Egg allergy

Egg allergy is an immune hypersensitivity to proteins found in chicken eggs, and possibly goose, duck, or turkey eggs.[1] Symptoms can be either rapid or gradual in onset. The latter can take hours to days to appear. The former may include anaphylaxis, a potentially life-threatening condition which requires treatment with epinephrine. Other presentations may include atopic dermatitis or inflammation of the esophagus.[1][3]

Egg allergy
Fried chicken egg
Frequency~1.5% (developed world)[1][2]

In the United States, 90% of allergic responses to foods are caused by cow's milk, eggs, wheat, shellfish, peanuts, tree nuts, fish, and soy beans.[4] The declaration of the presence of trace amounts of allergens in foods is not mandatory in any country, with the exception of Brazil.[5][6][7]

Prevention is by avoiding eating eggs and foods that may contain eggs, such as cake or cookies.[1] It is unclear if the early introduction of the eggs to the diet of babies aged 4–6 months decreases the risk of egg allergies.[8][9][10][11]

Egg allergy appears mainly in children but can persist into adulthood. In the United States, it is the second most common food allergy in children after cow's milk. Most children outgrow egg allergy by the age of five, but some people remain allergic for a lifetime.[12][13] In North America and Western Europe egg allergy occurs in 0.5% to 2.5% of children under the age of five years.[1][2] The majority grow out of it by school age, but for roughly one-third, the allergy persists into adulthood. Strong predictors for adult-persistence are anaphylaxis, high egg-specific serum immunoglobulin E (IgE), robust response to the skin prick test and absence of tolerance to egg-containing baked foods.[1][14]

Signs and symptoms

Food allergies usually have a fast onset (from seconds to one hour). Symptoms may include: rash, hives, itching of mouth, lips, tongue, throat, eyes, skin, or other areas, swelling of lips, tongue, eyelids, or the whole face, difficulty swallowing, runny or congested nose, hoarse voice, wheezing, shortness of breath, diarrhea, abdominal pain, lightheadedness, fainting, nausea, or vomiting.[15] Symptoms of allergies vary from person to person and may vary from incident to incident.[15] Serious danger regarding allergies can begin when the respiratory tract or blood circulation is affected. The former can be indicated by wheezing, a blocked airway and cyanosis, the latter by weak pulse, pale skin, and fainting. When these symptoms occur the allergic reaction is called anaphylaxis.[15] 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 severe symptoms.[15][16] Untreated, this can proceed to vasodilation, a low blood pressure situation called anaphylactic shock, and death (very rare).[12][16]

Young children may exhibit dermatitis/eczema on face, scalp and other parts of the body, in older children knees and elbows are more commonly afflicted. Children with dermatitis are at greater than expected risk of also exhibiting asthma and allergic rhinitis.[17]


Eating egg

The cause is typically the eating of eggs or foods that contain eggs. Briefly, the immune system over-reacts to proteins found in eggs. This allergic reaction may be triggered by small amounts of egg, even egg incorporated into cooked foods, such as cake. People with an allergy to chicken eggs may also be reactive to goose, duck, or turkey eggs.[1]


Influenza vaccines are created by injecting a live virus into fertilized chicken eggs.[18] The viruses are harvested, killed and purified, but a residual amount of egg white protein remains. Each year, vaccines are created to provide protection against the flu viruses expected to be prevalent in the upcoming cold weather months.[18] For the 2017-2018 flu season, the vaccines are described as IIV3 and IIV4 for resistance to the expected three or four viruses. For adults ages 18 and older there is also an option to receive recombinant flu vaccines (RIV3 or RIV4) which are grown on mammalian cell cultures instead of in eggs, and so are no risk for people with severe egg allergy.[19] Recommendations are that for people with a history of mild egg allergy should receive any IIV or RIV vaccine. People with a more severe allergic reaction may also receive any IIV or RIV, but in an inpatient or outpatient medical setting, administered by a healthcare provider. People with a known severe allergic reaction to influenza vaccine (which could be egg protein or the gelatin or the neomycin components of the vaccine) should not receive a flu vaccine.[19]

Each year the American Academy of Pediatrics (AAP) publishes recommendations for prevention and control of influenza in children.[20][21][22] In the most recent guidelines, for 2016-2017, a change was made, that children with a history of egg allergy may receive the IIV3 or IIV4 vaccine without special precautions. It does, however, state that "Standard vaccination practice should include the ability to respond to acute hypersensitivity reactions."[20] Prior to this, AAP recommended precautions based on egg allergy history: if no history, immunize; if a history of mild reaction, i.e., hives, immunize in a medical setting with healthcare professionals and resuscitative equipment available; if a history of severe reactions, refer to an allergist.[21][22]

The measles and mumps parts of the "MMR vaccine" (for measles, mumps, and rubella) are cultured on chick embryo cell culture and contain trace amounts of egg protein. The amount of egg protein is lower than in influenza vaccines and the risk of an allergic reaction is much lower.[23] One guideline stated that all infants and children should get the two MMR vaccinations, mentioning that "Studies on large numbers of egg-allergic children show there is no increased risk of severe allergic reactions to the vaccines."[24] Another guideline recommended that if a child has a known medical history of severe anaphylaxis reaction to eggs, then the vaccination should be done in a hospital center, and the child be kept for observation for 60 minutes before being allowed to leave.[23] The second guideline also stated that if there was a severe reaction to the first vaccination - which could have been to egg protein or the gelatin and neomycin components of the vaccine - the second is contraindicated.[23]


