Aging in the air we breathe: mechanisms and consequences of air pollution exposure for biological aging.

Abstract

Air pollution is the leading environmental cause of disease burden worldwide and is increasingly recognized as a potent driver of accelerated biological aging. Rather than acting through organ-specific toxicity alone, air pollutants appear to affect the fundamental hallmarks of aging itself, including oxidative stress, chronic inflammation, epigenetic dysregulation, telomere attrition, mitochondrial dysfunction, and cellular senescence. The pollutants of greatest concern are fine and ultrafine particulate matter (PM2.5, PM0.1), traffic-related air pollution, and household combustion emissions. This review synthesizes epidemiological and mechanistic evidence linking ambient and household air pollution to biological aging across the full spectrum of biomarker classes, including molecular measures (epigenetic clocks, telomere length, transcriptomic signatures), system-level indices (composite clinical biomarkers, proteomic aging clocks, inflammatory markers), and whole-organism measures (frailty). The strength of evidence varies meaningfully across biomarker classes. System-level composite measures, particularly the Klemera-Doubal method biological age, PhenoAge, and frailty scores, show the most robust and consistent associations with air pollution. Causal mediation analyses across independent cohorts support the role of biological aging as a mechanistic pathway linking air pollution exposure to clinical disease outcomes, including cardiovascular disease, neuropsychiatric disorders, and chronic kidney disease. Epigenetic clock findings remain inconclusive at the meta-analytic level despite strong biological plausibility, likely reflecting differences in exposure assessment methods, study design, and cell composition of the target tissue. Life-course vulnerability windows are also examined, with prenatal and early-life exposures shown to shape biological aging trajectories that persist into later life. Key research gaps include underrepresentation of household air pollution and low-income settings, and the shortage of longitudinal multimarker or multi-omics study designs. Air quality improvements and clean cooking fuel transitions have been shown to partially reverse air pollution-associated aging acceleration, reinforcing the public health relevance of these findings. Reducing air pollution thus remains the most equitable strategy for slowing biological aging at the population level, and incorporating aging-focused endpoints into environmental health research and regulatory policy is both a scientific and public health priority.