Respiratory and cardiovascular effects of ambient particulate matter from dust storm and non-dust storm periods in Kuwait

Abstract

Epidemiological studies demonstrate a positive association between daily changes in concentrations of ambient airborne particulate matter (PM) and adverse respiratory and cardiovascular health effects. However, physicochemical properties of PM can vary greatly across geographical, atmospheric, and temporal conditions and influence the relative toxicity of airborne PM. The purpose of this study was to investigate the adverse pulmonary and cardiovascular health effects of ambient PM collected from discrete sampling sites in Kuwait during dust storm (DS) and non-dust storm (NDS) conditions. Collected dust samples were characterized for their chemical composition using atomic absorption, GC–MS, and HPLC–MS analyses. Male BALB/cJ mice were exposed to 100 µg of either NDS or dust storm (DS) PM in 50 µl of PBS by oropharyngeal aspiration. Lung function was measured and bronchoalveolar lavage was conducted at 1, 7, and 14 days post-exposure. Ischemia–reperfusion injury was performed 24 h after exposures by obstructing the left main coronary artery approximately 4 mm distal to its origin for 20 min, followed by 2 h. of reperfusion. Exposure to either NDS or DS PM resulted in airway hyperresponsiveness to acetylcholine compared to PBS controls. Total protein and cells in BAL fluid were elevated in both dust groups one day after exposure; however, DS PM induced a greater increase in cell numbers than did NDS PM, particularly in neutrophils, eosinophils, and lymphocytes. Representative lung sections exhibited positive staining for mucus in large airways at 7 days which resolved by 14 days in dust storm-exposed mice but persisted in NDS-exposed animals. Our findings suggest that NDS PM may be more effective in producing an adaptive immune response, while the early inflammation induced by DS PM may better resolve. We also observed a prolonged airway mucus response after exposure to NDS PM, suggesting it may produce more asthma-like features than dust storm PM. PM-induced changes to cardiac ischemia–reperfusion injury were not observed in this study. The lack of cardiovascular response may have been due to the limited exposure and single time point used in this study.