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

Abstract 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.