Influence of prenatal air pollutant and stress exposures on sleep outcomes in urban preschool-aged children

项目总结/摘要 睡眠问题是幼儿父母最常见的健康问题之一。足够 睡眠对正常生长发育很重要，持续的幼儿期睡眠问题 许多行为、认知和身体健康结果，具有潜在的终身后果。研究 在少数种族/民族中，尤其是非洲人中，睡眠障碍的患病率更高 与白人相比，美国人和拉丁美洲人独立于社会经济地位。睡眠的病因 在幼年生活中出现的困难以及观察到的差异在很大程度上仍然不为人所知。睡眠是 被概念化为“发育神经可塑性的复杂表型”。神经发育 睡眠的结构始于子宫内，经过一系列精心安排的阶段。当胎儿 暴露于环境神经毒素，中枢神经系统编程，包括神经连接 参与睡眠调节的框架，可以被破坏，导致睡眠结构和效率的改变， 童年早期产前神经毒素和产后睡眠障碍之间的联系可能取决于 暴露的时间以及剂量。候选神经毒素包括产前暴露于环境罚款 颗粒物（PM2.5）和母亲压力。此外，产前污染的影响可以通过以下方式得到加强： 同时暴露于压力下。子宫内暴露于环境空气污染物对神经发育的影响 根据人种/种族或胎儿性别进一步修改。早期生活的气质特征也是重要的决定因素 包括睡眠障碍在内的新出现的行为问题，研究表明， 调节环境危险因素与睡眠行为之间的关系。我们利用 纵向城市多种族妊娠队列（n=450对母婴），详细描述了 产前暴露于环境PM2.5，母体心理压力（终身和当前不良生活事件， 母亲的心理功能，以及由母亲毛发皮质醇指数化的生物应激反应），以及 婴儿气质，开始检查这些因素和儿童睡眠结果之间的关联。 这项倡议将支持4-5岁的睡眠表型，通过标准化的父母- 报告的睡眠问卷/日记，可穿戴加速度计和家庭多导睡眠图（PSG）， 为了：（1）检查产前PM2.5暴露与不良儿童睡眠结果之间的关联， 解释暴露的时间;（2）检查母体压力和心理生物学是否相关， 在怀孕期间进行评估，独立考虑和混合考虑，预测不良儿童睡眠结果;（3） 检查PM2.5的影响是否会受到产前压力的影响;（4）探索这些关联是否 通过i）种族/民族或ii）胎儿性别进一步修改;以及（5）检查产前空气污染和/或压力是否 婴儿期的难相处性格会对这些影响起到调节和/或调节作用。研究结果可能会开始阐明 社会和物理环境之间的相互作用导致儿童早期睡眠差异。

Project Summary/Abstract Sleep problems are one of the most common health concerns among parents of young children. Adequate sleep is important to normal growth and development and persistent early childhood sleep problems impact a host of behavioral, cognitive, and physical health outcomes, with potential lifelong consequences. Studies demonstrate a higher prevalence of sleep disturbances in racial/ethnic minorities, particularly African Americans and Latinos when compared to whites, independent of socioeconomic status. The etiology of sleep difficulties emerging in early life, as well as observed disparities, remain largely unknown. Sleep can be conceptualized as “a complex phenotype of developmental neural plasticity”. Development of the neural architecture of sleep begins in utero, through a sequence of carefully orchestrated stages. When the fetus is exposed to environmental neurotoxins, central nervous system programming, including the neural connectivity framework involved in sleep regulation, can be disrupted resulting in altered sleep architecture and efficiency in early childhood. Associations between prenatal neurotoxins and postnatal sleep disorders may depend on timing of exposure as well as dose. Candidate neurotoxins include prenatal exposure to ambient fine particulate matter (PM2.5) and maternal stress. Moreover, effects of prenatal pollution can be enhanced by concomitant exposure to stress. Neurodevelopmental effects of in utero exposure to ambient air pollutants can be further modified by race/ethnicity or fetal sex. Early life temperament traits are also important determinants of emerging behavior problems including disordered sleep, with studies showing both mediating and moderating effects on associations between environmental risk factors and sleep behaviors. We leverage a longitudinal urban multi-ethnic pregnancy cohort (n=450 mother-child pairs), with detailed characterization of prenatal exposure to ambient PM2.5, maternal psychological stress (lifetime and current adverse life events, maternal psychological functioning, and biological stress response indexed by maternal hair cortisol), and infant temperament, to begin to examine associations among these factors and childhood sleep outcomes. This initiative will support sleep phenotyping at age 4-5 years, ascertained through standardized parent- reported sleep questionnaires/diaries, wearable accelerometers, and in-home polysomnography (PSG) in order to: (1) examine associations between prenatal PM2.5 exposure and adverse child sleep outcomes, accounting for timing of exposure; (2) examine whether maternal stress and psychobiological correlates, assessed in pregnancy, considered independently and as mixtures, predict adverse child sleep outcomes; (3) examine whether PM2.5 effects are modified by prenatal stress; (4) explore whether these associations are further modified by i) race/ethnicity or ii) fetal sex; and (5) examine whether prenatal air pollution and/or stress effects are mediated and/or modified by difficult temperament in infancy. Findings may begin to elucidate how interactions among social and physical environments contribute to early childhood sleep disparities.