Exhaled carbon monoxide is not elevated in patients with asthma or cystic fibrosis.
Increased levels of exhaled carbon monoxide (fractional concentration of CO in expired gas (FE,CO)), measured with an electrochemical sensor, have been reported in patients with inflammatory airway disorders, such as asthma, rhinitis and cystic fibrosis. This study aimed to evaluate these findings by using a fast-response nondisperse infrared (NDIR) analyser, and to compare these measurements with the fractional concentration of nitric oxide in exhaled air (FE,NO). Thirty-two steroid-naïve asthmatics, 24 steroid-treated asthmatics (16 patients with allergic rhinitis, nine patients with cystic fibrosis), and 30 nonsmoking healthy controls were included. CO measurements with the NDIR analyser were performed simultaneously with nitric oxide (NO) analysis (chemiluminescence technique). After 15 s of breath-hold, single-breath exhalations over 10 s were performed at two flow rates and end-tidal plateau concentrations were registered. An electrochemical CO sensor was used independently with an exhalation to residual volume, after a 15 s breath-hold. None of the two CO analysers gave a significant increase in FE,CO in the groups of patients with inflammatory airway disorders compared to controls. FE,NO was significantly elevated in steroid-naïve asthmatics and subjects with allergic rhinitis, but not in steroid-treated asthmatics and subjects with cystic fibrosis. Reducing exhalation flow rate by 50% gave a two-fold increase in FE,NO, while FE,CO was unaffected. A significant increase was seen in FE.CO, but not in FE,NO, when comparing with and without a 10 s breath-hold. In conclusion, the fractional concentration of carbon monoxide in expired gas was not increased in any of the patient groups, while the fractional concentration of nitric oxide in expired gas was significantly elevated in patients with steroid-naïve asthma and allergic rhinitis. Moreover, carbon monoxide was unaffected by flow rate but increased with breath-hold, suggesting an origin in the alveoli rather than the conducting airways.
Zetterquist
W
W
Dept of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden. wilhelm.zetterquist@fyfa.ki.se
Marteus
H
H
Johannesson
M
M
Nordval
S L
SL
Ihre
E
E
Lundberg
J O N
JO
Alving
K
K
D000293:Adolescent; D000328:Adult; D001249:Asthma / Q000378:metabolism*; D001944:Breath Tests / Q000295:instrumentation*; D001993:Bronchodilator Agents / Q000032:analysis; D002248:Carbon Monoxide / Q000032:analysis*; D005591:Chemical Fractionation; D002648:Child; D003550:Cystic Fibrosis / Q000378:metabolism*; D004563:Electrochemistry / Q000295:instrumentation*; D005260:Female; D006801:Humans; D008163:Luminescent Measurements; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000032:analysis; D006255:Rhinitis, Allergic, Seasonal / Q000378:metabolism*; D013997:Time Factors
D001993:Bronchodilator Agents; D009569:Nitric Oxide; D002248:Carbon Monoxide