Tobacco and Public Health - TCSC Indonesia

580
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
have specific scientific definitions but are commonly used in medical and scientific discourse
to include all forms of tobacco-induced chronic lung injury, occurs for all of the
common names for smoking-induced lung disease; and it causes confusion in the
medical and lay literature. In this chapter we will use the term COPD to encompass all
of the patterns of lung injury produced by cigarette smoking.
A second pathophysiological pattern is that of inflammatory changes in the smaller
and more distal airways of the lung which narrows these airways and increases their
resistance to airflow. These changes can progress to produce the decreased expiratory
airflow characteristic of clinically significant COPD.
Inflammatory cells present in the peribronchiolar spaces release digestive enzymes
that ultimately damage and disrupt the alveolar walls producing emphysema, the third
pathophysiological pattern of injury. As the alveolar walls rupture, the lung becomes
composed of a smaller number of much larger airspaces with a reduced surface area
and decreased elastic recoil. When examined at autopsy, this digested lung appears full
of holes of various sizes. During life, it functions poorly for gas exchange and ventilation.
The decreased elastic recoil of an emphysematous lung reduces the pressure available
to drive expiratory airflow and allows the airways to collapse during expiration,
further worsening the rate of expiratory airflow produced by the inflammatory
changes in the small airways described above.
Composition of tobacco smoke
Tobacco smoke is a complex aerosol with particles largely within the range of 0.1–1.0
microns in diameter (Stratton et al. 2001). These particles are small enough that they
are not removed in the upper airway and deposit largely on the alveolar and airway
surfaces of the lung. The pattern of lung deposition is consistent with particles of a
somewhat larger size since there is more deposition in the airways and on the alveolar
surfaces than would be expected from extrapolations based on particle size alone
(Stratton et al. 2001). The difference in deposition location is likely due to aggregation
of particles in the very dense aerosol of mainstream smoke or because the particles
may grow in size as they are humidified in the airway.
Tobacco smoke contains over 4800 individual constituents and the composition of
the smoke is undergoing rapid chemical change as it is inhaled (IARC 1986).
Biologically active free radicals are generated as tobacco is burned, and they persist
long enough to interact with lung tissue following inhalation. The constituents of
smoke have at least three toxicities important for causing injury to the lung in COPD.
Tobacco smoke as whole smoke, and several of its constituents, are potent irritants to
the airways capable of creating an inflammatory response in the airways even with initial
use. This acute irritant response, manifest as a reflex cough in many adolescents with
their first inhalation of cigarette smoke, disappears as the airway adapts to repetitive
exposure to smoke. It is replaced by a chronic low-grade inflammation of the airways.