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

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 (ß=-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 (ß=0.25 Ln-kg/m2, p=0.02) and BMI was negatively associated with InB (ß=-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.