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

Abstract

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