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Updated: Jul 13, 2026

A Novel Inhalation Mask System to Deliver High Concentrations of Nitric Oxide Gas in Spontaneously Breathing Subjects
Published on: May 4, 2021
Nitric oxide and exhaled breath nitrite/nitrates in chronic obstructive pulmonary disease patients
Jia Liu1, Alessandra Sandrini, Michelle C Thurston
1Prince of Wales Hospital Clinical School, Faculty of Medicine, University of New South Wales, Randwick, Australia.
Background:
Measurement of nitric oxide (NO) and nitrite/nitrates (NOx) levels in exhaled breath condensate (EBC) are non-invasive techniques, which can be used to monitor airway inflammatory diseases. Production of NO is often increased in inflammatory diseases of the airways, including exacerbations of chronic obstructive pulmonary disease (COPD). COPD-associated airway inflammation may be affected by multiple factors, including cigarette smoking and glucocorticosteroid (GCS) treatment.
Objectives:
To test the hypothesis that total NOx levels in EBC and exhaled NO levels would be affected by cigarette smoking or the presence of COPD.
Methods:
Exhaled NO levels and NOx levels in EBC were measured in 96 COPD patients and in 80 normal subjects.
Results:
Exhaled NO levels in COPD patients were significantly higher than those of normal subjects when comparing either the total groups (9.8 +/- 0.7 vs. 5.5 +/- 0.4 ppb, p < 0.0005) or 2 appropriate subgroups, ex-smokers (10.3 +/- 1.0 vs. 5.4 +/- 0.6 ppb, p < 0.0005) and smokers (9.2 +/- 1.2 vs. 5.7 +/- 0.5 ppb, p = 0.002). There was no significant difference in NOx levels in EBC, however, between COPD patients and healthy subjects when analysed either together or as subgroups. No significant difference was found in either exhaled NO levels or NOx levels in EBC between GCS-naive subjects and those on GCS treatment in the ex-smoking or smoking COPD subgroups.
Conclusions:
COPD patients have higher exhaled NO levels than control subjects when either combined or analysed as non-smoking, ex-smoking and smoking subgroups. GCS treatment did not appear to affect these non-invasive markers of airway inflammation in COPD.
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