There is a condition called food-dependent, exercise-induced anaphylaxis (FDEIAn). Exercise can trigger hives and more severe symptoms of an allergic reaction. For some people with this condition, exercise alone is not sufficient, nor consumption of a food to which they are mildly allergic sufficient, but when the food in question is consumed within a few hours before high intensity exercise, the result can be anaphylaxis. Egg are specifically mentioned as a causative food.[25][26][27] One theory is that exercise is stimulating the release of mediators such as histamine from IgE-activated mast cells.[27] Two of the reviews postulate that exercise is not essential for the development of symptoms, but rather that it is one of several augmentation factors, citing evidence that the culprit food in combination with alcohol or aspirin will result in a respiratory anaphylactic reaction.[25][27]


Conditions caused by food allergies are classified into three groups according to the mechanism of the allergic response:[28]

  1. IgE-mediated (classic) – the most common type, manifesting acute changes that occur shortly after eating, and may progress to anaphylaxis
  2. Non-IgE mediated – characterized by an immune response not involving immunoglobulin E; may occur hours to days after eating, complicating diagnosis
  3. IgE and non-IgE-mediated – a hybrid of the above two types

Allergic reactions are hyperactive responses of the immune system to generally innocuous substances, such as proteins in the foods we eat. Why some proteins trigger allergic reactions while others do not is not entirely clear, although in part thought to be due to resistance to digestion. Because of this, intact or largely intact proteins reach the small intestine, which has a large presence of white blood cells involved in immune reactions.[29] The heat of cooking structurally degrades protein molecules, potentially making them less allergenic.[30] 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 more tissue damage.

In the early stages of acute allergic reaction, lymphocytes previously sensitized to a specific protein or protein fraction react by quickly producing a particular type of antibody known as secreted IgE (sIgE), which circulates in the blood and binds to IgE-specific receptors on the surface of other kinds of immune cells called mast cells and basophils. Both of these are involved in the acute inflammatory response.[31] Activated mast cells and basophils undergo a process called degranulation, during which they release histamine and other inflammatory chemical mediators called (cytokines, interleukins, leukotrienes, and prostaglandins) into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve stimulation, and smooth-muscle contraction. This results in runny nose, itchiness, shortness of breath, and potentially 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 while eczema is localized to the skin.[31]

After the chemical mediators of the acute response subside, late-phase responses can often occur due to the migration of other white blood cells such as neutrophils, lymphocytes, eosinophils, and macrophages to the initial reaction sites. This is usually seen 2–24 hours after the original reaction.[32] 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.[33]

Five major allergenic proteins from the egg of the domestic chicken (Gallus domesticus) have been identified; these are designated Gal d 1-5. Four of these are in egg white: ovomucoid (Gal d 1), ovalbumin (Gal d 2), ovotransferrin (Gal d 3) and lysozyme (Gal d 4). Of these, ovomucoid is the dominant allergen, and one that is less likely to be outgrown as children get older.[1] Ingestion of under-cooked egg may trigger more severe clinical reactions than well-cooked egg. In egg yolk, alpha-livetin (Gal d 5) is the major allergen, but various vitellins may also trigger a reaction. People allergic to alpha-livetin may experience respiratory symptoms such as rhinitis and/or asthma when exposed to chickens, because the yolk protein is also found in live birds.[1] In addition to IgE-mediated responses, egg allergy can manifest as atopic dermatitis, especially in infants and young children. Some will display both, so that a child could react to an oral food challenge with allergic symptoms, followed a day or two later with a flare up of atopic dermatitis and/or gastrointestinal symptoms, including allergic eosinophilic esophagitis.[1][2]

Non-allergic intolerance

Egg whites, which are potentially histamine liberators, also provoke a nonallergic response in some people. In this situation, proteins in egg white directly trigger the release of histamine from mast cells.[34][35] Because this mechanism is classified as a pharmacological reaction, or "pseudoallergy",[34] the condition is considered a food intolerance instead of a true immunoglobulin E (IgE) based allergic reaction.

The response is usually localized, typically in the gastrointestinal tract.[34] Symptoms may include abdominal pain, diarrhea, or any other symptoms typical to histamine release. If sufficiently strong, it can result in an anaphylactoid reaction, which is clinically indistinguishable from true anaphylaxis.[35] Some people with this condition tolerate small quantities of egg whites.[36] They are more often able to tolerate well-cooked eggs, such as found in cake or dried egg-based pasta, than incompletely cooked eggs, such as fried eggs or meringues, or uncooked eggs.[36]


Diagnosis of egg allergy is based on the person's history of allergic reactions, skin prick test (SPT), patch test and measurement of egg-specific serum immunoglobulin E (IgE or sIgE). Confirmation is by double-blind, placebo-controlled food challenges.[2][14] SPT and sIgE have sensitivity greater than 90% but specificity in the 50-60% range, meaning these tests will detect an egg sensitivity, but will also be positive for other allergens.[37] For young children, attempts have been made to identify SPT and sIgE responses strong enough to avoid the need for a confirming oral food challenge.[38]


