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Fathead minnows (Pimephales promelas) and oligochaetes (Lumbriculus variegatus) were exposed in the laboratory to sediment samples from the lower Fox River/Green Bay, and their bioaccumulation of PCBs was compared with PCB concentrations in synoptic collections of fish (black bullhead, Ameiurus melas) and oligochaetes (primarily Limnodrilus sp.) from the field. Total PCBs and PCB homologues (expressed as lipid-normalized tissue concentrations/organic carbon-normalized sediment concentrations) were qualitatively and quantitatively similar in the laboratory-exposed and field-collected oligochaetes. PCB concentrations in A. melas generally were greater than in any of the other test species, due possibly to differences in exposure (e.g. biomagnification) compared with the other organisms. PCB concentrations in P. promelas were consistently smaller than in any of the other species investigated. These results indicate that, under the exposure regime used in this study, laboratory tests with L. variegatus can provide a reasonable quantitative estimate of the bioaccumulation of PCBs in field populations of oligochaetes. However, the use of P. promelas in laboratory sediment tests may result in significant underprediction of the exposure of indigenous benthic invertebrates and fishes to bioaccumulable contaminants.

The toxic effects of 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) to fathead minnow (Pimephales promelas), channel catfish (Ictalurus punctatus), lake herring (Coregonus artedii), medaka (Oryzias latipes), white sucker (Catastomus commersoni), northern pike (Esox lucius), and zebrafish (Danio danio) were observed during early life‐stage development after waterborne exposure of fertilized eggs. Species sensitivity based on TCDD‐Cegg (TCDD concentration in eggs) was determined by effects observed over a 32‐d period for all species except lake herring in which a 100‐d period was used. Signs of TCDD toxicity, including edema, hemorrhaging, and craniofacial malformations were essentially identical to those observed in salmonids following TCDD egg exposure and preceded or accompanied mortality most often during the period from hatch through swim‐up. The no‐observed‐effect concentrations and lowest‐observed‐effect concentrations, based on significant decreases in survival and growth as compared to the controls, ranged from 175 and 270 pg/g for lake herring to 424 and 2,000 pg/g for zebrafish, respectively. Shapes of concentration–response curves, expressed as TCDD‐Cegg versus percent mortality, were similar for all species and were consistently steep suggesting that the mechanism of action of TCDD is the same among these species. The LCegg50s (concentrations in eggs causing 50% lethality to fish at test termination) ranged from 539 pg/g for the fathead minnow to 2,610 pg/g for zebrafish. Comparisons of LCegg50s indicate that the tested species were approximately 8 to 38 times less sensitive to TCDD than lake trout, the most sensitive species evaluated to date. When LCegg50s are normalized to the fraction lipid in eggs (LCegg,l50s), the risk to early life stage survival for the species tested ranges from 16‐ to 180‐fold less than for lake trout.

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.