Author: Ward-Caviness CK1, Nwanaji-Enwerem JC2, Wolf K1, Wahl S1,3, Colicino E4, Trevisi L5, Kloog I6, Just AC7, Vokonas P8, Cyrys J1, Gieger C1,3, Schwartz J2, Baccarelli AA4, Schneider A1, Peters A1
Affiliation:
1Institute of Epidemiology II, Helmholtz Zentrum München, Neuherberg, Bavaria, Germany.
2Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
3Research Unit Molecular Epidemiology, Helmholtz Zentrum München, Neuherberg, Bavaria, Germany.
4Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York, NY, USA.
5Department of Global Health and Social Medicine, Harvard Medical School, Boston, MA, USA.
6Department of Geography and Environmental Development, Ben-Gurion University of the Negev, Beer Sheva, Israel.
7Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
8VA Normative Aging Study, Veterans Affairs Boston Healthcare System and the Department of Medicine, Boston University School of Medicine, Boston, MA, USA.
Conference/Journal: Oncotarget.
Date published: 2016 Oct 25
Other:
Special Notes: doi: 10.18632/oncotarget.12903. [Epub ahead of print] , Word Count: 252
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 PM10, PM2.5, PM2.5 absorbance/black carbon (BC), and NOx 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/m3) increase in PM2.5 was associated with a 0.33 y increase in EEAA (CI = 0.01, 0.64; P = 0.04). BC and NOx (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 PM10 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.
KEYWORDS: Gerotarget; air pollution; biological aging; black carbon; epigenetic aging; telomere length
PMID: 27793020 DOI: 10.18632/oncotarget.12903
