Hubbry Logo
Allergic rhinitisAllergic rhinitisMain
Open search
Allergic rhinitis
Community hub
Allergic rhinitis
logo
8 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Allergic rhinitis
Allergic rhinitis
Allergic rhinitis
View on Wikipedia
from Wikipedia
Allergic rhinitis
Other namesHay fever, pollenosis
SEM Microscope image of pollen grains from a variety of common plants: sunflower (Helianthus annuus), morning glory (Ipomoea purpurea), prairie hollyhock (Sidalcea malviflora), oriental lily (Lilium auratum), evening primrose (Oenothera fruticosa), and castor bean (Ricinus communis).
SpecialtyAllergy and immunology
SymptomsStuffy itchy nose, sneezing, red, itchy, and watery eyes, swelling around the eyes, itchy ears[1]
Usual onset20 to 40 years old[2]
CausesGenetic and environmental factors[3]
Risk factorsAsthma, allergic conjunctivitis, atopic dermatitis[2]
Diagnostic methodBased on symptoms, skin prick test, blood tests for specific antibodies[4]
Differential diagnosisCommon cold[3]
PreventionExposure to animals early in life[3]
MedicationNasal steroids, antihistamines such as loratadine, cromolyn sodium, leukotriene receptor antagonists such as montelukast, allergen immunotherapy[5][6]
Frequency~20% (Western countries)[2][7]
Approximately 10% to 40% of the global population[8]

Allergic rhinitis, of which the seasonal type is called hay fever, is a type of inflammation in the nose that occurs when the immune system overreacts to allergens in the air.[6] It is classified as a type I hypersensitivity reaction.[9] Signs and symptoms include a runny or stuffy nose, sneezing, red, itchy, and watery eyes, and swelling around the eyes.[1] The fluid from the nose is usually clear.[2] Symptom onset is often within minutes following allergen exposure, and can affect sleep and the ability to work or study.[2][10] Some people may develop symptoms only during specific times of the year, often as a result of pollen exposure.[3] Many people with allergic rhinitis also have asthma, allergic conjunctivitis, or atopic dermatitis.[2]

Allergic rhinitis is typically triggered by environmental allergens such as pollen, pet hair, dust mites, or mold.[3] Inherited genetics and environmental exposures contribute to the development of allergies.[3] Growing up on a farm and having multiple older siblings are associated with a reduction of this risk.[2] The underlying mechanism involves IgE antibodies that attach to an allergen, and subsequently result in the release of inflammatory chemicals such as histamine from mast cells.[2] It causes mucous membranes in the nose, eyes and throat to become inflamed and itchy as they work to eject the allergen.[11] Diagnosis is typically based on a combination of symptoms and a skin prick test or blood tests for allergen-specific IgE antibodies.[4] These tests, however, can give false positives.[4] The symptoms of allergies resemble those of the common cold; however, they often last for more than two weeks and, despite the common name, typically do not include a fever.[3]

Exposure to animals early in life might reduce the risk of developing these specific allergies.[3] Several different types of medications reduce allergic symptoms, including nasal steroids, intranasal antihistamines such as olopatadine or azelastine, 2nd generation oral antihistamines such as loratadine, desloratadine, cetirizine, or fexofenadine; the mast cell stabilizer cromolyn sodium, and leukotriene receptor antagonists such as montelukast.[12][5] Oftentimes, medications do not completely control symptoms, and they may also have side effects.[2] Exposing people to larger and larger amounts of allergen, known as allergen immunotherapy, is often effective and is used when first line treatments fail to control symptoms.[6] The allergen can be given as an injection under the skin or as a tablet under the tongue.[6] Treatment typically lasts three to five years, after which benefits may be prolonged.[6]

Allergic rhinitis is the type of allergy that affects the greatest number of people.[13] In Western countries, between 10 and 30% of people are affected in a given year.[2][7] It is most common between the ages of twenty and forty.[2] The first accurate description is from the 10th-century physician Abu Bakr al-Razi.[14] In 1859, Charles Blackley identified pollen as the cause.[15] In 1906, the mechanism was determined by Clemens von Pirquet.[13] The link with hay came about due to an early (and incorrect) theory that the symptoms were brought about by the smell of new hay.[16][17]

Signs and symptoms

[edit]
Illustration depicting inflammation associated with allergic rhinitis

The characteristic symptoms of allergic rhinitis are: rhinorrhea (excess nasal secretion), itching, sneezing fits, and nasal congestion/obstruction.[18] Characteristic physical findings include conjunctival swelling and erythema, eyelid swelling with Dennie–Morgan folds, lower eyelid venous stasis (rings under the eyes known as "allergic shiners"), swollen nasal turbinates, and middle ear effusion.[19] Nasal endoscopy may show findings such as pale and boggy inferior turbinates from mucosal edema, stringy mucus throughout the nasal cavities, and cobblestoning.[20][21]

There can also be behavioral signs; in order to relieve the irritation or flow of mucus, people may wipe or rub their nose with the palm of their hand in an upward motion: an action known as the "nasal salute" or the "allergic salute". This may result in a crease running across the nose (or above each nostril if only one side of the nose is wiped at a time), commonly referred to as the "transverse nasal crease", and can lead to permanent physical deformity if repeated enough.[22]

People might also find that cross-reactivity occurs.[23] For example, people allergic to birch pollen may also find that they have an allergic reaction to the skin of apples or potatoes.[24] A clear sign of this is the occurrence of an itchy throat after eating an apple or sneezing when peeling potatoes or apples. This occurs because of similarities in the proteins of the pollen and the food.[25] There are many cross-reacting substances. Hay fever is not a true fever, meaning it does not cause a core body temperature in the fever over 37.5–38.3 °C (99.5–100.9 °F).[citation needed]

Cause

[edit]

Pollen is often considered as a cause of allergic rhinitis, hence called hay fever (See sub-section below).[citation needed]

Predisposing factors to allergic rhinitis include eczema (atopic dermatitis) and asthma. These three conditions can often occur together which is referred to as the atopic triad.[26] Additionally, environmental exposures such as air pollution and maternal tobacco smoking can increase an individual's chances of developing allergies.[26]

[edit]

Allergic rhinitis triggered by the pollens of specific seasonal plants is commonly known as "hay fever", because it is most prevalent during haying season. However, it is possible to have allergic rhinitis throughout the year. The pollen that causes hay fever varies between individuals and from region to region; in general, the tiny, hardly visible pollens of wind-pollinated plants are the predominant cause. The study of the dispersion of these bioaerosols is called Aerobiology. Pollens of insect-pollinated plants are too large to remain airborne and pose no risk. Examples of plants commonly responsible for hay fever include:

Allergic rhinitis may also be caused by allergy to Balsam of Peru, which is in various fragrances and other products.[28][29][30]

Genetic factors

[edit]

The causes and pathogenesis of allergic rhinitis are hypothesized to be affected by both genetic and environmental factors, with many recent studies focusing on specific loci that could be potential therapeutic targets for the disease. Genome-wide association studies (GWAS) have identified a number of different loci and genetic pathways that seem to mediate the body's response to allergens and promote the development of allergic rhinitis, with some of the most promising results coming from studies involving single-nucleotide polymorphisms (SNPs) in the interleukin-33 (IL-33) gene.[31][32] The IL-33 protein that is encoded by the IL-33 gene is part of the interleukin family of cytokines that interact with T-helper 2 (Th2) cells, a specific type of T cell. Th2 cells contribute to the body's inflammatory response to allergens, with specific ST2 receptors—also known as IL1RL1—on these cells binding to the ligand IL-33. This IL-33/ST2 signaling pathway has been found to be one of the main genetic determinants in bronchial asthma pathogenesis, and because of the pathological linkage between asthma and rhinitis, the experimental focus of IL-33 has now turned to its role in the development of allergic rhinitis in humans and mouse models.[33] Recently, it was found that allergic rhinitis patients expressed higher levels of IL-33 in their nasal epithelium and had a higher concentration of ST2 serum in nasal passageways following their exposure to pollen and other allergens, indicating that this gene and its associated receptor are expressed at a higher rate in allergic rhinitis patients.[34] In a 2020 study on polymorphisms of the IL-33 gene and their link to allergic rhinitis within the Han Chinese population, researchers found that five SNPs specifically contributed to the pathogenesis of allergic rhinitis, with three of those five SNPs previously identified as genetic determinants for asthma.[35]

Another study focusing on Han Chinese children found that certain SNPs in the protein tyrosine phosphatase non-receptor 22 (PTPN22) gene and cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) gene can be associated with childhood allergic rhinitis and allergic asthma.[36] The encoded PTPN22 protein, which is found primarily in lymphoid tissue, acts as a post-translational regulator by removing phosphate groups from targeted proteins. Importantly, PTPN22 can affect the phosphorylation of T cell responses, and thus the subsequent proliferation of the T cells. As mentioned earlier, T cells contribute to the body's inflammatory response in a variety of ways, so any changes to the cells' structure and function can have potentially deleterious effects on the body's inflammatory response to allergens. To date, one SNP in the PTPN22 gene has been found to be significantly associated with allergic rhinitis onset in children. On the other hand, CTLA-4 is an immune-checkpoint protein that helps mediate and control the body's immune response to prevent overactivation. It is expressed only in T cells as a glycoprotein for the Immunoglobulin (Ig) protein family, also known as antibodies. There have been two SNPs in CTLA-4 that were found to be significantly associated with childhood allergic rhinitis. Both SNPs most likely affect the associated protein's shape and function, causing the body to exhibit an overactive immune response to the posed allergen. The polymorphisms in both genes are only beginning to be examined, therefore more research is needed to determine the severity of the impact of polymorphisms in the respective genes.[citation needed]

