Dioxins and endometriosis: a plausible hypothesis.

Linda S. Birnbaum, Audrey M. Cummings, Cummings AM
Environmental health perspectives · 2002 · vol. 110(1) , pp. 15–21 · doi:10.1289/ehp.0211015 · PMID:11781160 · PMC1240688 · W2069233447
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This review integrates evidence from animal models and epidemiological studies to support the hypothesis that dioxin exposure may increase the incidence and severity of endometriosis by affecting growth factors, cytokines, and hormones.

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Abstract

A potential connection exists between exposure to organochlorine chemicals and the increasing prevalence of endometriosis. Evidence shows that dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin) can increase the incidence and severity of the disease in monkeys and can promote the growth or survival of endometrial tissue implanted into rodents in a surgically induced model of endometriosis. The mechanism of the connection between organochlorine chemicals and endometriosis is not clear. Effects on growth factors, cytokines, and hormones (components of the immune and endocrine systems) are potential means of mediating the possible promotion of endometriosis by dioxins. Studies on epidemiology and on structure-activity relationships of organochlorine chemicals and endometriosis have been additional approaches to this problem. In this regard, toxic equivalence (TEQ) appears to be an important determinant of the effects of organochlorine chemicals on endometriosis. In this article, we review the literature related to endometriosis and dioxins and attempt to integrate the various sources of information that bolster the hypothesis connecting dioxins and endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Dioxins Endometriosis Environmental Exposure Environmental Pollutants Animals Dioxins Endometriosis Endometriosis Environmental Pollutants Female Humans Incidence Mice Rats Risk Assessment Structure-Activity Relationship

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (54)

Cited by (48)

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