PCB exposure has been associated with a reduction in circulating thyroid hormones via several different mechanisms. While thyroid hormones can influence many physiological endpoints in adults, precise concentrations during critical periods of gestation are crucial to normal development. Maternal consumption of PCB contaminated fish has been associated with developmental problems in animals and humans. Alterations of thyroid hormones is postulated to be one possible source of the developmental latencies associated with PCB exposure. Thus, this study investigated the influence of maternal thyroxine supplements in rodents exposed to a low dose of commercial PCBs; Pregnant Long-Evans rats were exposed to one of four doses including: Aroclor 1016 (IP); Aroclor and thyroxine (oral); thyroxine plus saline (IP), or saline. The offspring of all groups were observed for developmental landmarks and were put through a battery of behavior tests. Data were statistically analyzed using SPSS. Litters born to PCB exposed dams had significantly less males than those born to dams in all other dose groups. After receiving Aroclor, pinna unfolding, incisor eruption, and negative geotaxis were delayed and foot splay was wider than the controls. The group receiving both the Aroclor and thyroxine exhibited no statistically significant changes in these endpoints compared to controls. Overall response to startle stimuli was greater in pups after maternal exposure to Aroclor, and this group habituated significantly less than the other groups. Pups in the Aroclor group were most active in the figure 8 maze on average, and least active (and least accurate) in the 5-choice task, although these trends were not statistically significant; The supplementation of thyroxine to PCB exposed rats has provided some insight to the mechanisms underlying thyroid mediated PCB toxicity and suggests further examination into the efficacy of thyroxine to prevent or minimize developmental and behavioral effects in maternally exposed populations
