DNA methylation in context: Racial inequities in social adversity and vulnerability to the health impact of air pollution

DNA 甲基化背景：社会逆境中的种族不平等以及空气污染对健康影响的脆弱性

• 批准号: 10625337
• 负责人: Margaret Takako Hicken
• 金额: $ 61.08万
• 依托单位: UNIVERSITY OF MICHIGAN AT ANN ARBOR
• 依托单位国家: 美国
• 财政年份: 2021
• 资助国家: 美国
• 起止时间: 2021-07-15 至 2026-04-30
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10625337
• 关键词: Acceleration; Address; Adult; Age; Aging; Air Pollution; Area; Biological; Black race; Blood; Cardiovascular Diseases; Chemicals; Chronic; Chronic Disease; Complex; Crows; DNA Methylation; Data; Data Set; Diabetes Mellitus; Disease; Elderly; Environmental Epidemiology; Environmental Exposure; Environmental Science; Epigenetic Process; Etiology; Exposure to; Genes; Health; Health and Retirement Study; Hypertension; Immune system; Impaired cognition; Imprisonment; Industrialization; Inequity; Intervention; Knowledge; Laws; Link; Literature; Measures; Modeling; Neighborhoods; Outcome; Pathway interactions; Pattern; Play; Policies; Pollution; Population; Poverty; Prevalence; Race; Racial Segregation; Research; Resources; Risk; Role; Site; Social Environment; Social Sciences; Source; Stress; Time; Work; early onset; effective intervention; epigenomics; experience; health inequalities; healthy aging; innovation; member; methylation pattern; multi-ethnic; racial determinant; racial disparity; segregation; social; social adversity; social epidemiology; social stressor; social vulnerability; stressor

Black-White inequities in healthy aging are well-known with Black adults experiencing greater risk of developing and earlier onset of chronic conditions such as cardiovascular disease (CVD), hypertension, and diabetes compared to White adults. Neighborhood context has emerged as a potentially powerful determinant of racial inequities in aging-related health conditions, including cognitive decline, and may be a key intervention site. Neighborhoods include both social and environmental exposures important for healthy aging. Evidence indicates stark racial inequities in exposure to segregated, under-resourced but over-surveilled and polluted neighborhoods. Pollution and aspects of social adversity are often correlated and may operate cumulatively to result in racial health inequities. Importantly, however, these chemical (i.e. pollution) and non-chemical (i.e., social adversity) stressors may act synergistically, whereby exposure to social adversity can heighten vulnerability to the deleterious health impact of even low levels of pollution. Yet, the environmental and social science literatures – even the environmental and social epidemiology literatures – are largely separate. There is a pressing need to integrate the study of these exposures given their likely cumulative and synergistic effects on racial health inequities in order to direct effective interventions and policies. In addition to the gaps in our knowledge about the combined impact of chemical and non-chemical stressors on racial inequities in healthy aging, there is a need to focus on outcomes that may serve as biological pathways to numerous diseases. Research on either pollution or social adversity has tended to focus on specific health outcomes. Focus on a single disease may underestimate the overall health impact of these racially unequal exposures. It is critical to clarify the shared biological mechanisms that underlie numerous chronic diseases to understand the full impact of pollution and social adversity on racial health inequities. A growing literature points to the importance of epigenetic factors, particularly DNA methylation, linking socioenvironmental context to health. Indeed, it may be that epigenetic processes are an important mechanism through which inequities in both air pollution and social adversity are embodied. Our objective is to identify underlying DNA methylation mechanisms linking neighborhood segregation and ambient and industrial air pollution and social adversity to measures of healthy aging. Clarifying the role of neighborhood in racial health inequities is critical, as neighborhoods are amenable to intervention. Identifying the role of DNA methylation patterns reflecting racial segregation, including chemical and non-chemical stressors, can point to specific disease etiologies and causal mechanisms effective interventions to eliminate racial inequities in healthy aging.

健康衰老中的黑白不平等是众所周知的，黑人成年人的风险更大 发展和更早的慢性病发作，例如心血管疾病（CVD），高血压和 与白人成年人相比，糖尿病。邻里环境已经成为潜在的强大确定的 与衰老相关的健康状况（包括认知能力下降）中种族不平等现象，可能是关键干预措施 地点。社区包括对健康衰老很重要的社会和环境暴露。证据 表明暴露于隔离，资源不足但污染的种族不平等现象 社区。污染和社交广告的各个方面通常是相关的，可能会累计运作 导致种族健康不平等。但是，重要的是，这些化学（即污染）和非化学（即 社交广告）压力源可能会协同行动，从而接触社交广告可以增强 易受污染水平的微妙影响的脆弱性。但是，环境和社会 科学文献 - 甚至环境和社会流行病学文献 - 基本上是分开的。那里 鉴于它们可能累积和协同作用，需要整合这些暴露的研究 关于种族健康不平等，以指导有效的干预措施和政策。除了我们的差距 关于化学和非化学压力源对健康不平等的综合影响的知识 衰老，有必要专注于可以作为多种疾病的生物学途径的结果。 关于污染或社交广告的研究倾向于专注于特定的健康结果。专注于 单个疾病可能会低估这些大致不平等暴露的总体健康影响。这是至关重要的 澄清共同的生物学机制，这些机制是众多慢性慢性疾病的基础，以了解全部影响 关于种族健康不平等的污染和社会广告。越来越多的文献指出了 表观遗传因素，尤其是DNA甲基化，将社会环境环境与健康联系起来。确实，它可能 这是表观遗传过程是一个重要的机制，在空气污染和 社交广告体现了。我们的目标是识别连接的潜在DNA甲基化机制 邻里种族隔离，环境和工业空气污染和社会广告，以衡量健康 老化。澄清邻里在种族健康不平等中的作用至关重要，因为社区是可正常的 干预。确定反映大鼠分离的DNA甲基化模式的作用，包括化学 和非化学应力源可以指出特定的疾病病因和因果机制有效 消除健康衰老中大鼠摄入量的干预措施。