text:
Zamindar
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For other uses, see Zamindar (disambiguation).
Sir Khwaja Salimullah was a zamindar with the title of Nawab. His family's landholdings in Bengal were one of the largest and richest in British India.
A zamindar in the Indian subcontinent was an aristocrat. The term means "land owner" in Persian. Typically hereditary, zamindars held enormous tracts of land and control over their peasants, from whom they reserved the right to collect tax on behalf of imperial courts or for military purposes. Their families carried titular suffixes of lordship, such as Babu, Sri, Rai, Pillai, Rao, Chaudhuri, Khan, Sardar, Malik, Thakur, Wadero, Reddy, Thevar and Naidu. In the 19th and 20th centuries, with the advent of British imperialism, many wealthy and influential zamindars were bestowed with princely and royal titles such as Maharaja (Great King), Raja (King) and Nawab.
During the Mughal Empire, zamindars belonged to the nobility[1] and formed the ruling class. Emperor Akbar granted them mansabs and their ancestral domains were treated as jagirs.[2] Under British colonial rule in India, the permanent settlement consolidated what became known as the zamindari system. The British rewarded supportive zamindars by recognizing them as princes. Many of the region's princely states were pre-colonial zamindar holdings elevated to a greater protocol. However, the British also reduced the land holdings of many pre-colonial aristocrats, demoting their status to a zamindar from previously higher ranks of nobility.
The system was abolished during land reforms in East Bengal (Bangladesh) in 1950,[3] India in 1951[4] and West Pakistan in 1959.[5]
The zamindars often played an important role in the regional histories of the subcontinent. One of the most notable examples is the 16th century confederation formed by 12 zamindars in the Bhati region, which, according to the Jesuits and Ralph Fitch, earned a reputation for successively repelling Mughal invasions through naval battles. The confederation was led by a zamindar-king, Isa Khan, and included both Muslims and Hindus, such as Pratapaditya. The zamindars were also patrons of the arts. One of the zamindar of Bundelkhand had control over more than 52 villages.[6] The Tagore family produced India's first Nobel laureate in literature in 1913, Rabindranath Tagore, who was often based at his estate. The zamindars also promoted neoclassical and Indo-Saracenic architecture.
Contents
[hide]
1 Mughal era
2 British era
2.1 Accession
3 Abolition
4 See also
5 References
Mughal era[edit]
Mehtab Chand (1820-79) (zamindar of the Burdwan Raj) as a young man, c. 1840-45 A.D.
Before Mughal rule in India, the aristocracy collected and retained revenue from land and production. The Mughals appointed people to act as tax officers, sending them around the country to oversee collection of revenue and remit it to the capital city of Delhi.[7] These people were known as the zamindari (intermediaries)[8] and they collected revenue primarily from the Ryots (peasants)[9] The zamindari system was more prevalent in the north of India because Mughal influence in the south was less apparent.[8]
The zamindari system ensured proper collection of taxes in a period when the power and influence of the Mughal emperors were in decline. With the Mughal conquest of Bengal, "zamindar" became a generic title embracing people with different kinds of landholdings, rights and responsibilities ranging from the autonomous or semi-independent chieftains to the peasant-proprietors. All categories of zamindars under the Mughals were required to perform certain police, judicial and military duties. Zamindars under the Mughals were, in fact, more the public functionaries than revenue collecting agents. Although zamindaris were allowed to be held hereditarily, the holders were not considered to be the proprietors of their estates.[citation needed]
The territorial zamindars had judicial powers also. This conferred status with attendant power, which really made them the lords of their domains. They held regular courts, called zamindari adalat. The courts gave them not only power and status but some income as well by way of fines, presents and perquisites. The petty zamindars had some share in the dispensation of civil and criminal justice. The Chowdhurys, who were zamindars in most cases, had authority to deal with the complaints of debts, thefts and petty quarrels and to impose paltry fines.[citation needed]
British era[edit]
circa 1898-1901. Jagirdar Mustafa Ali Khan rais, a prominent zamindar (with the honorary title of Nawab) of old city Barielly (United Provinces) British India.
