The widespread contamination of the environment with PCB, a compound used extensively by industry in hydraulic and heat transfer fluids as well as plasticizers and solvents in adhesives and sealants, has resulted in detectable tissue levels in a large portion of the human population, domestic animals, and wildlife. Intoxication with PCB produces severe hepatic necrosis, degeneration of lymphoid tissues and kidney, skin lesions, decreased reproductive performance, reduced feed efficiency, and decreased weight gain. PCB also has been reported to reduce the binding of thyroid hormone to serum proteins and enhance the peripheral metabolism of thyroxine with increased excretion of thyroxine-glucuronide in the bile (Bastomsky, Endocrinology 95: 1150-1155, 1974).The objectives of this investigation were (1) to investigate the histopathologic, histochemical, and ultrastructural changes in thyroid FC produced by the acute (4 week) and chronic (12 week) administration of low (50 ppm) and high (500 ppm) doses of PCB to rats, (2) to correlate these alterations to changes in serum immunoreactive thyroxine concentration, and (3) to investigate the persistence of the effects of PCB on the thyroid gland.
