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Exposure to bushfire and biomass smoke and the risk of bacterial and viral lung infection

From September 2019 to March 2020, Australia experienced one of its worst bushfire seasons which became known as the Black Summer. An area of 186 000 km, more than twice the size of the island of Ireland, was burned with a loss of over 30 lives and 5000 buildings, half of which were private dwellings. In terms of health impacts, bushfire smoke releases hazardous particulate matter ≤10 μm in diameter (PM10), and fine particulate matter ≤2.5 μm in diameter (PM2.5). PM10 and PM2.5 increase the risk of hospitalization and emergency department visits in individuals with chronic airway illnesses, in particular, asthma and chronic obstructive pulmonary disease (COPD) as reviewed recently. But in regard to communicable illnesses, data on the role of bushfire smoke in infection are currently limited. Regarding the latter, as previously noted, standardized techniques are needed for the generation of reproducible biomass smoke in the laboratory. Extension of these techniques to bushfire smoke will assist in determining the impact of bushfire smoke on the respiratory system at the cellular and molecular levels including the process of infection by pathogenic microorganisms. Using an approach in which leaves and trees from a variety indigenous Australian tree species were combined and ignited, Hamon et al. applied a vacuum pump to bubble the smoke produced through saline which was then diluted into tissue culture growth media. This led them to determine that bushfire smoke suppresses the phagocytic activity of an human acute monocytic leukemia cell line (THP-1) and monocytederived macrophages (MDM) towards respiratory pathogen non-typeable Haemophilus influenzae (NTHi). Using a filter collection set-up, together with co-investigators, we recently found that exposure of human bronchial epithelial cells to biomass smoke led to increased adhesion by NTHi. As NTHi is a major bacterial cause of acute exacerbations of COPD, any events that increase its ability to evade the innate immune response and colonize respiratory epithelial surfaces could result in a heightened susceptibilityof host airways to NTHi infection. In terms of viruses, evidence collated by Gordon and colleagues indicates that exposure to biomass smoke is associated with an increased risk of respiratory viral infection. This may occur through a number of mechanisms, including epithelial barrier dysfunction, pulmonary and systemic inflammation, increased glutathione levels and decreased anti-viral defences. A study by Capistrano et al. examined the effect on human primary lung fibroblasts of smoke from softwood species, Pinus radiata (standard pine), and from hardwood species, Intsia bijuga (Merbau wood/Kwila). They reported a significant increase in the release of pro-inflammatory cytokines interleukin (IL)-6 and IL-8, as measured by enzyme-linked immunosorbent assay (ELISA), from fibroblasts that were treated with either 1% hardwood or softwood smoke extracts. In particular, the investigators found that infection of the fibroblasts with human rhinovirus-16 further increased biomass smoke-induced IL-8 expression. However, rhinoviral replication remained unaffected following biomass smoke exposure. This indicates that an increase in airway inflammation due to biomass smoke exposure does not necessarily equate with a heightened viral load and that a more complex relationship exists between smoke exposure, inflammation and rhinoviral infection. A 2019 study by Rebuli and colleagues of healthy adults (n = 39) aged between 18 and 40 years examined whether acute exposure to wood smoke particles modified nasal inflammatory responses to influenza. The investigators found with aggregated data that there was no detectable change in the expression of pro-inflammatory cytokines after wood smoke exposure in contrast to the earlier in vitro study. However, when the investigators de-aggregated the data with respect to the sex of the participants, they reported that in males, 13 genes, most of which were pro-inflammatory, were upregulated by wood smoke particles more than twofold in males compared to females. The authors then assessed whether sex differences extended to nasal challenge with live attenuated influenza virus (LAIV). They determined that nasal lavage fluid from subjects challenged with LAIV following wood smoke exposure exhibited differential expression of a considerably higher number of immune and inflammatory genes in females (78 genes) than in males (16 genes) at Day 2. The investigators hypothesized that different thresholds may exist in males and females with regard to the stimulus level required to trigger inflammatory mediators after wood smoke exposure, versus influx and activation of neutrophils in response to infection of a pathogen such as influenza virus. Again the complexity of the interaction between host, smoke exposure and viral pathogen challenge requires further extensive research. An ongoing study from Harvard University led by Wu et al. has examined coronavirus disease 2019 (COVID19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in relation to air pollution exposure. The authors analysed COVID-19 mortalities recorded across >3000 counties in the USA which encompass 98% of the population using data from the