The British colonists of India generally adopted the extant zamindari system of revenue collection in the north of the country. They recognised the zamindars as landowners and in return required them to collect taxes. Although some zamindars were present in the south, they were not so in large numbers and the British administrators used the ryotwari (cultivator) method of collection, which involved selecting certain farmers as being land owners and requiring them to remit their taxes directly.[8]
The Zamindars of Bengal were influential in the development of Bengal. They played pivotal part during the Indian Rebellion of 1857.[10]
Accession[edit]
Unlike the autonomous or frontier chiefs, the hereditary status of the zamindar class was circumscribed by the Mughals, and the heir depended to a certain extent on the pleasure of the sovereign.[11] Heirs were set by descent or a times even adoption by religious laws.[12] Under the British Empire, the zamindars were to be subordinate to the crown and not act as hereditary lords, but at times family politics was at the heart of naming an heir.[13] At times, a cousin could be named an heir with closer family relatives present;[14] a lawfully wedded wife could inherit the zamindari if the ruling zamindar named her as an heir.[15][16]
Abolition[edit]
The zamindari system was mostly abolished in India soon after its creation with the first amendment to the constitution of India which amended the right to property as shown in Articles 19 and 31.[17] This allowed the states to make their own "Zamindari Abolition Acts".[citation needed] In Bangladesh, the East Bengal State Acquisition and Tenancy Act of 1950 had a similar effect of ending the system.[citation needed]
See also[edit]
Indian feudalism
Indian honorifics
Maratha titles
Jagirdar
Mankari
List of amendments of the Constitution of India
References[edit]
Jump up ^ Metcalf, Barbara Daly (1984). Moral conduct and authority: the place of adab in South Asian Islam. University of California Press. p. 269.
Jump up ^ Acharya, Shreya. "Give an account of the Ruling Classes of Mughal Empire". www.preservearticles.com. Archived from the original on 2013-05-21.
Jump up ^ Baxter, C (1997). Bangladesh, from a Nation to a State. Westview Press. p. 72. ISBN 0-8133-3632-5.
Jump up ^ "Abolition of Zamindari in India - General Knowledge Today". www.gktoday.in. Archived from the original on 2016-11-30.
Jump up ^ Newspaper, From the (11 October 2010). "Land reforms in Pakistan". dawn.com. Archived from the original on 30 November 2016.
Jump up ^ Baxter first=c (1980). A legend man. Radha press. More than one of |author= and |last= specified (help)CS1 maint: Missing pipe (link)
Jump up ^ Hansen, Valerie; Curtis, Kenneth R. "The Politics of Empire in Southern and Eastern Asia". Voyages in World History, Volume 2: Since 1500. p. 461.
^ Jump up to: a b c Jaffrelot, Christophe (September–October 2000). "Sanskritization vs. Ethnicization in India: Changing Indentities and Caste Politics before Mandal". Asian Survey. 40 (5): 756–766. doi:10.1525/as.2000.40.5.01p0100d. JSTOR 3021175.
Jump up ^ Habib, Irfan (2000) [1963]. The Agrarian System of Mughal India, 1526-1707 (2nd revised ed.). Oxford University Press. ISBN 0-19-562329-0. For the meanings of zamindar see pp. 140ff.
Jump up ^ "Patriotic And Comprador Zamindars In The Great Rebellion Of 1857". pd.cpim.org. Archived from the original on 2012-05-05.
Jump up ^ Islam, Sirajul; Akhter, Shirin (2012). "Zamindar". In Islam, Sirajul; Jamal, Ahmed A. Banglapedia: National Encyclopedia of Bangladesh (Second ed.). Asiatic Society of Bangladesh. Archived from the original on 2015-07-03.
Jump up ^ The Indian Law Reports: Madras series. Controller of Stationery and Print. 1888. p. 385.
Jump up ^ McLane, John R. (2002). Land and Local Kingship in Eighteenth-Century Bengal. Cambridge University Press. p. 223. ISBN 978-0-521-52654-8.
Jump up ^ Madras High Court Reports: 1870 and 1871. J. Higgingbotham. 1872. p. 209.
Jump up ^ Great Britain. Privy Council. Judicial Committee.; India. Courts. (1908). "Kashi Prasad v. Indar Kunwar". Allahabad Law Journal. Indian Press. 5: 596.
Jump up ^ Woodman, Joseph Vere; Monnier, Emile Henry (1902). A Digest of Indian Law Cases: Containing High Court Reports, 1862-1900, and Privy Council Reports of Appeals from India, 1836-1900, with an Index of Cases. Volume III: J-M. Superintendent of Government Printing, India. p. 5498.
Jump up ^ Guha, Ramachandra (2011). India After Gandhi. Ecco. pp. 219–220. ISBN 978-0-330-54020-9.
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Food allergy
From Wikipedia, the free encyclopedia
Jump to: navigation, search
Food allergy
Hives on the back are a common allergy symptom.
