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Hazards of E-cigarettes/Climate change/WHO Air Quality Guidelines/Ethical issues in science

Ilaria Cattoni; Gabriella Guarnieri; Alessandro Tosetto; Paola Mason; Maria C. Scarpa; Marina Saetta; Piero Maestrelli

Chest. 2013. doi:10.1378/chest.12-1374

Abstract Exhaled nitric oxide (FeNO50), a biomarker of airway inflammation, is affected by changes in airway calibre. Whether lower FeNO50 levels during bronchoconstriction is only an artifact due to the strong flow-dependence of this parameter is controversial.We aimed to evaluate the dynamics of airway and alveolar NO during acute bronchoconstriction induced by methacholine.Exhaled NO was measured at expiratory flows of 10, 50, 100, 150 and 250 ml/s before and after metacholine in 26 responders to methacholine and 37 non-responders. Flow-independent parameters (airway wall NO flux, airway NO diffusing capacity, airway wall NO concentration, alveolar NO concentration) were calculated using two-compartment model and correction for NO axial back-diffusion was applied.Bronchoconstriction in responders was associated with a decrease in FeNO50 (-28%, p<0.0001), in airway wall NO flux (-34%, p<0.0001) and in airway NO diffusing capacity (-15%, p<0.05). In contrast, alveolar NO concentration was not affected by bronchoconstriction. Post-methacholine changes in FeNO50 were more strictly related to the ventilation distribution, assessed by single breath carbon monoxide uptake, than to larger airways caliber, assessed by FEV1. When bronchoconstriction was reversed by salbutamol, airway wall NO flux and airway NO diffusing capacity returned to values comparable to those measured pre-methacholine.In conclusion, the changes in airway caliber induced by non-inflammatory stimuli alters NO transport in the lung. The changes in NO dynamics are limited to conductive airways and are characterized by a reduction of NO flow to luminal space.