The pathogenesis of chronic obstructive pulmonary disease

Am J Med Sci. 1999 Aug;318(2):74-8. doi: 10.1097/00000441-199908000-00002.

Abstract

Cigarette smoking is the main risk factor for the development of chronic obstructive pulmonary disease (COPD). An accelerated rate of lung function decline that causes clinically significant COPD, however, is present in only a minority of smokers. In addition to the cumulative amount of cigarettes smoked, other environmental and genetic properties contribute to this variable physiological response. This article reviews the role of airway hyperresponsiveness, mucus hypersecretion, infection, and proteases in the development of COPD.

Publication types

  • Review

MeSH terms

  • Bronchi / metabolism
  • Bronchial Hyperreactivity / complications
  • Bronchial Hyperreactivity / etiology
  • Dust / adverse effects
  • Endopeptidases / metabolism
  • Humans
  • Lung Diseases, Obstructive / complications
  • Lung Diseases, Obstructive / etiology*
  • Lung Diseases, Obstructive / metabolism
  • Mucus / metabolism
  • Occupational Exposure / adverse effects
  • Oxidants / metabolism
  • Protease Inhibitors / metabolism
  • Respiratory Tract Infections / complications
  • Risk Factors
  • Smoking / adverse effects
  • Tobacco Smoke Pollution / adverse effects

Substances

  • Dust
  • Oxidants
  • Protease Inhibitors
  • Tobacco Smoke Pollution
  • Endopeptidases