Differential inflammatory and toxic effects in-vitro of wood smoke and traffic-related particulate matter from Sydney, Australia

Background: It is well known that PM2.5 generated by traffic or burning wood is pro-inflammatory and induces various adverse health outcomes in humans. In Sydney, New South Wales, Australia, the main anthropogenic contributors to particulate matter (PM) air pollution are wood combustion heaters, on-road vehicles, and coal-fired power stations. However, the relative toxicity of these local sources has not to date been investigated. Method: PM2.5 was collected on filters from the same sampling site in Liverpool, one suburb of Sydney. According to the positive matrix factorisation and collection season, filters were representative of either day with high traffic-related air pollution (TRAP), wood smoke, or both TRAP and woodsmoke (mixed air pollution). The elemental composition of the PM was assessed by accelerator-based ion beam analysis techniques (i.e. PIXE & PIGE) and size by Dynamic Light Scattering. Toxicity and inflammation were assessed in-vitro in human bronchial epithelial cells by measuring interleukin-6 (IL-6), interleukin-8 (IL-8) release, and MTT. Results: Mixed air pollution (TRAP/wood smoke) PM had more nanometer (nm) sized PM than the other two groups. Using an in-vitro model of the lungs, the mixed air pollution PM was the most toxic, whereas the PM from woodsmoke induced greater IL-6 release than TRAP PM. There was no difference in the induction of IL-8 between the three sources of PM. Conclusion: Marked differences occur in the cellular response to PM from different sources, with differences in both toxicity and inflammation. Crown Copyright (C) 2021 Published by Elsevier Ltd. All rights reserved.

Automated summary

The study investigates the relative toxicity of PM2.5 from different local sources in Sydney, Australia. The researchers found that mixed air pollution (TRAP/wood smoke) had the smallest nanometer-sized particles and induced the highest toxicity in a lung model, while wood smoke PM induced greater IL-6 release than traffic-related air pollution (TRAP) PM. There was no difference in IL-8 induction among the three sources of PM.