263588 Prenatal Tobacco Smoke Exposure and Reproductive Hormones Near the Onset of Puberty in US Girls

Tuesday, October 30, 2012 : 2:35 PM - 2:50 PM

Audra L. Gollenberg, PhD , Department of Public Health, Shenandoah University, Winchester, VA
O. Yaw Addo, PhD , Rollins School of Public Health, Hubert Dept of Global Health, Emory University, Atlanta, GA
John H. Himes, PhD , School of Public Health, University of Minnesota, Minneapolis, MN
Peter A. Lee, MD, PhD , Department of Pediatrics, Penn State College of Medicine/Milton S. Hershey Medical Center, Hershey, PA
Mary L. Hediger, PhD , Epidemiology Branch/Division of Epidemiology, Statistics, and Prevention Research, NICHD/NIH/DHHS, Rockville, MD
Mixed evidence suggests that prenatal smoking may disrupt development and delay age at menarche, though peripubertal hormone measurements have not been widely studied.

Objective: We examined reports of prenatal smoking and current environmental tobacco smoke (ETS) exposures in relation to luteinizing hormone (LH) and inhibin B (InB) in stored blood specimens from 6-11 year-old girls in the 3rd National Health and Nutrition Examination Survey (NHANES III).

Methods: Participants in the cross-sectional NHANES III (1988-1994) were recruited using a multi-stage, clustered sampling procedure to create a representative population. We used appropriate statistical techniques to account for laboratory limits of detection, sampling weights that reflect the availability of stored biospecimens, and recursive structural equation models (SEM) to analyze hypothesized structural pathways linking the observed variables and unobserved (latent) factors.

Results: Of 660 girls with complete information, 19% and 39% were exposed to prenatal smoke and current ETS, respectively. Accounting for pathways involving height, BMI-for-age, health status, ETS and demographics, girls exposed prenatally to smoking had significantly lower LH (=-0.25 NaturalLog(Ln)-mIU/mL, p<0.001). Prenatal smoking influenced InB indirectly through BMI-for-age, i.e. girls exposed prenatally had greater BMI-for-age (=0.25 Ln-kg/m2, p=0.02) and BMI was negatively associated with InB (=-0.13 Ln-pg/mL, p<0.0001). Neither exposure to ETS nor both ETS/prenatal smoke was associated with either hormone after accounting for other direct/indirect pathways.

Conclusion: Little is known regarding early origins of pubertal onset. Exposure to prenatal smoke may disrupt reproductive development manifesting in altered hormone levels, such as LH, which are primary indicators of pubertal onset.

Learning Areas:
Epidemiology

Learning Objectives:
Participants will explain the importance of considering early origins of pubertal development in girls. Participants will identify direct pathways and indirect pathways in which prenatal smoke exposure may influence reproductive hormones in young girls.

Keywords: Adolescent Health, Reproductive Health

Presenting author's disclosure statement:

Qualified on the content I am responsible for because: I have completed a PhD in Epidemiology in 2008 and have several years of experience conducting research and teaching in reproductive epidemiology.
Any relevant financial relationships? No

I agree to comply with the American Public Health Association Conflict of Interest and Commercial Support Guidelines, and to disclose to the participants any off-label or experimental uses of a commercial product or service discussed in my presentation.