Risk of weathered residual Exxon Valdez oil to pink salmon embryos in Prince William Sound.

It has been hypothesized that pink salmon eggs incubating in intertidal streams transecting Prince William Sound (PWS) beaches oiled by the Exxon Valdez oil spill were exposed to lethal doses of dissolved hydrocarbons. Since polycyclic aromatic hydrocarbon (PAH) levels in the incubation gravel were too low to cause mortality, the allegation is that dissolved high-molecular-weight hydrocarbons (HPAH) leaching from oil deposits on the beach adjacent to the streams were the source of toxicity. To evaluate this hypothesis, we placed pink salmon eggs in PWS beach sediments containing residual oil from the Exxon Valdez oil spill and in control areas without oil. We quantified the hydrocarbon concentrations in the eggs after three weeks of incubation. Tissue PAH concentrations of eggs in oiled sediments were generally < 100 ppb and similar to background levels on nonoiled beaches. Even eggs in direct contact with oil in the sediment resulted in tissue PAH loads well below the lethal threshold concentrations established in laboratory bioassays, and very low concentrations of HPAH compounds were present. These results indicate that petroleum hydrocarbons dissolved from oil deposits on intertidal beaches are not at concentrations that pose toxic risk to incubating pink salmon eggs. The evidence does not support the hypothesis that interstitial pore water in previously oiled beaches is highly toxic.

Biomarkers of PAH exposure in an intertidal fish species from Prince William Sound, Alaska: 2004-2005.

Polycyclic aromatic hydrocarbon (PAH) exposure biomarkers were measured in high cockscomb prickleback (Anoplarchus purpurescens) fish collected from both previously oiled and unoiled shore in Prince William Sound (PWS), Alaska, to test the hypothesis that fish living in the nearshore environment of the sound were no longer being exposed to PAH from the Exxon Valdez oil spill. Pricklebacks spend their entire lives in the intertidal zone of rocky shores with short-term movements during feeding and breeding restricted to an area of about 15 meters in diameter. Fish were assayed for the PAH exposure biomarkers, bile fluorescent aromatic compounds (FAC), and liver ethoxyresorufin O-deethylase (EROD) activity (a measure of cytochrome P450 1A (CYP1A) monooxygenase activity). Bile FAC concentrations and EROD activities were low and not significantly different in fish from previously oiled and unoiled sites. The similar low EROD activity and bile FAC concentrations in fish from oiled and unoiled shores, supports the hypothesis that these low-level biomarker responses were not caused by exposure of the fish to residues of the spilled oil.

Toxicity of weathered Exxon Valdez crude oil to pink salmon embryos.

Research was conducted at the University of Idaho (Moscow, ID, USA) on the toxicity of weathered Exxon Valdez crude oil to embryos of pink salmon from 2001 to 2003 for the purpose of comparing these data with those from the National Oceanic and Atmospheric Administration Fisheries Laboratory at Auke Bay (AK, USA). Mortality reported at Auke Bay for embryos chronically exposed to very low concentrations of aqueous solutions of weathered oil, measured as dissolved polycyclic aromatic hydrocarbons (PAHs), was inconsistent with that in other published research. Using the Auke Bay experimental design, we found that toxicity is not evident in pink salmon embryos until chronic exposure to laboratory weathered and naturally weathered oil concentrations exceeding 1,500 and 2,250 ppm, respectively, representing a total PAH tissue burden in excess of 7,100 ppb. Effluent hydrocarbons also drop well below concentrations sufficient to cause harm over the time frame of a few weeks, regardless of oiling level. Resolution of differences with Auke Bay involved the source of contributing hydrocarbons. The experimental design did not exclude dispersed oil droplets from the aqueous solution; thus, toxicity was not limited to the dissolved hydrocarbon fraction. The implications of the present results are discussed regarding the toxic risk of weathered oil to pink salmon embryos in streams of Prince William Sound (AK, USA).

Results from a sixteen year study on the effects of oiling from the Exxon Valdez on adult pink salmon returns.

For sixteen years following the 1989 Exxon Valdez oil spill adult returns of pink salmon in Prince William Sound, Alaska were monitored to assess spill effects on survival. No evidence of spill effects was detected for either intertidal or whole-stream spawning fish. From 1989 through 2004 mean densities for oiled and reference streams tracked each other, illustrating similar responses of oiled and reference stream adult populations to naturally changing oceanographic and climactic conditions. Hatchery fish strayed into the study streams, but similar incursions occurred in oiled and reference streams, and their presence was compensated for to eliminate their influence on determining the success of the returning natural populations. These results, showing no detectable effects of oiling on pink salmon spawning populations, are supported by published field studies on pink salmon incubation success in oiled streams.

Polycyclic aromatic hydrocarbon sources related to biomarker levels in fish from Prince William Sound and the Gulf of Alaska.

