The committee concludes that there is limited/suggestive evidence of no association between exposure to uranium and clinically significant renal dysfunction.
The committee carefully examined the studies on neurological outcomes as these outcomes are of interest in the study of Gulf War-related illnesses. Uranium has been shown in several animal studies to enter the brain of animals exposed through either inhalation or implantation of fragments of depleted uranium (see toxicology section). The mortality experiences of uranium processing workers (Table 4.15) generally show no excess neurologic disease mortality risks, with the exception of one study in which workers at a nuclear fuels fabrication plant had an SMR of 346 (95% CI 126–753) for death from diseases of the nervous system (Hadjimichael et al., 1983). There were 6 deaths from diseases of the central and peripheral nervous system and only 1.7 expected deaths. However, the number of cases was small, and the 95% CI was very wide. It is important to note that mortality is not a good measure for neurologic outcomes as they may not be the cause of death noted on the death certificate.
Several case studies have examined neurological outcomes or symptoms. Moore and Kathren (1985) studied three individuals 38 years after they were exposed to high concentrations of uranium (estimates of initial lung deposition of 40–50 mg of uranium) after an industrial accident. Shortly after the accident an examination found “mental status changes believed in excess of what which would be caused by fear reaction.” No other details were provided. Examination of two of these individuals 38 years after the accident revealed no clinical findings attributable to uranium exposure (Moore and Kathren, 1985; Kathren and Moore, 1986). Neurological symptoms were also absent in an examination of a male worker 6 days after he had a 5-minute accidental exposure to uranium tetrafluoride powder (an estimated radioactivity of 197 nCi/m3; 6,905.6 Bq/m3) (Lu and Zhao, 1990).
A case report described a 44-year-old man who developed foot cramps, leg pain, a gait disorder, and a tendency to fall backward (Goasguen et al., 1982). The symptoms progressed and he developed an extrapyramidal syndrome with ataxia, nystagmus, and peripheral neuropathy. Although the authors claimed that the etiology of his illness was related to a bar of metallic uranium that he handled frequently during the first 3 years of his illness, they presented no estimates of the level of exposure of this patient to uranium and did not make a convincing argument for its causal role in his illness.
The committee found no studies of neurological symptoms after human exposure to uranium by either the oral or the dermal route.
McDiarmid and colleagues (2000) studied a cohort of Gulf War veterans who had fragments of depleted uranium in their soft tissues. As noted in the preceding section, the veterans excreted substantial amounts of uranium, presuma-