TY  - JOUR
A1  - Pavlova, Viola
A1  - Grimm, Volker
A1  - Dietz, Rune
A1  - Sonne, Christian
A1  - Vorkamp, Katrin
A1  - Riget, Frank F.
A1  - Letcher, Robert J.
A1  - Gustavson, Kim
A1  - Desforges, Jean-Pierre
A1  - Nabe-Nielsen, Jacob
T1  - Modeling Population-Level Consequences of Polychlorinated Biphenyl Exposure in East Greenland Polar Bears
JF  - Archives of environmental contamination and toxicology
N2  - Polychlorinated biphenyls (PCBs) can cause endocrine disruption, cancer, immunosuppression, or reproductive failure in animals. We used an individual-based model to explore whether and how PCB-associated reproductive failure could affect the dynamics of a hypothetical polar bear (Ursus maritimus) population exposed to PCBs to the same degree as the East Greenland subpopulation. Dose-response data from experimental studies on a surrogate species, the mink (Mustela vision), were used in the absence of similar data for polar bears. Two alternative types of reproductive failure in relation to maternal sum-PCB concentrations were considered: increased abortion rate and increased cub mortality. We found that the quantitative impact of PCB-induced reproductive failure on population growth rate depended largely on the actual type of reproductive failure involved. Critical potencies of the dose-response relationship for decreasing the population growth rate were established for both modeled types of reproductive failure. Comparing the model predictions of the age-dependent trend of sum-PCBs concentrations in females with actual field measurements from East Greenland indicated that it was unlikely that PCB exposure caused a high incidence of abortions in the subpopulation. However, on the basis of this analysis, it could not be excluded that PCB exposure contributes to higher cub mortality. Our results highlight the necessity for further research on the possible influence of PCBs on polar bear reproduction regarding their physiological pathway. This includes determining the exact cause of reproductive failure, i.e., in utero exposure versus lactational exposure of offspring; the timing of offspring death; and establishing the most relevant reference metrics for the dose-response relationship.
Y1  - 2016
U6  - https://doi.org/10.1007/s00244-015-0203-2
SN  - 0090-4341
SN  - 1432-0703
VL  - 70
SP  - 143
EP  - 154
PB  - Springer
CY  - New York
ER  -