Recent Surveys on Food Allergy Prevalence : Nutrition Today (original) (raw)
Immunoglobulin E (IgE)–mediated food allergy is a significant public health issue that affects an estimated 3% to 10% of adults and 8% of children worldwide.1–4 Not all evidence5,6 indicates that food allergy may be on the rise. This review deals only with IgE-mediated food allergy. While data on prevalence of IgE-mediated allergy are discussed, it must be remembered that there is a vast difference between confirmed clinical food allergy and food sensitization.
The National Institute of Allergy and Infectious Diseases (NIAID) divides adverse food reactions into immune-mediated (food allergies) and non–immune-mediated (food intolerances) reactions. Food allergies are defined as “an adverse health effect arising from a specific immune response that occurs reproducibly on exposure to a given food.”7 This definition includes both IgE-mediated food allergy and non–IgE-mediated food allergies. Immunoglobulin E–mediated food allergy refers to an allergic reaction to a food that is immune mediated and occurs within 2 hours of consumption. Non–IgE-mediated is also immune mediated but occurs over a timeline usually more than 1 to 2 hours after consuming a food. Food intolerances, for example, lactose intolerance, do not involve any immune-mediated reactions. Food sensitivities, other than nonceliac gluten sensitivities, are not a recognized term by any of the national or international allergy or gastrointestinal societies or associations.8
The dietetic management of any type of food allergy typically involves information on food avoidance and label reading, identifying substitute foods and ensuring the diet is nutritionally sound.9 The type of food allergy (IgE or non–IgE mediated), possible cross-reactive and coexisting allergies, and knowledge of tolerance levels are important points to address individualized food allergen avoidance and tailor information on food labeling (Table 1).
List of Abbreviations
While more than 200 foods have been shown to be allergenic,10 regulatory agencies have recognized the need to focus allergen labeling regulations on a limited set of priority allergens. In 2004, the US Congress passed the Food Allergen Labeling and Consumer Protection Act (FALCPA), which mandates that the label of a food that contains an ingredient that is or is derived protein from a “major food allergen” must declare the presence of the allergen in the manner described by the law.
Eight allergenic foods, commonly referred to as the “Big 8,” fall under the FALCPA. The Big 8 foods that must be declared on product labels in the United States are milk/dairy, eggs, fish, crustacean shellfish, tree nuts, peanuts, wheat, and soy. The labeling requirement passed by Congress has undoubtedly increased awareness of the foods responsible for most food-allergic reactions in the United States. However, the significant degree to which the prevalence of these 8 allergies to food proteins varies may not be fully appreciated. From a public health perspective, the failure to recognize this variation takes on added significance because the prevalence of perceived (self-reported [SR]) food allergy is greater than prevalence estimates based on rigorous diagnostic methods.11,12 For example, a very recent survey involving 40 443 US adults found 10.8% of respondents were likely to have a food allergy, that is, to have signs and symptoms to specific allergens that were consistent with IgE-mediated reactions, whereas 19.0% SR a food allergy.13
Consequently, many consumers may be unnecessarily avoiding foods to which they are not allergic. The food industry has responded by developing foods based on consumers' perceived food allergy prevalence, rather than on actual prevalence. Therefore, dietary intake is potentially being shaped by a misunderstanding of food allergy prevalence, the consequences of which are difficult to assess, but potentially detrimental. For example, the adoption of gluten-free diets, which is more common than dictated by the actual prevalence of celiac disease and nonceliac gluten sensitivity, has been reported to adversely affect nutriture.11 On the other hand, those with true food allergies need to be vigilant in their efforts to avoid offending foods. It is important to establish conditions so that doing so is as easy as realistically possible.
This brief review addresses current understanding about the prevalence of IgE-mediated food allergy (see Table 2 for definition) based on recently published surveys.3,4,12–14 Before discussing these surveys, some background information on food allergy is provided to set the data in context.