Finally, epigenetic alterations and associations are of particular interest to the study and ultimate treatment of allergic rhinitis. Specifically, microRNAs (miRNA) are hypothesized to be imperative to the pathogenesis of allergic rhinitis due to the post-transcriptional regulation and repression of translation in their mRNA complement. Both miRNAs and their common carrier vessel exosomes have been found to play a role in the body's immune and inflammatory responses to allergens. miRNAs are housed and packaged inside of exosomes until they are ready to be released into the section of the cell that they are coded to reside and act. Repressing the translation of proteins can ultimately repress parts of the body's immune and inflammatory responses, thus contributing to the pathogenesis of allergic rhinitis and other autoimmune disorders. There are many miRNAs that have been deemed potential therapeutic targets for the treatment of allergic rhinitis by many different researchers, with the most widely studied being miR-133, miR-155, miR-205, miR-498, and let-7e.[32][37][38][39]

Air pollution

[edit]

Numerous studies confirm that ambient air pollution particularly traffic-related pollutants like nitrogen dioxide (NO2), carbon monoxide (CO), sulfur dioxide (SO2), and fine particulate matter (PM2.5 and PM10) is significantly associated with both the prevalence and severity of allergic rhinitis. One Taiwanese study found that a 10 ppb increase in NOx corresponded to an 11% higher odds of physician‑diagnosed allergic rhinitis, with smaller yet significant associations for CO, SO2, and PM10.[40] Chinese meta-analysis data echoed this trend: increases in SO2 (OR ≈ 1.03), NO2 (OR ≈ 1.11), PM10 (OR ≈ 1.02), and PM2.5 (OR ≈ 1.15) all correlated with heightened risk of childhood allergic rhinitis, while ozone exposure showed no significant association.[41]

Air pollutants impair the respiratory epithelial barrier, increasing permeability and inflammation. This occurs through mechanisms such as oxidative stress, immune modulation, and epigenetic changes. Diesel exhaust particles (DEP), for example, have been shown to enhance allergic inflammation by boosting eosinophil activation when allergens are present. Meanwhile, damaged nasal mucosa facilitates deeper allergen penetration, intensifying rhinitis symptoms.[42] Urbanization, vehicle emissions, and fossil fuel combustion have accelerated in recent decades, coinciding with a steady rise in allergic rhinitis prevalence. For instance, in Southeast Asia and parts of Latin America, higher AR rates align strongly with poorer air quality.[43]

Pathophysiology

[edit]

The pathophysiology of allergic rhinitis involves Th2 Helper T cell and IgE mediated inflammation with overactive function of the adaptive and innate immune systems.[12] The process begins when an aeroallergen penetrates the nasal mucosal barrier. This barrier may be more permeable in susceptible individuals. The allergen is then engulfed by an antigen presenting cell (APC) (such as a dendritic cell).[12] The APC then presents the antigen to a Naive CD4+ helper T cell stimulating it to differentiate into a Th2 helper T cell. The Th2 helper T cell then secretes inflammatory cytokines including IL-4, IL-5, IL-13, IL-14, and IL-31. These inflammatory cytokines stimulate B cells to differentiate into plasma cells and release allergen specific IgE immunoglobulins.[12] The IgE immunoglobulins attach to mast cells. The inflammatory cytokines also recruit inflammatory cells such as basophils, eosinophils and fibroblasts to the area.[12] The person is now sensitized, and upon re-exposure to the allergen, mast cells with allergen specific IgE will bind the allergens and release inflammatory molecules including histamine, leukotrienes, platelet activating factor, prostaglandins and thromboxane with these inflammatory molecules' local effects on blood vessels (dilation), mucous glands (secrete mucous) and sensory nerves (activation) leading to the clinical signs and symptoms of allergic rhinitis.[12]

Disruption of the nasal mucosal epithelial barrier may also release alarmins (a type of damage associated molecular pattern (DAMP) molecule) such as thymic stromal lymphopoietin, IL-25 and IL-33 which activate group 2 innate lymphoid cells (ILC2) which then also releases inflammatory cytokines leading to activation of immune cells.[12]

Diagnosis

[edit]
Patch test

Allergy testing may reveal the specific allergens to which an individual is sensitive. Skin testing is the most common method of allergy testing.[44] [failed verification] This may include a patch test to determine if a particular substance is causing the rhinitis, or an intradermal, scratch, or other test. Less commonly, the suspected allergen is dissolved and dropped onto the lower eyelid as a means of testing for allergies. This test should be done only by a physician, since it can be harmful if done improperly. In some individuals not able to undergo skin testing (as determined by the doctor), the RAST blood test may be helpful in determining specific allergen sensitivity. Peripheral eosinophilia can be seen in differential leukocyte count.[citation needed]

Allergy testing is not definitive. At times, these tests can reveal positive results for certain allergens that are not actually causing symptoms, and can also not pick up allergens that do cause an individual's symptoms. The intradermal allergy test is more sensitive than the skin prick test, but is also more often positive in people that do not have symptoms to that allergen.[45]

Even if a person has negative skin-prick, intradermal and blood tests for allergies, they may still have allergic rhinitis, from a local allergy in the nose. This is called local allergic rhinitis.[46] Specialized testing is necessary to diagnose local allergic rhinitis.[47]

Classification

[edit]
  • Seasonal allergic rhinitis (hay fever): Caused by seasonal peaks in the airborne load of pollens.
  • Perennial allergic rhinitis (nonseasonal allergic rhinitis; atopic rhinitis): Caused by allergens present throughout the year (e.g., dander).

Allergic rhinitis may be seasonal, perennial, or episodic.[10] Seasonal allergic rhinitis occurs in particular during pollen seasons. It does not usually develop until after 6 years of age. Perennial allergic rhinitis occurs throughout the year. This type of allergic rhinitis is commonly seen in younger children.[48]

Allergic rhinitis may also be classified as mild-intermittent, moderate-severe intermittent, mild-persistent, and moderate-severe persistent. Intermittent is when the symptoms occur <4 days per week or <4 consecutive weeks. Persistent is when symptoms occur >4 days/week and >4 consecutive weeks. The symptoms are considered mild with normal sleep, no impairment of daily activities, no impairment of work or school, and if symptoms are not troublesome. Severe symptoms result in sleep disturbance, impairment of daily activities, and impairment of school or work.[49]

Local allergic rhinitis

[edit]

Local allergic rhinitis is an allergic reaction in the nose to an allergen, without systemic allergies. So skin-prick and blood tests for allergy are negative, but there are IgE antibodies produced in the nose that react to a specific allergen. Intradermal skin testing may also be negative.[47]

The symptoms of local allergic rhinitis are the same as the symptoms of allergic rhinitis, including symptoms in the eyes. Just as with allergic rhinitis, people can have either seasonal or perennial local allergic rhinitis. The symptoms of local allergic rhinitis can be mild, moderate, or severe. Local allergic rhinitis is associated with conjunctivitis and asthma.[47]

In one study, about 25% of people with rhinitis had local allergic rhinitis.[50] In several studies, over 40% of people having been diagnosed with nonallergic rhinitis were found to actually have local allergic rhinitis.[46] Steroid nasal sprays and oral antihistamines have been found to be effective for local allergic rhinitis.[47]

As of 2014, local allergenic rhinitis had mostly been investigated in Europe; in the United States, the nasal provocation testing necessary to diagnose the condition was not widely available.[51]: 617 

Prevention

[edit]

Prevention often focuses on avoiding specific allergens that cause an individual's symptoms. These methods include not having pets, not having carpets or upholstered furniture in the home, and keeping the home dry.[52] Specific anti-allergy zippered covers on household items like pillows and mattresses have also proven to be effective in preventing dust mite allergies.[44]

Studies have shown that growing up on a farm and having many older siblings are associated with a reduction in individual's risk for developing allergic rhinitis.[2]

Studies in young children have shown that there is higher risk of allergic rhinitis in those who have early exposure to foods or formula or heavy exposure to cigarette smoking within the first year of life.[53][54]

Treatment

[edit]

The goal of rhinitis treatment is to prevent or reduce the symptoms caused by the inflammation of affected tissues. Measures that are effective include avoiding the allergen.[18] Intranasal corticosteroids are the preferred medical treatment for persistent symptoms, with other options if this is not effective.[18] Second line therapies include antihistamines, decongestants, cromolyn, leukotriene receptor antagonists, and nasal irrigation.[18] Antihistamines by mouth are suitable for occasional use with mild intermittent symptoms.[18] Mite-proof covers, air filters, and withholding certain foods in childhood do not have evidence supporting their effectiveness.[18]

Antihistamines

[edit]

Antihistamine drugs can be taken orally and nasally to control symptoms such as sneezing, rhinorrhea, itching, and conjunctivitis.[55]

It is best to take oral antihistamine medication before exposure, especially for seasonal allergic rhinitis. In the case of nasal antihistamines like azelastine antihistamine nasal spray, relief from symptoms is experienced within 15 minutes allowing for a more immediate 'as-needed' approach to dosage. There is not enough evidence of antihistamine efficacy as an add-on therapy with nasal steroids in the management of intermittent or persistent allergic rhinitis in children, so its adverse effects and additional costs must be considered.[56]

Ophthalmic antihistamines (such as azelastine in eye drop form and ketotifen) are used for conjunctivitis, while intranasal forms are used mainly for sneezing, rhinorrhea, and nasal pruritus.[57]

Antihistamine drugs can have undesirable side-effects, the most notable one being drowsiness in the case of oral antihistamine tablets. First-generation antihistamine drugs such as diphenhydramine cause drowsiness, while second- and third-generation antihistamines such as fexofenadine and loratadine are less likely to.[57][58]

