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University of Edinburgh, Respiratory Unit, Western General Hospital, Edinburgh, UK
To the Editor:
It was with interest that we read the study of Paredi et al. 1 which reports a slower rise in exhaled breath temperature in patients with chronic obstructive pulmonary disease (COPD). It is intriguing to think that altered airway heat transfer may provide a noninvasive marker of airways inflammation or remodelling. However, heat transfer in the airway has long been known to be a complex process and we feel this study leaves important questions unanswered.
The authors hypothesise that patients with COPD have alterations in bronchial blood flow that affect the rise in exhaled air temperature. Heat transfer in the airways in the context of respiratory disease was studied by Walker et al. 2 in 1961, and since in COPD 3, cystic fibrosis 4 and thermally induced asthma 5. There is still controversy over the relative roles of the upper airway, bronchial circulation and pulmonary circulation in airway heat exchange. Under conditions of high ventilation, the work of Baile et al. 6, Solway et al. 7 and, more recently, Serikov and Fleming 8 showed pulmonary circulation to be the dominant heat source to the airways. Furthermore, using invasive measurements of intra-airway temperature, McFadden et al. 9 showed that airways down to subsegmental level are actively involved in heat exchange only at high minute ventilation with extremely cold inspired air. In contrast, when breathing indoor room air at normal tidal flow rates, virtually all heat transfer occurs in the upper airway (above the glottis) 10. It has therefore yet to be established whether changes in bronchial blood flow caused by disease are a significant determinant of breath temperature under normal ambient conditions. In the study of Paredi et al. 1, subjects were respiring warm room air (21–23°C) at low flow rates (10 L·min–1). Previous work would suggest that the airway below the glottis (which the authors seek to test) would not be contributing significantly to heat exchange under these conditions.
Regarding the methodology of the temperature washout technique, the authors acknowledge the extreme sensitivity of the rate of temperature rise to expiratory flow rate but do not report the method of flow targeting or indeed the flow rates achieved in controls versus COPD groups. Expiratory flow patterns rather than airway heat transfer may therefore contribute to the differences seen between the groups and are crucial to the interpretation of the temperature washout data. Finally, heat is consumed in two ways during inspiration: 
25% of the energy is used in heating the air (convective) and 75% in evaporating moisture from the mucosal surface to humidify the air stream (evaporative). On expiration, the reverse of both processes occurs, namely, convective cooling and condensation of water vapour on the mucosa. This dominance of energy transfer through evaporation and condensation suggests that attempts to characterise the thermodynamic performance of the airways by temperature measurement alone, without accompanying humidity measurements, may be misleading.
As with all new noninvasive breath measurements, it is important that methods and protocols are standardised and optimised in a way that takes into account the known underlying physical mechanisms.
References
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