W9 PM Residual Oil and its Effects
Wednesday, 16 November 2005: 1:50 PM - 5:30 PM in 339-340

(SHO-1117-853248) Lingering Exxon Valdez oil remains the dominant cause of CYP1A induction in Prince William Sound, Alaska.

Short, Jeffrey¹, Rice, Stanley¹, Springman, Kathrine², Sloan, Catherine³, Kahn, Colin⁴, Hodson, Peter⁴, ¹ Alaska Fisheries Science Center, National Marine Fisheries Service, NOAA, Juneau, Alaska, USA² Center for Health and the Environment, University of California, Davis, Davis, California, USA³ Northwest Fisheries Science Center, National Marine Fisheries Service, NOAA, Seattle, Washington, USA⁴ Queen's University, Kingston, Ontario, Canada

ABSTRACT- We measured the induction of cytochrome P450 (CYP1A) in rainbow trout injected with extracts from semi-permeable membrane devices (SPMD) deployed in Prince William Sound, Alaska, to compare the potency of lingering oil from the 1989 Exxon Valdez oil spill (EVOS) with pollutants from alternative sources. Arrays of SPMD were deployed at intertidal sites where EVOS oil remains, at other intertidal sites impacted by present or historical human activity, at salmon streams to assess pollutants imported to PWS by migrating salmon, at Constantine Harbor where a suite of natural petrogenic hydrocarbons is present in intertidal sediments, and at randomly-selected sites to assess inputs from atmospheric transport or from ambient seawater. CYP1A induction was measured by the EROD assay applied to homogenized rainbow trout livers two days following injection. SPMD extracts were also analyzed for polycyclic aromatic hydrocarbons (PAH) and for a suite of persistent organic pollutants (POP) including chlorinated pesticides and PCBs. The magnitude of CYP1A induction caused by SPMD extracts from the EVOS sites ranged from 28 - 72 pmol/mg/min, much greater than elsewhere (1.5 - 6.5 pmol/mg/min; median 2.5). The CYP1A induction from the oiled sites was significantly (P < 0.01) related to total PAH concentrations of the extracts, and these all fingerprinted to EVO. Of the 9 human activity sites (hatcheries, old mine sites), only one current use site registered significant loads of PAH and stimulated a CYP1A response. At 45 un-impacted sites (salmon streams, non-oiled areas, random marine sites), background concentrations of PAH and POP stimulated a weak (< 6.5 pmol/mg/min) to negligible CYP1A response. These results indicate that POPs are negligible as CYP1A induction agents in PWS, as are PAH associated with historical human use sites (except at Sawmill Bay), whereas oil from the EVOS remains a potent CYP1A induction agent.

Key words: Exxon Valdez, Cytochrome P450, PAH, POP