Crude oil toxicity and interactions with chemical dispersants
Tools for assessing exposure and effects (biomarkers)
Toxic equivalent factors based on structure-activity; bioassays of short-term indicators
Transfer of sediment mercury through aquatic food webs in the St. Lawrence River.
Responses of fish populations to chemical stress
Role of chemical contamination in the decline of the American Eel
My primary interest is the role of metabolism in chemical toxicity to fish, with a focus on the reactive by-products of polycyclic aromatic hydrocarbon (PAH) metabolism by liver mixed function oxygenases enzymes (i.e. the cytochrome P450 or CYP1A enzymes). The goal is to understand the mechanism of PAH toxicity to the early life stages (embryos and larvae) of fish and the consequences for larval survival and recruitment. Research on mechanisms has extended to the role of alkyl substitution in PAH toxicity, the role of PAH in causing toxicity of crude and refined oils to fish, and the effect of chemical dispersion on oil toxicity. The results are directly applicable to ecological risk assessment of PAHs from oil, coal tar, creosote, soot and the by-products of microbial degradation of resin acids from pulp mill effluents. I have also been involved in studies of the transfer of mercury from point sources and from contaminated sediments through aquatic food webs of the St. Lawrence River, the contamination of St. Lawrence River sediments by pesticides used at EXPO 67, and the potential role of chemical contamination in the declining abundance of American eel in Lake Ontario.
The Beaty Water Research Centre 58 University Ave, Queen's University, Kingston, ON, K7M 9H7 (613) 533-3412 email@example.com