 is typically 0.2% to 0.3%, the deficit enables one to use analytic methods to identify uranium found in the urine of veterans as depleted, not natural. Uranium-238 has a half-life of 4.51E+9 years, or 4,510,000,000 years. One gram of pure uranium-238 has a specific activity of 12.4 kBq, which means that there are 12,400 atomic transformations every second, each of which releases an energetic alpha particle. Each atomic transformation produces another radioactive element. 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 account for much of the radioactivity in the depleted uranium. If uranium-238 were chemically separated from the mix of isotopes described above, the thorium-234 and protactinium-234 would again build up to approximate equilibrium within 6 months. 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.

Uranium and all of its products of decay, with the exception of the inert gas radon, are heavy metals. Unlike some other heavy metals that 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 amount of uranium, usually from food, is inescapable in the normal Earth environment. We humans basically take in, on average, 5 Bq per year of uranium-238 in equilibrium with its decay products. The ingested amount is about 0.000436 Bg a year [UNSCEAR 1988, 58-59], a mixture of soluble and insoluble compounds, absorbed mostly through the gut.

Regulatory limits, as recommended by the International Commission on Radiological Protection [ICRP], assume that the maximum permissible dose for the public will be the one which gives the individual 1.0 mSv dose per year. This is in addition to the natural exposure dose from the uranium in food. Assuming that the 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 the limit of intake of 1.2 mg (0.0012 g) per year for the general public.

This added radiation dose of 1.0 mSv of uranium is almost 2.75 times that from the natural uranium intake. According to the ICRP permissible maximum, nuclear workers would be allowed to reach an annual dose of 20 mSv, comparable to an intake of 24 mg of uranium or 55 times that of the normal yearly intake.

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

The maximum dose per year from anthropogenic sources can be converted to the maximum concentration permissible in air by using the fact that the adult male breathes in about 23 cubic m of air in a day [ICRP 1977]. Assuming the Gulf War situation of continuous occupancy rather than an eight-hour day, 40-hour workweek, the maximum permissible concentration of a uranium aerosol in air for the general public would be 0.14 microgram per cu m, and for workers would be 2.9 micrograms per cu m.

In order to understand the scale of the ceramic uranium released in Desert Storm, where at least 300 million grams were “lost” – breathing in only 0.023 g would be equivalent to the 1990 recommendations of ICRP maximum permissible inhalation dose for a nuclear worker to receive in one year.

MEDICAL TESTING FOR DEPLETED URANIUM CONTAMINATION:

Potential testing for depleted uranium contamination includes: chemical analysis of uranium in urine, feces, blood and hair; test 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. But, since this test only measures the amount of depleted uranium that has been circulating in the blood or kidneys within one or two weeks prior to the testing time, it cannot be directly used to reconstruct the veteran’s dose received during the Gulf War. Nor can it test the true body burden. However, this seems to be the best diagnostic tool at this time, eight years after the exposure.

A feces test for uranium is used for rapid detection of intake in an emergency situation and must be undertaken within hours or days of the exposure in order to be useful for dose reconstruction. Fecal and blood analyses 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, may be used to detect the isotope uranium-235, the isotope of uranium partially removed from depleted uranium. For lung counting, again it is the uranium-235 that is detected, and the minimum detection limit is about 7.4 Bq or 200 pCi. Since humans normally take in only 5 Bq per year, this is not a very sensitive measure. This method of detection is most likely useless for veterans now seven or eight years after the Gulf War exposure.

Routine blood counts are useful shortly after exposure or during a chelating process for decontamination of the body. These counts are not a search for uranium in blood, but rather for a complete blood count with differential. This procedure is done to discover potentially abnormal blood counts, since the stem cells, which produce the circulating lymphocytes and erythrocytes are found in the bone marrow – close 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 iron deficient anemia, since they recycle heme from discarded red blood cells, as well as 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 shampoos, conditioners, hair coloring or permanent waves used. 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 if and how the analysis would differentiate between the various uranium isotopes.

The testing of bone or lymph nodes during an 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 bronchoscope is recommended for medical reasons, it would be advisable to also take tissue samples for analysis for depleted uranium from the veteran at that time.

If 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 nonprotein nitrogen is 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 methodology, 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 in 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 or not the regulatory limits for exposure to ionizing radiation apply in a war situation, and, if they do, whether or not the veteran should be considered to have been “general public” or “nuclear worker”. Beyond this, the question that needs to be addressed is “Should international standards or US standards be used in a multinational situation?”

The second methodology would require ranking veterans on an ordinal scale of 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 or not any medical problems show an increase with the ordinal scale increase of exposure, determined through urine analysis; and secondly, whether or not there is a correlation between the descriptive accounts of potential depleted uranium exposure and the assigned ordinal scale.

Using Non-Parametric Statistics, one could determine the statistical significance of various medical problems being depleted uranium exposure related. This would undoubtedly eliminate the consideration of some medical problems 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 deaths, 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, page 2238 under uranium alloys and compounds, 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.

