Susan L Hefle. Cambridge World History of Food. Editor: Kenneth F Kiple & Kriemhild Conee Ornelas. Volume 1. Cambridge, UK: Cambridge University Press, 2000.
Adverse Food Reactions and Allergies
An adverse food reaction is defined as any untoward reaction following the ingestion of food (Lifshitz 1988). These reactions generally fall into two categories: food intolerance and food hypersensitivity. Intolerances are nonimmunologic (Sampson and Cooke 1990) and are responsible for most adverse food reactions. They may be idiosyncratic, due to metabolic disorders, or caused by pharmacological substances such as toxins or drugs present in food. Food additives can also be a cause of food intolerance or hypersensitivity and can produce respiratory and gastrointestinal complaints (Lifshitz 1988).
True food hypersensitivity, or allergy, is an adverse food reaction involving immunologic mechanisms. It is initiated by production of specific antibodies, otherwise known as immunoglobulins, in reaction to food constituents. The body manufactures antibodies as part of its regular defense system against foreign invaders such as viruses and bacteria. In certain individuals, the immune system is triggered to elicit a specific antibody, called immunoglobulin E (IgE), against various environmental substances like pollens, pet dander, insect venoms, and foods. The common immunologic mechanisms involved can cause food-allergic reactions to resemble allergic reactions to honeybee stings or penicillin.
In food-allergic individuals, IgE antibodies are produced against food components and circulate in the blood. Upon reaching certain cells, known as mast cells and basophils, the IgE becomes fixed to the cell surface and remains there. These cells contain high quantities of special receptors for IgE; rat mast cells have been found to contain 2-5 • 105receptors per cell (Mendoza and Metzger 1976). A large portion of the IgE in the body is fixed to these cells, and when they become armed with IgE, they are said to be “sensitized.”
Mast cells are present in many tissues of the body, and basophils are present in the blood. When certain food components, or allergens, are ingested and circulate in the blood, they come in contact with the IgE bound to the mast cell or basophil surface. This contact causes a chain of events to occur in the cells, leading to the release of granules containing certain mediators that are responsible for the clinical manifestations of the allergic reaction. This immediate allergic reaction is classified as a Type I hypersensitivity reaction according to the Gell and Coombs classification (Coombs and Gell 1975). Most food-allergic reactions are of this type (Moneret-Vautrin 1986), although other mechanisms have been shown to be responsible in some cases (Chandra and Shah 1984).
The substances released from the cells include histamine and serotonin, but many other mediators are also released (Barrett and Metcalfe 1988). The major inf luences of these mediators are vasodilation, smooth muscle contraction, and a general increase in vascular permeability.
A small amount of any food protein remains undigested and passes through the gut wall and into the circulatory system (Steinmann, Wottge, and MullerRuchholz 1990). During the neonatal period the gastrointestinal barrier to protein uptake and transport is immature. Therefore, excessive amounts of food proteins may be transported into the circulatory system. In addition, it is possible that a large quantity of protein is not broken down intracellularly due to immature cell function. During this period, infants may become sensitized to ingested allergens; and later, when the mucosal barrier is mature, small amounts of allergen absorbed by the gut can cause a reaction.
It has been suggested that food-allergic reactions are caused by pathologically increased gut permeability (Sampson 1990a); this claim has been refuted by studies with cow’s milk–allergic children in which the gut was not shown to be more permeable than in control children (Walker 1984; Powell et al. 1989). However, the permeability of the gastrointestinal barrier does increase following mast cell activation, thereby allowing more allergen through the barrier and, perhaps, increasing the allergic response (Barrett and Metcalfe 1988).
Mast cells located on the mucous surfaces of the gastrointestinal tract are thought to play a major role in IgE-mediated food hypersensitivity reactions (Barrett and Metcalfe 1988).The gastrointestinal tract contains comparatively large numbers of mast cells – for example, the human duodenum contains 20,000 per cubic millimeter (Norris, Zamchek, and Gottlieb 1962), whereas human skin contains 7,000 per cubic millimeter (Mikhail and Miller-Milinska 1964).
