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The decline of the populations of otters in Western Europe is assumed to be related to the accumulation of polychlorinated biphenyls (PCBs) in this species. A study was conducted to investigate the trophic transfer of non‐ortho, mono‐ortho‐, and di‐ortho‐substituted PCBs in the food web of the otter (Lutra lutra) in the Oude Venen lake system in the Netherlands, with relatively low PCB contamination. This area was one of the last strongholds of otters in the Netherlands and the species is considered to be virtually extinct since 1988. A marked increase in concentration of chlorinated biphenyls (CBs) was observed with successive trophic levels of the aquatic food web. Mean concentrations of the sum of 28 CB congeners (ΣCB) increased from 142 ng CB/g (organic carbon basis) in sediment and particulate matter to 588 ng CB/g (lipid weight basis) in invertebrates, to 2,450 ng CB/g (lipid weight) in fish, and 70,940 ng CB/g (lipid weight) in otter. A diet‐specific biomagnification factor (BMF) of 14 was calculated from fish to otter based on ΣCB; however, on the basis of toxic equivalent concentrations (ΣTEQ), a BMF of 41 was found. This higher BMF on TEQ basis was mainly due to the enrichment of non‐ortho‐substituted CB 126 in otter, compared to fish. In fish CB 126 contributed 30 to 50% to ΣTEQ, while this congener contributed 60 to 80% in otters. A shift in the CB patterns was found from relatively high concentrations of lowly chlorinated CBs in the abiotic compartments to the higher chlorinated CBs (five to seven chlorine atoms) at the highest trophic level. The relatively low concentrations of CB 77 and CBs with vicinal H‐atoms at the meta‐para position in otter compared to fish indicates that otters can metabolize these CBs and have P4501A‐like and P4502B‐like enzyme systems. It appears that even in an ecosystem with relatively low CB contamination, concentrations of CBs can be relatively high in aquatic top predators. The non‐ortho‐substituted CBs seem to be the most important toxic threat for otters, firstly because of the relatively high BMFs of CB 126 and CB 169 and secondly because of the formation of metabolites of CB 77.

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This paper describes an attempt to derive a median effect level (EC50) of PCBs for reproduction of mink based on experimental literature data. Unfortunately, the conditions of the mink studies carried out during the last two decades vary widely, which makes it difficult to establish unequivocal dose-effect relationships. This study describes an attempt to correct for the differences in exposure time using a one-compartment bioaccumulation model. This model estimates the whole-body concentration of PCBs in mink. Two approaches are tested. First, the whole-body concentration of 10 isomer groups of PCBs in mink were estimated and compared with reproduction data to calculate an ECSO value. Alternatively, estimates for the whole-body concentration in mink of 1 1 individual biologically active PCB congeners were made. With these, the toxic equivalent concentration (TEC) in mink was estimated using the 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) equivalent factor (TEF) approach. Whole-body dose-effect relationships were estimated and EC50 values for litter size and kit survival were calculated. The application of the one-compartment bioaccumulation model of the first approach resulted in a significant improvement in the doseeffect relationship in comparison to the raw data set. A further improvement in this relationship was achieved using the congener-specific bioaccumulation model in combination with the TEF approach. This study proposes a critical body residue (EC50) for mink litter size of 1.2 pg/g (total PCBs/wet weight). From the second approach a critical body residue (EC5O) expressed in TCDD equivalency for litter size of 160 pg/g (TCDD equivalence/wet weight) and 200 ng/g (TCDD equivalence/wet weight) for kit survival is proposed.