Chapter 28
ALLERGENS

David C. Caretto*

ENZYMES

Common names: Detergents, digestive aids, dough improvers, papain, others

Occupational setting

Enzymes are used in the chemical, pharmaceutical, cosmetic, textile, medical, detergent, and food and beverage industries. Paper and pulp industries use enzymes to break down wastes. Cellulase is used as a digestive aid. Aspergillus-derived alpha-amylase and cellulase are added to flour as dough improvers. Enzymes derived from Bacillus subtilis, such as alcalase (subtilisin A), are used in the detergent industry as an aid in removing stains from clothing. Papain and other enzymes are used in pharmaceutical products where the manufacturing process may involve sieving, blending, and compressing powders. Papain also has uses as a meat tenderizer (which use has resulted in illness in industrial kitchens), in the treatment of wool and silk for textiles, and in clarifying beer. Trypsin, a pancreatic enzyme, is used in the rubber industry.

Exposure (route)

Enzyme powders tend to be fine and easily airborne. Exposure to enzymes may occur through inhalation of enzyme dusts or through skin contact with liquid enzyme preparations or airborne dust. Dust may impact the upper airways or be carried directly into the lungs.

Pathobiology

Enzymes are proteins that catalyze chemical reactions. They are usually high-molecular-weight proteins and are effective in very small quantities. Cellulase catalyzes the cellulose to glucose reaction, xylanase catalyzes the breakdown of xylan, and alpha-amylase also has carbohydrate-cleaving activity. Papain and bromelain are proteolytic enzymes derived from the latex of ripe fruit of the pawpaw tree and the pineapple, respectively. Alcalase is a proteolytic enzyme derived from B. subtilis bacteria. Enzyme preparations may be contaminated with by-products of their production, such as growth media material, microorganisms, and preservatives.

Enzymes are potent respiratory sensitizers that may cause immediate, delayed, or dual allergy consisting of rhinoconjunctivitis and several patterns of asthma. In addition to respiratory allergy, immediate and delayed types of skin allergy have been described from enzyme exposure. Respiratory allergy may occur from exposure to cellulase, xylanase, papain, flaviastase, trypsin, bromelain, pepsin, alpha-amylase, and other enzymes. Asthmatic illnesses occur in a portion of sensitized workers who all typically have rhinitis and conjunctivitis along with nasal congestion. The pattern of asthma symptoms may be immediate (Type I, IgE mediated), biphasic with both early and late reactions, or delayed. Hypersensitivity pneumonitis may also occur. The occurrence of systemic symptoms along with delayed resolution of symptoms after removal from exposure and the presence of precipitins provide evidence for Type III hypersensitivity. In papain-induced asthma, the pathology seems to involve small airways, alveolar, and interstitial lung tissue in an inflammatory manner. Higher doses of enzyme seem to cause more intense pulmonary symptoms. Atopic individuals are thought to be at higher risk of developing enzyme-related allergies, such as that to papain, and to develop antibody and symptoms sooner than nonatopics.

Skin disorders from enzyme exposure may be irritant, digestive (commonly), or allergic. Skin allergy may be of the immediate (Type I, IgE mediated) variety, manifested by urticaria following skin contact with enzymes in liquid or powder form. Papain, cellulase, and xylanase are among the enzymes that cause contact urticaria.

Contact dermatitis, a delayed (Type IV) allergy that can be verified by positive patch tests, may also occur following exposure to enzymes. Contact dermatitis consists of an itchy, raised, red skin rash that may be slow to resolve. Although alcalase skin disorders may be irritant or digestive in nature, the combination of detergent with alcalase may be more allergenic than alcalase alone. Some enzymes, such as cellulase and xylanase, have been found to cause both urticaria and contact dermatitis. Patients with enzyme-related contact dermatitis may or may not be able to eat related products without problem.

Allergy to enzymes may develop after months to years of exposure. Allergic individuals exhibit rhinorrhea, conjunctivitis, and often shortness of breath, cough, chest tightness, and wheezing that occurs minutes to hours following exposure to enzymes. Oculonasal complaints typically precede the development of chest symptoms.

