II. DEPLETED URANIUM - A SHORT COURSE

The following sections discuss DU’s chemical and radiological properties, the ways those properties may affect human health, and the principles and standards for protecting soldiers and the public from harm. These discussions address DU’s chemical toxicity, which is the metal’s property of most concern, followed by a summary of DU’s radiological toxicity.

It should be emphasized that DU’s chemical and radiological properties, and their health and environmental implications, had been carefully evaluated as part of the standard acquisition, test, and evaluation process for new weapon systems. Throughout the development of the DU weapons program, the DoD has adhered to a highly regulated development and procurement process that involved extensive hazard assessments, tests, and evaluations. A comprehensive discussion of the DU research and development program, including specific test and evaluation efforts, is found in Tab E, Development of DU Munitions and in Tab L, Research Report Summaries.

A. Health Effects From the Chemical Toxicity of Depleted Uranium

1. Chemical Properties of DU

Uranium is all around us. It is a heavy metal similar to tungsten, lead, and cadmium, occurring in soils at an average concentration of 3 parts per million, equivalent to a tablespoon of uranium in a truckload of dirt.[2] All of us take in uranium every day from the air we breathe, the water we drink, and the foods we eat. On average, each of us takes in 1.9 micrograms (about two millionths of a gram) of uranium a day from food and water, and inhales a very small fraction (7 X 10-3 or 0.007) of a microgram every day.[3]

DU’s ability to self-sharpen as it penetrates armor is the primary reason why DU is a more potent weapon than alternate tungsten munitions, which tend to mushroom upon impact. Fragments and uranium oxides are generated when DU rounds strike an armored target. The size of the particles varies greatly; larger fragments can be easily observed, while very fine particles are smaller than dust and can be inhaled and taken into the lungs. Whether large enough to see, or too small to be observed, DU particles and oxides contained in the body are all subject to various degrees of solubilization—they dissolve in bodily fluids, which act as a solvent.

Figure 4. Cutaway of DU Sabot Round

The solubility of uranium varies greatly depending on the particular compound—or form of uranium—and the solvent. The human body’s natural fluids, which are water-based, provide the solvent that acts on DU that has entered the body. In this report, references to "soluble" and "insoluble" forms of depleted uranium are relative generalizations about depleted uranium’s overall solubility; over time, all uranium is soluble. The three uranium oxides of primary concern (UO3, UO2, and U3O8) all tend to dissolve slowly (days for UO3 to years for UO2 and U3O8) in bodily fluids.[4] Once dissolved, uranium may react with biological molecules and, in the form of the uranyl ion, may exert its toxic effects. Those toxic effects are: cellular necrosis (death of cells) in the kidney and atrophy in the tubular walls of the kidney resulting in a decreased ability to filter impurities from the blood.[5]

2. Chemical Effects

Once dissolved in the blood, about 90% of the uranium present will be excreted by the kidney in urine within 24-48 hours.[6] The 10% of DU in blood that is not excreted is retained by the body, and can deposit in bones, lungs, liver, kidney, fat and muscle. Insoluble uranium oxides, if inhaled, can remain in the lungs for years, where they are slowly taken into the blood and then excreted in urine.

Although heavy metals are not attracted to single biological compounds, they are known to have toxic effects on specific organs in the body. Previous research has demonstrated that the organ that is most susceptible to damage from high doses of uranium is the kidney. The uranyl-carbonate complexes decompose in the acidic urine in the kidney. This reaction forms the basis for the primary health effects of concern from uranium. The effects on the kidney from uranium resemble the toxic effects caused by other heavy metals, such as lead or cadmium.

So far, very few Gulf War veterans have been diagnosed with types of kidney damage in which DU would be on the list of possible causative agents. Diabetes and lupus would be the most likely causes on the list, however. Among the first 20,000 veterans who were evaluated in the CCEP, there were only 25 individuals (0.1%) who were diagnosed with these types of kidney damage. These included 13 individuals with glomerulonephritis and 12 individuals with renal insufficiency.[7] None of these 25 individuals were among the group of 33 veterans with the highest DU exposures who have been followed in the Baltimore VA program. The rates of these diagnoses in this self-selected population are consistent with the rates of similar kidney problems in the general US population.

