Chapter 5 
the air sacs, resulting in further airflow obstruction. These changes can 
cause significant respiratory impairment, disability, and death. Although 
individual patients vary in the relative contribution of these three changes, 
those with clinically severe COLD typically have all three. 
Although a minority of cigarette smokers will develop clinically 
severe COLD, some chronic deterioration in lung structure or function is 
demonstrable in most long-term smokers (U.S. Department of Health and 
Human Services, 1984a). Some smokers show more chronic cough and 
phlegm, others more airway obstruction. In general, breathing function 
declines with the increase in a person's cumulative exposure to smoke, 
measured in pack-years (Dockery et al., 1988). 
Cigarette smoke produces pathological changes in the lungs of smokers 
by a number of different mechanisms (U.S. Department of Health and 
Human Services, 1990). Cigarette smoke is toxic to the cilia that line the 
central breathing passages. These cilia, in combination with mucus 
secretions, defend against deep inhalation of foreign material (U.S. 
Department of Health and Human Services, 1984a). Smoking also induces 
many abnormalities in the inflammatory and immune systems within the 
lung (U.S. Department of Health and Human Services, 1985). In particular, 
cigarette smoke causes inflammatory cells to produce an enzyme called 
elastase, which in turn breaks down elastin, an important protein that lines 
the elastic walls of the air sacs (Fera et al. 1986; U.S. Department of Health 
and Human Services, 1984a). Moreover, oxidants present in cigarette smoke 
can inactivate a separate protective enzyme called alpha^-antitrypsin, which 
inhibits the destructive action of elastase Qanoff, 1985; U.S. Department of 
Health and Human Services, 1984a). 
Many organic and inorganic chemicals in the gaseous, volatile, and 
particulate phases of cigarette smoke appear to contribute to smoke's 
toxicity to the respiratory system, including hydrocarbons, aldehydes, 
ketones, organic acids, phenols, cyanides, acrolein, and nitrogen oxides. 
Some components contribute to the development of chronic mucus 
hypersecretion in the central airways, whereas others play a greater role 
in the production of small airway abnormalities and emphysematous injury 
to the peripheral air sacs. Oxidizing agents in smoke inhibit the enzymes 
that defend against the destruction of lung elastin (U.S. Department of 
Health and Human Services, 1984a). 
ATHEROSCLEROTIC Cigarette smoking is a major contributing cause to CHD, stroke, 
CARDIOVASCULAR and other atherosclerotic diseases of the circulatory system (U.S. 
DISEASES Department of Health and Human Services, 1984b and 1989). 
Atherosclerosis is a chronic disease that can affect the arterial blood 
vessels in virtually every part of the human body. The most important 
form of atherosclerosis in the United States is coronary atherosclerosis. 
Its manifestations, which include angina, heart attack, heart failure, and 
sudden death, are described by the inclusive term coronary heart disease. 
Atherosclerosis involving the arteries supplying the brain is a form of 
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