Project Details


Obstructive sleep apnea (OSA) occurs in 5-20% of the adult population. The pathophysiology of OSA ismultifactorial and includes impaired upper airway anatomy, low arousal threshold, respiratory control instability,and/or altered neuro-muscular control of upper airway muscles. A validated method has been pioneered byWellman and Sands to calculate the relative contribution of each of these components from diagnosticpolysomnography and this approach may define pathophysiologic phenotypes of the syndrome. We and othershave shown that WTC dust-exposed subjects have a high prevalence of conditions such as chronicrhinosinustis, gastroesophageal reflux disease, post-traumatic stress disorder and obesity that increase risk forOSA. Our goal is to define how these comorbid conditions might act via individual pathophysiologicmechanisms defined as a “phenotype of OSA.” Our current data in over 600 WTC responders shows anextraordinary prevalence of OSA of 75 %. We have also found an association between new or worseningchronic rhinosinusitis (CRS) symptoms since 9/11 and OSA that is significant even after controlling for knownrisk factors for OSA such as age, gender and BMI. This association is not explained by increased nasalresistance in those with CRS, suggesting other mechanisms could impact upper airway function in CRSincluding neuropathy, fibrosis and reduced upper airway sensitivity that impairs mechanoreflexes to negativepressure. We propose that an impaired afferent limb of upper airway reflexes impairs the ability to perceiveand/or process upper airway loading and contributes to failure of upper airway stiffening. Furthermore, the highprevalence of OSA even in subjects without CRS highlights the need to identify the mechanisms of OSA inthese subjects. The aims of this proposal are to 1. Examine the mechanism by which CRS increases the riskfor OSA. Building on our previous findings of increased prevalence of OSA in subjects with CRS symptoms, wewill examine the role of sensory function (2-point discrimination and vibration sensitivity threshold) in the upperairway in four groups of 50 subjects each with and without OSA and with and without CRS. 2. Examine therelationship of the mechanistic OSA phenotype components to CRS in WTC responders. In 100 subjectsdiagnosed with OSA (50 with CRS and 50 without CRS) we will test if upper airway muscle compensation islower in subjects with CRS. 3. Examine differences in the distribution of OSA pathophysiologic phenotypesbetween WTC responders and matched patients from a sleep clinic population without exposure to WTC dust.In 100 subjects in each group we will test the hypothesis that WTC subjects have a greater proportion ofsubjects with a) mild UA collapsibility b) low arousal threshold and c) low muscle compensation compared tonon-WTC subjects. This proposal will provide insight into the pathophysiologic mechanisms and mechanisticcomponents of OSA in WTC Responders, which could help identify groups responding to non-PAP therapiesand contribute to a more rational approach to developing and combining non-CPAP therapies.

Effective start/end date1/07/1830/06/21


  • National Institute for Occupational Safety and Health: $495,244.00


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