Adult male mallards were exposed to 0, 4, 20, 100, 250, and 500 mg/kg Aroclor 1254 by gavage twice per week for 5 weeks. Immunotoxic effects, as measured by antibody titers to sheep erythrocytes, natural killer cell activity and lymphocyte mitogenesis to phytohemagglutinin, were not detected as a consequence of polychlorinated biphenyl (PCB) exposure. Hepatic cytochrome P450 activities were measured as microsomal dealkylations of ethoxyresorufin (EROD) and pentoxyresorufin (PROD). Significant elevations in EROD and PROD were noted at 20 mg/kg and peaked in birds treated with 100 mg/kg. Total P450 was induced beginning at 100 mg/kg and peaked at 250 mg/kg. Relative liver weights were dose-dependently increased following treatment with 100 mg/kg or more. Thyroid weights were significantly increased in PCB-treated birds treated with 100 mg/kg or greater, but no significant histological abnormalities were observed, except at the highest dose. Plasma total triiodothyronine (T3) was decreased in a dose-dependent manner, with a significant lowest-observed-adverse-effect level (LOAEL) of 20 mg/kg. T3 was decreased following 7 days treatment with 100 mg/kg. The no-observed-adverse-effect level (NOAEL) was 4 mg/kg for decreased T3. Plasma glucose levels were decreased on days 28 and 35 in mallards treated with 500 mg/kg, while other clinical plasma biochemistry parameters were unaltered by PCB treatment. Plasma corticosterone levels were unchanged by PCB treatment. These results indicate that thyroid hormone levels and P450 activity in mallards are sensitive to subchronic PCB exposure in the absence of gross toxic effects and immunotoxicity.