Secondhand smoke exposure induces acutely airway acidification and oxidative stress
AuthorKostikas, K.; Minas, M.; Nikolaou, E.; Papaioannou, A. I.; Liakos, P.; Gougoura, S.; Gourgoulianis, K. I.; Dinas, P. C.; Metsios, G. S.; Jamurtas, A. Z.; Flouris, A. D.; Koutedakis, Y.
Previous studies have shown that secondhand smoke induces lung function impairment and increases proinflammatory cytokines. The aim of the present study was to evaluate the acute effects of secondhand smoke on airway acidification and airway oxidative stress in never-smokers. In a randomized controlled cross-over trial, 18 young healthy never-smokers were assessed at baseline and 0, 30, 60, 120, 180 and 240 min after one-hour secondhand smoke exposure at bar/restaurant levels. Exhaled NO and CO measurements, exhaled breath condensate collection (for pH, H2O2 and NO2-/NO3- measurements) and spirometry were performed at all time-points. Secondhand smoke exposure induced increases in serum cotinine and exhaled CO that persisted until 240 min. Exhaled breath condensate pH decreased immediately after exposure (p < 0.001) and returned to baseline by 180 min, whereas H2O2 increased at 120 min and remained increased at 240 min (p = 0.001). No changes in exhaled NO and NO2/NO3 were observed, while decreases in FEV1 (p <0.001) and FEV1/FVC (p < 0.001) were observed after exposure and returned to baseline by 180 min. A 1-h exposure to secondhand smoke induced airway acidification and increased airway oxidative stress, accompanied by significant impairment of lung function. Despite the reversal in EBC pH and lung function, airway oxidative stress remained increased 4 h after the exposure. Clinical trial registration number (EudraCT): 2009-013545-28. (C) 2012 Elsevier Ltd. All rights reserved.