Chapter 31

Environmental and Food Allergies

John W. Distler

Environmental Allergies

Definition and Epidemiology

Environmental allergens are responsible for a wide range of signs and symptoms ranging from rhinitis, eczema, urticaria, and bronchospasm to anaphylaxis. With repeated exposure, immediate type 1 hypersensitivity reactions may occur through the development of immunoglobulin E (IgE). Allergens can be found both indoors and outdoors and fluctuate among households, with the change of seasons, by weather patterns including heat and humidity, and by the area in which one lives in the United States. Common indoor allergens include dust mites, indoor molds, and animal dander. The more common outdoor allergens are pollen (i.e., grass, trees, and weeds) and outdoor molds, including mold smuts in wheat, corn, oat, and barley fields.¹ The incidence of environmental allergies with subsequent symptom development has been on the rise.² Allergic rhinitis may affect up to 20% of the U.S. population and up to 40% of children.¹ Atopic dermatitis was found to have a direct cost to the U.S. health care system ranging from $1 billion to $4 billion, with an average cost per patient of approximately $609.³ The potential psychosocial effects of atopic dermatitis are also staggering.

Allergic rhinitis may be considered the first step in the development of allergic asthma.⁴ The Centers for Disease Control and Prevention (CDC) reported a steady increase in the development of asthma in both adults and children from 1996 to 2007.⁵ However, symptom development may be secondary to other non–IgE-mediated environmental factors, such as urbanization, toxins, air pollution, and tobacco smoke exposure.¹ Occupational exposure has also become an increasingly important patient consideration.⁶ It is important to make the clinical distinction between a true IgE-mediated cause and those symptoms that result in irritation and subsequent inflammation of the mucous membranes in the nose, lungs, and skin.⁷

Common Environmental Allergens

Recurrent exposure to an environmental allergen and subsequent sensitization result in the typical presenting signs and symptoms of patients with a genetically determined atopic disorder. Environmental allergens may be either indoor or outdoor and are influenced by a variety of factors.

Common indoor allergens include molds, dust mites, cockroaches, and animal dander. Prominent indoor molds include Penicillium, Alternaria, Cladosporium, and Aspergillus. Indoor molds are fungi and are found in warm, moist, and humid environments of bathrooms, basements, and laundry rooms.⁸ Molds thrive in these conditions and spread through the production of spores. The mold spores become airborne in certain conditions, resulting in exposure to the host. Molds are hearty in that they can survive environmental conditions adverse to their growth, such as dry air and exposure to sunshine. No growth occurs under these conditions, but molds also do not die. Dust mites are microscopic relatives of the spider and are common in all households. Two common dust mites responsible for triggering of an atopic reaction are Dermatophagoides pteronyssinus and Dermatophagoides farinae. Like molds, dust mites also thrive in warm, moist environments; they survive through the ingestion of flakes of skin from humans and live in bedding, mattresses, carpets, curtains, and upholstered furniture.⁸ The total eradication of dust mites from the home is impossible. Pet dander is created by the oil glands, saliva, and urine of animals, not the fur. In combination, these excreted substances become allergenic to some individuals. An important consideration for patients with animal dander allergy is that dander is a sticky allergen and may remain in the home weeks or months after an animal has been removed. Cat dander and dog dander are among the most common allergens in schools, brought in by students with an animal in their home.⁸ Animals such as rabbits, gerbils, hamsters, guinea pigs, horses, and cows are also potentially allergenic, depending on exposure. Cockroaches are another indoor allergen and can cause severe asthma reactions in children living in crowded urban environments and older dwellings. The allergenic protein that cockroaches create is from their saliva and feces.⁸

