Allergic Rhinitis

Allergic rhinitis (AR) is an inflammatory condition of the nasal lining that develops when an immune system already sensitized to a harmless airborne substance, such as pollen, house dust mite, or animal dander, reacts to that substance again. The reaction is mediated mainly by immunoglobulin E antibodies and the immune-system, and it produces nasal congestion, runny nose, sneezing, and itching. It is one of the most common chronic conditions worldwide and is widely known as hay fever when triggered by pollen.

The condition matters because it reduces quality of life, sleep, school and work performance, and it generates large health-care costs. It is also closely linked to asthma, a relationship captured by the "one airway, one disease" concept that shapes how clinicians treat the upper and lower airways together. Understanding AR therefore requires knowledge of antibody biology, epidemiology, and clinical diagnosis, as well as the pharmacology of the medications used to control it.

This entry begins with the clinical picture and the immunological mechanisms behind it, then turns to the classification of AR by allergen exposure, duration, and severity, and to the allergens most often responsible. It then covers diagnosis, drug treatment, allergen avoidance and immunotherapy, the links with other airway diseases, and the epidemiological and economic burden. It closes with the evolution of the ARIA guidelines and the questions that remain open.

Definition and Clinical Features

Allergic rhinitis (AR) is an inflammatory disorder of the nasal lining in which immunoglobulin E (IgE) antibodies, directed against inhaled allergens, drive the reaction. Allergic rhinitis is an IgE-mediated disorder of the nose caused by the interaction of airborne allergens with specific IgE type antibodies on the surface of mast cells. The disease is therefore conditional on a prior immune state: only patients with a genetic predisposition to developing allergies develop it, since everyone is exposed to environmental allergens but only those with the innate ability to become sensitized develop symptoms.

The classic nasal symptom set is nasal congestion, rhinorrhea, sneezing, and nasal itching. Postnasal drip occurs commonly, as do associated symptoms involving the ears, eyes, and throat. Rhinorrhea may be anterior or posterior, and nasal congestion is usually the most bothersome complaint. Nasal congestion is reported as the most common and bothersome symptom; it is often associated with sleep-disordered breathing, a likely cause of sleep impairment in rhinitis-affected individuals.

Ocular involvement is frequent. Patients typically report reddened, itchy and watery eyes. In one study of seasonal AR, allergic conjunctivitis symptoms were found in more than 75% of patients with seasonal allergic rhinitis. Eye itching and tearing are useful clinical clues: because allergic rhinitis is frequently associated with allergic conjunctivitis, the presence of eye pruritus and lacrimation is a helpful indication that a patient's rhinitis has an allergic basis.

Distinguishing AR from infectious rhinitis rests largely on the history. Viral upper respiratory infections bring their own pattern: acute viral upper respiratory tract infection presents with nasal symptoms and constitutional symptoms such as fever, myalgias, and malaise. Pruritus is typically absent, and symptoms resolve within 7 to 10 days. By contrast, the presence of a recurrent seasonal pattern of symptoms, the presence of an obvious allergic trigger, and symptoms of nasal or ocular pruritus strongly suggest the diagnosis of AR. The distinction matters because it prevents inappropriate treatment. Clinicians should also recognize that separating viral from bacterial infections based on clinical presentation is often not possible.

Persistent symptoms extend beyond the nose. Nasal obstruction disturbs sleep, and in a survey of patients with moderate or severe AR, sleep disturbances were reported by 66% of adults and 43% of children. Polysomnography has documented changes in sleep architecture: patients with moderate to severe AR have a reduction of 38.5 ± 6.2 min in slow-wave sleep time and an increase of 22.4 ± 5.1 min in the latency of rapid eye movement sleep. Daytime consequences include fatigue and impaired attention. Allergic rhinitis, in addition to the nasal and ocular symptoms, is crucially linked to impairments in information processing and changes in attention-related cognitive processes. In children, nocturnal nasal congestion and sleep fragmentation directly lead to daytime sleepiness, poor concentration, and memory decline, severely affecting their academic performance. Ocular symptoms add less to sleep loss than nasal symptoms do: in one cross-sectional study, the association between ocular symptoms and poorer sleep disappeared once nasal severity was adjusted for.

Immunological Mechanisms

Sensitization

Sensitization is the silent priming step that precedes any symptoms. In the nasal lining, antigen-presenting cells capture allergen fragments and display them on MHC class II molecules to naive CD4+ T cells, which then differentiate into allergen-specific Th2 cells Antigen-presenting cells such as dendritic cells in the mucosal surface take up, process, and present allergen peptides on MHC class II molecules, and the complex then engages naive CD4+ T cells, which differentiate into allergen-specific Th2 cells. These Th2 cells secrete IL-4 and IL-13, which signal B cells to produce allergen-specific IgE Cytokines such as IL-4 and IL-13 released from the activated Th2 cells interact with B cells to produce allergen-specific IgE. The IgE then coats the surface of mast cells and circulating basophils. Once bound, the antibody is positioned to recognize the same allergen on the next exposure The IgE antibodies then bind to receptors on tissue mast cells and circulating basophils.

