Some chemicals appear to have hormonally active properties in animals, but data in humans are sparse. Therefore, we examined ovarian function in relation to organochlorine compound levels.
During 1997–1999, 50 Southeast Asian immigrant women of reproductive age collected urine samples daily. These samples were assayed for metabolites of estrogen and progesterone, and the women's menstrual cycle parameters were assessed. Organochlorine compounds (including DDT, its metabolite DDE, and 10 polychlorinated biphenyl [PCB] congeners) were measured in serum.
All samples had detectable DDT and DDE, with mean levels higher than typical U.S. populations. Mean cycle length was approximately 4 days shorter at the highest quartile concentration of DDT or DDE compared with the lowest. After adjustment for lipid levels, age, parity, and tubal ligation, and exclusion of a particularly long cycle, the decrements were attenuated to less than 1 day, with wide confidence intervals (CIs). The adjusted mean luteal phase length was shorter by approximately 1.5 days at the highest quartile of DDT (95% CI = −2.6 to −0.30) or DDE (−2.6 to −0.20). With each doubling of the DDE level, cycle length decreased 1.1 day (−2.4 to 0.23) and luteal phase length decreased 0.6 days (−1.1 to −0.2). Progesterone metabolite levels during the luteal phase were consistently decreased with higher DDE concentration. PCB levels were not generally associated with cycle length or hormone parameters after adjustment, and they did not alter the DDE associations when included in the same models.
This study indicates a potential effect of DDE on ovarian function, which may influence other end points such as fertility, pregnancy, and reproductive cancers.
Supplemental Digital Content is Available in the Text.
From the *Environmental Health Investigations Branch, Department of Health Services, Oakland, California; the †Public Health Institute, Berkeley, California; ‡Impact Assessment Inc., La Jolla, California; the §Hazardous Materials Laboratory, Department of Toxic Substances Control, California Environmental Protection Agency, Berkeley, California; and the ∥Institute of Toxicology and Environmental Health, School of Medicine, University of California, Davis, California.
Submitted 15 January 2004; final version accepted 16 November 2004.
This study was funded by the National Institute of Environmental Health Sciences (R01 ES08324) and the Office of Women's Health, administered through the Public Health Institute of Berkeley, CA.
Supplemental material for this article is available with the online version of the Journal at www.epidem.com.
Correspondence: Gayle C. Windham, Environmental Health Investigations Branch, Department of Health Services, 1515 Clay St., Suite 1700, Oakland, CA 94612. E-mail: firstname.lastname@example.org.