Definition of Immunoglobulin E (IgE)–Mediated Food Allergy
GENERATING ALLERGY PREVALENCE DATA
The Big 8 was based on comparative prevalence data at the time it was established (see following section), but 2 decades ago when that occurred, the available data were extremely limited. Even today, there is an imperfect understanding because generating accurate prevalence data on food allergy is quite challenging. On the other hand, it should be acknowledged that efforts are underway to improve this understanding.15
A rigorous estimate of the prevalence of food allergy would need to involve several critical features: a study of the general population; clinical demonstration of adverse reactions to a food, preferably by double-blind, placebo-controlled food challenges (DBPCFCs); and clinical documentation of an IgE-mediated mechanism for the adverse reaction. For obvious reasons, conducting a large-scale study utilizing this approach may not be feasible. For a detailed discussion of the problems inherent in generating accurate prevalence data, the reader is referred to the reference.16
In lieu of DBPCFCs involving the generally healthy population, early prevalence studies often incorporated selected cohorts from hospital-based or allergy practices and extrapolated the results to the general population, which typically led to inflated prevalence figures.17 Skin prick tests (SPTs) are often employed in these settings because they are safe and relatively inexpensive.
A positive SPT alone is insufficient for diagnosing food allergy; the patient must also have a supportive history or undergo an oral food challenge. For example, in the case of soy, protein, which is classified as a major allergen in the United States and Canada, research suggests that fewer than 15% of individuals with a positive SPT will react clinically to a food challenge.18,19 On the other hand, the negative predictive value of SPT is greater than 95%. Therefore, a negative SPT generally confirms the absence of IgE-mediated reactions.20,21
A second commonly used method for generating prevalence data is population-based surveys, which typically rely on less expensive approaches such as telephone surveys based on SR data, and tens of thousands of individuals can be included in such surveys. Because these studies rely on self-reporting of specific food allergies, or “perceived prevalence,” they produce higher prevalence rates than do studies incorporating more rigorous diagnostic methods such as challenge tests.22 Despite the limitations of population-based surveys, as discussed below, 5 recently published such surveys, 4 from the United States3,4,6,13 and 1 from Canada,14 provide considerable insight into the relative prevalence of allergy to the major food allergens.
ORIGINS OF THE BIG 8
An understanding of the historical origins of the creation of the Big 8 serves to highlight the limited prevalence data that were available at the time it was established. In 1993, a working paper on food allergens was presented to the Codex Committee on Food Labeling, which was followed by a Food and Agriculture Organization (FAO) Technical Consultation on Food Allergens in 1995. These efforts led to the adoption of a list of foods of concern in 1999 as part of the Codex General Standard for the Labeling of Prepackaged Food (Codex Alimentarius, 2001). The FAO report, which relied heavily upon pediatric data on comparative prevalence of food allergies in clinic populations, was pivotal and eventually led to the creation of the Big 8.23
However, data on adults and on the prevalence of specific food allergies in the general population were lacking at that time. In fact, in the 1995 FAO report, despite the listing of individual foods, including soy, as allergens, no specific data were cited as support for its inclusion. Subsequently, an International Life Sciences Institute–Europe Task Force on Food Allergy took a more in-depth look at foods that merited placement on the priority allergenic foods list.24 The task force determined that the priority list should include milk, egg, fish, crustacean shellfish, peanut, soy, tree nuts, wheat, and sesame. The criteria used by this group included clinical evidence of an allergic reaction through DBPCFCs and published evidence of severe and/or fatal anaphylactic reactions. However, data on prevalence were considered by the task force to be insufficient. The justification for including soy protein on this priority list is especially illustrative, because although 11 references were cited in support of including soy,25–35 none of these allowed conclusions to be made about the relative prevalence of clinically relevant soy protein allergy, although 1 small study not cited did provide prevalence data on soy.23
The Big 8 list adopted by Congress was that established by Codex in 1999. No specific data in support of this list were cited in the 2004 report published by Congress associated with the establishment of the Big 8. One year later, a report from the US Food and Drug Administration (FDA) entitled “Approaches to Establish Thresholds for Major Food Allergens and for Gluten in Food” included prevalence data for the Big 8. However, as can be seen from Table 3, prevalence data were not available for wheat or for soy among adults. Furthermore, the references in support of the prevalence data do not allow for accurately drawing conclusions about the prevalence of soy allergy among children.36–41 Thus, it is clear that the Big 8 was established on the basis of relatively few prevalence data overall and was especially limited in the case of soy and wheat.
