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 (TEC(egg)s) 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 TEC(egg)s 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 TEC(egg)s. 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.

Two methods for deriving bioaccumulation factors (BAFs) used by the U.S. Environmental Protection Agency in development of water quality criteria were evaluated using polychlorinated biphenyl (PCB) data from the Hudson River and Green Bay ecosystems. One method predicts BAF(L)fd values (BAFs based upon concentrations of freely dissolved chemical in ambient water and in the lipid fraction of tissue) using field-measured biota-sediment accumulation factors (BSAFs): greater than 90% of the predicted BAF(L)fd values were within a factor of 5 of their measured values for both ecosystems. The second method predicts BAF(L)fd values as the chemical's 1-octanol/water partition coefficient (Kow) times a food chain multiplier: greater than 90% of the predicted BAF(L)fd values were within a factor of 5 of their measured values for the Green Bay ecosystem and for three of the six sampling locations on the Hudson River. Poorer predictive ability with the Kow method for the other three sampling locations was believed to be due to the existence of environmental conditions not representative of the longer term ecosystem conditions assumed for the method. BAF(L)fd and BAF(T)t values (BAFs based upon concentrations of total chemical in ambient water and in wet tissue) were compared. The within ecosystem and across ecosystems comparisons demonstrated a 2-5-fold decrease in variability (expressed as ratios of coefficients of variation, percentile ranges, and confidence ranges) for predicted BAF(L)fd values in comparison to BAF(T)t values.

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