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Physiological and biochemical biomarker responses were studied in juvenile whitefish (Coregonus lavaretus L. s.l.) exposed experimentally to effluent from the forest industry. The large study area (609 km2), Southern Lake Saimaa, in Southeast Finland, receives 330,000 m3 d-1 of biologically and 55,000 m3 d-1 of chemically treated effluents, discharged from two integrated elementary chlorine free (ECF) bleached kraft pulp and paper mills, from one ECF pulp mill, and from one mill producing unbleached pulp and cardboard. The assessment of exposure to effluent discharged from the mills was based on lake water chlorophenolics (CPs) and resin acids (RAs) measured in samples collected from the 22 experimental sites along the area. Despite the low levels of effluent constituents in the lake, they were still accumulated in detectable levels in fish bile, indicating an exposure to the bioactive compounds of effluents. In comparison to the reference area, a two- to four-fold increase in ethoxyresorufin O-deethylase (EROD) activity was observed in whitefish exposed in the vicinity (1-6 km) of all the mills. However, cytochrome P450 1A1 (CYP1A1) gene expression was increased in only one of the receiving areas, indicating higher sensitivity of the EROD activity in the present study. There were no statistically significant correlations between EROD activity and the ambient water concentrations of the CPs, the RAs, or effluent dilution expressed by water sodium concentration. Neither bile chlorophenolics nor bile resin acids showed a significant correlation with EROD. No significant changes in circulating reproductive steroids, 17beta-estradiol and testosterone, in juvenile whitefish were observed. The vitellogenin gene was expressed in the vicinity of the pulp mill discharging the most wood-derived compounds, i.e. resin acids and wood-sterols, including beta-sitosterol. No differences were observed in plasma immunoglobulin M, glucose, or lactate concentrations between the effluent sources.

Retene (7-isopropyl-1-methylphenanthrene) is a naturally formed polycyclic aromatic hydrocarbon (PAH) that causes teratogenicity in fish larvae and induction of cytochrome P450 (CYP1A) enzymes. Retene occurs at high concentrations (< or =3,300 microg/g dry wt) in surface sediments contaminated by resin acids from pulp mill effluents. To assess the environmental risks of retene, it is important to evaluate conditions affecting its bioavailability and accumulation by fish. Fingerling rainbow trout were exposed to retene-spiked or naturally contaminated sediments and sampled after 4 d to determine liver CYP1A activity and concentrations of retene metabolites in bile as indicators of retene accumulation. Industrially contaminated sediments collected near a bleached kraft pulp and paper mill discharging to Lake Saimaa, Finland, significantly induced trout liver CYP1A activity, indicating accumulation of arylhydrocarbon receptor (AhR)-active ligands. Bile of these fish contained retene metabolites, providing direct evidence that retene is bioavailable, presumably via desorption from sediments. Induction of CYP1A in fish exposed to sediments spiked with retene or benzo[k]fluoranthene supported this conclusion. While the extent of CYP1A induction by spiked sediments declined after storage (i.e., aging), a portion of the spiked PAHs remained bioavailable. However, retene was not the sole CYP1A inducer in industrially contaminated sediments, as shown by induction in fish injected with sediment extracts oxidized to remove labile PAHs but not persistent organochlorine compounds such as chlorinated dioxins and furans.

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