Abstract

BACKGROUND AND AIM Ambient air pollution (AP) has been associated with shorter telomere length (TL), which is a hallmark of biological aging and may lead to respiratory and cardiovascular disease, and lung cancer. We investigated the association between AP and TL and associated health outcomes. METHODS Data was from the UK Biobank (n=412,575). Participants aged 40 to 70 were recruited from 2006-2010. Baseline leukocyte TL was measured as T/S ratio. Residential AP estimates from 2010 included annual means of NO2, PM10, and PM2.5 in μg/m3. AP levels were associated with TL using linear regression models. Logistic regression models were used to link AP or TL to incident coronary artery disease (CAD) (n=26,345 cases) and lung cancer (n=4,079 cases) through 2021. Covariates included age, sex, ethnicity, education, Townsend deprivation index, BMI, smoking status, alcohol intake, physical activity, and greenspace (1000m buffer). RESULTS We confirmed that longer TL was associated with reduced risk of incident CAD (OR=0.95 per SD increase in TL, p=1.51×10-15) but increased risk of incident lung cancer (OR=1.05 per SD increase in TL, p=0.003). Higher NO2 or PM2.5 was significantly associated with shorter TL (β=-0.021, -0.020, 0.002 SD comparing NO2 in (20, 30], (30, 40], >40 to NO2≤20, overall p=4×10-6; β=-0.010 SD comparing PM2.5>10 to PM2.5≤10, p=0.012). Both also were associated with increased risk of CAD (OR=1.11, 1.11, 1.09 comparing NO2 in (20, 30], (30, 40], >40 to NO2≤20, overall p=1.3×10-5; OR=1.04 comparing PM2.5 >10 to PM2.5≤10, p=0.027) but not risk of lung cancer. In contrast, PM10 was not associated with TL, incident CAD or lung cancer. CONCLUSIONS NO2 or PM2.5 concentrations were associated with shorter TL and risk of CAD. TL may play a mediation role in the relationship between AP and CAD. KEYWORD coronary artery disease, lung cancer, NO2, PM10, PM2.5

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