Anaphylaxis has followed the ingestion of papain in sensitized individuals. Cellulase and xylanase exhibit some cross-reactivity, as do chymopapain, papain, and bromelain. There is conflicting evidence regarding cross-reactivity between alcalase, sarinase, and esperase.1

Diagnosis

Medical and occupational history can be used to diagnose this disorder when the temporal relationship to exposure is elucidated in association with allergic symptoms. Symptoms that appear following exposure may resolve on weekends and holidays. Physical examination may reveal mucous membrane inflammation and respiratory wheeze. In patients with skin allergy, an itchy, red skin rash may be observed on exposed surfaces.

Pre- and postshift spirometry can be used to document the association of bronchoconstriction with exposure. One case report documented a 48–50% decrement in peak expiratory flow rate (PEFR) in a patient following entry into rooms where xylanase was handled.2 Confirmation of the diagnosis of enzyme allergy may be obtained through specific immunologic testing. RAST, skin prick, and skin patch testing may demonstrate specific IgE and hyperreactivity, respectively. Skin prick tests have been used to document reactivity of allergic patients to enzymes including cellulase, xylanase, papain, bromelain, and trypsin. In some cases, skin prick testing has resulted in a systemic reaction.1 Specific IgE measurements using RAST have been done for antibodies to cellulase, xylanase, alpha-amylase, alcalase, and papain.

ELISA has been reported to measure specific IgE antibody to alcalase in exposed detergent workers. In one study, ELISA was more sensitive than RAST, detecting 85% versus 68.4% of skin test positive workers.1 IgG antibodies to papain have been documented. Bronchial provocation has been used to diagnose alpha-amylase, cellulase,3 trypsin, and papain asthma.

Treatment

The preferred treatment for enzyme allergies is removal from exposure until corrective measures in work practice or engineering controls are implemented. In sensitized workers with symptoms, job change should be the ultimate goal. In severe cases, there is no alternative to a job change. In workers who remain in exposure situations, conventional allergy treatments may be tried. Cromolyn sodium reportedly prevented immediate papain-related symptoms in allergic workers, although steroids were needed to control the late response.4 Long-acting bronchodilators may abate late symptoms.

Medical surveillance

In the detergent industry, the goals of the medical surveillance program is to identify employees who have become sensitized to enzymes prior to the development of symptoms and to identify problems with the enzyme industrial hygiene program.5 All employees undergo annual pulmonary function testing, respiratory questionnaires, and monitoring by prick testing for specific IgE antibodies to enzymes. Total IgE and enzyme-specific IgE antibodies are also measured, typically by RAST.1 Although persons with IgE antibodies to enzymes are at higher risk of developing symptoms during prolonged, repeated, or high-dose exposures, skin prick test positive workers can continue to work with enzymes as long as they remain symptom-free.6 If an employee is found to be sensitized and symptomatic, an investigation of work practices and engineering controls should be conducted. The employee should be removed from the workplace until symptoms resolve, and the exposure is identified and corrected.

Prevention

The problem of respiratory sensitization in the detergent industry has led to the implementation of engineering controls that reduced exposures and the incidence of disease. Enzyme encapsulation, fume hoods, and other containment devices can prevent powder from becoming airborne and inhaled. When possible, enzymes should be handled in liquid preparations rather than powders to prevent airborne exposures to the respiratory tract and skin. Personal protective equipment may be used to further reduce the risk of exposure.

References

  1. 1. Sarlo K, Clark ED, Ryan CA, et al. ELISA for human IgE antibody to subtilisin A (alcalase): correlation with RAST and skin test results with occupationally exposed individuals. J Allergy Clin Immunol 1990; 86:393–9.
  2. 2. Tarvoinen K, Kanerva L, Tupasela O, et al. Allergy from cellulase and xylanase enzymes. Clin Exp Allergy 1991; 21:609–15.
  3. 3. Quirce S, Caevas M, Diez-Gome ML, et al. Respiratory allergy to Aspergillus-derived enzymes in bakers asthma. J Allergy Clin Immunol 1992; 90:970–8.
  4. 4. Novey HS, Keenan WJ, Fairshter RD, et al. Pulmonary disease in workers exposed to papain: clinico-physiological and immunological studies. Clin Allergy 1980; 10:721–31.
  5. 5. Sarlo K, Kirchner DB. Occupational asthma and allergy in the detergent industry: new developments. Curr Opin Allergy Clin Immunol 2002; 2(2):97–101.
  6. 6. Vanhanen M, Tuomi T, Tupasela O, et al. Cellulase allergy and challenge tests with cellulase using immunologic assessment. Scand J Work Environ Health 2000; 26(3):250–6.