When eggs are introduced to a baby's diet is thought to affect risk of developing allergy, but there are contradictory recommendations. A 2016 review acknowledged that introducing peanuts early appears to have a benefit, but stated "The effect of early introduction of egg on egg allergy are controversial."[9] A meta-analysis published the same year supported the theory that early introduction of eggs into an infant's diet lowers risk,[8] and a review of allergens in general stated that introducing solid foods at 4–6 months may result in the lowest subsequent allergy risk.[10] However, an older consensus document from the American College of Allergy, Asthma and Immunology recommended that introduction of chicken eggs be delayed to 24 months of age.[11]


The mainstay of treatment is total avoidance of egg protein intake.[39] This is complicated because the declaration of the presence of trace amounts of allergens in foods is not mandatory (see regulation of labelling).

Treatment for accidental ingestion of egg products by allergic individuals varies depending on the sensitivity of the person. An antihistamine such as diphenhydramine (Benadryl) may be prescribed. Sometimes prednisone will be prescribed to prevent a possible late phase Type I hypersensitivity reaction.[40] Severe allergic reactions (anaphalaxis) may require treatment with an epinephrine pen, i.e., an injection device designed to be used by a non-healthcare professional when emergency treatment is warranted. A second dose is needed in 16-35% of episodes.[41]


There is active research on trying oral immunotherapy (OIT) to desensitize people to egg allergens. A Cochrane Review concluded that OIT can desensitize people, but it remains unclear whether long-term tolerance develops after treatment ceases, and 69% of the people enrolled in the trials had adverse effects. They concluded there was a need for standardized protocols and guidelines prior to incorporating OIT into clinical practice.[42] A second review noted that allergic reactions, up to anaphylaxis, can occur during OIT, and recommends this treatment not be routine medical practice.[43] A third review limited its scope to trials of baked egg-containing goods such as bread or cake as a means of resolving egg allergy. Again, there were some successes, but also some severe allergic reactions, and the authors came down on the side of not recommending this as treatment.[44]

Avoiding eggs

Prevention of egg-allergic reactions means avoiding eggs and egg-containing foods. People with an allergy to chicken eggs may also be allergic to other types of eggs, such as goose, duck, or turkey eggs.[1] In cooking, eggs are multifunctional: they may act as an emulsifier to reduce oil/water separation (mayonnaise), a binder (water binding and particle adhesion, as in meatloaf), or an aerator (cakes, especially angel food). Some commercial egg substitutes can substitute for particular functions (potato starch and tapioca for water binding, whey protein for aeration or particle binding, or soy lecithin or avocado for emulsification). Food companies produce egg-free mayonnaise and other replacement foods. Alfred Bird invented egg-free Bird's Custard, the original version of what is known generically as custard powder today.[45]

Most people find it necessary to strictly avoid any item containing eggs, including:[13]

  • Albumin (egg white protein)
  • Apovitellin (egg yolk protein)
  • Egg Beaters (cholesterol-free, uses egg whites)
  • Dried egg solids, powdered egg
  • Egg, egg white, egg yolk
  • Egg wash
  • Eggnog
  • Fat substitutes (some)
  • Livetin (egg yolk protein)
  • Lysozyme (egg white protein)
  • Mayonnaise
  • Meringue or meringue powder
  • Ovalbumin (egg white protein)
  • Ovoglobulin (egg white protein)
  • Ovomucin (egg white protein)
  • Ovomucoid (egg white protein)
  • Ovotransferrin (egg white protein)
  • Ovovitelia (egg yolk protein)
  • Ovovitellin (egg yolk protein)
  • Silici albuminate
  • Simplesse
  • Vitellin (egg yolk protein)

Ingredients that sometimes include egg protein include: artificial flavoring, natural flavoring, lecithin and nougat candy.

Probiotic products have been tested, and some found to contain milk and egg proteins which were not always indicated on the labels.[46]


The majority of children outgrow egg allergy. One review reported that 70% of children will outgrow this allergy by 16 years.[14] In subsequently published longitudinal studies, one reported that for 140 infants who had challenge-confirmed egg allergy, 44% had resolved by two years.[47] A second reported that for 203 infants with confirmed IgE-mediated egg allergy, 45% resolved by two years of age, 66% by four years, and 71% by six years.[48] Children will be able to tolerate eggs as an ingredient in baked goods and well-cooked eggs sooner than under-cooked eggs.[14] Resolution was more likely if baseline serum IgE was lower, and if the baseline symptoms did not include anaphylaxis.[14][48]


In countries in North America and western Europe, where use of cow's milk based infant formula is common, chicken egg allergy is the second most common food allergy in infants and young children after cow's milk.[2][14][49] However, in Japan, egg allergy is first and cow's milk second, followed by wheat and then the other common allergenic foods.[12] A review from South Africa reported egg and peanut as the two most common allergenic foods.[50]

Incidence and prevalence are terms commonly used in describing disease epidemiology. Incidence is newly diagnosed cases, which can be expressed as new cases per year per million people. Prevalence is the number of cases alive, expressible as existing cases per million people during a period of time.[51] Egg allergies are usually observed in infants and young children, and often disappear with age (see Prognosis), so prevalence of egg allergy may be expressed as a percentage of children under a set age. One review estimates that in North American and western European populations the prevalence of egg allergy in children under the age of five years is 1.8-2.0%.[2] A second described the range in young children as 0.5-2.5%.[1] Although the majority of children develop tolerance as they age into school age years, for roughly one-third the allergy persists into adulthood. Strong predictors for adult-persistent allergy are anaphylactic symptoms as a child, high egg-specific serum IgE, robust response to the skin prick test and absence of tolerance to egg-containing baked foods.[14][1] Self-reported allergy prevalence is always higher than food-challenge confirmed allergy.