Food allergy can develop only if the allergen crosses the gastrointestinal barrier. The clinical manifestations of food allergy depend on the transport of allergens across the barrier, giving rise either to local allergic reactions or, from the systemic circulation, to systemic responses. Penetration of the gut depends on the size and structure of the allergen, changes occurring as a result of digestion, gut permeability (depending on age and preexisting disease), and interaction with other antibodies located in the gut. More factors to be considered are individual responses to various amounts of allergen, sufficient IgE binding at the mast cell or basophil, and the susceptibility of the affected organs to the mediators that are released.
Clinical manifestations of mediator release depend on the part of the body that is affected. Table IV.E.3.1 lists symptoms associated with food-allergic reactions. The most common manifestations are gastrointestinal, dermal, and respiratory (Sampson and Cooke 1990), and they represent contact of allergen with populations of sensitized mast cells present in the affected tissues.
Gastrointestinal symptoms, including nausea and vomiting, cramping, abdominal distension, flatulence, and diarrhea, are especially frequent in infants and young children (Barrett and Metcalfe 1988). Chronic ingestion of offending foods by sensitive people may cause fecal blood loss, malabsorption, and other long-term manifestations (Buckley and Metcalfe 1982). Skin reactions to food allergens in such individuals can include pruritus, edema of the lips, tongue, gums, oral mucosa, and pharynx. Urticaria (hives) is the most common skin manifestation and can be diffuse or localized.
The reactions are very individualistic and diverse (Collins-Williams and Levy 1984). Initially, some individuals may experience immediate contact reactions on their lips and tongue, whereas others do not experience a reaction until the offending food has moved farther down the gastrointestinal tract.
Respiratory symptoms can be divided into two categories: upper airway distress, which in food-allergic reactions is usually caused by laryngeal edema, and middle airway distress, produced as a consequence of bronchoconstriction, with resulting edema and pulmonary mucus production (Collins-Williams and Levy 1984). Respiratory symptoms are infrequent with food allergies, although asthma has been associated with allergies to cow’s milk, soybeans, and peanuts (Minford, MacDonald, and Littlewood 1982; Chiaramonte and Rao 1988).
Atopic dermatitis, a chronic inflammatory skin disease, is characterized by dry, easily irritated, intensely pruritic skin. The role of food hypersensitivity in atopic dermatitis has been debated for decades (Burks et al. 1988). IgE-mediated reactions to foods may contribute to the pathogenesis of atopic dermatitis (Sampson and McCaskill 1985); A.W. Burks and coworkers (1988) reported that 96 percent of atopic dermatitis subjects examined in their study developed skin reactions after food challenge.
Anaphylactic shock is a rare, acute, and potentially fatal form of food-allergic response. It is a generalized vasodilation triggered by significant mast cell degranulation and can involve a number of organ systems. If the cardiovascular system is affected, shock and low cardiac output result, and involvement of the respiratory tract can induce bronchospasm, pulmonary edema, and laryngeal edema. In food-induced anaphylactic shock, the gastrointestinal tract can respond with abdominal cramping and vomiting. Anaphylactic reactions may advance rapidly, beginning with mild symptoms that can progress to cardiorespiratory arrest and shock over a one- to three-hour period.
For example, an individual experiencing an anaphylactic food-allergic reaction may notice tongue itching and swelling, or palatal itching at first, then throat tightening, perhaps followed by wheezing and cyanosis. Chest pain and urticaria may be noted, and the individual may have gastrointestinal symptoms such as abdominal pain, vomiting, or diarrhea. A progression of symptoms can lead to potentially life-threatening hypotension and shock.
As there are no official means of reporting anaphylactic episodes, the actual frequency of these reactions is unknown, although J. W. Yunginger and colleagues at the Mayo Clinic (1988) documented 8 cases of fatal food-induced anaphylaxis in a period of 16 months. Exercise-induced food anaphylaxis is a type of reaction that develops during or shortly after exercise following the ingestion of certain foods. In documented cases, exercise most often occurred within 2 hours of ingestion. The foods implicated have included celery, lentils, peaches, shellfish, and wheat. Neither exercise alone nor food alone were sufficient to induce anaphylaxis (Maulitz, Pratt, and Schocket, 1979; Buchbinder et al. 1983; Kushimoto and Aoki 1985; Silverstein et al. 1986).