Pseudoephedrine is also indicated for vasomotor rhinitis. It is used only when nasal congestion is present and can be used with antihistamines. In the United States, oral decongestants containing pseudoephedrine must be purchased behind the pharmacy counter in an effort to prevent the manufacturing of methamphetamine.[57] Desloratadine/pseudoephedrine can also be used for this condition[citation needed]

Steroids

[edit]

Intranasal corticosteroids are used to control symptoms associated with sneezing, rhinorrhea, itching, and nasal congestion.[26] Steroid nasal sprays are effective and safe, and may be effective without oral antihistamines. They take several days to act and so must be taken continually for several weeks, as their therapeutic effect builds up with time.[citation needed]

In 2013, a study compared the efficacy of mometasone furoate nasal spray to betamethasone oral tablets for the treatment of people with seasonal allergic rhinitis and found that the two have virtually equivalent effects on nasal symptoms in people.[59]

Systemic steroids such as prednisone tablets and intramuscular triamcinolone acetonide or glucocorticoid (such as betamethasone) injection are effective at reducing nasal inflammation, [citation needed] but their use is limited by their short duration of effect and the side-effects of prolonged steroid therapy.[60]

Others

[edit]

Other measures that may be used second line include: decongestants, cromolyn, leukotriene receptor antagonists, and nonpharmacologic therapies such as nasal irrigation.[18]

Topical decongestants may also be helpful in reducing symptoms such as nasal congestion, but should not be used for long periods, as stopping them after protracted use can lead to a rebound nasal congestion called rhinitis medicamentosa.[citation needed]

For nocturnal symptoms, intranasal corticosteroids can be combined with nightly oxymetazoline, an adrenergic alpha-agonist, or an antihistamine nasal spray without risk of rhinitis medicamentosa.[61]

Nasal saline irrigation (a practice where salt water is poured into the nostrils), may have benefits in both adults and children in relieving the symptoms of allergic rhinitis and it is unlikely to be associated with adverse effects.[62]

Allergen immunotherapy

[edit]

Allergen immunotherapy, also called desensitization, treatment involves administering doses of allergens to accustom the body to substances that are generally harmless (pollen, house dust mites), thereby inducing specific long-term tolerance.[63] Allergen immunotherapy is the only treatment that alters the disease mechanism.[64] Immunotherapy can be administered orally (as sublingual tablets or sublingual drops), or by injections under the skin (subcutaneous). Subcutaneous immunotherapy is the most common form and has the largest body of evidence supporting its effectiveness.[65]

Alternative medicine

[edit]

There are no forms of complementary or alternative medicine that are evidence-based for allergic rhinitis.[44] Therapeutic efficacy of alternative treatments such as acupuncture and homeopathy is not supported by available evidence.[66][67] While some evidence shows that acupuncture is effective for rhinitis, specifically targeting the sphenopalatine ganglion acupoint, these trials are still limited.[68] Overall, the quality of evidence for complementary-alternative medicine is not strong enough to be recommended by the American Academy of Allergy, Asthma and Immunology.[44][69]

Epidemiology

[edit]

Allergic rhinitis is the type of allergy that affects the greatest number of people.[13] In Western countries, between 10 and 30 percent of people are affected in a given year.[2] It is most common between the ages of twenty and forty.[2]

History

[edit]

The first accurate description is from the 10th century physician Rhazes.[14] Pollen was identified as the cause in 1859 by Charles Blackley.[15] In 1906 the mechanism was determined by Clemens von Pirquet.[13] The link with hay came about due to an early (and incorrect) theory that the symptoms were brought about by the smell of new hay.[16][17] Although the scent per se is irrelevant, the correlation with hay checks out, as peak hay-harvesting season overlaps with peak pollen season, and hay-harvesting work puts people in close contact with seasonal allergens.

See also

[edit]

References

[edit]

Further reading

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Allergic rhinitis

View on Grokipedia
from Grokipedia
Allergic rhinitis, also known as hay fever, is an (IgE)-mediated inflammatory disorder of the triggered by exposure to environmental allergens, resulting in symptoms such as sneezing, nasal itching, , and congestion. This condition affects 10% to 30% of the global population, with rates higher in industrialized countries and increasing over recent decades, impacting up to 400 million people worldwide. Allergic rhinitis is classified into seasonal (intermittent) and perennial (persistent) forms based on the timing and persistence of symptoms, as well as into mild or moderate-to-severe categories depending on their impact on daily activities. Seasonal allergic rhinitis is primarily caused by outdoor aeroallergens like pollen from trees, grasses, and weeds, while perennial forms are driven by indoor triggers such as house dust mites, animal , cockroach allergens, and molds. Pathophysiologically, inhaled allergens cross-link IgE antibodies bound to high-affinity receptors on mast cells and in the , prompting the release of , leukotrienes, and cytokines that induce , increased , and nerve stimulation, leading to the acute symptoms. Beyond nasal manifestations, symptoms often extend to ocular itching and watering (), postnasal drip, and , with severe cases causing sleep disturbances, fatigue, and reduced cognitive performance. The disorder substantially impairs health-related quality of life, productivity, and school performance, while increasing risks for comorbidities including (present in up to 40% of cases), chronic rhinosinusitis, and . Diagnosis relies on a thorough clinical history of allergen exposure and symptoms, supported by skin prick testing or measurement of specific IgE levels to confirm . Effective management encompasses allergen avoidance measures, with intranasal corticosteroids as first-line treatment for persistent symptoms, oral or intranasal antihistamines for pruritus and sneezing, and allergen-specific for disease modification in selected patients.

Signs and symptoms

Nasal manifestations

Allergic rhinitis primarily manifests through a cluster of nasal symptoms triggered by exposure to allergens, including sneezing, rhinorrhea characterized by clear and watery nasal discharge, nasal itching, itchy throat, and congestion. Unlike infectious conditions such as viral rhinitis, allergic rhinitis does not cause fever. These symptoms arise from inflammation of the nasal mucosa and can vary in intensity depending on the individual's sensitization and environmental factors. The presentation of these symptoms is differentiated into intermittent and persistent patterns based on frequency and duration of allergen exposure. Intermittent allergic rhinitis involves symptoms occurring fewer than four days per week or for less than four consecutive weeks, often aligning with seasonal allergens such as pollen. In contrast, persistent allergic rhinitis features symptoms more than four days per week and for more than four consecutive weeks, typically linked to perennial indoor allergens like dust mites or pet dander. Nasal congestion, in particular, obstructs airflow through the nasal passages, leading to reduced breathing efficiency and often prompting as a compensatory mechanism. This obstruction can exacerbate discomfort during daily activities and contribute to secondary issues like dry mouth. While symptoms of allergic rhinitis, such as clear nasal discharge, sneezing, nasal congestion, and nasal itching, do not occur solely from exposure to cold air, they may worsen in cold environments. Cold air can irritate the nasal mucosa, drying the lining and prompting increased mucus production to maintain moisture, thereby exacerbating rhinorrhea. Additionally, cold weather often leads to more time spent indoors with windows closed, heightening exposure to indoor allergens and intensifying overall symptoms, including associated itchy eyes. Symptoms of allergic rhinitis frequently intensify at night or in the early morning, influenced by circadian variations in allergen levels or inflammatory mediators such as . This temporal pattern can disrupt and heighten overall symptom burden upon waking.

Associated systemic effects

Allergic rhinitis often manifests with ocular symptoms collectively termed , including itchy and watery eyes, redness, and periorbital swelling. These symptoms arise from the same IgE-mediated inflammatory response affecting the , with airborne allergens triggering conjunctival . Ocular involvement occurs in 40% to 60% of patients with allergic rhinitis, significantly impacting and frequently co-occurring with nasal symptoms. The chronic in allergic rhinitis extends beyond local effects, contributing to systemic symptoms such as , , sleep disturbances, and reduced concentration. Nasal disrupts sleep architecture, leading to frequent awakenings and non-restorative sleep, which in turn causes daytime and . Studies report that up to 46% of patients experience , 32% face concentration difficulties, and many exhibit heightened due to persistent discomfort and inflammatory mediators. Complications from allergic rhinitis include , which irritates the throat and induces or . This mucus drainage can also promote secondary infections, increasing the incidence of and , resulting in ear fullness, pressure, or pain. Untreated allergic rhinitis elevates the risk of infectious by promoting mucosal edema and bacterial overgrowth. Additionally, 20% to 40% of patients with allergic rhinitis have comorbid , with rhinitis exacerbating lower airway symptoms through shared inflammatory pathways. Allergic rhinitis can also cause headaches, particularly nasogenic or sinus headaches, through inflammation and swelling of the nasal mucosa leading to severe congestion. This congestion impairs sinus drainage and increases sinus pressure, resulting in pain in the forehead, eye sockets, and nose bridge. Long-term congestion may contribute to mild hypoxia or postnasal drip, which can irritate the throat and nerves, further exacerbating headache symptoms. Additionally, allergic rhinitis is associated with migraines due to shared inflammatory mechanisms, and many cases of sinus headaches are actually disguised migraines. Allergic rhinitis has also been associated with cardiovascular effects. Chronic allergic rhinitis is linked to increased odds of hypertension and coronary heart disease; for example, a large U.S. survey-based study found that allergic rhinitis was independently associated with 25% greater odds of coronary heart disease (OR 1.25, 95% CI 1.18-1.28). Histories of allergic disorders have also been associated with increased risk of high blood pressure and coronary heart disease. Short-term exposure to high pollen concentrations has been linked to modest increases in blood pressure in individuals with pollen allergies, due to inflammatory responses, with one study reporting increases of approximately 2 mmHg in systolic and 1.5 mmHg in diastolic blood pressure at higher exposure levels over 96 hours. Indirect effects, such as the use of oral decongestants which can elevate blood pressure and sleep disruption from nasal congestion, can also contribute to elevated blood pressure readings.

