Contaminants are important stressors in the aquatic environment and may exert selective pressures on organisms. We hypothesized that snails originating from a metal-contaminated habitat (B) would have increased tolerance to harbour contaminants (e.g. metals from antifouling paints), compared to snails originating from a relatively clean habitat (A). We assessed tolerance to metals in terms of survival and histopathological alterations after 2, 4 and 8 weeks of in situ exposure in three Baltic Sea boat harbours and three reference sites. We also hypothesized that any potential tolerance to contaminants would be associated with differences in genetic diversity between the two snail populations (evaluated as mitochondrial cytochrome c oxidase subunit I, COI). The results show that snails from population A survived to a higher extent compared to population B, possibly indicating either a lack of adaptation to metals in snails B or impaired health condition due to contaminant pre-exposure or a higher resilience of snails A. Moreover, the genetic diversity of COI was low within each population and did not differ between populations. In general, 83% of all the types of histopathological alterations (e.g. lysis and necrosis of gonads and digestive gland or granulocytoma and phagocytosis in the storage tissue, among others) had a higher probability of occurrence among harbour-exposed snails compared to reference exposed snails, regardless of snail population origin. The only significant difference in histological effects between the two populations was in the frequency of parasite infestations and shell fouling, both being larger for population A than B. Interestingly, the rate of parasite infestations was higher for males than females from population A, whereas no sexual dichotomy was observed for population B. Our results show that exposure to harbour contaminants causes both lethal and sublethal toxicity to snails, and the association between many of the toxic responses and metals substantiates that antifouling substances contribute to the observed effects, although there is a large proportion of variation in our data that remains unexplained.

Oil spills occur commonly, and chemical compounds originating from oil spills are widespread in the aquatic environment. In order to monitor effects of a bunker oil spill on the aquatic environment, biomarker responses were measured in eelpout (Zoarces viviparus) sampled along a gradient in Goteborg harbor where the oil spill occurred and at a reference site, 2 weeks after the oil spill. Eelpout were also exposed to the bunker oil in a laboratory study to validate field data. The results show that eelpout from the Goteborg harbor are influenced by contaminants, especially polycyclic aromatic hydrocarbons (PAHs), also during normal conditions. The bunker oil spill strongly enhanced the biomarker responses. Results show elevated ethoxyresorufin-O-deethylase (EROD) activities in all exposed sites, but, closest to the oil spill, the EROD activity was partly inhibited, possibly by PAHs. Elevated DNA adduct levels were also observed after the bunker oil spill. Chemical analyses of bile revealed high concentrations of PAH metabolites in the eelpout exposed to the oil, and the same PAH metabolite profile was evident both in eelpout sampled in the harbor and in the eelpout exposed to the bunker oil in the laboratory study.