Pulmonary function responses to ozone in smokers with a limited smoking history

In non-smokers, ozone (O₃) inhalation causes decreases in forced expiratory volume (FEV₁) and dead space (V_D) and increases the slope of the alveolar plateau (S_N). We previously described a population of smokers with a limited smoking history that had enhanced responsiveness to brief O₃ boluses and aimed to determine if responsiveness to continuous exposure was also enhanced. Thirty smokers (19 M, 11 F, 24 ± 4 years, 6 ± 4 total years smoking,4 ± 2 packs/week) and 30 non-smokers (17 M, 13 F, 25 ± 6 years) exercised for 1 h on a cycle ergometer while breathing 0.30 ppm O₃. Smokers and non-smokers were equally responsive in terms of FEV₁ (− 9.5 ± 1.8% vs − 8.7 ± 1.9%). Smokers alone were responsive in terms of V_D (− 6.1 ± 1.2%) and S_N (9.1 ± 3.4%). There was no difference in total delivered dose. Dead space ventilation (V_D/V_T) was not initially different between the two groups, but increased in the non-smokers (16.4 ± 2.8%) during the exposure, suggesting that the inhaled dose may be distributed more peripherally in smokers. We also conclude that these cigarette smokers retain their airway responsiveness to O₃ and, uniquely, experience changes in V_D that lead to heterogeneity in airway morphometry and an increase in S_N. - Highlights: • We previously found lung function responses to O₃ bolus exposure in smokers. • Here, we describe their responsiveness to continuous O₃ exposure with exercise. • Spirometry and capnography were used to assess pulmonary function changes. • Enhanced bronchoconstriction in smokers increases parenchymal delivery of O₃