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

• 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.

In non-smokers, ozone (O3) inhalation causes decreases in forced expiratory volume (FEV1) and dead space (VD) and increases the slope of the alveolar plateau (SN). 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 VD (− 6.1 ± 1.2%) and SN (9.1 ± 3.4%). There was no difference in total delivered dose. Dead space ventilation (VD/VT) 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 VD that lead to heterogeneity in airway morphometry and an increase in SN.