Chronic exposure to aerosolized PM2.5 in rats alters plasma protein levels and ex vivo coronary artery response to Sphingosine-1-phosphate.

Growing evidence shows that air pollution exposure plays a critical role in the development and progression of cardiovascular disease. Pollutants such as airborne particles smaller than 2.5 μm (PM2.5) are linked to systemic inflammation, oxidative stress and vascular dysfunction, thereby increasing the risk of hypertension, atherosclerosis, stroke and myocardial infarction. Understanding the pathology and the disease progression is essential for developing targeted interventions to mitigate the global cardiovascular burden associated with polluted air. We aimed to study how different PM2.5 exposure regimes may affect vasomotor response in coronary arteries. Using well-characterized PM2.5 collected in an urban environment, we exposed rats to re-aerosolized PM2.5, mimicking different potential scenarios of air pollution exposures such as acute high-dose exposure compared to chronic exposure at a lower dose. Vascular tone was studied ex vivo from the PM2.5 exposed rats and their corresponding controls, employing a wire myograph. Also, systemic effects were assessed through plasma biomarkers of soluble Sphingosine-1-phosphate (S1P) and Endothelin-1 (ET-1) together with immunohistochemical assessment of coronary arteries. In our translational experimental set-up, we observed that only the accumulative dose from the chronic exposure played a significant role on the studied outcomes in the vasculature and plasma biomarkers. Following chronic exposure, S1P vasomotor response was altered in coronary arteries, as well as plasma total protein levels and ET-1 concentration, which were significantly decreased. This indicates the importance of prolonged PM2.5 exposure effects on cardiovascular health, highlighting medical intervention options alongside the importance of improving air pollution management.