Causes

Environmental triggers

Allergic rhinitis is commonly triggered by environmental allergens, particularly airborne particles that provoke an inflammatory response in susceptible individuals. Seasonal allergens, such as from trees, grasses, and s, are primary culprits, with tree peaking in spring, grass in summer, and weed in late summer and fall. In , , a highly allergenic weed , typically begins in early August, peaks from mid-September to October, and declines by November, contributing significantly to fall allergy symptoms. Perennial indoor allergens provide year-round exposure and exacerbate symptoms regardless of season. House dust mites, thriving in warm, humid environments like and , release potent allergens through their and body fragments. Pet dander, consisting of flakes, saliva, and urine from cats, dogs, and other animals, disperses easily in indoor air and adheres to surfaces. Mold spores, produced by fungi in damp areas such as bathrooms and basements, also act as persistent triggers, especially in water-damaged buildings. Additionally, cold air is not a primary trigger for allergic rhinitis but can exacerbate symptoms by drying the nasal passages, leading to increased mucus production, and by increasing time spent indoors, which heightens exposure to perennial allergens such as house dust mites and pet dander. Occupational exposures represent a subset of environmental triggers, particularly in healthcare and industrial settings where repeated contact occurs. Natural rubber from gloves and medical devices can induce rhinitis in sensitized workers, with symptoms arising from airborne latex particles; prevalence among healthcare personnel reaches 8-12%. Chemicals such as isocyanates in or in may similarly provoke occupational allergic rhinitis through inhalation. Air pollution compounds the impact of these allergens by acting as an adjuvant, enhancing their potency and facilitating . Particulate matter (PM) and can bind to grains or indoor allergens, increasing their allergenicity and promoting epithelial damage in the , thereby worsening symptoms during co-exposure. further intensifies these triggers by altering exposure patterns. Rising temperatures and elevated CO2 levels have extended seasons across by an average of 20 days and increased concentrations by 21%, with seasons starting earlier and lasting longer in recent decades.

Genetic and immunological factors

Allergic rhinitis is strongly influenced by genetic predispositions, particularly , which represents a hereditary tendency toward IgE-mediated reactions. Atopy is considered a polygenic trait, with multiple genetic loci contributing to its expression and increasing susceptibility to allergic diseases, including . Family history plays a significant role in transmission; children with one atopic parent have an approximately 3- to 4-fold increased of developing allergic rhinitis compared to those without such history, while the is further elevated (up to 4- to 8-fold) when both parents are affected. Twin studies further underscore this , demonstrating concordance rates of 45% to 60% in monozygotic twins versus 25% or less in dizygotic twins for allergic rhinitis, indicating that genetic factors account for 40% to 60% of the variance in disease susceptibility. Key genes implicated in the pathogenesis include those regulating IgE production and T-helper 2 (Th2) immune skewing, such as IL4 and IL13 on chromosome 5q31, which promote B-cell class switching to IgE and eosinophil recruitment, and HLA-DR variants on chromosome 6p21, which enhance antigen presentation to Th2 cells. These genetic elements interact with environmental allergens to initiate sensitization, but their primary role lies in predisposing individuals to exaggerated immune responses. The atopic march, a sequential progression of allergic manifestations, exemplifies this genetic underpinning; approximately 50% of children with early-onset atopic dermatitis (eczema) and a family history of atopy develop allergic rhinitis by school age. The posits that reduced early-life exposure to diverse microbial agents impairs maturation, favoring Th2 dominance and elevating allergic rhinitis risk. Studies support this, showing that children in microbially rich environments, such as farms, exhibit lower incidence of due to enhanced regulatory T-cell development and reduced IgE responses. exacerbates this vulnerability, correlating with substantially higher prevalence rates of allergic rhinitis (up to 3 times greater in urban vs. rural areas, with ratios around 4) through diminished microbial diversity, increased indoor exposure, and lifestyle changes that limit protective early exposures.

Pathophysiology

Sensitization phase

The sensitization phase of allergic rhinitis represents the initial immune priming upon first exposure to allergens, establishing a foundation for subsequent allergic responses. When airborne allergens such as or dust mites are inhaled, they are captured by epithelial cells in the and processed by antigen-presenting cells, primarily dendritic cells. These dendritic cells migrate to regional lymph nodes, where they present allergen peptides via class II molecules to naive + T cells, promoting their differentiation into T helper 2 (Th2) cells under the influence of a Th2-biased microenvironment. Activated Th2 cells release signature cytokines, including interleukin-4 (IL-4) and IL-13, which drive class-switch recombination in B cells toward production of allergen-specific (IgE). IL-4 specifically induces the expression of activation-induced deaminase in B cells, facilitating the genetic rearrangement necessary for IgE synthesis, while IL-13 amplifies this process and contributes to mucosal inflammation priming. The resulting IgE antibodies circulate and bind with high affinity to the FcεRI receptors on the surface of mast cells and , primarily in the nasal tissues, sensitizing these effector cells for future encounters. This phase culminates in the establishment of immunological memory, where allergen-specific Th2 cells and plasma cells persist, enabling rapid IgE-mediated responses upon re-exposure. typically begins in childhood, with studies showing that allergen-specific IgE development often emerges by age 7 in susceptible individuals, influenced by early environmental exposures. between structurally similar allergens, such as pollen proteins (e.g., Bet v 1) and those in apples (e.g., Mal d 1), complicates this process and affects approximately 50-75% of pollen-allergic patients, leading to symptoms.

Effector phase

Upon re-exposure to allergens in individuals previously sensitized, the effector phase of allergic rhinitis initiates an acute inflammatory cascade in the . This phase is triggered when allergens bind to IgE antibodies attached to high-affinity FcεRI receptors on the surface of mast cells and , leading to cross-linking of IgE molecules. This cross-linking rapidly induces , releasing preformed mediators such as , as well as newly synthesized lipid mediators including leukotrienes (e.g., LTC4, LTD4, LTE4) and prostaglandins (e.g., PGD2). Histamine release occurs swiftly, peaking within 5-10 minutes of exposure, and contributes to immediate symptoms by binding to H1 receptors on endothelial cells, sensory nerves, and glandular cells, resulting in increased , , and hypersecretion. Leukotrienes and prostaglandins further amplify these effects by promoting , contraction, and enhanced production, exacerbating and during the early-phase response, which typically lasts 15-30 minutes but can extend up to 1-2 hours. The nasal mucosa inflammation and swelling during this phase lead to severe congestion, which impairs sinus drainage and increases sinus pressure, resulting in nasogenic or sinus headaches characterized by pain in the forehead, eye sockets, and bridge of the nose. Long-term congestion may also contribute to mild hypoxia or postnasal drip, irritating the throat and nerves, thereby exacerbating headache symptoms. Furthermore, allergic rhinitis is associated with migraines due to shared inflammatory mechanisms, including the release of histamine and other mediators that activate trigeminal nociceptors, with studies indicating that up to 90% of purported sinus headaches in allergic rhinitis patients may actually represent disguised migraines. The late-phase response, emerging 4-8 hours after initial exposure, involves the recruitment and activation of additional inflammatory cells, including , , and T helper 2 (Th2) cells, driven by and cytokines released during the early phase. , in particular, are attracted via interleukin-5 (IL-5) mediation, leading to their accumulation in the nasal tissues and release of cytotoxic proteins like major basic protein, which sustains tissue damage and inflammation. This late-phase inflammation contributes substantially to the persistence of symptoms in allergic rhinitis, contributing to chronic nasal obstruction and hyperresponsiveness.

Diagnosis

Clinical assessment

The clinical assessment of allergic rhinitis begins with a detailed patient history to evaluate symptoms, their onset, duration, and impact. Patients typically report nasal symptoms such as sneezing, itching, , and congestion, often accompanied by ocular symptoms like itchy or watery eyes. The history focuses on timing, with symptoms occurring seasonally or perennially, and triggers including environmental allergens like pollen, dust mites, or animal dander. For persistent symptoms such as ongoing nasal itching, teary eyes, and swelling, consultation with a specialist is recommended. An allergist/immunologist is the primary specialist for diagnosing and managing allergic rhinitis, including performing allergen testing and offering treatments like sublingual immunotherapy to address root causes. An ear, nose, and throat (ENT) specialist, or otolaryngologist, should be consulted if symptoms suggest structural nasal issues, such as chronic sinusitis or polyps complicating the allergic response. For severe or isolated ocular symptoms, an ophthalmologist may be involved to evaluate and treat allergic conjunctivitis. Severity is assessed using validated scales, such as the Total Nasal Symptom Score (TNSS), which quantifies the intensity of the four cardinal nasal symptoms (sneezing, , nasal itching, and congestion) on a scale from 0 to 12, helping to gauge overall burden.31187-X/fulltext) The Allergic Rhinitis and its Impact on () classification system guides this evaluation by categorizing the condition as intermittent (symptoms present less than 4 days per week or for less than 4 consecutive weeks) or persistent (more than 4 days per week and for more than 4 consecutive weeks), and as mild (no interference with , daily activities, , or leisure) or moderate-severe (disturbance in at least one of these areas). This framework aids in determining the and potential comorbidities, such as .31187-X/fulltext) Additionally, into family history of and personal history of other allergic conditions helps identify risk factors. Physical examination reveals characteristic findings, including pale, boggy (edematous) inferior turbinates with clear mucoid discharge, indicating mucosal . Extranasal signs may include allergic shiners (periorbital venous congestion causing dark circles under the eyes) and Dennie-Morgan lines (transverse folds below the lower eyelids due to chronic rubbing). The nasal mucosa appears hyperemic or bluish, and patients may exhibit an "allergic salute" (upward rubbing of the nose, leading to a transverse nasal crease). Differential diagnosis distinguishes allergic rhinitis from non-allergic rhinitis (e.g., or drug-induced, lacking triggers), acute viral or bacterial infections (which often include fever or purulent discharge), and structural issues like deviated septum or nasal polyps (causing unilateral obstruction). Local allergic rhinitis presents with similar nasal symptoms but without systemic , as evidenced by negative skin prick tests or serum IgE levels.02949-0/fulltext) Confirmation of allergic etiology may require subsequent diagnostic testing.

