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Depleted Uranium: Weapon of Mass Destruction
In the 1991 Persian Gulf War, U.S. forces used depleted uranium as both armor piercing bullets and as tank armor for the first time. These weapons are both radioactive and toxic. Uranium Oxide particles formed during production, testing, and battlefield use pose a long term threat to human health and the environment.
Uranium weapons are effective antitank “penetrators” because they are extremely dense. A slug of uranium weighs twice as much as a piece of lead the same size. When alloyed with titanium, uranium is extremely hard. Uranium is also “pyrophoric”, which means it burns upon impact.
The U.S. Military chose to develop uranium weapons not only because they are promised to be effective, but because the metal itself is very cheap. Depleted uranium is material that remains when enriched fissionable uranium- that is, capable of generating a nuclear explosion or nuclear power- is separated from natural uranium. The U.S. stockpile exceeds a billion pounds. Uranium weapons production is the nuclear bombmakers’ idea of “recycling”.
The Agent Orange of the 90’s
Depleted Uranium is not capable of an atomic chain reaction. It is not considered a high-level radioactive material. As a metal slab, like the armor plates in the U.S. Army’s M1 Abrams tanks, it is a relatively harmless. Though constant exposure could cause problems. But especially in particulate form, it can be extremely hazardous.
When uranium weapons burn, when they corrode, and when they are machined, uranium oxide dust is created. When inhaled, small particles-those less than 5 millionths of a meter-can lodge in a human lung tissue, exposing the host to a growing dose of alpha radiation. This can cause lung cancer in people of all ages, and is particularly hazardous to children.
Uranium, like lead and other heavy metals, is a chemical poison. The ingestion of minute quantities of uranium in food or drinking water can cause irreparable damage to the kidneys. Some experts consider this is a greater risk than radiation from depleted uranium.
Uranium weapons may be the “Agent Orange of the 90’s” because large numbers of people, friend and foe are being exposed to uranium oxide dust. We won’t know for 20-30 years the full significance of that exposure, but by then it will be too late. Here are a few examples of that exposure:
The U.S. Military, which fired thousands of uranium shells during the Persian Gulf War, left at least 387 tons of spent uranium munitions in Kuwait and southern Iraq after the war. The U.S. Government believes, based upon weapons tests in the U.S. and general knowledge about wind patterns, that there is no health or environmental hazard, but it has not undertaken any study of battlefield areas.
After the Persian Gulf War, contaminated U.S. armored vehicles were prepared for disposal in the United States. The U.S. soldiers–at least 25– who handled those vehicles were not warned of DU hazards or wore any protective gear.
Army weapons testers at the Jefferson Proving Ground in Indiana fired DU rounds at soft targets-cloth or plywood- to avoid combustion. Still, only 22,000kg of the 91,000kg fired there between 1984 and 1992 were recovered in biannual clearance operations. The Army will have to strip away several feet of soil during decontamination. This will increase soil erosion and the migration of DU.
The NRC permitted Nellis Air Force Base to receive and process up to 77,000 lbs. of DU rounds. These rounds were used in testing on the base’s Range 63 using tanks as targets. In 1980, NL Industries Uranium Weapons factory in Clonie, New York was forced to close. Uranium particles were found as far as 26 miles downwind.
In 1981, workers at Aerojet’s TNS Uranium Weapons Plant in Jonesborough, Tennessee went on strike because of plant conditions that caused an epidemic of uranium poisoning.
At Nuclear Metals Inc., which manufactures uranium weapons in Concord, Massachusetts, radioactive materials have contaminated surface water, ground water, and land. Independent testing done by Citizens Research and Environmental Watch(CREW), a local grassroots organization, found DU 18 times the background level and up to 9/10ths of a mile away. Concord has the second highest level of thyroid cancer in the state, 2 1/2 times the state average. — Military Toxics Project
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Alexandra C. Miller is a senior scientist with the Armed Forces Radiobiology Research Institute and an assistant professor at the Uniformed Services University of the Health Sciences in Bethesda, Maryland. Dr. Miller has numerous publications in the area of depleted uranium health hazards and is the author of Depleted Uranium, Properties, Uses, and Health Consequences from the CRC Press.