Seafloor sediments in Prince William Sound (PWS) and the eastern Gulf of Alaska (GOA) have a substantial regional hydrocarbon background from natural sources including oil seeps and eroding sedimentary rocks along the eastern GOA coast. Polycyclic aromatic hydrocarbons (PAH) from that background appear to be bioavailable to fish. Fish collected from PWS and the GOA in a 1999--2000 biomarker study (bile fluorescent aromatic contaminants and liver ethoxyresorufin O-deethylase) show evidence of exposure to low levels of PAH at all categories of sites sampled. Seafloor sediments at fish sampling sites in the GOA east of PWS and at three PWS site categories (nonspill path, spill path oiled, and spill path not oiled) contain hydrocarbons from four principal sources: regional background, combustion products, residues from the 1989 Exxon Valdez oil spill (EVOS), and Monterey (CA) petroleum residues. GOA sediments between PWS and Yakutat Bay, approximately 350 km to the east, are dominated by regional petrogenic background hydrocarbons (total PAH (TPAH) range approximately 60-3400 ng/g) that are the probable cause of low biomarker levels measured in halibut from this area. PWS sediments contain varying proportions of regional background, combustion products, Monterey residues, and EVOS residues at some spill path sites. Rockfish caught in PWS embayments in 1999 have liver EROD activities that correlate positively with the pyrogenic PAH indicator ratio (FI+Py)/C24Ph. Although traces (<5-100 ng/g TPAH) of EVOS residues were detected in seafloor sediments at some nearshore spill path sites, biomarker levels in fish from those sites are not elevated relative to other sites in PWS.

Biomarkers in fish from Prince William Sound and the Gulf of Alaska: 1999-2000.

To test the hypothesis that biomarker levels in fish collected at Prince William Sound (PWS) sites impacted by the 1989 Exxon Valdez oil spill were higher than those collected at unimpacted sites, a 1999-2000 study collected five fish species and associated benthic sediments from 21 sites in PWS and the eastern Gulf of Alaska (GOA). PWS sites were divided in three oiling categories based upon 1989 shoreline assessments: nonspill path (NSP), spill path oiled (SPO), and spill path not oiled (SPNO). Rockfish (N = 177), rock sole (N = 30), and kelp greenling (N = 49) were collected at near-shore locations (approximately 50-500 m from shore); Pacific halibut (N = 131) and Pacific cod (N = 81) were collected further offshore (approximately 500-7000 m). Fish were assayed for bile fluorescent aromatic contaminants (FAC) and cytochrome P4501A (CYP1A) levels measured as liver ethoxyresorufin O-deethylase (EROD) activity and by immunohistochemistry (IHC) of various tissues. For all species studied at all sites, bile FAC concentrations and CYP1A levels were low and in the same range for fish collected at PWS SPO and SPNO sites relative to NSP sites in PWS and the GOA. Consequently, the hypothesis is rejected for the species studied. The bile FAC results further indicate a pervasive exposure of fish at all sites, including those in the GOA far removed from the effects of the spill, to low levels of polycyclic aromatic hydrocarbons. Analysis of the benthic sediments indicates that the probable sources of this exposure are petrogenic hydrocarbons derived from natural oil seeps and eroding sedimentary rocks in the eastern GOA.

Hydrocarbon composition and toxicity of sediments following the Exxon Valdez oil spill in Prince William Sound, Alaska, USA.

An 1-year study of the 1989 Exxon Valdez oil spill found that spill residues on the oiled shorelines rapidly lost toxicity through weathering. After 1990, toxicity of sediments remained at only a few heavily oiled, isolated locations in Prince William Sound (AK, USA), as measured by a standard amphipod bioassay using Rhepoxynius abronius. Data from 648 sediment samples taken during the 1990 to 1993 period were statistically analyzed to determine the relationship between the total concentration of 39 parent and methyl-substituted polycyclic aromatic hydrocarbons (defined as total polycyclic aromatic hydrocarbons [TPAH]) and amphipod mortality and the effect of oil weathering on toxicity. A logistic regression model yielded estimates of the lower threshold, LC10 (lethal concentration to 10% of the population), and LC50 (median lethal concentration) values of 2,600, 4,100, and 10,750 ng/g TPAH (dry wt), respectively. Estimates of the threshold and LC50 values in this field study relate well to corresponding sediment quality guideline (SQG) values reported in the literature. For sediment TPAH concentrations >2,600 ng/g, samples with high mortality values (>90%) had relatively high fractions of naphthalenes and those with low mortality (<20%) had relatively high fractions of chrysenes. By 1999, the median sediment TPAH concentration of 117 ng/g for the post-1989 worst-case sites studied were well below the 2,600 ng/g toxicity threshold value, confirming the lack of potential for long-term toxic effects. Analysis of biological community structure parameters for sediment samples taken concurrently found that species richness and Shannon diversity decreased with increasing TPAH above the 2,600 ng/g threshold, demonstrating a correspondence between sediment bioassay results and biological community effects in the field. The low probability of exposure to toxic concentrations of weathered spill residues at the worst-case sites sampled in this study is consistent with the rapid overall recovery of shoreline biota observed in 1990 to 1991.