| Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental contaminants that are produced by natural processes and anthropogenic activities. Most vertebrate species (including fish) have a detoxifying mechanism that is induced following the binding of PAH to the arylhydrocarbon-receptor protein. The cytochrome P4501A (CYP1A) enzyme system is responsible for the detoxification and activation of several toxicants, including PAHs and 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD). Laboratory and field studies suggest that exposure of the early life stages (ELS) of fish to PAHs can mimic the toxic effects of TCDD. Since PAHs are widespread pollutants and highly abundant in Athabasca oil sands and tailings, these sediments may present a potential risk to fish populations.; To assess the risk of Athabasca oil sands and wastewater pond (WWP) sediments to fish, exposure and toxicity were evaluated. We observed that exposure of the ELS of fathead minnow (Chapter 2) and white sucker ( Chapter 3) to natural oil sands and WWP sediments caused exposure-related increases in toxicity, which was associated with the prevalence of fractions rich in alkyl-PAHs. Lethal and sublethal effects increased significantly with increasing oil sands exposure, and included: alterations in hatching times, reduced size, increased mortality, and larval malformations such as edemas, hemorrhages, skeletal, and eye defects. The signs of toxicity observed in oil sands-exposed fish mirrors the blue-sac disease (BSD) response of larval fish exposed to alkylPAHs and those caused by planar chlorinated aromatics. In addition, CYP1A was expressed in eye (retina, lens) and kidney endothelial tissues, as indicated by immunohistochemistry (Chapter 4). Although the kinetics of exposure-response curves for mortality and CYP1A expression were similar in both species, species differences in the magnitude and sensitivity of the responses were observed. For both species, eye pathology and larval mortality were significantly related to CYP1A protein concentrations, and severity of these effects rose with oil sands exposure. This research suggests that the toxicity of natural oil sands might be related to alkyl-substituted PAHs, and emphasizes the need to isolate the compounds of greatest concern and to examine potential interactive effects with other oil sands-related compounds. Toxicity of oil sands to the early life stages of fish. |