Early-Phase Response

When sensitized mast cells encounter the allergen again, cross-linking of surface IgE triggers rapid degranulation. Within minutes of contact with allergen, IgE-sensitized mast cells degranulate, releasing both preformed and newly synthesized mediators. Histamine is the principal preformed mediator. Its accumulation produces the classic symptoms of sneezing, itching, rhinorrhea and congestion This results in an accumulation of histamine which gives rise to the characteristic symptoms of rhinitis - sneezing, itching, rhinorrhoea and congestion. Histamine, proteases and cytokines such as TNF are released within about five minutes of allergen exposure Histamine, proteases, and some cytokines, such as tumor necrosis factor (TNF), are released within five minutes of the allergen. Mediator effects on vessels explain the watery discharge and swelling: they make vessels leak, producing edema and watery rhinorrhea, and dilate vascular channels, causing congestion These mediators stimulate the vessels to leak and produce edema plus watery rhinorrhea, and dilate arteriole venule anastomoses causing nasal congestion. In nasal challenge studies, tryptase, a marker of mast cell activity, typically peaks around five minutes and returns toward baseline within about two hours Existing data from multiple studies consistently reported peak induction of tryptase at 5-minutes post challenge, followed by rapidly declining levels within 60 minutes and then dropping back to baseline within 2 hours.

Late-Phase Response

The late phase develops after the early reaction has subsided and is driven by cell recruitment rather than preformed mediators. Mast cells release cytokines and chemokines that draw additional cells into the mucosa During the early and late phase responses, MCs release cytokines and chemokines to attract additional inflammatory cell types to the nasal mucosa, including neutrophils and eosinophils, group 2 innate lymphoid cells (ILC2), and Th2 cells. IL-4 and IL-13 upregulate adhesion molecules such as VCAM-1 on endothelial cells, which helps eosinophils, T lymphocytes and basophils enter the tissue These cytokines can upregulate the expression of 'adhesion molecules' like vascular cell adhesion molecule 1 (VCAM-1) on the endothelial cells facilitating the infiltration of eosinophils, T lymphocytes and basophils into the nasal mucosa. Th2 cells contribute mainly through IL-5, which activates eosinophils and draws them into the nasal mucosa Activated Th2 cells contribute to allergic inflammation mainly via the release of IL-5, which activates and further recruits eosinophils to the nasal mucosa. Eosinophils then become the dominant cell type of the chronic late-phase process Eosinophils are the predominant cell in the chronic inflammatory process characteristic of the late-phase allergic response. Their release of cationic proteins and leukotrienes sustains swelling. Clinically, this phase is associated with prolonged congestion, which one review describes as lasting roughly 18 to 24 hours The late phase response is characterized by a prolongation of symptoms - sneezing, rhinorrhea but most predominantly a sustained nasal congestion which lasts for about 18-24 h. Reported timing varies between sources: some place onset at 4–6 hours after exposure After 4–6 h of allergens exposure, the late phase of allergic response is initiated., while others give 6–9 hours the late phase response that may occur 6–9 hours after allergen exposure.

Tissue Remodeling and Nasal Hyperreactivity

Persistent disease reflects more than repeated early reactions. Repeated exposure produces priming, meaning the nose responds more strongly to the same allergen over time Priming is the term used to describe increased nasal responsiveness to an allergen with repeated allergen exposure. A repetitive nasal challenge study found that priming occurred both clinically and immunologically, with increases in tissue eosinophils and IL-5 but no detectable structural change There was an increase in early and late-phase symptoms after every allergen challenge compared to diluent, with evidence of both clinical and immunological priming. Nasal tissue eosinophils and IL-5 in nasal secretion increased significantly after RAC compared to corresponding diluent challenges. Eosinophils are considered central to mucosal swelling and hyperreactivity Among them, activated eosinophils is the main player of mucosal swelling and hyperreactivity.

Whether AR involves true airway remodeling is contested. Nasal biopsies in active disease show accumulations of mast cells, eosinophils and basophils, and the reticular basement membrane may thicken slightly, though less than in the lower airways in asthma Nasal biopsies of patients with active AR show accumulations of mast cells, eosinophils, and basophils in the epithelium and an accumulation of eosinophils in the deeper lamina propria. In time, the reticular basement membrane may appear slightly but significantly thickened, but not to the extent seen in the lower airways in asthma. Epithelial damage may also perpetuate disease, since Th2 cytokines can hinder the barrier from resealing, which may keep inflammatory antigens in contact with the mucosa Th2 cytokines also hinder the epithelial barrier from resealing which may maintain the inflammation and exposure to inflammatory antigens. Overall, the evidence on remodeling is described as conflicting, which is why this point remains an open research question.

Classification

Allergic rhinitis (AR) has been sorted in more than one way, and the schemes are not interchangeable. The older system divided the disease by timing of exposure into seasonal and perennial forms. A WHO-coordinated report argued that these subdivisions were unsatisfactory and proposed a classification based on symptoms instead (The authors proposed a new classification for allergic rhinitis, arguing that the current subdivisions (i.e., seasonal and perennial) were not satisfactory.). The Allergic Rhinitis and its Impact on Asthma (ARIA) initiative later built its grid on symptom duration and severity, but the older labels have not disappeared. US drug approvals for AR still follow the seasonal/perennial framework (it is this classification system that the US Food and Drug Administration (FDA) uses when approving new medications for AR.).

Temporal classification: seasonal, perennial and episodic

Seasonal AR is driven mainly by outdoor allergens. Tree, grass, and weed pollens and outdoor mold spores are common seasonal allergens. Because its onset and resolution follow pollen release so closely, it is the form most easily recognized (Seasonal allergic rhinitis (SAR) is fairly easy to identify because of the rapid and reproducible onset and offset of symptoms in association with pollen exposure.).

Perennial AR is driven by allergens that are present all year, such as indoor allergens such as dust mites, pet dander, and molds usually cause perennial symptoms. The boundary between the two is blurred. In some regions, pollen and mold are present year-round (in some places, such as California and Florida, these allergens are present year-round.), and in different climatic regions, the same aeroallergen can be either seasonal or perennial. Mixed patterns are also common. In a large study of young men assessed at a navy hospital, up to 80% of allergic rhinitics have a mixed form, although older estimates from other populations put the mixed group at roughly 40% (approximately 20% of all cases are strictly seasonal, 40% perennial, and 40% mixed (perennial with seasonal exacerbations).).