3. Chemical Toxicity Standards

For uranium, the Occupational Safety and Health Administration (OSHA) and the American Conference of Governmental Industrial Hygienists (ACGIH) have established protection standards for workers based on the chemical toxicity to the kidney. The standards are based on the assumption that they will provide adequate protection for workers over a normal working (40 hours per week) lifetime. Additionally, levels for short-term exposures are also defined to limit acute exposure effects. The Permissible Exposure Limits (PELs) listed in Table 2 are from the Code of Federal Regulations dealing with occupational exposures to toxic and hazardous substances. Table 2 is intended only for a general comparison of the relative toxicity of the various metals. Although the PEL was derived for natural uranium, the chemical effects of the various isotopes of uranium are expected to be identical.

Table 2. Comparison of OSHA PELs for Metals from Inhalation Exposures.[8]

Element Soluble Compounds (mg/m3) Insoluble Compounds (mg/m3)
Lead* 0.05 0.05
Cobalt - metal, dust and fume (as Co)* 0.1 0.1
Uranium 0.05 0.25
Nickel 1 1
Tungsten 1 5
Mercury 0.01  
Titanium Dioxide total dust*   15
* No distinction is made between soluble and insoluble compounds.

In addition to OSHA’s limits, ACGIH has established a Threshold Limit Value (TLV ) of 0.2 mg/m3 (for both soluble and insoluble compounds). For brief periods of exposure, ACGIH has set a short-term exposure limit (STEL)(an average concentration over a 15 minute period that allows for brief excursion above the TLV) of 0.6 mg/m3.[9] PELs and TLVs are based on the principle that there is a threshold below which no adverse health effects occur. As the exposure increases above the threshold, the adverse health effect becomes more severe. PELs and TLVs are called time-weighted-average values because they are averaged over an 8-hour workday, for a 40-hour workweek over a working lifetime.

The OSHA PELs and ACGIH TLVs were intended to apply to the common workplace, not to the battlefields of Desert Storm. Nevertheless, these limits provide a set of guidelines for use as a starting point in evaluating hazards. However, since only limited environmental data are available from the operational environment, the guidelines serve as reference points for comparison with experimental data.

4. Implications for the Military

DU exposures for the Level II and Level III exposure categories are believed to be well below levels expected to produce either temporary or permanent kidney damage. The friendly fire victims (Level I exposures) are believed to have had the highest exposures during the Gulf War (Reference Section III.B.1.c.). It is impossible to assess temporary DU-related kidney dysfunction in these soldiers immediately following their accidents, because traumatic injuries and major surgeries may also cause temporary renal abnormalities. In addition, routine urinalysis tests do not detect subtle, early renal damage that might be associated with DU heavy metal toxicity. However, no kidney abnormalities have been documented in any of the 33 veterans studied in the Baltimore VA program, including their most recent examinations in 1997.

B. Health Effects From the Radiological Toxicity of Depleted Uranium

1. Radiological Properties of DU

Depleted uranium—described above as a metallic remnant of one of several processes that begin with uranium ore—is composed of three isotopes of uranium (234U, 235U, and 238U). Depleted uranium, like all uranium and other elements, is composed of atoms; the basic building block of nature. Atoms consist of atomic particles called neutrons (neutral particles), protons (positively charged particles), and electrons (negatively charged and relatively massless). For any element, like uranium, the number of protons and electrons determine the chemical properties. Atoms of the same element can have different numbers of neutrons. These different atoms of the same element are called isotopes. Isotopes of an element have the same chemical properties, but may have different nuclear or radiological properties. In nature, uranium consists of the isotopes 234U, 235U, and 238U in a certain ratio. Depleted uranium has a lower content of 234U and 235U, which have been removed in the enrichment process.

The number of heavy particles (protons and neutrons) in the nucleus of an atom determines the stability of the element. Unstable elements ‘decay’ through a nuclear transformation process into new elements called progeny or daughter products. Each daughter product has a lower atomic weight than the unstable parent isotope. This process of decay—radioactivity—emits one or more forms of ionizing radiation (among them, alpha particles, beta particles, neutrons, X-rays, or gamma rays) during each nuclear transformation. This decay process continues until a stable (non-radioactive) element is produced. For example, after completing several stages of the radioactive decay process, 238U becomes lead. A more thorough description of the origins of depleted uranium can be found at Tab C.