Self-reported Food Allergy Prevalence (Percent) of the US Populationa
RECENT PREVALENCE DATA ON FOOD ALLERGY IN THE UNITED STATES AND CANADA
Despite the limitations of telephone surveys based on SR data, which likely overestimate prevalence data, the 5 large telephone surveys described below that have been published within the past 8 years provide a basis for drawing conclusions about the prevalence of food allergy among North Americans. Table 3 summarizes data from these studies.
The National Health and Nutrition Examination Survey (US NHANES) is a periodic survey conducted by the National Center for Health Statistics of the Centers for Disease Control and Prevention. The prevalence of SR food allergy was assessed by a positive response to the question, “Do you have any food allergies?” If the subjects answered yes, they were asked, “What foods are you allergic to?” with options including allergies to wheat, cow's milk, eggs, fish, shellfish, corn, peanuts, other nuts, soy products, and other foods. A total of 20 686 individuals were surveyed between 2007 and 2010.12
A cross-sectional, list-assisted, random-digit-dial telephone survey of US consumers conducted by the FDA (US FDA) known as the Food Safety Surveys (FSS) involved 4568 adults (data for year 2010).13 The respondents were 18 years or older. Participants were asked a variation of the question, “Do you currently have any food allergy or suspect that you have a food allergy?” Respondents who answered “yes” were defined as adult respondents with SR food allergy. No definition for food allergy was provided to respondents. This self-identified food allergy group was further subdivided based on whether they reported yes to the question “was your allergy diagnosed by a doctor?” hereafter referred to as SR doctor-diagnosed (SRDD) food allergy.
A population-based survey was administered between October 2015 and September 2016 to a sample of US households that was funded in part by the NIAID.3 Eligible participants included adults (≥18 years old) able to complete the survey in English or Spanish via web or telephone who resided in a US household. Prevalence estimates were based on responses from the National Opinion Research Center at the University of Chicago's nationally representative, probability-based AmeriSpeak Panel (51% completion rate), which were augmented by non–probability-based responses via calibration weighting to increase precision. Parent-reported data were collected for 41 341 children; 2933 children were excluded because of incomplete data on food allergy outcomes resulting in a total of 38 408 children and adolescents.
The Surveying Canadians to Assess the Prevalence of Food Allergies and Attitudes Towards Food LAbelling and Risk (SCAAALAR) invited 10 596 households to complete a survey on food allergy; of those invited, 3666 responded (35% response rate), and 3613 completed the survey, representing 9667 individuals (7469 adults and 2198 children). Data were collected for years 2008 to 2009.14
In a cross-sectional survey of US adults, surveys were administered via the internet and telephone from October 9, 2015, to September 18, 2016. Participants were first recruited from the National Opinion Research Center at the University of Chicago's probability-based AmeriSpeak panel, and additional participants were recruited from the non–probability-based Survey Sampling International panel.4 Surveys were completed by 40 443 adults (mean age, 46.6 (SD, 20.2) years.
As noted, the results of all 5 surveys are based on SR data, although the FSS conducted by the FDA also included data on SRDD food allergy. The method by which food allergy was physician-diagnosed in the FSS was not determined; however, it is unlikely that in most cases an oral food challenge, the criterion standard, was conducted.
PREVALENCE DATA—ADULTS
As can be seen from Table 4, the prevalence of self-reported food allergy in adults varies greatly from food to food. In all 4 surveys involving adults, soy protein allergy is the least prevalent, whereas milk/dairy and shellfish are the most prevalent. The prevalence of soy allergy ranged from a low of 0.1%13 to a high of 0.6%,4 while the prevalence of milk/dairy allergy ranged from a low of 1.89%14 to a high of 2.64%.12 Data for the 5 assessments in these 4 surveys show the prevalence of milk/dairy allergy was 41 (SR),13 20 (SRDD),13 11.8,14 7.5,12 and 3.24 times greater than the prevalence of soy allergy.
