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

健康老龄化中的黑白不平等是众所周知的，黑人成年人面临更大的风险， 发展中和早期发作的慢性疾病，如心血管疾病（CVD），高血压， 与白色成年人相比。邻里环境已经成为一个潜在的强有力的决定因素 种族不平等的老龄化相关的健康状况，包括认知能力下降，并可能是一个关键的干预措施， 绝佳的价钱社区包括对健康老龄化很重要的社会和环境暴露。证据 这表明，在面临种族隔离、资源不足、但受到过度监视和污染的环境中， 邻里关系污染和社会逆境的各个方面往往是相互关联的，并可能累积起来， 导致种族健康不平等。然而，重要的是，这些化学（即污染）和非化学（即， 社会逆境）压力源可能会协同作用，从而暴露于社会逆境可以提高 即使是低水平的污染也会对健康产生有害影响。然而，环境和社会 科学文献-甚至环境和社会流行病学文献-在很大程度上是分开的。那里 考虑到这些接触可能产生的累积和协同效应， 种族卫生不平等问题，以指导有效的干预措施和政策。除了我们的差距之外， 了解化学品和非化学品压力因素对健康和营养方面种族不平等的综合影响 随着老龄化的加剧，有必要重点关注可能成为许多疾病的生物学途径的结果。 关于污染或社会逆境的研究往往侧重于具体的健康结果。专注于一个 单一疾病可能低估了这些种族不平等的暴露对健康的总体影响。至关重要 阐明许多慢性疾病的共同生物学机制，以了解其全面影响 污染和社会逆境对种族健康不平等的影响。越来越多的文献指出， 表观遗传因素，特别是DNA甲基化，将社会环境背景与健康联系起来。的确， 表观遗传过程是一种重要的机制，通过这种机制，空气污染和 社会逆境体现。我们的目标是确定潜在的DNA甲基化机制， 邻里隔离、环境和工业空气污染以及社会逆境对健康措施的影响 衰老澄清邻里在种族健康不平等中的作用至关重要，因为邻里是可以接受的。 干预。确定DNA甲基化模式反映种族隔离的作用，包括化学 和非化学应激源，可以指向特定的疾病病因和因果机制有效 采取干预措施，消除健康老龄化中的种族不平等现象。

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.