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Environmental contaminants, fertility, and multioocytic follicles: a lesson from wildlife?

The overall contribution of environmental exposures to infertility is unknown, but a growing scientific database suggests that exposure to various environmental factors, both in utero and neonatally, could dramatically affect adult fertility. Studies of various contaminant-exposed wildlife populations suggest that multiple mechanisms contribute to changes in gonadal development, maturation of germ cells, fertilization, and pregnancy; specifically, the endocrine processes supporting these events. Although great debate and extensive research has occurred during the last decade surrounding fertility, fecundity, and semen quality, much less work has focused on environmental alterations in oocyte development and maturation. Exposure of the developing ovary to estrogens, whether of pharmaceutical (e.g., diethylstilbesterol) or environmental (e.g., phytoestrogens, pesticides with estrogenic action) origin, can disrupt early oogenesis and folliculogenesis leading to a pathology termed the multioocytic follicle (polyovular follicle), which in rodents reduces fertilization and embryonic survival rates. The mechanism underlying this pathology is hypothesized to involve a disruption in the gonadotropin-estrogen-inhibin/activin signaling pathway. Given the conserved nature of vertebrate oogenesis and folliculogenesis, we suggest that perturbations of these phenomena in humans, caused by environmental contaminant exposure, could lead to altered fertility, as has been reported in wildlife and laboratory rodent models.