Investigating Mechanisms of Redox Stress Induced in Human Airway Epithelial Cells (HAEC) exposed to woodsmoke at an Air-Liquid Interface (ALI)
On this page:
Background: Exposure to airborne fine particulate matter (PM2.5) is a leading cause of morbidity and mortality worldwide. Exposure to PM2.5 is associated with a wide range of adverse outcomes such as exacerbation of cardiovascular disease, respiratory infections, and premature death. A major contributor ambient air pollution is wildfire smoke which is a complex mixture of PM, gases such as carbon monoxide and nitrogen oxides, and semi-volatile organic compounds. Epidemiological data has demonstrated that ambient wood smoke exposure is associated with cardiovascular mortality and an increase in asthmatic events. In vitro studies have shown that wood smoke condensates induce inflammation and cytotoxicity, which is proposed to be underlain by oxidative stress. However, the mechanisms by which wood smoke induces redox stress and the ensuing responses have not been characterized. In the present study, we hypothesize that HAEC exposure to wood smoke induces oxidative stress specifically through the initiation of lipid peroxidation reactions.
Methods: We recently reported the use of a tube furnace to generate wood smoke and its novel interface to a live cell imaging system. We studied live-cell imaging of HAEC derived from human volunteers using an IRB- approved protocol. Total lipid extracts (TLE) prepared from HAEC exposed at an air liquid interface were used to treat naïve HAEC expressing the glutathione redox potential (EGSH) sensor roGFP.
Results: TLE from wood smoke exposed primary HAEC induced glutathione oxidation in naïve HAEC expressing roGFP. Using the fluorescent sensor Liperfluo, which specifically reports on the formation of lipid hydroperoxides, we observed that TLE of wood smoke exposed HAEC also induced increased lipid hydroperoxide generation.
Conclusions: These data indicate that wood smoke induces oxidative stress and the formation of lipid hydroperoxides in HAEC. Taken together, these findings further our understanding of the mechanisms involved in the generation of redox stress in the human airway epithelium exposed to inhaled wood smoke.
This abstract of a proposed presentation does not necessarily reflect EPA policy.