Urinary and serum mutagenicity studies with rats implanted with depleted uranium or tantalum pellets
During the 1991 Persian Gulf War several US military personnel were wounded by shrapnel fragments consisting of depleted uranium. These fragments were treated as conventional shrapnel and were not surgically removed to spare excessive tissue damage. Uranium bioassays conducted over a year after the initial uranium injury indicated a significant increase in urine uranium levels above natural background levels. The potential mutagenic effects of depleted uranium are unknown. To assess the potential mutagenic effects of long-term exposure to internalized depleted uranium, Sprague-Dawley rats were implanted with depleted uranium and their urine and serum were evaluated for mutagenic potential at various times after pellet implantation using the Ames Salmonella reversion assay. Tantalum, an inert metal widely used in prosthetic devices was used for comparison. Enhancement of mutagenic activity in Salmonella typhiurium strain TA98 and the Ames II™ mixed strains (TA7001-7006) was observed in urine samples from animals implanted with depleted uranium pellets. In contrast, urine samples from animals implanted with tantalum did not show a significant enhancement of mutagenic activity in these strains. In depleted uranium-implanted animals, urine mutagenicity increased in a dose- and time-dependent manner demonstrating a strong positive correlation with urine uranium levels (r = 0.995, P < 0.001). There was no mutagenic enhancement of any bacterial strain detected in the sera of animals implanted with either depleted uranium or tantalum pellets. The results suggest that uranium content in the urine is correlated with urine mutagenicity and that urinary mutagenicity might be used as a biomarker to detect exposure to internalized uranium.
Depleted uranium-catalyzed oxidative DNA damage: absence of significant alpha particle decay
Depleted uranium (DU) is a dense heavy metal used primarily in military applications. Published data from our laboratory have demonstrated that DU exposure in vitro to immortalized human osteoblast cells (HOS) is both neoplastically transforming and genotoxic. DU possesses both a radiological (alpha particle) and a chemical (metal) component. Since DU has a low-specific activity in comparison to natural uranium, it is not considered to be a significant radiological hazard. In the current study we demonstrate that DU can generate oxidative DNA damage and can also catalyze reactions that induce hydroxyl radicals in the absence of significant alpha particle decay. Experiments were conducted under conditions in which chemical generation of hydroxyl radicals was calculated to exceed the radiolytic 6 generation by 10 -fold. The data showed that markers of oxidative DNA base damage, thymine glycol and 8-deoxyguanosine could be induced from DU-catalyzed reactions of hydrogen peroxide and ascorbate similarly to those occurring in the presence of iron catalysts. DU was 6-fold more efficient than iron at catalyzing the oxidation of ascorbate at pH 7. These data not only demonstrate that DU at pH 7 can induced oxidative DNA damage in the absence of significant alpha particle decay, but also suggest that DU can induce carcinogenic lesions, e.g. oxidative DNA lesions, through interaction with a cellular oxygen species. Published by Elsevier Science Inc.
Effect of the militarily-relevant heavy metals, depleted uranium and heavy metal tungsten-alloy on gene expression in human liver carcinoma cells (HepG2)
Depleted uranium (DU) and heavy-metal tungsten alloys (HMTAs) are dense heavy-metals used primarily in military applications. Chemically similar to natural uranium, but depleted of the higher activity 235U and 234U isotopes, DU is a low specific activity, high-density heavy metal. In contrast, the non-radioactive HMTAs are composed of a mixture of tungsten (91–93%), nickel (3–5%), and cobalt (2–4%) particles. The use of DU and HMTAs in military munitions could result in their internalization in humans. Limited data exist however, regarding the long-term health effects of internalized DU and HMTAs in humans. Both DU and HMTAs possess a tumorigenic transforming potential and are genotoxic and mutagenic in vitro. Using insoluble DU-UO2 and a reconstituted mixture of tungsten, nickel, cobalt (rWNiCo), we tested their ability to induce stress genes in thirteen different recombinant cell lines generated from human liver carcinoma cells (HepG2). The commercially available CAT-Tox (L) cellular assay consists of a panel of cell lines stably transfected with reporter genes consisting of a coding sequence for chloramphenicol acetyl transferase (CAT) under transcriptional control by mammalian stress gene regulatory sequences. DU, (5–50 μg/ml) produced a complex profile of activity demonstrating significant dose-dependent induction of the hMTIIA FOS, p53RE, Gadd153, Gadd45, NFκBRE, CRE, HSP70, RARE, and GRP78 promoters. The rWNiCo mixture (5–50 μg/ml) showed dose-related induction of the GSTYA, hMTIIA, p53RE, FOS, NFκBRE, HSP70, and CRE promoters. An examination of the pure metals, tungsten (W), nickel (Ni), and cobalt (Co), comprising the rWNiCo mixture, demonstrated that each metal exhibited a similar pattern of gene induction, but at a significantly decreased magnitude than that of the rWNiCo mixture. These data showed a synergistic activation of gene expression by the metals in the rWNiCo mixture. Our data show for the first time that DU and rWNiCo can activate gene expression through several signal transduction pathways that may be
involved in the toxicity and tumorigenicity of both DU and HMTAs.