For all age groups, a review of fifty studies conducted in Europe estimated 2.5% for self-reported egg allergy and 0.2% for confirmed.[49] National survey data in the United States collected in 2005 and 2006 showed that from age six and older, the prevalence of serum IgE confirmed egg allergy was under 0.2%.[52]

Adult-onset of egg allergy is rare, but there is confirmation of cases. Some were described as having started in late teenage years; another group were workers in the baking industry who were exposed to powdered egg dust.[53]

Society and culture

Whether food allergy prevalence 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.[54][55][56][57] 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.[58] 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.[59] Food fear has a significant impact on quality of life.[56][57] 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.[60]

Regulation of labelling

An example of a list of allergens in a food item

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 among the ingredients intentionally added to foods. Nevertheless, there are no labeling laws to mandatory declare the presence of trace amounts in the final product as a consequence of cross-contamination, except in Brazil.[7][61][62][63][64][65][5][6]

Ingredients intentionally added

In the United States, the Food Allergen Labeling and Consumer Protection Act of 2004 (FALCPA) requires companies to disclose on the label whether a packaged food product contains any of these eight major food allergens, added intentionally: cow's milk, peanuts, eggs, shellfish, fish, tree nuts, soy and wheat.[61] This list originated in 1999 from the World Health Organisation Codex Alimentarius Commission.[5] To meet FALCPA labeling requirements, if an ingredient is derived from one of the required-label allergens, then it must either have its "food sourced name" in parentheses, for example "Casein (milk)," or as an alternative, there must be a statement separate but adjacent to the ingredients list: "Contains milk" (and any other of the allergens with mandatory labeling).[61][63] The European Union requires listing for those eight major allergens plus molluscs, celery, mustard, lupin, sesame and sulfites.[62]

FALCPA applies to packaged foods regulated by the FDA, which does not include poultry, most meats, certain egg products, and most alcoholic beverages.[6] However, some meat, poultry, and egg processed products may contain allergenic ingredients. These products are regulated by the Food Safety and Inspection Service (FSIS), which requires that any ingredient be declared in the labeling only by its common or usual name. Neither the identification of the source of a specific ingredient in a parenthetical statement nor the use of statements to alert for the presence of specific ingredients, like "Contains: milk", are mandatory according to FSIS.[64][65] FALCPA also does not apply to food prepared in restaurants.[66][67] 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.[68]

In the United States, there is no federal mandate to address the presence of allergens in drug products. FALCPA does not apply to medicines nor to cosmetics.[69]

Trace amounts as a result of cross-contamination

The value of allergen labeling other than for intentional ingredients is controversial. This concerns labeling for ingredients present unintentionally as a consequence of cross-contact or cross-contamination at any point along the food chain (during raw material transportation, storage or handling, due to shared equipment for processing and packaging, etc.).[5][6] Experts in this field propose that if allergen labeling is to be useful to consumers, and healthcare professionals who advise and treat those consumers, ideally there should be agreement on which foods require labeling, threshold quantities below which labeling may be of no purpose, and validation of allergen detection methods to test and potentially recall foods that were deliberately or inadvertently contaminated.[70][71]

Labeling regulations have been modified to provide for mandatory labeling of ingredients plus voluntary labeling, termed precautionary allergen labeling (PAL), also known as “may contain” statements, for possible, inadvertent, trace amount, cross-contamination during production.[5][72] PAL labeling can be confusing to consumers, especially as there can be many variations on the wording of the warning.[72][73] As of 2014 PAL is regulated only in Switzerland, Japan, Argentina, and South Africa. Argentina decided to prohibit precautionary allergen labeling since 2010, and instead puts the onus on the manufacturer to control the manufacturing process and label only those allergenic ingredients known to be in the products. South Africa does not permit the use of PAL, except when manufacturers demonstrate the potential presence of allergen due to cross-contamination through a documented risk assessment and despite adherence to Good Manufacturing Practice.[5] In Australia and New Zealand there is a recommendation that PAL be replaced by guidance from VITAL 2.0 (Vital Incidental Trace Allergen Labeling). A review identified "the eliciting dose for an allergic reaction in 1% of the population" as ED01. This threshold reference dose for foods such as cow's milk, egg, peanut and other proteins) will provide food manufacturers with guidance for developing precautionary labeling and give consumers a better idea of might be accidentally in a food product beyond "may contain."[74][75] VITAL 2.0 was developed by the Allergen Bureau, a food industry sponsored, non-government organization.[76] The European Union has initiated a process to create labeling regulations for unintentional contamination but is not expected to publish such before 2024.[77]

