While polychlorinated biphenyls (PCB) are fat-soluble environmental pollutants stored breast fatty tissue and secreted in milk; the precise evidence of breast carcinoma from exposure to PCBs remains unclear. The aim of this study was to investigate the dose-response relationship in-utero and lactational exposure of PCBs congener for dimethlbenz[a]anthracene (DMBA)-induced rat mammary carcinogenesis. Female SD rats were injected (i.g.) with 25 pg, 2.5 ng, 250 ng, 7.5 μg of 3,3',4,4',5-pentachlorobiphenyl (PCB126)/kg, or the vehicle, on days 13 to 19 post-conception. Fifty-day-old female offspring were injected (i.g.) with 20 mg DMBA. The concentration of PCB in the liver of the 50-day-old was compared to the vehicle-group, found to be 530-fold higher in the 7.5 μg-group, nearly 21-fold higher in the 250 ng-group, nearly 2.4-fold in the 2.5 ng-group, and nearly 1.2-fold in the 25 pg-group. The expression of CYP1A1 in the liver of the 50-day-old was intensive in the 7.5 μg- and 250 ng-groups, and slight in the 2.5 ng-group, and not observed in the other groups. The observation was terminated when the pups were 170-day-old or the tumor size reached 20mm in diameter. The 7.5 μg-group showed a reduction of mammary carcinogenesis, but the 250 ng- and 2.5 ng-groups revealed increases incidence of carcinoma, while the 25 pg-group showed a similar incidence of the vehicle-group. The time course of tumor development of the 7.5 μg-group was significantly lower than that of the other groups, but that of the 250 ng-group was significantly higher, and that of the 2.5 ng- and 25 pg-groups was similar to that of the vehicle-group. Moreover, the tumors of the 250 ng-group showed the highest cell proliferation, anuploid tumor index, and nuclear grade when compared to those of the other groups. The present studies indicate that in-utero and lactational exposure of relatively low dose PCB acts as an enhancing agent toward DMBA-induced rat mammary carcinogenesis, but that of high dose PCB acts as an inhibiting agent. This effect partly may be due to the in vivo difference at the day of DMBA exposure (50-day-old); between the concentration of PCB and the expression of phase I drug-metabolize enzymes (CYP1A1) converting DMBA into the ultimate carcinogen.