ABSTRACT
Endometriosis is a common gynecologic problem of unknown etiology. Estrogen dependence
and immune modulation are established features of this disease, and environmental
contaminants have been suggested to play a role in the pathobiology of this disease
as well. Previous work in nonhuman primates has shown that exposure to the dioxin
2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) is associated with an increased prevalence and severity of endometriosis.
Further animal experiments have implicated dioxin and dioxin-like compounds in this
disease. Rodent studies support the plausibility of a role of environmental contaminants
in the pathophysiology of endometriosis, although a convincing mechanistic hypothesis
has yet to be advanced. Small hospital-based case-control studies have failed to provide
compelling evidence for or against an association of environmental contaminants and
endometriosis. Herein we review evidence that dioxin and dioxin-like compounds are
potent modulators of immune and endocrine function critical to the pathobiology of
endometriosis. Furthermore, perspectives on the potential mechanism(s) of dioxin and
dioxin-like compound;ndinduced toxicity in endometriosis, important knowledge needs,
potential animal models for endometriosis studies, and considerations integral to
future human case-control studies are discussed.
KEYWORDS
endometriosis - environmental dioxins - TCDD - dioxin-like polychlorinated biphenyls