In Brazil since April 2016, the declaration of the possibility of cross-contamination is mandatory when the product does not intentionally add any allergenic food or its derivatives, but the Good Manufacturing Practices and allergen control measures adopted are not sufficient to prevent the presence of accidental trace amounts. These allergens include wheat, rye, barley, oats and their hybrids, crustaceans, eggs, fish, peanuts, soybean, milk of all species of mammalians, almonds, hazelnuts, cashew nuts, Brazil nuts, macadamia nuts, walnuts, pecan nuts, pistaches, pine nuts, and chestnuts.[7]

See also


  1. Caubet JC, Wang J (2011). "Current understanding of egg allergy". Pediatr. Clin. North Am. 58 (2): 427–43, xi. doi:10.1016/j.pcl.2011.02.014. PMC 3069662. PMID 21453811.
  2. Urisu A, Kondo Y, Tsuge I (2015). Hen's Egg Allergy. Chem Immunol Allergy. Chemical Immunology and Allergy. 101. pp. 124–30. doi:10.1159/000375416. ISBN 978-3-318-02340-4. PMID 26022872.
  3. National Report of the Expert Panel on Food Allergy Research, NIH-NIAID 2003 "June 30 2003.pdf" (PDF). Archived from the original (PDF) on 2006-10-04. Retrieved 2006-08-07.
  4. "Food Allergy Facts" Archived 2012-10-06 at the Wayback Machine Asthma and Allergy Foundation of America
  5. Allen KJ, Turner PJ, Pawankar R, Taylor S, Sicherer S, Lack G, Rosario N, Ebisawa M, Wong G, Mills EN, Beyer K, Fiocchi A, Sampson HA (2014). "Precautionary labelling of foods for allergen content: are we ready for a global framework?". World Allergy Organ J. 7 (1): 1–14. doi:10.1186/1939-4551-7-10. PMC 4005619. PMID 24791183.
  6. FDA (18 December 2017). "Food Allergies: What You Need to Know". Retrieved 12 January 2018.
  7. "Agência Nacional de Vigilância Sanitária Guia sobre Programa de Controle de Alergênicos" (in Portuguese). Agência Nacional de Vigilância Sanitária (ANVISA). 2016. Archived from the original on 29 April 2018. Retrieved 7 April 2018.
  8. Ierodiakonou D, Garcia-Larsen V, Logan A, Groome A, Cunha S, Chivinge J, Robinson Z, Geoghegan N, Jarrold K, Reeves T, Tagiyeva-Milne N, Nurmatov U, Trivella M, Leonardi-Bee J, Boyle RJ (2016). "Timing of Allergenic Food Introduction to the Infant Diet and Risk of Allergic or Autoimmune Disease: A Systematic Review and Meta-analysis". JAMA. 316 (11): 1181–1192. doi:10.1001/jama.2016.12623. hdl:10044/1/40479. PMID 27654604.
  9. Fiocchi A, Dahdah L, Bahna SL, Mazzina O, Assa'ad A (2016). "Doctor, when should I feed solid foods to my infant?". Curr Opin Allergy Clin Immunol. 16 (4): 404–11. doi:10.1097/aci.0000000000000291. PMID 27327121.
  10. Anderson J, Malley K, Snell R (2009). "Is 6 months still the best for exclusive breastfeeding and introduction of solids? A literature review with consideration to the risk of the development of allergies". Breastfeed Rev. 17 (2): 23–31. PMID 19685855.
  11. Fiocchi A, Assa'ad A, Bahna S (2006). "Food allergy and the introduction of solid foods to infants: a consensus document. Adverse Reactions to Foods Committee, American College of Allergy, Asthma and Immunology". Ann. Allergy Asthma Immunol. 97 (1): 10–20, quiz 21, 77. doi:10.1016/s1081-1206(10)61364-6. PMID 16892776.
  12. Urisu A, Ebisawa M, Ito K, Aihara Y, Ito S, Mayumi M, Kohno Y, Kondo N (2014). "Japanese Guideline for Food Allergy 2014". Allergol Int. 63 (3): 399–419. doi:10.2332/allergolint.14-RAI-0770. PMID 25178179.
  13. "Egg Allergy Facts" Archived 2013-01-12 at the Wayback Machine Asthma and Allergy Foundation of America
  14. Hasan SA, Wells RD, Davis CM (2013). "Egg hypersensitivity in review". Allergy Asthma Proc. 34 (1): 26–32. doi:10.2500/aap.2013.34.3621. PMID 23406934.
  15. MedlinePlus Encyclopedia Food allergy
  16. Sicherer SH, Sampson HA (2014). "Food allergy: Epidemiology, pathogenesis, diagnosis, and treatment". J Allergy Clin Immunol. 133 (2): 291–307. doi:10.1016/j.jaci.2013.11.020. PMID 24388012.
  17. Pols DH, Wartna JB, van Alphen EI, Moed H, Rasenberg N, Bindels PJ, Bohnen AM (2015). "Interrelationships between Atopic Disorders in Children: A Meta-Analysis Based on ISAAC Questionnaires". PLoS ONE. 10 (7): e0131869. doi:10.1371/journal.pone.0131869. PMC 4489894. PMID 26135565.