Self-reported Prevalence of Food Allergy Reported by US and Canadian Adults for Major Food Allergens (Percent of Population)
In contrast, both surveys that reported sesame allergy prevalence found it to be considerably lower than the prevalence of soy allergy, 0.16% versus 0.07%14 and 0.6% versus 0.2%.4 Sesame seed is classified as a major allergen in Europe, Canada, and Australia. In October 2018, the FDA announced it is advancing a new effort for the consideration of labeling for sesame.42
It is notable that in the FSS the prevalence of allergy to pea protein (Linda Verrill, personal communication, April 7, 2018) was identical to the prevalence of soy allergy despite pea protein not being a major allergen. Allergy to pea protein has been previously noted;26,43 however, pea protein allergy has not been extensively studied. That the prevalence of pea protein allergy is the same as the prevalence of soy allergy is noteworthy because in recent years the number of foods in the United States containing pea protein has markedly increased. Pea protein has replaced soy protein in many instances because the former is perceived as being nonallergenic. Pea protein can now be found in a wide range of foods including plant-based milks, yogurts, plant-based burgers, and energy bars. It is therefore especially noteworthy that a recent Canadian case series suggests the increase in the number of products containing concentrated sources of pea protein has resulted in an increase in the number of severe reactions to pea.44
PREVALENCE DATA—CHILDREN/ADOLESCENTS
As was the case for adults, the prevalence of soy allergy among US children/adolescents was very low in comparison to the other Big 8 food proteins (Table 5). Data from the National Health and Nutrition Examination Survey show it to have the lowest prevalence (0.25%) among the Big 8; the prevalence of milk/dairy allergy was 7.8 times greater.12 Interestingly, in this study, the prevalence of allergy to corn, which is not a major allergen, was similar to the prevalence of soy allergy (corn vs soy; 0.28% vs 0.25%). In the US NIAID-Children, the reported prevalence of soy allergy was twice as high (0.5%) and similar to wheat, but milk/dairy allergy was still 3.8 times higher than soy allergy prevalence.3 Finally, in Canada, the prevalence of soy allergy (0.32%) was intermediate between the 2 US surveys, although the prevalence of milk/dairy allergy was still 7 times higher than the prevalence of soy allergy.14 Both surveys that reported sesame allergy found the prevalence to be numerically lower than soy allergy, 0.5% versus 0.2%3 and 0.32% versus 0.23%.14
Self-reported (or Proxy Reported) Prevalence of Food Allergy Among US and Canadian Children and Adolescents for the Major Food Allergens (Percent of Population)
In general, there is a tendency for children to outgrow their food allergies, although this is not evident from the US survey of children in the case of peanuts, shellfish, and fin fish (Table 5). It is likely that the overall prevalence of peanut allergy will begin to decline as more clinicians recommend the early introduction (4-6 months) of peanuts for infants with mild or severe eczema, egg allergy, or both.16 In contrast to peanuts, shellfish, and fin fish, the prevalence of soy allergy decreased by 60% when comparing the average prevalence for all ages with the prevalence for adolescents 14 to 17 years of age.3 These data are consistent with estimates, based on clinical experience, that approximately 70% of children outgrow their soy allergy by age 10 years.45 In fact, when comparing the age at peak prevalence of soy allergy with prevalence for those aged 14 to 17 years, the change is even more striking (Figure). The peak prevalence of soy allergy was 1.5% at age 1 year; after age 1 year, prevalence rates steadily decreased to a low of 0.2% at age 14 to 17 years.
Change in the prevalence (percent of population) of self- or proxy-reported soy allergy by age among US children and adolescents.3
The prevalence of soy allergy among children of all ages was the same as wheat (0.5%) but higher than the prevalence of allergy to sesame seed (0.2%). However, by age 14 to 17 years, only the prevalence of sesame allergy was lower than that for soy (0.2% vs 0.1%). Although it is problematic to compare surveys, the fact that the FFS found the prevalence of soy allergy to be only 0.1% among adults suggests soy allergy prevalence continues to decline beyond that age of 17 years. However, in the NIAID survey, there was no evidence that soy allergy continued to decline during adulthood as the prevalence (%) for ages 18 to 29, 30 to 39, 40 to 49, 50 to 59, and 60 years or older was 0.7, 0.8, 0.6, 0.7, and 0.4, respectively.4
DISCUSSION
There is a need to better educate both health professionals and the public about the prevalence of food allergy overall as well as the relative prevalence of allergy of specific foods so that consumers, who are demanding greater transparency about the foods they eat, can make more informed choices (see Table 6 for key points). The Big 8 serves a useful purpose in this regard; however, it also has its limitations. One is that when it was created, it was based on very limited prevalence data. Two, it does not inform consumers about the relative prevalence of each of the foods designated as major allergens because all are treated equally in labeling. As was discussed, there is a large variation in prevalence among the foods in the Big 8, with data showing that soy allergy is the least prevalent. Health professionals need to help their patients and clients correctly identify the food proteins to which they are allergic. Doing so requires that health professionals better understand the signs and symptoms of food allergy and understand the diagnostic tests best suited for determining the existence of food allergy.
