Quantitative Risk Model for Polycyclic Aromatic Hydrocarbon Photoinduced Toxicity in Pacific Herring Following the Exxon Valdez Oil Spill

2013 ◽  
Vol 47 (10) ◽  
pp. 5450-5458 ◽  
Author(s):  
Marlo K. Sellin Jeffries ◽  
Carrie Claytor ◽  
William Stubblefield ◽  
Walter H. Pearson ◽  
James T. Oris
2010 ◽  
Vol 60 (8) ◽  
pp. 1359-1363 ◽  
Author(s):  
Abílio Soares-Gomes ◽  
Roberta L. Neves ◽  
Ricardo Aucélio ◽  
Paulo H. Van Der Ven ◽  
Fábio B. Pitombo ◽  
...  

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.


2001 ◽  
Vol 2001 (1) ◽  
pp. 551-557 ◽  
Author(s):  
David S. Page ◽  
Edward S. Gilfillan ◽  
William A. Stubblefield ◽  
Paul D. Boehm ◽  
Keith R. Parker ◽  
...  

ABSTRACT Beginning in 1989, scientists supported by ExxonMobil conducted a number of scientific studies to assess the fate and effects of the Exxon Valdez oil spill on shorelines in Prince William Sound (PWS), Alaska. The 1990, 1991, and 1993 field programs included concurrent sediment sampling for hydrocarbon chemistry and sediment toxicity. This sediment quality assessment found that spill residues on the oiled shorelines rapidly lost toxicity through weathering. The relative amounts of naphthalenes and chrysenes in the polycyclic aromatic hydrocarbons (PAH) in the sediments were found to be good indicators of weathering and toxicity. Using a standard sediment amphipod bioassay on the field samples increased mortality above background was found at exposure levels above approximately 2,600 ng/g total PAH (TPAH) for oil that had weathered a year or more. For samples with TPAH > 2,600 ng/g, fractions of naphthalenes (R = +0.76) and chrysenes (R = −0.63) significantly correlated with amphipod mortality where samples with high mortalities (> 80%) were dominated by relatively high fractions of naphthalenes (median = 0.26), and the low mortality category (< 30%) was dominated by relatively high fractions of chrysenes (median = 0.24). The amphipod mortality data fit significantly to a logistic model. Estimated LC10 and LC50 values were approximately 4,100 and 10,750 ng/g TPAH, respectively. Sediment grain size and total organic carbon were also found to contribute to increased amphipod mortality and were covariates in the data analysis. As petroleum weathers through exposure to the environment and lighter hydrocarbon fractions are lost, the results of this study show that the Exxon Valdez spill oil rapidly lost toxicity as the fractions of chrysenes increased and fractions of naphthalenes decreased.


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