J King et al 2009 J. Breath Res. 3 027006 doi:10.1088/1752-7155/3/2/027006
J King1,2,3, A Kupferthaler1,2, K Unterkofler2,3, H Koc2,3,5, S Teschl4, G Teschl5, W Miekisch2,6, J Schubert2,6, H Hinterhuber2,7 and A Amann1,2,8,9
Show affiliationsA real-time recording setup combining exhaled breath volatile organic compound (VOC) measurements by proton transfer reaction-mass spectrometry (PTR-MS) with hemodynamic and respiratory data is presented. Continuous automatic sampling of exhaled breath is implemented on the basis of measured respiratory flow: a flow-controlled shutter mechanism guarantees that only end-tidal exhalation segments are drawn into the mass spectrometer for analysis. Exhaled breath concentration profiles of two prototypic compounds, isoprene and acetone, during several exercise regimes were acquired, reaffirming and complementing earlier experimental findings regarding the dynamic response of these compounds reported by Senthilmohan et al (2000 Redox Rep. 5 151–3) and Karl et al (2001 J. Appl. Physiol. 91 762–70). While isoprene tends to react very sensitively to changes in pulmonary ventilation and perfusion due to its lipophilic behavior and low Henry constant, hydrophilic acetone shows a rather stable behavior. Characteristic (median) values for breath isoprene concentration and molar flow, i.e., the amount of isoprene exhaled per minute are 100 ppb and 29 nmol min−1, respectively, with some intra-individual day-to-day variation. At the onset of exercise breath isoprene concentration increases drastically, usually by a factor of ~3–4 within about 1 min. Due to a simultaneous increase in ventilation, the associated rise in molar flow is even more pronounced, leading to a ratio between peak molar flow and molar flow at rest of ~11. Our setup holds great potential in capturing continuous dynamics of non-polar, low-soluble VOCs over a wide measurement range with simultaneous appraisal of decisive physiological factors affecting exhalation kinetics. In particular, data appear to favor the hypothesis that short-term effects visible in breath isoprene levels are mainly caused by changes in pulmonary gas exchange patterns rather than fluctuations in endogenous synthesis.
Issue 2 (June 2009)
Received 18 March 2009, accepted for publication 20 May 2009
Published 9 June 2009
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