Jauhonen P, Baraona E, Miyakawa H, Lieber C S
J Lab Clin Med. 1982 Dec;100(6):908-16.
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.
口咽微生物群和肺微粒体可将乙醇转化为乙醛。因此，我们评估了通过呼气乙醛分析来估算血液中乙醛含量的适用性。我们发现，在饮酒后乙醛浓度会升高（超过50微摩尔）的个体（如东方的“脸红者”）中，呼气末空气中的乙醛浓度反映了血液中的水平。然而，在大多数血液中乙醛浓度非常低（低于5微摩尔）的非东方受试者中，呼吸道中乙醛的生成占呼气末样本中乙醛的大部分。在后一种情况下，呼气乙醛与血液水平不相关。长期吸烟者呼吸道中乙醇生成乙醛的过程明显加剧。在采样前用吡唑（一种乙醇脱氢酶抑制剂）冲洗口咽腔可减少但不能消除局部对呼气乙醛的影响，尤其是在吸烟者中。在狒狒中，只有通过气管内导管收集呼出气体以完全排除上呼吸道的影响时，才能通过呼气分析准确估算血液中的乙醛含量。因此，为了评估血液中的乙醛含量，除了已知与非常高的血液水平相关的少数情况外，呼气乙醛测量不能替代直接测量。
