Tobacco and Public Health - TCSC Indonesia

DAVID M. BURNS
rate of growth in lung function may be worsened, and the age of peak lung growth may
be reached earlier, if the adolescent begins to actively smoke cigarettes. There is considerable
concern that these changes in the developing lung may predispose the adult lung
to a more rapid decline in function with increasing age, particularly with continued
smoking during adulthood.
When the entire population of adult smokers is examined, their rate of lung function
decline with age is substantially steeper than that for nonsmokers, reflecting progressive
damage to the airways and alveoli of the their lungs. This change with advancing
age and duration of smoking is presented in Fig. 33.1 as a dashed line labeled ‘all
smokers’. However, the rate of decline is not sufficient to cause respiratory disability
for the majority of smokers, in part because of the large ventilatory reserve of the
lung. When an abnormal FEV 1 is used as the criteria for diagnosis of COPD, approximately
one-third of smokers over age 55 (Sherrill et al. 1994) have COPD, and that
percentage increases to over 45 per cent when smokers over age 65 are examined
(Higgins et al. 1993). These high prevalences of abnormal lung function are supported
by autopsy studies which show evidence of at least some emphysema in the lungs of
approximately 90 per cent of long-term cigarette smokers (Auerbach et al. 1972;
Sutinen et al. 1978).
Many smokers with abnormal lung function may be unaware of the presence of lung
injury and may have no symptoms related to their lung damage. A minority of cigarette
smokers, in the range of 15 per cent, will have a more rapid decline in lung function
and will develop clinically significant COPD. These smokers are more likely to
have smoked more cigarettes per day and to have smoked for a longer duration, but
known characteristics of smoking behavior do not fully explain why some smokers will
develop COPD and others with similar smoking patterns do not. Differences in genetic
susceptibility or differences in response to inflammation have been postulated as
reasons for the differences in the rate of progression to clinically significant disease.
The thin solid line in Fig. 33.1 represents those smokers who go on to develop
COPD. They have a more rapid decline in lung function with time, as must be expected
since they have developed more extensive disease. Having an abnormal FEV 1 by early
middle age (age 45) is a strong predictor of developing COPD, but it is less clear that
the rate of decline over one period of time is a good predictor of the future rate of
decline or of the likelihood of developing COPD. Identification of smokers with
abnormal lung function in early middle age offers the opportunity to intervene with
smoking cessation assistance before clinically significant ventilatory limitation develops.
Those who quit smoking are likely to have a small improvement in lung function during
the first year of abstinence, and their rate of decline in lung function slows to that
of the never smoker (Anthonisen et al. 1994; Scanlon et al. 2000). This pattern of
change is depicted by the thin solid line in Fig. 33.1 labeled ‘quit at age 40’. If smokers
quit before there is extensive lung damage and remain abstinent, it is likely that most of
them will never develop clinically significant COPD.
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