You are here:
DECLINE AND EXTINCTION OF LAKE TROUT IN THE GREAT LAKES: CAN BIOLOGICAL INDICATORS HELP DIAGNOSE CAUSES, IDENTIFY REMEDIAL ACTIONS, AND PREDICT FUTURE CONDITIONS?
Citation:
Cook, P. M. DECLINE AND EXTINCTION OF LAKE TROUT IN THE GREAT LAKES: CAN BIOLOGICAL INDICATORS HELP DIAGNOSE CAUSES, IDENTIFY REMEDIAL ACTIONS, AND PREDICT FUTURE CONDITIONS? Presented at Indicators in Health and Ecological Risk Assessment, 5th NHEERL Symposium, RTP, NC, June 6-8, 2000.
Description:
The lake trout, Salvelinus namaycush, is the predominant top predator native fish species of the Great Lakes. Lake trout are valued for commercial and recreational use in addition to their ecological importance. In the last half of the 20th century, population declines lead to virtual extinction of lake trout in all the Great Lakes except for Lake Superior. In 1991 NHEERL's research on bioaccumulation of 2,3,7,8-tetrachlorodibenzo (TCDD) in Lake Ontario and the University of Wisconsin's discovery of the extreme sensitivity of lake trout for early life stage mortality associated with exposure of embryos to TCDD lead to a collaborative risk assessment effort. Concentrations in lake trout eggs of TCDD and structurally related polyhalogenated aromatic chemicals that may act through an aryl hydrocarbon receptor (AhR) mediated mechanism of action thus became specific indicators of toxicity risks. A lake trout-specific additive toxicity equivalence model and a reconstruction of historical lake trout embryo exposures in Lake Ontario from the sediment record and congener specific biota sediment accumulation factors (BSAFs) were developed. 100% mortality of sac fry from the 1940s into the 1970s with partial mortality continuing into the 1980s was predicted. This was consistent with the decline of lake trout populations to extinction by 1960 and the failure to achieve natural reproduction following reintroduction of large numbers of adult fish through stocking of yearlings since 1973. Chemical residue data for herring gull eggs confirmed the presence of supra lethal exposures for lake trout in the early 1970s. Evidence of dioxin toxicity to sac fry reared from eggs collected from stocked lake trout in the early 1980s and progressive improvement in survival of feral sac fry in the 1990s supported the TCDD toxicity predictions. Uncertainty for levels of TCDD and other AhR agonists that may cause decreased survival of young lake trout through chronic effects makes it - - - -