Specialty
Emergency medicine
Symptoms
Itchiness, swelling of the tongue, vomiting, diarrhea, hives, trouble breathing, low blood pressure[1]
Usual onset
Minutes to several hours of exposure[1]
Duration
Long term, some may resolve[2]
Causes
Immune response to food[1]
Risk factors
Family history, vitamin D deficiency, obesity, high levels of cleanliness[1][2]
Diagnostic method
Based on a medical history, elimination diet, skin prick test, oral food challenge[1][2]
Similar conditions
Food intolerance, food poisoning[1]
Prevention
Early exposure to potential allergens[2][3]
Treatment
Avoiding the food in question, having a plan if exposure occurs, medical alert jewelry[1][2]
Medication
Adrenaline (epinephrine)[1]
Frequency
~6% (developed world)[1][2]
[edit on Wikidata]
A food allergy is an abnormal immune response to food.[1] The signs and symptoms may range from mild to severe.[1] They may include itchiness, swelling of the tongue, vomiting, diarrhea, hives, trouble breathing, or low blood pressure.[1] This typically occurs within minutes to several hours of exposure.[1] When the symptoms are severe, it is known as anaphylaxis.[1] Food intolerance and food poisoning are separate conditions.[1]
Common foods involved include cow's milk, peanuts, eggs, shellfish, fish, tree nuts, soy, wheat, rice, and fruit.[1][2][4] The common allergies vary depending on the country.[1] Risk factors include a family history of allergies, vitamin D deficiency, obesity, and high levels of cleanliness.[1][2] Allergies occur when immunoglobulin E (IgE), part of the body's immune system, binds to food molecules.[1] A protein in the food is usually the problem.[2] This triggers the release of inflammatory chemicals such as histamine.[1] Diagnosis is usually based on a medical history, elimination diet, skin prick test, blood tests for food-specific IgE antibodies, or oral food challenge.[1][2]
Early exposure to potential allergens may be protective.[2][3] Management primarily involves avoiding the food in question and having a plan if exposure occurs.[2] This plan may include giving adrenaline (epinephrine) and wearing medical alert jewelry.[1] The benefits of allergen immunotherapy for food allergies is unclear, thus is not recommended as of 2015.[5] Some types of food allergies among children resolve with age, including that to milk, eggs, and soy; while others such as to nuts and shellfish typically do not.[2]
In the developed world, about 4% to 8% of people have at least one food allergy.[1][2] They are more common in children than adults and appear to be increasing in frequency.[2] Male children appear to be more commonly affected than females.[2] Some allergies more commonly develop early in life, while others typically develop in later life.[1] In developed countries, a large proportion of people believe they have food allergies when they actually do not have them.[6][7][8]
Contents
[hide]
1 Signs and symptoms
2 Cause
2.1 Sensitization
2.2 Atopy
2.3 Cross-reactivity
3 Pathophysiology
3.1 Acute response
3.2 Late-phase response
4 Diagnosis
4.1 Differential diagnosis
5 Prevention
5.1 Inhalation exposure
6 Treatment
6.1 Epinephrine
6.2 Antihistamines
6.3 Steroids
7 Epidemiology
7.1 United States
8 Society and culture
8.1 Regulation of labelling
8.2 Genetically modified food
9 Research
10 See also
11 References
12 External links
Signs and symptoms[edit]
Food allergies usually have a fast onset (from seconds to one hour) and may include:[9]
Rash
Hives[9]
Itching of mouth, lips, tongue, throat, eyes, skin, or other areas[9]
Swelling (angioedema) of lips, tongue, eyelids, or the whole face[9]
Difficulty swallowing[9]
Runny or congested nose[9]
Hoarse voice[9]
Wheezing and/or shortness of breath[9]
Diarrhea, abdominal pain, and/or stomach cramps[9]
Lightheadedness[9]
Fainting[9]
Nausea[9]
Vomiting[9]
In some cases, however, onset of symptoms may be delayed for hours.[9]
Symptoms of allergies vary from person to person. The amount of food needed to trigger a reaction also varies from person to person.
