TOXICOLOGY STUDIES OF LEAD

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A study was conducted to compare the toxicity and bioavailability of lead in male F344 rats exposed to pure lead salts or to lead ore from Skagway, AK. The chemicals were fed to rats for 30 days. At study termination lead concentrations in blood, bone, kidney, and brain, and urinary aminolevulinic acid were measured. The soluble lead salts, lead oxide and lead acetate, accumulated to a greater degree in bone and soft tissues than the insoluble lead sulfide or the lead ore from Skagway, AK. there was a strong correlation between dose and bone lead concentration for either soluble or insoluble lead samples when the data were graphed on a long- linear scale. Use of the aminolevulinic acid biomarker was ineffective at bone lead concentrations below 20 mug/g. Blood lead concentrations were ~ 80 mug/dl in rats fed the soluble lead salts, and ~ 10 mug/dl in rats fed lead sulfide or lead ore. The highest lead concentrations in soft tissue occurred in kidney, followed by brain. Rats fed soluble lead salts accumulated about 10-fold higher lead concentrations in the soft tissues compared to those fed lead sulfide or lead ore. However, detectable and potentially toxic concentrations of lead accumulated in a dose-related fashion in kidney and brain of rats fed the less soluble lead samples, and to a higher degree in rats fed lead ore compared to those fed lead sulfide. These data suggest that longer exposure periods might result in continual and greater accumulations of lead. Kidney lesions occurred in rats dosed with 30 or 100 ppm lead acetate but not in other treatment groups. Lead ore samples from three other mining sites, Alaska, Missouri, and Colorado, are being fed to rats for longer periods (90 days) to compare the bioavailability and toxicity or ores from different geographical areas. Assays of blood ?-aminolevulinic acid dehydratase enzyme activity, a sensitive and specific biomarker for lead toxicity, and determinations of lead in blood, kidney, and brain are being conducted at 30, 60, and 90d exposure. Data from the 30d samples indicate that at 100ppm in the feed two samples, Alaskan lead ore and Missouri lead ore, significantly inhibited blood ALAD enzyme activity.