Various preparative techniques were used to extract nonpolar organic compounds from the muscle tissue of Lake Ontario rainbow trout (Oncorhynchus mykiss). In this extract, PCBs and organochlorine compounds were detected in nanogramper-milliliter quantities, and polychlorinated dibenzo-p-dioxins and dibenzofurans were detected in picogram-per-milliliter quantities. The extract and various subfractions of the extract were tested for embryotoxicity in a bioassay with embryos of Japanese medaka (Oryzius (atrpes). The whole extract was embryotoxic to medaka, as were an extract fraction containing PCBs (fraction A) and extract fractions containing nonpolar organochlorine compounds (fractions B and C). When subfractions prepared from fraction A were tested for embryotoxicity, a subfraction containing non-ortho-substituted PCB congeners was embryotoxic, whereas subfractions containing mono-ortho-and di-ortho-substituted PCB congeners were relatively nontoxic. Pathological lesions characteristic of exposure to planar halogenated aromatic hydrocarbons were observed only in embryos exposed to the non-ortho-PCB subfraction. The non-ortho-PCB subfraction of fraction A was more toxic than the original fraction A, which indicates that nontoxic PCBs reduce the toxicity of the non-ortho-PCBs through some unknown mechanism. This study indicates that organochlorine compounds and non-ortho-substituted PCBs have the potential to be embryotoxic to early life stages of Great Lakes fish, but nontoxic contaminants can modify this toxic response. These data are relevant to the interpretation of correlations between embryo mortalities and concentrations of persistent organic contaminants in Great Lakes salmonids.

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Various preparative techniques were used to extract nonpolar organic compounds from the muscle tissue of Lake Ontario rainbow trout (Oncorhynchus mykiss). In this extract, PCBs and organochlorine compounds were detected in nanogramper‐milliliter quantities, and polychlorinated dibenzo‐p‐dioxins and dibenzofurans were detected in picogram‐per‐milliliter quantities. The extract and various subfractions of the extract were tested for embryotoxicity in a bioassay with embryos of Japanese medaka (Oryzias latipes). The whole extract was embryotoxic to medaka, as were an extract fraction containing PCBs (fraction A) and extract fractions containing nonpolar organochlorine compounds (fractions B and C). When subfractions prepared from fraction A were tested for embryotoxicity, a subfraction containing non‐ortho‐substituted PCB congeners was embryo‐toxic, whereas subfractions containing mono‐ortho‐ and di‐ortho‐substituted PCB congeners were relatively nontoxic. Pathological lesions characteristic of exposure to planar halogenated aromatic hydrocarbons were observed only in embryos exposed to the non‐ortho‐PCB subfraction. The non‐ortho‐PCB subfraction of fraction A was more toxic than the original fraction A, which indicates that nontoxic PCBs reduce the toxicity of the non‐ortho‐PCBs through some unknown mechanism. This study indicates that organochlorine compounds and non‐ortho‐substituted PCBs have the potential to be embryotoxic to early life stages of Great Lakes fish, but nontoxic contaminants can modify this toxic response. These data are relevant to the interpretation of correlations between embryo mortalities and concentrations of persistent organic contaminants in Great Lakes salmonids.

PCB congener 81 (3,4,4′,5‐tetrachlorobiphenyl) has been detected in fish tissues from various sites in North America. The embryotoxicity of this compound to medaka (Oryzias latipes) and the induction of hepatic aryl hydrocarbon hydroxylase (AHH) in rainbow trout (Oncorhynchus mykiss) were determined to assess the toxic potency of this compound relative to 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) and two other non‐ortho‐substituted PCB compounds, congener 77 (3,3′,4,4′‐tetrachlorobiphenyl) and congener 126 (3,3′,4,4′,5‐pentachlorobiphenyl). The TCDD toxic equivalency factors (TEFs) estimated for congener 81 from two end points in the medaka embryotoxicity assay were 0.0014 (from mortality data) and 0.006 (from swim bladder inflation data). The TEF estimated for congener 81 from data on AHH induction in rainbow trout was 0.004. All TEFs were greater than those estimated for congener 77 but were less than the TEFs estimated for congener 126. On the basis of these toxicity data, it is suggested that this congener may contribute significantly to the toxic burden of planar halogenated aromatic hydrocarbons in fish.

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