Research Paper Advance Articles pp 24141—24155
Accelerated epigenetic age as a biomarker of cardiovascular sensitivity to traffic-related air pollution
- 1 Center for Public Health and Environmental Assessment, US Environmental Protection Agency, Chapel Hill, NC 27709, USA
- 2 Department of Civil and Environmental Engineering, Georgia Institute of Technology, Atlanta, GA 30332, USA
- 3 Oak Ridge Associated Universities at the US Environmental Protection Agency, Chapel Hill, NC 27709, USA
- 4 Department of Environmental Sciences and Engineering, Gillings School of Public Health, University of North Carolina, Chapel Hill, NC 27599, USA
- 5 Institute for Environmental Health Solutions, University of North Carolina, Chapel Hill, NC 27599, USA
- 6 Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, NC 27710, USA
- 7 Department of Psychiatry and Behavioral Sciences, Duke University School of Medicine, Durham, NC 27710, USA
- 8 Department of Biostatistics and Bioinformatics, Duke University School of Medicine, Durham, NC 27710, USA
- 9 Cooperative Studies Program Epidemiology Center, Durham Veterans Affairs Medical Center, Durham, NC 27705, USA
- 10 Division of Cardiology, Department of Medicine, School of Medicine, Duke University, Durham, NC 27710, USA
Received: July 9, 2020 Accepted: October 27, 2020 Published: December 7, 2020https://doi.org/10.18632/aging.202341
How to Cite
Copyright: © 2020 Ward-Caviness 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.
Background: Accelerated epigenetic age has been proposed as a biomarker of increased aging, which may indicate disruptions in cellular and organ system homeostasis and thus contribute to sensitivity to environmental exposures.
Methods: Using 497 participants from the CATHGEN cohort, we evaluated whether accelerated epigenetic aging increases cardiovascular sensitivity to traffic-related air pollution (TRAP) exposure. We used residential proximity to major roadways and source apportioned air pollution models as measures of TRAP exposure, and chose peripheral arterial disease (PAD) and blood pressure as outcomes based on previous associations with TRAP. We used Horvath epigenetic age acceleration (AAD) and phenotypic age acceleration (PhenoAAD) as measures of age acceleration, and adjusted all models for chronological age, race, sex, smoking, and socioeconomic status.
Results: We observed significant interactions between TRAP and both AAD and PhenoAAD. Interactions indicated that increased epigenetic age acceleration elevated associations between proximity to roadways and PAD. Interactions were also observed between AAD and gasoline and diesel source apportioned PM2.5.
Conclusion: Epigenetic age acceleration may be a biomarker of sensitivity to air pollution, particularly for TRAP in urban cohorts. This presents a novel means by which to understand sensitivity to air pollution and provides a molecular measure of environmental sensitivity.