Episodic AR is a third category used in some European taxonomies, which divide AR into seasonal (SAR), perennial (PAR) and episodic (EAR) types. It describes symptoms that arise from sporadic, short-lived exposure, such as visiting a home with pets. It is not a separate category in the ARIA scheme.

Duration: intermittent and persistent AR

ARIA's duration-based classification uses two thresholds. "intermittent" AR as symptoms that are present less than 4 days per week or for less than 4 consecutive weeks, and "persistent" AR as symptoms that are present more than 4 days/week and for more than 4 consecutive weeks. Symptoms must also be substantial to count: AR patients must encounter two or more of the following clinical symptoms for more than 1 h on most days. Secondary sources sometimes restate the second threshold as weeks per year rather than consecutive weeks (for example, patients with persistent disease have symptoms for more than 4 days/week for more than 4 weeks/year), so the wording should be checked against the original guideline.

Severity: mild and moderate-to-severe AR

Severity is judged by impact on quality of life rather than by symptom count. "Mild" means that none of the following items are present: Sleep disturbance, Impairment of daily activities, leisure and/or sport, Impairment of school or work, Troublesome symptoms. The moderate-severe category is triggered by any one of these items. ARIA's approach was notable because it explicitly used HRQL criteria to assess severity. A 2007 analysis of the same items suggested a finer split, treating patients with 1 to 3 affected items as moderate and those with all four as severe. This was a proposal and did not replace the two-tier ARIA scheme.

Distinguishing IgE-mediated AR from non-allergic rhinitis

AR is defined by its immune mechanism: it is defined as an IgE-mediated, type 1 hypersensitivity response to a spectrum of inhaled environmental allergens. Non-allergic rhinitis (NAR) is a heterogeneous group that does not depend on this pathway. The categories listed in one classification include infectious, perennial (or vasomotor rhinitis), NARES (non allergic rhinitis with eosinophilia syndrome), reflex induced (such as chemical), occupational or caused by atrophy, hormones, exercise or medication induced. Because symptoms overlap, the separation relies on demonstrating sensitization. A small subgroup, local allergic rhinitis, is characterized by nasal mucosa localized allergic response type 2 with the presence of nasal-specific IgE (NsIgE), which means patients may have negative systemic allergy tests yet still have an allergic process confined to the nose.

Occupational rhinitis

Occupational rhinitis is a related category defined by workplace exposure. Allergen-related occupational rhinitis clearly is in the allergic rhinitis category, whereas irritant-related occupational rhinitis is better categorized as nonallergic rhinitis. Allergen sources in workplaces include laboratory animals (e.g., rats, mice, guinea pigs), grains, coffee beans, and wood dust. Clinically, a useful clue is that symptoms improve when away from the workplace.

Allergens and Triggers

Pollen allergens

Pollen is the classic trigger of seasonal AR, and its timing follows the flowering calendar of local plants. Tree pollen is usually associated with the onset of the growing season. Grass pollens appear after local tree pollination, and this may occur earlier in locales where winters are short. Weeds come last. Weed pollen is associated with the late-summer pollen peak, and ragweed is the primary weed pollen in eastern and central North America. Among weeds, ragweed is the most consequential: it accounts for about half of all pollen-associated allergic rhinitis cases in North America. Its major allergen, Amb a 1, is identified in short ragweed, the most allergenic weed.

Grass pollen is especially widespread. Grass pollen is a ubiquitous allergen source worldwide, and in Europe timothy grass is the most prevalent sensitizing pollen. Because grass pollen is light, the wind can carry it easily, so the grass in a neighbor's yard can cause symptoms. Species composition matters as well. Subtropical grasses, including Bermuda, Johnson and para grass, are clinically important in subtropical zones across the Americas, Africa, Asia and Australia. People in subtropical regions show stronger sensitivity to these grasses than to temperate grass species.

Indoor perennial allergens

Indoor allergens cause symptoms throughout the year. Perennial allergic rhinitis is mainly caused by dust mites and animal dander. House dust mites are present in virtually all households, and they tend to be more numerous in bedding, upholstery and carpets. Their growth depends on the environment: they thrive indoors when temperature and humidity are suitable and when shed skin cells, their main food, are available. The main mite species is Dermatophagoides pteronyssinus, and its Der p1 protein is the most allergenic component.

Cockroach allergens come from the insect's saliva and waste. Mold spores are the other common indoor trigger. Outdoor molds are mostly seasonal, dominated by Alternaria alternata, with less frequent species such as Cladosporium herbarum and Botrytis cinerea. Pet allergens are proteins found in animal skin cells (dander), saliva, urine, or sweat on fur. When an animal sheds, fine particles spread into the air and stay suspended for a long time.

Episodic and occupational exposures

Some patients react only when they meet an allergen by chance. Episodic rhinitis arises from an indoor allergen that is infrequently encountered, such as staying overnight in a house with pets, molds, dust mites, cockroaches, or feathers. Pet exposure in another home is therefore a common episodic scenario. The relationship is not simple, however. In one study of adolescents, keeping pets did not increase the risk of sensitization, although sensitization itself was linked to lower-airway inflammation.

Occupational AR is a separate category. Occupational rhinitis is triggered by exposure to irritants and allergens. Allergen-related occupational rhinitis clearly belongs to the allergic rhinitis category. Examples of occupational allergens include animals and wood dust. In laboratory settings, workers exposed to proteins from laboratory animals, including urine, dander and saliva, as well as bedding, feed, mold and insects, may develop allergic symptoms.

Regional differences

The dominant allergens vary widely by geography, and this shapes both prevalence patterns and clinical choices. In a national Brazilian...

