Nonallergic rhinitis refers to rhinitis that is not due to an allergy. The category was formerly referred to as vasomotor rhinitis, as the first cause discovered was vasodilation due to an overactive parasympathetic nerve response. As additional causes were identified, additional types of nonallergic rhinitis were recognized. Vasomotor rhinitis is now included among these under the more general classification of nonallergic rhinitis. The diagnosis is made upon excluding allergic causes. 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. Vasomotor rhinitis appears to be significantly more common in women than men, leading some researchers to believe that hormones play 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. The antihistamine cyproheptadine is also effective, probably due to its antiserotonergic effects.

A Cochrane review on non-allergic rhinitis reports improvement of overall function after treatment with capsaicin (the active component of chili peppers). The quality of evidence is low, however.

Nonallergic rhinitis is inflammation of the inner part of the nose that is not caused by an allergy. Nonallergic rhinitis involves symptoms including chronic sneezing or having a congested, drippy nose without an identified allergic reaction. Other common terms for nonallergic rhinitis are vasomotor rhinitis and perennial rhinitis. The prevalence of nonallergic rhinitis in otolaryngology is 40%. Allergic rhinitis is more common than nonallergic rhinitis; however, both conditions have similar presentation, manifestation and treatment. Nasal itching and paroxysmal sneezing are usually associated with nonallergic rhinitis in comparison to allergic rhinitis.

Nasal mucosa has rich blood supply and has venous sinusoids or "lakes" surrounded by smooth muscle fibers. These smooth muscle fibers act as sphincters and control the filling and emptying of sinusoids. Sympathetic stimulation causes vasoconstriction and shrinkage of mucosa, which leads to decongestion of nose. Parasympathetic stimulation causes not only excessive secretion from the nasal gland but also vasodilatation and engorgement, which lead to rhinorrhoea and congestion of nose. The autonomic nervous system, which supplies the nasal mucosa, is under the control of the hypothalamus. Therefore, emotions play significant role in nonallergic rhinitis.

Rhinitis medicamentosa is a form of drug-induced nonallergic rhinitis which is associated with nasal congestion brought on by the use of certain oral medications (primarily sympathomimetic amine and 2-imidazoline derivatives) and topical decongestants (e.g., oxymetazoline, phenylephrine, xylometazoline, and naphazoline nasal sprays) that constrict the blood vessels in the lining of the nose.

Causes can be remembered by mnemonic HERNIA:

- Hereditary factors: the disease runs in families

- Endocrine imbalance: the disease tends to start at puberty and mostly involves females

- Racial factors: whites are more susceptible than natives of equatorial Africa

- Nutritional deficiency: vitamins A or D, or iron

- Infection: "Klebsiella ozaenae", diphtheroids, "Proteus vulgaris", "E. coli", etc.

- Autoimmune factors: viral infection or some other unidentified insult may trigger antigenicity of the nasal mucosa.

One way to prevent allergic rhinitis is to wear a respirator or mask when near potential allergens.

Growing up on a farm and having multiple brothers and or sisters decreases the risk.

Specific infections, such as syphilis, lupus, leprosy and rhinoscleroma, may cause destruction of the nasal structures leading to atrophic changes. Atrophic rhinitis can also result from long-standing purulent sinusitis or radiotherapy of the nose, or as a complication of surgery of the turbinates. The United Kingdom National Health Service has stated that "Most cases of atrophic rhinitis in the UK occur when the turbinates are damaged or removed during surgery". Some authors refer to as Atrophic rhinitis secondary to sinus surgery as the empty nose syndrome.

Rhinorrhea can be a symptom of other diseases, such as the common cold or influenza. During these infections, the nasal mucous membranes produce excess mucus, filling the nasal cavities. This is to prevent infection from spreading to the lungs and respiratory tract, where it could cause far worse damage. It has also been suggested that rhinorrhea is a result of viral evolution, and may be a response that is not useful to the host, but which has evolved by the virus to maximise its own infectivity. Rhinorrhea caused by these infections usually occur on circadian rhythms. Over the course of a viral infection, sinusitis (the inflammation of the nasal tissue) may occur, causing the mucous membranes to release more mucus. Acute sinusitis consists of the nasal passages swelling during a viral infection. Chronic sinusitis occurs when one or more nasal polyps appear. This can be caused by a deviated septum as well as a viral infection.

