In nonsmokers, ozone (O3) is removed primarily by the epithelial lining fluid (ELF) of the conducting airways. We hypothesized that cigarette smokers, whose ELF antioxidant capacity may be limited by smoking, would remove less O3 from their conducting airways than nonsmokers. We recruited 29 nonsmokers (17M, 12F) and 30 smokers (19M, 11F, 4 ± 4 pack-years) with similar anthropometric characteristics and measured the longitudinal distribution of O3 using the bolus inhalation method. We also assessed the physiological effect of this transient exposure regimen using forced spirometry and capnography. Contrary to our hypothesis, the penetration volume at which 50% of a bolus was absorbed was not different between smokers and nonsmokers (97.1 ± 5.4 mL versus 97.9 ± 5.8 mL, p = 0.92). However, smokers did experience an increase in the slope of the alveolar plateau of the capnogram (SN) (8.1 ± 3.2%, p = 0.02) and a small decrease in FEV1 (- 1.3 ± 0.6%, p = 0.03), whereas nonsmokers did not (ΔFEV1 - 0.1 ± 0.5% and ΔSN - 0.2 ± 2.5%, p > 0.10). Thus, smokers are more sensitive to inhaled O3 boluses than nonsmokers, despite a similar internal dose distribution.
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