Age at Pubertal Onset in Girls and Tobacco Smoke Exposure During Pre- and Postnatal Susceptibility Windows

Abstract

Background Tobacco smoke contains known hormonally active chemicals and reproductive toxicants. Several studies have examined prenatal maternal smoking and offspring age at menarche, but few examined earlier pubertal markers, nor accounted for exposure during childhood. Our objective was to examine pre- and post-natal smoke exposure in relation to timing of early pubertal events. Methods An ethnically diverse cohort of 1239 girls was enrolled at age 6–8 years for a longitudinal study of puberty at three U.S. sites. Girls participated in annual or semi-annual exams to measure anthropometry and Tanner breast and pubic hair stages. Prenatal and current tobacco smoke exposures, as well as covariates, were obtained from parent questionnaire. Cotinine was measured in urine collected at enrollment. Using accelerated failure time models, we calculated adjusted time ratios for age at pubertal onset (maturation stages 2 or higher) and smoke exposure. Results Girls with higher prenatal (≥5 cigarettes/day) or secondhand smoke exposure had earlier pubic hair development than unexposed (adjusted time ratio = 0.92 (95% CI 0.87–0.97) and 0.94 (95% CI 0.90–0.97), respectively). Including both exposures in the same model yielded similar associations. Higher urinary cotinine quartiles were associated with younger age at breast and pubic hair onset in unadjusted models, but not after adjustment. Conclusions Greater prenatal and childhood secondhand smoke exposure were associated with earlier onset of pubic hair, but not breast, development. These exposures represent modifiable risk factors for early pubertal development that should be considered for addition to the extensive list of adverse effects from tobacco smoke.

Maternal Smoking During Pregnancy and Timing of Puberty in Sons and Daughters: A Population-Based Cohort Study

“…This is corroborated by the similar associations for both early and late milestones. The only exception was the null finding for Tanner stage 2 for pubic hair in girls, which is in line with former data on girls of white ethnicity (26, 40). Despite this, we cannot rule out that the null finding for Tanner stage 2 for pubic hair in girls is due to left censoring and a skewed distribution of the residuals for this specific milestone.…”

“…Other important markers of puberty are less well studied. These markers include breast and pubic hair development in daughters (26, 37, 40) and genital and pubic hair development in sons (39, 41).…”

Urinary polycyclic aromatic hydrocarbons in relation to anthropometric measures and pubertal development in a cohort of Northern California girls

“…Prenatal and secondhand tobacco smoke exposure in young girls resulted in earlier public hair development in the full BCERP cohort; among girls overweight/obese at baseline, pubic hair development was even earlier. 24 Measured urinary cotinine concentrations, a nicotine metabolite and established biomarker of secondhand smoke exposure, at baseline were not associated with age at breast and public hair onset. 24 Another exposure, residential proximity to higher levels of traffic metrics as indicators of air pollution exposure (e.g., traffic volume, traffic density) was found to be associated with earlier pubic hair development and the association was not mediated by BMI in the same cohort.…”

“… 24 Measured urinary cotinine concentrations, a nicotine metabolite and established biomarker of secondhand smoke exposure, at baseline were not associated with age at breast and public hair onset. 24 Another exposure, residential proximity to higher levels of traffic metrics as indicators of air pollution exposure (e.g., traffic volume, traffic density) was found to be associated with earlier pubic hair development and the association was not mediated by BMI in the same cohort. 25 The null findings for measured urinary cotinine concentrations are consistent with our null findings between measured baseline PAHs metabolites and pubertal onset among all girls.…”

“… 23 To date, there have been no longitudinal studies examining childhood exposure to PAH metabolites and obesity. Early pubertal development has been associated both with childhood environmental tobacco smoke exposure 24 and residential traffic-related air pollution exposure, 25 respectively, which could in part reflect PAH exposure, yet the association between PAH metabolites and pubertal onset has not been studied directly.…”