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

1997 ◽  
Vol 54 (8) ◽  
pp. 1846-1857 ◽  
Author(s):  
G D Marty ◽  
J E Hose ◽  
M D McGurk ◽  
E D Brown ◽  
D E Hinton

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.

1999 ◽  
Vol 56 (4) ◽  
pp. 711-737 ◽  
Author(s):  
W H Pearson ◽  
R A Elston ◽  
R W Bienert ◽  
A S Drum ◽  
L D Antrim

Following record harvests of Pacific herring (Clupea pallasi) in Prince William Sound, Alaska, in the 3 years after the Exxon Valdez oil spill, the fishery failed in 1993. The hypotheses advanced to explain this dramatic 1993 decline occur in three categories: (i) effects associated with the 1989 oil spill, (ii) harvesting effects, and (iii) natural phenomena. Based on our review, we are convinced that a combination of increasing Prince William Sound herring biomass and decreasing food supply led to poor condition of Prince William Sound herring, which resulted in the 1993 decline. Other natural causes could have contributed to the decline, including disease, cold water temperatures, increased predation, and other natural stochastic processes. No evidence supports hypotheses that the decline resulted solely from overharvesting or underharvesting. The record high population levels and harvests of Prince William Sound herring in the years after the 1989 oil spill, the lack of change from the expected age-class distribution, and the low level of oil exposure documented for herring in 1989 and the following years all indicate that the 1989 oil spill did not contribute to the 1993 decline. Poor nutritional status, either alone or in combination with disease or other natural factors, was most likely responsible for the 1993 collapse.


1999 ◽  
Vol 56 (3) ◽  
pp. 419-426 ◽  
Author(s):  
Gary D Marty ◽  
Mark S Okihiro ◽  
Evelyn D Brown ◽  
David Hanes ◽  
David E Hinton

Pacific herring (Clupea pallasi) sampled from oiled sites in Prince William Sound, Alaska, U.S.A., 3 weeks after the 1989 Exxon Valdez oil spill had multifocal hepatic necrosis and significantly increased tissue concentrations of polynuclear aromatic hydrocarbons (PAH). By comparison, Pacific herring from reference sites in 1989 and from all sites in 1990 and 1991 did not have hepatic necrosis or increased PAH concentrations. Adult Pacific herring were sampled for histopathology of liver, spleen, and kidney from oiled and reference sites in April (1989 and 1991) and October (1990 and 1991). Increased scores for macrophage aggregates contributed to significant differences in 1990, but these differences probably resulted from sampling older fish from the oiled site. Naphthalenes were the predominant PAH in all tissue samples. The development of hepatic necrosis and the predominance of naphthalenes in samples from 1989 is consistent with recent laboratory study in which crude oil exposure resulted in dose-dependent expression of viral hemorrhagic septicemia virus (VHSV). We conclude that Pacific herring were exposed to Exxon Valdez oil in 1989 and that development of hepatic necrosis in exposed fish probably was a result of VHSV expression.


1993 ◽  
Vol 1993 (1) ◽  
pp. 325-328 ◽  
Author(s):  
Adam D. Moles ◽  
Stanley D. Rice ◽  
Mark S. Okihiro

ABSTRACT We examined the intensity and prevalence of larval nematodes (Anisakis simplex,) and alterations in selected tissues of spawning Pacific herring (Clupea harengus pallasi) exposed to crude oil, in the laboratory under controlled conditions and in Prince William Sound 14 days after the Exxon Valdez oil spill. In the laboratory, intensity and prevalence of nematodes in the body cavities of herring exposed to the water-soluble fraction of oil declined when exposed to doses above 1.2 mg/L total aromatics. In Prince William Sound, nematodes were rare in spawning herring from oiled sites and abundant among herring from areas outside the spill. Oil exposure apparently induced the nematodes to migrate from the body cavity to the body wall with the lower intensity reflecting a change in parasite location. A coccidian Eimeria clupearum was found in greater numbers in oil exposed herring. To verify exposure effects and to link parasite and tissue alteration with oil exposure, histological examination was used. Liver coagulative necrosis indicated hepatotoxic exposure. Necrosis was followed by macrophage aggregation in the resolution phase. The laboratory exposures allowed confirmation of oil exposure in Prince William Sound and permitted analysis of effects on two internal parasites.


The Condor ◽  
2000 ◽  
Vol 102 (4) ◽  
pp. 723-737 ◽  
Author(s):  
David B. Irons ◽  
Steven J. Kendall ◽  
Wallace P. Erickson ◽  
Lyman L. McDonald ◽  
Brian K. Lance

Abstract We compared post Exxon Valdez oil-spill densities of marine birds in Prince William Sound from 1989–1991, 1993, 1996, and 1998 to pre-spill densities from 1984–1985. Post-spill densities of several species of marine birds were lower than expected in the oiled area of Prince William Sound when compared to densities in the unoiled area. These negative effects continued through 1998 for five taxa: cormorants, goldeneyes, mergansers, Pigeon Guillemot (Cepphus columba), and murres. Black Oystercatchers (Haematopus bachmani) and Harlequin Ducks (Histrionicus histrionicus) exhibited negative effects in 1990 and 1991. Loons showed a weak negative effect in 1993. Black-legged Kittiwakes (Rissa tridactyla) showed relative decreases in 1989, 1996, and 1998 which may have been caused by shifts in foraging distribution rather than declines in populations. Glaucous-winged Gulls (Larus glaucescens) showed positive effects in most post-spill years. Murrelets and terns showed relative increases in 1993, 1996, and 1998. Generally, taxa that dive for their food were negatively affected, whereas taxa that feed at the surface were not. Effects for some taxa were dependent upon the spatial scale at which they were analyzed. Movements of birds and the mosaic pattern of oiling reduced our ability to detect oil-spill effects, therefore our results may be conservative. Several marine bird species were negatively affected at the population level and have not recovered to pre-spill levels nine years after the oil spill. The reason for lack of recovery may be related to persistent oil remaining in the environment and reduced forage fish abundance.


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