FARM ANIMALS

Common names: Cows, horses, pigs, reindeer, sheep, chickens

Occupational setting

The raising of livestock occurs in various settings ranging from indoor to outdoor and small, family-run enterprises to large, commercial facilities. Reindeer herding is an important and prevalent occupation in Scandinavia. Horse exposure occurs in mounted law enforcement personnel and racetrack workers as well as agricultural workers. Livestock exposure is also a risk for veterinarians.

Exposure (route)

Exposure to farm animal antigens may be through inhalation of airborne particles or through skin contact with animals. Housekeeping tasks cause increased airborne dust concentrations, which may result in inhalation exposure. Fomite transmission of livestock allergens can occur when work clothes are brought into household living spaces.

Pathobiology

Animal proteins from farm animals may cause occupational allergy. Farm animals include various species of domesticated animals. Animals whose antigenic dander is associated with occupational allergy include horses, cows, sheep, pigs, and reindeer.

Skin contact with farm animal antigens may cause immediate or delayed skin allergy that produces dermatitis. Delayed dermatitis can be predicted to be an IgG-mediated process following skin exposure. One case report described delayed hypersensitivity in a piggery worker to pig epithelium that resulted in hand and body eczema.1 This contact dermatitis was substantiated by positive patch test to pig epithelium.1

Allergic respiratory disease has been associated with exposure to farm animals including cows, horses, and reindeer. Dander from these animals is allergenic. Respiratory disorders in hog farmers are not thought to be IgE or IgG allergic illnesses2 but rather inflammatory responses consisting of cytokine-mediated lymphocytes directed against endotoxin and dust associated with swine containment facilities.3 Pork allergens are associated with occupational asthma in hog farmers and pork processing plant employees. In one case study, a pork processing plant employee presented with occupational asthma from Type I hypersensitivity and contact dermatitis from Type IV hypersensitivity.4

Poultry workers have been found to have rhinitis and asthma in association with poultry-related antigens.5 This IgE antibody mediated allergy may result from chicken antigens such as serum, dander, and droppings. Other related antigens include the northern fowl mite antigen (see section on “Mites”). Bird fanciers and pigeon breeders have been shown to have bird-related immediate respiratory symptoms associated with immediate wheal and flare reactions. Although 19% of allergic patients reportedly react to horse allergens by intracutaneous testing, clinical disorders from horse allergy seem to be relatively infrequent.6

Diagnosis

Contact dermatitis from farm animal exposure may be diagnosed through a thorough medical and occupational history and physical examination along with patch skin testing. Workers with occupational dermatitis develop red, raised, itchy, often lichenified patches of skin inflammation in areas where direct skin contact with an allergen has occurred. Hand dermatitis is more common. This condition can also occur on other exposed areas, such as limbs, face, and thorax. The dermatitis can be chronic, with clearing associated with time away from the work site.

In immediate hypersensitivity disorders, rhinitis and asthma may develop following months to years of exposure. Workplace challenge can be used to demonstrate signs of allergy, such as bronchoconstriction as measured by pre- and postshift peak flow measurements. Skin prick test and specific IgE antibody measurements with reindeer epithelium have been used to document reindeer allergy in herders.7 Skin prick test antigens from cow, sheep, goat, and horse are also available. Nasal provocation has been used to confirm cow dander allergy.6 Skin prick test and RAST have also been used to demonstrate antibody to poultry-related antigens in poultry workers and cow dander in farmers.

Treatment

Avoidance of antigen exposure should be the ultimate goal in the treatment of occupational animal allergies. Since this solution is normally not practical, conventional treatments for dermatitis and asthma may be tried.

Medical surveillance

Farm workers tend to be self-employed or employed in relatively small numbers per facility. Medical surveillance using allergy symptom questionnaires would be appropriate for larger employers.

Prevention

Farmers need to be educated about the risks of allergy in association with farm work. Informed workers are more likely to avoid antigen exposure. Gloves, protective clothing, and respirators may decrease exposure. Work practice controls that minimize the generation of airborne dust and the need for direct skin contact should be instituted. Additional controls include showering and changing of clothes prior to entry into the home to prevent fomite transmission. An increased risk of symptoms in winter associated with closed quarters may necessitate increased vigilance in protective measures.

