Long-term exposure to air pollution is associated with biological aging

// Cavin K. Ward-Caviness 1 , Jamaji C. Nwanaji-Enwerem 2 , Kathrin Wolf 1 , Simone Wahl 1,3 , Elena Colicino 4 , Letizia Trevisi 5 , Itai Kloog 6 , Allan C. Just 7 , Pantel Vokonas 8 , Josef Cyrys 1 , Christian Gieger 1,3 , Joel Schwartz 2 , Andrea A. Baccarelli 4 , Alexandra Schneider 1 and Annette Peters 1 1 Institute of Epidemiology II, Helmholtz Zentrum München, Neuherberg, Bavaria, Germany 2 Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA 3 Research Unit Molecular Epidemiology, Helmholtz Zentrum München, Neuherberg, Bavaria, Germany 4 Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York, NY, USA 5 Department of Global Health and Social Medicine, Harvard Medical School, Boston, MA, USA 6 Department of Geography and Environmental Development, Ben-Gurion University of the Negev, Beer Sheva, Israel 7 Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA 8 VA Normative Aging Study, Veterans Affairs Boston Healthcare System and the Department of Medicine, Boston University School of Medicine, Boston, MA, USA Correspondence to: Annette Peters, email: // Keywords : epigenetic aging, telomere(definition) length, biological aging, air pollution, black carbon, Gerotarget Received : June 10, 2016 Accepted : October 13, 2016 Published : October 25, 2016 Abstract Long-term exposure to air pollution is associated with age-related diseases. We explored the association between accelerated biological aging and air pollution, a potential mechanism linking air pollution and health. We estimated long-term exposure to PM 10 , PM 2.5 , PM 2.5 absorbance/black carbon (BC), and NO x via land-use regression models in individuals from the KORA F4 cohort. Accelerated biological aging was assessed using telomere length (TeloAA) and three epigenetic measures: DNA methylation age acceleration (DNAmAA), extrinsic epigenetic age acceleration (correlated with immune cell counts, EEAA), and intrinsic epigenetic age acceleration (independent of immune cell counts, IEAA). We also investigated sex-specific associations between air pollution and biological aging, given the published association between sex and aging measures. In KORA an interquartile range (0.97 µg/m 3 ) increase in PM 2.5 was associated with a 0.33 y increase in EEAA (CI = 0.01, 0.64; P = 0.04). BC and NO x (indicators or traffic exposure) were associated with DNAmAA and IEAA in women, while TeloAA was inversely associated with BC in men. We replicated this inverse BC-TeloAA association in the Normative Aging Study, a male cohort based in the USA. A multiple phenotype analysis in KORA F4 combining all aging measures showed that BC and PM 10 were broadly associated with biological aging in men. Thus, we conclude that long-term exposure to air pollution is associated with biological aging measures, potentially in a sex-specific manner. However, many of the associations were relatively weak and further replication of overall and sex-specific associations is warranted.