Summary of Salient Points for Clinicians
The FALCPA states that the major food allergens account for 90% of food allergies. But as pointed out by Gendel,46 it is not clear why 90% is considered an appropriate level of public health concern. This cutoff seems to have been determined rather arbitrarily. Given the low prevalence of soy allergy, an argument could be made that soy could be left off the list without meaningfully affecting public health. In Japan, 7 food allergens, of which soy is not one, require mandatory labeling. However, in contrast to Japan, the European Union has classified 14 foods (Big 14) as major allergens requiring labeling. In addition to the 8 foods classified as major allergens in the United States, the European major allergen list includes celery, lupin, mustard, sesame, and sulfur dioxide. As dietary habits associated with different cultures increasingly merge, and migration continues to increase, for simplicity sake, there may be some advantage to coordinating allergen lists throughout the world.47
Interestingly, although soy is one of the Big 14, the prevalence of IgE-mediated soy allergy among Europeans appears to be quite low, lower than for other commonly consumed foods not classified as major allergens.48,49 This point was emphasized by a report from EuroPrevall (the prevalence, cost, and basis of food allergy across Europe), which stated that the data “… indicate that some allergens for which labeling is mandated and for which management measures are therefore instituted (eg, soy, mustard) appear to have a lower public health impact than some which are not required to be declared (eg, some fruits).” In a recent report from EuroPrevall, it was found that among 6 European cities, the prevalence of probable soy allergy was 0.08% and 0.03% in Zurich and Utrecht, respectively, whereas no soy allergy was reported in Madrid, Reykjavik, Lodz, and Athens.50
Three complementary epidemiological studies, covering the period 2005 to 2009, based on SR prevalence were conducted in EuroPrevall: a birth cohort study conducted in 9 countries, a general population survey in schoolchildren and adults in 8 countries (community surveys), and a cross-sectional study in allergy clinics in 12 countries.51 In the community and the outpatient clinic studies, food allergies were diagnosed by assessing sensitization to a panel of 24 foods using serum IgE measurements and complemented by skin prick testing. In a second step, clinical reactivity to foods was assessed by standardized DBPCFCs. These challenges will continue to be in those infants and children from the birth cohorts showing suspected food allergic reactions. For the outpatient clinic studies and a randomly selected sample of schoolchildren and adults from the community-based surveys, DBPCFCs were undertaken with those foods responsible for the preponderance of the food-allergic reactions. EuroPrevall may serve as a template for research in the United States that can provide more accurate data on food allergy prevalence. Regardless of when or if more accurate prevalence data become available, further effort is needed to educate the public about the relative prevalence of each of the major food allergens.
REFERENCES
1. Zarkadas M, Scott WF, Salminen J, et al. Common allergenic foods and their labelling in Canada—a review. Can J Allergy Clin Immunol. 1999;4118–4141.
2. Sicherer SH. Epidemiology of food allergy. J Allergy Clin Immunol. 2011;127(3):594–602.
3. Gupta RS, Warren CM, Smith BM, et al. The public health impact of parent-reported childhood food allergies in the United States. Pediatrics. 2018;142(6).
4. Gupta RS, Warren CM, Smith BM, et al. Prevalence and severity of food allergies among US adults. JAMA Netw Open. 2019;2(1):e185630.
5. Jackson KD, Howie LD, Akinbami LJ. Trends in allergic conditions among children: United States, 1997-2011. NCHS Data Brief 2013;(121):1–8.
6. McGowan EC, Peng RD, Salo PM, et al. Changes in food-specific IgE over time in the National Health and Nutrition Examination Survey (NHANES). J Allergy Clin Immunol Pract. 2016;4(4):713–720.
7. Boyce JA, Assa'a A, Burks AW, et al. Guidelines for the diagnosis and management of food allergy in the United States: summary of the NIAID-sponsored expert panel report. Nutrition. 2011;27(2):253–267.