  18. "Recommendations for the production and control of influenza vaccine (inactivated)" (PDF). World Health Organization. Archived (PDF) from the original on October 28, 2013. Retrieved May 27, 2013.
  19. "Prevention and Control of Seasonal Influenza with Vaccines: Recommendations of the Advisory Committee on Immunization Practices — United States, 2017–18 Influenza Season" Grohskopf LA, Sokolow LZ, Broder KR, et al. Prevention and Control of Seasonal Influenza with Vaccines. MMWR Recomm Rep 2017;66(No. RR-2):1–20.
  20. COMMITTEE ON INFECTIOUS DISEASES (2016). "Recommendations for Prevention and Control of Influenza in Children, 2016-2017". Pediatrics. 138 (4): e20162527. doi:10.1542/peds.2016-2527. PMID 27600320.
  21. Committee On Infectious Diseases, American Academy of Pediatrics (2015). "Recommendations for Prevention and Control of Influenza in Children, 2015-2016". Pediatrics. 136 (4): 792–808. doi:10.1542/peds.2015-2920. PMID 26347430.
  22. American Academy of Pediatrics Committee on Infectious Diseases (2011). "Recommendations for prevention and control of influenza in children, 2011-2012". Pediatrics. 128 (4): 813–25. doi:10.1542/peds.2011-2295. PMID 21890834.
  23. Piquer-Gibert M, Plaza-Martín A, Martorell-Aragonés A, Ferré-Ybarz L, Echeverría-Zudaire L, Boné-Calvo J, Nevot-Falcó S (2007). "Recommendations for administering the triple viral vaccine and anti-influenza vaccine in patients with egg allergy". Allergol Immunopathol (Madr). 35 (5): 209–12. doi:10.1157/13110316. PMID 17923075.
  24. Clark AT, Skypala I, Leech SC, Ewan PW, Dugué P, Brathwaite N, Huber PA, Nasser SM (2010). "British Society for Allergy and Clinical Immunology guidelines for the management of egg allergy". Clin. Exp. Allergy. 40 (8): 1116–29. doi:10.1111/j.1365-2222.2010.03557.x. PMID 20649608.
  25. Feldweg AM (2017). "Food-Dependent, Exercise-Induced Anaphylaxis: Diagnosis and Management in the Outpatient Setting". J Allergy Clin Immunol Pract. 5 (2): 283–288. doi:10.1016/j.jaip.2016.11.022. PMID 28283153.
  26. Pravettoni V, Incorvaia C (2016). "Diagnosis of exercise-induced anaphylaxis: current insights". J Asthma Allergy. 9: 191–198. doi:10.2147/JAA.S109105. PMC 5089823. PMID 27822074.
  27. Kim CW, Figueroa A, Park CH, Kwak YS, Kim KB, Seo DY, Lee HR (2013). "Combined effects of food and exercise on anaphylaxis". Nutr Res Pract. 7 (5): 347–51. doi:10.4162/nrp.2013.7.5.347. PMC 3796658. PMID 24133612.
  28. "Food allergy". NHS Choices. 16 May 2016. Retrieved 31 January 2017. A food allergy is when the body's immune system reacts unusually to specific foods
  29. Food Reactions. Allergies Archived 2010-04-16 at the Wayback Machine. Kent, England. 2005. Accessed 27 Apr 2010.
  30. Mayo Clinic. Causes of Food Allergies. Archived 2010-02-27 at the Wayback Machine April 2010.
  31. Janeway, Charles; Paul Travers; Mark Walport; Mark Shlomchik (2001). Immunobiology; Fifth Edition. New York and London: Garland Science. pp. e–book. ISBN 978-0-8153-4101-7. Archived from the original on 2009-06-28.
  32. Grimbaldeston MA, Metz M, Yu M, Tsai M, Galli SJ (2006). "Effector and potential immunoregulatory roles of mast cells in IgE-associated acquired immune responses". Curr. Opin. Immunol. 18 (6): 751–60. doi:10.1016/j.coi.2006.09.011. PMID 17011762.
  33. Holt PG, Sly PD (2007). "Th2 cytokines in the asthma late-phase response". Lancet. 370 (9596): 1396–8. doi:10.1016/S0140-6736(07)61587-6. PMID 17950849.
  34. Arnaldo Cantani (2008). Pediatric Allergy, Asthma and Immunology. Berlin: Springer. pp. 710–713. ISBN 978-3-540-20768-9.
  35. Joris, Isabelle; Majno, Guido (2004). Cells, tissues, and disease: principles of general pathology. Oxford [Oxfordshire]: Oxford University Press. p. 538. ISBN 978-0-19-514090-3.
  36. Carina Venter; Isabel Skypala (2009). Food Hypersensitivity: Diagnosing and Managing Food Allergies and Intolerance. Wiley-Blackwell. pp. 129–131. ISBN 978-1-4051-7036-9.
  37. Soares-Weiser K, Takwoingi Y, Panesar SS, Muraro A, Werfel T, Hoffmann-Sommergruber K, Roberts G, Halken S, Poulsen L, van Ree R, Vlieg-Boerstra BJ, Sheikh A (2014). "The diagnosis of food allergy: a systematic review and meta-analysis". Allergy. 69 (1): 76–86. doi:10.1111/all.12333. PMID 24329961.