2. Radiological Effects

As it decays, DU emits alpha, beta, and gamma radiation. An understanding of how DU’s emissions may cause health effects can be drawn from existing knowledge of how radiation, in general, causes health effects.

Radiation is everywhere. People live their lives being bombarded by gamma rays, neutrons, and charged particles produced by materials in nature and even in their own bodies. This ever-present background radiation has persisted for as long as the earth has existed. Humans have evolved and developed in this ionizing radiation environment.

In discussing health effects relating to ionizing radiation, the term "dose" is used. "Dose" comes from the early medical use of x-rays, much as a dose of medicine is measured in grains or ounces. It refers to the amount of radiation energy absorbed by an organ, tissue, or cell, measured in rems.[10] Today, the average American receives a dose of 0.3 rem every year from natural sources—radioactive materials in rocks and soil, cosmic radiation, radon, and radioactivity in our bodies. Over a 70-year lifetime, the average dose is 21 rems. In some areas of the world, people receive much higher doses from background radiation. For example, in areas of India and Brazil the ground is covered with monazite sand, a radioactive ore. Radiation exposure rates there are many times the average background levels elsewhere. People who live in these areas receive doses of up to about 0.7 rem each year from the gamma radiation alone.[11] These levels combined with the other sources of background radiation (cosmic rays, radon, etc.), cause average doses that are about three times more than the US average. Yet these people show no unusual rates of cancer or other diseases linked to radiation.[12]

The effects of ionizing radiation can be categorized as either prompt or delayed, based on the time frame in which the effects are observed. Prompt effects, like rapid death, occur when high doses are received in a short period of hours to weeks. Delayed effects, such as cancer, can occur when the combination of dose and dose rate is too small to cause prompt effects. Both animal experiments and human exposures to high levels of radiation show that ionizing radiation can cause some cancers.[13] All of the observed effects of ionizing radiation in humans occur at relatively high doses. At the low doses that are of interest to radiation workers and the general public (that is, below a few rems), studies to date are inconclusive.[14] Although adverse health effects have not been observed at low doses, the carcinogenic nature of ionizing radiation makes it wise to limit the dose.

For low-doses, there is no reliable data relating dose to health effects or showing a threshold, or minimum, level for cancer. Because of this, experts who study radiation effects have decided that the results from high-dose, high-dose-rate studies must be used to control the low-dose, low-dose-rates experienced by workers and the public. The easiest way to do this is to assume that no effects occur at zero dose. Also, since the rate at which effects occur is extrapolated from higher doses, it is also assumed that the effect increases linearly with dose. These two assumptions are known as the "linear-dose-response, non-threshold" (LNT) hypothesis. This implies that the same number of additional cancers would occur from exposing 100 persons to 100 rems, or 10 thousand persons to 1 rem, or 10 million persons to 0.001 rem. No threshold effects have ever been reliably observed in humans below about 10 rems[15] , but reports from the Japanese atomic bomb survivor studies conclude that the location and reality of such a threshold, if one does exist, are difficult to assess.[16]

3. Radiological Protection Standards and Guidelines

Ionizing radiation offers many benefits to society in medical diagnosis and treatment, greenhouse-gas-free power, food safety, etc. At the same time, it carries risks to safety and health as discussed above.

Within the first 30 years after the discovery of x-rays, standards were developed for the measurement of radiation. At about the same time, acceptable levels of dose were set. The first level, known as the ‘tolerance dose,’ or that amount of radiation that could be tolerated, was set at one-tenth of a unit (about 0.1 rem in today’s units) per day for 300 days a year.

From World War II to the early 1980s, radiation dose limits were adjusted downward in response to increased concern about radiation effects, the increased uses of radiation, and because improved radiation protection technologies appeared. The National Council on Radiation Protection and Measurements (NCRP, established in the 1930s) developed the recommended changes for the United States. During that time, the dose limit was reduced from three-tenths of a rem in a six-day period in 1946 to 5 rems per year in the mid-1950s. Also, a limit for the public was set at one-tenth of the worker limit to provide an additional margin of safety.