8. Volta U, Caio G, Karunaratne TB, et al. Non-coeliac gluten/wheat sensitivity: advances in knowledge and relevant questions. Expert Rev Gastroenterol Hepatol. 2017;11(1):9–18.
9. Nowak-Węgrzyn A, Chehade M, Groetch ME, et al. International consensus guidelines for the diagnosis and management of food protein-induced enterocolitis syndrome: executive summary—Workgroup Report of the Adverse Reactions to Foods Committee, American Academy of Allergy, Asthma & Immunology. J Allergy Clin Immunol. 2017;139(4):1111–1126.e4.
10. Hefle SL, Nordlee JA, Taylor SL. Allergenic foods. Crit Rev Food Sci Nutr. 1996;(36 suppl):S69–S89.
11. Vici G, Belli L, Biondi M, Polzonetti V. Gluten free diet and nutrient deficiencies: a review. Clin Nutr. 2016;35(6):1236–1241.
12. McGowan EC, Keet CA. Prevalence of self-reported food allergy in the National Health and Nutrition Examination Survey (NHANES) 2007-2010. J Allergy Clin Immunol. 2013;132(5):1216–1219.e5.
13. Verrill L, Bruns R, Luccioli S. Prevalence of self-reported food allergy in U.S. adults: 2001, 2006, and 2010. Allergy Asthma Proc. 2015;36(6):458–467.
14. Soller L, Ben-Shoshan M, Harrington DW, et al. Overall prevalence of self-reported food allergy in Canada. J Allergy Clin Immunol. 2012;130(4):986–988.
15. Perkin MR, Logan K, Marrs T, et al. Enquiring About Tolerance (EAT) study: feasibility of an early allergenic food introduction regimen. J Allergy Clin Immunol. 2016;137(5):1477–1486.e8.
16. Sicherer SH, Sampson HA. Food allergy: a review and update on epidemiology, pathogenesis, diagnosis, prevention, and management. J Allergy Clin Immunol. 2018;141(1):41–58.
17. Bock SA. Prospective appraisal of complaints of adverse reactions to foods in children during the first 3 years of life. Pediatrics. 1987;79(5):683–688.
18. Magnolfi CF, Zani G, Lacava L, Patria MF, Bardare M. Soy allergy in atopic children. Ann Allergy Asthma Immunol. 1996;77(3):197–201.
19. Celakovska J, Krcmova I, Bukac J, et al. Sensitivity and specificity of specific IgE, skin prick test and atopy patch test in examination of food allergy. Food Agricult Immunol. 2017;28(2):238–247.
20. Sicherer SH, Sampson HA. Food allergy. J Allergy Clin Immunol. 2010;125(2 suppl 2):S116–S125.
21. Scurlock AM, Lee LA, Burks AW. Food allergy in children. Immunol Allergy Clin North Am. 2005;25(2):369–388, vii-viii.
22. Nwaru BI, Hickstein L, Panesar SS, et al. Prevalence of common food allergies in Europe: a systematic review and meta-analysis. Allergy. 2014;69(8):992–1007.
23. Sampson HA, McCaskill CC. Food hypersensitivity and atopic dermatitis: evaluation of 113 patients. J Pediatr. 1985;107(5):669–675.
24. Bousquet J, Bjorksten B, Bruijnzeel-Koomen CA, et al. Scientific criteria and the selection of allergenic foods for product labelling. Allergy. 1998;53(47 suppl):3–21.
25. Foucard T, Edberg U, Malmheden Yman I. Fatal and severe food hypersensitivity. Peanut and soya underestimated allergens. Lakartidningen. 1997;94(30–31):2635–2638.
26. Bernhisel-Broadbent J, Sampson HA. Cross-allergenicity in the legume botanical family in children with food hypersensitivity. J Allergy Clin Immunol. 1989;83(2 pt 1):435–440.
27. Bernhisel-Broadbent J, Taylor S, Sampson HA. Cross-allergenicity in the legume botanical family in children with food hypersensitivity. II. Laboratory correlates. J Allergy Clin Immunol. 1989;84(5 pt 1):701–709.
28. Eigenmann PA, Burks AW, Bannon GA, et al. Identification of unique peanut and soy allergens in sera adsorbed with cross-reacting antibodies. J Allergy Clin Immunol. 1996;98(5 pt 1):969–978.
