Rats that received Cd 300 ppm in drinking water (average daily Cd intake = 4.5 mg/rat) for 12 wk attained peak Cd levels of 112, 34 and 19 .mu.g/g in hair, liver and kidney, respectively, at wk 4. Rats that ingested Cd 200 ppm (average daily Cd intake = 3.6 mg/rat) for 13 wk attained peak Cd levels of 29 .mu.g/g in kidney at wk 7, and 94 and 27 .mu.g/g in hair and liver, respectively, at wk 9. Despite continuous exposure to the heavy metal, tissue Cd concentrations declined to steady-state levels of 24-33 .mu.g/g in hair and 10-17 .mu.g/g in liver and kidney. Histopathologic effects were not observed in liver or kidney. In contrast to Cd in hair, blood Cd levels, which remained consistently low (< 0.04 .mu.g/ml) throughout the study, did not correlate with changes in Cd levels in liver and kidney. [Cd in humans due to environmental and occupational exposure is discussed.].
