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Polybrominated Biphenyl Exposure and Menstrual Cycle Function

Howards, Penelope P.a; Terrell, Metrecia L.a; Jacobson, Melanie H.a; Taylor, Kira C.a,b; Kesner, James S.c; Meadows, Juliana W.c; Spencer, Jessica B.d; Manatunga, Amita K.e; Marcus, Michelea,f,g

doi: 10.1097/EDE.0000000000001045
Reproductive Epidemiology
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Background: Brominated flame retardants, including polybrominated biphenyls (PBB), are persistent compounds reported to affect sex hormones in animals; less is known about potential effects in humans. An industrial accident in 1973–1974 exposed Michigan residents to PBB through contaminated food. We examined whether this exposure to PBB had long-term effects on menstrual cycle function.

Methods: In 2004–2006, we recruited reproductive-aged women in the Michigan PBB Registry who were not pregnant, lactating, or taking hormonal medications. Participants kept daily diaries and provided daily urine samples for up to 6 months. We assayed the urine samples for estrone 3-glucuronide (E13G), pregnanediol 3-glucuronide (Pd3G), and follicle stimulating hormone (FSH). We fit linear mixed models among women aged 35–42 years to describe the relation between serum PBB levels and log-transformed, creatinine-adjusted daily endocrine levels among women who were premenarchal during the exposure incident in 1973–1974 (n = 70).

Results: We observed that high (>3.0 parts per billion [ppb]) and medium (>1.0–3.0 ppb) PBB exposure were associated with lower E13G levels across the menstrual cycle and lower FSH levels during the follicular phase, compared with low PBB exposure (≤1.0 ppb). High PBB exposure was also associated with lower Pd3G levels across the cycle compared with low PBB exposure, whereas Pd3G levels were similar in women with medium and low PBB exposure.

Conclusion: Our results are consistent with a hypothesized effect of exposure to an exogenous estrogen agonist but the modest sample size of the study requires cautious interpretation.

From the aDepartment of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA

bEpidemiology and Population Health, School of Public Health and Information Sciences, University of Louisville, Louisville, KY

cNational Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Cincinnati, OH

dReproductive Endocrinology and Infertility, Department of Gynecology and Obstetrics, Emory University, Atlanta, GA

eDepartment of Biostatistics and Bioinformatics, Rollins School of Public Health, Emory University, Atlanta, GA

fDepartment of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA

gPediatrics, School of Medicine, Emory University, Atlanta, GA.

Submitted June 26, 2018; accepted May 21, 2019.

The results reported herein correspond to specific aims of grant R01 ES08341 and R01 ES012014 to investigator M.M. from the National Institutes of Health (NIH). Supported by grant R 82530 from the U.S. Environmental Protection Agency, grant U37/CCU500392 from the Centers for Disease Control and Prevention, and grant P30 ES019776 from NIH.

The findings and conclusions in this report are those of the authors and do not necessarily represent the views of NIOSH. Mention of any company or product does not constitute endorsement by NIOSH.

Requests for access to data and code used in these analyses should be addressed to Michele Marcus, Emory University, 1518 Clifton Rd NE CNR 4045, Atlanta, GA 30322. Phone: 404-727-8010. E-mail: mmarcus@emory.edu

The authors report no conflicts of interest.

Supplemental digital content is available through direct URL citations in the HTML and PDF versions of this article (www.epidem.com).

Correspondence: Penelope Howards, Epidemiology Department, Emory University, 1518 Clifton Rd, NE, CNR 3029, Atlanta, GA 30322. E-mail: penelope.howards@emory.edu.

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