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.
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 EC50 value. Alternatively, estimates for the whole‐body concentration in mink of 11 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 dose‐effect 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 μg/g (total PCBs/wet weight). From the second approach a critical body residue (EC50) 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.
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AbstractOrganisms in contaminated aquatic ecosystems are often exposed to toxicants for their entire lifetime. In order to evaluate the ecological consequences of long-term exposure to metals, we studied the relation between short-term and long-term effects of Zn and Pb on the filtration rate and survival of zebra mussels (Dreissena polymorpha) in laboratory experiments. The results indicated that the effects of Zn and Pb on the filtration rate of D. polymorpha increased when the exposure time was increased, but it remained unclear whether the decrease in filtration rate is caused by accumulation of metals by the mussels or by the metal concentration in the water, or both. The capacity ofD. polymorpha to regulate the body concentration of the essential metal Zn decreased when the exposure time was increased, whereas the non-essential metal Pb could not be regulated by the zebra mussel. Not only the concentration of metal accumulated is of importance for survival, but also the rate of accumulation. It was concluded that the relation between short-term and long-term toxicity was different for each metal and could not be predicted from the results of the short-term experiments.
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