Abstract
Air pollution is associated with morbidity and mortality induced by respiratory diseases. However, the mechanisms therein involved are not yet fully clarified. Thus, we tested the hypothesis that a single acute exposure to low doses of fine particulate matter (PM2.5) may induce functional and histological lung changes and unchain inflammatory and oxidative stress processes. PM2.5 was collected from the urban area of São Paulo city during 24 h and underwent analysis for elements and polycyclic aromatic hydrocarbon contents. Forty-six male BALB/c mice received intranasal instillation of 30 μL of saline (CTRL) or PM2.5 at 5 or 15 μg in 30 μL of saline (P5 and P15, respectively). Twenty-four hours later, lung mechanics were determined. Lungs were then prepared for histological and biochemical analysis. P15 group showed significantly increased lung impedance and alveolar collapse, as well as lung tissue inflammation, oxidative stress and damage. P5 presented values between CTRL and P15: higher mechanical impedance and inflammation than CTRL, but lower inflammation and oxidative stress than P15. In conclusion, acute exposure to low doses of fine PM induced lung inflammation, oxidative stress and worsened lung impedance and histology in a dose-dependent pattern in mice.
Acknowledgments
The authors are grateful to Joao Luiz Coelho Rosas Alves and Antonio Carlos de Souza Quaresma for their skillful technical assistance.
Declaration of interest
This study was supported by: The Centers of Excellence Program (PRONEX- MCT/FAPERJ), The Brazilian Council for Scientific and Technological Development (MCT/CNPq), The Carlos Chagas Filho Rio de Janeiro State Research Supporting Foundation (FAPERJ). They are all governmental research supporting agencies that did not interfere with the study at any point. The authors do not have any actual or potential conflict of interest including any financial, personal or other relationships with other people or organizations within 3 years of beginning the work submitted that could inappropriately influence (bias) their work.