Endometriosis is a common disease that affects women of reproductive age. Polychlorinated dibenzo-p-dioxins (PCDn) are a group of estrogenic toxicants produced as byproducts during many Industrial and combustion processes. A study released in 1993 found that rhesus monkeys exposed to the prototype dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or dioxin), developed endometriosis with incidence and severity related to dose. Dioxins are believed to affect the pathobiology of endometriosis through their effects on growth factors/cytokines, steroidogenic enzymes, remodeling enzymes, and xenobiotic enzymes resulting in inflammation, increased local estrogen levels, and activation of pro-carcinogens. Rodent studies have provided a cost-effective means of exploring the pathophysiology behind the dioxin and endometriosis relationship, but have failed to produce a clear association. Previous research in nonhuman primates claimed exposure to dioxin was associated with increased prevalence and severity of endometriosis. However, current research has not confirmed a cause and effect relationship between dioxin exposure and endometeriosis in the nonhuman primate model. A number of human studies, including data from the Seveso population-based historical cohort study, indicate the argument for dioxin as a causative agent of endometriosis is weak. This paper will provide an extensive literature review of the published evidence both supporting and refuting ,a link . between dioxin and the development of endometriosis. In addition, it will discuss possible areas for future research and how the genetics of endometriosis may play a role.
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