Outdoor allergens consist mainly of pollen from trees, grass, and weeds in addition to molds and mold smuts. Tree pollen, grass pollen, and weed pollen are the only seasonal environmental allergens. The pollination season varies from one area of the United States to another. In the spring, trees are typically the first to shed their pollen. Southern states may have detectable levels of tree pollen as early as late January, whereas northern states may not have measurable levels until May or June. Not all tree pollen is allergenic. Trees that release allergenic pollen include oak, elm, maple, hickory, poplar, willow, box elder, and walnut.⁸ As with trees, only a small number of the many species of grass are allergenic. For the most part, grass pollen season tends to follow tree season, and again the variability is dependent on the area of the United States. Some common grasses that release allergic pollen are Kentucky bluegrass, Johnson grass, Bermuda grass, orchard grass, sweet vernal grass, and timothy. Grass pollen levels are affected by temperature, moisture, humidity, and time of day. Weeds are typically fall pollen producers and may begin to pollinate as early as August and into November, depending on the type of weed and location in the United States. Common allergenic weeds include ragweed, pigweed, plantain, sheep’s sorrel, sagebrush, and lamb’s quarters. Like grass pollen counts, weed pollen counts are higher at dawn and dusk and also on hot, dry, windy days.⁸ Flower pollens are rarely allergenic because their pollen is heavier and is dispersed by insects that carry the pollen from plant to plant.⁹ Outdoor molds tend to be more allergenic than indoor molds. Common outdoor molds include Alternaria and Hormodendrum (i.e., Cladosporium). Alternaria is a common mold that can be brought indoors by humans and pets. Like indoor molds, outdoor molds produce spores for growth and are found commonly on fallen leaves and rotting vegetation. Mold smuts grow in the soil and roots of wheat, corn, oat, and barley fields. Mold counts tend to be higher from July into late summer, depending on the geographic location. In the colder months, mold becomes dormant but does not die with snow or frost. When it is covered with snow or ice, mold is less likely to release its spores into the wind.⁸ Therefore a warmer, more humid late fall and early winter may produce more mold spores.

Pathophysiology

With repeated exposure to an environmental allergen through the respiratory tract, genetically predisposed people begin to develop IgE as an inappropriate means to protect the body from the protein allergen (antigen). Antigen-specific T cells are activated through the lymphatic system in response to the antigen. The activated antigen-specific T cells then activate B cells, and IgE is created in lymphoid tissue or at local tissue sites.³^,¹⁰ The newly created antigen-specific IgE is released by plasma cells and binds to high-affinity IgE receptors located on the basophils and mast cells. This leads to the sensitization of the cells in the tissues of the nose, lung, or skin.⁴^,¹⁰

Although other immunoglobulins, such as IgG, IgA, and IgM, are produced to appropriately protect the body, circulating levels of IgE and the attachment to the allergen are responsible for the atopic reaction.¹⁰ With repeated exposure and further sensitization, IgE binds with the antigen protein, and degranulation of the mast cells and basophils begins, starting the allergic cascade. Mediators, including histamine, proteoglycans, enzymes, cytokines, and many others, are released as a result of the degranulation. The chain in the release of mediators is responsible for the immediate and late-phase responses of the cells. Histamine may be fully released within 30 minutes of degranulation, whereas cytokines may be released over many hours.¹^,⁹^,¹⁰

Atopic diseases are typically genetically determined, yet individual responses to antigen exposure are also based on environmental factors and susceptibility of the host as well. For instance, the timing of the exposure to an allergen may affect the exposure response. High-level exposure to allergens early on may predispose a person to develop a more severe atopic response. The period of sensitivity is highly variable among people. In addition, exposure to cigarette smoke and pathogens may also alter the body’s immune response, modifying the level of IgE activation.

Clinical Presentation and Physical Examination

Patients with environmental allergies may have a variety of signs and symptoms. Typical presenting signs and symptoms include rhinitis, eczema, urticaria, bronchospasm, and anaphylaxis.¹ Exposure to environmental allergens may also exacerbate other non–IgE-mediated symptoms.

A cause-and-effect relationship must be determined; a patient may have rhinitis because of grass pollen, bronchospasm from cat exposure, or urticaria from dust mite sensitivity.¹¹ An important diagnostic consideration is to determine whether a patient’s symptoms are seasonal or perennial or both. A patient may live with dust mite sensitivity and have subclinical symptoms, yet the symptoms become bothersome only during the spring when the seasonal flare results in further IgE activation. Similarly, patients may become symptomatic only in the winter when doors and windows are closed and their exposure to dust mites and animal dander increases. Understanding of the patient’s individualized IgE activation triggers and the environmental timing is essential in helping patients control their symptoms.

