Cough Reflex Sensitivity in Cigarette Smokers

Peter V. Dicpinigaitis, MD, FCCP

Disclosures

CHEST. 2003;123(3) 

In This Article

Abstract and Introduction

Abstract

Study objectives: To evaluate cough reflex sensitivity in a population of young, healthy, male cigarette smokers.
Design: Cross-sectional comparison.
Setting: Academic medical center.
Participants: Twenty healthy, male current-smokers (mean [± SEM] age, 32.2 ± 1.2 years).
Measurements: Subjects underwent baseline spirometry followed by capsaicin cough challenge testing, which involved the inhalation of capsaicin in ascending, doubling concentrations until the concentrations inducing two or more coughs (C2) and those inducing five or more coughs (C5) were reached. The data were compared to those from a group of 50 healthy, male nonsmokers who had undergone identical cough challenge testing.
Results: The two groups did not differ in terms of age or baseline pulmonary function. Cough sensitivity was significantly diminished in the current-smokers compared to control subjects. The mean ( ± SEM) log C2 values in smokers and nonsmokers were 1.26 ± 0.13 and 0.81 ± 0.08, respectively (p = 0.004). The mean log C5 values in smokers and nonsmokers were 2.03 ± 0.10 and 1.20 ± 0.08, respectively (p < 0.000001).
Conclusions: Cough reflex sensitivity is significantly diminished in young, healthy, male current-smokers compared to a similar population of nonsmokers. The mechanism of cough suppression in smokers remains speculative but may involve long-term tobacco smoke-induced desensitization of the cough receptors within the airway epithelium.

Introduction

Cough results from the stimulation of sensory receptors within the respiratory tract the afferent impulses of which activate a brainstem cough center. The following two types of receptors are involved in cough production: rapidly adapting pulmonary stretch receptors (RARs) with thin, myelinated, afferent fibers; as well as pulmonary and bronchial C-fiber receptors with unmyelinated afferent fibers. RARs are believed to induce cough via a primary sensory pathway, whereas C fibers, the central pathways of which inhibit cough, may stimulate cough peripherally by causing the release of sensory neuropeptides that activate RARs.[1]

The cough reflex serves a protective function by preventing foreign material from entering the respiratory tract and by facilitating the expulsion of mucus from the airways. To date, relatively little attention has been paid to the effect of cigarette smoking on cough reflex sensitivity. Animal studies have suggested that long-term exposure to tobacco smoke enhances the sensitivity of the cough reflex, perhaps by stimulating tachykinin synthesis and release within the airways.[2,3,4] However, two small studies in humans have demonstrated higher cough thresholds (ie, diminished cough sensitivity) in smokers compared to nonsmokers.[5,6]

To further investigate the effect of long-term cigarette smoking on cough reflex sensitivity, we prospectively performed capsaicin cough challenge testing in a group of healthy, male current-smokers, and compared the data with those of healthy, male nonsmokers. The tussive agent capsaicin has been shown in humans to induce cough in a safe, reproducible, and dose-dependent manner,[7] thereby rendering it an excellent tool for the measurement of cough reflex sensitivity. Unlike previous studies, only subjects of one gender (male) were compared because of the well-documented gender differences in cough reflex sensitivity.[8,9]

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