Air Pollution and Pulse Wave Velocity in Young and Middle-Aged Asymptomatic Adults: The Kangbuk Samsung Health Study

摘要

Objective: Long-term exposure to fine particulate matter less than 2.5 μm in diameter (PM2.5) and less than 10 μm in diameter (PM10) are associated with cardiovascular risk. The mechanisms underlying these associations remains uncertain. We evaluated the association between long-term exposure to particulate matter and brachial-ankle pulse wave velocity (PWV), a marker of arterial stiffness, in a large sample of asymptomatic men and women. Methods: Cross-sectional analysis of 102,316 participants in the Kangbuk Samsung Health Study (KSHS) who underwent a comprehensive health screening examination in Seoul or Suwon, South Korea, between 2011 and 2016. We used participant-specific spatiotemporal pollution concentration models, incorporating agency monitoring data and geographical predictors, to estimate PM10 and PM2.5 concentrations between 2008 and 2016. We measured PWV using an oscillometry method with cuffs placed on both arms and ankles. Results: The monthly average particulate matter concentrations over 2011-2016 ranged from 22.6-113.2 and 4.8-57.9 μg/m3 for PM10 and PM2.5, respectively. The average PWV was 1307.2 cm/sec. In fully adjusted models, a 10 μg/m3 increase in 12-, 36-, and 60-month PM10 exposure was associated with a PWV increase of 4.11 (95% CI 0.75, 7.48), 6.19 (2.86, 9.53), and 4.87 (1.47, 8.26) cm/s, respectively. The corresponding increases in PWV associated with a 10 μg/m3 increase in 12- and 36-month PM2.5 exposure were 6.31 (1.61, 11.00) and 3.14 (-2.49, 8.76) cm/s, respectively. The association of particulate matter with PWV was evident in men and women, but it was significantly stronger in men compared to women. Conclusions: Increased concentrations of particulate matter were independently associated with brachial-ankle PWV in a large sample of young and middle-aged asymptomatic adults. Our findings add to the increasing body of evidence that identifies arterial stiffness as a mediator of the cardiovascular effects of air pollution.