Neighborhood Stressors and Epigenetic Age Acceleration among Older Americans

Abstract Objectives Exposure to stressful neighborhood environments is a well-established risk factor for health deterioration and premature death. However, the biological underpinnings are not fully understood. Epigenetic aging may function as a key molecular pathway to adverse health outcomes among residents of high-stress neighborhoods. This study examines the associations between neighborhood social stressors (socioeconomic deprivation, observed and perceived disorder, and low social cohesion) and epigenetic age (DunedinPACE and Principal component adjusted [PC] PCHorvath, PCHannum, PCPhenoAge, PCGrimAge). Further, we identify subpopulations most vulnerable to neighborhood stressors. Methods Respondent data are from the 2016 Health and Retirement Study (HRS) DNA methylation subsample. Neighborhood data come from respondent reports (2014/2016) and the census (2012–2016 ACS). The analytic sample included 3,146 adults ages 56 and older (mean age = 68.8), of whom 54.9% were women and 19.3% were non-White. Results In multilevel regression models adjusting for sociodemographic covariates, all neighborhood stressors were associated with faster DunedinPACE (B = 0.008 to 0.017). Neighborhood deprivation, perceived disorder, and low cohesion were associated with PCPhenoAge (B = 0.27 to 0.40) or PCGrimAge acceleration (B = 0.23). Health behaviors explained these associations to some degree. However, no significant associations were found with PCHorvath and PCHannum. In interaction analyses, adverse associations with deprivation, observed disorder, and low cohesion were more pronounced for women. No consistent interactions were found for race/ethnic and education groups. Discussion Our findings indicate that neighborhood stressors can accelerate epigenetic aging, with older women particularly vulnerable to their effects. These findings provide insights into the biological foundations of health disparities rooted in neighborhood environments.