Many people hear the word uranium (U) and think of Chernobyl, or more recently Fukushima. The risk of possible nuclear disasters is a difficult one to communicate to the public. Nevertheless, risk incorporates both effects and probability of exposure, which is an important distinction needed in assessing the risk of U use in society. Exposure to U from nuclear energy production (and resulting “nuclear disaster”) may produce more severe adverse effects, but are less likely to occur than effects associated with exposure to U via metal mining, U containing fertilizers, or from depleted uranium (DU) incorporated into ammunition and military armour. Thus, the risk of U should focus on both effects of U exposure and the likelihood of U exposure.
U is a naturally occurring metal that displays both chemically toxic and radiotoxic properties. U consists of three radioactive isotopes (238U -99.27%, 235U –0.72%, and 234U –0.0057% abundance), emitting alpha particles in the decay process. Thus, U particles do not easily penetrate and are considered to be weakly radioactive due to the long half-lives of U isotopes (105-109 years) (ATSDR, 1999). Radiotoxic effects can thus only occur from internal exposure of U because alpha particles cannot travel far through air and do not penetrate clothing.
Investigation of the radiotoxic and chemotoxic effect of U peaked in the 1990’s due to the increasing use of DUenhanced armour and munitions. DU is a by-product of U enrichment processes, and as a result contains less 235U than natural U and has 60% less radioactivity than natural U (Bleise et al. 2003; McDiarmid et al. 2000). Due to the high density of DU, its availability, and low cost, DU is favoured for military use and is considered effective because of its self-sharpening and pyrophoric abilities. DU is incorporated in defensive armour plating and armour-piercing projectiles. However, there is a growing concern regarding the potential long-term impacts on human health for both military personnel and civilians exposed to or surrounding high conflict areas. Particular interest arose from veterans that fought in the Gulf War and reported a variety of symptoms that are referred to as the “Gulf war syndrome” (Bleise et al. 2003). Conflicting reports have been published over the last two decades suggesting two extremes; (1) there is no evidence that DU is causing adverse effects, and (2) DU exposure is responsible for a number of cancer and non-cancer health effects.
It is generally concluded that due to the low- specific activ ity of DU, chemical toxicity is the more significant contributor to DU effects in humans, with the kidney considered to act as the critical target organ (McDiarmid et al. 2000; Squibb et al. 201 2). Howev er, effects from radiation should not be completely disregarded as results from in vitro tests with human osteoblast cells hav e shown that radiation can play a role in DU- induced biological effects (Miller et al. 2002). Other target receptors of DU exposure in humans include the brain, liv er, heart, lung, and other sy stems (Lestaev el et al. 2005; Bleise et al. 2003; WHO, 2001 ). The pathway s for exposure of DU include ingestion, inhalation and dermal routes. Ingestion of DU can occur from direct ingestion of contaminated soil and consumption of contaminated water, but is not considered a major exposure pathway (Bliese et al. 2003). Dermal exposure can occur via embedded fragments, shrapnel contamination, or wound contamination from depleted U oxides in the form of dust. Nev ertheless, dermal exposure is considered a relativ ely unimportant route since little DU will pass across the skin into the blood (WHO, 2001 ). Inhalation is considered the major route of exposure for DU in both combat and non- combat situation.DU aerosols arise from impacts of DU- enhanced projectiles with hard surfaces creating dust containing U oxides, which can accumulate in the lungs.
Debate has arisen with regard to the actual outcomes of acute and chronic exposure of DU. Some believe and have concluded that the human epidemiological evidence is in support of increased risk of birth defects in offspring from those exposed to DU (Hindi et al. 2005). In addition to reproductive effects conclusions from epidemiological studies and animal toxicity tests have suggested DU has immunotoxic, neurotoxic, carcinogenic and leukemogenic potential (Briner and Murray 2005; Lestaevel et al. 2005; Miller et al. 2005). In contrast, the World Health Organization and other studies have concluded that there is no risk of reproductive, developmental, or carcinogenic effects in humans due to DU exposure (Bleise et al. 2003, McDiarmid et al. 2013; WHO, 2001). A twenty year follow-up of a DU exposed military cohort confirmed previous evidence that there are no U-related health effects in organ systems known to be targets of U in an extensive general health assessment in veterans (McDiarmid et al. 2013). Criticism of reproductive toxicity arise in the difficulty to establish a causal pathway between human parental DU exposure and the birth defects of offspring. Hindi et al. (2005) highlights that the mechanism by which DU is internalized and reaches reproductive cells is still not fully understood. Another drawback is that epidemiological studies must deal with the separation of DU exposure from other teratogens and the limited available documentation of individual parental exposure to DU. There is also an uncertainty regarding the long term radiation effects, with little information stated in the literature about dose-response curves for health effects caused by radiation exposure.
It is understandable that society likes to be caution when it comes to health effects in connection with possible radiation and/or chemical toxicity of uranium. Studies are needed to improve our understanding of the extent, reversibility, and possibility of threshold levels for kidney and other target organ damage. Toxicity will be a function of route of exposure, particle solubility, contact time, and rate of elimination. WHO (2001) has set a tolerable daily intake (TDI) of 0.5 μg/kg BW/d for soluble U (more toxic) and 5 μg/kg BW/d for insoluble (less toxic), with an inhalation limit of 1 μg/m3 (either U solubility). As discussed in class, background exposure may also be important in assessing the estimated exposure to a contaminant and should be considered. Background exposure of DU to civilians include use of DU in counterweights of aircrafts, industrial radiography equipment, radiation shielding in medical radiation therapy, and containers used to transport radioactive materials (Bleise et al. 2003). One of the uncertainties in the population studies of veterans in the Gulf war includes pre-war exposure of DU and overall health assessments. Better characterisation of exposure before, during and after use in conflict will allow countries to better assess the risk associated with DU use for military purposes. However, a bias might exist in countries that put more weight on the benefit of DU use in their militaries, while others are concerned with the potential but unproven long-term health effects of DU. Overall, the risk of DU is a controversial topic with many viewpoints, some of which should be considered with caution.
[ATSDR] Agency for Toxic Substances and Disease Registry. 2013. Toxicological profile for Uranium. Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service. http://www.atsdr.cdc.gov/toxprofiles/TP.asp?id=440&tid=77
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Briner, W., and Murray, J. (2005). Effects of short-term and long-term depleted uranium exposure on open-field behavior and brain lipid oxidation in rats. Neurotoxicology and teratology, 27(1), 135-144. http://www.sciencedirect.com/science/article/pii/S0892036204001321
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McDiarmid, M. A., Engelhardt, S., Oliver, M., Gucer, P., Wilson, P. D., Kane, R., and Squibb, K. S. (2004). Health effects of depleted uranium on exposed Gulf War veterans: a 10-year follow-up. Journal of Toxicology and Environmental Health, Part A, 67(4), 277-296. https://18.104.22.168/downloads/Env_Health%20Effects_DU.pdf
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Miller, A. C., Bonait-Pellie, C., Merlot, R. F., Michel, J., Stewart, M., and Lison, P. D. (2005). Leukemic transformation of hematopoietic cells in mice internally exposed to depleted uranium. Molecular and cellular biochemistry, 279(1-2), 97-104. http://www.nukewatchinfo.org/du/leukemiainmice2005.pdf
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[WHO] World Health Organization. (2001). Depleted Uranium, Sources, Exposure and Health Effects. WHO, Geneva. http://www.who.int/ionizing_radiation/pub_meet/en/DU_Eng.pdf