References

  1. 1. Bovenschen HJ, Peters B, Koetsier MI, et al. Occupational contact dermatitis due to multiple sensitizations in a pig farmer. Contact Dermatitis 2009; 61(2):127–8.
  2. 2. Matson SC, Swanson MC, Reed CE, et al. IgE and IgG-immune mechanisms do not mediate occupation-related respiratory or systemic symptoms in hog farmers. Allergy Clin Immunol 1983; 72:299.
  3. 3. Dosman JA, Fukushima Y, Senthilselvan A, et al. Respiratory response to endotoxin and dust predicts evidence of inflammatory response in volunteers in a swine barn. Am J Ind Med 2006; 49(9):761–6.
  4. 4. Labrecque M, Coté J, Cartier A, et al. Occupational asthma due to pork antigens. Allergy 2004; 59(8):893–4.
  5. 5. Viegas S, Faísca VM, Dias H, et al. Occupational exposure to poultry dust and effects on the respiratory system in workers. J Toxicol Environ Health A 2013; 76:230–9.
  6. 6. Bardana EJ Jr. Occupational asthma and related conditions in animal workers. In: Bardana EJ Jr., Montanaro A, O’Hollaren MT, eds., Occupational Asthma. Philadelphia: Hanley & Belfus, 1992:225–35.
  7. 7. Reijula K, Halmepuro L, Hannaksela M, et al. Specific IgE to reindeer epithelium in Finnish reindeer herders. Allergy 1991; 46:577–81.

GRAIN DUST

Common names: Rye grass, soybeans, buckwheat, oat grass, barley

Occupational setting

Grain dust allergy occurs in any occupation where grains are handled, stored, or used. Farming, cereal manufacturing, and grain loading and unloading operations are examples of settings associated with occupational grain dust allergy. Rye flour is used in agglomerate board manufacturing glue and therefore may be an allergen in wood dust. Buckwheat hulls are sometimes used as fillers in pillow and cushion manufacturing.1 Aspergillus-derived enzymes are used to enhance baked products.2 Brewery workers have developed occupational asthma after exposure to grain dust in the workplace.3

Exposure (route)

Inhalation exposure to respirable dust is the route of exposure in the development of occupational respiratory sensitization to grain dust. Grain dust results from the abrasion of kernels during handling; it forms at an estimated rate of 3–4 lb per ton of grain handled.4 Airborne dust measurements made during wheat and oat loading in Canada showed a mean particle size of 1.7–3.1 µm, which is respirable.5 Some grain-associated allergens, such as cellulase and buckwheat, may also cause skin reactions from skin contact.

Pathobiology

Grain dust is a product of various grass species used primarily in food manufacturing. It contains fractured grain kernels as well as various contaminants and additives, including molds, fungi, Aspergillus-derived enzymes (high-molecular-weight proteins with catalytic activity), bacteria, insects such as grain weevil, storage mites, pollens, fractured weed seeds, and mineral particles.2,6 Wheat dust and storage mites are covered separately in other sections of this chapter.

Because there are many allergenic components of grain dust, the etiology of grain-related allergy varies. Potential allergens range from contaminants such as insects, bacteria, and fungi to components of the grains themselves, such as soybean flour (which contains a number of antigens) and buckwheat flour. Wheat, rye, and triticale grasses are closely related species that have significant cross-antigenicity. Rye, barley, and oat are less closely related but still exhibit some cross-reactivity.6 Allergic individuals may be sensitized to more than one grain-related antigen. Most grain-associated antigens cause an immediate-type IgE-mediated hypersensitivity that may result in grain-associated rhinoconjunctivitis and asthma. Symptoms typically occur within minutes of exposure. A late-phase aggravation of symptoms after the workday may occur. Buckwheat and cellulase have also been associated with contact urticaria. One patient with prior symptoms related to occupational buckwheat and kapok exposure experienced an anaphylactic episode after buckwheat ingestion. Community asthma epidemics have been associated with soybean loading and unloading in Barcelona, Spain.7,8 A case of occupational allergy to oilseed rape dust has been documented.9

Among grain workers, grain dust exposure is a well-documented cause of nonallergic respiratory symptoms, including cough, shortness of breath, and decrease in lung function. Grain elevator workers have been found to have lower forced expiratory volume in 1 second (FEV1) and lower forced vital capacity (FVC) than nonexposed controls on a chronic basis.10 Severity of symptoms tends to be related to duration of exposure. Nonallergic acute grain-related respiratory disorders also occur, including an asthma-like acute syndrome and grain fever. These conditions of the bronchial airways should be considered when assessing a case of possible allergic disease from grain dust.

