Tobacco and Public Health - TCSC Indonesia

584
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
In contrast to interventions early in the course of lung injury from smoking, getting
smokers to quit once they have developed disease extensive enough to be disabling has
more limited benefits. Even for this group with extensive damage, there is a slowing in
the rate of decline in lung function with cessation of smoking; but the individuals usually
remain symptomatic. The effect is simply to prolong the interval between the onset of
symptoms and death rather than to eliminate the disability. This effect is depicted by
the thin solid line in Fig. 33.1 labeled ‘Quit with onset of disability’.
Chronic cough is a less disabling but far more common result of cigarette smoking
than is ventilatory limitation. Increased prevalence of chronic cough is evident even
among adolescent and young adult smokers. The prevalence increases with increasing
duration of smoking and is present in the majority of moderate to heavy smokers over age
60 years (Lebowitz and Burrows 1977). This cough begins as a dry cough but progresses
with longer duration of smoking to become productive of small amounts of mucus.
Mechanisms of lung injury
Airway inflammation and enzymatic digestion of lung structural proteins (elastin and
collagen) are mechanisms that define the injury to the lung in COPD. Early in the
smoking exposure, the changes are edema and inflammatory cell (cytotoxic T lymphocytes
and macrophages) infiltration in the walls of the small airways of the lung.
Inflammation is due to epithelial cell injury that increases permeability and releases
proinflammatory mediators. These mediators draw in neutrophils, and the result is a
pathological picture typical of chronic inflammation. The vast majority of smokers
develop these changes, and many develop them within the first year or two of smoking.
These early changes can reverse within one year following cessation among smokers
with a short smoking duration (Buist et al. 1976, 1979). With longer duration of smoking,
epithelial hyperplasia, smooth muscle hypertrophy, and peribronchiolar fibrosis
are commonly found in most smokers (Cosio et al. 1978, 1980). At least modest degree
of emphysema is found in most continuing smokers over the age of 60 years (Auerbach
et al. 1972; Sutinen et al. 1978), and the severity of the emphysematous change increases
with the number of cigarettes smoked per day.
The neutrophils and macrophages that characterize the inflammatory response to
cigarette smoke in the lung release enzymes capable of digesting the elastin and collagen
that make up the structural elements of the lung. Antiproteases, released from
macrophages and found in the blood, block the action of these enzymes (Barnes 2000).
The result is a balance that preserves the integrity of normal lung while allowing the
lung to respond to external infectious agents by releasing digestive enzymes. Oxidants
in cigarette smoke inactivate the antiproteases unbalancing this relationship and leading
to digestion of lung tissue, rupture of alveolar walls, and emphysematous dilation
of the alveolar spaces (Barnes 2000).
In contrast to the inflammatory changes in the small airways, emphysema is usually
manifested later in life (over age 50) and is not reversible.