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The present study examines the effects of exposure to oil sands on the early life stages (ELS) of fathead minnows (Pimephales promelas). Sediments within and outside natural oil sand deposits were collected from sites along the Athabasca River (AB, Canada). The ELS toxicity tests were conducted with control water, natural oil sands, reference sediments, and oil-refining wastewater pond sediments. Eggs and larvae were exposed to 0.05 to 25.0 g sediment/L and observed for mortality, hatching, malformations, growth, and cytochrome P4501A induction as measured by immunohistochemistry. Natural bitumen and wastewater pond sediments caused significant hatching alterations and exposure-related increases in ELS mortality, malformations, and reduced size. Larval deformities included edemas, hemorrhages, and spinal malformations. Exposure to reference sediments and controls showed negligible embryo mortality and malformations and excellent larval survival. Sediment analyses using gas chromatography-mass spectrometry revealed high concentrations of alkyl-substituted polyaromatic hydrocarbons (PAHs) compared to unsubstituted PAHs in natural oil sands (220-360 microg/g) and oil-mining wastewater pond sediments (1,300 microg/g). The ELS sediment toxicity tests are rapid and sensitive bioassays that are useful in the assessment of petroleum toxicity to aquatic organisms.

The objectives of this study were to evaluate the influence of natural oil sands on the early developmental stages of white sucker (Catostomus commersoni) and to determine whether biochemical responses in this species were similar to native fish caught in the Athabasca Oil Sands area. Early life stage (ELS) sediment toxicity tests were conducted using controls, reference sediments, natural oil sands, and industrially contaminated (wastewater pond) sediments collected from sites along the Athabasca River, Alberta (Canada). Eggs and larvae were observed for mortality, hatching, deformities, growth, and cytochrome P-4501A (CYP1A) activity using immunohistochemistry. E-Nat-, S-Nat-, and wastewater pond sediment-exposed groups showed significant premature hatching, reduced growth, and exposure-dependent increases in ELS mortality and larval malformations relative to controls. The most common larval deformities included edemas (pericardial, yolk sac, and subepidermal), hemorrhages, and spinal defects. Juveniles exposed to oil sands and wastewater pond sediments (96 h) demonstrated significantly increased 7-ethoxyresorufin-O-deethylase (EROD) activity (30- to 50-fold) as compared to controls. Reference sediment-exposed groups and water controls demonstrated reliable embryo and larval survival, minimal malformations, and negligible CYP1A staining. These observed signs of blue sac disease (ELS mortality, malformations, growth reductions, CYP1A activity induction) may produce deleterious reproductive effects in natural fish populations exposed to oil sands mixtures.

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Exposure of the early life stages of fish to oil sands constituents is associated with mortality and larval malformations such as edemas, hemorrhages, and skeletal, craniofacial, and eye defects. In fathead minnow (Pimephales promelas) and white sucker (Catostomus commersoni) larvae, indices of total eye pathology increased significantly following oil sands exposure. Structural, cytoplasmic, inflammatory, and degenerative eye alterations included poor retinal differentiation, microphthalmia, optic fissures, dysphasic retinas and lenses, inflammatory infiltrates, retinal epithelial lifting, and necrotic foci. Cytochrome P-4501A (CYP1A) was expressed in ocular (retina, lens) and kidney endothelial tissues, as indicated by immunohistochemistry. 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. Oil sands were twofold more toxic to fathead minnows (TPAH LC50 = 47-330 microg/g) than to white sucker (TPAH LC50 = 95-860 microg/g) larvae. For both species, larval mortality was significantly related to CYP1A protein concentrations in kidneys, and severity of these effects rose with oil sands exposure. The relationships among eye damage, mortality, and CYP1A indices warrants further investigation, and may lead to the use of CYP1A induction as an indicator of adverse effects rather than just contaminant exposure.