Diagnosis

The presence of rhinitis, conjunctivitis, sneezing, coughing, wheezing, and shortness of breath upon exposure to grain dust provides evidence for grain dust allergy. However, a medical history should be taken to exclude the existence of an underlying respiratory illness. Grain-exposed workers are known to have a high prevalence of respiratory symptoms, including productive cough, wheezing, and shortness of breath from nonallergic grain-related pathology (e.g., exposure to toxic gases, pesticides, fertilizers)

Conjunctivitis, rhinitis, edematous mucosa, and wheezing may be present on physical examination. Serial peak flow measurements may be used to establish reversibility of airflow obstruction and the temporality of symptoms in relation to exposure. Also, a trial of removal from the workplace to watch for resolution of symptoms may be useful. Demonstration of atopic status by history or prick skin test to common allergens is useful, since atopic individuals are at increased risk of some types of grain dust allergy.

Demonstrating positive skin prick test or RAST or positive bronchial challenge to grain-related antigens can support the diagnosis of grain dust hypersensitivity. Prick skin tests and reverse enzyme immunoassay have been used to demonstrate hypersensitivity to fungal alpha-amylase and cellulase in bakers who were also sensitized to wheat flour.2 Specific IgE antibodies to some cereal grains, including wheat and rye, can be measured through commercially available tests. Prick skin test methods and specific IgE tests have been developed for a number of research applications in grain dust allergy. Prick skin tests and RAST have been used for barley and rye flour. Bronchial challenge has been used to demonstrate reactions in individuals sensitized to alpha-amylase, cellulase, and wheat flour. Because of coincident exposures in the grain industry, nonallergenic causes of respiratory pathology should be ruled out.

Treatment

Treatment for grain dust allergy focuses on the avoidance of exposure. If workers are unable or unwilling to change occupations, various standard preventive and symptomatic therapies for allergies and asthma may be instituted. However, when the allergic disorder is severe, avoidance of exposure is prudent. If specific antigens are identified to which the patient is allergic, immunotherapy could be considered; however, this is not standard treatment.

Medical surveillance

An occupational history, concentrating on recent tasks, exposures, and respiratory symptoms, may be taken as part of routine medical surveillance. Periodic spirometry is indicated in workers exposed to grain dust. Although other screening tests for surveillance purposes have not been well studied, prick skin testing or RAST should be considered.

Prevention

Occupational allergy develops following exposure to antigenic materials. Therefore, avoidance of inhalation of and skin contact with these substances is the best way to prevent the development of hypersensitivity. The American Conference of Governmental Industrial Hygienists (ACGIH) has recommended 4 mg/m3 8-hour TWA (time-weighted average) as an exposure limit for oat, wheat, and barley dust. For buckwheat, however, allergic illness has been documented among workers exposed to as little as 1–2 mg/m3 of airborne dust.11 Work practice, engineering, housekeeping, and personal protective equipment controls can help to minimize dust exposure in the food and other grain handling industries. Recent studies have identified the N95 elastomeric respirator as preferable for protecting agricultural workers from aerosolized particulates of all particle size ranges.12,13