Serious danger regarding allergies can begin when the respiratory tract or blood circulation is affected. The former can be indicated through wheezing and cyanosis. Poor blood circulation leads to a weak pulse, pale skin and fainting.[10]
A severe case of an allergic reaction, caused by symptoms affecting the respiratory tract and blood circulation, is called anaphylaxis. When symptoms are related to a drop in blood pressure, the person is said to be in anaphylactic shock. Anaphylaxis occurs when IgE antibodies are involved, and areas of the body that are not in direct contact with the food become affected and show symptoms.[11] Those with asthma or an allergy to peanuts, tree nuts, or seafood are at greater risk for anaphylaxis.[12]
Cause[edit]
Although sensitivity levels vary by country, the most common food allergies are allergies to milk, eggs, peanuts, tree nuts, seafood, shellfish, soy, and wheat.[13] These are often referred to as "the big eight".[14] Allergies to seeds — especially sesame — seem to be increasing in many countries.[15] An example an allergy more common to a particular region is that to rice in East Asia where it forms a large part of the diet.[16]
One of the most common food allergies is a sensitivity to peanuts, a member of the bean family. Peanut allergies may be severe, but children with peanut allergies sometimes outgrow them.[17] Tree nuts, including cashews, Brazil nuts, hazelnuts, macadamia nuts, pecans, pistachios, pine nuts, coconuts, and walnuts, are also common allergens. Sufferers may be sensitive to one particular tree nut or to many different ones.[18] Also, seeds, including sesame seeds and poppy seeds, contain oils where protein is present, which may elicit an allergic reaction.[18]
Egg allergies affect about one in 50 children but are frequently outgrown by children when they reach age five.[19] Typically, the sensitivity is to proteins in the white, rather than the yolk.[18]
Milk from cows, goats, or sheep is another common food allergen, and many sufferers are also unable to tolerate dairy products such as cheese. A small portion of children with a milk allergy, roughly 10%, have a reaction to beef. Beef contains a small amount of protein that is also present in cow's milk.[20]
Seafood is one of the most common sources of food allergens; people may be allergic to proteins found in fish, crustaceans, or shellfish.[21]
Other foods containing allergenic proteins include soy, wheat, fruits, vegetables, maize, spices, synthetic and natural colors,[citation needed] and chemical additives.
Balsam of Peru, which is in various foods, is in the "top five" allergens most commonly causing patch test reactions in people referred to dermatology clinics.[22][23][24]
Sensitization[edit]
An Institute of Medicine report says that food proteins contained in vaccines, such as gelatin, milk, or egg can cause sensitization (development of allergy) in vaccine recipients, to those food items.[25]
Atopy[edit]
Food allergies develop more easily in people with the atopic syndrome, a very common combination of diseases: allergic rhinitis and conjunctivitis, eczema, and asthma.[26] The syndrome has a strong inherited component; a family history of allergic diseases can be indicative of the atopic syndrome.[medical citation needed]
Cross-reactivity[edit]
Some children who are allergic to cow's milk protein also show a cross-sensitivity to soy-based products.[27] Some infant formulas have their milk and soy proteins hydrolyzed, so when taken by infants, their immune systems do not recognize the allergen and they can safely consume the product. Hypoallergenic infant formulas can be based on proteins partially predigested to a less antigenic form. Other formulas, based on free amino acids, are the least antigenic and provide complete nutritional support in severe forms of milk allergy.
People with latex allergy often also develop allergies to bananas, kiwifruit, avocados, and some other foods.[28]
Pathophysiology[edit]
A histamine, the structure shown, causes a person to feel itchy during an allergic reaction. A common medication to stop this is an antihistamine, which fights the histamines in the person's system.
Conditions caused by food allergies are classified into three groups according to the mechanism of the allergic response:[29]
IgE-mediated (classic) – the most common type, occurs shortly after eating and may involve anaphylaxis.
Non-IgE mediated – characterized by an immune response not involving immunoglobulin E; may occur some hours after eating, complicating diagnosis
IgE and/or non-IgE-mediated – a hybrid of the above two types
Allergic reactions are hyperactive responses of the immune system to generally innocuous substances. When immune cells encounter the allergenic protein, IgE antibodies are produced; this is similar to the immune system's reaction to foreign pathogens. The IgE antibodies identify the allergenic proteins as harmful and initiate the allergic reaction. The harmful proteins are those that do not break down due to the strong bonds of the protein. IgE antibodies bind to a receptor on the surface of the protein, creating a tag, just as a virus or parasite becomes tagged. Why some proteins do not denature and subsequently trigger allergic reactions and hypersensitivity while others do is not entirely clear.[30]
Hypersensitivities are categorized according to the parts of the immune system that are attacked and the amount of time it takes for the response to occur. The four types of hypersensitivity reaction are: type 1, immediate IgE-mediated; type 2, cytotoxic; type 3, immune complex-mediated; and type 4, delayed cell-mediated.[31] The pathophysiology of allergic responses can be divided into two phases. The first is an acute response that occurs immediately after exposure to an allergen. This phase can either subside or progress into a "late-phase reaction" which can substantially prolong the symptoms of a response, and result in tissue damage.
Many food allergies are caused by hypersensitivities to particular proteins in different foods. Proteins have unique properties that allow them to become allergens, such as stabilizing forces in their tertiary and quaternary structures which prevent degradation during digestion. Many theoretically allergenic proteins cannot survive the destructive environment of the digestive tract, thus do not trigger hypersensitive reactions.[32]
Acute response[edit]
Degranulation process in allergy.
