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Changzhong Chen,¹ Xiaobin Wang,² Lihua Wang,³ Fan Yang,⁴ Genfu Tang,⁴ Houxun Xing,⁴ Louise Ryan,⁵ Bill Lasley,⁶ James W. Overstreet,⁶ Joseph B. Stanford,⁷ and Xiping Xu¹

¹Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA; ²Department of Pediatrics, Northwestern University Feinberg School of Medicine and Children’s Memorial Hospital and Children’s Memorial Research Center, Chicago, Illinois, USA; ³Center for Ecogenetics and Reproductive Health, Beijing Medical University, Beijing, China; ⁴Institute for Biomedicine, Anhui Medical University, Anhui, China; ⁵Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts, USA; ⁶Institute of Toxicology and Environmental Health and Department of Obstetrics and Gynecology, School of Medicine, University of California, Davis, California, USA; ⁷Health Research Center, Department of Family and Preventive Medicine, University of Utah, Salt Lake City, Utah, USA

Abstract
Our recent study showed a dose-response relationship between environmental tobacco smoke (ETS) and the risk of early pregnancy loss. Smoking is known to affect female reproductive hormones. We explored whether ETS affects reproductive hormone profiles as characterized by urinary pregnanediol-3-glucuronide (PdG) and estrone conjugate (E₁C) levels. We prospectively studied 371 healthy newly married nonsmoking women in China who intended to conceive and had stopped contraception. Daily records of vaginal bleeding, active and passive cigarette smoking, and daily first-morning urine specimens were collected for up to 1 year or until a clinical pregnancy was achieved. We determined the day of ovulation for each menstrual cycle. The effects of ETS exposure on daily urinary PdG and E₁C levels in a ±10 day window around the day of ovulation were analyzed for conception and nonconception cycles, respectively. Our analysis included 344 nonconception cycles and 329 conception cycles. In nonconception cycles, cycles with ETS exposure had significantly lower urinary E₁C levels (β = -0.43, SE = 0.08, p < 0.001 in log scale) compared with the cycles without ETS exposure. There was no significant difference in urinary PdG levels in cycles having ETS exposure (β = -0.07, SE = 0.15, p = 0.637 in log scale) compared with no ETS exposure. Among conception cycles, there were no significant differences in E₁C and PdG levels between ETS exposure and nonexposure. In conclusion, ETS exposure was associated with significantly lower urinary E₁C levels among nonconception cycles, suggesting that the adverse reproductive effect of ETS may act partly through its antiestrogen effects. Key words: environmental tobacco smoke, estrone conjugates (E₁C) , pregnanediol-3-glucuronide (PdG) , prospective study, urinary hormone levels. Environ Health Perspect 113:412-417 (2005) . doi:10.1289/ehp.7436 available via http://dx.doi.org/ [Online 14 January 2005]

Address correspondence to X. Wang, The Mary Ann and J. Milburn Smith Child Health Research Program, Children’s Memorial Hospital and Children’s Memorial Research Center, 2300 Children’s Plaza, #157, Chicago, IL 60614 USA. Telephone: (312) 573-7738. Fax: (312) 573-7825. E-mail: xbwang@childrensmemorial.org

This study is supported in part by grants 1R01 HD32505 from the National Institute of Child Health and Human Development ; 1R01 ES08337, ES-00002, P01 ES06198, and 1R01 ES11682 from the National Institute of Environmental Health Sciences ; and 20-FY98-0701 and 20-FY02-56 from the March of Dimes Birth Defects Foundation.

The authors declare they have no competing financial interests.

Received 21 July 2004 ; accepted 13 January 2005.

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