Environmental Influences on the Development of Endometriosis

Abstract

Purpose Several environmental toxicants (ETs), including dioxins and dioxin-like compounds (DLCs), perfluorochemicals, organochlorine pesticides, phthalates, and heavy metals (especially cadmium with its estrogen-like properties in animal models) have been investigated as possibly being related to endometriosis. Methods Systematic review of pertinent literature. Results DLCs have been the most investigated ETs. DLCs are persistent organic pollutants with highly toxic potential and include three types of compounds: polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs) or furans, and polychlorinated biphenyls (PCBs). The most toxic is 2, 3, 7, 8- tetrachlorodibenzo-p-dioxin (TCDD). The connection mechanism between dioxins and endometriosis is still unclear. However, dioxins and DLCs are endocrine-disrupting compounds that can affect the pathobiology of endometriosis at multiple levels. Part of the dioxin and DLCs toxic effects can be accounted for by their interaction with the aryl hydrocarbon receptor (AhR). It has been proposed that dioxin can initiate or promote endometriosis by means of interaction with estrogen receptors or by suppressing the expression of progesterone receptors. Furthermore, TCDD alters the expression of cytokines and growth factors, remodeling enzymes and cytochrome P450 expression and activity. Conclusions Studies in rhesus models have revealed a correlation between dioxin exposure and endometriosis. However, evidence from epidemiologic studies is inconclusive.