MCNABB, F.M.A.: Avian Thyroid Development In Organochlorine-Polluted Environments: Is There Evidence Of Thyroid Disruption And Teratogenesis?

Developmental abnormalities, reduced reproduction, and behavioral alterations in wild birds in some areas of the Great Lakes (GL) have led to >25 years of toxicological monitoring of herring gull populations. Organochlorine pollutants, especially polychlorinated biphenyls (PCBs), are widespread contaminants in some parts of the GL. Since manufacture of PCBs was halted in the late 1970s, their concentrations in avian eggs and tissues has decreased, although PCBs are far higher in the most polluted sites than the reference sites. Developmental abnormalities, thyroid gland histopathology and increases in liver enzymes in embryos and chicks of herring gulls from high PCB sites in the GL have led to speculation that PCBs are altering thyroid development and function, and subsequently altering other developmental processes in these birds. However, although PCB exposure is associated with hypothyroidism in laboratory rats, much less is known of PCB effects on avian thyroid development or function. Our studies of thyroid development in herring gull populations from the GL show that both embryonic and prefledgling herring gulls from high PCB sites have marked depletion of thyroid gland hormone stores compared to gulls at the reference sites. Developing gulls at most sites do not show evidence of overt hypothyroidism but the consequences of thyroid gland hormone depletion may only be apparent under stressful environmental conditions. Studies of other avian species in GL and western Europe also show a more variable relationship between thyroid alterations and environmental PCB exposure than has been shown in studies of rats. This paper will examine the evidence for avian thyroid disruption and developmental abnormalities in relation to PCB exposure in the environment and in laboratory studies.