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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• 作者：Philip M. Cook ; John A. Robbins ; Douglas D. Endicott ; Keith B. Lodge ; Patrick D. Guiney ; Mary K. Walker ; Erik W. Zabel ; and Richard E. Peterson
• 刊名：Environmental Science & Technology
• 出版年：2003
• 出版时间：September 1, 2003
• 年：2003
• 卷：37
• 期：17
• 页码：3864 - 3877
• 全文大小：550K
• 年卷期：v.37,no.17(September 1, 2003)
• ISSN：1520-5851

文摘

Lake trout embryos and sac fry are very sensitive totoxicity associated with maternal exposures to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and structurally relatedchemicals that act through a common aryl hydrocarbonreceptor (AHR)-mediated mechanism of action. The loadingof large amounts of these chemicals into Lake Ontarioduring the middle of the 20th century coincided with apopulation decline that culminated in extirpation of thisspecies around 1960. Prediction of past TCDD toxicityequivalence concentrations in lake trout eggs (TEC_eggs)relative to recent conditions required fine resolutionof radionuclide-dated contaminant profiles in two sedimentcores; reference core specific biota-sediment accumulationfactors (BSAFs) for TCDD-like chemicals in lake trouteggs; adjustment of the BSAFs for the effect of temporalchanges in the chemical distributions between water andsediments; and toxicity equivalence factors based ontrout early life stage mortality. When compared to the dose-response relationship for overt early life stage toxicity ofTCDD to lake trout, the resulting TEC_eggs predict an extendedperiod during which lake trout sac fry survival wasnegligible. By 1940, following more than a decade ofpopulation decline attributable to reduced fry stockingand loss of adult lake trout to commercial fishing, thepredicted sac fry mortality due to AHR-mediated toxicityalone explains the subsequent loss of the species. Reducedfry survival, associated with lethal and sublethal adverseeffects and possibly complicated by other environmentalfactors, occurred after 1980 and contributed to a lack ofreproductive success of stocked trout despite graduallydeclining TEC_eggs. Present exposures are close to the mostprobable no observable adverse effect level (NOAELTEC_egg = 5 pg TCDD toxicity equivalence/g egg). The toxicitypredictions are very consistent with the available historicaldata for lake trout population levels in Lake Ontario,stocking programs, and evidence for recent improvementin natural reproduction concomitant with declininglevels of persistent bioaccumulative chemicals in sedimentsand biota.