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EFFECTS OF ARYL HYDROCARBON RECEPTOR MEDIATED EARLY LIFE STAGE TOXICITY ON LAKE TROUT POPULATIONS IN LAKE ONTARIO DURING THE 20TH CENTURY
Citation:
Cook, P. M., J. A. Robbins, D D. Endicott, K. B. Lodge, P. D. Guiney, M. K. Walker, E. W. Zabel, AND R. E. Peterson. EFFECTS OF ARYL HYDROCARBON RECEPTOR MEDIATED EARLY LIFE STAGE TOXICITY ON LAKE TROUT POPULATIONS IN LAKE ONTARIO DURING THE 20TH CENTURY. ENVIRONMENTAL SCIENCE & TECHNOLOGY. American Chemical Society, Washington, DC, 37(17):3864-3877, (2003).
Description:
Lake trout embryos and sac fry are very sensitive to toxicity associated with maternal exposures to 2,3,7,8-tetrachlorodibenza-p-dioxin (TCDD) and structurally related chemicals that act through a common aryl hydrocarbon receptor (AHR)- mediated mechanism of action. The presence of large amounts of these chemicals in Lake Ontario during the later half of the twentieth century coincided with a population decline that culminated in extirpation of this species around 1960. A retrospective risk assessment was conducted in order to establish and validate a model for prediction of exposure conditions under which AHR-mediated toxicity will not contribute to future sac fry mortality. Past TCDD toxicity equivalence concentrations in lake trout eggs (TECeggS) were predicted from radionuclide dated sediment core sections. Assessment of exposures of lake trout embryos over time relative to recent conditions required fine resolution of radionuclide dating profiles in two sediment cores; reference core specific biota-sediment accumulation factors (BSAFs) for TCDD-like chemicals in lake trout eggs; adjustment of BSAFs for the effect of temporal changes in the chemical distributions between water and sediments; and toxicity equivalence factors (TEFs) based on trout early life stage mortality. When compared to the dose-response relationship for overt early life stage toxicity of TCDD to lake trout, the resulting TECeggS predict an extended period during which lake trout sac fry survival was negligible. By 1940, following more than a decade of population decline attributable to reduced fry stocking and loss of adult lake trout to commercial fishing, the predicted sac fry mortality due to AHR-mediated toxicity alone explains the subsequent loss of the species. Reduced fry survival, associated with lethal and sub-lethal adverse effects and possibly complicated by other environmental factors, occurred after 1980 and contributed to a lack of reproductive success of stocked trout despite gradually declining TECeggS. Present exposures are close to the most probable no observable adverse effect level (NOAEL TECegg = 5 pg TCDD toxicity equivalence/g egg). These predictions are very consistent with the available historical data for lake trout population levels in Lake Ontario, stocking programs, and evidence for recent improvement in natural reproduction concomitant with declining levels of persistent bioaccumulative chemicals in sediments and biota.