Symptoms of food-induced anaphylaxis may include cutaneous erythema, itching, and urticaria, which can progress to vascular collapse or upper respiratory obstruction (Schocket 1991).The pathophysiological mechanism of these reactions has not been elucidated, but heightened mast cell responsiveness to physical stimuli may be involved (Sheffer et al. 1983). It has been shown that avoidance of the offending food 8 to 12 hours prior to exercise usually eliminates difficulties.
Incidence and Natural History
The incidence of true food allergy is probably less than the general population perceives. Although studies have shown that at least one in four adults with allergies believe that they have experienced adverse reactions following ingestion or handling of foods (Sampson and Metcalfe 1992), it is estimated that just 2 to 3 percent (Bock 1987; Sampson and Cooke 1990) of the pediatric population and 1 to 2 percent of the adult population suffer from allergic reactions to food (Sampson and Cooke 1990). The true prevalence is unknown, however, and other estimates range from 0.3 to 10 percent of the total population (Taylor 1980; Johnstone 1981; Taylor 1985; Barrett and Metcalfe 1988; Schreiber and Walker 1989).
Food allergy is also influenced by culture and eating habits. For example, allergies to fish are more common in Japan and Norway than elsewhere because consumption of fish is higher in those countries (Aas 1966).The frequency of food hypersensitivity varies by ethnic group and socioeconomic class (Lieberman and Barnes 1990). Its etiology includes many factors, but genetics seem to play a large role. Studies with children have shown that the risk for allergy with one allergic parent is approximately 50 percent and for bilateral parental allergy 67 to 100 percent (Schatz et al. 1983).
Frequency of food allergy is highest in infancy and early childhood and diminishes with increasing age (Collins-Williams and Levy 1984). It is most prevalent between 1.5 and 3 years of age (Kjellman 1991). Although young children appear more likely to outgrow their food allergies, older children and adults may also lose their sensitivity if the offending food is removed from the diet. Investigations have shown that one-third of children and adults lose their clinical reactivity after one to two years of allergen avoidance (Sampson and Scanlon 1989).
Differences in disappearance rates depend on the allergen and the individual; for example, many children with allergy to cow’s milk can tolerate small amounts of milk by the time they are 3 years old, and egg allergy tends to decline before age 7. But allergies to nuts, legumes, fish, and shellfish tend to remain a problem for a much longer time (Bock 1982; Collins-Williams and Levy 1984).
Although exposure to food allergens can occur in utero through placental passage, most studies have shown that prenatal sensitization to food is infrequent (Halpern et al. 1973; Croner et al. 1982; Hamburger et al. 1983; Kjellman and Croner 1984). However, the case of an infant with strong skin-test reactivity to wheat and milk at the age of 5 hours has been reported (Kaufman 1971). Some fully breast-fed infants have been observed to have allergies to egg and cow’s milk (Warner et al. 1980), and significant amounts of cow’s milk casein have been detected in breast milk for up to 12 hours after maternal ingestion (Stuart et al. 1984).
There have been a number of studies on breast feeding to determine what benefit it might have in preventing food sensitization (Halpern et al. 1973; Saarinen et al. 1979; Juto and Bjorkstein 1980; Hide and Guyer 1981; Buscino et al. 1983). The results are conflicting, and the only consistent observation is that prolonged breast feeding (greater than four months and preferably six) and delayed introduction of solid food seem to be beneficial in the prevention of food allergy (Zeiger 1988). Breast feeding and maternal avoidance of common allergenic foods is suggested if there is a family history of allergy and a high serum IgE level at birth (Michel et al. 1980).
