Disrupted development in fathead minnow embryos exposed to wetland waters from the Athabasca Oil Sands Region, Alberta, Canada.

To assess aquatic toxicity of natural wetlands in the Athabasca oil sands region (AOSR) of northern Alberta, fifteen collected water samples were tested for their ability to affect survival and development of fathead minnow embryos. Wetland waters were also assessed for toxicants from natural oil sands bitumen deposits (Na, Cl, metals, naphthenic acids (NAs), naphthenic acid fraction compounds (NAFCs), polycyclic aromatic hydrocarbons (PAHs), and alkylated PAHs). Water samples from four wetlands caused toxicity to fish embryos. The most potent wetland water, HAT-S5, caused significantly decreased hatch success, decreased time-to-hatch, decreased embryonic heart rate and increased deformities (60 % vs controls 2 %). Exposure to wetland waters from Saline Lake (where conductivity was 2320 μS/cm and Na was high) resulted in fish with increased deformities (58 % vs controls 2 %) that were not the results of high conductivity alone. Two other wetland waters (Gateway Bridge and Crane Lake) also disrupted development in fathead minnow embryos. These combined findings suggest that for natural wetland waters causing effects in fish embryos, toxicants other than salinity/conductivity/ions were responsible for the observed effects. The general water chemistry of most wetlands was unremarkable. However, the most potent wetland, HATS5-wtl is a naturally occurring wetland with possible connections to ground water that makes contact with bitumen. The assessment of the toxicity and chemicals present in natural wetlands provides background data for future studies and for design of restoration wetlands for oil sands mining-disturbed landscapes.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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