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 (NO2), particulate matter with aerodynamic diameter ≤2.5μm (PM2.5), 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 NO2 and PM2.5 exposures levels. Each standard deviation (SD) increase in prenatal NO2 was associated with a −1.5% (95% CI: −2.8, −0.2) change in LTL. Prenatal PM2.5 was nonsignificantly associated with LTL (−0.7% per SD increase; 95% CI: −2.0, 0.6). For each SD increment in 1-y childhood NO2 and PM2.5 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.