Connecting the social and built environment to health and health inequalities

History

Since its inception in the early 1960s, the Social Environment and Health Program (SEH) has been a leader in the development of theory and research on the major role of psychosocial factors in the etiology and course of both mental and physical health and illness. Founded as a cross-disciplinary program, SEH was first led by psychologists John R. P. French, Jr., Robert Kahn, and Floyd Mann in the 1960s and 1970s, and joined by physician epidemiologist Sidney Cobb and several junior colleagues (especially Stanislav Kasl and Robert Caplan). One member of this founding group, Robert Kahn, remains an active and valued member of SEH, working on problems of productive activities and successful aging (Rowe and Kahn, 1998), as he continues to age successfully beyond his 90th birthday in 2008. We continue to expand this area of research, focusing on the importance of social context for health and well-being across the life course. Our work examines social disparities in health, including the role of racism, toxic and built environments, and the molecular pathways linking neighborhoods to health inequalities.

Racial inequalities in healthy aging have been well-documented. Compared to White Americans, Black Americans experience illness and death at early ages and show steeper age-related declines in health. Our neighborhoods, as the site of where we live, learn, play, and pray, may serve as a powerful source of these racial inequalities. Racial residential segregation (which is the sorting of different racial groups into different neighborhoods through historical and current discriminatory policies and practices) has resulted in a racially unequal American neighborhood landscape. Neighborhoods with mostly Black residents experience more poverty, civic and commercial disinvestment, and more exposure to environmental hazards compared to neighborhoods with mostly White residents. While more researchers are documenting the role of neighborhoods in health inequalities, we may actually be underestimating the true impact of neighborhood context, because we often focus on specific health outcomes, such as cardiovascular disease or diabetes. However, there are likely shared biological mechanisms within the body that drive many of these diseases – and one such mechanism may be changes to our genomic structure, called epigenomics. While our genes do not change, the environment can have an impact on whether our genes are actually “expressed”. We will determine whether the accumulation of adulthood lived experience in racially-segregated neighborhoods is related to epigenomic patterns called DNA methylation. We will also specifically determine whether the accumulation of adulthood exposure to neighborhood industrial air pollution and disadvantage together are related to these patterns of DNA methylation. Finally, we will determine whether the DNA methylation patterns we see are related to racial inequalities in healthy aging. We hypothesize that racially-segregation Black neighborhoods, with their greater levels of industrial air pollution and social disadvantage, will be related to the types of patterns in DNA methylation that have been shown to be related to chronic diseases in molecular studies. In fact, we further hypothesize that these patterns in DNA methylation will be related to racial inequalities in cognitive function and the number of chronic diseases one has had. Clarifying the role of neighborhood context in racial inequalities in healthy aging is critical, as neighborhoods are not naturally- occurring. They develop and change through policies and are amenable to intervention. Identifying the role of DNA methylation that likely underlies many chronic diseases, will clarify the importance of neighborhoods and point to potential effective interventions

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