Table 1.

Examples of human evidence that documents key principles in reproductive environmental health

The placenta does not protect the fetus from damaging chemicals: Methylmercury

In the 1950s, methylmercury exposure in utero resulted in severe neonatal neurological impairment in children after pregnant mothers consumed high levels methylmercury in fish and shellfish contaminated from toxic industrial releases in Minimata, Japan. [3] More recent evidence documents that developmental and cognitive effects can occur in children exposed prenatally to mercury at low doses that do not result in effects in the mother, [4] [5] [6] [7] and that the adverse neurological effects of methylmercury exposure may be delayed. [8, 9] As of 1992 there were 2252 officially recognized cases of Minimata disease. [10]

The fetus can be uniquely sensitive to chemical exposures: Thalidomide

In the 1960s, thalidomide, a drug given to pregnant women for morning sickness, with no adverse maternal consequences, resulted in a high rate of congenital limb and gastrointestinal malformations when taken day 28-42 post conception. [11, 12] It is estimated that more than 10,000 children in 46 countries where the drug had been approved were born with deformities as a consequence their mothers using the drug during pregnancy. [13]

Intergenerational harm can result from in utero chemical exposures: Diethylstilbestrol (DES)

Diethylstilbestrol (DES), which was prescribed in up to 10 million pregnancies from 1938 to 1971 to prevent miscarriage, was subsequently found to be a “transplacental carcinogen” causally-linked to post-pubertal benign and malignant reproductive tract abnormalities in the daughters and sons of DES exposed mothers. These adverse health impacts manifested only decades after exposure. [14] Established health impacts of in utero DES exposure include: vaginal clear cell adenocarcinoma, vaginal epithelial changes, reproductive tract abnormalities (e.g., gross anatomical changes of the cervix, T-shaped and hypoplastic uteri), ectopic pregnancies, miscarriages, and premature births, and infertility in females exposed in utero; reproductive tract abnormalities (e.g., epididymal cysts, hypoplastic testis, cryptorchidism) in males exposed in utero; and increased risk for breast cancer in women who took the drug while pregnant. [15] Recent cohort studies indicate that women who were exposed to DES prenatally have an increased risk of breast cancer after age 40. [16]Animal data predict inter-generational impacts (i.e., among granddaughters of DES exposed women) to-date supported by limited human data. [17]