Effects of commonly used air filters on secondhand tobacco smoke and the induction of oxidative stress and inflammation in mice.
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The annual number of deaths related to secondhand smoke (SHS) exposure exceeds 40,000 in the United States. Exposure to SHS primarily occurs in homes and work places. Public places of exposure to SHS include restaurants, bars and casinos due to lack of smoke-free laws. Approximately 7000 chemicals have been identified as constituents of SHS, of which 250 are known to be toxic and 70 as carcinogens. Exposure to these harmful chemicals can result in cardiovascular diseases and lung cancer. The critics of smoking bans have proposed air filtration systems as a viable solution to eliminate the risk of exposure to SHS. In this project, one of the primary objectives was to assess the effects of commonly used air filters, MERV 4 fiberglass, MERV 8 pleated and MERV 8 pleated activated charcoal on SHS and its biological effects. SHS was generated using a TE-10 smoke machine system, and the total suspended particulates, the smaller respirable particles and the carbon monoxide concentrations were measured in filtered smoke. Our results showed that these filters failed to remove these components of SHS. We also examined the physiological responses caused by exposure to SHS. Using murine models, the oxidative stress and the inflammatory responses caused by SHS exposure were assessed. In order to assess the oxidative stress response caused by the free radicals in SHS, superoxide dismutase (SOD), glutathione peroxidase (GPx), total glutathione (GSH) and lipid peroxidation products (MDA+HAE) in the lung homogenates were quantified. GSH and MDA+HAE in the lung tissues were chosen as the appropriate biomarkers to assess the oxidative stress by SHS. For the assessment of the inflammatory response, interleukin 1 beta (IL-1), interleukin 6 (IL-6), granulocyte macrophage colony stimulating factor (GM-CSF) and tumor necrosis factor alpha (TNF-) cytokines were quantified in the bronchoalveolarlavage (BAL) fluid. TNF-α in the BAL fluid was chosen the appropriate biomarker to assess the inflammatory response due to SHS. Exposure to SHS caused significantly upregulated oxidative stress response and a suppressed cytokine response. The attenuated cytokine response displayed characteristics of endotoxin tolerance/cross tolerance. The tested air filters were unable to remove the oxidative stress response in the lung homogenates. The tested filters also failed to protect against the suppression of cytokine response due to SHS. Our results showed that exposure to SHS causes a complex oxidative stress and an inflammatory response and that these commonly used air filters failed to protect against the SHS exposure.