In this issue of Journal of Clinical Sleep Medicine, two studies report on association between sleep apnea and hearing impairment. Chopra and colleagues present data associating hearing impairment and sleep apnea in a large population of individuals from Hispanic descent.1 The study clearly shows a relationship between hearing impairment and sleep apnea. The authors also discuss possible pathophysiologic mechanism(s) linking sleep apnea to hearing impairment. The second study by Seo and colleagues shows that in a small sample of patients with severe sleep apnea (defined as AHI > 30 per hour of sleep), nadir oxygen saturation during the sleep study was associated with higher risk of hearing impairment.2
Snoring has been proposed as a cause of hearing impairment (HI) in obstructive sleep apnea (OSA). However, data supporting such a relationship are mixed.3,4 The study by Chopra failed to show any additional effect for snoring beyond OSA on HI.1 Nonetheless, exposure to loud sounds is known to adversely affect hearing to the extent that regulations exist regarding exposure to loud sounds in the workplace.5 Objective measures showed that noise due to snoring sometimes exceed work place noise limits.6 Importantly, however, snoring noise in OSA occurs in the milieu of hypoxia. Even if snoring alone does not result in HI, effects of simultaneous presence of snoring sound and hypoxia is not clear. Various studies suggest hypoxia and ischemia as the common pathway for various insults to cause HI.7 Intense sound diminishes cochlear perilymph oxygenation and causes accumulation of hypoxia inducible factor 1 (HIF-1) in the inner ear.8,9 In a rodent model, presence of hypoxia potentiate effect of noise on producing hearing loss.10 So the jury is still out on the effect of snoring in patients with OSA and significant hypoxia.
One interesting and important result of Chopra's and Seo's studies is the association between hypoxia and HI. In Chopra's study, 44.7%, 42%, and 48% of all OSA, moderate OSA and severe OSA, respectively, had HI. Interestingly, the highest prevalence of HI (according to quartiles of hypoxia) was 52.5% in patients with SpO2 below 85.2% (Table S1 in the supplemental material). For all the other quartiles of SpO2 (above 85.2%) the prevalence of HI is much lower than what was found in OSA categories as mentioned above. In Seo's study, subjects with hearing impairment had significantly lower nadir oxyhemoglobin saturations. Thus, data provide strong support that severity of hypoxia is the main culprit linking OSA to HI.
The other possible mechanism linking OSA to HI involves changes in intracranial perfusion due to sleep apnea.11 It is known that increased intracranial pressure can present with hearing impairment.12,13 Auditory evoked potentials are disturbed with higher centers more affected than the lower hearing center (cochlea).14 An even more complex issue in sleep apnea is the effect of acute nightly change in intracranial pressure versus chronic changes in intracranial pressure that may happen in patients with OSA over years.
The comorbid illnesses associated with OSA can also contribute to HI. Hypertension, diabetes mellitus, and dyslipidemia are risk factors associated with hearing impairment.15 Obesity is a prevalent risk factor and comorbid condition in patients with OSA. The question may therefore relate more to an obesity threshold, obesity's relative contribution to HI beyond effects of snoring, and hypoxia. An animal study showed that weight gain activated hypoxia-induced factor 1 (HIF-1) and resulted in blood vessels with smaller diameters and thicker walls in the stria vascularis and increased inflammatory response at the middle and basal turns of the cochlea, with reduced cell densities in the spiral ganglion and spiral ligament at the cochlea.16 Both studies in this issue of the journal took a further step in adjusting for presence of vascular risk factors and BMI showing that only severe OSA is associated with increased odds of having HI.
The study by Chopra and colleagues showed a clear association between the HI and OSA with an even stronger association between severity of hypoxia and HI (Table S1 in the supplemental material). It also showed that the population studied may be different than a normal healthy population, as a quarter of the population has oxygen saturations below 85%. The study by Seo and colleagues provided additional evidence for relationship between hypoxia and HI. More data on association between hypoxia (for example length of time below 88%) and HI may help further elucidate the link. In addition, as snoring was not measured objectively, the effect of various levels of snoring on HI is not clear from this study, especially when snoring occurs during hypoxic episodes.
Clinically, the paramount question is how these data will improve care for our patients in day-to-day practice. The studies point to a potentially modifiable risk factor for HI. Although the studies did not aim at and evaluated effects of treatment of OSA on HI, a next logical step would be to assess such effects.
The authors have indicated no financial conflicts of interest. This work is supported by the office of Research and Development at the Department of Veterans Affairs.
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Seo YJ, Park SY, Chung HJ, et al., authors. Lowest oxyhemoglobin saturation may be an independent factor influencing auditory function in severe obstructive sleep apnea. J Clin Sleep Med. 2016;12:653–8.
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