References

  1. 1. Heffner E, Nebiolo F, Asero R, et al. Clinical manifestations, co-sensitizations, and immunoblotting profiles of buckwheat-allergic patients. Allergy 2011; 66(2):264–70.
  2. 2. Quirce S, Cuevas M, Díez-Gómez M, et al. Respiratory allergy to Aspergillus-derived enzymes in bakers’ asthma. J Allergy Clin Immunol 1992; 90:970–8.
  3. 3. Godnic-Cvar J, Zuskin E, Mustajbegovic J, et al. Respiratory and immunological findings in brewery workers. Am J Ind Med 1999; 35(1):68–75.
  4. 4. Chan Yeung M, Enarson D, Kennedy S. The impact of grain dust on respiratory health. Am Rev Respir Dis 1992; 145:476–87.
  5. 5. Williams N, Skoulas A, Merriman JE. Exposure to grain dust. I. A survey of the effects. J Occup Med 1964; 6:319–29.
  6. 6. Quirce S, Diaz-Perales A. Diagnosis and management of grain-induced asthma. Allergy Asthma Immunol Res 2013; 5(6):348–56.
  7. 7. Anto JM, Sunyer J, Rodrigues-Roisin R, et al. Community outbreaks of asthma associated with inhalation of soybean dust. N Engl J Med 1989; 320:1097–102.
  8. 8. Codina R, Ardusso L, Lockey RF, et al. Sensitization to soybean hull allergens in subjects exposed to different levels of soybean dust inhalation in Argentina. J Allergy Clin Immunol 2000; 105(3):570–6.
  9. 9. Suh CH, Park HS, Nahm, DH, et al. Oilseed rape allergy presented as occupational asthma in the grain industry. Clin Exp Allergy 1997; 28:1159–63.
  10. 10. Wild P, Dorribo V, Pralong J, et al. Respiratory effects of an exposure to wheat dust among grain workers and farmers: a longitudinal study. Occup Environ Med 2014; 71(Suppl 1):A18–9.
  11. 11. Goehte CJ, Wieslander G, Ancker K, et al. Buckwheat allergy: health food, an inhalation health risk. Allergy 1983; 38:155–9.
  12. 12. Lee SA, Adhikari A, Grinshpun SA, et al. Respiratory protection provided by N95 filtering facepiece respirators against airborne dust and microorganisms in agricultural farms. J Occup Environ Hyg 2005; 2(11): 577–85.
  13. 13. Cho KJ, Jones S, Jones G, et al. Effect of particle size on respiratory protection provided by two types of N95 respirators used in agricultural settings. J Occup Environ Hyg 2010; 7(11):622–7.

INSECTS

Common names: Moths, bees, beetles, cockroaches, others

Occupational setting

Exposure to insects occurs in a variety of occupational settings. Workers at risk of exposure include those who work directly with insects, those who work with materials that may be contaminated by insects, and those who work in outdoor environments where insects coincidentally live. Occupations involving direct work with insects include entomologists, lepidopterists, ecologists, aquarists, toxicologists, beekeepers, spice or dye factory workers, organic farmers, and pest control researchers. Occupations involving work with potentially contaminated materials include bakers, process and warehouse workers (e.g., honey processors, grain mill workers), silk weavers, dock loaders, and sewage treatment workers. Outdoor occupations where insects coincidentally occur include farmers, fishermen, gardeners, fire fighters, forestry workers, environmental researchers, hydroelectric plant workers, fruit pickers, and those involving waterside work.

Exposure (route)

Insect-related organic materials readily become airborne. Shedded insect exoskeletons and scales are thin, readily dried, and very friable. In environments where these and related materials are found, dust may be raised through nearly any activity. Particulates from insects may be inhaled, resulting in respiratory illnesses.

Skin contact with certain insect parts may result in irritant or allergic disorders. Such contact can arise through direct handling of insects or by contact with contaminated objects or surfaces. Bites, such as from beetles, can cause urticaria. Insect stings may also cause allergy.

Pathobiology

Insects are small, invertebrate animals that have an adult stage characterized by three pairs of legs, a segmented body with three major divisions, and usually two pairs of wings. Insect parts and by-products are the source of allergenic proteins that cause insect-related allergies and asthma.

Allergenic particles can arise from shed skeleton, scales, excretions, and secretions of insects. Caterpillar hairs and moth scales are known skin irritants that, upon repeated contact, can cause dermal sensitization. Insect hairs that are not irritants may also give rise to allergic disorders following repeated exposure. Larvae may contain the same antigenic material found in adult insects.1

Inhalation of insect fragments may result in respiratory sensitization, which may occur after weeks to years of exposure. Intensity and duration of exposure are important determinants of allergy development. The mechanism for most insect allergies is immediate-type IgE-related hypersensitivity. In one survey of entomologists, 25% of workers directly exposed to insects had allergic conditions.2 In evaluating other documents that estimate incidence, 30% is a representative figure. In moth and butterfly-rearing laboratories, an incidence of allergy of 53–75% has been documented.3

