TY - JOUR
T1 - Long-term exposure to air pollution is associated with biological aging
AU - Ward-Caviness, Cavin K.
AU - Nwanaji-Enwerem, Jamaji C.
AU - Wolf, Kathrin
AU - Wahl, Simone
AU - Colicino, Elena
AU - Trevisi, Letizia
AU - Kloog, Itai
AU - Just, Allan C.
AU - Vokonas, Pantel
AU - Cyrys, Josef
AU - Gieger, Christian
AU - Schwartz, Joel
AU - Baccarelli, Andrea A.
AU - Schneider, Alexandra
AU - Peters, Annette
PY - 2016/1/1
Y1 - 2016/1/1
N2 - 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 landuse 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 sexspecific 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 sexspecific associations is warranted.
AB - 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 landuse 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 sexspecific 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 sexspecific associations is warranted.
KW - Air pollution
KW - Biological aging
KW - Black carbon
KW - Epigenetic aging
KW - Gerotarget
KW - Telomere length
UR - http://www.scopus.com/inward/record.url?scp=84996605406&partnerID=8YFLogxK
U2 - 10.18632/oncotarget.12903
DO - 10.18632/oncotarget.12903
M3 - Article
C2 - 27793020
AN - SCOPUS:84996605406
SN - 1949-2553
VL - 7
SP - 74510
EP - 74525
JO - Oncotarget
JF - Oncotarget
IS - 46
ER -