Origin of breath acetaldehyde during ethanol oxidation. Effect of long-term cigarette smoking.

Oropharyngeal microflora and lung microsomes can produce acetaldehyde from ethanol. Therefore we evaluated the suitability of breath acetaldehyde analysis to estimate blood acetaldehyde. We found that in individuals who develop high acetaldehyde concentrations (over 50 micro M) after alcohol ingestion (such a s oriental "flushers"), the acetaldehyde concentration in end-expiratory air reflects the blood levels. However, in the majority of non-Oriental subjects who develop very small concentrations of acetaldehyde in the blood (less than 5 micro M), the production of acetaldehyde in the respiratory tract accounted for most of the acetaldehyde present in end-expiratory samples. Under the latter conditions, breath acetaldehyde did not correlate with blood levels. The production of acetaldehyde from ethanol in the respiratory tract was markedly exaggerated in long-term cigarette smokers. Rinsing the oropharyngeal cavity with pyrazole (an alcohol dehydrogenase inhibitor) prior to sampling reduced, but did not eliminate, the local contribution to breath acetaldehyde, especially in smokers. In baboons, blood acetaldehyde could be accurately estimated from breath analysis only when the upper respiratory tract was completely excluded by collecting the expired air through an endotracheal tube. Thus, to assess blood acetaldehyde, breath acetaldehyde measurements cannot be substituted for direct measurements, except for those few conditions known to be associated with very high blood levels.