In a national study of patients in a (sub)tropical country, patients in the tropical region were almost all sensitized to house dust mites (87%), while sensitization in the central agricultural zones was mainly to grass and tree pollen. In some areas pollens and molds are effectively perennial, such as grass pollen in southern California and Florida, or Parietaria pollen in the Mediterranean. Pet sensitization also differs by setting. In a Beijing series of nearly 48,000 patients, pets were the second most common indoor allergen, with cat (26.6%) and dog (13.7%) sensitization. Smaller series can show the opposite pattern; one small Indian cohort found very low cat dander and dog fur sensitization (1.9% each), while house dust mite was the most common allergen there.

These differences matter in practice. Skin-test panels and immunotherapy extracts are usually built around the allergens that dominate in a given area, so a panel suited to a temperate, pollen-driven region may miss the mites or grasses that drive symptoms elsewhere. Local allergen surveillance therefore informs which tests are useful and which extracts are worth prescribing.

Diagnosis and Differential Diagnosis

Clinical history and examination as the core

Diagnosis rests first on the patient's history and physical examination. The diagnosis is based on the clinical history and, if needed in patients with uncontrolled rhinitis despite medications or with long-lasting symptoms, on skin tests or the presence of serum-specific IgE antibodies to allergens. In a typical presentation, routine laboratory testing or imaging is not required. Testing is instead considered when the diagnosis is in doubt, when symptoms stay poorly controlled despite appropriate treatment, when identifying specific triggers would shape avoidance measures, or when allergen immunotherapy is being considered (Medscape).

Skin prick testing and serum allergen-specific IgE

Skin prick testing (SPT) is generally the preferred method. It is minimally invasive, inexpensive, results are immediately available and when carried out by trained health professionals, reproducible. A positive reaction is read at 15 to 20 minutes, with a wheal of at least 3 mm defined as positive. Serum allergen-specific IgE (sIgE) testing serves as the alternative when skin testing is contraindicated or cannot be interpreted reliably (Medscape). Total serum IgE has little diagnostic value, because normal levels do not exclude AR and elevated levels are nonspecific (Medscape).

The main limitation of both tests is that they show sensitization rather than clinical allergy. These tests only denote sensitization, and atopy and allergy represent two different phenomena. A small retrospective Brazilian study of 42 patients reported 90% sensitivity for dust mite SPT versus 66.7% for dust mite sIgE, illustrating that the two methods do not perform identically (PMC4406598). Intradermal testing is considered unreliable for cat and timothy grass because of a high false-positive rate (PubMed 26708395). When results are discordant, the nasal provocation test is the reference method for local allergic rhinitis, a condition in which SPT and sIgE are negative but the nasal challenge is positive (PMC12653089). Because this test is not routinely performed, it is generally reserved for specialist settings.

Sinus imaging

Routine sinonasal imaging is discouraged. The 2015 AAO-HNSF guideline advises clinicians not to routinely perform sinonasal imaging in patients presenting with symptoms consistent with a diagnosis of allergic rhinitis. The international consensus on allergy and rhinology reached a similar conclusion, noting that there are no high-quality studies demonstrating a role for imaging in the diagnosis of AR. Cost and concern for ionizing radiation with CT scanning, along with risk for future malignancy also weigh against its use. Imaging is instead reserved for suspected chronic or complicated rhinosinusitis, structural abnormalities, neoplasm, or other conditions requiring anatomic assessment (Medscape).

Differential diagnosis

Non-allergic rhinitis (NAR) is a heterogeneous group. It includes infectious rhinitis, hormonal rhinitis, vasomotor rhinitis, non allergic rhinitis with eosinophilia syndrome (NARES), certain types of occupational rhinitis and gustatory and drug induced rhinitis. Clinically, NAR tends to differ from AR in age of onset and symptom profile. 70% of patients with non-allergic rhinitis present after the age of 20, and patients with NAR typically complain of nasal congestion and rhinorrhea and rarely have significant pruritus or sneezing. Mixed allergic and non-allergic rhinitis is also common, with one review estimating that from 44-87% of people with rhinitis have "mixed" allergic and non-allergic rhinitis. Some local allergic rhinitis cases are usually either underdiagnosed or misdiagnosed and assigned to the non-allergic rhinitis group.

Infectious rhinosinusitis must be separated from AR by the time course and inflammatory pattern. Acute rhinosinusitis is defined as up to four weeks of purulent nasal drainage (anterior, posterior or both) accompanied by nasal obstruction, facial pain-pressure-fullness or both. A diagnosis of chronic rhinosinusitis requires that inflammation be documented after evaluation of the nasal cavity and/or computerized tomography (CT) imaging, as well as symptoms less than 12 weeks. Histologically, neutrophilia infiltrates are usually seen with infectious rhinitis.

Structural nasal disease calls for a different workup. Persistent unilateral obstruction or drainage, recurrent epistaxis, a visible mass, marked facial pain, or suspected structural disease warrants further examination, nasal endoscopy, or imaging as clinically indicated. Persistent unilateral clear rhinorrhea after trauma or sinonasal surgery should also prompt evaluation for a cerebrospinal fluid leak (Medscape). Medication-induced rhinitis, including rhinitis caused by drugs that are not themselves allergens, falls under the NAR umbrella (JACI: In Practice), and it should be considered when a patient's symptoms begin or worsen after a new medication.

Pharmacological Treatment

Drug therapy for allergic rhinitis (AR) targets two components of the disease: the early histamine-driven response and the later inflammatory response that produces prolonged congestion. The ARIA–EAACI 2024–2025 revision, which is organised around intranasal treatments and oral and ocular treatments, reflects a clear move toward intranasal routes and fixed combinations, although much of the supporting evidence is of low or very low certainty.