Diagnostic testing

Diagnostic testing for allergic rhinitis involves objective methods to confirm IgE-mediated and identify specific allergens, complementing clinical . These tests include prick testing, measurement of serum-specific IgE, nasal provocation testing, and advanced techniques like component-resolved diagnostics, while aids in evaluating structural complications. Selection depends on factors such as conditions or use that may contraindicate certain procedures. Skin prick testing (SPT) is a first-line method that assesses immediate through the wheal-and-flare response elicited by introducing standardized extracts into the , typically on the or back. A positive result is defined as a wheal at least 3 mm larger than the negative control after 15-20 minutes, indicating the presence of allergen-specific IgE bound to mast cells. This test demonstrates high diagnostic accuracy, with pooled sensitivity of 85% and specificity of 77% in discriminating allergic from non-allergic based on of clinical studies. However, false positives occur in 10-20% of cases due to irritants or non-specific reactions, such as release from skin conditions or improper technique, necessitating correlation with symptoms. SPT is preferred for its speed and cost-effectiveness but requires discontinuation of antihistamines for 3-7 days prior. Serum-specific IgE testing, including (RAST) or more modern like ImmunoCAP, quantifies allergen-specific IgE antibodies in blood samples, providing an alternative when SPT is contraindicated, such as in patients with extensive , on beta-blockers, or unable to avoid antihistamines. ImmunoCAP uses solid-phase extracts to bind IgE, with results reported in kUA/L, offering high specificity (up to 90%) and sensitivity comparable to SPT (around 80-90%) for common aeroallergens like or dust mites. This method is particularly useful for confirming in pediatric or elderly patients and avoids risks associated with skin testing, though it may be less sensitive for some low-level sensitizations. Nasal provocation testing (NPT) evaluates local allergic responses by directly challenging the with escalating doses of allergens, measuring outcomes like symptom scores, nasal via rhinomanometry, or acoustic rhinometry; it is especially valuable for diagnosing local allergic rhinitis (LAR), where systemic SPT and serum IgE are negative despite persistent symptoms. In LAR cases, NPT induces significant nasal resistance increases and symptom exacerbation in 80-90% of confirmed patients, distinguishing it from non-allergic rhinitis. This procedure, performed under medical supervision, helps guide targeted therapies but is not routine due to potential discomfort and risk of severe reactions. Nasal , using a flexible or rigid scope, visualizes the to detect complications of allergic rhinitis such as mucosal , polyps, or sinus ostia obstruction, which may indicate progression to chronic rhinosinusitis. Pale, swollen turbinates or clear secretions are common findings supporting allergic , while structural abnormalities prompt further or intervention. This tool enhances diagnostic precision in refractory cases but is adjunctive rather than primary for allergen identification.70219-2/fulltext) Component-resolved diagnostics (CRD), often via multiplex arrays like ImmunoCAP ISAC, measures IgE to individual components rather than crude extracts, enabling identification of cross-reactive proteins such as profilins (e.g., Bet v 2 from birch pollen) that cause pan- sensitization without primary . This approach refines by distinguishing true sensitizers from cross-reactants with >70% , reducing misinterpretation in polysensitized patients and predicting reaction severity for selection. CRD is increasingly used in complex cases but requires specialized labs.

Management

Allergen avoidance

Allergen avoidance serves as the cornerstone of managing allergic rhinitis, aiming to reduce exposure to triggers such as , dust mites, and occupational irritants to alleviate symptoms and improve . This approach is particularly effective when tailored to identified allergens through diagnostic testing, forming the foundation before considering adjunctive therapies.

Environmental Controls for Indoor Allergens

For house mites, a primary indoor trigger, key strategies include encasing mattresses, pillows, and box springs in allergen-proof covers to prevent mite contact and reduce levels by over 90% within a month. Regular washing of bedding in hot water (at least 130°F or 54°C) weekly removes s and , while vacuuming with a -filtered minimizes airborne particles. High-efficiency particulate air (HEPA) filters in air purifiers or HVAC systems capture up to 99.97% of particles 0.3 microns and larger, significantly lowering mite in indoor air and reducing symptom severity in sensitized individuals. Maintaining indoor relative humidity below 50% through dehumidifiers or is crucial, as this level inhibits reproduction and can decrease concentrations by up to 90% over three months by limiting water availability for mites. with saline solution, performed daily, physically clears from nasal passages and reduces symptoms by approximately 20-30%.

Strategies for Outdoor Pollen Exposure

Pollen from trees, grasses, and weeds exacerbates seasonal allergic rhinitis, and avoidance involves monitoring daily pollen forecasts via apps or services to anticipate high-count days. Staying indoors with windows closed during peak pollen times (typically midday to evening) and using with clean filters prevents influx of outdoor allergens. After outdoor activities, showering, washing hair, and changing clothes remove adhered , while wearing wraparound or masks outdoors further limits exposure.

Occupational Avoidance Measures

In workplaces where allergens like , , or chemicals trigger , protective equipment such as masks, respirators, or minimizes and contact. Modifications like improved ventilation, regular cleaning, or relocating to low-allergen areas can reduce exposure, with employers often required to implement these under occupational guidelines. For instance, in or healthcare settings, using allergen-free alternatives or scheduling work during low-exposure periods helps prevent symptoms.

Dietary Considerations for Oral Allergy Syndrome

Oral allergy syndrome (OAS), a cross-reaction between pollen allergens and certain fresh fruits, vegetables, or nuts, affects up to 70% of pollen-allergic individuals and manifests as itching in the mouth or throat. Avoidance involves steering clear of raw triggers specific to the pollen type—for example, avoiding apples, carrots, or hazelnuts in birch pollen allergy—while cooked or processed forms of these foods are often tolerated due to heat denaturation of proteins. Consulting an allergist for personalized lists ensures balanced nutrition without unnecessary restrictions.

Pharmacological interventions

Pharmacological interventions for allergic rhinitis primarily aim to alleviate symptoms such as , , sneezing, and itching through targeted blockade of inflammatory mediators. These treatments are recommended as the cornerstone of following allergen avoidance, with selection based on symptom severity, persistence, and preferences. According to recent guidelines, intranasal formulations are preferred over oral options for superior efficacy in controlling nasal symptoms while minimizing systemic side effects. Intranasal corticosteroids, such as fluticasone propionate or mometasone, represent the first-line therapy for moderate-to-severe or persistent allergic rhinitis due to their potent effects. These agents inhibit multiple inflammatory pathways, including production and recruitment, leading to substantial symptom relief, including effective control of persistent runny nose. Fluticasone is available over-the-counter or by prescription, while mometasone requires a prescription. Clinical trials demonstrate that intranasal corticosteroids reduce total nasal symptom scores by approximately 30-40% compared to , with no significant differences in efficacy among commonly used formulations like fluticasone, mometasone, or . They are typically administered once or twice daily, with onset of action within 12 hours and maximal benefits after 1-2 weeks, and are well-tolerated with low risk of systemic absorption. Second-generation oral antihistamines, exemplified by , loratadine, and fexofenadine, are widely used for mild intermittent symptoms or as adjunctive therapy and are available over-the-counter at pharmacies. These medications competitively antagonize H1 , thereby blocking histamine-mediated effects like itching, sneezing, and , particularly helping to reduce persistent runny nose and itching, with minimal central nervous system penetration to avoid . They provide rapid onset (within 1-3 hours) and are effective in reducing ocular and nasal symptoms, though less so for congestion compared to corticosteroids; meta-analyses show improvements in total symptom scores of 15-25% over . For persistent ocular symptoms such as teary eyes and swelling, consultation with an ophthalmologist may be considered in addition to allergist management. Dosing is once daily, and they are suitable for long-term use in adults and children. Decongestants, such as oral or intranasal , target by activating alpha-adrenergic receptors to induce . They offer quick relief (within minutes for intranasal forms) but are recommended for short-term use (3-5 days) to prevent rebound congestion or . Oral decongestants such as pseudoephedrine can elevate blood pressure and should be used with caution in patients with hypertension or cardiovascular risks, or avoided in cases of severe or uncontrolled hypertension. For symptoms suggesting sinusitis complicating allergic rhinitis, a doctor may prescribe short-term decongestants along with antibiotics if a bacterial infection is suspected. Evidence supports their in reducing nasal airflow resistance by 20-30%, often in with antihistamines for broader symptom control. Leukotriene receptor antagonists like provide an alternative for patients with concomitant or inadequate response to antihistamines, by blocking cysteinyl receptors to attenuate inflammation and . Administered orally once daily, improves nasal symptoms and , with studies showing comparable efficacy to antihistamines in reducing total nasal symptom scores by 20-30%, particularly for perennial rhinitis. It is nonsedating and approved for use in children as young as 6 months. Nasal ipratropium bromide, an agent, is specifically indicated for excessive in both allergic and non-allergic . It inhibits muscarinic receptors to reduce glandular secretions, achieving a 30-50% decrease in runny nose severity without affecting other symptoms significantly. This spray acts rapidly (within ) and is safe for chronic use, often as an add-on to other therapies. therapies, such as fixed-dose intranasal -antihistamine sprays (e.g., fluticasone-azelastine), enhance outcomes by addressing multiple symptom pathways simultaneously. Randomized trials indicate that these combinations improve total nasal symptom scores by an additional 10-15% over monotherapy alone, with faster onset and better patient satisfaction. Current 2024 guidelines emphasize such intranasal combinations for persistent disease to optimize efficacy while prioritizing topical over oral routes.