  38. Calvani M, Arasi S, Bianchi A, Caimmi D, Cuomo B, Dondi A, Indirli GC, La Grutta S, Panetta V, Verga MC (2015). "Is it possible to make a diagnosis of raw, heated, and baked egg allergy in children using cutoffs? A systematic review". Pediatr Allergy Immunol. 26 (6): 509–21. doi:10.1111/pai.12432. hdl:10447/143352. PMID 26102461.
  39. Martorell A, Alonso E, Boné J, Echeverría L, López MC, Martín F, et al. (2013). "Position document: IgE-mediated allergy to egg protein". Allergol Immunopathol (Madr) (Review). 41 (5): 320–36. doi:10.1016/j.aller.2013.03.005. PMID 23830306.
  40. Tang AW (2003). "A practical guide to anaphylaxis". Am Fam Physician. 68 (7): 1325–1332. PMID 14567487.
  41. The EAACI Food Allergy and Anaphylaxis Guidelines Group (August 2014). "Anaphylaxis: guidelines from the European Academy of Allergy and Clinical Immunology". Allergy. 69 (8): 1026–45. doi:10.1111/all.12437. PMID 24909803.
  42. Romantsik, O; Tosca, MA; Zappettini, S; Calevo, MG (20 April 2018). "Oral and sublingual immunotherapy for egg allergy". The Cochrane Database of Systematic Reviews. 4: CD010638. doi:10.1002/14651858.CD010638.pub3. PMC 6494514. PMID 29676439.
  43. Ibáñez MD, Escudero C, Sánchez-García S, Rodríguez del Río P (2015). "Comprehensive Review of Current Knowledge on Egg Oral Immunotherapy". J Investig Allergol Clin Immunol. 25 (5): 316–28, quiz 2 p following 328. PMID 26727760.
  44. Lambert R, Grimshaw KE, Ellis B, Jaitly J, Roberts G (2017). "Evidence that eating baked egg or milk influences egg or milk allergy resolution: a systematic review". Clin. Exp. Allergy. 47 (6): 829–837. doi:10.1111/cea.12940. PMID 28516451.
  45. Carey, John (1997). Eyewitness to Science. Harvard University Press. p. 173. ISBN 9780674287556.
  46. Nanagas, VC; Baldwin, JL; Karamched, KR (July 2017). "Hidden Causes of Anaphylaxis". Current Allergy and Asthma Reports. 17 (7): 44. doi:10.1007/s11882-017-0713-2. PMID 28577270.
  47. Peters RL, Dharmage SC, Gurrin LC, Koplin JJ, Ponsonby AL, Lowe AJ, Tang ML, Tey D, Robinson M, Hill D, Czech H, Thiele L, Osborne NJ, Allen KJ (2014). "The natural history and clinical predictors of egg allergy in the first 2 years of life: a prospective, population-based cohort study". J. Allergy Clin. Immunol. 133 (2): 485–91. doi:10.1016/j.jaci.2013.11.032. PMID 24373356.
  48. Arik Yilmaz E, Cavkaytar O, Buyuktiryaki B, Sekerel BE, Soyer O, Sackesen C (2015). "Factors associated with the course of egg allergy in children". Ann. Allergy Asthma Immunol. 115 (5): 434–438.e1. doi:10.1016/j.anai.2015.08.012. PMID 26505933.
  49. Nwaru BI, Hickstein L, Panesar SS, Roberts G, Muraro A, Sheikh A (2014). "Prevalence of common food allergies in Europe: a systematic review and meta-analysis". Allergy. 69 (8): 992–1007. doi:10.1111/all.12423. PMID 24816523.
  50. Gray CL (2017). "Food Allergy in South Africa". Curr Allergy Asthma Rep. 17 (6): 35. doi:10.1007/s11882-017-0703-4. PMID 28470372.
  51. “Incidence and Prevalence” Advanced Renal Education Program (Accessed 17 October 2017).
  52. Liu AH, Jaramillo R, Sicherer SH, Wood RA, Bock SA, Burks AW, Massing M, Cohn RD, Zeldin DC (2010). "National prevalence and risk factors for food allergy and relationship to asthma: results from the National Health and Nutrition Examination Survey 2005-2006". J. Allergy Clin. Immunol. 126 (4): 798–806.e13. doi:10.1016/j.jaci.2010.07.026. PMC 2990684. PMID 20920770.
  53. Unsel M, Sin AZ, Ardeniz O, Erdem N, Ersoy R, Gulbahar O, Mete N, Kokuludağ A (2007). "New onset egg allergy in an adult". J Investig Allergol Clin Immunol. 17 (1): 55–8. PMID 17323866.
  54. Ravid NL, Annunziato RA, Ambrose MA, Chuang K, Mullarkey C, Sicherer SH, Shemesh E, Cox AL (2015). "Mental health and quality-of-life concerns related to the burden of food allergy". Psychiatr. Clin. North Am. 38 (1): 77–89. doi:10.1016/j.psc.2014.11.004. PMID 25725570.
  55. Morou Z, Tatsioni A, Dimoliatis ID, Papadopoulos NG (2014). "Health-related quality of life in children with food allergy and their parents: a systematic review of the literature". J Investig Allergol Clin Immunol. 24 (6): 382–95. PMID 25668890.
