Nasal congestion resulting from allergic rhinitis is associated with a 1.8-fold increase in the risk of developing moderate to severe OSA. The proposed mechanism for this enhanced risk includes increased airway resistance and mouth breathing. In OSA, the primary pathological obstructive sites are located at either the velopharyngeal or retropalatal segments of the upper airway; however, nasal resistance has also been shown to contribute up to 50% of the upper airway resistance. The Starling resistor model, which describes patterns of airflow through a collapsible tube, recognizes four determinants of airflow: pressure upstream, pressure downstream, pressure surrounding the tube, and resistance of the upstream segment. When nasal resistance is increased, it results in an increased pressure differential between the intraluminal space and the atmosphere, which induces airway collapse. The higher nasal resistance is accompanied by an increase in the resistance of the upstream segment that consequently decreases the airflow through the pharynx (the collapsible tube).