1 — antigen
2 — IgE antibody
3 — FcεRI receptor
4 — preformed mediators (histamine, proteases, chemokines, heparin)
5 — granules
6 — mast cell
7 — newly formed mediators (prostaglandins, leukotrienes, thromboxanes, PAF)
In the early stages of allergy, a type I hypersensitivity reaction against an allergen, encountered for the first time, causes a response in a type of immune cell called a TH2 lymphocyte, which belongs to a subset of T cells that produce a cytokine called interleukin-4 (IL-4). These TH2 cells interact with other lymphocytes called B cells, whose role is the production of antibodies. Coupled with signals provided by IL-4, this interaction stimulates the B cell to begin production of a large amount of a particular type of antibody known as IgE. Secreted IgE circulates in the blood and binds to an IgE-specific receptor (a kind of Fc receptor called FcεRI) on the surface of other kinds of immune cells called mast cells and basophils, which are both involved in the acute inflammatory response. The IgE-coated cells, at this stage, are sensitized to the allergen.[33]
If later exposure to the same allergen occurs, the allergen can bind to the IgE molecules held on the surface of the mast cells or basophils. Cross-linking of the IgE and Fc receptors occurs when more than one IgE-receptor complex interacts with the same allergenic molecule, and activates the sensitized cell. Activated mast cells and basophils undergo a process called degranulation, during which they release histamine and other inflammatory chemical mediators (cytokines, interleukins, leukotrienes, and prostaglandins) from their granules into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve stimulation, and smooth-muscle contraction. This results in rhinorrhea, itchiness, dyspnea, and anaphylaxis. Depending on the individual, the allergen, and the mode of introduction, the symptoms can be system-wide (classical anaphylaxis), or localized to particular body systems; asthma is localized to the respiratory system and eczema is localized to the dermis.[33]
Late-phase response[edit]
After the chemical mediators of the acute response subside, late-phase responses can often occur due to the migration of other leukocytes such as neutrophils, lymphocytes, eosinophils, and macrophages to the initial site. The reaction is usually seen 2–24 hours after the original reaction.[34] Cytokines from mast cells may also play a role in the persistence of long-term effects. Late-phase responses seen in asthma are slightly different from those seen in other allergic responses, although they are still caused by release of mediators from eosinophils, and are still dependent on activity of TH2 cells.[35]
Diagnosis[edit]
Skin testing on the arm is a common way for detecting an allergy, but it is not as effective as other tests.
Patch test
Diagnosis is usually based on a medical history, elimination diet, skin prick test, blood tests for food-specific IgE antibodies, or oral food challenge.[1][2]
For skin-prick tests, a tiny board with protruding needles is used. The allergens are placed either on the board or directly on the skin. The board is then placed on the skin, to puncture the skin and for the allergens to enter the body. If a hive appears, the person is considered positive for the allergy. This test only works for IgE antibodies. Allergic reactions caused by other antibodies cannot be detected through skin-prick tests.[36]
Skin-prick testing is easy to do and results are available in minutes. Different allergists may use different devices for testing. Some use a "bifurcated needle", which looks like a fork with two prongs. Others use a "multitest", which may look like a small board with several pins sticking out of it. In these tests, a tiny amount of the suspected allergen is put onto the skin or into a testing device, and the device is placed on the skin to prick, or break through, the top layer of skin. This puts a small amount of the allergen under the skin. A hive will form at any spot where the person is allergic. This test generally yields a positive or negative result. It is good for quickly learning if a person is allergic to a particular food or not, because it detects IgE. Skin tests cannot predict if a reaction would occur or what kind of reaction might occur if a person ingests that particular allergen. They can, however, confirm an allergy in light of a patient's history of reactions to a particular food. Non-IgE-mediated allergies cannot be detected by this method.
