A cross-sectional study on the relationship between electronic cigarette and combustible cigarette use with obstructive sleep apnea among U.S. adults: result from NHANES 2015–2018

Our current findings, based on a survey of a representative US population, demonstrate that smoking in adults is associated with a higher prevalence of OSA. Additionally, among adults with different smoking patterns, a significant association between c-cigarette use only and a high prevalence of OSA was observed. However, e-cigarette-only smoking did not affect the prevalence of OSA compared to non-smoking adults. In addition, we found the highest prevalence of OSA in participants who smoked both e-cigarettes and conventional cigarettes.

OSA is an unfavorable factor in multiple systems of the body, including the metabolic system, the neuropsychiatric system, and the cardiovascular system. The well-known etiology of OSA is primarily caused by recurrent episodes of the partial or complete collapse of the upper airway during sleep. OSA is increasingly being recognized as a significant cause of increased mortality [13]. It is noteworthy that despite the great progress made in the past in the recognition of OSA, 70–80% are still undiagnosed [14, 15]. Since patients are often unaware of their symptoms while sleeping, they are usually detected by their bed partners or family members, missing the best time for early intervention, which can lead to serious complications. Therefore, understanding the prevalence factors for OSA is crucial for the population to receive early diagnosis and treatment.

Recent research suggests that participants who smoke are more likely to snore and develop OSA [16]. A recent meta-analysis revealed that secondhand smoke exposure has been independently associated with OSA [17]. Cigarette smoke-induced airway inflammation and injury alter the mechanical and neurological properties of the upper airway and increase its collapsibility during sleep [13]. Overall, these cases support the view that participants who traditionally smoked were significantly associated with OSA. Our results are consistent with previous studies showing that smokers have a higher prevalence of OSA than non-smokers.

Recently, the use of e-cigarettes has been on the rise among young people and adults. In a previous study, 43% of young people reported that e-cigarettes were less harmful than cigarettes [18]. Even e-cigarettes are sometimes considered a quit-smoking tool. However, with reports of e-cigarette-related lung injury in 2019, various side effects produced by e-cigarettes in life are getting attention. To the best of our knowledge, there are no studies on the effects of different smoking patterns on OSA. In the present study, we planned to investigate whether e-cigarette users were positively associated with a higher prevalence of OSA. We found that e-cigarette smokers did not increase the prevalence of OSA (OR = 0.84, 95% CI = 0.52–1.37). Interestingly, the prevalence of e-cigarettes for OSA was different in the results of different years. The prevalence of OSA among e-cigarette smoking participants in 2015–2016 was 28.79%, which was higher than that of non-smokers. While the lowest OSA prevalence rate was 17.26% among e-cigarette smokers in 2017–2018. Similarly, the prevalence of OSA in e-cigarette users was not significantly different from that in non-smokers in a fully adjusted analysis. The prevalence of OSA is higher among e-cigarette smokers and dual users than among non-smokers. The difference in the prevalence of OSA among e-cigarette users between years may be due to the population bias in different years. More extensive population surveys are needed to verify.

The relationship between smoking and OSAS may be caused by the following factors: (1) smoking changes the sleep structure of the patient and reduces sleep stability; (2) nicotine in tobacco leaves the upper respiratory tract muscles loose, the nerve reaction weakened, and the respiratory tract collapses easily; (3) nicotine increases the threshold of sleep-wake; and (4) smoking stimulates the mucous membrane of the upper respiratory tract and aggravates the inflammatory reaction of the respiratory tract [19]. In addition, smoking causes edema and thickening of the hanging mucous membrane, leading to narrowing of the upper respiratory tract and oropharynx, which may also be the mechanism of a severe increase in OSAS [20]. In addition, studies have shown that 35% of OSA patients smoke, while only about 18% of non-OSA patients smoke [9]. Although no clinical studies have been conducted to assess if OSA will aggravate tobacco addiction, some studies have shown that some patients can relieve clinical manifestations of OSA such as drowsiness, anxiety, or depression by smoking, and smoking may become one of the methods for self-treatment of daytime symptoms in OSA patients [21]. At the same time, a small sample study showed that 60% of 65 patients with OSA successfully quit smoking during 5 years of continuous positive airway pressure treatment [22]. However, the specific mechanism still needs further study.

Despite the novel findings of this study from a US population sample, it has several limitations. First, records of related situations were a self-report of participants’ recollections, and thus, memory bias may exist. Second, the present study could not exclude all confounding factors, which would have an impact on the results, such as the effect of different geographical locations and lifestyles on OSA. Third, the differences in gender and age distribution between the two groups may affect the results.