A detailed history is required to determine a cause-and-effect relationship of environmental allergen exposure and the development of symptoms. Standard history questions include current medications, medication allergies, past medical history, family history, and surgeries and hospitalizations. In addition, further atopy, including the potential for stinging insect venom allergy and food allergies, must be understood; the presence of these conditions may trigger further IgE activation, potentially increasing a patient’s physical response.

To understand the entire allergic presentation, additional questions must be asked about the environment. The type of home in which one lives and the age of the dwelling may indicate the potential for mold or cockroaches. Heating and cooling sources must be identified because the use of forced hot air may add to the disbursement of dust mite and animal dander. Radiant heat may increase the humidity of the home, resulting in an increase in mold spore production and dust mites. The presence of a crawl space or unfinished damp basement may also increase the potential for indoor mold. Dust mites may be present in bed linens, older pillows, mattresses, and stuffed animals. The frequency of laundering of bed linens must also be recorded. Determination of the number and type of animals in the home and the area of the house in which they are allowed is essential. Recent renovations to the home could modify mold or dust mite exposure. Ideally, the humidity in the home should be 35% to 40% to decrease indoor mold spore growth and to control dust mite propagation.

A thorough physical examination must be performed after the environmental allergy history. The examination should always include a careful head, eyes, ears, nose, and throat (HEENT) examination to look for allergic symptoms of the nose and eyes, including sclera erythema and injection, allergic shiners from venous engorgement, swollen pink nasal turbinates, and tonsillar enlargement. Small, nontender movable posterior cervical nodes in the neck are a common finding in children. Direct visualization of the skin with ambient lighting should be performed to look for cutaneous symptoms of urticaria and eczema. Encouraging the patient and parents to take pictures of the cutaneous response would also be helpful in cases of intermittent symptoms. Pulmonary function tests (PFTs) should be performed, if they are available, to look for reversibility of symptoms and PFT results after bronchodilation. A heart and abdominal examination should also be conducted for each patient, looking for other diagnostic clues.

Diagnostics

History and physical examination includes the following.

• Skin testing

• A skin prick test (SPT) can be performed by either the scratch or intradermal method. Both histamine and normal saline controls are placed on patients at the time of testing. The reaction to histamine must be positive and the reaction to saline negative to ensure reliability of the test results.¹²

• Certain medications, such as antihistamines, H₂ blockers, and tricyclic antidepressants, must be discontinued for up to 5 days before skin testing because these may interfere with test result reliability.

• Skin tests are placed on the back, upper arm, or ventral surface of the forearms, depending on the amount of testing to be performed and the age of the patient.¹³ The use of the back in children is recommended because pruritus from a positive test result may make the patient scratch the area. Scratching of the area may mix allergens placed on the skin, interfering with evaluation of the results. Results are read within 15 to 20 minutes.

• Scratch testing involves scratching the surface of the skin with a single stylus for each allergen.¹² This form of allergy testing is safer, more rapid, and less uncomfortable to patients than intradermal testing but is not as sensitive as intradermal testing. Depending on the practice, providers may begin with scratch testing and proceed to intradermal testing if the results are negative.¹³ Scratch testing is also associated with a lower potential for anaphylaxis than intradermal testing.

• Intradermal testing is more sensitive and reproducible than scratch testing. This test involves the use of a 25-gauge needle with a small drop of allergen (0.02 to 0.05 mL) placed beneath the skin.⁹ Depending on the practice and the type of allergen, the concentration placed beneath the skin may be 1:10 or as high as 1:1000.¹² If the patient reacts to the allergen, that particular allergen (e.g., grass pollen) is not tested further, and the test result is considered positive. If the test result is negative, higher concentrations are used. A stepwise approach to intradermal testing should be taken to ensure safe patient outcomes. All providers and staff must be trained to handle any potential systemic reactions, including urticaria, bronchospasm, and full anaphylaxis.

• Serum IgE levels

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