Key result
High air pollution plus short telomeres linked to ~2.3-fold higher carotid plaque prevalence.
Why the study?
Higher air pollution exposure and shorter leukocyte telomere length (LTL) are both associated with increased cardiovascular disease risk, but whether air pollution exposure is associated with shorter LTL and whether LTL modulates the cardiovascular effects of pollution exposure was uncertain.
Does high air pollution exposure and shorter leukocyte telomere length increase atherosclerotic burden (cfPWV, cIMT, and carotid plaque) in adults from the Corinthia region in Greece?
Cross-Sectional (n=418)
Does high air pollution exposure and shorter leukocyte telomere length increase atherosclerotic burden (cfPWV, cIMT, and carotid plaque) in adults from the Corinthia region in Greece?
Prolonged exposure to high air pollution starting early in life negatively impacts telomere length, while longer telomeres may partially protect against the adverse vascular effects (increased arterial stiffness, intima-media thickness, and carotid plaque) of chronic air pollution.
Answers are grounded in this paper and cite their sources.
Early air pollution exposure (≤20 years) was associated with shorter LTL and rising carotid plaque; hypothesis-generating for mediation in pollution-CVD links.
Objective Higher air pollution exposure and shorter leukocyte telomere length (LTL) are both associated with increased risk of cardiovascular disease. In this study we examined whether air pollution exposure is associated with shorter LTL and whether LTL can modulate the effects of pollution exposure on cardiovascular state. Design and Method In this cross-sectional analysis we selected 418 individuals, aged 62.4 ± 11.8 years, from the "Corinthia" study which was conducted in the homonym region in Greece. Half of the participants lived in a high air pollution area (HAPA) according to the CO, NO2 and SO2levels and the other half in a low air pollution area (LAPA). LTL was measured from whole blood by Southern blot and carotid-femoral pulse wave velocity (cfPWV), carotid intima media thickness (cIMT) and presence of carotid plaque were determined to evaluate atherosclerotic burden. Results We found no difference in age and sex adjusted LTL between HAPA and LAPA groups (p=0.42). In multivariate analysis including age, sex, as co-factors, participants of HAPA whose exposure began at an earlier age (≤ 20 years) had significantly shorter LTL compared to those exposed at >20 years of age (B=-0.169, p=0.012). Using the median LTL (6.78 kb) as a cutoff, the cohort was divided into four groups: Group 1 - LAPA/Long LTL (108 subjects), Group 2 - LAPA/Short LTL (98 subjects), Group 3 - HAPA/ Long LTL (102 subjects), and Group 4 - HAPA/Short LTL (110 subjects). Group 4 patients had significantly greater cf-PWV and cIMT compared to the other three groups (p<0.05), whereas there was no intragroup difference between the other clusters. These differences subsisted after adjustment for age and sex. Carotid plaque prevalence increased from 17.9% for Group 1 to 22.5% for Group 2, 29.7% for Group 3 and 40.4% for Group 4 (p < 0.01). Conclusion Prolonged exposure to high air pollution starting early in life seems to display a negative effect on telomere dynamics. Presence of longer telomeres may at least partially protect from negative effects of high air pollution exposure on vascular health. These results could be used for personalized cardiovascular risk prevention.
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Sagris et al. (2026) conducted a cross-sectional in Atherosclerotic burden and cardiovascular risk (n=418). High air pollution exposure and short leukocyte telomere length vs. Low air pollution exposure and long leukocyte telomere length was evaluated on Atherosclerotic burden (carotid plaque prevalence, cfPWV, and cIMT) and leukocyte telomere length (p=<0.01). High air pollution exposure combined with short telomere length was associated with higher carotid plaque prevalence vs low pollution and long telomeres (40.4% vs 17.9%, p<0.01).
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