Why did the Prince William Sound, Alaska, Pacific herring (Clupea pallasi) fisheries collapse in 1993 and 1994? Review of hypotheses

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.

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.


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.


2001 ◽  
Vol 2001 (1) ◽  
pp. 569-575
Author(s):  
Ernest Brannon ◽  
Keya Collins ◽  
Lawrence Moulton ◽  
Keith R. Parker

ABSTRACT In the tenth year following the Exxon Valdez oil spill, differences of opinion still exist about injuries to pink salmon. It was alleged that exposure to oil reduced growth of fry and induced mortality in eggs. The authors reexamined the allegation that injury occurred and have concluded that insufficient consideration was given to other factors that affected results in the studies from which these allegations were drawn. The inability to track temperature differences and the unknown ages of fry precluded assessment of oil effects on growth during early marine residence. Reported higher egg mortality and long-term injury alleged to have resulted from oil exposure during incubation were confounded by the mortality of eggs that occurred as an artifact of the sampling procedure, unrelated to oil effects. The authors concluded that injury to incubating pink salmon embryos and reduced fry growth were based on an incomplete assessment of other factors that influenced these results. This evidence is supported by other research that has disclosed no oil effects on incubating eggs. Among these were studies that showed measured oil concentrations reaching the incubation substrate were 14 to 7,600 times below the lethal threshold. The seven largest runs in the history of Prince William Sound (PWS), Alaska have returned in the 10 years following the spill, which ultimately demonstrated the lack of measurable effect of the oil spill on pink salmon. The authors suggest that the allegation of oil-induced injury to PWS pink salmon needs to be reconsidered in light of these analyses.


2001 ◽  
Vol 2001 (1) ◽  
pp. 559-567 ◽  
Author(s):  
Edward S. Gilfillan ◽  
David S. Page ◽  
Keith R. Parker ◽  
Jerry M. Neff ◽  
Paul D. Boehm

ABSTRACT A shoreline ecology program was performed in Prince William Sound (PWS), Alaska in 1990 and 1991 (1 and 2 years after the Exxon Valdez oil spill, EVOS) to assess the fate and effects of the oil in the intertidal zone. Major components of the study were repeated in 1998 and 1999. This update included a sediment-sampling program at formerly oiled “worst-case” boulder/cobble (B/C) sites and randomly chosen unoiled B/C reference sites. The samples were analyzed for petroleum hydrocarbons and benthic infaunal community characteristics. This paper focuses on the results of the benthic infaunal community analysis. Analysis of Covariance (ANCOVA) was used to analyze the 1990–1999 infaunal species composition data. Very little effect of oiling was detected in either the analysis of community structure parameters or in individual species abundances. Oiling effects were detected at some sites in 1990 and 1991, but not in 1998 and 1999. Nearly all the change in intertidal community parameters between 1990 and 1999 was attributed to natural interannual variation. The composition of the intertidal community of B/C shores changed over time because of natural factors not related to the spill. A core group of species was found in each of the 4 years. This group of species represented between 9 to 30% of all species identified. Two other groups of species did not co-occur. One group was present in 1990 and 1991, but not in 1998 and 1999; the other group was present in 1998 and 1999, but not in 1990 and 1991. The progressive change in the animal community observed between 1990 and 1999 is very likely related to long-term climatic changes occurring in the study area and not the oil spill. This long-term study demonstrates the importance of study designs that allow separation of oiling effects from natural factors that can affect biological communities.


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.


2001 ◽  
Vol 58 (6) ◽  
pp. 1070-1076 ◽  
Author(s):  
Ernest L Brannon ◽  
Keya CM Collins ◽  
Lawrence L Moulton ◽  
Keith R Parker

The Exxon Valdez Oil Spill Trustee Council concluded that oil caused mortality of pink salmon (Oncorhynchus gorbuscha) eggs in Prince William Sound streams. Their conclusion was based primarily on Alaska Department of Fish and Game (ADF&G) studies which reported that mean mortality of embryos in eggs was higher in oiled than non-oiled streams when sampled shortly after spawning completion. However, developing embryos are vulnerable to shock mortality for a period of 20 days after fertilization, and the embryos in eggs from the latest spawners were still in the sensitive period at the time sampling took place. We argue that the original ADF&G analysis should have included sample timing in statistical comparisons of mortality between streams. Analysis of a subset of the ADF&G data showed that sampling shock was a major source of embryo mortality in these samples, and that source of mortality in the original survey would likely have been mistakenly interpreted as an oiling effect. Compensating for sample timing removed all statistical evidence for an oiling effect in the data subset. We conclude that the ADF&G study design confounded the ability to assess for the effect of oil exposure on pink salmon eggs.


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