<img height="1" width="1" style="display:none" src="https://www.facebook.com/tr?id=1717549828521399&amp;ev=PageView&amp;noscript=1">

«  View All Posts

Blog Feature

By: Regina Patrick, RPSGT, RST on August 7th, 2020

Print/Save as PDF

Possible Link Between Obstructive Sleep Apnea and the Sense of Smell

OSA | OSA and sense of smell

An overlooked symptom in people with obstructive sleep apnea (OSA) is olfactory dysfunction (i.e., impairment in the sense of smell) such as an inability to detect or distinguish between odors. A finding that the sense of smell improves soon after a person with OSA begins continuous positive airway pressure (CPAP) treatment corroborates a possible link between olfactory dysfunction and OSA.1,2

What is Obstructive Sleep Apnea (OSA)?

OSA is the intermittent cessation of breathing during sleep. It occurs because the upper airway muscles relax excessively during sleep, which allows structures supported by the muscles to collapse into and obstruct the upper airway. This blockage restricts airflow and consequently decreases the blood oxygen level. A person makes increasingly strong efforts to breathe. Despite this effort, the blockage remains. When the blood oxygen level falls to a certain point, the respiratory center in the brain triggers a brief arousal (lasting for a few seconds) during which the upper airway muscle tone is restored. The person can then take some deep, quick breaths that restore the blood oxygen level. 

Treatment Options for OSA

The most common treatment for OSA is continuous positive airway pressure (CPAP). In this treatment, a continuous flow of pressurized air is delivered through a mask that fits over the nose or nose and mouth. The force of the air prevents the upper airway structures from collapsing into the airway as a person relaxes during sleep, thereby effectively preventing OSA episodes. 

Another treatment for OSA is a surgery called uvulopalatopharyngoplasty (UPPP), which opens the upper airway by removing tissues (e.g., uvula, enlarged tonsils and adenoids) and reshaping the soft palate. With these tissues unable to collapse into and block the upper airway during sleep, OSA episodes can be reduced. An adverse effect of UPPP reported by some people is the loss of or a diminishment in the sense of smell.

Sense of Smell

The ability to perceive odors begins when chemical molecules come into contact with receptors on olfactory sensory neurons located in the upper nasal cavity. Chemical molecules can enter the nasal passage anteriorly after being inhaled through the nose or enter the nasal passage posteriorly from the nasopharynx with the ingestion of food. The molecules stimulate the olfactory sensory neurons to transmit signals to the olfactory bulb, which lies at the base of the brain. The olfactory bulb then relays the signals to different areas in the brain such as the primary olfactory cortex (which allows a person to perceive an odor before identifying it), hypothalamus (which allows smells to be associated with long-term memory) and limbic system (which allows smells to be associated with emotional responses). 

Sense of Smell Dysfunction

An olfactory dysfunction may be conductive (i.e., the molecules of an odorant are impeded in stimulating the olfactory sensory neurons), sensorineural (i.e., an impairment in the transmission of signals from the olfactory sensory neurons) or central (i.e., impairment in the transmission of signals from the olfactory bulb to various areas within the brain). Some factors that can contribute to conductive dysfunction are inflammation within the nasal cavity or structural defect of the nasal cavity (e.g., deviated septum). A factor that can contribute to sensorineural olfactory dysfunction is damage to the olfactory sensory neurons due to events such as viral infections, the use of certain medications, and head trauma. A factor that can contribute to central olfactory dysfunction is neurodegenerative disorders such as Parkinson’s disease or Alzheimer’s disease.

OSA and Impaired Sense of Smell

How OSA contributes to an impaired sense of smell is unclear. Two possibilities are inflammation and reduced olfactory bulb volume. 

People with OSA have higher than normal levels of inflammatory chemicals (e.g., cytokines) and airway hyperreactivity. Some factors that could contribute to these findings are increased immunoreactivity and a chronic inflammatory response induced by intermittent episodes of hypoxia-reoxygenation and damage to upper airway tissues caused by the vibration of upper airway tissues against each other during snoring. Inflammation can narrow the nasal cavity and reduce the airflow needed to properly stimulate olfactory sensory neurons, and thereby reduce odor perception. 

A reduction in olfactory bulb volume has been noted in people with olfactory dysfunction.3 With this in mind, Salihoglu4 and colleagues used magnetic resonance imaging to measure nasal structures in people with and without OSA. They demonstrated that the olfactory bulb was smaller in people with OSA. This finding may explain olfactory dysfunction in people with OSA. Salihoglu further found the olfactory bulb volume decreased with increasing severity of the condition.

UPPP and Sense of Smell

Some reports regarding the loss of smell in people with OSA have been in relation to patients who have undergone UPPP.5,6 However, the patients were not assessed for the type of olfactory dysfunction (i.e., conductive, sensorineural, central). On noting this lack, researchers Jiang7 et al. used olfactory testing to assess two patients who complained of loss of the sense of smell after UPPP.

They used the phenyl ethyl alcohol (PEA) odor detection threshold test to determine the patient’s odor threshold and used the University of Pennsylvania Smell Identification Test (UPSIT) to determine a patient’s ability to identify an odor. After the patients’ baseline olfactory function was obtained, they were treated with steroids — one patient was additionally treated with zinc gluconate. On re-evaluations two months later and two to three months afterward, both patients subjectively reported progressive improvements in their sense of smell, which was corroborated by their progressively improved performance on the PEA and UPSIT tests. However, Jiang noted that olfactory function did not fully recover in either patient.

CPAP and Sense of Smell

Continuous positive airway pressure treatment reduces inflammatory processes in people with OSA. Therefore, CPAP treatment, by reducing inflammatory processes, would theoretically improve the sense of smell in people with OSA.8 To this end, some researchers have investigated the impact of CPAP treatment on improving the sense of smell in people with OSA. 