  56. Lange L (2014). "Quality of life in the setting of anaphylaxis and food allergy". Allergo J Int. 23 (7): 252–260. doi:10.1007/s40629-014-0029-x. PMC 4479473. PMID 26120535.
  57. van der Velde JL, Dubois AE, Flokstra-de Blok BM (2013). "Food allergy and quality of life: what have we learned?". Curr Allergy Asthma Rep. 13 (6): 651–61. doi:10.1007/s11882-013-0391-7. PMID 24122150.
  58. Culinary Institute of America Allergen-free oasis comes to the CIA (2017)
  59. Shah E, Pongracic J (2008). "Food-induced anaphylaxis: who, what, why, and where?". Pediatr Ann. 37 (8): 536–41. PMID 18751571.
  60. Fong AT, Katelaris CH, Wainstein B (2017). "Bullying and quality of life in children and adolescents with food allergy". J Paediatr Child Health. 53 (7): 630–635. doi:10.1111/jpc.13570. PMID 28608485.
  61. "Food Allergen Labeling and Consumer Protection Act of 2004". FDA. August 2, 2004. Archived from the original on 2011-02-02.
  62. "Food allergen labelling and information requirements under the EU Food Information for Consumers Regulation No. 1169/2011: Technical Guidance" (April 2015).
  63. FDA (14 December 2017). "Have Food Allergies? Read the Label". Retrieved 14 January 2018.
  64. "Food Ingredients of Public Health Concern" (PDF). United States Department of Agriculture. Food Safety and Inspection Service. 7 March 2017. Retrieved 16 February 2018.
  65. "Allergies and Food Safety". United States Department of Agriculture. Food Safety and Inspection Service. 1 December 2016. Retrieved 16 February 2018.
  66. Roses JB (2011). "Food allergen law and the Food Allergen Labeling and Consumer Protection Act of 2004: falling short of true protection for food allergy sufferers". Food Drug Law J. 66 (2): 225–42, ii. PMID 24505841.
  67. FDA (18 July 2006). "Food Allergen Labeling And Consumer Protection Act of 2004 Questions and Answers". Retrieved 12 March 2018.
  68. "Allergy and intolerance: guidance for businesses". Archived from the original on 2014-12-08. Retrieved 2014-12-12.
  69. Shah AV, Serajuddin AT, Mangione RA (2017). "Making All Medications Gluten Free". J Pharm Sci. 107 (5): 1263–1268. doi:10.1016/j.xphs.2017.12.021. PMID 29287928.
  70. Mills EN, Valovirta E, Madsen C, Taylor SL, Vieths S, Anklam E, Baumgartner S, Koch P, Crevel RW, Frewer L (2004). "Information provision for allergic consumers--where are we going with food allergen labelling?". Allergy. 59 (12): 1262–1268. doi:10.1111/j.1398-9995.2004.00720.x. PMID 15507093.
  71. Taylor SL, Baumert JL (2015). Worldwide food allergy labeling and detection of allergens in processed foods. Chem Immunol Allergy. Chemical Immunology and Allergy. 101. pp. 227–234. doi:10.1159/000373910. ISBN 978-3-318-02340-4. PMID 26022883.
  72. DunnGalvin A, Chan CH, et al. (2015). "Precautionary allergen labelling: perspectives from key stakeholder groups". Allergy. 70 (9): 1039–1051. doi:10.1111/all.12614. PMID 25808296.
  73. Zurzolo GA, de Courten M, Koplin J, Mathai ML, Allen KJ (2016). "Is advising food allergic patients to avoid food with precautionary allergen labelling out of date?". Curr Opin Allergy Clin Immunol. 16 (3): 272–277. doi:10.1097/ACI.0000000000000262. PMID 26981748.
  74. Allen KJ, Remington BC, Baumert JL, Crevel RW, Houben GF, Brooke-Taylor S, Kruizinga AG, Taylor SL (2014). "Allergen reference doses for precautionary labeling (VITAL 2.0): clinical implications". J. Allergy Clin. Immunol. 133 (1): 156–164. doi:10.1016/j.jaci.2013.06.042. PMID 23987796.
  75. Taylor SL, Baumert JL, Kruizinga AG, Remington BC, Crevel RW, Brooke-Taylor S, Allen KJ, Houben G (2014). "Establishment of Reference Doses for residues of allergenic foods: report of the VITAL Expert Panel". Food Chem. Toxicol. 63: 9–17. doi:10.1016/j.fct.2013.10.032. PMID 24184597.
  76. The VITAL Program Allergen Bureau, Australia and New Zealand.
  77. Popping B, Diaz-Amigo C (2018). "European Regulations for Labeling Requirements for Food Allergens and Substances Causing Intolerances: History and Future". J AOAC Int. 101 (1): 2–7. doi:10.5740/jaoacint.17-0381. PMID 29202901.
This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.