Gestational exposure to PM2.5, NO2, and sex steroid hormones: Identifying critical windows of exposure in the Rochester UPSIDE Cohort.

IF 3.3 Q2 ENVIRONMENTAL SCIENCES
Environmental Epidemiology Pub Date : 2025-01-15 eCollection Date: 2025-02-01 DOI:10.1097/EE9.0000000000000361
Mariah Kahwaji, Luke Duttweiler, Sally W Thurston, Donald Harrington, Richard K Miller, Susan K Murphy, Christina Wang, Jessica Brunner, Yihui Ge, Yan Lin, Philip K Hopke, Thomas G O'Connor, Junfeng J Zhang, David Q Rich, Emily S Barrett
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引用次数: 0

Abstract

Background: Sex steroid hormones are critical for maintaining pregnancy and optimal fetal development. Air pollutants are potential endocrine disruptors that may disturb sex steroidogenesis during pregnancy, potentially leading to adverse health outcomes.

Methods: In the Environmental influences on Child Health Outcomes Understanding Pregnancy Signals and Infant Development pregnancy cohort (Rochester, NY), sex steroid concentrations were collected at study visits in early-, mid-, and late-pregnancy in 299 participants. Since these visits varied by the gestational age at blood draw, values were imputed at 14, 22, and 30 weeks gestation. Daily NO2 and PM2.5 concentrations were estimated using random forest models, with daily concentrations from each 1-km2 grid containing the subject's residence. Associations between gestational week mean NO2 and PM2.5 concentrations and sex steroid concentrations were examined utilizing distributed lag nonlinear models.

Results: Each interquartile range (IQR = 9 ppb) increase in NO2 during weeks 0-5 was associated with higher early-pregnancy total testosterone levels (cumulative β = 0.45 ln[ng/dl]; 95% CI = 0.07, 0.83), while each IQR increase in NO2 during weeks 12-14 was associated with lower early-pregnancy total testosterone levels (cumulative β = -0.27 ln[ng/dl]; 95% CI = -0.53, -0.01). Similar NO2 increases during gestational weeks 0-14 were associated with higher late-pregnancy estradiol concentrations (cumulative β = 0.29 ln[pg/ml]; 95% CI = 0.10, 0.49), while each IQR increase in NO2 concentrations during gestational weeks 22-30 was associated with lower late-pregnancy estradiol concentrations (cumulative β = -0.18 ln[pg/ml]; 95% CI = -0.34, -0.02). No associations with PM2.5 were observed, except for an IQR increase in PM2.5 concentrations (IQR = 4 µg/m3) during gestational weeks 5-11 which was associated with lower late-pregnancy estriol levels (cumulative β = -0.16 ln[ng/ml]; 95% CI = -0.31, -0.00).

Conclusions: Residential NO2 exposure was associated with altered sex steroid hormone concentrations during pregnancy with some indication of potential compensatory mechanisms.

妊娠期暴露于PM2.5、二氧化氮和性类固醇激素:确定罗切斯特上行队列暴露的关键窗口期。
背景:性类固醇激素对维持妊娠和最佳胎儿发育至关重要。空气污染物是潜在的内分泌干扰物,可能会干扰怀孕期间的性类固醇生成,可能导致不利的健康后果。方法:在了解妊娠信号和婴儿发育的环境对儿童健康结局的影响妊娠队列(Rochester, NY)中,299名参与者在妊娠早期、中期和晚期的研究访问中收集了性类固醇浓度。由于这些访问随抽血时的胎龄而变化,因此在妊娠14周、22周和30周时进行了数值计算。使用随机森林模型估计NO2和PM2.5的日浓度,每1平方公里网格包含受试者的住所。利用分布滞后非线性模型检验妊娠周平均NO2和PM2.5浓度与性类固醇浓度之间的关系。结果:0-5周NO2升高的每四分位数范围(IQR = 9 ppb)与妊娠早期总睾酮水平升高相关(累积β = 0.45 ln[ng/dl];95% CI = 0.07, 0.83),而12-14周NO2每增加1 IQR与妊娠早期总睾酮水平降低相关(累积β = -0.27 ln[ng/dl];95% ci = -0.53, -0.01)。妊娠0-14周NO2升高与妊娠后期雌二醇浓度升高相关(累积β = 0.29 ln[pg/ml];95% CI = 0.10, 0.49),而妊娠22-30周NO2浓度的每一次IQR增加与妊娠后期雌二醇浓度降低相关(累积β = -0.18 ln[pg/ml];95% ci = -0.34, -0.02)。除了妊娠5-11周PM2.5浓度IQR增加(IQR = 4µg/m3)与妊娠后期雌三醇水平较低(累积β = -0.16 ln[ng/ml])相关外,未观察到与PM2.5的关联;95% ci = -0.31, -0.00)。结论:居住NO2暴露与怀孕期间性类固醇激素浓度的改变有关,并有一些潜在的补偿机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Environmental Epidemiology
Environmental Epidemiology Medicine-Public Health, Environmental and Occupational Health
CiteScore
5.70
自引率
2.80%
发文量
71
审稿时长
25 weeks
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