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

• Published in: Environmental science & technology 2014-06, Vol.48 (12), p.7053-7061
• Main Authors: Mager, Edward M, Esbaugh, Andrew J, Stieglitz, John D, Hoenig, Ronald, Bodinier, Charlotte, Incardona, John P, Scholz, Nathaniel L, Benetti, Daniel D, Grosell, Martin
• Format: Article
• Language: English
• Subjects: Aerobiosis - drug effects; Agnatha. Pisces; Animal, plant and microbial ecology; Animals; Applied ecology; Basal Metabolism - drug effects; Biological and medical sciences; Biological Transport - drug effects; Chemical Fractionation; Crude oil; Ecotoxicology, biological effects of pollution; Effects of pollution and side effects of pesticides on vertebrates; Embryo, Nonmammalian - drug effects; Embryo, Nonmammalian - physiology; Fish; Fundamental and applied biological sciences. Psychology; Larva - drug effects; Larva - physiology; Motor ability; Nonnative species; Perciformes - embryology; Perciformes - physiology; Petroleum - toxicity; Petroleum Pollution; Polycyclic aromatic hydrocarbons; Polycyclic Aromatic Hydrocarbons - toxicity; Swimming - physiology; Toxicity; Toxicity Tests, Acute; Water Pollutants, Chemical - toxicity
• ISSN: 0013-936X; 1520-5851
• DOI: 10.1021/es501628k

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 (U crit), 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 U crit.