Nitrogen dioxide component of air pollution increases pulmonary congestion assessed by lung ultrasound in patients with chronic coronary syndromes

Abstract

Pulmonary congestion is an intermediate biomarker and long-term predictor of acute decompensated heart failure. To evaluate the effects of air pollution on pulmonary congestion assessed by lung ultrasound. In a single-center, prospective, observational study design, we enrolled 1292 consecutive patients with chronic coronary syndromes referred for clinically indicated ABCDE-SE, with dipyridamole (n = 1207), dobutamine (n = 84), or treadmill exercise (n = 1). Pulmonary congestion was evaluated with lung ultrasound and a 4-site simplified scan. Same day values of 4 pollutants were obtained on the morning of testing (average of 6 h) from publicly available data sets of the regional authority of environmental protection. Assessment of air pollution included fine (< 2.5 µm diameter) and coarse (< 10 µm) particulate matter (PM), ozone and nitrogen dioxide (NO2). NO2 concentration was weakly correlated with rest (r =.089; p = 0.001) and peak stress B-lines (r =.099; p < 0.001). A multivariable logistic regression analysis, NO2 values above the median (23.1 µg/m3) independently predicted stress B-lines with odds ratio = 1.480 (95% CI 1.118–1.958) together with age, hypertension, diabetes, and reduced (< 50%) ejection fraction. PM2.5 values were higher in 249 patients with compared to those without B-lines (median and IQR, 22.0 [9.1–23.5] vs 17.6 [8.6–22.2] µg/m3, p < 0.001). No other pollutant correlated with other (A-C-D-E) SE steps. Higher concentration of NO2 is associated with more pulmonary congestion mirrored by B-lines at lung ultrasound. Local inflammation mediated by NO2 well within legally allowed limits may increase the permeability of the alveolar-capillary barrier and therefore pulmonary congestion in susceptible subjects. ClinicalTrials.gov Identifier: NCT030.49995.