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Acute Embryonic or Juvenile Exposure to Deepwater Horizon Crude Oil Impairs the Swimming Performance of Mahi-Mahi (Coryphaena hippurus)

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Division of Marine Biology and Fisheries, University of Miami, Rosenstiel School of Marine and Atmospheric Science, 4600 Rickenbacker Causeway, Miami, Florida 33149, United States
Department of Marine Science, University of Texas, Marine Science Institute, 750 Channel View Drive, Port Aransas, Texas 78373, United States
§ Ecotoxicology Program, Northwest Fisheries Science Center, National Oceanic and Atmospheric Administration, 2725 Montlake Boulevard E, Seattle, Washington 98112, United States
*E. M. Mager. E-mail: [email protected]. Phone: 305-421-4823. Fax: 305-421-4600. Division of Marine Biology and Fisheries, University of Miami, Rosenstiel School of Marine and Atmospheric Science, 4600 Rickenbacker Cswy., Miami, FL 33149-1098, United States.
Cite this: Environ. Sci. Technol. 2014, 48, 12, 7053–7061
Publication Date (Web):May 23, 2014
https://doi.org/10.1021/es501628k
Copyright © 2014 American Chemical Society
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Abstract

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The Deepwater Horizon incident likely resulted in exposure of commercially and ecologically important fish species to crude oil during the sensitive early life stages. We show that brief exposure of a water-accommodated fraction of oil from the spill to mahi-mahi as juveniles, or as embryos/larvae that were then raised for ∼25 days to juveniles, reduces their swimming performance. These physiological deficits, likely attributable to polycyclic aromatic hydrocarbons (PAHs), occurred at environmentally realistic exposure concentrations. Specifically, a 48 h exposure of 1.2 ± 0.6 μg L–1 ΣPAHs (geometric mean ± SEM) to embryos/larvae that were then raised to juvenile stage or a 24 h exposure of 30 ± 7 μg L–1 ΣPAHs (geometric mean ± SEM) directly to juveniles resulted in 37% and 22% decreases in critical swimming velocities (Ucrit), respectively. Oil-exposed larvae from the 48 h exposure showed a 4.5-fold increase in the incidence of pericardial and yolk sac edema relative to controls. However, this larval cardiotoxicity did not manifest in a reduced aerobic scope in the surviving juveniles. Instead, respirometric analyses point to a reduction in swimming efficiency as a potential alternative or contributing mechanism for the observed decreases in Ucrit.

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Further information is available that provides PAH compositions and measurements (Tables S1 and S2; Figure S1), water quality measurements (Table S2), an example of larval pericardial edema (Figure S2), an example linear regression of metabolic rate vs swimming speed (Figure S3), methods for determining mass scaling constants and coefficients (Figure S4), and nonmass scaled metabolic rate and COT data (Figure S5). This material is available free of charge via the Internet at http://pubs.acs.org/.

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