Patch testing is used to determine if a specific substance causes allergic inflammation of the skin. It tests for delayed food reactions.[37][38][39]
Blood testing is another way to test for allergies; however, it poses the same disadvantage and only detects IgE allergens and does not work for every possible allergen. Radioallergosorbent testing (RAST) is used to detect IgE antibodies present to a certain allergen. The score taken from the RAST is compared to predictive values, taken from a specific type of RAST. If the score is higher than the predictive values, a great chance the allergy is present in the person exists. One advantage of this test is that it can test many allergens at one time.[40]
A CAP-RAST has greater specificity than RAST; it can show the amount of IgE present to each allergen.[41] Researchers have been able to determine "predictive values" for certain foods, which can be compared to the RAST results. If a person's RAST score is higher than the predictive value for that food, over a 95% chance exists that patients will have an allergic reaction (limited to rash and anaphylaxis reactions) if they ingest that food.[citation needed] Currently, predictive values are available for milk, egg, peanut, fish, soy, and wheat.[42][43][44] Blood tests allow for hundreds of allergens to be screened from a single sample, and cover food allergies as well as inhalants. However, non-IgE-mediated allergies cannot be detected by this method. Other widely promoted tests such as the antigen leukocyte cellular antibody test and the food allergy profile are considered unproven methods, the use of which is not advised.[45]
Food challenges test for allergens other than those caused by IgE allergens. The allergen is given to the person in the form of a pill, so the person can ingest the allergen directly. The person is watched for signs and symptoms. The problem with food challenges is that they must be performed in the hospital under careful watch, due to the possibility of anaphylaxis.[46]
Food challenges, especially double-blind, placebo-controlled food challenges, are the gold standard for diagnosis of food allergies, including most non-IgE-mediated reactions. Blind food challenges involve packaging the suspected allergen into a capsule, giving it to the patient, and observing the patient for signs or symptoms of an allergic reaction.
The best method for diagnosing food allergy is to be assessed by an allergist. The allergist will review the patient's history and the symptoms or reactions that have been noted after food ingestion. If the allergist feels the symptoms or reactions are consistent with food allergy, he/she will perform allergy tests. Additional diagnostic tools for evaluation of eosinophilic or non-IgE mediated reactions include endoscopy, colonoscopy, and biopsy.
Differential diagnosis[edit]
Important differential diagnoses are:
Lactose intolerance generally develops later in life, but can present in young patients in severe cases. It is due to an enzyme deficiency (lactase) and not allergy, and occurs in many non-Western people.
Celiac disease is an autoimmune disorder triggered by gluten proteins such as gliadin (present in wheat, rye, and barley). It is a non-IgE-mediated food allergy by definition.
Irritable bowel syndrome
C1 Esterase inhibitor deficiency (hereditary angioedema), a rare disease, generally causes attacks of angioedema, but can present solely with abdominal pain and occasional diarrhea.
Prevention[edit]
Breastfeeding for more than four months may prevent atopic dermatitis, cow's milk allergy, and wheezing in early childhood.[47] Early exposure to potential allergens may be protective.[2] Specifically, early exposure to eggs and peanuts reduces the risk of allergies to these.[3]
To avoid an allergic reaction, a strict diet can be followed. It is difficult to determine the amount of allergenic food required to elicit a reaction, so complete avoidance should be attempted. In some cases, hypersensitive reactions can be triggered by exposures to allergens through skin contact, inhalation, kissing, participation in sports, blood transfusions, cosmetics, and alcohol.[48]
Inhalation exposure[edit]
Allergic reactions to airborn particles or vapors of known food allergens have been reported as an occupational consequence of people working in the food industry, but can also take place in home situations, restaurants, or confined spaces such as airplanes. According to two reviews, respiratory symptoms are common, but in some cases there has been progression to anaphylaxis.[49][50] The most frequent reported cases of reactions by inhalation of allergenic foods were due to peanut, seafood, legumes, tree nut, and cow’s milk.[49] Steam rising from cooking of lentils, green beans, chickpeas and fish has been well documented as triggering reactions, including anaphylactic reactions.[49][51] One review mentioned case study examples of allergic responses to other foods, including examples in which oral consumption of the food is tolerated.[49]
Treatment[edit]
The mainstay of treatment for food allergy is total avoidance of the foods identified as allergens. An allergen can enter the body by consuming a food containing the allergen, and can also be ingested by touching any surfaces that may have come into contact with the allergen, then touching the eyes or nose. For people who are extremely sensitive, avoidance includes avoiding touching or inhaling the problematic food.
If the food is accidentally ingested and a systemic reaction (anaphylaxis) occurs, then epinephrine should be used. A second dose of epinephrine may be required for severe reactions. The person should then be transported to the emergency room, where additional treatment can be given. Other treatments include antihistamines and steroids.[52]
Epinephrine[edit]
Epinephrine autoinjectors are portable single-dose epinephrine-dispensing devices used to treat anaphylaxis.
