Research Paper Volume 13, Issue 6 pp 7883—7899
Neighborhood environment, social cohesion, and epigenetic aging
- 1 Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
- 2 Carolina Population Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
- 3 Center for Public Health and Environmental Assessment, US Environmental Protection Agency, Durham, NC 27709, USA
- 4 Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
- 5 Institute of Environmental Health Solutions, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
- 6 Department of Biostatistics, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
- 7 School of Public Health, Boston University, Boston, MA 02118, USA
- 8 Genomics Program, College of Public Health, University of South Florida, Tampa, FL 33612, USA
- 9 Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA
Received: November 2, 2020 Accepted: February 16, 2021 Published: March 14, 2021https://doi.org/10.18632/aging.202814
How to Cite
Copyright: © 2021 Martin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Living in adverse neighborhood environments has been linked to risk of aging-related diseases and mortality; however, the biological mechanisms explaining this observation remain poorly understood. DNA methylation (DNAm), a proposed mechanism and biomarker of biological aging responsive to environmental stressors, offers promising insight into potential molecular pathways. We examined associations between three neighborhood social environment measures (poverty, quality, and social cohesion) and three epigenetic clocks (Horvath, Hannum, and PhenoAge) using data from the Detroit Neighborhood Health Study (n=158). Using linear regression models, we evaluated associations in the total sample and stratified by sex and social cohesion. Neighborhood quality was associated with accelerated DNAm aging for Horvath age acceleration (β = 1.8; 95% CI: 0.4, 3.1), Hannum age acceleration (β = 1.7; 95% CI: 0.4, 3.0), and PhenoAge acceleration (β = 2.1; 95% CI: 0.4, 3.8). In models stratified on social cohesion, associations of neighborhood poverty and quality with accelerated DNAm aging remained elevated for residents living in neighborhoods with lower social cohesion, but were null for those living in neighborhoods with higher social cohesion. Our study suggests that living in adverse neighborhood environments can speed up epigenetic aging, while positive neighborhood attributes may buffer effects.