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

黑人和白人在健康老龄化中的不平等是众所周知的，黑人成年人经历更大的风险 慢性疾病，如心血管疾病(CVD)、高血压和 与白人成年人相比，糖尿病患者的比例更高。社区环境已经成为一个潜在的强大决定因素 与老龄化相关的健康状况中的种族不平等，包括认知能力下降，这可能是一项关键的干预措施 地点。社区包括对健康老龄化很重要的社会和环境暴露。证据 表明在隔离、资源不足但过度监督和污染的环境中暴露出明显的种族不平等 邻里关系。污染和社会逆境的各个方面往往是相关的，并可能累积作用于 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)压力源可以协同作用，由此暴露在社会逆境中可以增加 即使污染水平很低，也容易受到有害健康影响的影响。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 鉴于这些暴露可能产生的累积和协同影响，迫切需要整合对这些暴露的研究 关于种族健康不平等的问题，以指导有效的干预和政策。除了我们的差距之外 关于化学和非化学应激源对健康人群种族不平等的联合影响的认识 随着年龄的增长，有必要把重点放在可能成为多种疾病生物学途径的结果上。 对污染或社会逆境的研究往往集中在具体的健康结果上。把重点放在 单一疾病可能低估了这些种族不平等暴露对整体健康的影响。这是至关重要的 阐明许多慢性疾病背后的共同生物学机制，以了解其全部影响 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了 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。事实上，它可能会 表观遗传过程是一个重要的机制，通过它，空气污染和 体现了社会的逆境。我们的目标是确定潜在的DNA甲基化机制 社区隔离、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。澄清社区在种族健康不平等中的作用是至关重要的，因为社区是可以服从的 干杯干杯。确定反映种族隔离的DNA甲基化模式的作用，包括化学物质 和非化学应激源，可以指向特定的疾病病因和有效的致病机制 健康老龄化中消除种族不平等的干预措施。

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.