Transformation of Human Osteoblast Cells to the Tumorigenic Phenotype by Depleted Uranium-Uranyl Chloride
Depleted uranium (DU) is a dense heavy metal used primarily in military applications. Although the health effects of occupational uranium exposure are well known, limited data exist regarding the long-term health effects of internalized DU in humans. We established an in vitro cellular model to study DU exposure. Microdosimetric assessment, determined using a Monte Carlo computer simulation based on measured intracellular adn extracellular uranium levels, showed that few (0.0014%) cell nuclei were hit by alpha particles. We report the ability of DU-uranyl chloride to transform immortalized human osteoblastic cells (HOS) to the tumorigenic phenotype. DU-uranyl chloride-transformants are characterized by anchorage-indeendent growth, tumor formation in mice, expression of high levels of the k-ras oncogene, reduced production of the Rb tumor-suppressor protein, and elevated levels of sister chromatid exchanges per cell. DU-uranyl chloride treatment resulted in a 9.6 (± 2.8) -fold increase in transformation frequency compared to untreated cells. In comparison, nickel sulfate resulted in a 7.1 (± 2.1) -fold increase in transformation frequency. This is the first report showing that a DU compound caused human cell transformation to the neoplastic phenotype. Although additional studies are needed to determine if protracted DU exposure produces tumors in vivio, the implication from these in vitro results is that the risk of cancer induction from internalized DU exposure may be comparable to other biologically reactive and carcinogenic heavy-metal compounds (e.g., nickel). Environ Health Perspect 106:465-471 (1998). [Online 6 July 1998]
Genomic instability in human osteoblast cells after exposure to depleted uranium: delayed lethality and micronuclei formation
It is known that radiation can induce a transmissible persistent destabilization of the genome. We have established an in vitro cellular model using HOS cells to investigate whether genomic instability plays a role in depleted uranium (DU)-induced effects. Transmissible genomic instability, manifested in the progeny of cells exposed to ionizing radiation, has been characterized by de novo chromosomal aberrations, gene mutations, and an enhanced death rate. Cell lethality and micronuclei formation were measured at various times after exposure to DU, Ni, or gamma radiation. Following a prompt, concentration-dependent acute response for both endpoints, there was de novo genomic instability in progeny cells. Delayed reproductive death was observed for many generations (36 days, 30 population doublings) following exposure to DU, Ni, or gamma radiation. While DU stimulated delayed production of micronuclei up to 36 days after exposure, levels in cells exposed to gamma-radiation or Ni returned to normal after 12 days. There was also a persistent increase in micronuclei in all clones isolated from cells that had been exposed to nontoxic concentrations of DU. While clones isolated from gamma-irradiated cells (at doses equitoxic to metal exposure) generally demonstrated an increase in micronuclei, most clonal progeny of Ni-exposed cells did not. These studies demonstrate that DU exposure in vitro results in genomic instability manifested as delayed reproductive death and micronuclei formation.
Published by Elsevier Science Ltd.
Leukemic transformation of hematopoietic cells in mice internally exposed to depleted uranium
Depleted uranium (DU) is a dense heavy metal used in military applications. During military conflicts, US military personnel have been wounded by DU shrapnel. The health effects of embedded DU are unknown. Published data from our laboratory demonstrated thatDUexposure in vitro can transform immortalized human osteoblast cells (HOS) to the tumorigenic phenotype. Results from our laboratory have also shown that DU is genotoxic and mutagenic in cultured human cells. Internalized DU could be a carcinogenic risk and concurrent alpha particle and heavy metal toxic effects complicate this potential risk. Anecdotal reports have suggested that DU can cause leukemia. To better assess this risk, we have developed an in vivo leukemogenesis model. This model involves using murine hematopoietic cells (FDC-P1) that are dependent on stimulation by granulocytemacrophage colony stimulating factor (GM-CSF) or interleukin 3 (IL-3) and injected into mice to produce myeloid leukemia. Although immortalized, these cells are not tumorigenic on subcutaneous inoculation in mice. Intravenous injection of FDC-P1 cells into DU-implanted DBA/2 mice was followed by the development of leukemias in 76% of all mice implanted with DU pellets. In contrast, only 12% of control mice developed leukemia. Karyotypic analysis confirmed that the leukemias originated from FDC-P1 cells. The growth properties of leukemic cells from bone marrow, spleen, and lymph node were assessed and indicate that the FDC-P1 cells had become transformed in vivo. The kidney, spleen, bone marrow, muscle, and urine showed significant elevations in tissue uranium levels prior to induction of leukemia. These results demonstrated that a DU altered in vivo environment may be involved in the pathogenesis of DU induced leukemia in an animal model. (Mol Cell Biochem 279: 97–104, 2005)
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