Polychlorinated biphenyls (PCB) were added to the diets of mice at different concentrations. Mice fed these diets were given a sc or oral doses of 109Cd. The uptake and excretion of Cd was followed by whole-body counting. The gastrointestinal absorption of Cd after an oral dose of 109Cd was less in animals fed on 66 ppm PCB diet, compared with a control group, and the body elimination of Cd was faster. In the liver, the amount of Cd was reduced by dietary PCB exposure, after both oral and sc administration of 109Cd, and the data suggest a faster transport of Cd from liver to kidneys in PCB-exposed animals than in controls. The mobilized liver Cd was not quantitatively recovered in the kidneys, thus increased urinary excretion due to PCB exposure may have taken place. Histological examination of the livers revealed a dose-dependent induction of liver changes characterized by centrilobular enlargement of liver cells and centrilobular focal necroses. In four of eight livers from animals fed 200 ppm PCB for 32 weeks there were five liver cell tumors with cytological signs of malignancy. In the control group and in groups fed lower doses of PCB (10-100 ppm) no such tumors were found among 28 animals. The results support observations made with agents inducing acute liver damage, that liver damage increases the rate of redistribution of cadmium from the liver to the kidney.