Antihistamines

Second-generation H1-antihistamines, taken orally, are the usual choice for sneezing, itching, and watery rhinorrhea, because they block histamine at its receptor with less sedation than older agents. Intranasal antihistamines such as azelastine and olopatadine act directly on the nasal mucosa and are effective in both allergic and non-allergic rhinitis, according to a U.S. state drug-review document (Intranasal antihistamines, such as azelastine (Astepro®) and olopatadine (Patanase®), are effective treatments for AR and NAR.). Because histamine contributes little to the late-phase swelling that causes congestion, antihistamines help less with a blocked nose than with the other symptoms.

Intranasal corticosteroids

Intranasal corticosteroids (INCS) are the most effective single option for persistent disease. Their anti-inflammatory action suppresses the eosinophilic late-phase response that the allergy literature links to lasting obstruction. Guidance reserves them for patients whose symptoms impair quality of life, and a Texas review notes that they remain the preferred monotherapy for persistent AR (Intranasal corticosteroids (INCS) remain the preferred monotherapy for persistent AR; however, additional studies support the additive benefit of combination treatment with INCS and intranasal antihistamines.). When a clinician must choose a single spray, the 2024–2025 ARIA recommendations favour a corticosteroid over an antihistamine (Overall, we suggest using INAH+INCS over INAH or INCS and INCS over INAH.).

Fixed antihistamine–corticosteroid combinations

The most notable change in the 2024–2025 revision concerns combination sprays. The earlier 2010 and 2016 editions treated a combined spray and a corticosteroid alone as roughly equivalent options; the newer revision instead gives a conditional recommendation in favour of the combination (Recommendation changed from conditional recommendation either for either INAH + INCS or INCS (2010/2016 guidelines) to a conditional recommendation in favor of INAH + INCS (2024–2025 guidelines).). The rationale is that the combination addresses both the early and late phases, which is why the combination is positioned as a step-up option for moderate-to-severe disease. The certainty behind this advice differs by season: the panel's evidence rating is moderate for seasonal AR but very low for perennial AR. Commonly used products include azelastine–fluticasone and olopatadine–mometasone, and for seasonal AR the panel prefers azelastine–fluticasone ("In patients with AR, we suggest using azelastine‐fluticasone over olopatadine‐mometasone.").

Leukotriene receptor antagonists

Oral leukotriene receptor antagonists (LTRAs), chiefly montelukast, play a limited role. ARIA Part II favours oral antihistamines over LTRAs and advises against adding an LTRA to an oral antihistamine, since the combination shows no clinically relevant added benefit and costs more (OAH + LTRA show no added clinically relevant benefit over OAH alone and result in increased costs.). In the United States, the FDA added a boxed warning in 2020 for neuropsychiatric events, including suicidal thoughts, and advised reserving montelukast for allergic rhinitis in patients who have responded inadequately to, or cannot tolerate, other therapies (FDA is requiring a Boxed Warning stating that serious neuropsychiatric events that may include suicidal thoughts or actions have been reported in patients taking montelukast (Singulair).).

Intranasal decongestants

Topical decongestants such as oxymetazoline relieve congestion quickly, but they are generally not recommended for long-term use. Short courses of about three to five days work well, whereas prolonged use can lead to rebound congestion, known as rhinitis medicamentosa (When used briefly (<3–5 days consecutively), α-adrenergic decongestants provide fast and effective relief of nasal congestion. However, with chronic use, rebound nasal congestion can occur and can be severe.). Rebound typically appears after five to seven days of use, and nearly half of people who self-treat persistent rhinitis overuse these sprays (Typically, RM develops after 5 to 7 days of topical decongestant use.). The 2024–2025 ARIA guidance advises against adding a decongestant to an intranasal corticosteroid when the steroid alone is already being used (In patients with AR, we suggest against using a combination of an INCS + intranasal decongestant over an INCS alone. (Conditional recommendation based on very low certainty of evidence).). Some data suggest that daily steroid cover reduces the risk of rebound, but this does not change the guideline's view that the combination offers no clear efficacy gain.

Allergen Avoidance and Allergen Immunotherapy

Allergen avoidance

Avoidance is the first step in managing AR, but its benefits are limited. Physical and chemical measures can substantially lower allergen load, yet a systematic review found little evidence that these reductions lead to lasting clinical improvement significant reductions of allergen load can be achieved by physical and chemical means, but there is little evidence at present that these reductions translate into sustained improvements in clinical outcomes. Routine advice to use impermeable mattress covers is not supported: studies have not found any benefit to using mite-proof impermeable mattresses or pillow covers. For house dust mites, the evidence is weak overall. Reducing exposure does not necessarily reduce symptoms, and avoidance has not shown a clear clinical benefit for patients who already have perennial AR or asthma, although infants and children with a genetic predisposition to asthma may gain some benefit evidence on the efficacy of avoidance is poor, and reduction in mite exposure does not necessarily reduce symptoms. No overall clinical benefit has been demonstrated from avoidance measures to patients already suffering from HDM-related perennial AR and/or asthma, but babies and children with a genetic predisposition to asthma may benefit from mite avoidance. The limit is structural: pollen and mites are present in nearly every indoor and outdoor setting, so practical avoidance rarely removes exposure enough to control symptoms, which is why pharmacotherapy remains necessary.

Mechanism of allergen-specific immunotherapy

Allergen-specific immunotherapy (AIT) is the only approach that aims to change the underlying immune response to a specific allergen rather than simply suppress symptoms. Its central step is the induction of regulatory T cells (Treg) and the establishment of immune tolerance. Repeated exposure to the causative allergen generates allergen-specific Treg cells that secrete the anti-inflammatory cytokines IL-10 and TGF-β, which restrain effector cells such as Th2 cells Peripheral T cell tolerance is characterized by the generation of allergen-specific Treg cells that are able to produce anti-inflammatory cytokines such as IL-10 and TGF-β. A rapid effect also occurs early in treatment, when mast cell and basophil degranulation falls shortly after the first dose An early desensitization effect including decrease in mast cell and basophil degranulation soon after the first administration of allergens.

