Synthesis of the toxicological impacts of theExxon Valdezoil spill on Pacific herring (Clupea pallasi) in Prince William Sound, Alaska, U.S.A.

2002 ◽  
Vol 59 (1) ◽  
pp. 153-172 ◽  
Author(s):  
M G Carls ◽  
G D Marty ◽  
J E Hose

Pacific herring (Clupea pallasi) in Prince William Sound (PWS) were affected by two major events in the past decade: the Exxon Valdez oil spill in 1989 and a 75% collapse in the adult population in 1993. In this review we compare and reinterpret published data from industry and government sources. Combining site-specific estimates of exposure and recent laboratory effects thresholds, 0.4–0.7 µg·L–1total polynuclear aromatic hydrocarbons, we conclude that 25–32% of the embryos were damaged in PWS in 1989. Significant effects extended beyond those predicted by visual observation of oiling and by toxicity information available in 1989. Oil-induced mortality probably reduced recruitment of the 1989 year class into the fishery, but was impossible to quantify because recruitment was generally low in other Alaskan herring stocks. Significant adult mortality was not observed in 1989; biomass remained high through 1992 but declined precipitously in winter 1992–1993. The collapse was likely caused by high population size, disease, and suboptimal nutrition, but indirect links to the spill cannot be ruled out. These concepts have broad application to future oil spill assessments. For example, safety standards for dissolved aromatics should reflect the previously unrecognized high toxicity of polynuclear aromatic hydrocarbons to adequately protect critical life stages.

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.


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.


2003 ◽  
Vol 2003 (1) ◽  
pp. 275-283 ◽  
Author(s):  
Paul D. Boehm ◽  
John S. Brown ◽  
David S. Page ◽  
William A Burns ◽  
Jerry M. Neff ◽  
...  

ABSTRACT Studies of records and data pertaining to anthropogenic and natural sources of petroleum, and specifically of the polycyclic aromatic hydrocarbons (PAH), have indicated a generally constant background, with episodic input spikes of bioavailable PAH to the marine environment of Prince William Sound (PWS), Alaska. The Exxon Valdez oil spill (EVOS) was one such PAH spike. However, hundreds of smaller spills, occurring prior to and since the EVOS, contribute a background of bioavailable petrogenic PAH to PWS. The widespread historical and contemporary uses of PWS by man have left chronic, sizeable, and widespread petrogenic and pyrogenic PAH fingerprints and bioavailable PAH at many locations in PWS. Evidence from mussel samples, taken both prior to and since EVOS, and from subtidal sediments, indicates that bioavailable PAH are a constant feature of the PWS system. While EVOS may continue to add some bioavailable PAH to highly localized areas, most PAH inputs to the PWS marine environment are unrelated to EVOS. Such findings indicate that biological, sublethal effects studies, which rely on tissue body burdens and biomarkers as leading indicators of continuing effects from EVOS (e.g. CYP1A-P450, etc.) may have been misinterpreted, as they are confounded by this easily detectable, significant, and continuing background of bioavailable PAH. Therefore measurements of exposure to PAH as indicating lingering effects from EVOS, 13 years after the spill, are speculative and ignore the baseline PAH from non-EVOS inputs.


1999 ◽  
Vol 56 (6) ◽  
pp. 1133-1142 ◽  
Author(s):  
Christopher N Rooper ◽  
Lewis J Haldorson ◽  
Terrance J Quinn II

Recruitment for many marine fishes is believed to be determined at an early life history stage. Pacific herring (Clupea pallasi) spawn in the intertidal and shallow subtidal zones and have a demersal egg stage that is susceptible to egg removals during incubation. Data were collected by the Alaska Department of Fish and Game in four years in Prince William Sound, Alaska, to identify important factors contributing to egg removals. We constructed analysis of variance models based on physical and biological variables to determine which environmental factors control egg loss rates. The habitat variables examined at each study transect were depth, wave exposure, north-south location, substrate, vegetation, mean bird abundance, abundance of loose eggs, and fish predation. Depth of spawn was the primary factor determining egg loss. Cumulative time of air exposure over incubation was substituted into the model for depth. Using the model, the total estimated egg loss from spawning to hatching ranged from 67 to 100% with an average of 75% (SE = 3.3%) in 1995. Eggs were originally deposited from 4 to -6 m depth relative to mean low water. The majority of eggs that remained in the spawning beds to hatching were deposited from 1 to -4 m depth. Egg removals due to avian predation were probably responsible for extreme egg loss rates at shallow depths.


2007 ◽  
Vol 65 (1) ◽  
pp. 25-43 ◽  
Author(s):  
Peter-John F. Hulson ◽  
Sara E. Miller ◽  
Terrance J. Quinn ◽  
Gary D. Marty ◽  
Steven D. Moffitt ◽  
...  

Abstract Hulson, P-J. F., Miller, S. E., Quinn, T. J. II, Marty, G. D., Moffitt, S. D., and Funk, F. 2008. Data conflicts in fishery models: incorporating hydroacoustic data into the Prince William Sound Pacific herring assessment model. – ICES Journal of Marine Science, 65: 25–43. Data conflicts present difficulties in running integrated assessment models as shown by the age-structured assessment (ASA) model for the Pacific herring population in Prince William Sound (PWS), Alaska. After the 1989 “Exxon Valdez” oil spill in PWS, the Pacific herring (Clupea pallasi) ASA model indicated a significant decline in the population, starting in winter 1992. Back-calculated estimates from hydroacoustic abundance surveys that started in 1993 suggested that the ASA model overestimated herring biomass from 1990 to 1992 and that the population decline actually began in 1989. To expose data conflicts, we incorporated the hydroacoustic survey information with all available spawning population indices directly into the age-structured model. In this way, the substantial uncertainty about population parameters from 1989 to 1992 attributable to data conflicts was quantified. Consequently, the magnitude of declines for that period estimated from both linear and ASA models depend on the type of integrated datasets and weighting, particularly with indices of male spawners. Our view is that a major decline started in 1992 when disease affected a large population that was in weakened condition. Other views are consistent with the existing data too.


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