Because the ATSDR division was based of the duration of the presence of the external source of contamination, not its residence time in the body, 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 on humans.

It should not be assumed that lack of research on a particular system implies lack of effect on that 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 that might likely be raised.

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% 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 is DU-metal. When it burns it forms uranium dioxide or less likely, uranium trioxide. 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 single molecules of uranium dioxide. Of the portion of inhaled uranium which passes through the gastro-intestinal tract, only 0.2% 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 alpha particles. 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 chemical toxicity is largely due to the 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 supporting the US Veteran Administration’s claim that the insoluble uranium oxide to which the Gulf War Veterans were exposed will be primarily a renal chemical toxicant. Yet this is the criterion that 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 through 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 in this table.

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	H: rales, slight degeneration in lung epithelium; hemorrhagic lungs1 A: severe nasal congestion, hemorrhage; gasping in 100%2	A: slight degenerative changes in lung;3 pulmonary edema; hemorrhage; emphysema; inflammation of the bronchi; bronchial pneumonia; alveoli and alveolar interstices; edematous alveoli; hyperemia and atelectasis.; lung lesions; minimal pulmonary hyaline fibrosis and pulmonary fibrosis.2	A: minimal pulmonary fibrosis3 Lung cancer in dog3
Hepatic		A: moderate fatty livers in 5 of 8 animals that died; focal necrosis of liver.3	A:increased bromo-sulfalein retention2
Hematological	A: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)	A: lengthened blood clotting time, decreased blood fibinogen2
Gastro-intestinal	H: anorexia, abdominal pain, diarrhea, tenesmus or ineffective straining, and pus and blood in stool1		A: anorexia; vomited blood; ulceration of caecum.1,6
Renal	H: proteinuria, elevated levels of NPN, aminoacid nitrogen/creatinine, abnormal phenol-sulfonphthalein excretion. Increased urinary catalase; diuresis.1 A: Proteinuria, glucosuria and polyuria; severe degeneration of renal cortical tubules 5-8 days post exposure.2	A: diuresis, mild degeneration in glomerulus and tubules.3 proteinuria, increased NPN.3 minimal microscopic lesions in tubular epithelium1	A: slight azotemia4 slight degenerative changes3 minimal microscopic lesions1,5,6 tubular necrosis and regeneration6
Cardiovascular
Musculo-skeletal		A: severe muscle weakness; lassitude[3 with F]
Endocrine
Metabolic
Dermal
Ocular	A: conjunctivitis2	A: eye irritation2
Body Weight		A: 26% decrease in body weight; 14% decrease at 22 mg /cu m air;1,3 12% decrease at 2.1 mg/cu m air.2 2.9 to 27.9% decreased body weight guinea pig6
Other Systemic		A: weakness and unsteady gate,1 minimal lymph node fibrosis.3 rhinitis1	A: minimal lymph node fibrosis3 lung cancer (dog)3
Mortality	A: 20% for dogs at 2 mg per cu. m air2	A 10% rat and guinea pig4 17% dog4 60% rabbits3 67% rabbits4	A: 4.5% mortality dog3

Notes

¹ Uranium tertrafluoride, 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 there is a great deal of animal data. This was not as likely a pathway in the Gulf War as inhalation was, 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.

Note: No comments on the quality or extent of the research are implied by this table.

MORTALITY WITHIN 30 DAYS OF EXPOSURE:

The lowest acute duration lethal dose observed, with exposure to the soluble uraniumhexafluoride, was 637 mg per cu m 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 that 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 m of air. With soluble uranium hexachloride it was much lower, 2mg per cu m 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 m 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 m air. A generally sensitive indicator of exposure seems to be loss of body weight. However this finding is sometimes 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 two soluble compounds: uranium tetrafluoride and uranium hexafluoride (neither 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 m 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 that 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 – 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); and, antioxidants and modifiers of apoptosis (fragmentation of a cell into small membrane bound particles which are then eliminated 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 that an analysis be undertaken of both the questionnaire and clinical data of a sample from each of the following populations: US, Canadian, British Gulf War veterans and/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.

Each participant should complete a questionnaire 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 of individuals.

All questionnaire data will be entered into a computer using Epi Info Software (WHO) and transferred by 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)

The correlation between the questionnaire exposure estimates and the level of depleted uranium found in urine.

The association of medical problems related to damage of the blood and/or hepatic systems with exposure data and with the level of depleted uranium found in urine.

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

References:

Encyclopaedia of Occupational Health and Safety, Third (Revised) Edition. Technical Editor:
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 Registry, 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.
Dr. Luigi Parmeggiani, published by the International Labour Organization in 1983 (ISBN: 92-2-103289-2) Geneva, Switzerland.
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Dygert HP 1949. Pharmacology and Toxicology of Uranium Compounds. Pages: 647-652, 666-672, and 673-675. McGraw Hill Books Inc.
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, United Kingdom.
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, 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.
Stokinger HE, Baxter RC, Dygent HP, et al 1953. In: Toxicity Following Inhalation for 1 and 2 Years. Editors: Voegtlin C and Hodge HC.
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.