Many insect species have been implicated in occupational allergic disorders. Some examples include moths of various species, grasshoppers, locusts, screwworms, blowflies, beetles, parasitic wasps, Drosophila, yellow jackets, honeybees, bumblebees, houseflies, caddis flies, cochineal insect (source of carmine dye), red midges and larvae, and bloodworms, as well as cockroaches.4–7 Reactions that occur upon development of insect-related occupational allergy include eye symptoms, rhinitis, nasal congestion, urticaria, and often cough, wheezing, and shortness of breath. Once sensitized, workers develop illness within minutes of exposure to insect-related allergens.

The exoskeleton of many insect species is allergenic. The scales of butterflies and moths produce allergy. Hemoglobins are major allergens of red midge larvae and adults.1 In species where feces cause sensitization, the allergen arises from gut-derived cellular material, possibly the peritrophic membrane.8,9 Other insect by-products such as “bee dust” and cocoons are also allergenic.

Diagnosis

Diagnosis of insect allergy can be made presumptively by a thorough medical and occupational history along with physical examination. Immunological testing can be used to confirm that the suspected allergenic material will cause the signs and symptoms of the illness.

For example, prick skin tests, RAST, and bronchial provocation with honeybee whole-body extract have been used to document IgE-mediated occupational asthma in a honey processor.10 Intracutaneous tests produce reactions in bumblebee-allergic patients.11 ELISA has been used for the measurement of specific IgE and IgG antibodies to insect extracts from locust, mealworms, cockroaches, spring stick insects, and mulberry moon moths.8 Specific IgE can be documented by immunoblot. Skin prick tests and bronchial challenge have been used to document occupational asthma to cockroaches in international shipping deckhands, crickets in greenhouse staff, and blowflies in researchers.5,12,13 Nasal provocation in cockroach-sensitized workers demonstrated decreased nasal flow rates.3 Caution must be used in interpretation of skin prick test results in chironomid-exposed workers since cross-sensitization with other insect or crustacean species may occur.14

Treatment

Definitive treatment of occupational insect allergies is removal from exposure. Treatment by conventional therapies such as antihistamines, bronchodilators, and inhaled steroids may be used. In one survey, 28% of individuals reporting allergy indicated that job transfer or discontinuation was necessary.3 Desensitization injections have been successfully used to treat occupational insect allergies. Patients with anaphylactic reactions to bumblebees have been desensitized using honeybee venom.15 Injectable adrenaline kits are indicated for workers with history of anaphylaxis.

Medical surveillance

No literature is available on the application of surveillance methods to insect-handling workers. In theory, a program including a respiratory questionnaire and examination along with pulmonary function testing would be useful. Research programs could be conducted utilizing prick skin testing or RAST methods.

Prevention

Prevention of inhalation of or skin contact with insects and insect by-products will prevent insect-related allergies. Engineering and work practice controls may reduce the amount of airborne dust in occupational settings where insects are used. This includes institution of a formal integrated pest management program at the work site, which has been shown to decrease incidence of sensitization and occupational asthma in employee populations.16 Laboratories should be designed with appropriate air circulation, segregation of insects, and ease of maintenance and housekeeping in mind. Good hygiene is imperative.

Personal protective equipment may be useful in avoiding exposure and preventing symptoms. However, one survey found that individuals at institutions that reported no insect allergies were less likely to use protective equipment on either routine or as-needed bases than individuals at institutions that reported allergies.8 Protective equipment may include gloves, respirators, face masks, head nets, and lab coats.

Educating workers about the risk of insect allergy is important in preventing these disorders, particularly since the illnesses are not well known. Workers may be at risk of nonoccupational exposure to insects and may have illness because of antigenic cross-reactivity. In one case report, a butcher allergic to carmine developed food allergy from exposure to the dye while manufacturing sausages, which had initially produced rhinitis and respiratory symptoms from inhalation.17 Workers who are aware of the possibility of developing respiratory allergy are more likely to protect themselves from exposure.

