Embryonic Crude Oil Exposure Causes Cardiac Hypertrophy And Reduced Aerobic Performance In Juvenile Pink Salmon And Pacific Herring

Embryonic Crude Oil Exposure Causes Cardiac Hypertrophy And Reduced Aerobic Performance In Juvenile Pink Salmon And Pacific Herring

File size: 0.9 MB
Date: January 23, 2014
Author: John P. Incardona, Mark G. Carls, Larry Holland, Tiffany L. Linbo, David H. Baldwin, Mark S. Myers, Karen A. Peck, Mark Tagal, Stanley D. Rice, and Nathaniel L. Scholz
Category: Hydrocarbon Toxicity
Description: The 1989 Exxon Valdez disaster exposed the embryos of pink salmon and Pacific herring to weathered crude oil in shoreline habitats throughout Prince William Sound. The Pacific herring population collapsed four years later. The role of the oil spill, if any, in the forage fish decline has remained one of the most prominent unanswered questions in modern natural resource injury assessment. Studies subsequent to the spill identified disruption of heart morphogenesis as a major impact of polycyclic aromatic hydrocarbons (PAHs) derived from crude oil. Here we show that pink salmon and herring embryos exposed transiently to trace levels of Alaskan crude oil develop cardiac abnormalities that lead to permanent changes in heart anatomy and physiological performance. When assessed after 7 to 10 months of growth in clean water, both species showed reduced aerobic capacity and common changes in cardiac morphology, including evidence of ventricular hypertrophy. Therefore, the Exxon Valdez oil spill likely impacted pink salmon and herring more than previously appreciated. Moreover, the particular sensitivity of herring embryos to PAHs suggest that the catastrophic collapse of the Prince William Sound population may have been caused in part by delayed mortality due to developmental cardiotoxicity. These findings extend our understanding of the long-term impacts of oil spills, and apply also to more chronic inputs of PAH pollution to aquatic systems from land-based runoff and other sources.
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