The most commonly implicated foods in food allergy are listed in Table IV.E.3.2. The allergenic substances are usually proteins (Aas 1978b). Adults tend to be allergic to shellfish, legumes (especially peanuts), crustacea, tree nuts, and wheat (Bock and Atkins 1990; Sampson 1990a; Sampson and Cooke 1990). Children tend to be allergic to milk and eggs more frequently. Any food, however, has the potential to cause an IgE-mediated reaction. Very severe reactions are most often seen with peanuts, eggs, fish, and nuts (Collins-Williams and Levy 1984). In fact, peanuts are the most common cause of life-threatening reactions (Sampson 1990b). In a period of 16 months, a research team at the Mayo Clinic reported 4 cases of death due to peanut-induced anaphylactic shock (Yunginger et al. 1988).
With the widespread introduction of new and “exotic” foods into our diets, it is anticipated that newly described allergic reactions will be reported. D. A. Moneret-Vautrin (1986), for example, has noted that with the relatively recent introduction of soybeans to the diet in France, the incidence of observed soybean allergy has increased to the point where it has become the third most common food allergy. Another example is kiwi fruit, which is not indigenous to the United States and became available as a result of importation in the 1980s. Following its introduction, allergic reactions to kiwi fruit were suddenly reported (Fine 1981; Fallier 1983).
Genetically Engineered Foods
Some concerns are being raised regarding nontraditional foods produced using genetic engineering techniques. These techniques allow for the fast and easy transfer of proteins from one food into another and for increased nutritional or other benefits, such as viral resistance. But there also is the potential for allergenic proteins from some foods to be transferred into other foods; how or whether these foods should be labeled is still being debated. Another compelling issue is whether genetic engineering techniques could potentially change the protein structure so that it could become allergenic once transferred and reproduced in the engineered food.The United States Food and Drug Administration has been and will continue to be working on policies governing the regulation of bioengineered foods, with allergenicity a key issue (Kessler et al. 1992).
Most allergenic foods contain multiple allergens. For example, egg white is a complex mixture of at least 20 proteins, of which 5 or 6 are allergenic (Langeland 1982). The existence of multiple allergens in cow’s milk (Goldman 1963; Bleumink and Young 1968) and peanuts (Barnett, Baldo, and Howden 1983) is well known. Most major food allergens range from 14 to 70 kilodaltons (1,000 atomic mass units) in molecular weight (Aas 1976; King 1976; Chiaramonte and Rao 1988). The upper molecular size observed for these allergens may be due to the permeability limits involved in the gastrointestinal barrier of the host. The allergen must be of adequate molecular intricacy to interact with the elements of the immune system, but quite low limits of molecular size exist; for example, small fragments of the codfish allergen, 6,500 and 8,500 daltons in size, possess pronounced allergenic activity (Elsayad et al. 1972).T. Ishizaka and K. Ishizaka (1984) have shown that the release of mast cell mediators depends on the bridging of two cell-fixed IgE molecules by the allergen. If such bridging is critical, the allergic response should, in fact, depend on the number of allergenic determinants and their distribution on the surface of the allergen and not necessarily their size.
Common food allergens that have been fully or partially purified or characterized include codfish (Elsayad and Aas 1971), cow’s milk (Goldman et al. 1963; Bleumink and Young 1968), eggs (Anet et al. 1985), peanuts (Barnett and Howden 1986; Burks et al. 1991; Burks et al. 1992), soybeans (Shibaski et al. 1980; Herian, Taylor, and Bush 1990), and shrimp (Hoffman, Day, and Miller 1981; Daul et al. 1992).
Most common allergenic food proteins appear to be heat-stable and resistant to proteolytic processes, such as peanut, shrimp, and codfish allergens, although many lose their allergenic activity during digestion or cooking (Aas 1984). Therefore, the allergenicity of a food may be influenced by the way in which the food is prepared, processed, or stored. For example, ovalbumin, the third most important allergen of eggs, is moderately heat-labile and is found only in small amounts in cooked egg (Hoffman 1979). Similarly, heating denatures some cow’s milk allergens and makes them less allergenic (Bahna and Gandhi 1983). Individuals allergic to fresh fruits and vegetables can often tolerate these foods after they are cooked, canned, or frozen (Hannuksela and Lahti 1977; Eriksson 1978).
