allergic rhinitis allergic rhinitis 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. signs and symptoms include a runny or stuffy nose, sneezing, red, itchy, and watery eyes, and swelling around the eyes. the fluid from the nose is usually clear. symptom onset is often within minutes following allergen exposure, and can affect sleep and the ability to work or study. some people may develop symptoms only during specific times of the year, often as a result of pollen exposure. many people with allergic rhinitis also have asthma, allergic conjunctivitis, or atopic dermatitis. allergic rhinitisother nameshay fever, pollenosissem 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 immunologysymptomsstuffy itchy nose, sneezing, red, itchy, and watery eyes, swelling around the eyes, itchy earsusual onset20 to 40 years oldcausesgenetic and environmental factorsrisk factorsasthma, allergic conjunctivitis, atopic dermatitisdiagnostic methodbased on symptoms, skin prick test, blood tests for specific antibodiesdifferential diagnosiscommon coldpreventionexposure to animals early in lifemedicationnasal steroids, antihistamines such as diphenhydramine, cromolyn sodium, leukotriene receptor antagonists such as montelukast, allergen immunotherapyfrequency~20% (western countries) allergic rhinitis is typically triggered by environmental allergens such as pollen, pet hair, dust, or mold. inherited genetics and environmental exposures contribute to the development of allergies. growing up on a farm and having multiple siblings decreases this risk. 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. it causes mucous membranes in the nose, eyes and throat to become inflamed and itchy as they work to eject the allergen. diagnosis is typically based on a combination of symptoms and a skin prick test or blood tests for allergen-specific ige antibodies. these tests, however, can give false positives. 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. exposure to animals early in life might reduce the risk of developing these specific allergies. several different types of medications reduce allergic symptoms, including nasal steroids, antihistamines, such as diphenhydramine, cromolyn sodium, and leukotriene receptor antagonists such as montelukast. oftentimes, medications do not completely control symptoms, and they may also have side effects. exposing people to larger and larger amounts of allergen, known as allergen immunotherapy (ait), is often effective. the allergen can be given as an injection under the skin or as a tablet under the tongue. treatment typically lasts three to five years, after which benefits may be prolonged. allergic rhinitis is the type of allergy that affects the greatest number of people. in western countries, between 10 and 30% of people are affected in a given year. it is most common between the ages of twenty and forty. the first accurate description is from the 10th-century physician abu bakr al-razi. in 1859, charles blackley identified pollen as the cause. in 1906, the mechanism was determined by clemens von pirquet. 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. although the scent per se is irrelevant, the correlation with hay remains more than random, as peak hay-harvesting season overlaps with peak pollen season, and hay-harvesting work puts people in close contact with seasonal allergens. signs and symptoms illustration depicting inflammation associated with allergic rhinitis the characteristic symptoms of allergic rhinitis are: rhinorrhea (excess nasal secretion), itching, sneezing fits, and nasal congestion and obstruction. 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. 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. people might also find that cross-reactivity occurs. for example, people allergic to birch pollen may also find that they have an allergic reaction to the skin of apples or potatoes. 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. 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). cause pollen is often considered as a cause of allergic rhinitis, hence called hay fever (see sub-section below). 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. additionally, environmental exposures such as air pollution and maternal tobacco smoking can increase an individual's chances of developing allergies. pollen-related causes 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: trees: such as pine (pinus), mulberry (morus), birch (betula), alder (alnus), cedar (cedrus), hazel (corylus), hornbeam (carpinus), horse chestnut (aesculus), willow (salix), poplar (populus), plane (platanus), linden/lime (tilia), and olive (olea). in northern latitudes, birch is considered to be the most common allergenic tree pollen, with an estimated 15–20% of people with hay fever sensitive to birch pollen grains. a major antigen in these is a protein called bet v i. olive pollen is most predominant in mediterranean regions. hay fever in japan is caused primarily by sugi (cryptomeria japonica) and hinoki (chamaecyparis obtusa) tree pollen. "allergy friendly" trees include: female ash, red maple, yellow poplar, dogwood, magnolia, double-flowered cherry, fir, spruce, and flowering plum. grasses (family poaceae): especially ryegrass (lolium sp.) and timothy (phleum pratense). an estimated 90% of people with hay fever are allergic to grass pollen. weeds: ragweed (ambrosia), plantain (plantago), nettle/parietaria (urticaceae), mugwort (artemisia vulgaris), fat hen (chenopodium), and sorrel/dock (rumex) allergic rhinitis may also be caused by allergy to balsam of peru, which is in various fragrances and other products. genetic factors 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. 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, and specific st2 receptors, also known as il1rl1, on these cells bind to the ligand il-33 protein. 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. 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. 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. 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. 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. 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. diagnosis 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. 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. 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