Airway exposure to urban aerosolized PM_2.5 particles induces neuroinflammation and endothelin-mediated contraction of coronary arteries in adult rats

Ambient airborne particles with an aerodynamic diameter of <2.5 µm (PM_2.5), which contain particles from combustion processes, are linked to increased risks for cardiovascular and respiratory diseases. In this experimental study, the short-term and long-term physiologic consequences of PM_2.5 inhalation were investigated with the focus on inflammatory parameters and vascular tonus. PM_2.5 collected from urban environments in southern Sweden were aerosolized with a nebulizer and delivered to male Sprague Dawley rats. The rats were divided into two treatment groups (n=8 in each): short-term exposed (8 h with an estimated lung exposure rate of 90 μg PM_2.5/h); and long-term exposed (3 h/day, 5 days/week, for 8 weeks, with an estimated lung exposure rate of 30 μg PM_2.5/h). A group of non-particle-exposed control animals (n=8) was run in parallel with each test group. The results showed that short-term exposure increased the numbers of lymphocytes in the bronchoalveolar lavage fluids. Long-term exposure led to impaired substance P-induced relaxation and increased endothelin-1-induced contraction of the coronary arteries. The contractile response was found to be mediated by endothelin receptor A. Long-term exposure led to increased interleukin-6 levels in brain tissues, as compared to the controls. In summary, this explorative study reveals that exposure to aerosolized, ambient PM_2.5 leads to impaired coronary artery function and neuroinflammation. Further investigations into the impacts on health effects of short-term and long-term exposures to urban air pollution are warranted.