Female reproductive disorders: the roles of endocrine-disrupting compounds and developmental timing

Abstract

Objective To evaluate the possible role of endocrine-disrupting compounds (EDCs) on female reproductive disorders emphasizing developmental plasticity and the complexity of endocrine-dependent ontogeny of reproductive organs. Declining conception rates and the high incidence of female reproductive disruptions warrant evaluation of the impact of EDCs on female reproductive health. Design Publications related to the contribution of EDCs to disorders of the ovary (aneuploidy, polycystic ovary syndrome, and altered cyclicity), uterus (endometriosis, uterine fibroids, fetal growth restriction, and pregnancy loss), breast (breast cancer, reduced duration of lactation), and pubertal timing were identified, reviewed, and summarized at a workshop. Conclusion(s) The data reviewed illustrate that EDCs contribute to numerous human female reproductive disorders and emphasize the sensitivity of early life-stage exposures. Many research gaps are identified that limit full understanding of the contribution of EDCs to female reproductive problems. Moreover, there is an urgent need to reduce the incidence of these reproductive disorders, which can be addressed by correlative studies on early life exposure and adult reproductive dysfunction together with tools to assess the specific exposures and methods to block their effects. This review of the EDC literature as it relates to female health provides an important platform on which women’s health can be improved.

The effect of selected environmental Fusarium mycotoxins on the ovaries in the female wild boar (Sus scrofa)

“…Estrogens are found naturally in the body, and they also occur in the environment and in the form of xenobiotics. Environmental estrogens have been recently identified, some of them as undesirable compounds (Gajęcki et al 2010), and they are classified as endocrine disruptors (EDs) (Yurino et al 2004, Crain et al 2008). Exposure to high levels (above NOAEL) of EDs can lead to pathological processes, in particular in the reproductive system, specially in the ovaries.…”

Effects of age, nursing, and oral IGF1 supplementation on neonatal porcine cervical development

“…Mechanisms through which lactocrine programing of FRT development may affect reproductive capacity remain to be defined. Targeted disruption of FRT development during organizationally critical periods of postnatal life can have lasting effects on the form and function of adult reproductive tissues (Crain et al 2008, McLachlan et al 2012. In the hamster, neonatal exposure to diethylstilbesterol increased cervical diameter and altered LE histology, reflected by increased luminal epithelial height and cornification, in a manner that persisted into adulthood (Hendry et al 2004).…”

Defining Future Directions for Endometriosis Research: Workshop Report From the 2011 World Congress of Endometriosis in Montpellier, France

“…56 Animal studies also show that endometriosis can be promoted by adult exposures to organochlorines, a class of chemicals that includes the dioxin, tetrachlorodibenzo-p-dioxin, the pesticides methoxychlor and dichlorodiphenyltrichloroethane, and polychlorinated biphenyls with dioxin-like effects. 57 An equivocal literature exists regarding the relation between persistent organochlorine pollutants (POPs) and endometriosis in women, with differences attributed to methodologies. A recent study assessed the association between POPs and the odds of an endometriosis diagnosis and the consistency of findings by biological medium and study cohort.…”