The later changes concern antibody isotypes. IL-10 pushes B cells toward producing IgG4 instead of IgE IL-10, the major cytokine, suppresses IgE production through Treg cell–B cell interaction.. The IgG4 produced competes with IgE for allergen binding on mast cells and basophils Together with IgG_2, IgG_4 induced following AIT competes with IgE for binding of allergens on mast cells and basophils.. The clinical consequence is a durable benefit: The most prominent advantage of SIT compared with pharmacotherapy is the maintenance of its long-term efficacy after the end of treatment.

Subcutaneous versus sublingual immunotherapy

The two main routes differ mainly in how they are given and how they are monitored. SCIT involves injections in a clinical setting, whereas SLIT tablets are placed under the tongue and can be taken at home. SLIT's favorable safety profile permits home administration, significantly increasing convenience and accessibility for families, whereas SCIT mandates administration in a clinical setting equipped to manage potential systemic reactions. This difference drives the monitoring requirements. The main safety concern with SCIT is systemic reaction, and a systematic review found that SLIT consistently showed a more favorable safety profile (mainly local reactions), whereas SCIT carried a higher risk of systemic reactions. Uncontrolled severe asthma is among the frequent contributors to SCIT-related adverse events Severe, not controlled asthma, and medical error were the most frequent causes of SCIT-induced adverse events.

On efficacy, the two routes are broadly comparable for core symptoms, though not identical. One 2025 systematic review of children concluded that SLIT offers comparable efficacy for many outcomes with better safety/convenience, while SCIT may have advantages for certain outcomes but requires clinic administration. Adherence is a practical differentiator: Adherence can be a problem. for SLIT, while SCIT adherence is easier to verify. The licensed SLIT range has also been narrow in some markets; a 2015 review noted that sublingual products were then available only for a limited set of grass and ragweed pollens, a situation that has since widened.

Patient selection

AIT is considered for patients whose symptoms are significant despite avoidance and standard drug therapy. Both routes are indicated for patients who have evidence of clinically relevant allergen-specific IgE, and significant symptoms despite reasonable avoidance measures and/or maximal medical therapy. In practice, the clearest indication is moderate or severe persistent allergic rhinitis that is not responsive to usual treatments, along with patients who cannot tolerate standard drugs. The evidence base is strongest in adults, and in children evidence base in children is less convincing; more studies are needed. Questions about long-term outcomes and disease progression are discussed in the final section.

Comorbidities and the Unified Airway

Asthma

Allergic rhinitis (AR) and asthma are so often found together that clinicians treat them as linked conditions. A systematic review and meta-analysis of 29 studies, with about 274,000 participants, found that a history of AR was significantly associated with the later occurrence of asthma (pooled OR about 3.8). The relationship is also temporal: in a 1990s-era case-control study, about three-quarters of asthma patients reported rhinitis before their first wheezing episodes. In children, AR often comes first, a sequence described as the "asthma march," and the severity of AR has been linked to later asthma risk. In adults, a retrospective cohort found that AR at baseline strongly predicted new-onset asthma ten years later, after adjustment for other risk factors. Allergen immunotherapy was associated with a lower risk of new asthma in that cohort, but the design is observational, so a causal effect is not established.

The reverse direction also matters. Asthma onset in a child with AR appears to worsen the rhinitis, and AR is a recognized trigger for asthma exacerbations. Whether controlling AR can prevent asthma remains an open question: treating rhinitis to prevent asthma is a proposed strategy, but the knowledge of which factors drive progression from AR to asthma is limited.

Chronic Rhinosinusitis, Otitis Media with Effusion and Conjunctivitis

Chronic rhinosinusitis (CRS) frequently coexists with AR, and the combination appears to add to respiratory risk. In a large retrospective cohort of patients with nasal polyps, those with coexisting AR had a higher risk of new-onset asthma at one year than those with polyps alone, and the risk of asthma exacerbation was also greater. An earlier case-control study found that rhinitis and sinusitis together carried a higher odds of asthma than either condition alone.

Otitis media with effusion and conjunctivitis are generally linked to AR through shared mechanisms rather than through a single demonstrated causal pathway. The Eustachian tube drains and ventilates the middle ear through the nasopharyngeal mucosa, so nasal and nasopharyngeal swelling can impair middle-ear pressure regulation and favour fluid accumulation, a concern that is most relevant in children. Ocular itching and tearing reflect the same mast-cell and mediator activity that drives nasal symptoms in the conjunctiva. The strength of these associations varies across studies, and they are best described as clinically recognized overlaps rather than fully quantified risks.

Sleep, Fatigue and Cognition

Sleep disturbance is one of the most consequential effects of AR. Studies indicate that roughly 40–60% of patients with AR report sleep quality problems, which include difficulty falling asleep, frequent nocturnal awakening, fragmented sleep architecture and daytime sleepiness. Nasal obstruction raises upper-airway resistance, which encourages mouth breathing, snoring and non-restorative sleep. A placebo-controlled study of intranasal fluticasone propionate found that improvement in nasal congestion was accompanied by less daytime sleepiness and better cognitive performance, while the placebo group showed no significant change. Sedating antihistamines, by contrast, can worsen daytime somnolence and are generally advised against in these patients.

