Accelerated epigenetic age as a biomarker of cardiovascular sensitivity to traffic-related air pollution
| Autor: | Radhika Dhingra, Lucas M. Neas, Erik Slawsky, Wayne E. Cascio, Rong Jiang, Robert B. Devlin, Lydia Coulter Kwee, Elizabeth R. Hauser, Anne M. Weaver, Cavin K. Ward-Caviness, Svati H. Shah, Kenneth Olden, Armistead G. Russell, William E. Kraus, David Diaz-Sanchez |
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| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
Genetic Markers
Male environmental sensitivity Aging Traffic-Related Pollution Arterial disease air pollution Air pollution Blood Pressure medicine.disease_cause Risk Assessment Epigenesis Genetic Peripheral Arterial Disease cardiovascular disease Residence Characteristics Environmental health medicine North Carolina Humans Epigenetics Organ system Aged Vehicle Emissions traffic business.industry Age Factors Urban Health Cell Biology Chronological age DNA methylation age Environmental Exposure DNA Methylation Middle Aged Heart Disease Risk Factors Cohort Biomarker (medicine) Female business Research Paper Environmental Monitoring |
| Zdroj: | Aging (Albany NY) |
| ISSN: | 1945-4589 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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