Smoking and chronic obstructive pulmonary disease.
Smoking is overwhelmingly the major cause of chronic bronchitis and emphysema worldwide. Additional risk factors for developing COPD are presented, along with the variables that govern cigarette smoke deposition in the lung. Major paradigms for the pathogenesis of COPD, including the protease-antiprotease and oxidant-antioxidant theories are described, and evidence for impaired reparative mechanisms in the causation of emphysema is noted. A description of the natural history of declining lung function in smokers and in the susceptible subset of smokers that ultimately develop smoking-induced COPD is accompanied by a discussion of the effects of smoking cessation on preservation of lung health. The disordered ventilation and gas-exchange physiology in the cigarette smoke-damaged lung is explained on the basis of the observed morphological changes.
Sethi
J M
JM
Section of Pulmonary and Critical Care, Yale University School of Medicine, New Haven, Connecticut, USA.
Rochester
C L
CL
D000818:Animals; D001991:Bronchitis / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D002908:Chronic Disease; D005541:Forced Expiratory Volume; D020022:Genetic Predisposition to Disease; D006801:Humans; D008168:Lung / Q000473:pathology; D011656:Pulmonary Emphysema / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D011659:Pulmonary Gas Exchange / Q000502:physiology; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects* / Q000473:pathology / Q000503:physiopathology; D016540:Smoking Cessation; D019896:alpha 1-Antitrypsin Deficiency / Q000503:physiopathology