Landscape fire smoke airway exposure impairs respiratory and cardiac function and worsens experimental asthma

Background Millions of people are exposed to landscape fire smoke (LFS) globally and inhalation of LFS particulate matter is associated with poor respiratory and cardiovascular outcomes. However, how LFS affects respiratory and cardiovascular function is less well understood. Objective To characterize the pathophysiological effects of representative LFS airway exposure on respiratory and cardiac function and on asthma outcomes. Methods LFS was generated using a customized combustion chamber. 8-week old female Balb/C mice were administered low (25μg/m3, 24 hour equivalent) or moderate (100μg/m3, 24 hour equivalent) concentrations of LFS particulate matter (10μm and below; PM10) daily for 3 (short-term) and 14 (long-term) days in the presence and absence of experimental asthma. Lung inflammation, gene expression, structural changes and lung function were assessed. 8-week old male C57Bl/6 mice were administered low concentration LFS PM10 for 3 days. Cardiac function and gene expression were assessed. Results Short- and long-term LFS PM10 airways exposure increased airways hyperresponsiveness and induced steroid-insensitivity in experimental asthma, independent of significant changes in airway inflammation. Long-term LFS PM10 airways exposure also decreased gas diffusion. Short-term LFS PM10 airways exposure decreased cardiac function and the expression of gene changes relating to oxidative stress and cardiovascular pathologies. Conclusion We have characterised significant detrimental effects of physiologically relevant concentrations and durations of LFS PM10 airways exposure on lung and heart function. Our study provides a platform for assessment of mechanisms that underpin LFS PM10 airways exposure on respiratory and cardiovascular disease outcomes.