Immunotherapies

Allergen-specific immunotherapy (AIT) represents a disease-modifying treatment for allergic rhinitis, aiming to induce long-term tolerance to allergens rather than merely suppressing symptoms. Unlike pharmacological interventions that provide symptomatic relief, AIT addresses the underlying immune dysregulation by progressively exposing patients to increasing doses of allergens, thereby modulating the allergic response. The two primary established forms are subcutaneous immunotherapy (SCIT), involving injections under the skin, and sublingual immunotherapy (SLIT), administered as drops or tablets under the tongue. Patients with persistent symptoms such as nasal itching, teary eyes, and swelling should consult an allergist, ear, nose, and throat (ENT) specialist, or ophthalmologist for diagnosis, allergen testing, and initiation of advanced treatments like SLIT to address root causes. Both approaches build immune tolerance primarily through the induction and expansion of regulatory T-cells (Tregs), which suppress Th2-driven allergic inflammation by producing anti-inflammatory cytokines such as IL-10 and TGF-β, leading to reduced allergen-specific IgE production and enhanced IgG4 responses. SCIT and SLIT have demonstrated comparable efficacy in reducing allergic rhinitis symptoms and medication use, with long-term benefits persisting for years after treatment cessation. Meta-analyses indicate that typically achieves a 30-50% reduction in symptom scores and rescue medication requirements, particularly for perennial allergens like house dust mites and seasonal ones like . In children, not only alleviates rhinitis but also prevents the progression to , with studies showing a approximately 50% reduction in new-onset asthma risk ( of 0.51). These effects are most pronounced when treatment targets key sensitizing allergens such as grass or dust mites, which are common triggers in allergic rhinitis. Standard protocols for involve an initial buildup phase to reach maintenance doses, followed by a continuation period of 3-5 years to ensure durable tolerance. SCIT requires visits for injections, typically weekly during buildup and monthly thereafter, while SLIT allows home administration after the first dose under , improving adherence. A 2025 umbrella review of meta-analyses confirmed that SLIT is particularly superior for children with allergic rhinitis, offering similar symptom control to SCIT but with greater tolerability and feasibility in pediatric populations. profiles are favorable overall, with SCIT carrying a low risk of (less than 0.1% of patients or injections), mitigated by standardized extracts and observation periods post-injection.

Novel and alternative approaches

Biologic therapies targeting key inflammatory pathways represent a promising advancement for managing severe or refractory allergic rhinitis (AR). , a against the alpha (IL-4Rα), has shown efficacy in reducing Th2-mediated in patients with moderate-to-severe AR. In clinical trials, including a phase 2b study in patients with perennial allergic rhinitis and comorbid , dupilumab administered subcutaneously every two weeks has shown significant improvements in nasal symptoms compared to . It offers a potential targeted option for severe cases with unresponsive to standard treatments, though not yet approved specifically for allergic rhinitis. Photobiomodulation therapy (PBMT), also known as , utilizes non-thermal light energy to modulate immune responses and reduce nasal inflammation in AR. A 2025 placebo-controlled randomized demonstrated that PBMT significantly alleviated clinical symptoms, including nasal obstruction, in patients with AR, positioning it as a non-invasive alternative with minimal side effects. This approach works by inhibiting activation and release, thereby decreasing allergic responses in the . Complementary therapies such as and herbal remedies provide moderate evidence-based support for symptom relief in AR, though they are not recommended as first-line interventions. Systematic reviews indicate that can improve nasal symptoms, with meta-analyses showing significant reductions in total nasal symptom scores compared to sham treatments. Similarly, butterbur () extract has demonstrated efficacy in alleviating seasonal AR symptoms, with randomized trials reporting comparable effects to antihistamines like , supported by moderately strong evidence from multiple studies. Other herbal remedies include black cumin oil (Nigella sativa), which exhibits anti-inflammatory and antihistamine effects, with clinical studies demonstrating significant reductions in nasal symptoms. Nettle tea or extract (Urtica dioica) offers mild antihistamine action, supported by evidence from randomized trials showing improvements in symptom scores. Quercetin, obtainable from supplements or foods such as onions and apples and often combined with vitamin C, functions as a natural antihistamine and mast cell stabilizer, backed by preclinical and clinical studies. Local honey may aid in acclimating to regional pollen, with weak but positive evidence from trials indicating symptom improvement, and it is generally harmless. Steam inhalation with peppermint, eucalyptus, or chamomile can provide symptom relief, as indicated by phytotherapeutic studies. Emerging approaches aim to address the root causes of AR by modulating allergen-specific immune responses. The AAVITS (AAV-based Inducible System) platform, utilizing adeno-associated viral vectors, enables on-demand activation of therapeutic genes in nasal tissues to reduce . In 2025 preclinical studies, AAVITS delivering anti-IL-4 constructs (AAVITS-ΔmIL-4) effectively lowered inflammatory factors and improved nasal in AR mouse models, targeting Th2-driven pathways associated with IgE production. This inducible system offers potential for personalized, long-term control without continuous dosing. Research into climate-adapted allergen vaccines is underway to counter the prolongation of pollen seasons due to global warming, which exacerbates AR exposure. These vaccines incorporate modified s to account for shifting pollen profiles and increased allergenicity, with early developmental efforts focusing on enhanced sublingual formulations responsive to extended seasons.

Epidemiology

Global prevalence

Allergic rhinitis affects an estimated 10% to 30% of the global population, corresponding to approximately 400 to 500 million individuals worldwide. In the United States, around 81 million people were diagnosed with seasonal allergic rhinitis as of recent estimates. The median worldwide prevalence is approximately 18.1%, with consistent reports of an upward trend in most regions over recent decades. The incidence of allergic rhinitis has been rising globally, with increases attributed to factors such as and , which exacerbate exposure to allergens and pollutants. Studies indicate growth rates of around 0.4% to 1.4% per year in various populations, equating to roughly 4% to 14% per decade in affected areas. Prevalence varies significantly by region, with higher rates in developed countries—such as approximately 24% in —compared to 5% to 10% in rural areas of developing regions like parts of . The International Study of Asthma and Allergies in Childhood () has documented an average prevalence of about 14.6% for rhinoconjunctivitis symptoms among 13- to 14-year-old children globally, though rates can reach 20% or higher in urbanized settings. Recent 2025 analyses highlight how climate-driven extensions of pollen seasons in have contributed to increased cases, with projections indicating up to a 200% rise in -related allergic reactions by mid-century, amplifying the burden in the region.

Risk factors and disparities

Allergic rhinitis exhibits distinct patterns related to age and , with typically peaking between the ages of 20 and 40 years before declining in older adulthood. to allergens, a key driver of the condition, reaches its highest rates in the 20-29 age group and progressively decreases thereafter. Approximately 80% of symptoms manifest before age 20, underscoring the importance of early-life exposures in disease onset. influences emerge prominently around , with females showing a higher incidence post-puberty compared to males, at a ratio of approximately 1.5:1 in adulthood. Between ages 8 and 19, girls experience a notably higher incidence of allergic rhinitis—estimated at 10-15% greater than in boys—while boys demonstrate higher rates of remission during this period. Socioeconomic and racial disparities significantly contribute to inequities in the burden of allergic , often resulting in underdiagnosis and undertreatment among low-socioeconomic-status (SES) and minority populations despite higher underlying risks. Allergic is more frequently diagnosed among individuals with higher education and levels, as well as and non- patients, leading to underrepresentation of cases in low-SES groups. Racial and ethnic minorities, particularly in urban settings, face a 25% higher attributable to environmental factors like , according to recent NIH analyses. and individuals, especially women, exhibit elevated rates of aeroallergen , exacerbating symptoms in polluted urban environments. Lower SES correlates with greater severity due to limited access to clean air and allergen mitigation resources, widening these gaps. Comorbidities play a critical role in amplifying the risks and impacts of allergic rhinitis, with substantial overlap observed in respiratory conditions. Up to 80-90% of individuals with also have allergic rhinitis, creating a bidirectional risk where rhinitis increases asthma susceptibility by 2-3 times. Obesity further elevates the risk of developing allergic rhinitis by approximately 1.5-fold, potentially through alterations in immune responses and increased . These comorbidities often result in poorer symptom control and , particularly when unmanaged. Climate change exacerbates allergic rhinitis disproportionately in low-income areas, where communities face heightened exposure to prolonged pollen seasons and elevated aeroallergen levels without adequate adaptive measures. Warmer temperatures and increased CO2 concentrations extend pollen production periods, intensifying symptoms in urban low-SES neighborhoods with limited green spaces or air filtration. Low-income residents experience the greatest uptick in rhinitis-related healthcare utilization due to these environmental shifts, underscoring the need for targeted interventions in vulnerable populations.

