Pre- and postnatal chemical mixture exposure, adolescent sleep health, and allostatic load
产前和产后化学混合物暴露、青少年睡眠健康和稳态负荷
基本信息
- 批准号:10639218
- 负责人:
- 金额:$ 56.24万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2023
- 资助国家:美国
- 起止时间:2023-09-12 至 2028-06-30
- 项目状态:未结题
- 来源:
- 关键词:AdolescenceAdolescentAdolescent DevelopmentAdrenal GlandsAdultAgeBiologicalBiological MarkersBiometryBirthBody CompositionCardiovascular systemCatecholaminesCharacteristicsChemicalsChildChildhoodCortisoneDataDevelopmentDietDiseaseEnrollmentEnvironmentEnvironmental ExposureEnvironmental HealthEnvironmental Risk FactorEpidemiologyExposure toFoundationsGlycoproteinsGoalsGrowthHairHealthHomeostasisHydrocortisoneHypertensionHypothalamic structureImmuneIndividualInfantInflammationInterventionJointsKnowledgeLifeLinkLongitudinal StudiesLongitudinal cohortMeasuresMetabolicMetalsMiddle School StudentMorbidity - disease rateNeurobiologyNeurosecretory SystemsObesityOutcomeOutcome MeasurePathway interactionsPersonsPhysiologicalPituitary GlandPituitary-Adrenal SystemPoly-fluoroalkyl substancesPredispositionPregnancyPregnant WomenProcessProspective cohortQuestionnairesRegulationResearchRiskRisk FactorsRisk ReductionSchool-Age PopulationSerumShapesSleepSystemTestingToxic Environmental SubstancesToxicant exposureVisitactigraphyadequate sleepallostasisallostatic loadblood pressure elevationcardiometabolismcardiovascular disorder riskcardiovascular healthcardiovascular risk factorcohortconsumer productcritical developmental perioddesignearly childhoodearly life exposureenvironmental chemicalhigh schoolimprovedimprovement on sleepindexinginfancymodifiable riskmortalitymultidisciplinaryneurobiological mechanismneurodevelopmentneurotoxicnovelphthalatespollutantpoor sleeppostnatalpregnantprenatalprospectivepublic health interventionsleep healthsleep qualitysystemic inflammatory responsetoxic metaltoxicanturinary
项目摘要
PROJECT SUMMARY / ABSTRACT
A majority of U.S. adolescents are not getting sufficient sleep for optimal health. Sleep health is critical during
adolescence because of rapid neurodevelopment, growth, and body composition changes. Moreover,
inadequate and poor-quality sleep can increase allostatic load, or cumulative physiological ‘wear and tear’, from
disruptions across multiple regulatory systems that coordinate immune, cardiovascular, and metabolic function.
Evidence indicates that developmental exposures to ubiquitous environmental toxicants may disrupt
neurobiological mechanisms that regulate sleep and allostasis. However, whether these exposures are
modifiable risk factors for poor sleep during adolescence has not been rigorously examined. Our multidisciplinary
project brings together experts in pediatric environmental health, sleep, and cardiometabolic health to identify
whether early life exposure to environmental toxicant mixtures disrupts adolescent sleep health and increases
allostatic load. This project focuses on mixtures of phthalates, per-/polyfluoroalkyl substances (PFAS), and
metals. Most pregnant people, infants, and children are exposed to mixtures of these toxicants through diet and
consumer goods. The project leverages existing and new data from two well-characterized prospective
pregnancy and birth cohorts, the Health Outcomes and Measures of the Environment (HOME) Study and the
Maternal-Infant Research on Environmental Chemicals (MIREC) Study. Both cohorts previously enrolled
pregnant women and followed children until ages 7-9 (MIREC n=300) or 10-12 (HOME n=256) years with
additional visits underway at ages 10-12 (MIREC) and 16-18 (HOME) years. Sleep characteristics will be
examined at two timepoints in both cohorts using actigraphy. We will quantify relations between environmental
toxicant biomarkers during gestation, early childhood, school age, and adolescence with sleep characteristics
(Aim 1) and allostatic load (Aim 2) during adolescence. We will also examine whether exposure to environmental
toxicant mixtures is associated with hypothalamus-pituitary-adrenal (HPA) activity, catecholamines, and
systemic inflammation, biological intermediates of sleep-wake regulation and allostasis (Aim 3). Our analyses
will identify individual and joint effects of environmental toxicant mixtures and examine periods of heightened
susceptibility during critical developmental periods. Identifying modifiable environmental factors that contribute
to poor sleep health and allostatic load may inform novel interventions to reduce the risk of cardiovascular
disease, the leading cause of morbidity and mortality in adulthood worldwide.
项目摘要 /摘要
大多数美国青少年没有足够的睡眠来获得最佳健康。睡眠健康至关重要
青少年由于神经发育,生长和身体成分的快速变化。而且,
不足和质量不足的睡眠会增加同性恋负荷或累积的生理“磨损”
多个调节系统的破坏,这些调节系统是协调免疫学,心血管和代谢功能的。
证据表明,发育性暴露于无处不在的环境有毒物质可能会破坏
调节睡眠和同性恋的神经生物学机制。但是,这些暴露是
青少年期间睡眠不佳的可修改风险因素尚未进行严格检查。我们的多学科
项目汇集了儿科环境健康,睡眠和心脏代谢健康方面的专家
早期生命暴露于环境有毒物质混合物是否会破坏青少年睡眠健康并增加
同级负载。该项目的重点是邻苯二甲酸盐,每/多氟烷基物质(PFA)和
金属。大多数孕妇,婴儿和儿童都会通过饮食和
消费品。该项目利用两个特征良好的潜在的现有数据和新数据
怀孕和出生队列,环境的健康成果和措施(家庭)研究和
孕产妇环境化学研究(MIREC)研究。两个队列先前均已注册
孕妇并跟随儿童直到7-9岁(MIREC n = 300)或10-12(家庭n = 256)年
在10-12岁(MIREC)和16-18岁(家庭)年的额外访问中。睡眠特征将是
使用行为摄影在两个队列中的两个时间点检查。我们将量化环境之间的关系
妊娠,童年,学龄和青少年的毒物生物标志物具有睡眠特征
(AIM 1)和Allostatic载荷(AIM 2)在青少年期间。我们还将检查是否接触环境
毒物混合物与下丘脑 - 垂体 - 肾上腺(HPA)活性,儿茶酚胺和
系统性炎症,睡眠效果调节的生物学中间体和同性恋(AIM 3)。我们的分析
将确定环境有毒物质的个人和关节作用,并检查了增长的时期
关键发育时期的敏感性。确定可改变的环境因素
对于睡眠不良和同性恋负荷可能会导致新颖的干预措施,以降低心血管的风险
疾病,是全球成年期发病和死亡率的主要原因。
项目成果
期刊论文数量(0)
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