Common issues that lead to overuse of topical decongestants:

- Deviated septum

- Upper respiratory tract infection

- Vasomotor rhinitis

- Cocaine use and other stimulant abuse

- Pregnancy (these products are not considered safe for pregnancy)

- Chronic rhinosinusitis

- Hypertrophy of the inferior turbinates

Rhinorrhea can also occur when individuals with allergies to certain substances, such as pollen, dust, latex, soy, shellfish, or animal dander, are exposed to these allergens. In people with sensitized immune systems, the inhalation of one of these substances triggers the production of the antibody immunoglobulin E (IgE), which binds to mast cells and basophils. IgE bound to mast cells are stimulated by pollen and dust, causing the release of inflammatory mediators such as histamine. In turn, this causes, among other things, inflammation and swelling of the tissue of the nasal cavities as well as increased mucus production. Particulate matter in polluted air and chemicals such as chlorine and detergents, which can normally be tolerated, can make the condition considerably worse.

Rhinitis medicamentosa (or RM) is a condition of rebound nasal congestion brought on by extended use of topical decongestants (e.g., oxymetazoline, phenylephrine, xylometazoline, and naphazoline nasal sprays) and certain oral medications (e.g., sympathomimetic amines and various 2-imidazolines) that constrict blood vessels in the lining of the nose.

Allergic rhinitis is the type of allergy that affects the greatest number of people. In Western countries, between 10 and 30 percent of people are affected in a given year. It is most common between the ages of twenty and forty.

Some people have reported relief of symptoms by following a low-salicylate diet such as the Feingold diet. Aspirin is quickly converted in the body to salicylic acid, also known as 2-Hydroxybenzoic acid. Sommer "et al." reported a multi-center prospective randomized cross-over trial with 30 patients following a low-salicylate diet for 6 weeks. This study demonstrated a clinically significant decrease in both subjective and objective scoring of severity of disease, but made note of the challenge for patients in following what is a fairly stringent diet.

A diet low in omega-6 oils (precursors of arachidonic acid), and high in omega-3 oils, may also help. In a small study, aspirin-sensitive asthma patients taking 10 grams of fish oil daily reported relief of most symptoms after six weeks, however symptoms returned if the supplement was stopped.

Allergic diseases are strongly familial: identical twins are likely to have the same allergic diseases about 70% of the time; the same allergy occurs about 40% of the time in non-identical twins. Allergic parents are more likely to have allergic children, and those children's allergies are likely to be more severe than those in children of non-allergic parents. Some allergies, however, are not consistent along genealogies; parents who are allergic to peanuts may have children who are allergic to ragweed. It seems that the likelihood of developing allergies is inherited and related to an irregularity in the immune system, but the specific allergen is not.

The risk of allergic sensitization and the development of allergies varies with age, with young children most at risk. Several studies have shown that IgE levels are highest in childhood and fall rapidly between the ages of 10 and 30 years. The peak prevalence of hay fever is highest in children and young adults and the incidence of asthma is highest in children under 10.

Overall, boys have a higher risk of developing allergies than girls, although for some diseases, namely asthma in young adults, females are more likely to be affected. These differences between the sexes tend to decrease in adulthood.

Ethnicity may play a role in some allergies; however, racial factors have been difficult to separate from environmental influences and changes due to migration. It has been suggested that different genetic loci are responsible for asthma, to be specific, in people of European, Hispanic, Asian, and African origins.

Chronic stress can aggravate allergic conditions. This has been attributed to a T helper 2 (TH2)-predominant response driven by suppression of interleukin 12 by both the autonomic nervous system and the hypothalamic–pituitary–adrenal axis. Stress management in highly susceptible individuals may improve symptoms.

Nasal congestion is the blockage of the nasal passages usually due to membranes lining the nose becoming swollen from inflamed blood vessels.

Nasal decongestants target the discomfort directly. These come as nasal sprays, inhalers, and as oral pills.

