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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

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Mid-Continent Ecology Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, 6201 Congdon Boulevard, Duluth, Minnesota 55804, Great Lakes Environmental Research Laboratory, National Oceanographic and Atmospheric Administration, 2205 Commonwealth Boulevard, Ann Arbor, Michigan 48105-1593, Department of Chemical Engineering, University of MinnesotaDuluth, 1303 Ordean Court, Duluth, Minnesota 55812-3025, NIEHS Marine and Freshwater Biomedical Sciences Center, University of WisconsinMilwaukee, 600 East Greenfield Avenue, Milwaukee, Wisconsin 53204, Molecular and Environmental Toxicology Center, University of WisconsinMadison, 1710 University Avenue, Madison, Wisconsin 53726-4098, and School of Pharmacy, University of Wisconsin, 777 Highland Avenue, Madison, Wisconsin 53705-2222
Cite this: Environ. Sci. Technol. 2003, 37, 17, 3864–3877
Publication Date (Web):July 26, 2003
Copyright © 2003 American Chemical Society

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    Lake trout embryos and sac fry are very sensitive to toxicity associated with maternal exposures to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and structurally related chemicals that act through a common aryl hydrocarbon receptor (AHR)-mediated mechanism of action. The loading of large amounts of these chemicals into Lake Ontario during the middle of the 20th century coincided with a population decline that culminated in extirpation of this species around 1960. Prediction of past TCDD toxicity equivalence concentrations in lake trout eggs (TECeggs) relative to recent conditions required fine resolution of radionuclide-dated contaminant profiles in two sediment cores; reference core specific biota−sediment accumulation factors (BSAFs) for TCDD-like chemicals in lake trout eggs; adjustment of the BSAFs for the effect of temporal changes in the chemical distributions between water and sediments; and toxicity equivalence factors 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 sublethal 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). The toxicity 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.

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     Corresponding author phone:  (218)529-5202; fax (218)529-5003; e-mail:  [email protected].

     U.S. Environmental Protection Agency.

     National Oceanographic and Atmospheric Administration.


     Present address:  Great Lakes Environmental Center.

     University of MinnesotaDuluth.

     University of WisconsinMilwaukee.


     Present address:  S. C. Johnson & Son, Inc.

     University of WisconsinMadison.

     Present address:  College of Pharmacy, University of New Mexico.


     Present address:  Minnesota Department of Health.


     School of Pharmacy, University of Wisconsin.

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    Details of methods used for chemical analyses of fish, egg, and sediment samples and radionuclide dating of sediments. This material is available free of charge via the Internet at

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