Abstract：
BACKGROUND: Polycyclic aromatic hydrocarbons (PAHs) are endocrine disruptors resulting from incomplete combustion. Pregnancy represents a particularly vulnerable period to such exposures, given the significant influence of hormone physiology on fetal growth and pregnancy outcomes. Maternal thyroid hormones play crucial roles in fetal development and pregnancy outcomes. However, limited studies have examined gestational PAH exposure and maternal thyroid hormones during pregnancy.
METHODS: Our study included 439 women enrolled in the LIFECODES birth cohort in Boston, aiming to explore the relationship between urinary PAH metabolites and thyroid hormones throughout pregnancy. Urine samples for PAH metabolite analysis and plasma samples for thyroid hormone were measured up to four visits throughout gestation. Single pollutant analyses employed linear mixed effect models to investigate individual associations between each PAH metabolite and thyroid hormone concentration. Sensitivity analyses were conducted to assess potential susceptibility windows and fetal-sex-specific effects of PAH exposure. Mixture analyses utilized quantile g-computation to evaluate the collective impact of eight PAH metabolites on thyroid hormone concentrations. Additionally, Bayesian kernel machine regression (BKMR) was employed to explore potential non-linear associations and interactions between PAH metabolites. Subject-specific random intercepts were incorporated to address intra-individual correlation of serial measurements over time in both single pollutant and mixture analyses.
RESULTS: Our findings revealed positive trends in associations between PAH metabolites and thyroid hormones, both individually and collectively as a mixture. Sensitivity analyses indicated that these associations were influenced by the study visit and fetal sex. Mixture analyses suggested non-linear relationships and interactions between different PAH exposures.
CONCLUSIONS: This comprehensive investigation underscores the critical importance of understanding the impact of PAH exposures on thyroid hormone physiology during pregnancy. The findings highlight the intricate interplay between environmental pollutants and human pregnancy physiology, emphasizing the need for targeted interventions and public health policies to mitigate adverse outcomes associated with prenatal PAH exposure.
METHODS: Our study included 439 women enrolled in the LIFECODES birth cohort in Boston, aiming to explore the relationship between urinary PAH metabolites and thyroid hormones throughout pregnancy. Urine samples for PAH metabolite analysis and plasma samples for thyroid hormone were measured up to four visits throughout gestation. Single pollutant analyses employed linear mixed effect models to investigate individual associations between each PAH metabolite and thyroid hormone concentration. Sensitivity analyses were conducted to assess potential susceptibility windows and fetal-sex-specific effects of PAH exposure. Mixture analyses utilized quantile g-computation to evaluate the collective impact of eight PAH metabolites on thyroid hormone concentrations. Additionally, Bayesian kernel machine regression (BKMR) was employed to explore potential non-linear associations and interactions between PAH metabolites. Subject-specific random intercepts were incorporated to address intra-individual correlation of serial measurements over time in both single pollutant and mixture analyses.
RESULTS: Our findings revealed positive trends in associations between PAH metabolites and thyroid hormones, both individually and collectively as a mixture. Sensitivity analyses indicated that these associations were influenced by the study visit and fetal sex. Mixture analyses suggested non-linear relationships and interactions between different PAH exposures.
CONCLUSIONS: This comprehensive investigation underscores the critical importance of understanding the impact of PAH exposures on thyroid hormone physiology during pregnancy. The findings highlight the intricate interplay between environmental pollutants and human pregnancy physiology, emphasizing the need for targeted interventions and public health policies to mitigate adverse outcomes associated with prenatal PAH exposure.
摘要：
背景：多环芳烃（PAHs）是由不完全燃烧引起的内分泌干扰物。怀孕是一个特别容易受到这种暴露的时期，鉴于激素生理对胎儿生长和妊娠结局的显著影响。母体甲状腺激素在胎儿发育和妊娠结局中起着至关重要的作用。然而,有限的研究已经检查了妊娠期PAH暴露和妊娠期母体甲状腺激素。
方法：我们的研究纳入了波士顿LIFECODES出生队列中的439名女性，目的探讨妊娠期尿PAH代谢产物与甲状腺激素的关系。在整个妊娠期间，测量了用于PAH代谢物分析的尿液样本和甲状腺激素的血浆样本，直至四次就诊。单一污染物分析采用线性混合效应模型来研究每种PAH代谢物与甲状腺激素浓度之间的个体关联。进行敏感性分析以评估PAH暴露的潜在易感性窗口和胎儿性别特异性影响。混合物分析利用分位数g计算来评估八种PAH代谢物对甲状腺激素浓度的集体影响。此外,贝叶斯核机回归（BKMR）用于探索PAH代谢物之间潜在的非线性关联和相互作用。纳入了特定于受试者的随机截距，以解决单污染物和混合物分析中连续测量随时间变化的个体内相关性。
结果：我们的发现揭示了PAH代谢物与甲状腺激素之间的正相关趋势，无论是单独的和集体的混合物。敏感性分析表明，这些关联受研究访视和胎儿性别的影响。混合物分析表明，不同PAH暴露之间存在非线性关系和相互作用。
结论：这项全面的调查强调了了解妊娠期间PAH暴露对甲状腺激素生理的影响至关重要。研究结果强调了环境污染物与人类怀孕生理学之间的复杂相互作用，强调需要有针对性的干预措施和公共卫生政策，以减轻与产前PAH暴露相关的不良结局。
方法：我们的研究纳入了波士顿LIFECODES出生队列中的439名女性，目的探讨妊娠期尿PAH代谢产物与甲状腺激素的关系。在整个妊娠期间，测量了用于PAH代谢物分析的尿液样本和甲状腺激素的血浆样本，直至四次就诊。单一污染物分析采用线性混合效应模型来研究每种PAH代谢物与甲状腺激素浓度之间的个体关联。进行敏感性分析以评估PAH暴露的潜在易感性窗口和胎儿性别特异性影响。混合物分析利用分位数g计算来评估八种PAH代谢物对甲状腺激素浓度的集体影响。此外,贝叶斯核机回归（BKMR）用于探索PAH代谢物之间潜在的非线性关联和相互作用。纳入了特定于受试者的随机截距，以解决单污染物和混合物分析中连续测量随时间变化的个体内相关性。
结果：我们的发现揭示了PAH代谢物与甲状腺激素之间的正相关趋势，无论是单独的和集体的混合物。敏感性分析表明，这些关联受研究访视和胎儿性别的影响。混合物分析表明，不同PAH暴露之间存在非线性关系和相互作用。
结论：这项全面的调查强调了了解妊娠期间PAH暴露对甲状腺激素生理的影响至关重要。研究结果强调了环境污染物与人类怀孕生理学之间的复杂相互作用，强调需要有针对性的干预措施和公共卫生政策，以减轻与产前PAH暴露相关的不良结局。
