Mol. Hum. Reprod. Advance Access originally published online on September 10, 2009
Molecular Human Reproduction 2009 15(10):609-624; doi:10.1093/molehr/gap075
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This article appears in the following Molecular Human Reproduction issue: Special Issue: Mechanisms of Endometriosis [View the issue table of contents]
Reassessing the evidence for the link between dioxin and endometriosis: from molecular biology to clinical epidemiology
1 Institute of Obstetric and Gynecologic Research, and Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200001, China 2Leuven University Fertility Centre, Department of Obstetrics & Gynaecology, University Hospital Gasthuisberg, Leuven, Belgium 3Department of Obstetrics and Gynaecology, National Institute of Health, Budapest, Hungary 4Department of Obstetrics and Gynecology, Assiut Faculty of Medicine, Assiut, Egypt
5 Correspondence address. Tel: +32-16-343624; Fax: +32-16-343607; E-mail: thomas.dhooghe{at}uz.kuleuven.ac.be
A 1993 study reporting the link between exposure to dioxin and the risk of developing endometriosis in rhesus monkeys prompted many investigators to look suspiciously at dioxin. Since 1993, many in vitro, animal and epidemiological studies have been published, but the link between dioxin exposure and endometriosis is still unclear. The aim of our review is to present a summary of the biological effects of dioxin and its aryl hydrocarbon receptor, and to reassess the evidence presented in published, in vitro, preclinical and epidemiological studies regarding the association between dioxins and endometriosis. Although in vitro and animal studies provide results in support for a role of dioxins in the pathogenesis of endometriosis, caution should be exercised since these findings are mostly context dependent and since negative findings from these studies are rarely published. On the basis of our review of original epidemiological studies, no significant evidence can be found to support a link between dioxins and endometriosis in women. This observation can be explained by positive publication bias and by significant methodological problems associated with these studies, or by the absence of such a link. In conclusion, it seems that there is insufficient evidence at this moment in support of the hypothesis that dioxin exposure may lead to increased risk of developing endometriosis in women.
Key words: dioxin/endometriosis/epidemiology/risk/publication bias
Both authors contributed equally to this article. Submitted on June 4, 2009; resubmitted on August 17, 2009; accepted on August 18, 2009.