ABSTRACT

Uranium (U) and depleted uranium (DU) are only now being investigated in detail for their potential neurotoxicity. It is reasonable to assume that detailed studies of the clinical neurotoxicity of uranium are lacking because the kidney is historically considered to be the target organ of clinical uranium toxicity. The resultant renal failure and tumor formation from uranium poisoning were more important in uranium workers than potential CNS effects. The entry of DU into the environment, and the potential for chronic low-dose exposure to a slightly radioactive form of uranium, is shifting research to examine subclinical effects, with the brain a likely target. DU and native U are chemically identical. It is suspected that the neurotoxicity of DU is largely from its chemical activity.