Nickel ingestion by women resulted in an increase in interleukin-5 levels 4 h after ingestion and a decrease in CD4+ and an increase in CD8+ lymphocytes 24 h following the nickel intake. Thus, alterations in the immune response may be associated with excessive nickel ingestion, consistent with reports of tumor production in animals and humans by inhalation of nickel-containing dust or powders. The mechanism for nickel-associated toxicity is purported to be oxi-dative. For bismuth, neurotoxicity, including irritability, numbness and tingling of the extremities, insomnia, poor concentration, impairment of short-term memory, tremors, dementia masquerading as Alzheimer's disease, and abnormal electroencephalograms, has been reported. Discontinuation of the bismuth may result in restoration of normal neurological function. Production of these symptoms in animals was associated with a brain bismuth concentration of 8 mgg 1 brain tissue; a brain bismuth concentration of 4 mgg 1 brain tissue was not associated with these neurotoxic manifestations. However, hydrocephalus was reported. At 1 mg bismuth g-1 brain tissue, no neurotoxic features were observed in animals. Nephropathy, osteoar-thropathy, and thrombocytopenia have also been reported with bismuth toxicity.

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