Association between leukocyte telomere shortening and exposure to traffic pollution: a cross-sectional study on traffic officers and indoor office workers
Mirjam Hoxha 
Environmental Health 2009, 8:41doi:10.1186/1476-069X-8-41
| Published: | 21 September 2009 |
Abstract (provisional)
Background
Telomere shortening in blood leukocytes has been associated with increased morbidity and death from cardiovascular disease and cancer, but determinants of shortened telomeres, a molecular feature of biological aging, are still largely unidentified. Traffic pollution has been linked with both cardiovascular and cancer risks, particularly in older subjects. Whether exposure to traffic pollution is associated with telomere shortening has never been evaluated.
Methods
We measured leukocyte telomere length (LTL) by real-time PCR in blood DNA from 77 traffic officers exposed to high levels of traffic pollutants and 57 office workers (referents). Airborne benzene and toluene, as tracers for traffic exposure, were measured using personal passive samplers and gas-chromatography/flame-ionization detector analysis. We used covariate-adjusted multivariable models to test the effects of the exposure on LTL and obtain adjusted LTL means and 95% Confidence Intervals (CIs).
Results
Adjusted mean LTL was 1.10 (95%CI 1.04-1.16) in traffic officers and 1.27 in referents (95%CI 1.20-1.35) [p<0.001]. LTL decreased in association with age in both traffic officers (p=0.01) and referents (p=0.001), but traffic officers had shorter LTL within each age category. Among traffic officers, adjusted mean relative LTL was shorter in individuals working in high (n=45, LTL=1.02, 95%CI 0.96-1.09) compared to low traffic intensity (n=32, LTL=1.22, 95%CI 1.13-1.31) [p<0.001]. In the entire study population, LTL decreased with increasing levels of personal exposure to benzene (p=0.004) and toluene (p=0.008).
Conclusions
Our results indicate that leukocyte telomere length is shortened in subjects exposed to traffic pollution, suggesting evidence of early biological aging and disease risk.
