Nasal resistance and inflammation: mechanisms for obstructive sleep apnea from chronic rhinosinusitis

Study Objectives: We have previously estimated that the prevalence of obstructive sleep apnea (OSA) among World Trade Center rescue and recovery workers is 75% and identified that having symptoms of chronic rhinosinusitis (CRS) is an independent risk factor for OSA in this population. Nasal inflammation and/or elevated awake nasal resistance that carried over into sleep could explain this association. To understand the mechanism(s) for the elevated risk of OSA observed in World Trade Center responders with CRS symptoms we examined if elevated awake supine nasal resistance was associated with OSA, CRS and/or nasal inflammatory biomarkers. Methods: A total of 601 individuals (83% male, average age 53 years, body mass index = 29.9 ± 5.5 kg/m²) enrolled in the World Trade Center Health Program and without significant snoring prior to September 11, 2001 underwent 2 nights of home sleep apnea testing, measurements of anterior rhinomanometry in the supine position, and nasal lavage. Results: Awake supine nasal resistance was not associated with OSA; 74.8% and 74.4% of the participants with low and high nasal resistance respectively, had OSA. Patients with CRS had elevated nasal inflammatory markers (interleukin 6, interleukin 8, eosinophilic cationic protein, and neutrophil) but did not have high nasal resistance. Nasal inflammatory markers were not correlated with nasal resistance. Conclusions: As awake nasal resistance did not explain the relationship of CRS to OSA in this large and well characterized dataset, our findings suggest that either “sleep” nasal resistance or other factors such as increased supraglottic inflammation, perhaps through impairing upper airway reflex mechanisms, or systemic inflammation are involved in the pathophysiology of OSA in the World Trade Center population.