Polychlorinated biphenyl (PCB) exposure produces placental vascular and trophoblastic lesions in the mink (Mustela vison): a light and electron microscopic study.

Polychlorinated biphenyls (PCBs) cross the placenta and cause fetal death in mink. No indications of impaired implantation have been reported. To study the effects of PCB on mink placental morphology, 2 groups each of 10 animals were orally exposed to Clophen A50 at 0.65 mg (low dose) and 1.3 mg (high dose) per day for 54 days, starting before mating, with 10 control animals. Placentae from mid to late gestation were examined by light and electron microscopy. In the controls, 11% of placentae were degenerate compared to 31% (low dose) and 64% (high dose) in PCB-exposed mink. All control animals exhibited implantation sites, while one animal in the low dose and four in the high-dose group exhibited none. However, there was no difference between PCB-exposed and control animals in the number of placentation sites in implanted animals. Fetal death was markedly increased in PCB-exposed mink, with only four animals (low dose) having all viable fetuses and eight (low and high dose) having a mixture of viable and dead fetuses. Nine exposed animals displayed maternal vascular lesions in the placental labyrinthine zones of viable fetuses, comprising loss and degeneration of endothelial cells, thrombi and haemorrhages. Extracellular fluid was present between the interstitial layer of maternal vessels and the syncytiotrophoblast, and there was focal degeneration of the trophoblast and fetal vasculature. It appears, therefore, that exposure of the mink placenta to PCBs affects maternal vasculature and produces degenerative changes in the trophoblast and fetal vessels, leading to fetal growth retardation or death.