The major function of the nose is to warm and humidify air before it reaches to the lungs for gas exchange. Conditioning of inspired air is achieved through evaporation of water from the epithelial surface. The continuous need to condition air leads to a hyperosmolar environment on the surface of the epithelium. As ventilation increases, the hyperosmolar surface moves more distally, covering a larger surface area of the airway, and stimulates epithelial cells to release mediators that lead to inflammation. This inflammation is not identical to allergic inflammation, but causes both short-term and long-term changes in the epithelium. In the short-term, it increases paracellular water transport in an attempt to enhance conditioning, and it stimulates sensory nerves to initiate neural reflexes. It also disrupts channels in the cellular membrane, which might permit greater penetration of foreign proteins, such as allergens, leading to further inflammatory cascades. The long-term inflammation induced over time by the hyperosmolar milieu could worsen the ability of the nose to condition air, requiring more of the conditioning to occur in the lower airway and leading to adverse consequences for the respiratory system.