29. Barnett D, Bonham B, Howden ME. Allergenic cross-reactions among legume foods—an in vitro study. J Allergy Clin Immunol. 1987;79(3):433–438.
30. Bock SA, Atkins FM. The natural history of peanut allergy. J Allergy Clin Immunol. 1989;83(5):900–904.
31. Burks AW Jr., Brooks JR, Sampson HA. Allergenicity of major component proteins of soybean determined by enzyme-linked immunosorbent assay (ELISA) and immunoblotting in children with atopic dermatitis and positive soy challenges. J Allergy Clin Immunol. 1988;81(6):1135–1142.
32. Bock SA, Lee WY, Remigio LK, et al. Studies of hypersensitivity reactions to foods in infants and children. J Allergy Clin Immunol. 1978;62(6):327–334.
33. David TJ. Anaphylactic shock during elimination diets for severe atopic eczema. Arch Dis Child. 1984;59(10):983–986.
34. Yunginger JW, Nelson DR, Squillace DL, et al. Laboratory investigation of deaths due to anaphylaxis. J Forensic Sci. 1991;36(3):857–865.
35. Burks AW, Williams LW, Thresher W, et al. Allergenicity of peanut and soybean extracts altered by chemical or thermal denaturation in patients with atopic dermatitis and positive food challenges. J Allergy Clin Immunol. 1992;90(6 pt 1):889–897.
36. Cordle CT. Soy protein allergy: incidence and relative severity. J Nutr. 2004;134(5):1213S–1219S.
37. Sampson HA. Food allergy. JAMA. 1997;278(22):1888–1894.
38. Sampson HA. Update on food allergy. J Allergy Clin Immunol. 2004;113(5):805–819; quiz 20.
39. Sampson HA. Food allergy—accurately identifying clinical reactivity. Allergy. 2005;60(suppl 79):19–24.
40. Sicherer SH, Munoz-Furlong A, Sampson HA. Prevalence of peanut and tree nut allergy in the United States determined by means of a random digit dial telephone survey: a 5-year follow-up study. J Allergy Clin Immunol. 2003;112(6):1203–1207.
41. Sicherer SH, Munoz-Furlong A, Sampson HA. Prevalence of seafood allergy in the United States determined by a random telephone survey. J Allergy Clin Immunol. 2004;114(1):159–165.
42. Food and Drug Administration. Sesame as an allergen in foods. Fed Regist. 2018;83(210):54594–54596.
43. Hompes S, Köhli A, Nemat K, et al. Provoking allergens and treatment of anaphylaxis in children and adolescents—data from the anaphylaxis registry of German-speaking countries. Pediatr Allergy Immunol. 2011;22(6):568–574.
44. Lavine E, Ben-Shoshan M. Anaphylaxis to hidden pea protein: a Canadian pediatric case series. J Allergy Clin Immunol Pract. 2019;7(6):2070–2071.
45. Savage JH, Kaeding AJ, Matsui EC, Wood RA. The natural history of soy allergy. J Allergy Clin Immunol. 2010;125(3):683–686.
46. Gendel SM. Comparison of international food allergen labeling regulations. Regul Toxicol Pharmacol. 2012;63(2):279–285.
47. Venter C, Groetch M, Netting M, Meyer R. A patient-specific approach to develop an exclusion diet to manage food allergy in infants and children. Clin Exp Allergy. 2018;48(2):121–137.
48. Bartra J, Garcia-Moral A, Enrique E. Geographical differences in food allergy. Bundesgesundheitsbla. 2016;59(6):755–763.
49. Burney P, Summers C, Chinn S, et al. Prevalence and distribution of sensitization to foods in the European Community respiratory health survey: a EuroPrevall analysis. Allergy. 2010;65(9):1182–1188.
50. Lyons SA, Burney PGJ, Ballmer-Weber BK, et al. Food allergy in adults: substantial variation in prevalence and causative foods across Europe. J Allergy Clin Immunol Pract. 2019;7(6):1920–1928.e11.
51. Mills EN, Mackie AR, Burney P, et al. The prevalence, cost and basis of food allergy across Europe. Allergy. 2007;62(7):717–722.
Copyright © 2020 The Authors. Published by Wolters Kluwer Health, Inc.