History

Historical recognition

The earliest recorded observations of symptoms resembling allergic rhinitis date back to , where (c. 460–377 BCE) described seasonal episodes of sneezing, nasal discharge, and eye irritation, potentially linked to environmental triggers such as plant pollens during summer months. These accounts, found in the , portrayed such conditions as imbalances of bodily humors, including causing catarrhal of the nasal passages, though without explicit identification of allergens. In the , allergic rhinitis gained formal recognition as a distinct clinical entity. English physician John provided the first detailed description in , coining the term "hay fever" (or "summer catarrh") based on his own recurring symptoms of intense sneezing, lacrimation, and during the hay harvest season. Bostock initially attributed the condition to the odor of new hay or exposure to bright light and heat, misconceptions that persisted in early , and he noted its prevalence among the educated elite and urban dwellers, suggesting a link to refined lifestyles or nervous temperaments. Further advancements clarified the through experimental work. In 1873, British physician Charles Harrison Blackley conducted pioneering self-experiments, deliberately exposing his skin and to grass , which reproducibly induced hay fever symptoms; he concluded that airborne pollen grains were the primary cause, debunking prior theories and establishing a scientific basis for the disease. Blackley's findings, detailed in his monograph Experimental Researches on the Causes and Nature of Catarrhus Aestivus, marked a pivotal shift toward understanding allergic rhinitis as an airborne allergen-mediated disorder. The modern nomenclature emerged in the early 20th century, with "allergic rhinitis" formalized in the 1920s following the introduction of the term "allergy" by Clemens von Pirquet in 1906 to describe altered immune reactivity; this replaced "hay fever" to encompass a broader spectrum of pollen and other inhalant sensitivities.

Key scientific advancements

In 1911, Leonard Noon and John Freeman pioneered subcutaneous immunotherapy (SCIT) as a treatment for pollen-induced hay fever, marking the first systematic attempt to desensitize patients through graduated injections of grass pollen extracts.78276-6/fulltext)0417-X/fulltext) Noon proposed the concept based on the idea of countering pollen "toxins" with prophylactic inoculations, while Freeman reported initial clinical results in 18 patients, demonstrating symptom relief in a majority during the hay fever season.31214-X/fulltext) This approach laid the foundation for allergen-specific immunotherapy, which remains a cornerstone for long-term management of allergic rhinitis despite early challenges with standardization and safety. The 1960s brought a pivotal understanding of the immunological basis of allergic rhinitis through the identification of immunoglobulin E (IgE) by Kimishige and Teruko Ishizaka. Their work isolated reaginic antibodies—previously elusive factors in allergic reactions—as a distinct fifth class of immunoglobulins, IgE, which binds to mast cells and basophils to trigger immediate hypersensitivity upon allergen exposure.00029-6/fulltext) This discovery, confirmed in 1967, explained the mechanism of type I hypersensitivity central to allergic rhinitis and enabled subsequent diagnostic advancements like skin prick tests and serum IgE measurements. Building on IgE insights, the 1980s introduced the Th2 paradigm, elucidating the role of T helper 2 (Th2) cells in driving allergic inflammation. Tim Mosmann and Robert Coffman described functionally distinct Th1 and Th2 subsets, with Th2 cells producing cytokines like interleukin-4 (IL-4) and IL-5 that promote IgE class switching, recruitment, and mucosal inflammation in response to . This framework shifted allergy research toward cytokine-targeted therapies and underscored the Th2-skewed in allergic rhinitis pathogenesis.70345-5/fulltext) In recent decades, the Allergic Rhinitis and its Impact on (ARIA) guidelines, first published in 1999 and updated through 2024, have standardized evidence-based classification and management of allergic rhinitis.70191-X/fulltext) The initial ARIA framework integrated rhinitis with comorbidity using a severity-based approach (intermittent/persistent, mild/moderate-severe), while the 2024 update incorporates , mobile health tools, and patient-centered outcomes to address implementation gaps.31187-X/fulltext) Concurrently, biologics trials in the 2020s have explored targeted therapies; for instance, (anti-IL-4/IL-13) reduced nasal symptoms and improved in patients with allergic rhinitis comorbid with chronic in phase 3 studies, outperforming (anti-IgE) in head-to-head comparisons for polyp scores and control. similarly showed efficacy in reducing seasonal exacerbations, with ongoing trials evaluating combination regimens. Additionally, IPCC reports since 2014 have recognized climate change's influence on allergic rhinitis, noting prolonged pollen seasons and increased aeroallergen potency due to elevated CO2 levels and warming temperatures. This has prompted integrated environmental-allergy models to predict rising disease burden.01622-5/fulltext)

