Vascular remodeling and endothelial dysfunction in patients with occupational chronic obstructive pulmonary disease caused by exposure to industrial aerosol nanoparticles

BACKGROUND: The characteristics of vascular pathology in different phenotypes of occupational chronic obstructive pulmonary disease (COPD), as well as the causal role of various industrial aerosol components, especially nanoparticles, are poorly understood.

AIM: To determine the characteristics of arterial remodeling and endothelial function in patients with occupational COPD caused by exposure to aerosol nanoparticles.

METHODS: An observational, cohort cross-sectional study was performed in patients with occupational COPD caused by exposure to aerosols containing metal (n = 48) or silicon (n = 55) nanoparticles, compared with COPD caused by tobacco smoking (n = 50). Scanning electron microscopy and inductively coupled plasma atomic emission spectroscopy were used to measure the size and chemical composition of particles, respectively. The procedures used in the study included color-flow duplex scanning of the brachiocephalic arteries, brachial arteries, and aorta; flow-mediated dilation test of the brachial arteries; and enzyme-linked immunosorbent assay of molecular markers. Linear regression was used to determine relationships.

RESULTS: The group of occupational COPD caused by aerosols with silicon nanoparticles had the highest values of carotid intima-media thickness: 1.2 [0.9; 1.5] mm; in the group of occupational COPD caused by aerosols with metal nanoparticles and the control group, these values were 0.9 [0.7; 1.0] mm and 0.8 [0.7; 0.9] mm, respectively (p = 0.009). Moreover, the group of occupational COPD caused by aerosols with silicon nanoparticles had the highest incidence of atherosclerosis compared to the group of occupational COPD caused by aerosols with metal nanoparticles and the control group (41.8% vs. 22.9% and 18.0%, respectively; р = 0.003). The aortic pulse wave velocity in the three groups was 12.6 [11.2; 14.1], 9.3 [8.9; 10.7], and 7.2 [6.9; 8.4] m/s, respectively (р = 0.001). The minimum flow-mediated dilation of the brachial arteries was 2.5 [2.1; 3.4], 3.8 [3.3; 4.6], and 4.7 [4.5; 5.3]%, respectively (р = 0.001). Occupational COPD caused by aerosols with silicon nanoparticles was associated with the highest serum levels of vascular cell adhesion molecule 1, von Willebrand factor, transforming growth factor β1, procollagen III N-terminal propeptide, and fibroblast growth factor 2. Regression relationships were found between the intima-media thickness and the concentration of metal (adjusted R-squared [R²]: 0.36) and silicon (adjusted R²: 0.47) nanoparticles, as well as the length of employment (adjusted R²: 0.27). Moreover, regression relationships were found between the flow-mediated dilation of the brachial arteries and the concentration of metal (adjusted R²: 0.51) and silicon (adjusted R²: 0.71) nanoparticles, the length of employment (adjusted R²: 0.68), and the total concentration of silicon-containing dust (adjusted R²: 0.55).

CONCLUSION: Occupational COPD caused by exposure to aerosol nanoparticles (especially silicon-containing ones) is associated with significant vascular remodeling and endothelial dysfunction, which must be considered during follow-up care.