Abstract-Pacific herring eggs were exposed for 16 d to weathered Alaska North Slope crude oil. Exposure to an initial aqueous concentration of 0.7 parts per billion (ppb) polynuclear aromatic hydrocarbons (PAHs) caused malformations, genetic damage, mortality, and decreased size and inhibited swimming. Total aqueous PAH concentrations as low as 0.4 ppb caused sublethal responses such as yolk sac edema and immaturity consistent with premature hatching. Responses to less weathered oil, which had relatively lower proportions of high molecular weight PAH, generally paralleled those of more weathered oil, but lowest observed effective concentrations (LOECs) were higher (9.1 ppb), demonstrating the importance of composition. The LOEC for more weathered oil (0.4 ppb) was similar to that observed in pink salmon (1.0 ppb), a species with a very different development rate; by inference, other species may be similarly sensitive to weathered oil. Our methods simulated conditions observed in Prince William Sound (PWS) following the Exxon Valdez oil (EVO) spill. Biological effects were identical to those observed in embryolarval herring from PWS in 1989 and support the conclusion that EVO caused significant damage to herring in PWS. Previous demonstration by our laboratory that most malformed or precocious larvae die corroborates the decreased larval production measured after the spill.
Polycyclic aromatic hydrocarbons (PAHs), derived largely from fossil fuels and their combustion, are pervasive contaminants in rivers, lakes, and nearshore marine habitats. Studies after the Exxon Valdez oil spill demonstrated that fish embryos exposed to low levels of PAHs in weathered crude oil develop a syndrome of edema and craniofacial and body axis defects. Although mechanisms leading to these defects are poorly understood, it is widely held that PAH toxicity is linked to aryl hydrocarbon receptor (AhR) binding and cytochrome P450 1A (CYP1A) induction. Using zebrafish embryos, we show that the weathered crude oil syndrome is distinct from the well-characterized AhR-dependent effects of dioxin toxicity. Blockade of AhR pathway components with antisense morpholino oligonucleotides demonstrated that the key developmental defects induced by weathered crude oil exposure are mediated by low-molecular-weight tricyclic PAHs through AhR-independent disruption of cardiovascular function and morphogenesis. These findings have multiple implications for the assessment of PAH impacts on coastal habitats.
Teleost embryos develop a syndrome characterized by edema when exposed to water that weathers substrates contaminated with crude oil. Previous studies using zebrafish demonstrated that crude oil exposure causes cardiogenic edema, and that the most abundant polycyclic aromatic hydrocarbons (PAHs) in weathered crude oils (tricyclic fluorenes, dibenzothiophenes, and phenanthrenes) are cardiotoxic, causing arrhythmia through a pathway that does not require activation of the aryl hydrocarbon receptor (AHR). We demonstrate here for Pacific herring, a species impacted by the Exxon Valdez oil spill, that the developing heart is the primary target of crude oil exposure. Herring embryos exposed to the effluent of oiled gravel columns developed dose-dependent edema and irregular cardiac arrhythmia soon afterthe heartbeat was established. At a dose that produced cardiac dysfunction in 100% of exposed embryos, tissue levels of tricyclic PAHs were below 1 micromol/kg, suggesting a specific, high affinity target in the heart. These findings have implications for understanding the mechanism of tricyclic PAH cardiotoxicity, the development of biomarkers for the effects of PAH exposure in fish, and understanding the long-term impacts of oil spills and other sources of PAH pollution in aquatic environments.
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