Biomarker and histopathologic responses in flatfish following site remediation in Eagle Harbor, WA

Abstract Eagle Harbor is a designated Superfund site due to high sediment concentrations of creosote-derived polycyclic aromatic hydrocarbons (PAHs) released chronically from a nearby creosoting facility. Studies with English sole Pleuronectes vetulus from this site (1984–1986) demonstrated high prevalences of toxicopathic liver lesions including neoplasms in resident sole. Inducibility of neoplasia-related lesions by injections of a PAH-rich fraction extracted from Eagle Harbor sediment has also been shown. Further studies (1986–1988) also sampled starry flounder Platichthys stellatus and rock sole Lepidopsetta bilineata, and incorporated biomarkers of PAH exposure and effect, including hepatic CYP1A expression, biliary fluorescent aromatic compounds (FACs), and hydrophobic DNA adducts in liver. Hepatic lesion prevalences and biomarker values in these species from Eagle Harbor were among the highest found at Puget Sound sites. A cap of uncontaminated sediment was placed (September 1993–March 1994) over the most contaminated portions of Eagle Harbor in an attempt to sequester PAH-contaminated sediments. Lesion prevalences and biomarker values just before capping began were generally reduced compared to historical data, consistent with creosoting facility closure and site-based source controls. Similar data from fish collected immediately after capping, and, at 3, 6, 12, 16, 19, 21, 31, 44, and 49 months after cap completion, are presented to determine the efficacy of the capping in ameliorating PAH exposure and associated effects in resident flatfish species.