Accelerated epigenetic age as a biomarker of cardiovascular sensitivity to traffic-related air pollution
Cavin Ward‐Caviness, Armistead G. Russell, Anne M. Weaver, Erik D. Slawsky, Radhika Dhingra, Lydia Coulter Kwee, Rong Jiang, Lucas Neas, David Díaz-Sánchez, Robert B. Devlin, Wayne E. Cascio, Kenneth Olden, Elizabeth R. Hauser, Svati H. Shah, William E. Kraus
Abstract
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: . 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.