Cognitive effects are reported in adults more consistently than in children. AR can by itself produce sedation and impaired cognitive performance, and disturbed sleep adds to fatigue and reduced daytime function. Reviews describe a self-reinforcing cycle in which symptoms cause poor sleep, poor sleep worsens mood, and worsened mood heightens the perception of symptoms. In children, the evidence is mixed: some studies link AR to poorer attention and examination performance, while others find no clear association.

The Rationale for an Integrated Airway Approach

The concept of a "united airway" rests on the observation that the upper and lower airways share anatomical features, histology, causes and pathophysiological mechanisms, and they often respond similarly to therapy. The ARIA initiative was framed as a public-health effort to unify the management of rhinitis and asthma, which had long been handled separately. Proponents of the concept acknowledge that the two airway regions also differ, so the model is an organizing principle rather than a claim of identity. In practice, treating rhinitis is considered important in patients with asthma because it can improve control of both conditions. Scoping reviews, however, note that the interactions between upper and lower airways are still incompletely understood, and that more studies are needed. Integrated care pathways, which set out interdisciplinary milestones for patients with rhinitis and asthma, are one way to translate this rationale into routine care.

Epidemiology and Socioeconomic Burden

Prevalence across regions and age groups

Prevalence estimates vary with how AR is defined and which population is surveyed. The ARIA 2024–2025 documents put the worldwide total at about 400 million people, affecting an estimated 10%-30% of the adult population. Other reviews give a wider adult range of 10–40%, and an ARIA-Italy paper reports 5% and 35%, with marked regional differences linked to pollution and allergen exposure. In some high-income countries, lifetime prevalence has been reported at up to half the population.

Prevalence also differs by age. In a Malaysian pediatric study, overall symptom prevalence was 27%, with the 12–14-year-old group (38.2%) far above the 5–7-year-old group (18.2%). Trend data suggest the burden is growing: recent studies show a rising trend in physician-diagnosed AR, with rates nearly doubling in the last decade. In the United States, one widely cited estimate puts symptoms in 26 percent of adults and 19 percent of children.

Economic burden in the United States

Most detailed cost data come from the United States, and the estimates have shifted with each data source. A cost-of-illness analysis based on the 1987 National Medical Expenditure Survey estimated that approximately 39 million persons in the United States experienced allergic rhinitis in 1987. However, only 12.3% (4.8 million) sought medical treatment. The total cost was $1.23 billion, in 1994 dollars. Direct medical expenses accounted for 94% of total costs. A later estimate put direct costs at $3.4 billion, with the majority attributable to prescription medications (46.6%) and outpatient visits (51.9%).

Indirect costs are harder to measure. Productivity losses tied to a diagnosis were estimated at $601 million in the 1995 National Health Interview Survey, but when sedating over-the-counter antihistamine use and self-reported at-work impairment were included, at-work productivity losses were estimated to range from $2.4 billion to $4.6 billion. An employer-based study found that allergic rhinitis was associated with the highest costs from lost productivity, with a mean productivity loss of $593 per employee per year. A 2024 analysis of app users estimated a median cost of 507.8 US$ per person during poorly controlled weeks, and found that presenteeism contributed more to these costs than absenteeism.

These figures describe the American health system and labor market in different years, using different methods (national surveys, employer data, and app-based monitoring). They are not directly comparable with one another, and they should not be transferred to other countries without adjustment.

Risk factors

A family history of atopy is among the most consistently reported risk factors for AR. Early-life patterns also matter: the allergic march is a trend of atopic dermatitis and food allergies in babies that progresses to chronic respiratory problems in school-aged children, including AR and asthma. Urbanization is another factor. Rising prevalence has been particularly among urban populations, which is consistent with the role of traffic-related and other air pollution. Environmental exposures in early childhood, including microbial exposure (the basis of the hygiene hypothesis), are considered candidate influences, but the evidence for them is less settled.

Climate change and allergen exposure

Rising temperatures and carbon dioxide levels are altering pollen seasons. One projection for the continental United States estimates that warmer end-of-century temperatures (4–6 K) shift the start of spring emissions 10–40 days earlier and summer/fall weeds and grasses 5–15 days later and lengthen the season duration. The same model suggests that the annual total pollen emission could increase by 16–40%. Warmer conditions and air pollution may also make pollen more allergenic, and some new allergenic plant species are spreading into regions where they could not previously survive. Direct evidence of the effect of CO₂ is less certain, since much of the work on pollen output comes from chamber experiments on a limited number of species. A 2025 scoping review found that sixteen studies reported longer pollen seasons and/or higher pollen concentrations related to climate change, and that low-income residents were most impacted by increased usage of healthcare services for AR. As seasons lengthen, AR symptoms are present throughout the year for some patients, which has direct implications for treatment planning.

Guideline Development and Evolution

The Allergic Rhinitis and its Impact on Asthma (ARIA) initiative was started at a World Health Organization workshop in 1999. ARIA was initiated during a World Health Organization workshop in 1999 and has evolved in five phases. Its first edition appeared in print in 2001, and later revisions were published in 2008, 2010, 2016 and 2019 (some sources date the MASK-air integration to 2020). Asthma (ARIA) guidelines had their first edition in 1999 (published in 2001), with subsequent revisions published in 2008, 2010, 2016, and 2020. The early documents took a single-airway view, giving treatment advice for rhinitis on the basis of the concept of "one airway, one disease."

From consensus document to GRADE-based guideline

The 2010 revision was a methodological turning point. It was the first evidence-based guideline in allergy to follow the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) approach. GRADE links the strength of a recommendation to the certainty of the evidence and also records the benefits, harms and assumed patient values behind it. ARIA 2010 and 2016 devised a medication algorithm, which made the pharmacological advice more directly usable in clinical practice.

