A Reinvestigation of the Usefulness of Breath Analysis in the Determination of Blood Acetaldehyde Concentrations

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Abstract
Human volunteers were given ethanol (0.4 g/gk) either i.v. or per os [by mouth]. They were also given ethanol (0.2 g/kg) i.v. 4 h after receiving a dose of 50 mg citrated calcium carbimide, an aldehyde dehydrogenase inhibitor. During the 1st h after starting the administration of ethanol, ethanol and acetaldehyde concentrations were determined in expired air, blood from the right atrium, arterial blood and venous blood. In the absence of calcium carbimide treatment, the respective maximal blood acetaldehyde concentrations were (range): 6-30 .mu.M (calculated from breath analysis using a blood:breath partition ratio of 190 for acetaldehyde); 0-3.5 .mu.M (right atrium blood); and 0 .mu.M (arterial and venous blood). After calcium carbimide treatment, the maximal blood acetaldehyde concentrations were 10-220 .mu.M (calculated from concentrations in expired air), 38-280 .mu.M (right atrium), 31-250 .mu.M (arterial blood) and 7-186 .mu.M (venous blood). With aldehyde dehydrogenase inhibition, a clear correlation existed between breath concentrations and blood concentrations. Without this inhibition, no such correlation was found. A clear arterio-venous difference was seen for acetaldehyde concentrations while they were artificially elevated by calcium carbimide. Factors other than the equilibrium of acetaldehyde between alveolar air and pulmonary blood evidently are of great importance in determining the concentration of acetaldehyde in expired air.