Department of Pediatrics, Penn State University Hershey Medical Center, Hershey, Pennsylvania 17033-0850, USA.
Environ Health Perspect. 2012 Jun;120(6):916-20. doi: 10.1289/ehp.1104175. Epub 2012 Feb 14.
Bisphenol A (BPA), an endocrine-disrupting chemical that is routinely detected in > 90% of Americans, promotes experimental asthma in mice. The association of prenatal BPA exposure and wheeze has not been evaluated in humans.
We examined the relationship between prenatal BPA exposure and wheeze in early childhood.
We measured BPA concentrations in serial maternal urine samples from a prospective birth cohort of 398 mother-infant pairs and assessed parent-reported child wheeze every 6 months for 3 years. We used generalized estimating equations with a logit link to evaluate the association of prenatal urinary BPA concentration with the dichotomous outcome wheeze (wheeze over the previous 6 months).
Data were available for 365 children; BPA was detected in 99% of maternal urine samples during pregnancy. In multivariable analysis, a one-unit increase in log-transformed creatinine-standardized mean prenatal urinary BPA concentration was not significantly associated with child wheeze from birth to 3 years of age, but there was an interaction of BPA concentration with time (p = 0.003). Mean prenatal BPA above versus below the median was positively associated with wheeze at 6 months of age [adjusted odds ratio (AOR) = 2.3; 95% confidence interval (CI): 1.3, 4.1] but not at 3 years (AOR = 0.6; 95% CI: 0.3, 1.1). In secondary analyses evaluating associations of each prenatal BPA concentration separately, urinary BPA concentrations measured at 16 weeks gestation were associated with wheeze (AOR = 1.2; 95% CI: 1.0, 1.5), but BPA concentrations at 26 weeks of gestation or at birth were not.
Mean prenatal BPA was associated with increased odds of wheeze in early life, and the effect diminished over time. Evaluating exposure at each prenatal time point demonstrated an association between wheeze from 6 months to 3 years and log-transformed BPA concentration at 16 weeks gestation only.
双酚 A（BPA）是一种内分泌干扰化学物质，超过 90%的美国人的尿液中都能检测到这种物质，它会促进实验性哮喘的发生。但是，产前 BPA 暴露与喘息之间的关联尚未在人类中得到评估。
我们研究了产前 BPA 暴露与儿童早期喘息之间的关系。
我们在一个前瞻性的母婴队列中，对 398 对母婴对的连续母亲尿液样本进行了 BPA 浓度测量，并在 3 年内每 6 个月评估一次儿童父母报告的喘息情况。我们使用广义估计方程和对数链接评估了产前尿液 BPA 浓度与二分类结局（过去 6 个月内的喘息）之间的关联。
数据可用于 365 名儿童；在妊娠期间，99%的母亲尿液样本中检测到 BPA。在多变量分析中，对数转换的肌酐标准化平均产前尿液 BPA 浓度每增加一个单位，与儿童从出生到 3 岁的喘息无关，但 BPA 浓度与时间之间存在交互作用（p=0.003）。高于中位数与低于中位数的平均产前 BPA 浓度与 6 个月龄时的喘息呈正相关（调整后的优势比（AOR）=2.3；95%置信区间（CI）：1.3，4.1），但与 3 岁时无关（AOR=0.6；95%CI：0.3，1.1）。在评估每个产前 BPA 浓度分别的关联的二次分析中，妊娠 16 周时的尿液 BPA 浓度与喘息相关（AOR=1.2；95%CI：1.0，1.5），而妊娠 26 周或出生时的 BPA 浓度则没有。
平均产前 BPA 与生命早期喘息的发生几率增加有关，并且这种影响随着时间的推移而减弱。评估每个产前时间点的暴露情况仅表明，从 6 个月到 3 岁的喘息与妊娠 16 周时的 BPA 浓度对数之间存在关联。
