It is an umbrella term of rhinitis of multiple causes, such as occupational (chemical), smoking, gustatory, hormonal, senile (rhinitis of the elderly), atrophic, medication-induced (including rhinitis medicamentosa), local allergic rhinitis, non-allergic rhinitis with eosinophilia syndrome (NARES) and idiopathic (vasomotor or non-allergic, non-infectious perennial allergic rhinitis (NANIPER), or non-infectious non-allergic rhinitis (NINAR).In vasomotor rhinitis, certain nonspecific stimuli, including changes in environment (temperature, humidity, barometric pressure, or weather), airborne irritants (odors, fumes), dietary factors (spicy food, alcohol), sexual arousal, exercise, and emotional factors trigger rhinitis. There is still much to be learned about this, but it is thought that these non-allergic triggers cause dilation of the blood vessels in the lining of the nose, which results in swelling and drainage. Non-allergic rhinitis can co-exist with allergic rhinitis, and is referred to as "mixed rhinitis". The pathology of vasomotor rhinitis appears to involve neurogenic inflammation and is as yet not very well understood. The role of transient receptor potential ion channels on the non-neuronal nasal epithelial cells has also been suggested. Overexpression of these receptors have influence the nasal airway hyper-responsiveness to non-allergic irritant environmental stimuli (e.g., extremes of temperature, changes in osmotic or barometric pressure). Vasomotor rhinitis appears to be significantly more common in women than men, leading some researchers to believe that hormone imbalance plays a role. In general, age of onset occurs after 20 years of age, in contrast to allergic rhinitis which can be developed at any age.
Individuals with vasomotor rhinitis typically experience symptoms year-round, though symptoms may be exacerbated in the spring and autumn when rapid weather changes are more common. An estimated 17 million United States citizens have vasomotor rhinitis.Drinking alcohol may cause rhinitis as well as worsen asthma (see alcohol-induced respiratory reactions). In certain populations, particularly those of East Asian countries such as Japan, these reactions have a nonallergic basis. In other populations, particularly those of European descent, a genetic variant in the gene that metabolizes ethanol to acetaldehyde, ADH1B, is associated with alcohol-induced rhinitis. It is suggested that this variant metabolizes ethanol to acetaldehyde too quickly for further processing by ALDH2 and thereby leads to the accumulation of acetaldehyde and rhinitis symptoms. In these cases, alcohol-induced rhinitis may be of the mixed rhinitis type and, it seems likely, most cases of alcohol-induced rhinitis in non-Asian populations reflect true allergic response to the non-ethanol and/or contaminants in alcoholic beverages, particularly when these beverages are wines or beers. Alcohol-exacerbated rhinitis is more frequent in individuals with a history of rhinitis exacerbated by aspirin.Aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs), particularly those that inhibit cyclooxygenase 1 (COX1), can worsen rhinitis and asthma symptoms in individuals with a history of either one of these diseases. These exacerbations most often appear due to NSAID hypersensitivity reactions rather than NSAID-induced allergic reactions.The antihistamine azelastine, applied as a nasal spray, may be effective for vasomotor rhinitis. Fluticasone propionate or budesonide (both are steroids) in nostril spray form may also be used for symptomatic treatment.