Research does not show a clear threshold dose for cancers from radiation, so the small risk per person at low doses had to be considered in relation to the large number of workers who were receiving those doses.[17]

The NCRP adopted three radiation protection principles: (a) no practice shall be carried out unless it produces a positive net benefit (sometimes called justification); (b) all exposures shall be kept as low as reasonably achievable (ALARA), economic and social factors being taken into account (called optimization); and (c) the dose equivalent to individuals shall not exceed the recommended limits (called limitation). These principles work together to protect against both prompt and delayed effects in large groups of workers and the public.

In 1993, the NCRP released a new set of national recommendations based on International Council on Radiation Protection’s (ICRP) 1990 recommendations. Those limits for non-threshold effects differ slightly from the earlier recommendations: 50 rems per year to any tissue or organ and 15 rems to the lens of the eye to avoid cataract formation. The recommended occupational limits on whole-body doses (total effective dose equivalent), first set at 5 rems per year in 1958, are now set at no more than 5 rems in any one year and a lifetime average of no more than 1 rem per year.[18]

Occupational radiation exposure limits for federal agencies are currently established in "Radiation Protection Guidance to Federal Agencies for Occupational Exposure," 52FR 1717, signed by President Reagan on January 20, 1987. The Nuclear Regulatory Commission implemented that guidance in its regulations on radiation protection (Title 10, Code of Federal Regulations, Part 20). These limits apply to all licensed uses of radioactive material under NRC's jurisdiction. Similarly, other Federal agencies as a matter of policy and directive, including the DoD in DODI 6055.8, Occupational Radiation Protection Program, also observe this guidance.[19]

The current established protection standards are:[20]

These limits are in addition to the radiation doses a person normally receives from natural background, medical testing and treatment, and other sources.

Because any amount of radiation dose is assumed to lead to some health effects (regardless of how small), guidance also requires that doses be kept "as low as reasonably achievable" (ALARA). This means that one should try to reduce doses to as far below the limits as reasonably possible.

For DU, the annual occupational limit of 5 rems was selected as the benchmark for evaluating the consequences of exposure in the Gulf War. This benchmark has been shown to be well below the levels at which any effects from ionizing radiation have ever been observed in people. Furthermore, the limit is consistent with the safe practices in the radiation industry.

4. Implications for the Military

External radiation exposures may occur when personnel are close to DU due to its beta and gamma radiation. Studies of external radiation measurements inside tanks show that the tank commander, gunner, and loader receive a radiation dose rate of 0.00001-0.00002 rem/hour, an amount which is somewhat less than the average natural background rate of about 0.00003 rem/hour.[21] The tank driver may receive slightly higher dose rates of 0.00003 (gun pointed forward) to 0.00013 rem/hour (bustle fully loaded with DU ammunition pointed forward), when the driver’s hatch is open.[22] This means the driver inside a fully loaded "heavy armor" tank (a model using DU armor panels) continuously, 24 hours a day, 365 days a year, would still receive a dose of less than 25% of the current, annual occupational limit of 5 rems. Studies have also shown that the maximum dose rate outside the tank approaches 0.0003 rem/hr at the front of a HA turret or over a fully loaded bustle. Continuous exposure at that level would produce an annual dose of about 2.6 rems or slightly more than one-half the occupational limit. Fortunately, these exposure scenarios represent very unlikely situations. Actual exposures based on realistic times spent in the tanks are likely to be less than 0.1 rem in a year.

Figure 5. M1A1s in the Gulf

Another external radiation hazard from DU is from contact with the bare skin. DU produces a dose rate of 0.2 rem/hour when it is located in contact with bare skin. The current dose limit for skin (50 rems in a year) would only be exceeded if unshielded DU remains in direct contact with the skin for more than 250 hours. Some reports have mistakenly applied the total effective dose equivalent (whole body dose) criteria of 0.1 rem/year for individual members of the public to this exposure. This leads to the erroneous conclusion that the exposure from one exposed DU penetrator could subject an individual to a dose of radiation thousands of times higher than the recommended maximum permissible dose. The correct criteria is the NRC’s occupational dose limit of a shallow-dose equivalent of 50 rems/year to the skin or to each of the extremities.

In fires and during impact, DU forms both soluble and insoluble oxides. The inhalation of the insoluble oxides presents an internal hazard from radiation if they are retained in the lungs. Sustained exposure to the alpha and beta radiation from the material could damage lung tissue. As indicated in the following assessment section, the worst exposures in the Gulf were less than one-fifth the annual occupational limit and well below the level known to cause health effects in people.


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