When a sensitive individual produces IgE antibodies directed against a certain food component and then encounters another food with similar components, an allergic response may occur. Structural allergenic similarities may exist within families of biologically related foods. Since dietary elimination of the offending food is the only “tried-and-true” method of preventing an allergic reaction, cross-allergenicity among related foods is of concern to allergists and patients. Food-allergic individuals often report cross-reactivity among other foods in the same families and are cautioned to avoid eating other closely related foods.
The most common food families associated with cross-reactions are fish, citrus fruits, legumes, shellfish, mollusks, and crustaceans (Chiaramonte and Rao 1988). Certain allergens are also apparently common to both foods and pollens. Common allergens have been reported in melon, banana, and ragweed pollen (Anderson et al. 1970), celery and mugwort pollen (Pauli et al. 1985), and apple and birch pollen (Lahti, Bjorkstein, and Hannuksela 1980).
“True” clinical cross-reactivity, however, is often difficult to establish without performing oral challenge studies. Reports in the literature seem to indicate that the occurrence of clinical cross-reaction is infrequent (Bock 1991). Extensive in vitro “allergenic cross-reactivity” (binding of IgE antibody that is specific for a different food allergen) has been documented. For example, D. Barnett, B. Bonham, and M. E. H. Howden (1987) found that 25 percent of sera from legume-sensitive patients reacted strongly with peanut, garden pea, soybean, and chickpea extracts. Another research team also found extensive in vitro cross-allergenicity with peanuts, soybeans, peas, and lima beans in patients with legume sensitivity (Bernhisel Broadbent,Taylor, and Sampson 1989).
However, an earlier study by the same researchers indicated that clinical results and in vitro results did not correlate well in evaluating allergenic cross-reactivity in the legume family (Bernhisel-Broadbent and Sampson 1989). Fifty-nine percent of skin-test-positive patients reacted to oral challenge, but only (approximately) 3 percent reacted in oral challenges to more than one legume. These studies show that although IgE antibodies can cross-react with related foods and cause positive skin tests in some cases, clinical manifestations are rare, and being allergic to one food does not necessarily rule out the consumption of biologically related foods.
Occupational Food Allergy
Development of allergic disease can be associated with occupational exposure to food proteins, and most occupational sensitizing agents are food-derived protein allergens (O’Neil and Lehrer 1991). Exposure is facilitated through inhalation and contact, and syndromes include occupational asthma, hypersensitivity pneumonitis, and skin reactions, including contact dermatitis and contact urticaria.
But although allergen levels in the workplace can be very high, only a small percentage of exposed workers develop occupational responses, suggesting that host factors play an influential role. For example, a history of allergy seems to influence development of sensitivity in some instances of occupational allergic disease, such as occupational asthma caused by exposure to green coffee beans (Jones et al. 1982). By contrast, however, family or individual history of allergy has not been shown to be a factor in the development of occupational asthma due to exposure to snow crab (Cartier et al. 1984).
Although the pathophysiology of many occupational food reactions has not been ascertained, the role of IgE in occupational asthma in bakers is well known (Hendrick, Davies, and Pepys 1976; Block et al. 1983). Most occupational allergens that are also foods have not been shown to induce symptoms following ingestion by workers sensitized via inhalation. Occupational asthma related to food products has been most often associated with seafood, eggs, grains, spices, herbs, coffee, tea, and mushrooms, whereas hypersensitivity pneumonitis, although low in occurrence, has been associated with molds used in cheese production, poultry proteins, fish meal, and mushroom spores. Dermatological reactions precipitated by food have been most often linked with fish, seafood, mustard, garlic, onion, cashews, and lettuce.
Diagnosis of Food Allergy
The diagnosis of food allergy is complicated. As we have seen, adverse food reactions can be caused by immunologic, nonimmunologic, and unknown factors (Hawrylko and Murali 1988). Substantiation of food allergy involves meticulous medical evaluation, since self-diagnosis is often unreliable. Elimination diets are frequently the initial approach to diagnosis of food allergy. The suspected offending food is first eliminated for two to four weeks, then reintroduced in small quantities and the patient’s response is recorded (Cummings and Bock 1988).
