Can smoking worsen Obstructive Sleep Apnea (OSA)?

Can Smoking Worsen Obstructive Sleep Apnea?

Yes, smoking significantly worsens obstructive sleep apnea through multiple pathophysiologic mechanisms including upper airway inflammation, increased mucosal edema, and altered sleep architecture, with current smokers showing nearly 80% increased odds of OSA compared to non-smokers.

Evidence for Smoking's Detrimental Effect on OSA

Epidemiologic Association

• Current smokers have 1.79 times higher odds of OSA compared to non-smokers (95% CI 1.10-2.89), with former smokers showing 1.53 times higher odds (95% CI 1.01-2.32) in male populations 1

• Among men specifically, current smoking is associated with severe OSA risk (OR: 1.88,95% CI 1.07-3.29), while former smoking correlates with moderate OSA risk (OR: 1.61,95% CI 1.05-2.48) 1

• The duration of smoking correlates significantly with OSA severity, suggesting a dose-response relationship 2

Pathophysiologic Mechanisms

Smoking worsens OSA through four primary mechanisms:

• Upper airway inflammation and edema: Smoking induces increased thickness and edema of the uvular mucosa lamina propria, causing oropharyngeal narrowing that exacerbates upper airway collapse during sleep 2

• Neurogenic inflammation: Smokers demonstrate increased calcitonin gene-related peptide (CGRP) staining in uvular mucosa, indicating heightened neuroinflammatory responses that contribute to airway dysfunction 2

• Altered sleep architecture: Nicotine disrupts normal sleep patterns by prolonging total sleep and REM latency while reducing sleep efficiency, total sleep time, and slow wave sleep 3

• Impaired neuromuscular function: Smoking affects upper airway neuromuscular responses and arousal mechanisms, compromising the compensatory mechanisms that normally maintain airway patency 4

Clinical Manifestations in Smokers with OSA

OSA patients with smoking history demonstrate worse clinical parameters:

• Higher Epworth Sleepiness Scale scores (9.3 ± 4.0 vs 8.5 ± 5.1 in non-smokers, p<0.05), indicating greater daytime sleepiness 5

• Longer sleep latency [20.5 minutes vs 18.5 minutes in non-smokers, p<0.05] 5

• Lower nocturnal mean oxygen saturation (91.8 ± 3.6% vs 92.8 ± 3.4%, p<0.001), reflecting more severe hypoxemia 5

• Importantly, the apnea-hypopnea index (AHI) may not differ significantly between smokers and non-smokers, suggesting that smoking worsens OSA through mechanisms beyond simple apnea frequency 5

Increased Comorbidity Burden

Smoking compounds the already substantial comorbidity burden of OSA:

• OSA patients who smoke have significantly increased risk of hypertension (OR=2.09,95% CI: 1.46-3.01) 5

• Chronic obstructive pulmonary disease risk is dramatically elevated (OR=9.80,95% CI: 4.73-20.33), creating the particularly dangerous "overlap syndrome" 5

• Gastroesophageal reflux disease risk increases (OR=1.97,95% CI: 1.19-3.27) 5

• Chronic pharyngitis risk is elevated (OR=1.83,95% CI: 1.32-2.54) 5

Nicotine Replacement Therapy Considerations

The evidence on nicotine's direct effect on OSA is mixed and should not influence smoking cessation recommendations:

• While nicotine is a breathing stimulant that increases upper airway muscle activity, randomized controlled trials show no significant effect of nicotine replacement on AHI 6

• One early study suggested nicotine gum at bedtime prevented OSA in the first 2 hours of sleep, but subsequent RCTs failed to confirm this benefit 6

• The lack of benefit from isolated nicotine suggests that the harmful effects of smoking on OSA are primarily due to smoke-induced inflammation and tissue changes rather than nicotine itself 6

Clinical Implications and Recommendations

Smoking cessation should be aggressively pursued in all OSA patients:

• The histological changes in upper airway mucosa caused by smoking (edema, inflammation) are potentially reversible with cessation 2

• Smoking cessation may reduce upper airway edema and improve OSA severity, though robust evidence for this hypothesis remains limited 3

• Given the clear association between smoking duration and OSA severity, earlier cessation is preferable 2

Important Clinical Pitfalls

• Do not rely solely on AHI to assess smoking's impact on OSA—smokers may have similar AHI values but worse oxygen desaturation, sleep quality, and symptom burden 5

• Screen smoking OSA patients more aggressively for cardiovascular and pulmonary comorbidities, as their risk is substantially elevated compared to non-smoking OSA patients 5

• Recognize that smoking cessation itself may temporarily worsen sleep quality due to nicotine withdrawal, but this should not deter cessation efforts as the long-term benefits outweigh short-term sleep disruption 3

• The "overlap syndrome" (COPD + OSA) carries particularly high mortality risk—when present, patients should be treated with continuous positive airway pressure as this has been shown to decrease mortality 6