For example, Koseoglu1 and colleagues examined the impact of positive airway pressure (PAP) treatment on olfactory function in patients who had polysomnographically confirmed OSA. Sniffin’ Sticks (felt-tipped pen devices manufactured by Burghardt in Wedel, Germany), which contain different odorants, were used to assess the patients’ olfactory function before and three months after initiating PAP treatment.

The Sniffin’ Stick test is used to determine three aspects of olfactory function: at what concentration a person can detect an odor (olfactory threshold), whether a person can distinguish between odors (olfactory discrimination) and whether a person can distinguish what a particular odor is (olfactory identification). Three months after initiating PAP treatment, the patients’ odor threshold, odor discrimination and odor identification had improved.

Based on their findings, the authors suggested people with OSA can have olfactory dysfunction and this dysfunction can improve with PAP therapy. However, they had no explanation for the pathogenesis of olfactory dysfunction in OSA or how PAP therapy contributes to the improvement of olfactory function.

In a similar study, Boemer2 and colleagues assessed whether odor threshold, odor discrimination and odor identification would improve after three months of nasal CPAP treatment in people with moderate or severe OSA. The researchers similarly used Sniffin’ Sticks to assess the patients’ olfactory function before and after three months of CPAP treatment. As in the Koseoglu study, the patients’ olfactory function had improved significantly at three months.

Boemer then had a small group of CPAP-compliant patients undergo subtherapeutic air pressure treatment. At three weeks, their sense of smell had somewhat deteriorated. This finding indicated that improvement in the sense of smell is reversible. Thus, consistent treatment compliance may be necessary to maintain the improvement in the sense of smell. 

The Sniffin’ Stick test involves some subjective input from an individual. A more objective measurement of olfactory function is chemosensory event-related potentials (CSERPs), which are recorded on an electroencephalogram while a person is exposed to different odors. After the exposure, certain waveforms (i.e., potentials) appear at specific times (i.e., latency) such as 100 ms or 300 ms and with a characteristic amplitude. A change in a waveform’s latency or in a waveform’s amplitude indicates olfactory dysfunction. The first waveforms that appear after odor exposure (i.e., early components) are modulated by the concentration of the odorant, whereas waveforms that appear later (i.e., the late positive complex) reflect the significance of the odor to the person (e.g., whether the odor is “pleasant” or “unpleasant.”)

Researchers Invitto9 and colleagues recently used CSERPs to more objectively assess olfactory perception in nonsmoking patients with polysomnographically confirmed OSA. Their results were compared with those nonsmoking volunteers without OSA. Invitto focused on two waveforms: N1 (an early signal) and the late positive complex (LPC; a late signal). A comparison of these waveforms between the OSA patients and the controls revealed that the N1 latency occurred sooner and the LPC amplitude was deeper in the OSA patients than in the controls. Invitto believes that the finding of the shorter N1 latency may reflect the patients’ difficulty in odor perception and the deeper amplitude of the LPC may reflect an impairment in the patient’s subjective experience of an odor (e.g., its pleasantness).

The link between OSA and olfactory dysfunction is an interesting finding. Once scientists learn more about this association, it may prove to be important in OSA treatment. For example, OSA patients who have a pre-existing loss of smell and plan to undergo surgery for sleep apnea or snoring may need to avoid certain types of surgery or, to reduce any further loss in the sense of smell, they may first need to be treated for the olfactory dysfunction before undergoing the surgery. As the Boemer study suggests, consistent compliance with CPAP treatment may help restore and/or preserve the sense of smell in people with OSA. Future studies may soon clarify how olfactory dysfunction can be used beneficially in the treatment and possibly the diagnosis of OSA. 

Original article was published in the A2Zzz Magazine Quarter 1, 2019


  1. Koseoglu S, Derin S, Yilmaz M, et al. Does positive airway pressure therapy improve olfactory function? International Forum of Allergy and Rhinology. 2017;7:557-560.
  2. Boerner B, Tini GM, Fachinger P, et al. Significant improvement of olfactory performance in sleep apnea patients after three months of nasal CPAP therapy—observational study and randomized trial. PLoS One. 2017;12:e0171087.
  3. Haehner A, Rodewald A, Gerber JC, Hummel T. Correlation of olfactory function with changes in the volume of the human olfactory bulb. Archives of Otolaryngology and Head Neck Surgery. 2008;134(6):621-624.
  4. Salihoglu M, Kendirli MT, Altundag, A, et al. The effect of obstructive sleep apnea on olfactory functions. Laryngoscope. 2014;124:2190-2194.
  5. Hagert B, Wikblad K, Odkvist L, et al. Side effects after surgical treatment of snoring. ORL: Journal for Otorhinolaryngology and Its Related Specialties. 2000;62:76-80.
  6. Rombaux P HM, Bertrand B, et al. Postoperative pain and side effects after uvulopalatopharyngoplasty, laserassisted uvulopalatoplasty, and radiofrequency tissue volume reduction in primary snoring. Laryngoscope. 2003;113:2169-2173.
  7. Jiang RS, Chang YH. Olfactory loss after uvulopalatopharyngoplasty: a report of two cases with review of the literature. Case Reports in Otolaryngology. 2014;2014:546317.
  8. Wu KM, Lin CC, Chiu CH, et al. Effect of treatment by nasal continuous positive airway pressure on serum high mobility group box-1 protein in obstructive sleep apnea. Chest. 2010;137:303-309.
  9. Invitto S, Calcagni A, Piraino G, et al. Obstructive sleep apnea syndrome and olfactory perception: An OERP study. Respiration Physiology Neurobiology. 2018: doi: 10.1016/j.resp.2018.1007.1002