Bisphenol A and phthalates and endometriosis: the Endometriosis: Natural History, Diagnosis and Outcomes Study

  • University of California, San Francisco ROR
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development ROR
  • Zhejiang Chinese Medical University ROR
  • Wadsworth Center ROR
  • New York State Department of Health ROR
  • University of Utah ROR

Fertility and sterility, 99(3), 790-795

DOI 10.1016/j.fertnstert.2013.03.026

Abstract

Objective

To assess in utero exposures and the odds of an endometriosis diagnosis.

Design

Matched cohort design.

Setting

Fourteen participating clinical centers in geographically defined areas in Utah and California. PATIENT(S): Operative cohort comprised 473 women undergoing laparoscopy/laparotomy, and an ageand residence-matched population cohort comprising 127 women undergoing pelvic magnetic resonance imaging (MRI), 2007-2009. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Women completed standardized interviews before surgery or MRI regarding in utero

exposures: mothers' lifestyle during the index pregnancy, and the index woman's gestation and birth size. Endometriosis was defined as visually confirmed disease in the operative cohort, and MRI visualized disease in the population cohort. The odds of an endometriosis diagnosis and corresponding 95% confidence intervals (CI) were estimated for each exposure by cohort using logistic regression and adjusting for current smoking, age at menarche, body mass index, and study site. RESULT(S): Endometriosis was diagnosed in 41% and 11% of women in the operative and population cohorts, respectively. In the primary analysis, adjust odds ratios (AORs) were elevated for maternal vitamin usage (1.27; 95% CI, 0.85-1.91), maternal cigarette smoking (1.16; 95% CI = 0.61-2.24), and low birth weight (1.1; 95% CI, 0.92-1.32). Reduced odds were observed for maternal usage of caffeine (0.99; 95% CI, 0.64-1.54), alcohol (0.82; 95% CI, 0.35-1.94), paternal cigarette smoking (0.72; 95% CI, 0.43-1.19), and preterm delivery (0.98; 95% CI, 0.47-2.03). Sensitivity analyses mostly upheld the primary results except for a decreased AOR for preterm birth (0.41; 95% CI, 0.18-0.94) when restricting to visualized and histologically confirmed endometriosis in the operative cohort. CONCLUSION(S): In utero exposures were not statistically significantly associated with the odds of an endometriosis diagnosis in either cohort.

Topics

bisphenol A phthalates endometriosis risk exposure, environmental endocrine disruptors endometriosis diagnosis, in utero exposure endometriosis ENDO study, Buck Louis endometriosis natural history diagnosis outcomes, BPA phthalate urinary biomarkers endometriosis women, environmental chemical exposure endometriosis matched cohort, endocrine disrupting chemicals reproductive health endometriosis, prenatal exposure endometriosis developmental origins, laparoscopy confirmed endometriosis environmental risk factors, Stanford endometriosis cohort study Utah California
DOI 10.1016/j.fertnstert.2013.03.026 10.1016/j.fertnstert.2013.03.026

Cite this article

Wolff, E. F., Sun, L., Hediger, M. L., Sundaram, R., Peterson, C. M., Chen, Z., & Buck Louis, G. M. (2013). In utero exposures and endometriosis: the Endometriosis, Natural History, Disease, Outcome (ENDO) Study. *Fertility and sterility*, *99*(3), 790-795. https://doi.org/10.1016/j.fertnstert.2012.11.013

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