Nasal congestion has many causes and can range from a mild annoyance to a life-threatening condition. Most people prefer to breathe through the nose (historically referred to as "obligate nasal breathers"). Nasal congestion in an infant in the first few months of life can interfere with breastfeeding and cause life-threatening respiratory distress; in older children and adolescents it is often just an annoyance but can cause other difficulties.

Nasal congestion can interfere with the hearing and speech. Significant congestion may interfere with sleep, cause snoring, and can be associated with sleep apnea. In children, nasal congestion from enlarged adenoids has caused chronic sleep apnea with insufficient oxygen levels and hypoxia, as well as right-sided heart failure. The problem usually resolves after surgery to remove the adenoids and tonsils, however the problem often relapses later in life due to craniofacial alterations from chronic nasal congestion.

Nasal congestion can also cause mild facial and head pain, and a degree of discomfort, often from allergies or the common cold.

The disorder is thought to be caused by an anomaly in the arachidonic acid metabolizing cascade which leads to increased production of pro-inflammatory cysteinyl leukotrienes, a series of chemicals involved in the body's inflammatory response. When medications like NSAIDs or aspirin block the COX-1 enzyme, production of thromboxane and some anti-inflammatory prostaglandins is decreased, and in patients with aspirin-induced asthma this results in the overproduction of pro-inflammatory leukotrienes to causes severe exacerbations of asthma and allergy-like symptoms. The underlying cause of the disorder is not fully understood, but there have been several important findings:

- Abnormally low levels of prostaglandin E (PGE), which is protective for the lungs, has been found in patients with aspirin-induced asthma and may worsen their lung inflammation.

- In addition to the overproduction of cystinyl leukotrienes, overproduction of 15-lipoxygenase-derived arachidonic acid metabolites viz., 15-hydroxyicosatetraenoic acid and eoxins by the eosinophils isolated from the blood of individuals with AERD; certain of these products may help promote the inflammatory response.

- Overexpression of both the cysteinyl leukotriene receptor 1 and the leukotriene C synthase enzyme has been shown in respiratory tissue from patients with aspirin-induced asthma, which likely relates to the increased response to leukotrienes and increased production of leukotrienes seen in the disorder.

- The attachment of platelets to certain leukocytes in the blood of patients with aspirin-sensitive asthma has also been shown to contribute to the overproduction of leukotrienes.

- There may be a relationship between aspirin-induced asthma and "TBX21", "PTGER2", and "LTC4S".

- Eosinophils isolated from the blood of aspirin-induced asthma subjects (as well as severe asthmatic patients) greatly overproduce 15-hydroxyicosatetraenoic acid and eoxin C4 when challenged with arachidonic acid or calcium ionophore A23187, compared to the eosinophils taken from normal or mildly asthmatic subjects; aspirin treatment of eosinophils from aspirin intolerant subjects causes the cells to mount a further increase in eoxin production. These results suggest that 15-lipoxygenase and certain of its metabolites, perhaps eoxin C4, as contributing to aspirin-induced asthma in a fashion similar to 5-lipoxygenase and its leukotriene metabolites.

Some examples:

- Allergic asthma

- Allergic conjunctivitis

- Allergic rhinitis ("hay fever")

- Anaphylaxis

- Angioedema

- Urticaria (hives)

- Eosinophilia

- Penicillin allergy

- Cephalosporin allergy

- Food allergy

- Sweet itch

The treatment of nasal congestion frequently depends on the underlying cause.

Alpha-adrenergic agonists are the first treatment of choice. They relieve congestion by constricting the blood vessels in the nasal cavity, thus resulting in relieved symptoms. Examples include oxymetazoline and phenylephrine.

Both influenza and the common cold are self-limiting conditions that improve with time; however, drugs such as acetaminophen (paracetamol), aspirin, and ibuprofen may help with the discomfort.

A cause of nasal congestion may also be due to an allergic reaction caused by hay fever, so avoiding allergens is a common remedy if this becomes a confirmed diagnosis. Antihistamines and decongestants can provide significant symptom relief although they do not cure hay fever. Antihistamines may be given continuously during pollen season for optimum control of symptoms. Topical decongestants should only be used by patients for a maximum of 3 days in a row, because rebound congestion may occur in the form of rhinitis medicamentosa.

