Airborne particulate matter exposure impairs lung redox metabolism involved in tissue damage repair mechanism

Abstract

Is estimated that 91% of the world's population breathes polluted air leading to more than 7 million premature deaths per year. Airborne pollutants such as particulate matter (PM) are associated with enhanced health risk as they can trigger or aggravate several pulmonary diseases. Our aim was to assess if alterations in the lung oxidative metabolism initiated by toxicological mechanisms triggered after PM inhalation were associated with a delayed tissue injury repair. To characterize our model, BALB/c mice were exposed to filtered air (FA) or urban air (UA) from Buenos Aires City, in whole-body exposure chambers. Results showed that after 8 weeks of UA exposure, mice developed lung redox alterations and local inflammation without histological damage, therefore that was the time point selected to further evaluate the oxidative metabolism after a moderate lung injury induced by intratracheal instillation of 0.1 N hydrochloric acid (HCl). Pulmonary tissue was evaluated 5 days after HCl treatment. Tissue oxygen consumption was assessed as a whole lung metabolism marker, and the increase observed in mice breathing FA by HCl treatment, was not detected in HCl-mice exposed to UA (p<0.05). Interestingly, SOD activity showed the same trend (p<0.05), even though transcription factor Nrf2 expression was higher after the injury in the UA group (p<0.05). While no edema was observed in any group, local inflammation measured as total cell count in bronchoalveolar lavage (BAL), was significantly increased only after UA exposure and HCl instillation (p<0.05) compared to control values. Hence, mice breathing UA might not be able to modulate the redox metabolism involved in lung damage repair mechanisms. Our results highlight the importance of tissue healing mechanisms evaluation as valuable knowledge for developing adequate therapeutic approaches aiming to ensure restoration of normal alveolar architecture required for proper lung function.