Allergen Management in the Food Industry

Joyce I. Boye, Samuel Benrejeb Godefroy, Samuel Benrejeb Godefroy

• Publisher: Wiley
• Year: 2011
• Print ISBN:
  9780470227350
• Edition: 1
• eBook ISBN:
  9781118060285
• Topic: Technology & Engineering
• Subtopic: Food Science
• Index: Technology & Engineering

This book comprehensively addresses the sources of allergenic contaminants in foods, their fate during processing, and the specific measures that need to be taken to minimize their occurrence in foods. The book provides up-to-date information on the nine major allergens (as well as other emerging allergens) and practical guidelines on how these allergens can be identified and controlled during production and processing. Starting with an introduction to food allergens, the book follows with sections on food allergen management during production and processing, guidelines for the processing of specific allergen-free foods, techniques for hypo-allergenization and allergen detection, and allergen-free certification.

Part I: FOOD ALLERGY AND THE CONSUMER

1

IMMUNE-MEDIATED ADVERSE REACTIONS TO DIETARY PROTEINS

Olga M. Pulido

1.1. INTRODUCTION

An adverse reaction to food is a general term applied to the clinically abnormal response to an ingested food, food ingredient, or food additive. Adverse reactions to food may or may not be mediated by the immune system [1–6]. Nonimmune-mediated adverse reactions to food mimicking food allergy are termed food intolerances and can be the result of toxicity, for example, histamine in scromboid fish poisoning or nonallergic food hypersensitivity (Fig. 1.1) [4–7]. In turn, nonallergic food hypersensitivity (Fig. 1.1) can result from (1) chemical/pharmacological action of food ingredients (e.g., caffeine in coffee, tyramine in aged cheese, sulfites in wine, phenylethylamine in chocolate, or the flavor enhancer monosodium glutamate [8–10]; (2) physiological factors associated with specific characteristics of the host (e.g., lactase deficiency leading to lactose intolerance and deficiency of glucose-6-phosphate dehydrogenase in favism) [5, 11–13]; or (3) others such as psychogenic causes (e.g., eating disorders may present clinical symptoms suggestive of an adverse reaction to food) [6, 14]. Conversely, an adverse reaction to food (Table 1.1) may be mediated by an immunologic response and should be distinguished from food intolerances that do not have an immune basis, but may be similar in clinical presentation [2, 7, 15–17].

TABLE 1.1 Food Allergies: Immune-Mediated Mechanisms, Associated Clinical Presentations, and Most Often Offending Foods

Fig. 1.1 Nonimmune-mediated adverse reaction to food “Food Intolerances.” See text and Glossary of Terms for further explanation and references.

Allergy is defined as a hypersensitivity reaction to intrinsically harmless antigens, most of which are environmental, and the process is initiated by specific immunologic mechanisms [3]. The term food allergy has been recommended when an adverse reaction to food is mediated by immunologic mechanisms [1, 3, 5, 18]. Food allergens are defined as the antigenic molecules giving rise to the immunologic response [3, 19–21]. Proteins are the food constituents responsible for eliciting immune-mediated adverse responses to food [3, 19–21]. Hence, the eliciting dietary proteins are known as allergens. The term IgE-mediated food allergy is used when immunoglobulin E (IgE) is involved in the reaction [3, 5, 6]. Allergies to food contaminants such as dust mites, mold, and parasites should also be distinguished from food allergy elicited by dietary proteins.

Under the above definitions, all immune-mediated adverse reactions to dietary proteins are considered food allergy. Together, food allergy encompasses a wide range of clinical disorders, which are grouped in Table 1.1 as IgE, non-IgE, and mixed IgE/non-IgE [2, 5, 6, 22]. These include IgE-mediated food allergy, celiac disease, dermatitis herpetiformis (DH), and clinical conditions such as allergic eosinophilic esophagitis and food protein-induced enterocolitis syndrome (FPIES) [14, 23–25]. Many factors are implicated in the basic pathophysiological mechanisms of food allergy, such as host genetics, biochemical characteristics of the proteins, exposure, changes induced through food processing, or genetic engineering in “genetically modified foods” (Table 1.2) [20, 21, 26–28].