Skin testing is the most popular diagnostic tool for evaluating food allergy. It was first used in 1966 to identify children allergic to codfish (Aas 1966). The techniques for skin tests are varied and include puncture, prick, scratch, and intradermal methods. A positive response results in a skin reaction forming a “wheal-and-flare.” Results are recorded by measuring the wheal-and-flare diameter and comparing them to negative (saline solution) and positive (histamine) controls. Clinically significant wheals are 3 millimeters or more in diameter (Cummings and Bock 1988). But the use of skin testing is precluded in the face of anaphylactic or other severe reactions, as well as generalized dermatitis, and positive skin tests may be inhibited by the use of some medications, especially certain antihistamines and drugs with antihistamine effects (Chodirker 1985).
A major problem with skin testing is that food allergen extracts have not been standardized. Food skin-test extracts are usually crude preparations of unknown composition, and accurate diagnosis of food allergy has, in part, been impeded by the lack of standardized extracts. This may ultimately be responsible for the variability in the predictive accuracy of food skin tests. H. A. Sampson (1988), for example, compared extracts from three commercial firms for their positive predictive accuracy against oral-food-challenge results and discovered that they ranged from 0 to 79 percent. Negative predictive accuracies were much better, ranging from 85 to 100 percent. C. Ortolani and co-workers (1989) found that skin-test extracts prepared with fresh foods produced more sensitive results when compared to commercial extracts. As an increasing number of food allergens are isolated and fully characterized, the potential for use of standardized food extracts increases.
Double-Blind, Placebo-Controlled Food Challenge
The double-blind, placebo-controlled food challenge (DBPCFC), in which a suspected offending food or placebo is administered in capsules or masked in other food, has been called the “gold standard” for the diagnosis of food allergy (Collins-Williams and Levy 1984; Cummings and Bock 1988; Sampson 1988; Bock 1991).This method was initially used in the investigation of immediate hypersensitivity reactions to foods in asthmatic children (May 1976). But S. A. Bock and F. M. Atkins (1990) recently reported a study of a group of food-allergic children over a period of 16 years. Fully 39 percent had positive DBPCFC results. Other investigators have reported good correlation of DBPCFC results with other laboratory methods for diagnosing food allergy (Bernstein, Day, and Welsh 1982; Sampson 1988; Parker et al. 1990).
Although controversy exists regarding the use of skin tests alone for diagnosis (Bernstein, Day, and Welsh 1982; Bock and Atkins 1990), some investigators have found good correlation between food-challenge studies and skin-test results. For example, one such study, which focused on a group of adults with histories of immediate adverse reactions to foods, discovered that 90 percent of those in the group who were food-challenge-positive were also skin-test-positive (Atkins, Steinberg, and Metcalfe 1985). Similarly, Bock and Atkins (1990) noted that 98 percent of positive food reactions to oral challenge were accompanied by a positive skin test in children past their third birthday. But in younger children the correlation dropped to 83 percent.
Nonetheless, other investigators have found false-positive skin tests in patients who were food-challenge-negative (Bernstein et al. 1982; Sampson and Albergo 1984). In general, a negative skin-test result is a good indicator of absence of IgE-mediated hypersensitivity (Sampson 1988; Parker et al. 1990).
The first assay developed for measuring IgE blood levels was the radioallergosorbent assay (RAST), which was initially described in 1967 (Wide, Bennich, and Johansson 1967). RAST is specific and reproducible (Hawrylko and Murali 1988); however, it measures only circulating, and not tissue-bound, IgE. For this reason, it is less sensitive than skin tests for the detection of specific IgE. In addition, a RAST test is not necessary if the skin test is negative, as circulating IgE will not be present if there is no tissue-bound IgE (May 1976; Sampson and Albergo 1984; Chodirker 1985; Bock and Atkins 1990). Generally, sensitivity of RAST for food allergens varies from 50 percent to more than 90 percent (May 1976). RAST is still widely used in the allergy field to augment skin testing in diagnosis. Sensitivity of RAST for food allergens could be improved, as could skin-test reliability, if there were technical advances in the purification of food allergens.