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK538186/
  2. https://www.mayoclinic.org/diseases-conditions/hay-fever/symptoms-causes/syc-20373039
  3. https://www.aaaai.org/about/news/for-media/allergy-statistics
  4. https://pmc.ncbi.nlm.nih.gov/articles/PMC10582485/
  5. https://pmc.ncbi.nlm.nih.gov/articles/PMC9021509/
  6. https://www.aaaai.org/tools-for-the-public/allergy%2C-asthma-immunology-glossary/allergic-rhinitis-defined
  7. https://pmc.ncbi.nlm.nih.gov/articles/PMC9599528/
  8. https://pubmed.ncbi.nlm.nih.gov/20209315/
  9. https://pubmed.ncbi.nlm.nih.gov/27083099/
  10. https://pmc.ncbi.nlm.nih.gov/articles/PMC6036679/
  11. https://pmc.ncbi.nlm.nih.gov/articles/PMC9301683/
  12. https://www.nlm.nih.gov/medlineplus/ency/article/000813.htm
  13. https://pubmed.ncbi.nlm.nih.gov/38470381/
  14. https://www.aaaai.org/tools-for-the-public/conditions-library/allergies/rhinitis-%28hay-fever%29
  15. https://my.clevelandclinic.org/health/diseases/8622-allergic-rhinitis-hay-fever
  16. https://pmc.ncbi.nlm.nih.gov/articles/PMC6156899/
  17. https://www.entofga.com/how-does-cold-weather-affect-your-allergies/
  18. https://pubmed.ncbi.nlm.nih.gov/15536446/
  19. https://pmc.ncbi.nlm.nih.gov/articles/PMC7126948/
  20. https://pubmed.ncbi.nlm.nih.gov/21785348/
  21. https://aacijournal.biomedcentral.com/articles/10.1186/s13223-020-0403-9
  22. https://journals.lww.com/co-allergy/_layouts/15/oaks.journals/downloadpdf.aspx?an=00130832-201110000-00014
  23. https://pmc.ncbi.nlm.nih.gov/articles/PMC4460099/
  24. https://www.jacionline.org/article/S0091-6749%2804%2902300-0/fulltext
  25. https://pubmed.ncbi.nlm.nih.gov/12140359/
  26. https://www.heraldopenaccess.us/openaccess/impacts-of-allergic-rhinitis-in-social-communication-quality-of-life-and-behaviours-of-the-patients
  27. https://my.clevelandclinic.org/health/diseases/23082-postnasal-drip
  28. https://pmc.ncbi.nlm.nih.gov/articles/PMC7123453/
  29. https://med.stanford.edu/ohns/OHNS-healthcare/earinstitute/conditions-we-treat/eustachian-tube-dysfunction.html
  30. https://pubmed.ncbi.nlm.nih.gov/22179899/
  31. https://www.jacionline.org/article/S0091-6749%2800%2944364-2/fulltext
  32. https://pmc.ncbi.nlm.nih.gov/articles/PMC4762930/
  33. https://pmc.ncbi.nlm.nih.gov/articles/PMC3634285/
  34. https://pmc.ncbi.nlm.nih.gov/articles/PMC3809225/
  35. https://pubmed.ncbi.nlm.nih.gov/38341139/
  36. https://www.acc.org/About-ACC/Press-Releases/2022/04/11/13/40/History-of-Allergies-May-Be-Associated-with-Increased-Risk-of-High-Blood-Pressure-Heart-Disease
  37. https://pubmed.ncbi.nlm.nih.gov/38797464/
  38. https://www.health.harvard.edu/heart-health/dont-let-decongestants-squeeze-your-heart
  39. https://www.mayoclinic.org/diseases-conditions/allergies/symptoms-causes/syc-20351497
  40. https://acaai.org/allergies/management-treatment/living-with-allergies/environmental-allergy-avoidance/
  41. https://www.epa.gov/climate-indicators/climate-change-indicators-ragweed-pollen-season
  42. https://allergyasthmanetwork.org/allergies/pollen-allergy/ragweed-allergy/
  43. https://www.aaaai.org/tools-for-the-public/conditions-library/allergies/indoor-allergens-ttr
  44. https://aafa.org/allergies/prevent-allergies/control-indoor-allergens/
  45. https://pubmed.ncbi.nlm.nih.gov/18417052/
  46. https://www.jacionline.org/article/S0091-6749%2802%2900108-2/fulltext
  47. https://www.osha.gov/latex-allergy
  48. https://pmc.ncbi.nlm.nih.gov/articles/PMC7457822/
  49. https://www.frontiersin.org/journals/allergy/articles/10.3389/falgy.2024.1387525/full
  50. https://pubmed.ncbi.nlm.nih.gov/33558232/
  51. https://www.cdc.gov/climate-health/php/effects/allergens-and-pollen.html
  52. https://pubmed.ncbi.nlm.nih.gov/1520004/
  53. https://pmc.ncbi.nlm.nih.gov/articles/PMC1661616/
  54. https://pmc.ncbi.nlm.nih.gov/articles/PMC8700872/
  55. https://pmc.ncbi.nlm.nih.gov/articles/PMC3650954/
  56. https://pmc.ncbi.nlm.nih.gov/articles/PMC2841828/
  57. https://pmc.ncbi.nlm.nih.gov/articles/PMC3339357/
  58. https://link.springer.com/article/10.1007/s11882-020-00977-7
  59. https://www.atsjournals.org/doi/full/10.1513/pats.201008-057RN
  60. https://www.nature.com/articles/s41392-023-01344-4
  61. https://pmc.ncbi.nlm.nih.gov/articles/PMC8974858/
  62. https://www.aaaai.org/tools-for-the-public/conditions-library/allergies/oral-allergy-syndrome-%28oas%29
  63. https://emedicine.medscape.com/article/134825-clinical
  64. https://acaai.org/allergies/allergic-conditions/hay-fever/
  65. https://www.jaxallergy.com/visit-allergist-or-ent/
  66. https://www.westbocaeyecenter.com/post/when-to-see-ophthalmologist-if-you-suffer-from-allergies
  67. https://aacijournal.biomedcentral.com/articles/10.1186/s13223-018-0280-7
  68. https://publications.aap.org/pediatriccare/book/348/chapter/5776334/Allergic-Rhinitis-Chapter-212
  69. https://www.clinicaladvisor.com/features/stat-consult-allergic-rhinits/
  70. https://www.aafp.org/pubs/afp/issues/2006/0501/p1583.html
  71. https://aacijournal.biomedcentral.com/articles/10.1186/s13223-024-00923-6
  72. https://www.frontiersin.org/journals/allergy/articles/10.3389/falgy.2021.721851/full
  73. https://pmc.ncbi.nlm.nih.gov/articles/PMC4848807/
  74. https://www.mayoclinic.org/tests-procedures/allergy-tests/about/pac-20392895
  75. https://pmc.ncbi.nlm.nih.gov/articles/PMC4291909/
  76. https://www.thermofisher.com/phadia/us/en/our-solutions/immunocap-allergy-solutions/specific-ige-single-allergens.html
  77. https://emedicine.medscape.com/article/134825-workup
  78. https://pmc.ncbi.nlm.nih.gov/articles/PMC7874866/
  79. https://pubmed.ncbi.nlm.nih.gov/26163237/
  80. https://entgasouth.com/blog/can-a-nasal-endoscopy-help-with-allergy-management
  81. https://pmc.ncbi.nlm.nih.gov/articles/PMC5898957/
  82. https://www.jacionline.org/article/S0091-6749%2803%2902837-9/fulltext
  83. https://pmc.ncbi.nlm.nih.gov/articles/PMC9955395/
  84. https://www.achooallergy.com/blog/learning/dust-mites-fact-sheet/
  85. https://www.jacionline.org/article/S0091-6749%2899%2970298-8/pdf
  86. https://eymj.org/DOIx.php?id=10.3349/ymj.2020.61.8.689
  87. https://sleepandsinuscenters.com/blog/humidifier-vs-dehumidifier-for-allergies-which-is-better
  88. https://journals.lww.com/ebp/fulltext/2016/05000/does_nasal_saline_irrigation_decrease_the_symptoms.9.aspx
  89. https://www.aaaai.org/tools-for-the-public/conditions-library/allergies/allergic-rhinitis
  90. https://emedicine.medscape.com/article/134825-treatment
  91. https://pmc.ncbi.nlm.nih.gov/articles/PMC8496442/
  92. https://journals.lww.com/co-allergy/fulltext/2009/04000/rhinitis_guidelines_and_implications_for.6.aspx
  93. https://acaai.org/allergies/allergic-conditions/food/pollen-food-allergy-syndrome/
  94. https://pmc.ncbi.nlm.nih.gov/articles/PMC2917934/
  95. https://my.clevelandclinic.org/health/diseases/23996-oral-allergy-syndrome
  96. https://pmc.ncbi.nlm.nih.gov/articles/PMC10242043/
  97. https://pmc.ncbi.nlm.nih.gov/articles/PMC8436259/
  98. https://pubmed.ncbi.nlm.nih.gov/28234147/
  99. https://www.mayoclinic.org/drugs-supplements/fluticasone-nasal-route/description/drg-20070965
  100. https://www.mayoclinic.org/drugs-supplements/mometasone-nasal-route/description/drg-20064895
  101. https://acaai.org/allergies/allergic-conditions/eye-allergy/
  102. https://pmc.ncbi.nlm.nih.gov/articles/PMC9356736/
  103. https://pubmed.ncbi.nlm.nih.gov/9951950/
  104. https://www.mayoclinic.org/diseases-conditions/allergies/in-depth/allergy-medications/art-20047403
  105. https://www.aafp.org/pubs/afp/issues/2015/1201/p985.html
  106. https://jamanetwork.com/journals/jamaotolaryngology/fullarticle/484089
  107. https://www.aafp.org/pubs/afp/issues/2011/0501/p1057.html
  108. https://www.ema.europa.eu/en/news/ema-confirms-measures-minimise-risk-serious-side-effects-medicines-containing-pseudoephedrine
  109. https://newsnetwork.mayoclinic.org/discussion/mayo-clinic-q-and-a-decongestants-can-sometimes-cause-more-harm-than-good/
  110. https://pmc.ncbi.nlm.nih.gov/articles/PMC1936314/
  111. https://pubmed.ncbi.nlm.nih.gov/32915441/
  112. https://pubmed.ncbi.nlm.nih.gov/7751529/
  113. https://pubmed.ncbi.nlm.nih.gov/18254486/
  114. https://acaai.org/allergies/management-treatment/allergy-immunotherapy/immunotherapy-with-allergy-tablets/
  115. https://www.mayoclinic.org/diseases-conditions/allergies/diagnosis-treatment/drc-20351503
  116. https://www.nature.com/articles/s41577-022-00786-1
  117. https://www.frontiersin.org/journals/allergy/articles/10.3389/falgy.2021.747323/full
  118. https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2025.1658826/full
  119. https://pmc.ncbi.nlm.nih.gov/articles/PMC6132438/
  120. https://www.mayoclinic.org/tests-procedures/allergy-shots/about/pac-20392876
  121. https://pmc.ncbi.nlm.nih.gov/articles/PMC9100360/
  122. https://www.mdpi.com/1422-0067/26/10/4509
  123. https://pubmed.ncbi.nlm.nih.gov/39828891/
  124. https://www.jkslms.or.kr/journal/view.html?uid=373&vmd=Full
  125. https://eurjmedres.biomedcentral.com/articles/10.1186/s40001-022-00682-3
  126. https://www.sciencedirect.com/science/article/abs/pii/S1081120610603754
  127. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11315530/
  128. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5963652/
  129. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6273625/
  130. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6074882/
  131. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3259400/
  132. https://www.atsjournals.org/doi/full/10.1165/rcmb.2025-0241ED
  133. https://www.atsjournals.org/doi/10.1165/rcmb.2025-0085OC
  134. https://www.jacionline.org/article/S0091-6749%2825%2900268-4/fulltext
  135. https://www.sciencedirect.com/science/article/abs/pii/S1081120625001802
  136. https://aafa.org/wp-content/uploads/2025/04/aafa-allergy-facts-and-figures.pdf
  137. https://www.expertmarketresearch.com/epidemiology-reports/allergic-rhinitis-epidemiology-forecast
  138. https://pmc.ncbi.nlm.nih.gov/articles/PMC9606573/
  139. https://www.mdpi.com/2313-5786/3/4/14
  140. https://www.sciencedirect.com/science/article/abs/pii/S0301054617300708
  141. https://www.nace.org.au/knowledge-hub/news-media/2024/nothing-to-sneeze-at-why-so-many-australians-suffer-from-hay-fever/
  142. https://www.jaci-inpractice.org/article/S2213-2198%2817%2930953-4/abstract
  143. https://pubmed.ncbi.nlm.nih.gov/19132975/
  144. https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370%2825%2900259-7/fulltext
  145. https://www.explorationpub.com/uploads/Article/A100987/100987.pdf
  146. https://www.sciencedirect.com/science/article/pii/S0091674997800401
  147. https://pubmed.ncbi.nlm.nih.gov/32425054/
  148. https://www.frontiersin.org/journals/medicine/articles/10.3389/fmed.2022.874114/full
  149. https://pmc.ncbi.nlm.nih.gov/articles/PMC11963224/
  150. https://pmc.ncbi.nlm.nih.gov/articles/PMC12371843/
  151. https://www.jacionline.org/article/S0091-6749%2823%2901431-8/fulltext
  152. https://pmc.ncbi.nlm.nih.gov/articles/PMC10923006/
  153. https://jcsm.aasm.org/doi/10.5664/jcsm.10114
  154. https://www.healio.com/news/allergy-asthma/20230217/comorbid-asthma-worsens-quality-of-life-among-patients-with-allergic-rhinitis
  155. https://pmc.ncbi.nlm.nih.gov/articles/PMC10941053/
  156. https://onlinelibrary.wiley.com/doi/abs/10.1002/lary.32124
  157. https://karger.com/books/book/217/chapter/5146063/History-of-Allergy-in-Antiquity
  158. https://aai.org.tr/pdf.php?id=90
  159. https://pmc.ncbi.nlm.nih.gov/articles/PMC3110966/
  160. https://pmc.ncbi.nlm.nih.gov/articles/PMC4617537/
  161. https://hekint.org/2017/01/28/charles-harrison-blackley-the-man-who-put-the-hay-in-hay-fever/
  162. https://link.springer.com/article/10.1007/BF02136147
  163. https://onlinelibrary.wiley.com/doi/10.1111/all.12174
  164. https://pmc.ncbi.nlm.nih.gov/articles/PMC5332128/
  165. https://pmc.ncbi.nlm.nih.gov/articles/PMC11166500/
  166. https://pubmed.ncbi.nlm.nih.gov/41033334/
  167. https://www.cureus.com/articles/307041-efficacy-of-biologic-therapies-in-the-management-of-allergic-rhinitis-a-systematic-review
  168. https://pmc.ncbi.nlm.nih.gov/articles/PMC12111765/
  169. https://www.ipcc.ch/site/assets/uploads/2018/02/WGIIAR5-Chap11_FINAL.pdf
Add your contribution
Related Hubs
User Avatar
No comments yet.