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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 (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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The concentration of 19 PCB congeners was analysed in biota, sediments, water, and suspended solids in four central Ontario lakes in which atmospheric deposition was the major source of PCB contamination. Input from the atmosphere resulted in total congener concentrations of 1–2 ng∙L−1 dissolved in water, 10–50 μg∙kg−1 (dry weight} in sediment, 5–10 μg∙kg−1 (wet weight) in biota from lower trophic levels (i.e. zooplankton, golden shiner (Notemigonus crysoleucas)), and 10–30 μg∙kg−1 (wet weight) in fish from upper trophic levels (yellow perch (Perca fiavescens), smallmouth bass (Micropterus dolomieui)). The dominant PCB congeners in the lakes were the trichlorobiphenyl congeners 31(28} and the hexachlorobiphenyl congeners 153 and 138, consistent with congener distributions reported for vapour- and particulate-bound PCBs in the atmosphere. Discriminant analysis indicated slight differences in congener patterns between the study lakes, but the general pattern for isolated lakes was substantially different from point-source contaminated lakes, primarily due to the high proportion of congeners 31(28). There was no significant difference in the total PCB concentrations in biota (lipid basis) between lakes, but within the lakes, total PCB concentrations were significantly higher in yellow perch than in biota from lower trophic levels.

Sediments from Hamilton Harbour and an uncontaminated control site were collected and extracted for organic contaminants to investigate the putative association between chemical contaminants and high incidences of fish tumours in Hamilton Harbour. Sediment extract from Hamilton Harbour had high levels of polynuclear aromatic hydrocarbons and was mutagenic in the Ames bacterial mutagenicity assay. In two sets of experiments using a trout sac-fry microinjection route of exposure, Hamilton Harbour sediment extract induced hepatocellular carcinomas in rainbow trout (Salmo gairdneri).

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