Endometriosis has many hypothesized etiologies. Known risk factors include genetic predisposition, uterine outflow abnormalities, and iatrogenic causes. Of increasing concern is prenatal environmental exposures. However, the findings of studies investigating the relationships between prenatal environmental exposures and the development of endometriosis have not always been conclusive, and therefore, the relationships are debatable.
Effects of Prenatal Environmental Exposures on the Development of Endometriosis in Female Offspring, National Institutes of Health, NCBI PubMed PMID: 26905420, 2016 Feb 22.
This review presents a summary and analysis of the current studies that investigated the effects of prenatal environmental exposures on the development of endometriosis in female offspring.
Prenatal exposure to estrogenic substances (such as ethinyl estradiol and diethylstilbestrol) and environmental toxins (such as 2,3,7,8-tetrachlorodibenzo-p-dioxin, polychlorinated biphenyls, and bisphenol A) may increase the incidence of endometriosis in female offspring. However, exposure to cigarette smoke may protect against the development of endometriosis in female offspring mainly because of its antiestrogenic effects.
Certain prenatal environmental exposures might result in the development of endometriosis in female offspring. In addition to known environmental exposures that predispose the development of endometriosis in adulthood, such as dioxin and radiation exposure (animal models), prenatal exposures are of increasing concern.
More DES DiEthylStilbestrol Resources
- DES studies on cancers and screening.
- DES studies on epigenetics and transgenerational effects.
- DES studies on fertility and pregnancy.
- DES studies on gender identity and psychological health.
- DES studies on in-utero exposure to DES and side-effects.
- DES studies on the genital tract.
- Papers on DES lawsuits.
- DES videos and posts tagged DES, the DES-exposed, DES victims.