PCB Effects on Brain Type II 5'Deiodinase Activity in Developing Brids

PCBs are known to cause thyroid disruption in laboratory rats and are thought to be the causal agent in thyroid gland alterations in herring gulls in the Great Lakes. This study examined the regulation of thyroid hormone supply during development in (1) domestic chicken embryos (Gallus domesticus) exposed to a specific dioxin-like PCB congener (PCB-126) and (2) herring gull (Larus argentatus) embryos and pre-fledglings from Great Lakes sites with different chemical pollutant exposures. Specifically, PCB effects on thyroid status were evaluated by measuring plasma thyroid hormone concentrations and brain type II 5'D activity (to determine if PCB exposure was associated with alteration in brain 5'D type II activity that could maintain local T3 supply to the brain). If PCB-126 and PCB mixtures altered thyroid function, we expected to see decreased plasma thyroid hormone concentrations and subsequent increases in 5'D-II activity. Chicken eggs were injected (into the air cell) before incubation with five dose levels (0.0512, 0.128, 0.32, 0.64, 0.8 ng/g) of PCB-126 (3,3, 4,4',5-pentachlorobiphenyl), or vehicle (sunflower oil); sampling was on day 20 of the 21-day incubation period. Studies on PCB-treated embryos included a preliminary study and a larger study encompassing a serious of smaller studies. Herring gull embryos (at pipping, on day 25 of the 26 day incubation), and 28-day pre-fledgling chicks were sampled (for two field seasons) at several Great Lakes sites with different contaminant exposures (with Kent Island being the reference site). In PCB-treated chicken embryos, there were no statistically significant decreases in plasma T4 or T3 concentrations and no significant increases in brain 5'D-II activity in either the preliminary or the larger study. We found no clear pattern of altered thyroid function in herring gulls from polluted Great Lakes' sites. Plasma TH concentrations were not significantly decreased and 5'D-II activity did not significantly increase in birds from more contaminated sites in comparison to birds from Kent Island or sites with less contamination. Although pipped embryos from Strachnan Island had a significant increase in 5'D-II activity when compared to Kent Island, there were no differences in plasma TH concentrations, and brain 5'D-II activity was not significantly increased in birds from sites with greater PCB loads than Strachnan Island. Plasma T4 and T3 concentrations were significantly decreased in prefledglings from West Sister Island and Detroit Edison in comparison to Kent Island, but there was no subsequent increase in brain 5'D-II activity. The present study is the first to evaluate the potential effects of PCBs, alone and in a mixed environmental exposure, on circulating THs and brain 5'D-II activity in developing birds. Although thyroid function was not altered by the specific PCB congener used in my study or by exposure to environmental pollutants, more complete evaluations are needed before determining whether PCBs alter thyroid function in birds.