Basophil Histamine Release
In this technique, blood basophils are obtained from an allergic patient. They are incubated with an allergen for a specified time, and the release of mediating histamine, caused by the presence of the allergen, is measured (May et al. 1970; Hirsch and Zastrow 1972). In one study employing purified cow’s milk proteins, wheat, soybean, and ovalbumin extracts, release of histamine from cells was found in 25 to 50 percent of pediatric subjects who also had positive skin tests, and no histamine was released in skin-test-negative patients (May and Alberto 1972).
In another study, however, food extracts did not induce release of histamine in patients with food allergy (Dockhorn 1969). H. Nolte and colleagues (1989), using gut mast cells obtained during biopsies of food-allergic patients, found that histamine release from intestinal mast cells could not be correlated with histamine release by blood basophils.Therefore, there are differences in the ability of food extracts to elicit a response in mast cells from different organs.
As with other diagnostic allergy assays, the sensitivity of the basophil histamine release assay could probably be improved by the use of purified food-allergen preparations. In addition, the technique is neither convenient nor easy to perform and, therefore, is not used widely for diagnosis.
Treatment and Prevention of Food Allergy
Elimination diets are the only proven effective therapy for food allergy, once the offending food is identified (Chodirker 1985; Schreiber and Walker 1989). In patients with severe reactions to foods, strict avoidance is indicated, which may include cross-reacting foods, prepared foods (unless one is absolutely certain of all ingredients), and the inhalation of aerosols of the implicated food (Rao and Bahna 1988).
Despite the apparent low incidence of clinical cross-reactivity, food-allergic persons are encouraged to use caution when eating a biologically related food for the first time. The recommendation is usually to avoid the offending food for a number of years, if not for the remainder of the patient’s life. However, this advice may be adjusted for children, as they tend to outgrow certain food allergies, such as those to eggs and milk.
Food-allergic individuals must read food labels and ingredient listings diligently, as these usually reveal the presence of the offending ingredient. This task can be difficult, and a certain amount of “education” in reading labels is necessary, because particular terms used by food processors can camouflage the presence of allergenic proteins. “Natural flavorings” may include soybean and/or milk proteins, and “caramel f lavoring” may contain milk proteins. “Hydrogenated vegetable protein” commonly contains soybean proteins but can be comprised of other types of vegetable protein. In addition, it can be difficult to identify and avoid some types of allergenic foods. An example is peanuts, which after pressing and deflavoring, are then reflavored and sold as other types of nuts, such as almonds. Though they smell, taste, and look like tree nuts, these deflavored peanuts have been found to retain their allergenic qualities (Nordlee et al. 1981) and can pose a serious threat to unsuspecting peanut-allergic people.
Sensitive individuals may also be inadvertently exposed to foods contaminated with allergenic proteins during processing. In one documented case, for example, the inadequate cleaning of common equipment caused sunflower butter to become contaminated with peanut butter and elicited an allergic reaction in a peanut-sensitive patient (Yunginger et al.1983).
Antihistamines have been suggested for use in children with mild food allergies before mealtime (Bahna and Furukawa 1983). However, since antihistamines work by competitive inhibition (Furukawa 1988), they cannot completely prevent allergic reactions, and individuals with severe reactions should not rely on them.
Perspective on the Development of Allergy
Allergic disease is difficult to trace in archaeological or historical records. Evidence of foods or medicines used in the past is very limited (Lieberman and Barnes 1990), and the symptoms of allergy can mimic those of other diseases, thereby concealing accounts of allergic reactions in records and notes.
It has been theorized that allergy is a fairly recent development in the history of the human race. A prominent characteristic of parasitic infections in humans is an elevated level of IgE (Johansson, Bennich, and Berg 1972). But because parasitic infections and allergic disease seem to be mutually exclusive (Merrett, Merrett, and Cookson 1976), allergy could be the result of an ecological transition from endemic parasitosis to improved sanitary conditions that eliminate or reduce parasitic exposure (Lieberman and Barnes 1990). An interesting discovery is a higher frequency of allergies among urban than rural residents in developing countries, but higher IgE levels in rural people than among urban asthmatics and individuals with allergies (Godfrey 1975; Merrett et al. 1976).The advent of modern, hygienic conditions and the elimination of parasitic infection could, therefore, be responsible for spawning production of IgE against other substances in our environment.