摘要：Background: Telomere length is a molecular marker of biological aging. Objective: Here we investigated whether early-life exposure to residential air pollution was associated with leukocyte telomere length (LTL) at 8 y of age. Methods: In a multicenter European birth cohort study, HELIX (Human Early Life Exposome) ( n = 1,396 ), we estimated prenatal and 1-y childhood exposure to nitrogen dioxide ( NO 2 ), particulate matter with aerodynamic diameter ≤ 2.5 μ m ( PM 2.5 ), and proximity to major roads. Average relative LTL was measured using quantitative real-time polymerase chain reaction (qPCR). Effect estimates of the association between LTL and prenatal, 1-y childhood air pollution, and proximity to major roads were calculated using multiple linear mixed models with a random cohort effect and adjusted for relevant covariates. Results: LTL was inversely associated with prenatal and 1-y childhood NO 2 and PM 2.5 exposures levels. Each standard deviation (SD) increase in prenatal NO 2 was associated with a − 1.5 % (95% CI: − 2.8 , − 0.2 ) change in LTL. Prenatal PM 2.5 was nonsignificantly associated with LTL ( − 0.7 % per SD increase; 95% CI: − 2.0 , 0.6). For each SD increment in 1-y childhood NO 2 and PM 2.5 exposure, LTL shortened by − 1.6 % (95% CI: − 2.9 , − 0.4 ) and − 1.4 % (95% CI: − 2.9 , 0.1), respectively. Each doubling in residential distance to nearest major road during childhood was associated with a 1.6% (95% CI: 0.02, 3.1) lengthening in LTL. Conclusion: Lower exposures to air pollution during pregnancy and childhood were associated with longer telomeres in European children at 8 y of age. These results suggest that reductions in traffic-related air pollution may promote molecular longevity, as exemplified by telomere length, from early life onward.
