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On March 24, 1989, the Exxon Valdez grounded on Bligh Reef in Prince William Sound, Alaska, spilling an estimated 10.8 million gallons of crude oil. Contrary to early projections, subsequent studies over several decades have shown subsurface oil persisting on impacted beaches. Here we present findings from a lingering oil survey conducted during the summer of 2015 at a small set of beaches in Prince William Sound known to have persistent subsurface Exxon Valdez oil. The objectives of the survey were to estimate how much oil remains at these sites, the oil composition, and oil retention rates compared to previous studies. Results from the survey found lingering oil was present at 8 of 9 sites that were revisited. Surveys revealed little evidence of change in oil area or mass over the last 14 years, nor has there been a change in the distribution of oiling intensities or their location on the beach. Detailed analysis of the oil indicated it has not weathered since 2001. Subsurface oils collected in 2015 have enriched concentrations of phenanthrenes and chrysenes relative to oil originating in the cargo hold indicating that buried oil has retained some toxic potential over the last two decades, but it is not currently bioavailable. Subsurface oil appears to be sequestered in sediments and protected from hydrological washing and low oxygen and nutrient levels inhibiting biodegradation. These findings are consistent with previous surveys and predictive geomorphic models suggesting the estimated 0.6% Exxon Valdez oil remaining is sequestered and not bioavailable unless disturbed and will likely persist in the environment on a decadal scale.

Extracts from semi-permeable membrane devices (SPMDs) deployed on beaches in Prince William Sound (PWS), Alaska, were used to evaluate if complex contaminant mixtures from different sources can be distinguished by the resulting cytochrome P450 1A (CYP1A) activity in exposed test animals. Deployment sites included canneries, salmon hatcheries, and beaches where lingering oil remains from discharges during the 1964 earthquake or the 1989 Exxon Valdez oil spill. Other sites were selected at random to evaluate region-wide contaminant inputs or were located in salmon streams to evaluate contaminants carried and released by migrating salmon carcasses following reproduction. Following standard deployments of approximately 28 d, an aliquot of the accumulated contaminants was intraperitoneally injected without cleanup into juvenile rainbow trout (Oncorhynchus mykiss). After 2 d and 7 d, the activity of CYP1A was measured by the ethoxyresorufin-o-deethylase (EROD) assay. Exposure to extracts from the oiled sites and one hatchery site with numerous creosote pilings elicited strong EROD responses, whereas fish exposed to salmon stream extracts elicited weak but significant responses during late summer compared to late spring. Responses from the other sites were not significant, indicating contaminants from these sources are unlikely to cause CYP1A induction in resident biota. Rather than simply assessing extant contaminants, this method evaluates the potency of the different sites for bringing about aryl hydrocarbon receptor responses in resident biota.