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John P. Incardona,¹ Mark G. Carls,² Hiroki Teraoka,³ Catherine A. Sloan,⁴ Tracy K. Collier,¹ and Nathaniel L. Scholz¹

¹Ecotoxicology and Environmental Fish Health Program, Environmental Conservation Division, Northwest Fisheries Science Center, National Oceanic and Atmospheric Administration, Seattle, Washington, USA; ²Auke Bay Laboratory, Alaska Fisheries Science Center, National Oceanic and Atmospheric Administration, Juneau, Alaska, USA; ³Department of Toxicology, School of Veterinary Medicine, Rakuno Gakuen University, Ebetsu, Japan; ⁴Environmental Assessment Program, Environmental Conservation Division, Northwest Fisheries Science Center, National Oceanic and Atmospheric Administration, Seattle, Washington, USA

Abstract
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. Key words: cardiovascular function, fish development, non-point source pollution, oil spill. Environ Health Perspect 113:1755-1762 (2005) . doi:10.1289/ehp.8230 available via http://dx.doi.org/ [Online 10 August 2005]

Address correspondence to J.P. Incardona, Environmental Conservation Division, Northwest Fisheries Science Center, National Oceanic and Atmospheric Administration, 2725 Montlake Blvd. E, Seattle, WA 98112 USA. Telephone: (206) 860-3347. Fax: (206) 860-3335. E-mail: john.incardona@noaa.gov

Supplemental Material is available online at http://ehp.niehs.nih.gov/docs/2005/8230/supplement.pdf

We thank J. Stegeman and B. Woodin for providing monoclonal antibody 1-12-3 ; T. Linbo for fish husbandry ; and P. Swanson and K. Peck-Miller for manuscript reviews.

This work was supported by the National Oceanic and Atmospheric Administration Coastal Storms Program ; by grants to J.P.I. and N.L.S. from the California Department of Fish and Game's Oil Spill Response Trust Fund through the Oiled Wildlife Care Network, University of California, Davis ; and by a grant to H.T. from the Japanese Ministry of Education, Culture, Sports, Science and Technology, and Cooperative Research from Active Research in Rakuno Gakuen University. J.P.I. was supported by the National Academies/National Research Council Research Associateships Program.

The authors declare they have no competing financial interests.

Received 19 April 2005 ; accepted 10 August 2005.