Smoking induces oropharyngeal narrowing and increases the severity of obstructive sleep apnea syndrome.

OBJECTIVE: Smoking is a known risk factor for snoring, and is reported to be associated with an increased prevalence of obstructive sleep apnea syndrome (OSAS). The purpose of this was to determine the relationship of smoking to the severity of OSAS and examine what local histological changes in the uvular mucosa of OSAS patients might influence this relationship.

STUDY DESIGN AND METHODS: Fifty-seven OSAS subjects were included and classified according to smoking history and OSAS severity. Twenty-eight subjects were heavy smokers and 29 were nonsmokers; these 57 patients were divided according to moderate or severe OSAS. Histologic changes in the uvular mucosa were evaluated in all subjects as well as smoking duration and OSAS severity.

RESULTS: Among smokers, moderate-to-severe OSAS was more common, and apnea, hypopnea, and oxygen desaturation indices were higher. Moreover, smoking duration and OSAS severity were significantly correlated. Increased thickness and edema of the uvular mucosa lamina propria were observed in moderate and severe OSAS patients, and only smokers had significant changes in uvular mucosa histology. Positive staining for calcitonin gene-related peptide (CGRP), a neuroinflammatory marker for peripheral nerves, was increased in the uvular mucosa of smokers.

CONCLUSIONS: Our results suggest that smoking may worsen OSAS through exacerbation of upper airway collapse at the level of the uvula, and that histological changes of the uvular mucosa correlated with smoking might be due to increased CGRP-related neurogenic inflammation.