Epinephrine (adrenaline) is the first-line treatment for severe allergic reactions (anaphylaxis). If administered in a timely manner, epinephrine can reverse its effects. Epinephrine relieves airway swelling and obstruction, and improves blood circulation; blood vessels are tightened and heart rate is increased, improving circulation to body organs. Epinephrine is available by prescription in an autoinjector.[53]
Antihistamines[edit]
Antihistamines can alleviate some of the milder symptoms of an allergic reaction, but do not treat all symptoms of anaphylaxis.[54] Antihistamines block the action of histamine, which causes blood vessels to dilate and become leaky to plasma proteins. Histamine also causes itchiness by acting on sensory nerve terminals. The most common antihistamine given for food allergies is diphenhydramine.
Steroids[edit]
Glucocorticoid steroids are used to calm down the immune system cells that are attacked by the chemicals released during an allergic reaction. This treatment in the form of a nasal spray should not be used to treat anaphylaxis, for it only relieves symptoms in the area in which the steroid is in contact. Another reason steroids should not be used is the delay in reducing inflammation. Steroids can also be taken orally or through injection, by which every part of the body can be reached and treated, but a long time is usually needed for these to take effect.[55]
Epidemiology[edit]
The most common food allergens account for about 90% of all allergic reactions;[56] in adults they include shellfish, peanuts, tree nuts, fish, and egg.[57] In children, they include milk, eggs, peanuts, and tree nuts.[57] Six to 8% of children under the age of three have food allergies and nearly 4% of adults have food allergies.[57]
For reasons not entirely understood, the diagnosis of food allergies has apparently become more common in Western nations recently.[58] In the United States, food allergy affects as many as 5% of infants less than three years of age[59] and 3% to 4% of adults.[60] A similar prevalence is found in Canada.[61]
About 75% of children who have allergies to milk protein are able to tolerate baked-in milk products, i.e., muffins, cookies, cake, and hydrolyzed formulas.[62]
About 50% of children with allergies to milk, egg, soy, peanuts, tree nuts, and wheat will outgrow their allergy by the age of 6. Those who are still allergic by the age of 12 or so have less than an 8% chance of outgrowing the allergy.[63]
Peanut and tree nut allergies are less likely to be outgrown, although evidence now shows[64] that about 20% of those with peanut allergies and 9% of those with tree nut allergies will outgrow them.[65]
In Japan, allergy to buckwheat flour, used for soba noodles, is more common than peanuts, tree nuts or foods made from soy beans.[66]
United States[edit]
In the United States, an estimated 12 million people have food allergies. Food allergy affects as many as 5% of infants less than three years of age[59] and 3% to 4% of adults.[60][67] The prevalence of food allergies is rising.[58][68][69] Food allergies cause roughly 30,000 emergency room visits and 150 deaths per year.[70]

Society and culture[edit]
Whether rates of food allergy is increasing or not, food allergy awareness has definitely increased, with impacts on the quality of life for children, their parents and their immediate caregivers.[71][72][73][74] In the United States, the Food Allergen Labeling and Consumer Protection Act of 2004 causes people to be reminded of allergy problems every time they handle a food package, and restaurants have added allergen warnings to menus. The Culinary Institute of America, a premier school for chef training, has courses in allergen-free cooking and a separate teaching kitchen.[75] School systems have protocols about what foods can be brought into the school. Despite all these precautions, people with serious allergies are aware that accidental exposure can easily occur at other peoples' houses, at school or in restaurants.[76] Food fear has a significant impact on quality of life.[73][74] Finally, for children with allergies, their quality of life is also affected by actions of their peers. There is an increased occurrence of bullying, which can include threats or acts of deliberately being touched with foods they need to avoid, also having their allergen-free food deliberately contaminated.[77]
Regulation of labelling[edit]
In response to the risk that certain foods pose to those with food allergies, some countries have responded by instituting labeling laws that require food products to clearly inform consumers if their products contain major allergens or byproducts of major allergens. Some countries also require companies to warn customers when food has been prepared around certain allergens that have been known to cause severe reactions.[78]
An example of a list of allergens in a food item
Under the U.S. Food Allergen Labeling and Consumer Protection Act of 2004 (Public Law 108-282), companies are required to disclose on the label whether the product contains a major food allergen in clear, plain language.The eight major allergens are cow's milk, peanuts, eggs, shellfish, fish, tree nuts, soy and wheat. The allergens have to clearly be called out in the ingredient statement. Most companies list allergens in a statement separate from the ingredient statement.[79]
The European Union requires listing for those eight plus molluscs, celery, mustard, lupin, sesame and sulfites.[80] The EU Food Information for Consumers Regulation 1169/2011 – requires food businesses to provide allergy information on food sold unpackaged, for example, in catering outlets, deli counters, bakeries and sandwich bars.[81]
On 4 January 2011, President Barack Obama signed into federal law the Food Safety and Modernization Act of 2010 (S510/HR2751, 111th Congress). Section 112 of this Act establishes voluntary food allergy and anaphylaxis management guidelines for public kindergartens and elementary and secondary schools.
