Project 1: Multi-Exposure Epidemiology Across the Life Course

项目 1：生命历程中的多重暴露流行病学

基本信息

批准号：
9270435
负责人：
Antonella Zanobetti
金额：
$ 12.55万
依托单位：
HARVARD SCHOOL OF PUBLIC HEALTH
依托单位国家：
美国
项目类别：
财政年份：
资助国家：
美国
起止时间：
至
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/9270435
关键词：
Accident and Emergency department Accounting Acute Address Adult Affect Age Air Pollution Biological Birth Birth Weight Boston Carbon Black Cardiovascular system Caregivers Cessation of life Characteristics Chemicals Child Child health care Childhood Clinic Communities Coronary Artery Risk Development in Young Adults Study Data Data Sources Enrollment Environmental Health Epidemiology Epigenetic Process Ethnic Origin Exposure to Food Green space Growth Health Housing Individual Infiltration Knowledge Life Cycle Stages Longevity Low Income Population Massachusetts Measures Medical Records Medical center Methods Modeling Modification Neighborhoods Nitrogen Dioxide Noise Outcome Premature Birth Public Health Race Registries Site Small for Gestational Age Infant Socioeconomic Status Specific qualifier value Statistical Methods Temperature Time Uncertainty United States Vulnerable Populations Work built environment density early childhood environmental stressor epidemiology study fine particles genome wide methylation health disparity high dimensionality improved innovation mortality novel particle racial diversity residence social social health determinants stressor study population urban children walkability

项目摘要

PROJECT SUMMARY Several epidemiological studies have found an association between exposure to chemical stressors (such as air pollution) and non-chemical stressors (such as temperature, noise, green space, socioeconomic status [SES], race, and ethnicity), and health outcomes. However, few of these studies have: 1) estimated the health effects across the life course associated with simultaneous exposure to multiple chemical stressors; 2) characterized confounding/effect modification by non-chemical stressors and social determinants of health disparities, particularly factors such as housing conditions and food insecurity; and 3) investigated whether exposure to these chemical stressors can affect health through epigenetic modifications. Moreover, there is a need for new statistical methods that can account for the high dimensionality of the exposures, confounders, and interaction terms in order to understand the effect on health outcomes. We have assembled four unique study populations, three in the Commonwealth of Massachusetts (MA), with data on health outcomes spanning from birth to death, as well as a wealth of information on potential determinants of health disparities. In Aim 1, we will develop innovative statistical methods to estimate health effects associated with a large number of exposures (chemical stressors), while also accounting for large number of potential confounders and interactions. In Aim 2, we will estimate the association between exposure to multiple chemical stressors on birth outcomes, childhood growth rates, and cardiovascular mortality. We will examine effect modification by non-chemical stressors at an individual residence level, including temperatures, noise, green space, and the built environment (neighborhood walkability). We will also examine effect modification by a rich host of individual-level social determinants of health disparities (e.g., age, race/ethnicity, SES). In addition, through the work of Projects 2 and 3, we will have access to housing features that may influence particle infiltration or indoor thermal conditions and measures of environmental health disparities , including housing, neighborhood, material hardship, and sociodemographic stressor constructs. In Aim 3, we will study whether longitudinal changes in epigenetic profiles are associated with air pollution exposures, and how these profiles are modified by determinants of health disparities. The successful completion of this study will address the urgent need for: 1) methods to quantify the health effects of simultaneous exposure to multiple chemical stressors; 2) identifying which non-chemical stressors and social determinants of health disparities exacerbate these effects; 3) identifying disparities in effects; and 4) elucidating potential underlying biological mechanism for environmentally driven health disparities. The knowledge produced upon the successful completion of this project will be essential in mitigating environmentally driven health disparities and improving the health of vulnerable populations and communities.

项目概要多项流行病学研究发现，接触化学应激源（例如空气污染）和非化学压力源（例如温度、噪音、绿地、社会经济地位 [SES]、种族和民族）和健康结果。然而，这些研究很少有：1）估计健康状况与同时暴露于多种化学应激源相关的整个生命周期的影响； 2）非化学压力源和健康社会决定因素造成的混杂/效应修改的特征差异，特别是住房条件和粮食不安全等因素； 3）调查是否暴露于这些化学应激源会通过表观遗传修饰影响健康。此外，还有一个需要新的统计方法来解释暴露、混杂因素的高维性，和交互术语，以了解对健康结果的影响。我们集合了四种独特的研究人群，其中三个来自马萨诸塞州 (MA)，其健康结果数据涵盖从出生到死亡，以及有关健康差异潜在决定因素的大量信息。在目标 1 中，我们将开发创新的统计方法来估计与大量相关的健康影响暴露（化学压力源），同时也考虑了大量潜在的混杂因素和互动。在目标 2 中，我们将估计暴露于多种化学应激源之间的关联出生结果、儿童期增长率和心血管死亡率。我们将通过以下方式检查效果修改个人居住水平的非化学压力源，包括温度、噪音、绿地和建成环境（社区步行能力）。我们还将通过丰富的主机来检查效果修改个人层面的健康差异社会决定因素（例如年龄、种族/民族、社会经济地位）。此外，通过通过项目 2 和 3 的工作，我们将能够获得可能影响颗粒渗透或室内热条件和环境健康差异的衡量标准，包括住房、邻里、物质困难和社会人口压力源结构。在目标 3 中，我们将研究纵向是否表观遗传特征的变化与空气污染暴露有关，以及这些特征是如何改变的健康差异的决定因素。这项研究的成功完成将解决以下迫切需求： 1）量化同时暴露于多种化学应激源对健康影响的方法； 2）识别哪些非化学压力源和健康差异的社会决定因素会加剧这些影响； 3）确定效果的差异； 4）阐明潜在的潜在生物学机制环境驱动的健康差异。成功完成本课程后产生的知识该项目对于减少环境驱动的健康差异和改善人们的健康至关重要弱势群体和社区。