Cigarette smoke-induced airway inflammation as sampled by the expired breath condensate

Am J Med Sci. 2003 Oct;326(4):174-8. doi: 10.1097/00000441-200310000-00004.


Airways exposed to smoke respond with inflammatory processes. The airway inflammation generally present in smokers causes persistent cough and phlegm production, reactive airway disease, and tissue infiltration by inflammatory cells. Although the short-term response may be protective, long-term pathological consequences include swelling of the airway epithelium, mucus hypersecretion, and increased airway reactivity characteristic of chronic bronchitis and chronic obstructive lung disease and the tissue destruction characteristic of emphysema. The natural history of these diseases is poorly understood, because human airway tissue is available for study only at autopsy, from surgical specimens, or from procedures such as bronchoscopy or thoracotomy. A noninvasive method of monitoring the inflammation is by analyzing expired breath condensate, which contains a diluted sample of airway surface liquid. The study of expired breath condensate may offer a more practical approach to sampling airway chemistry and make it possible to study the detailed inflammatory response to airborne particulates.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Breath Tests*
  • Emphysema
  • Genetic Predisposition to Disease
  • Humans
  • Inflammation / diagnosis
  • Inflammation / etiology*
  • Inflammation / pathology
  • Reactive Oxygen Species / analysis
  • Respiratory Tract Diseases / diagnosis
  • Respiratory Tract Diseases / etiology*
  • Respiratory Tract Diseases / pathology
  • Smoke / adverse effects*
  • Smoke / analysis
  • Tobacco*
  • alpha 1-Antitrypsin


  • Reactive Oxygen Species
  • Smoke
  • alpha 1-Antitrypsin