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Dept of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
From the authors:
We appreciate the interest P. Paredi and colleagues have shown in our article. In their letter, they describe some differences in the methodologies used and suggest that these differences may explain why our results on exhaled carbon monoxide (CO) in asthma and cystic fibrosis 1 contrast with their previous findings. We agree that it is preferable to use standardised methods, but there is as yet no consensus on standardised methods for exhaled CO measurements.
With regard to possible contamination with nasal CO, we did have our patients exhale against a resistance using one of the two methods. However, in another study, we had not been able to detect any nasal CO formation whatsoever 2, so this may be a minor problem.
Although we used a 15-s breathhold time before exhalation and they did not, the methods are more or less equivalent in that the patients in their studies exhaled for 
25 s in contrast to 10 s in our study, resulting in the same time for CO diffusion in the alveoli when recording endtidal CO values. Furthermore, other researchers have used a 20-s breathhold and still reported elevated CO levels in various respiratory conditions 3–5.
We used COfree air for inhalation in one of the setups because we do not believe that subtraction of inhaled (ambient) CO is a correct procedure. The inhaled CO concentration will affect the concentration gradient for CO over the alveolar membranes (and possibly in the airways), and should not be compensated for by direct subtraction.
Our data primarily indicate an alveolar origin of exhaled CO. For many years now, exhaled CO has been used to detect smoking behaviour, for which this method is sometimes superior, even to urinary cotinine measurements 6. Exhaled CO is also used to detect haemolysis in the newborn with high sensitivity 7. In both these cases, the increase in exhaled CO is due to increased levels of carboxyhaemoglobin. Interestingly, it was recently suggested that the increase in exhaled CO in respiratory diseases like asthma is also due to increased carboxyhaemoglobin 8, again indicating an alveolar origin of exhaled CO. The cause of the increased carboxyhaemoglobin levels in respiratory conditions, increased haem breakdown or increased uptake/reduced elimination of inhaled CO, remains to be clarified. However, the latter is indicated by several studies 9–11, and it is well known that exposure to ambient CO (passive smoking, car exhaust) is sufficient to increase exhaled CO 12–13.
In conclusion, we do not agree that the contrasting results in our study depend on the suggested methodological differences. The reason for the disparate findings should be studied further. In any case, we believe that the profound alveolar contribution of CO derived from carboxyhaemoglobin, will make it difficult to use exhaled CO as a marker of airway inflammation.
REFERENCES
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