Tobacco and Public Health - TCSC Indonesia

Many of the constituents in both the gas phase and the particulate phase of smoke
paralyse the cilia lining the airways. Cilia are the hair-like structures on the surface of
airway cells that rhythmically beat to move mucus up and out of the lung aiding in the
removal of particles deposited on the surface of the airways. Paralysis interferes
with the clearance process of the lung and results in a longer residence time in the
airway for toxic smoke constituents. Lastly, smoke can oxidatively inactivate some
of the protective proteins in the blood, most notably the antiproteases that prevent
lung digestion.
Early responses of the lung to cigarette smoking
Acute cough and bronchoconstriction are common reactions to the first inhalation of
cigarette smoke. When this protective warning of the airways is ignored and regular
smoking is begun, inflammatory changes appear in the small (>2 mm) airways of the
lung. These changes are evident in some smokers within the first few years of smoking;
and, after smoking for 10–15 years, the majority of smokers have evidence of abnormal
function in these small airways. Much of the functional limitation of expiratory airflow
in COPD results from increased resistance to expiratory airflow in these same small
airways (Hogg et al. 1968). However, development of inflammatory changes in the
small airways early in the smoking experience is not a useful predictor of the likelihood
of subsequently developing clinically significant COPD. These early changes are likely a
nearly universal response to the inhaled irritants in the smoke, and it is other biologic
or genetic determinants of how the lung responds to chronic irritation that define
which smokers will go on to develop COPD.
Even during adolescence and early adulthood, cigarette smoking is associated with a
lower level of lung function and an increased frequency of respiratory symptoms,
particularly cough (USDHHS 1994). Adolescent smokers have a lower rate of increase
in lung function as they grow into adulthood when compared to nonsmoking adolescents,
and there is evidence that they reach a lower level of peak lung function (Tager
et al. 1988). There is also concern that their decline in lung function may begin at an
earlier age. Changes in lung development documented in actively smoking adolescents
are likely superimposed on similar changes produced by exposure to environmental
tobacco smoke during infancy and early childhood.
Changes in lung function in smokers and nonsmokers
DAVID M. BURNS
The most widely used measure of lung function abnormality in COPD is the volume of
air that can be expired during the first second with a maximal effort (FEV 1 ). Among
populations of heavy smokers, an excess decline in the FEV 1 is first seen at age 25–34
for both males and females in comparison with never smokers. An excess decline
in FEV 1 is seen among both light and heavy smokers by age 35–44 (Beck et al. 1981).
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