From the aCA Department of Public Health, Richmond, CA; bImpact Assessment Inc., La Jolla, CA; cIcahn School of Medicine at Mount Sinai, New York City, NY; dUniversity of Cincinnati College of Medicine, Cincinnati, OH; eCenters for Disease Control and Prevention, Atlanta, GA; fUniversity of California San Francisco, San Francisco, CA; gKaiser Permanente, San Francisco, CA; and hKaiser Permanente Division of Research, Oakland, CA.
Epidemiology. 2017 Sep;28(5):719-727. doi: 10.1097/EDE.0000000000000704.
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 postnatal smoke exposure in relation to timing of early pubertal events.
An ethnically diverse cohort of 1239 girls was enrolled at age 6-8 years old for a longitudinal study of puberty at three US 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.
Girls with higher prenatal (≥5 cigarettes per 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.
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.
烟草烟雾中含有已知的具有激素活性的化学物质和生殖毒物。有几项研究检查了产前母亲吸烟和子女初潮年龄,但很少有研究检查更早的青春期标志物,也没有考虑到儿童时期的暴露。我们的目的是研究产前和产后吸烟暴露与早期青春期事件发生时间的关系。
在三个美国地点,对 1239 名女孩进行了一项关于青春期的纵向研究,这些女孩在 6-8 岁时被纳入该研究。女孩们每年或每半年参加一次考试,以测量身高和乳房及阴毛发育的 Tanner 分期。从父母的调查问卷中获得产前和当前的吸烟暴露以及协变量。在入组时收集尿液以测量可替宁。使用加速失效时间模型,我们计算了青春期起始年龄(发育阶段 2 或更高)和吸烟暴露的调整时间比。
与未暴露的女孩相比,具有更高的产前(每天≥5 支香烟)或二手烟暴露的女孩阴毛发育更早(调整后的时间比:0.92 [95%可信区间 0.87,0.97]和 0.94 [95%可信区间 0.90,0.97])。在同一个模型中包括这两种暴露也会产生类似的关联。未调整模型中,更高的尿可替宁四分位数与乳房和阴毛起始年龄更小有关,但调整后则不然。
更大的产前和儿童时期二手烟暴露与阴毛更早发育有关,但与乳房发育无关。这些暴露是可改变的青春期早期发育风险因素,应该考虑添加到烟草烟雾的大量不良影响列表中。