Nasal decongestants target discomfort directly. These come as nasal sprays like naphazoline (Privine), oxymetazoline (Afrin, Dristan, Duramist), as inhalers, or phenylephrine (Neo-Synephrine, Sinex, Rhinall) or as oral pills (Bronkaid, Sudafed, Neo-Synephrine, Sinex, Rhinall). Oral decongestants may be used for up to a week without consulting a doctor, with the exception of Bronkaid and Sudafed, which can be taken as long as needed, but nasal sprays can also cause "rebound" (Rhinitis medicamentosa) and worsen the congestion if taken for more than a few days. Therefore, you should only take nasal sprays when discomfort cannot be remedied by other methods, and never for more than three days.

If an infant is unable to breathe because of a plugged nose, a nasal aspirator may be useful to remove the mucus. The mucus might be thick and sticky, making it difficult to expel from the nostril.

Treatment usually involves adrenaline (epinephrine), antihistamines, and corticosteroids.

If the entire body is involved, then anaphylaxis can take place, which is an acute, systemic reaction that can prove fatal.

This is a rare condition, probably caused by an allergic reaction, in which there is sudden swelling of the salivary glands. It is associated with other allergic conditions such as asthma, urticaria, allergic rhinitis and food allergy.

Smoking, especially heavy smoking, is an important predisposing factor but the reasons for this relationship are unknown. One hypothesis is that cigarette smoke contains nutritional factors for "C. albicans", or that local epithelial alterations occur that facilitate colonization of candida species.

First-generation antihistamine has been suggested as first-line therapy to treat post-nasal drip.

Allergic inflammation is an important pathophysiological feature of several disabilities or medical conditions including allergic asthma, atopic dermatitis, allergic rhinitis and several ocular allergic diseases. Allergic reactions may generally be divided into two components; the early phase reaction, and the late phase reaction. While the contribution to the development of symptoms from each of the phases varies greatly between diseases, both are usually present and provide us a framework for understanding allergic disease.

The early phase of the allergic reaction typically occurs within minutes, or even seconds, following allergen exposure and is also commonly referred to as the immediate allergic reaction or as a Type I allergic reaction. The reaction is caused by the release of histamine and mast cell granule proteins by a process called degranulation, as well as the production of leukotrienes, prostaglandins and cytokines, by mast cells following the cross-linking of allergen specific IgE molecules bound to mast cell FcεRI receptors. These mediators affect nerve cells causing itching, smooth muscle cells causing contraction (leading to the airway narrowing seen in allergic asthma), goblet cells causing mucus production, and endothelial cells causing vasodilatation and edema.

The late phase of a Type 1 reaction (which develops 8–12 hours and is mediated by mast cells) should not be confused with delayed hypersensitivity Type IV allergic reaction (which takes 48–72 hours to develop and is mediated by T cells). The products of the early phase reaction include chemokines and molecules that act on endothelial cells and cause them to express Intercellular adhesion molecule (such as vascular cell adhesion molecule and selectins), which together result in the recruitment and activation of leukocytes from the blood into the site of the allergic reaction. Typically, the infiltrating cells observed in allergic reactions contain a high proportion of lymphocytes, and especially, of eosinophils. The recruited eosinophils will degranulate releasing a number of cytotoxic molecules (including Major Basic Protein and eosinophil peroxidase) as well as produce a number of cytokines such as IL-5. The recruited T-cells are typically of the Th2 variety and the cytokines they produce lead to further recruitment of mast cells and eosinophils, and in plasma cell isotype switching to IgE which will bind to the mast cell FcεRI receptors and prime the individual for further allergic responses.

Sialodochitis (also termed ductal sialadenitis), is inflammation of the duct system of a salivary gland. This is compared to sialadenitis, which is inflammation of the gland parenchyma.

Sialodochitis may be associated with salivary duct strictures and salivary stones.

It is common in both the parotid glands and submandibular glands.

The treatment is as for sialadenitis.