TABLE 1.2 Food Allergies

Food allergens are generally glycoproteins with molecular weights ranging from 10 to 70 kDa. Innate allergenic capacity of foods may be determined by a combination of factors, for example, solubility, resistance to pH, heat, and proteolysis by digestive enzymes. Allergenic capacity of food allergens may be modified (increase or decrease) by food processing and manipulation, for example, heating. The individual must first be sensitized by exposure to the allergenic protein. The route of initial exposure and sensitization can be oral, respiratory (aeroallergens), or dermal (skin) contact. In infants, the route of initial exposure and sensitization can occur in utero or through breast milk. Food allergy occurs when a sensitized individual is exposed to the same or a cross-reactive protein through food ingestion. Food allergies are often encountered by infants or children during a developmental window of immunologic immaturity. IgE-mediated food allergies are characterized by the rapid release of powerful cellular chemicals such as histamine. In IgE-mediated food, allergy reactions can occur within minutes or up to 4 hours after ingestion. Clinical disorders associated to non-IgE-mediated mechanisms or to mixed IgE and non-IgE, typically have delayed onset of symptoms (>2 hours) and a chronic, relapsing course. Severity of reactions and presenting symptoms may vary with time and exposure.

During the last two decades, there has been an increasing trend in the prevalence of food allergy in Western countries. It is estimated that food allergy affects between 5% and 8% of infants and young children and approximately 2–4% of adults [2, 7, 15, 17, 29]. Today, food allergies, both IgE and non-IgE mediated, are important health concerns from the point of view of risk management, policy setting, public health, diagnosis, and treatment for the consumers, their families, and the communities where they live, and for the food industry at large [13, 18, 30–32].

An understanding of the basic mechanisms underlying adverse reactions to foods and an enhanced awareness of the various clinical presentations is important for the overall management of food allergies. To this extent, this chapter presents an overview of the current understanding of the basic immune mechanisms mediating adverse reactions to food proteins and their various clinical presentations. For further clarification, refer to the Glossary of Terms on pages xix–xxvii.

Discussion of other aspects relevant to food allergy, such as allergen thresholds dose, clinical diagnostic tests, and methods used to detect specific allergenic proteins in food, are beyond the scope of this chapter. The chapter is organized in sections based on the implicated immune-mediated mechanism and associated clinical conditions. With the exception of celiac disease, which is discussed separately, a brief description of symptoms and medical conditions associated with food allergies is presented under each category throughout the text or in the Glossary of Terms.

1.2. ORAL IMMUNE TOLERANCE

The gut is responsible for the digestion and absorption of nutrients while acting as the first line of immune defense against pathogenic microbes within the gastrointestinal tract. The gut mucosal immune system accomplishes this task partly by establishing a tolerance to macronutrients [28, 33]. The gastrointestinal tract is the largest immune organ in the body and is constantly exposed to dietary proteins from ingested food. Immune tolerance to dietary proteins is maintained by active suppressive mechanisms involving antigen-specific regulatory T cells. In the first few years of life, humans gradually develop an intricate balance between tolerance and immune reactivity in the gut mucosa, along with a tremendous expansion of gut-associated lymphoid tissue (GALT). GALT is comprised predominantly of clusters of organized lymphoid tissue in the terminal ileum (Peyer’s patches), appendix, and isolated lymphoid follicles located beneath the epithelium throughout the gut [34].

Several factors can cause disturbances at different steps in the process of developing oral tolerances, disrupting intestinal barrier function, and contributing to disease pathogenesis [35]. The factors implicated in the development and/or altering the risk of adverse immune reactions to dietary proteins can include genetic susceptibility, gastrointestinal infection, age, exposure (route, dose, and time), timing and length of initial exposure, association with breast-feeding, gastric pH, and type of protein [2, 13, 36–38]. Food allergies may be the result of a breach in oral tolerance to ingested food or from cross-reactivity between food and nonfood allergens. For example, individuals with allergies to fruits and vegetables may have been sensitized by pollen exposure known as pollen-food allergy syndrome or oral allergy syndrome (OAS) [5, 13].

1.3. FOOD ALLERGY

Food allergy is defined as an exaggerated immune response (hypersensitivity) to dietary proteins [1–3]. Allergies to food develop when exposure to a food protein is mistakenly identified as harmful by the human body. Failure of the development of gut tolerance for a specific food protein leads to hypersensitivity to that protein [21, 28, 33]. Food allergies are often seen during the early period of life that coincides with the critical period of development of immune tolerance and typically occurs during this period of immunologic immaturity [2, 15, 17, 28, 39].

Host factors, for example, genetics, age, gut flora, asthma, history of atopy, exercise, and extrinsic factors such as characteristics and dose of the protein (threshold), all influence the potential allergic reaction [2, 5, 33, 36, 40, 41]. The allergenic capacity of the protein may be modified by food processing and manipulation (e.g., heating) [27, 42, 43]. Food proteins that are resistant to digestion are considered to be the most allergenic. The ability of the allergenic protein to trigger direct oral sensitization is modulated by gastric acidity [37].

