Smoking is overwhelmingly the major cause of chronic bronchitis and emphyse
ma worldwide. Additional risk factors for developing COPD are presented, al
ong with the variables that govern cigarette smoke deposition in the lung.
Major paradigms for the pathogenesis of COPD, including the protease-antipr
otease and oxidant-antioxidant theories are described, and evidence for imp
aired reparative mechanisms in the causation of emphysema is noted. A descr
iption of the natural history of declining lung function in smokers and in
the susceptible subset of smokers that ultimately develop smoking-induced C
OPD is accompanied by a discussion of the effects of smoking cessation on p
reservation of lung health. The disordered ventilation and gas-exchange phy
siology in the cigarette smoke-damaged lung is explained on the basis of th
e observed morphological changes.