Analysis of expired air for oxidation products.
Chronic inflammation is a critical feature of chronic obstructive pulmonary disease, cystic fibrosis, and asthma. This inflammation is associated with the increased production of reactive oxygen species or oxidative stress in the lungs. Oxidative stress may have several adverse effects and may amplify the inflammatory process; however, monitoring oxidative stress is difficult and may not be reflected by changes in blood markers. We have therefore developed several noninvasive markers in the exhaled breath that may indicate oxidative stress in the lungs, and we studied these in relationship to the severity of chronic inflammatory lung diseases. We analyzed the exhaled breath for the content of nitric oxide as a marker of inflammation, carbon monoxide as a marker of oxidative stress, and ethane, which is one of the end products of lipid peroxidation. In addition, we measured the concentration of markers of oxidative stress such as isoprostanes in exhaled breath condensate. Our results confirm that there are increased inflammation, oxidative stress, and lipid peroxidation in lung disease, as shown by elevated levels of nitric oxide, carbon monoxide, and ethane, respectively. The finding of lower levels of these gases in patients on steroid treatment and of higher levels in those with more severe lung disease, as assessed by lung function tests and clinical symptoms, reinforces the hypothesis that the noninvasive measurement of exhaled gases maybe useful in monitoring the underlying pathologic pathways of lung disease. Longitudinal studies are required to assess the clinical usefulness of these measurements in the monitoring of chronic inflammatory lung disease.
Paredi
Paolo
P
Department of Thoracic Medicine, National Heart and Lung Institute, Imperial College School of Science, Technology and Medicine, London, United Kingdom.
Kharitonov
Sergei A
SA
Barnes
Peter J
PJ
D001249:Asthma / Q000378:metabolism*; D015415:Biomarkers / Q000032:analysis*; D001944:Breath Tests / Q000379:methods*; D002248:Carbon Monoxide / Q000032:analysis; D003550:Cystic Fibrosis / Q000378:metabolism*; D006801:Humans; D006838:Hydrocarbons / Q000032:analysis; D015227:Lipid Peroxidation / Q000502:physiology; D018384:Oxidative Stress / Q000502:physiology*; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism*
D015415:Biomarkers; D006838:Hydrocarbons; D002248:Carbon Monoxide