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


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: <sup>1</sup>Institute of Epidemiology II, Helmholtz Zentrum München, Neuherberg, Bavaria, Germany.

<sup>2</sup>Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA.

<sup>3</sup>Research Unit Molecular Epidemiology, Helmholtz Zentrum München, Neuherberg, Bavaria, Germany.

<sup>4</sup>Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York, NY, USA.

<sup>5</sup>Department of Global Health and Social Medicine, Harvard Medical School, Boston, MA, USA.

<sup>6</sup>Department of Geography and Environmental Development, Ben-Gurion University of the Negev, Beer Sheva, Israel.

<sup>7</sup>Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

<sup>8</sup>VA 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