Although any food protein can potentially provoke an immune reaction, relatively few food proteins are responsible for the vast majority of significant food-induced allergic reactions [21]. The most common food allergens in the pediatric population include cow’s milk, eggs, peanuts, tree nuts, soy, wheat, fish, and shellfish, whereas peanuts, tree nuts, fish, and shellfish predominate in adults [2, 5, 13, 14, 25, 44]. Gluten from wheat, barley, and rye are the proteins of most concern for celiac disease, DH, and other gluten-induced conditions (Section 1.4), while rice is emerging as a food of concern for FPIES [45, 46].

The most common food allergies in a given population and the criteria for identification of priority allergenic proteins will vary based on world regions, individual countries, dietary habits, and regulatory systems [30].

1.3.1. IgE-Mediated Food Allergy

IgE-mediated food allergies constitute the majority of food allergic reactions and are the best studied. An IgE-mediated reaction develops when an allergenic protein binds with specific IgE antibodies on mast cells and basophils activating the release of potent compounds such as histamine. The first step in the development of IgE food allergies is sensitization. The first time the susceptible individual is exposed to the specific food allergen, the body’s immune system misidentifies the protein as harmful and responds by creating specific antibodies (IgE) to that allergen. Repeat exposures to the same food protein trigger an immune reaction with the release of IgE antibodies [2, 5, 17, 33]. The conjugation of the IgE antibody with the allergens triggers a stimulus to mast cells and basophils, which degranulate, releasing mediators (e.g., histamine) and promoting the synthesis of prostaglandins, leukotrienes, and cytokines [2, 18, 33]. This reaction represents an effort by the immune system to reject/remove the protein, mistakenly identified as harmful, from the body. In turn, the chemicals released have powerful effects on the respiratory system, gastrointestinal tract, skin, and cardiovascular system.

Histamine is a powerful biogenic amine, released during IgE-mediated allergic reactions. It is synthesized by mast cells, basophils, platelets, and other cells such as histaminergic neurons and enterochromaffin cells, where it is stored in the cytoplasm in vesicles and released upon stimulation. Conversely, histamine exerts its effects by binding to a family of receptors on target cells in various tissues mediating numerous biological reactions. These biological reactions include smooth muscle contraction, vasodilation, increased vascular permeability, mucus secretion, tachycardia, alterations of blood pressure, arrhythmias, and stimulation of gastric acid secretion [12]. This mechanism explains the fast onset of symptoms and potential severity of clinical symptoms observed with IgE-mediated food allergies.

IgE-mediated reactions can start within minutes to 1 hour (rarely past 2 hours) of exposure. Reactions often affect the skin (urticaria, angioedema, morbilliform eruptions, flushing, pruritus) [47] and can involve the respiratory tract (sneezing, rhinorrhea, congestion, cough, wheezing, difficulty breathing) [48], the gastrointestinal tract (OAS, nausea, vomiting, diarrhea, cramping, abdominal pain) [17, 49], and the cardiovascular system (tachycardia, hypotension) [50, 51]. Severe systemic reactions can result in anaphylactic shock and death [52].

A late-phase response may follow the immediate reaction beginning 4–6 hours after contact with the allergen and continuing for several days. This response is caused by chemotactic mediators released at the same time as the immediate reaction, which promote selective recruitment of inflammatory cells, mainly eosinophils and neutrophils, which infiltrate the tissue producing an inflammation that can last for a few days [6].

1.3.1.1. Anaphylaxis.

Anaphylaxis is a serious generalized allergic reaction that may cause death. Anaphylaxis represents the most severe form of IgE-mediated food allergy and is clinically defined as a food allergic reaction involving two or more organ systems [50–52]. It can include cutaneous (skin), respiratory, cardiovascular, and gastrointestinal s...

Table of contents

• Cover
• Half title page
• Title page
• Copyright page
• DEDICATION
• PREFACE
• CONTRIBUTORS
• GLOSSARY OF TERMS
• Part I: FOOD ALLERGY AND THE CONSUMER
• Part II: GENERAL PRINCIPLES FOR ALLERGEN MANAGEMENT AND CONTROL
• Part III: PROCESSING FOODS FREE FROM SPECIFIC ALLERGENS
• Part IV: RISK ASSESSMENT AND RISK MANAGEMENT
• Index