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Carbon monoxide (CO) can be detected in the exhaled breath and has been proposed as a marker of airway inflammation or reactivity. Several studies have been done recently to investigate the role of this gas in lung physiology and diseases. As it has been hypothesized that CO is produced within the human airways and may increase in the inflammatory airway diseases, we measured exhaled CO (eCO) in patients with asthma and chronic obstructive pulmonary diseases (COPD) before and after a one-month inhaled steroid therapy. Smoker and non-smoker healthy individuals were taken as control groups. In the healthy smoker group concentration of eCO was higher than the other groups (eCO ppm; healthy smokers, 9.5±2.5; healthy non-smokers, 2.1±0.4; asthma, 5.5±1.2; asthma attack, 5.2±0.7; COPD, 5.1±0.8; p<0.05). The patients with asthma (including attack group) and COPD had higher eCO levels than the healthy nonsmoker group before the corticosteroid therapy (p<0.05). Although there was no significant change in eCO in patients with COPD after a one-month corticosteroid therapy (eCO ppm; 5.1±0.8 and 4.8±0.6 p<0.277), there was a significant decrease in both asthma groups (eCO ppm; asthma 5.5±1.2 and 2.4±0.5 p<0.001 and asthma attack 5.2±0.7 and 2.5±0.4 p<0.001). In conclusion we suggest that eCO measurements may be used as a noninvasive tool in the diagnosis and the follow-up of therapy in the inflammatory airway diseases such as asthma and COPD.