Endothelial function in relation to low-level chronic residential air pollution in a general population: a cohort study.

BACKGROUND: Given the recently updated clean-air targets, this population study assessed endothelial function at low exposure to particulate matter with an aerodynamic diameter of ≤10 µm (PM10) and ≤2.5 µm (PM2.5), nitrogen dioxide (NO2), and black carbon (BC). METHODS: In 453 Flemish participants (47.7% women; mean age, 52.8 years), endothelial function was assessed by finger photoplethysmography after 5 minutes of ischaemia. The outcome measures were the maximal ischaemic-to-control ratio (Rmax) and the maximal difference (Dmax) in pulse amplitude between the test and control fingers. The air pollutants were related to Rmax and Dmax using mixed models accounting for coresidence, to cardiovascular endpoints by proportional hazards regression, and to residential address by high-resolution spatiotemporal interpolation. RESULTS: From 2010 to 2015, PM10, PM2.5, NO2 and BC decreased (p < 0.0001) with 6-year levels averaging 15.9, 12.8, 14.3, and 1.04 μg/m3. Irrespective of adjustment for risk factors, Dmax was inversely correlated with PM2.5, while associations of Rmax with PM2.5 and associations of both Dmax and Rmax with other pollutants were weaker (p-values <0.10), but consistently inverse. Association sizes of Rmax and Dmax with PM10 and PM2.5 weakened over 6 years, paralleling the decreasing air pollutants (p ≤ 0.044). In adjusted analyses, the risk of a composite cardiovascular endpoint decreased (p ≤ 0.043) with higher Rmax and Dmax with hazard ratios ranging from 0.27 to 0.49. Finally, in the geographical analysis, endothelial dysfunction followed the spatial gradients in PM2.5. CONCLUSIONS: Long-term low-level air pollution is associated with subclinical endothelial dysfunction, the initial and critical step leading to adverse cardiovascular outcomes.