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REDUCING EXPOSURE UNCERTAINTY FOR ASSESSMENT OF DIOXIN TOXICITY RISKS TO LAKE TROUT POPULATIONS IN THE GREAT LAKES
Citation:
Cook, P. M. REDUCING EXPOSURE UNCERTAINTY FOR ASSESSMENT OF DIOXIN TOXICITY RISKS TO LAKE TROUT POPULATIONS IN THE GREAT LAKES. Presented at 21st SETAC Annual Meeting, Nashville, TN, November 12-16, 2000.
Description:
During the 20th century, declines of lake trout (Salvelinus namaycush) populations to virtual extinction in all the Great Lakes except Lake Superior were followed by failure of stocked lake trout to achieve recruitment through natural reproduction. Stresses such as excessive harvesting, sea lamprey predation, habitat and water quality degradation, and thiamine deficiency associated with exotic species in the diet have been implicated in different stages o fthe problems faced by this keystone species. Lake trout were found in the early 1990s to be the most sensitive fish species known for early life stage mortality caused by embryo exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The toxicity symptoms were identical to "blue sac disease" observed in sac fry from stocked lake trout in Lake Ontario. Trout early life stage mortality-specific toxicity equivalence factors (TEFs) were developed for other polychlorinated dibenzo-p-dioxins, dibenzofurans,and biphenyls that could actthrough the same arylhydrocarbon receptor (AhR) mediated mechanism as TCDD. The additive toxicity equivalence model, applied to measured congener concentrations in lake trout eggs, indicated that lake trout in the 1990s were likely below the threshold for overt mortality in the sac fry stage. Concern for dioxin toxicity contributions to present lake trout recruitment problems hinges in part on uncertainty for extrapolation of toxicology research results to lake trout under ecological conditions in the Great Lakes and in part on uncertainty for chronic effects. Retrospective risk analysis for Lake Ontario indicates that exposures of lake trout to TCDD and related AhR agonists from approximately 1940 to 1985 would cause reproductive failure independent of effects from other stressors. Temporal and spatial uncertainty for theexposure predictions, based on estensive contemporary and historical monitoring data, radionuclide dated sediment core analyses, and interpretation of biota - - -