dysfunction in patients with chronic bronchitis after cessation of
smoking has also been reported in a small prospective study (Camner
et al. 1973b).

Thus, both patients with chronic bronchitis and healthy smokers
exhibit an impaired mucociliary function. However, the magnitude
of the impairment is not the same as suggested by Goodman et al.
(1978), who demonstrated a greater impairment of tracheal mucocili-
ary transport rates in smokers and nonsmokers with chronic
bronchitis than in healthy smokers (Figure 2).

The consequences of airway mucociliary dysfunction have not
been satisfactorily examined, but may include increased susceptibili-
ty to respiratory infections, airflow obstruction by excessive airway
secretions, and increased risk of carcinogenesis resulting from
prolonged contact between inhaled carcinogens and the respiratory
epithelium (Matthys et al. 1983; Hilding 1957; Moersch and McDon-
ald 1953).

Summary and Conclusions

1. Increased numbers of inflammatory cells are found in the
lungs of cigarette smokers. These cells include macrophages
and, probably, neutrophils, both of which can release elastase
in the lung.

2.Human neutrophil elastase produces emphysema when in-
stilled into animal lungs.

3. Alpha,-antiprotease inhibits the action of elastase, and a very
small number of people with a homozygous deficiency of a,-
antiprotease are at increased risk of developing emphysema.
The a,-antiprotease activity has been shown to be reduced in
the bronchoalveolar fluids obtained from cigarette smokers
and from rats exposed to cigarette smoke.

4. The protease-antiprotease hypothesis suggests that emphyse-
ma results when there is excess elastase activity as the result
of increased concentrations of inflammatory cells in the lung
and of decreased levels of a,-antiprotease secondary to oxida-
tion by cigarette smoke.

5. Cigarette smokers have been shown to have a more rapid fall in
antibody levels following immunization for influenza than
nonsmokers. Whole cigarette smoke has been shown to depress
the number of antibody-forming cells in the spleens of experi-
mental animals.

6. Cigarette smoke produces structural and functional abnormali-
ties in the airway mucociliary system.

7. Short-term exposure to cigarette smoke causes ciliostasis in
vitro, but has inconsistent effects on mucociliary function in
man. Long-term exposure to cigarette smoke consistently

301
causes an impairment of mucociliary clearance. This impair-
ment is associated with epithelial lesions, mucus hypersecre-

tion, and ciliary dysfunction.

8. Chronic bronchitis in smokers and ex-smokers is characterized
by an impairment of mucociliary clearance.

9. Both the particulate phase and the gas phase of cigarette
smoke are ciliotoxic.

302
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