Geologically distinct crude oils cause a common cardiotoxicity syndrome in developing zebrafish.

Crude oils from different geological formations vary in composition, yet most crude oils contain a polycyclic aromatic hydrocarbon (PAH) fraction that would be expected to produce cardiotoxic effects in developing fish. To determine whether different crude oils or PAH compositions produce common or distinct effects, we used zebrafish embryos to directly compare two crude oils at different states of weathering. Iranian heavy crude oil (IHCO) spilled in the Yellow Sea following the 2007 Hebei Spirit accident was compared to the intensively studied Alaska North Slope crude oil (ANSCO) using two different exposure methods, water-accommodated fractions containing dispersed oil microdroplets and oiled gravel effluent. Overall, both crude oils produced a largely overlapping suite of defects, marked by the well-known effects of PAH exposure on cardiac function. Specific cardiotoxicity phenotypes were nearly identical between the two oils, including impacts on ventricular contractility and looping of the cardiac chambers. However, with increased weathering, tissue-specific patterns of aryl hydrocarbon receptor (AHR) activation in the heart changed, with myocardial AHR activation evident when alkyl-PAHs dominated the mixture. Our findings suggest that mechanisms of cardiotoxicity may shift from a predominantly AHR-independent mode during early weathering to a multiple pathway or synergistic mode with prolonged weathering and increased proportions of dissolved alkyl-PAHs. Despite continued need for comparisons of crude oils from different sources, the results here indicate that the body of knowledge already acquired from studies of ANSCO is directly relevant to understanding the impacts of other crude oil spills on the early life history stages of fish.

Sublethal exposure to crude oil during embryonic development alters cardiac morphology and reduces aerobic capacity in adult fish.

Exposure to high concentrations of crude oil produces a lethal syndrome of heart failure in fish embryos. Mortality is caused by cardiotoxic polycyclic aromatic hydrocarbons (PAHs), ubiquitous components of petroleum. Here, we show that transient embryonic exposure to very low concentrations of oil causes toxicity that is sublethal, delayed, and not counteracted by the protective effects of cytochrome P450 induction. Nearly a year after embryonic oil exposure, adult zebrafish showed subtle changes in heart shape and a significant reduction in swimming performance, indicative of reduced cardiac output. These delayed physiological impacts on cardiovascular performance at later life stages provide a potential mechanism linking reduced individual survival to population-level ecosystem responses of fish species to chronic, low-level oil pollution.