Long-term exposure to ambient air pollution and epigenetic age acceleration in children

Wenli Ni; Anne K Bozack; Sheryl L Rifas-Shiman; Emily Oken; Marie-France Hivert; Nicholas J Nassikas; Joanne Sordillo; Wei Perng; Diane R Gold; Andres Cardenas; Mary B Rice

doi:10.1093/aje/kwaf006

Long-term exposure to ambient air pollution and epigenetic age acceleration in children

Am J Epidemiol. 2025 Jan 14:kwaf006. doi: 10.1093/aje/kwaf006. Online ahead of print.

Authors

Wenli Ni^{1

2}, Anne K Bozack³, Sheryl L Rifas-Shiman⁴, Emily Oken^{4

5}, Marie-France Hivert^{4

6}, Nicholas J Nassikas¹, Joanne Sordillo⁴, Wei Perng⁷, Diane R Gold^{5

8}, Andres Cardenas³, Mary B Rice^{1

2}

Affiliations

¹ Division of Pulmonary and Critical Care Medicine, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
² Center for Climate, Health, and the Global Environment, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.
³ Department of Epidemiology and Population Health, Stanford University, Stanford, California.
⁴ Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, Massachusetts.
⁵ Environmental Health Department, Harvard T. H. Chan School of Public Health, Boston, Massachusetts.
⁶ Diabetes Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
⁷ Department of Epidemiology and the Lifecourse Epidemiology of Adiposity and Diabetes (LEAD) Center, Colorado School of Public Health, University of Colorado Anschutz Medical Campus, Aurora, Colorado.
⁸ Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.

PMID: 39814684
DOI: 10.1093/aje/kwaf006

Abstract

Long-term exposure to ambient air pollution has been associated with epigenetic age acceleration (EAA) in adults, but its impact on children remains less understood. This study analyzed data from 457 children (mean age: 7.9 years) in the Project Viva cohort (2007-2010, eastern Massachusetts, USA). We calculated EAA from leukocytes: Horvath's Epigenetic Age Acceleration (HorvathEAA), Intrinsic Epigenetic Age Acceleration (IEAA), and Skin and Blood Epigenetic Age Acceleration (Skin&BloodEAA). We applied generalized additive models to evaluate associations of prior 365-day average and lifetime average exposure to PM2.5, NO2, and O3, and distance to major roadways with EAA. Results indicated that each interquartile range of prior 365-day average of PM2.5 corresponded with 0.26 years (95% CI: -0.49, -0.03) lower HorvathEAA, although it did not survive multiple testing adjustment. Similar patterns but with wider confidence intervals were observed for IEAA (-0.22, 95% CI: -0.44, 0.01) and Skin&BloodEAA (-0.04, 95% CI: -0.19, 0.11). No associations were observed of exposure to lifetime average PM2.5, prior-year or lifetime average NO2 or O3, or distance to major roadways with EAA. These findings suggest higher prior 365-day average PM2.5 exposure may relate to lower HorvathEAA in children.

Keywords: EAA; ambient air pollution; children; long-term exposure; particulate matter.