Genetically modified food[edit]
There are concerns that genetically modified foods, also described as foods sourced from genetically modified organisms (GMO), could be responsible for allergic reactions, and that the widespread acceptance of GMO foods may be responsible for what is a real or perceived increase in the percentage of people with allergies.[82][83][84] One concern is that genetic engineering could make an allergy-provoking food more allergic, meaning that smaller portions would suffice to set off a reaction.[84] Of the food currently in widespread GMO use, only soybeans are identified as a common allergen. However, for the soybean proteins known to trigger allergic reactions, there is more variation from strain to strain than between those and the GMO varieties.[83] The same review quoted a 2016 U.S. National Academy of Sciences report that concluded, “The committee did not find a relationship between consumption of GE foods and the increase in prevalence of food allergies."[83]
A second concern is that genes transferred from one species to another could introduce an allergen in a food not thought of as particularly allergenic. Research on an attempt to enhance the quality of soybean protein by adding genes from Brazil nuts was terminated when human volunteers known to have tree nut allergy reacted to the modified soybeans.[82] A second example was the 1998 introduction of a Bacillus thuringiensis gene coding for Cry9c protein into Starlink brand corn to provide insect resistance. The U.S. Environmental Protection Agency had restricted its use to corn intended as animal feed, but in 2000 it was found in the human food supply, leading to first a voluntary and then a FDA mandated recall, referred to as the StarLink corn recall.[85] At present, prior to a new GMO food receiving government approval, certain criteria need to be met. These include: Is the donor species known to be allergenic? Does the amino acid sequence of the transferred proteins resemble the sequence of known allergenic proteins? Are the transferred proteins resistant to digestion - a trait shared by many allergenic proteins?[83] Finally, there are requirements in some countries and recommendations in others that all foods containing GMO ingredients be so labeled, and that there be a post-launch monitoring system to report adverse effects (much there exists in some countries for drug and dietary supplement reporting).[82] According to a 2015 report from the Center for Food Safety, 64 countries require labeling of GMO products in the marketplace.[86]
Research[edit]
A number of desensitization techniques are being studied.[87] Areas of research include anti-IgE antibody (omalizumab), specific oral tolerance induction (SOTI, also known as OIT for oral immunotherapy), and sublingual immunotherapy (SLIT). The benefits of allergen immunotherapy for food allergies is unclear, thus is not recommended as of 2015.[5]
There is research on the effects of increasing intake of polyunsaturated fatty acids (PUFAs) during pregnancy, lactation, via infant formula and in early childhood on the subsequent risk of developing food allergies during infancy and childhood. From two reviews, maternal intake of omega-3, long-chain fatty acids during pregnancy appeared to reduce the risks of medically diagnosed IgE-mediated allergy, eczema and food allergy per parental reporting in the first 12 months of life,[88][89] but the effects were not all sustained past 12 months.[89] The reviews characterized the literature's evidence as inconsistent and limited.[88][89] Results when breastfeeding mothers were consuming a diet high in PUFAs were inconclusive.[90] For infants, supplementing their diet with oils high in PUFAs did not affect the risks of food allergies, eczema or asthma either as infants or into childhood.[91]
There is research on probiotics, prebiotics and the combination of the two (synbiotics) as a means of treating or preventing infant and child allergies. From reviews, there appears to be a treatment benefit for eczema,[92][93][94] but not asthma, wheezing or rhinoconjunctivitis.[95] The evidence was not consistent for preventing food allergies and this approach cannot yet be recommended.[93][94][96][97]
See also[edit]
List of allergens (food and non-food)
SEICAP (Spanish Society of Pediatric Allergy, Asthma and Clinical Immunology)
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Notes
Nester, Eugene W.; Anderson, Denise G.; Roberts Jr, C. Evans; Nester, Martha T. (2009). "Immunologic Disorders". Microbiology: A Human Perspective (6th ed.). New York: McGraw-Hill. pp. 414–428.
Sicherer, Scott H. (2006). Understanding and Managing Your Child's Food Allergy. Baltimore: Johns Hopkins University Press.
External links[edit]
Classification
V · T · D
ICD-10: T78.0
ICD-9-CM: V15.01-V15.05
OMIM: 147050
MeSH: D005512
External resources
MedlinePlus: 000817
eMedicine: med/806

Food Allergy, Merck Manual
"Food Allergies and Intolerances Resource List for Consumers" (PDF). Food and Nutrition Information Center, National Agricultural Library. December 2010. – a collection of resources on the topic of food allergies and intolerances
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