Background

Exposure to ambient air pollution is associated with cardiovascular risk, potentially via atherosclerosis promotion. The disease mechanisms underlying these associations remain uncertain.

Objectives

We aim to investigate the relationship of air pollution and traffic proximity with subclinical atherosclerosis, using coronary plaque phenotypes to gain insight into potential mechanisms.

Methods

Coronary plaque total and component volumes, high-risk plaque (HRP) appearance, and luminal stenosis were characterized by coronary computed tomography angiography in 2279 patients with atherosclerosis at baseline between 2014 and 2017. Annual average exposure to air pollutants including fine particulate matter (PM_2.5), nitrogen dioxide (NO₂), and ozone (O₃) was estimated by air pollution models for individual participants. Multiple linear regression models were used to assess the association of each exposure with plaque phenotypes and coronary stenosis, controlling for potential confounders. Multiple logistic regression models were used to estimate associations with plaque vulnerability.

Results

The studied population was 60.2±9.2 years old. PM_2.5 and NO₂ concentrations were significantly associated with a 5.0% (95%CI: 0.3, 9.9%, per 15 μg/m³ increase for PM_2.5), 12.0% (95%CI: 2.5, 22.5% per 20 μg/m³ for NO₂) larger volume of non-calcified plaque, respectively. Increase in O₃ concentration was associated with a 12.2% (95%CI: 2.2, 23.2%, per 5 μg/m³ O₃) larger volume of calcified plaque and a 12.8% (95%CI: 0.9, 26.2%) greater lumen narrowing. Increased PM_2.5 and NO₂, was also associated with increase in HRP, determined by the napkin ring sign (odds ratio: 1.41 [95%CI: 1.10, 1.80] for PM_2.5 and 1.78 [95%CI: 1.20, 2.63] for NO₂) and positive remodeling index (OR: 1.11 [95%CI: 1.01, 1.21] for PM_2.5 and 1.20 [95%CI: 1.02, 1.42] for NO₂), respectively, indicating increased plaque vulnerability.

Conclusion

Long-term exposures to air pollution were associated with greater plaque volume and luminal stenosis, and increased plaque vulnerability with attendant risk of plaque rupture and erosion.