Exposure to synthetic environmental chemicals (e.g., DDT and its metabolites, especially p,p`-DDE, alkylphenol ethoxylates, PCBs and dioxins) produces reproductive problems in a variety of vertebrate species via endocrine mechanisms.
Naturally occurring environmental chemicals (e.g., phytoestrogens and estrogenic mycotoxins) induce infertility in domestic animal species and can alter human reproductive function. Concerns over these findings have been compounded by a series of publications suggesting that in utero exposure to environmental chemicals may have contributed to the reported decline in human sperm counts, the increased incidences of urogenital malformations (e.g., hypospadias, testicular cancer and undescended testes) and altered sex ratio over the last 40–50 years.
It is postulated that in utero exposure to environmental estrogens could be responsible for the increased incidences of these alterations. This hypothesis is biologically plausible because hormones play critical roles as regulators of development in vertebrates and exposure to hormonally active toxicants during sexual differentiation is known to produce abnormal reproductive phenotypes in humans and other animals.