Exposure to urban air pollution, ultrafine particles or gas, is associated with acute cardiovascular mortality and morbidity. We investigated the effects of ambient air pollution on endothelial function in 40 healthy Caucasian men, previously described in the KLK study (JCI 2005), who spontaneously breathed ambient air pollution in Paris.

Endothelial function was measured by the % of brachial artery dilatation (dDr) and the absolute variation of shear stress (dSS) after hyperhemia following 5 min hand ischemia and after 150 μg of TNT sublingual, using RF-bases echotracking device, at two visits 2 weeks apart. Air pollution level, (CO, NO, NO₂, SO₂, PM 2.5) were extracted from “Airparif” database, the day of vascular measurement (J0”Pollutant”) and 5 days before (mean “pollutant”). The ranks of pollutants were added to form SPOL score.

Baseline dDr was significantly and negatively correlated with mean and J0 NO (P <0.001 for both), mean and J0 SO2 (P <0.0001 for both), mean and J0 CO (P <0.0001 for both), and SPOL(P < 0.001). SPOL explained 19% of the variance of baseline dDr. Baseline dSS was significantly correlated with mean NO2 (P = 0.003), mean SO2 (P = 0.004), J0 SO2 (P = 0.05), and J0 PM 2.5 (P = 0.02). Changes in dDr between the two visits was significantly correlated with delta NO (P = 0.001) and delta SPOL (P = 0.006). Delta SPOL explained 8% of the variance of Delta DdLir. Changes in diameter or shear stress after TNT were not correlated with changes in air pollutants levels.

Endothelial function is significantly impaired by ordinary levels of pollutant in healthy young males, in urban area.