Author:
Cardenas Andres,Ecker Simone,Fadadu Raj P.,Huen Karen,Orozco Allan,McEwen Lisa M.,Engelbrecht Hannah-Ruth,Gladish Nicole,Kobor Michael S.,Rosero-Bixby Luis,Dow William H.,Rehkopf David H.
Abstract
AbstractSmoking-associated DNA methylation (DNAm) signatures are reproducible among studies of mostly European descent, with mixed evidence if smoking accelerates epigenetic aging and its relationship to longevity. We evaluated smoking-associated DNAm signatures in the Costa Rican Study on Longevity and Healthy Aging (CRELES), including participants from the high longevity region of Nicoya. We measured genome-wide DNAm in leukocytes, tested Epigenetic Age Acceleration (EAA) from five clocks and estimates of telomere length (DNAmTL), and examined effect modification by the high longevity region. 489 participants had a mean (SD) age of 79.4 (10.8) years, and 18% were from Nicoya. Overall, 7.6% reported currently smoking, 35% were former smokers, and 57.4% never smoked. 46 CpGs and five regions (e.g. AHRR, SCARNA6/SNORD39, SNORA20, and F2RL3) were differentially methylated for current smokers. Former smokers had increased Horvath’s EAA (1.69-years; 95% CI 0.72, 2.67), Hannum’s EAA (0.77-years; 95% CI 0.01, 1.52), GrimAge (2.34-years; 95% CI1.66, 3.02), extrinsic EAA (1.27-years; 95% CI 0.34, 2.21), intrinsic EAA (1.03-years; 95% CI 0.12, 1.94) and shorter DNAmTL (− 0.04-kb; 95% CI − 0.08, − 0.01) relative to non-smokers. There was no evidence of effect modification among residents of Nicoya. Our findings recapitulate previously reported and novel smoking-associated DNAm changes in a Latino cohort.
Funder
National Institute of Environmental Health Sciences
National Institute on Aging
National Institute on Minority Health and Health Disparities
Publisher
Springer Science and Business Media LLC
Reference79 articles.
1. Rodgman, A., Smith, C. J. & Perfetti, T. A. The composition of cigarette smoke: A retrospective, with emphasis on polycyclic components. Hum. Exp. Toxicol. https://doi.org/10.1191/096032700701546514 (2016).
2. Centers for Disease Control and Prevention (US), National Center for Chronic Disease Prevention and Health Promotion (US), & Office on Smoking and Health (US). How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease: A Report of the Surgeon General. (Centers for Disease Control and Prevention (US), 2010).
3. Morris, P. B. et al. Cardiovascular effects of exposure to cigarette smoke and electronic cigarettes: Clinical perspectives from the prevention of cardiovascular disease section leadership council and early career councils of the American college of cardiology. J. Am. Coll. Cardiol. 66, 1378–1391 (2015).
4. Yoshida, T. & Tuder, R. M. Pathobiology of cigarette smoke-induced chronic obstructive pulmonary disease. Physiol. Rev. 87, 1047–1082 (2007).
5. Onor, I. O. et al. Clinical effects of cigarette smoking: Epidemiologic impact and review of pharmacotherapy options. Int. J. Environ. Res. Public Health 14, 1147 (2017).
Cited by
18 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献