Histopathology and cytogenetic evaluation of Pacific herring larvae exposed to petroleum hydrocarbons in the laboratory or in Prince William Sound, Alaska, after the Exxon Valdez oil spill

Abstract

Following the 1989 Exxon Valdez oil spill in Prince William Sound, Alaska, USA, Pacific herring (Clupea pallasi) larvae sampled from oiled sites had ascites, pericardial edema, and genotoxic damage. Laboratory study confirmed that these lesions were consistent with oil exposure. Pacific herring larvae were trawled from two oiled and two unoiled sites in Prince William Sound in May 1989. Larvae from oiled sites were shorter, had ingested less food, had slower growth (oiled, 0.07-0.10 mm/day; unoiled, 0.15-0.18 mm/day), and had higher prevalence of cytogenetic damage (oiled, 56-84%; unoiled, 32-40%) and ascites (oiled, 16%; unoiled, 1%) than from unoiled sites. In the laboratory experiment, Pacific herring eggs were exposed to an oil-water dispersion of Prudhoe Bay crude oil (initial concentrations of 0.0, 0.10, 0.24, 0.48, and 2.41 mg/L) and sampled for histopathology <24 h after hatching. Effects were significant at the 0.48 mg/L dose (Dunnett's procedure, P < 0.05). Lesions included ascites; hepatocellular vacuolar change; and degeneration or necrosis of skeletal myocytes, retinal cells, and developing brain cells. Lesions in field-sampled larvae were consistent with higher mortality rates documented in larvae from oiled sites.