The oxidative capacity of indoor source combustion derived particulate matter and resulting respiratory toxicity

Indoor air pollution sources with emissions of fine particles (PM2.5), including environmental tobacco smoke (ETS) and incense (IS) deteriorate indoor quality may cause respiratory diseases in humans. This study characterized the emission factors (EFs) five types Hong Kong using an chamber. Human alveolar epithelial cells (A549) were exposed to PM2.5 collected from different determine their cytotoxicity. The EF ETS (109.7±36.5 mg/g) was higher than IS (97.1±87.3 mg/g). EFs total polycyclic aromatic hydrocarbons (PAHs) carbonyls for ETS, these two combustion showed similar distributions individual PAHs carbonyls. Oxidative damage inflammatory responses (i.e. DNA damage, 8-hydroxy-desoxyguanosine (8-OHdG), tumor necrosis factor-? (TNF-?) interlukin-6 (IL-6)) A549 triggered by exposure generated IS. Different oxidative stress inflammations due accumulation effects mixed organic compounds. High molecular weight correlations markers, most demonstrated significant inflammation. Exposure anthropogenic produced such as results risks (e.g. lung cancer) epithelium within distal human tract, which posed a