We deployed semi-permeable membrane devices (SPMDs) on beaches for 28 days at 53 sites in Prince William Sound (PWS), Alaska, to evaluate the induction potential from suspected sources of cytochrome P450 1A (CYP1A)-inducing contaminants. Sites were selected to assess known point sources (23 sites in total), or were chosen randomly to evaluate the region-wide sources (30 sites). After deployment, SPMD extracts were analyzed chemically for suites of persistent organic pollutants (POP) and polycyclic aromatic hydrocarbons (PAH). Results of chemical analyses were compared with hepatic CYP1A enzyme activity (ethoxyresorufin-O-deethylase; EROD) of juvenile rainbow trout injected with the same extracts. Increased CYP1A activity (induction) was associated most strongly with concentrations of PAH in extracts, especially chrysene homologues. There were no correlations between induction and concentrations of persistent organic pollutants such as PCBs. EROD activity levels followed a simple power curve of the form y = ax^b, where x is the amount of total PAH or of chrysene homologues injected. The only apparent sources of chrysene homologues were lingering oil from Exxon Valdez, bunker fuels released from storage tanks during the 1964 Alaska earthquake, creosote leaching from numerous pilings at one site, and PAH-contaminated sediments at Cordova Harbor. Our results indicate that PWS is remarkably free of pollution from PAH, as well as from pesticides and PCBs, when an obvious nearby source is absent.