The 2016 revision was a targeted update rather than a full rewrite. By using a modified Delphi process, the ARIA guideline panel selected new questions that required answering with recommendations or the existing recommendations that required an updated review of the evidence. Its certainty ratings were modest: most of the recommendations are based on low- or very low-certainty evidence, mainly because of the imprecision of the estimated effects due to few patients being studied.

The 2019 next-generation guidelines marked a further shift. They used real-life MASK-air data and allergen exposure chamber studies and proposed digitally enabled, person-centred care for the first time. Real-world evidence was used alongside randomized trials, which are often narrow in their applicability.

The 2024–2025 ARIA–EAACI revision

The current revision is developed with the European Academy of Allergy and Clinical Immunology (EAACI) and follows the GRADE framework. Its evidence base is broader than in earlier editions: it draws on systematic reviews and meta-analyses, mHealth data and pharmacovigilance data, among others. Patient-generated data are also counted as evidence, because they better reflect the affected individuals' perspectives. Question generation used expert surveys and artificial intelligence (AI)-based tools to analyse web searches on allergic rhinitis. Each prioritised question is assessed in an evidence-to-decision framework with 12 criteria. In ARIA-EAACI 2024-2025, 42 questions on AR management were voted by guideline panel members as "prioritised questions". The output is being published in parts, and the first two reports cover intranasal treatments and oral and ocular treatments.

Comparison with other guideline bodies

The Joint Task Force on Practice Parameters (JTFPP), representing the American Academy of Allergy, Asthma and Immunology and the American College of Allergy, Asthma and Immunology, is the main US counterpart. Its 2017 update made specific recommendations for seasonal allergic rhinitis. For patients aged 12 years or older, clinicians should routinely prescribe monotherapy with an INCS rather than a combination of oral antihistamines and INCSs. In its 2020 update, the only GRADE recommendations were those previously published in the 2017 rhinitis guideline update. The remainder of the recommendations are consensus-based statements. This reflects a practical constraint: it was cost prohibitive to attempt to conduct a GRADE analysis for all of the questions. Where ARIA emphasises a formal, evidence-graded approach across many questions, the JTFPP relies more heavily on expert judgement where evidence is thin.

Their treatment algorithms also differ in detail. The JTFPP summary advises that moderate/severe persistent symptoms should have INAH and INCS combination therapy, and that leukotriene receptor antagonists are not recommended for initial treatment of allergic rhinitis. The American Academy of Otolaryngology–Head and Neck Surgery Foundation guideline, written from an ENT perspective, is not compared point by point here.

Gaps between guidance and prescribing

Recommendations do not always reach routine care. An analysis of ARIA implementation found that they have not yet found their way into the daily routine of general practitioners. In that analysis, only 16% of the general practitioners followed the guideline recommendations. By contrast, more than 50% of patients with rhinitis and concomitant asthma were treated according to the guidelines in post-2001 studies of ENT specialists. The gap is therefore largest in primary care, where most patients with allergic rhinitis are first seen.

Open Questions and Future Directions

The 2024–2025 ARIA–EAACI revision was built as a person-centred, digitally enabled guideline that is assisted by artificial intelligence and uses the GRADE approach. Its structure also makes the guideline a living document rather than a fixed edition. One unresolved question is how far recommendations should be tailored by region. Pollen seasons, allergen mixes, and drug availability differ between countries, and the ARIA group has moved toward regionally tailored recommendations within this living format. The evidence I reviewed does not show whether such local algorithms produce better outcomes than a single global standard. The balance between local adaptation and consistent guidance is therefore still a matter of judgment.

Digital tools are the second open area. A systematic review of 120 studies published between 2010 and 2025, most of them randomized trials, found that digital approaches improved symptom control and medication adherence in many settings. Telemedicine reduced the number of visits, and wearable devices that record measures such as fractional exhaled nitric oxide and nasal resistance increased diagnostic accuracy. The same review noted that current AI systems rely largely on what patients report about themselves and their environment. An AI-enabled smartwatch trial showed better adherence and lower symptom scores than self-report, but the authors of a separate systematic review pointed to a concentration of studies in a few regions, weak external validation, and poor reporting of model calibration. Tool quality is also uneven. An automated search of app stores in three countries retrieved 1,593 apps, only 21 of which were relevant, and only two could calculate the combined symptom-medication score that is used in trials. A 60-day pilot of a pollen-based self-management app found that two-thirds of its 46 participants felt better informed, but a pilot of this size cannot establish effects on outcomes. The central task is therefore to validate these tools and to determine how they can support shared decision-making without replacing clinical judgment.

Long-term outcomes of allergen-specific immunotherapy form the third area. Immunotherapy remains the only disease-modifying treatment for IgE-mediated diseases, and one review estimated that long-term symptomatic relief occurs in about 65–90% of patients, while a small subset does not respond. Follow-up studies suggest that some protective effects persist after treatment stops; in one study, inhibitory antibody activity remained for two years after discontinuation. Evidence that treatment in childhood reduces the later development of asthma is encouraging, but long-term real-life data, especially for pollen immunotherapy in asthma, remain limited. Key questions include the optimal duration and dosing, whether preventive effects last into adulthood, and whether the immune changes seen during treatment translate into durable slowing of disease progression.

The fourth area is the search for biomarkers that predict response. Earlier reviews reported that no surrogate biomarker was yet predictive of clinical response to immunotherapy. More recent work has examined ratios of allergen-specific to total IgE, functional IgG4 activity, cytokines such as IL-10 and IL-35, and basophil-based tests, and some proposals combine these into composite scores. These markers still require prospective validation before clinical use. The same need applies to drug therapy, where predicting which patients benefit from particular agents would help avoid trial-and-error prescribing. Finally, the value of co-medication strategies and of as-needed rather than continuous treatment, in terms of symptom control, cost, and adherence, is still under evaluation, and the conclusions drawn so far are provisional.

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