We hypothesized that populations exposed to chronic levels of genotoxins for many generations in situ will accumulate latent heritable genetic damage leading to increases in mutational load and decreased population fitness. Common pulmonate snails (Lymnaea stagnalis) were collected from three sites that differed in pollution level [Manitoulin Island (reference), Beauharnois (moderate pollution), and Varennes (highly polluted)]. These organisms have a rapid generation time and are capable of self-fertilization. Fitness indicators were clutch size, survival (hatching to day 30) and growth (length from hatching to day 90). Recessive deleterious mutations that have accumulated through time are masked as snails preferentially outcrossed, but are expressed when snails self-fertilize. Results obtained by comparing fitness components of snails derived from selfing and outcrossing experiments showed that in sites with higher levels of pollution inbreeding depression increased for clutch size and survival. Results for growth rate were similar to those for clutch size and survival in the two least polluted sites, but not for the most polluted site, due possibly to biased mortality of smaller snails at this site. After correction for size biased mortality, the growth estimates showed patterns similar for the two polluted sites when compared to the reference site. This study suggests that long-term in situ exposure to genotoxic pollution may effect population fitness due to the accumulation of latent heritable genetic damage.

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The goal of this thesis was to examine the sources and ecological behaviour of genotoxic organics in the St. Lawrence river system. A rapid and effective version of the SOS Chromotest was developed to accomplish the task of genotoxicity assessment. The method, validated with standard reference materials, is particularly well suited to complex environmental extracts. The endpoint investigated throughout the thesis, SOS genotoxicity, is empirically related to more familiar endpoints such as mutagenicity and carcinogenicity. Analyses of literature data confirmed correlations between SOS genotoxicity and both Ames/Salmonella mutagenicity and animal carcinogenicity. Analyses of industrial and municipal wastewaters revealed that organic and inorganic chemical production facilities, metal refining and founding facilities and petroleum refineries release high potency wastes. Loading values indicate that low potency sources (e.g. municipal wastewater and pulp & paper facilities) often have exceptionally high loadings. A substantial portion (2.3-99.8%) of industrial genotoxins are associated with suspended particulates. Sorption partition efficients (K$ sb{ rm d-genotox}$) indicate that municipal wastewater and pulp & paper facilities release particularly soluble genotoxins. Extracts of suspended particulate matter collected near industrial discharges are direct-acting. Bottom sediment extracts are less potent and usually require S9 metabolic activation. Genotoxicity of both bottom sediment and suspended particulates are empirically related to the genotoxicity of regional industrial emissions. Direct-acting substances in the water column appear to be less stable and may be converted to more stable pro-genotoxic substances present in the bottom sediments. A mass balance of genotoxicity for St. Lawrence surface waters revealed that domestic, rather than industrial sources make the largest contribution to observed genotoxicity. The importance of domestic wastes was confirmed

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