Introduction: Australian bushfires are increasing in frequency and severity. Bushfire smoke contains organic/inorganic compounds including aldehydes, acrolein, and carbon monoxide. Little is known about its effects on airway cells. We have previously described effects of tobacco smoke, including increased apoptosis of bronchial epithelial cells and defects in macrophage phagocytic function. We hypothesised that exposure to bushfire smoke would result in changes to airway cells similar to cigarette smoke.

Methods: THP-1 macrophages and 16HBE bronchial epithelial cells were exposed to 1%-10% ‘Bushfire’ smoke extract (BFSE); prepared from dried leaves and stems of 5 commonly occurring native plant species of Acacia and Eucalyptus. Cigarette smoke extract served as positive control. Efferocytosis of apoptotic 16HBE cells and phagocytosis of NTHi was assessed by Flow Cytometry. Cell viability was studied using 7AAD and Annexin V, LDH assay and western blot analysis of caspase-3 and PARP cleavage. IL-8 was measured in supernatants from BFSE-exposed macrophages using a cytometric bead array.

Results(p<0.05): Efferocytosis by macrophages was significantly decreased (10.4% controls, 6.4% BFSE 5%; p<0.05). There was a trend towards decreased phagocytosis of NTHi. BFSE significantly increased LDH release from epithelial cells (2.8% controls, 6.4% and 36.6%, for BFSE% and 10%; p<0.0001). IL-8 secretion was significantly increased by 75% and 82%, respectively;(p<0.05).

Conclusions: Bushfire smoke exposure can impair macrophage function and reduce epithelial cell viability while increasing pro-inflammatory cytokines. This preliminary data highlights the need for further research into the harmful effects of exposure to bushfire smoke. This has implications for patients with pre-existing lung diseases but also for the normal population.