Smoking influences the severity of obstructive sleep apnoea independently from COPD
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Carol Davila University of Medicine and Pharmacy, Bucharest, Romania
Ovidius University of Constanta, Constanta, Romania
Publication date: 2020-10-22
Tob. Prev. Cessation 2020;6(Supplement):A100
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The influence of smoking on the incidence and/or severity of the obstructive sleep apnoea (OSA) is still being debated, and remains a controversial matter. Some studies explained the relationship between OSA severity and smoking as a consequence of the lung function impairment caused by chronic obstructive pulmonary disease (COPD).

To assess the impact of smoking on OSA severity in patients without COPD.

A cross-sectional study of OSA severity among outpatients was conducted. Demographics (age, gender), anthropometric data (body mass index, waist circumference, neck circumference), smoking exposure, symptoms, spirometry and nocturnal polygraphy parameters were recorded. All COPD cases were excluded. The severity of OSA was estimated by apnoea-hypopnoea index (AHI) thresholds (AHI ≥5 for mild, AHI ≥15 for moderate, AHI ≥30 for severe) and markers of desaturation [TS90O2 (90% of O2 saturation level) and ODI (O2 desaturation index)]. Data were processed by SPPS software. Current smokers (CS) and never smokers (NS) were compared using Mann Whitney and chi-squared tests.

Study group included 112 OSA cases (50 CS and 62 NS), with no difference in gender distribution (χ2=2.66; p=0.10) or anthropometric characteristics (p<0.05). CS were significantly younger (mean age 44.23 years vs 52.28 years in NS, U=1972; p=0.014), had significant higher daytime sleepiness (χ2=4.46; p=0.03), great frequency of severe OSA (78% vs 56%, χ2=5.73; p=0.02), with significant difference in supine AHI (p=0.009), associated with longer TS90O2 (median=17.5 in CS vs 7 in NS, U=1138.5; p=0.05) and higher ODI (median=54 vs 34.5 in NS, U=1138; p=0.02).

Current smokers developed severe OSA almost one decade earlier than non-smokers. All outcomes of this study are supporting the influence of smoking on OSA severity, independent of the mechanisms initiated by COPD.