OBJECTIVES/HYPOTHESIS: The effects of smoking on endonasal geometry and airflow remain largely unknown. Our study examined the relationship between smoking status and objective measures of nasal cavity dimensions, nasal congestion, and nasal airflow, using acoustic rhinometry (AR) and peak nasal inspiratory flow (PNIF). STUDY DESIGN: Cross-sectional study. METHODS: Included in the study were 2,523 consecutive patients referred for evaluation of chronic nasal or sleep-related complaints. Smoking history was recorded, and AR and PNIF were measured at baseline and after decongestion of the nasal mucosa. Minimal cross-sectional areas (MCA), nasal cavity volumes (NCV), and PNIF, as well as quantified reversible mucosal congestion based on nasal congestion indexes (NCI) were analyzed to reveal possible associations with smoking status. Linear and logistic regressions were applied adjusting for possible confounders. RESULTS: Smokers exhibited lower values of MCA, NCV, and PNIF than nonsmokers, both at baseline and after decongestion. Further, smokers had a lower decongestive capacity of the nasal mucosa, reflected by lower NCI for AR measures. Cigarette consumption, expressed as either pack-years or cigarettes smoked per day, showed a similar inverse relationship with the rhinometric measures even though a linear dose-response relationship could not be established. CONCLUSIONS: We have clearly demonstrated that smokers exhibit lower MCA and NCV, achieve lower PNIF values, and have a less-compliant nasal mucosa than nonsmokers. Our results are unique, and provide evidence that smoking has adverse effects on the nasal airway, possibly due to mucosal inflammation. This might have further implications because altered nasal function could compromise the lower airways.
OBJECTIVES/HYPOTHESIS: The effects of smoking on endonasal geometry and airflow remain largely unknown. Our study examined the relationship between smoking status and objective measures of nasal cavity dimensions, nasal congestion, and nasal airflow, using acoustic rhinometry (AR) and peak nasal inspiratory flow (PNIF). STUDY DESIGN: Cross-sectional study. METHODS: Included in the study were 2,523 consecutive patients referred for evaluation of chronic nasal or sleep-related complaints. Smoking history was recorded, and AR and PNIF were measured at baseline and after decongestion of the nasal mucosa. Minimal cross-sectional areas (MCA), nasal cavity volumes (NCV), and PNIF, as well as quantified reversible mucosal congestion based on nasal congestion indexes (NCI) were analyzed to reveal possible associations with smoking status. Linear and logistic regressions were applied adjusting for possible confounders. RESULTS: Smokers exhibited lower values of MCA, NCV, and PNIF than nonsmokers, both at baseline and after decongestion. Further, smokers had a lower decongestive capacity of the nasal mucosa, reflected by lower NCI for AR measures. Cigarette consumption, expressed as either pack-years or cigarettes smoked per day, showed a similar inverse relationship with the rhinometric measures even though a linear dose-response relationship could not be established. CONCLUSIONS: We have clearly demonstrated that smokers exhibit lower MCA and NCV, achieve lower PNIF values, and have a less-compliant nasal mucosa than nonsmokers. Our results are unique, and provide evidence that smoking has adverse effects on the nasal airway, possibly due to mucosal inflammation. This might have further implications because altered nasal function could compromise the lower airways.