Tollefsen et al. (2008) studied the cytotoxicity

of a range of APs in cultures of primary hepatocytes from rainbow trout. Toxicity measured as metabolic inhibition and loss of membrane integrity increased with the hydrophobicity of the APs for compounds with logKOW < 4.9, but deviated from this for more hydrophobic compounds (logKOW > 4.9). Metabolic inhibition occurred at lower concentrations than loss of membrane integrity for most of the APs, which suggests that effects on cellular metabolic functions were the main causes of the cytotoxicity. The study gives insight into the structure–toxicity relationship of important PW components, but it is difficult to extrapolate to real PW exposure. Still, for chemicals with logKOW < 2–3 MG-132 clinical trial the metabolic Selleckchem SAHA HDAC inhibition and to a lesser degree also loss of membrane integrity was claimed to correspond to reported in vivo acute toxicity in fathead minnow (Pimpehales promelas) ( Schultz et al., 1986). The in vitro toxicity of the more hydrophobic compounds underestimated the in vivo toxicity in this fish. Meier et al. (2010) found that exposure of Atlantic cod to PW during the embryonic and early larval stages (up to 3 months of age) and during the early juvenile stage (from 3 to 6 months of age) had no effect on embryo survival or hatching success, but 1% PW interfered with the development of normal

larval pigmentation. After hatching most of the larvae exposed to 1% PW failed to begin feeding and died of starvation. This inability to feed may be linked to an increased frequency of jaw deformities in the exposed larvae. No similar effects were seen at exposure to 0.1% and 0.01% PW. Analysis

of DNA adducts in fish tissue has been recommended for assessment of genotoxic effects of contaminants in PW (Balk et al., 2011 and Hylland et al., 2006). Similarly, the micronuclei frequency method has been found sensitive and feasible for use as a biomarker of genotoxicity in blue mussel exposed to PW contaminants (Brooks et al., 2009). Holth et al. (2009) found time and dose dependent formation of DNA adducts in Atlantic cod exposed for 44 weeks to APs and a WSF of oil. Elevated DNA adduct values have been measured Chlormezanone in wild haddock in the Tampen region in 2002, 2005 and 2008 (Balk et al., 2011, Grøsvik et al., 2010 and Hylland et al., 2006). The cause of the effect was unclear, as the DNA adduct signal could possibly stem from recent PW discharges or from fish being in contact with PAHs or other contaminants in deposits of drill cuttings. Monitoring surveys at the Ekofisk field have detected elevated micronuclei frequencies in blue mussel caged up to 1.6 km from the discharge point (Sundt et al., 2008). After implementation of a new PW treatment system elevated micronuclei frequencies were only detected in cages at 500 m distance (Brooks et al., 2009). Brooks et al. (2011a) studied the biological impact of treated PW under laboratory conditions in the blue mussel.