References

  1. 1. Galindo PA, Feo F, Gomez E, et al. Hypersensitivity to chironomid larvae. Invest Allergol Clin Immunol 1998; 8(4):219–25.
  2. 2. Bauer M, Patnode R. NIOSH HHE Report No. HETA-81-121-1421, Insect Rearing Facilities, Agricultural Research Service, U.S. Department of Agriculture, Cincinnati, OH, 1984. Available at: http://www.cdc.gov/niosh/nioshtic-2/00149683.html (accessed on July 13 2016).
  3. 3. Wirtz RA. Occupational allergies to arthropods – documentation and prevention. Bull Entomol Soc Am 1980; 26:356–60.
  4. 4. Arruda LK, Vailes LD, Ferriani VP, et al. Cockroach allergens and asthma. J Allergy Clin Immunol 2001; 107(3):419–28.
  5. 5. Oldenburg M, Latza U, Baur X. Occupational health risks due to shipboard cockroaches. Int Arch Occup Environ Health 2008; 81(6):727–34.
  6. 6. Focke M, Hemmer W, Wöhrl S, et al. Specific sensitization to the common housefly (Musca domestica) not related to insect panallergy. Allergy 2003; 58(5):448–51.
  7. 7. Linares T, Hernandez D, Bartolome B. Occupational rhinitis and asthma due to crickets. Ann Allergy Asthma Immunol 2008; 100(6):566–9.
  8. 8. Edge G, Burge PS. Immunological aspects of allergy to locusts and other insects. Clin Allergy 1980; 10:347.
  9. 9. Tee RD, Gordon DJ, Hawkins ER, et al. Occupational allergy to locusts: an investigation of the sources of the allergen. J Allergy Clin Immunol 1988; 81(3):517–25.
  10. 10. Ostrom NK, Swanson MC, Agarwal MK, et al. Occupational allergy to honey bee-body dust in a honey-processing plant. J Allergy Clin Immunol 1986; 77:736–40.
  11. 11. de Groot H. Allergy to bumblebees. Curr Opin Allergy Clin Immunol 2006; 6(4):294–7.
  12. 12. Lopata AL, Fenemore B, Jeebhay MF, et al. Occupational allergy in laboratory workers caused by the African migratory grasshopper Locusta migratoria. Allergy 2005; 60(2):200–5.
  13. 13. Kaufman GL, Baldo BA, Tovey ER, et al. Inhalant allergy following occupational exposure to blowflies. Clin Allergy 1986; 16:65–71.
  14. 14. Galindo PA, Lombardero M, Mur P, et al. Patterns of immunoglobulin E sensitization to chironomids in exposed and unexposed subjects. Invest Allergol Clin Immunolog 1999; 9(2):117–22.
  15. 15. Kochuyt AM, Van Hoeyveld E, Stevens EAM. Occupational allergy to bumble bee venom. Clin Exp Allergy 1993; 23:190–5.
  16. 16. Portnoy J, Chew GL, Phipatanakul W, et al. Environmental assessment and exposure reduction of cockroaches: a practice parameter. J Allergy Clin Immunol 2013; 132(4):802–8.
  17. 17. Ferrer A, Marco FM, Andreu C, et al. Occupational asthma to carmine in a butcher. Int Arch Allergy Immunol 2005; 138(3):243–50.

LABORATORY ANIMALS

Common names: Rats, mice, guinea pigs, rabbits, hamsters, monkeys

Occupational setting

Laboratory animal allergy (LAA) is an important work-related illness that occurs in 11–44% of exposed workers. It occurs in workers who have laboratory animal contact ranging from casual, indirect exposure, through infrequent animal handling, to full-time daily care of animals and their housing facilities. Laboratory animals are housed and handled at many types of research institutions, including academic centers, medical schools, and private sector research facilities such as pharmaceutical companies. LAA may also result from work in other settings where rodents are present such as pet shops, vivariums, and veterinary offices.

Exposure (route)

Laboratory animal allergy may result from skin exposure or respiratory exposure. Percutaneous exposures may result from animal bites or allergen contamination of wounds, which may result in anaphylaxis. Different routes of exposure result in different disorders with different mechanisms.

Exposure to allergens may result from direct contact through handling contaminated animal bedding and laboratory animals as well as from indirect contact through airborne dust.

Inhalation exposure may result from general contamination of air within the facilities or from airborne dust created through animal handling or care. Allergens, such as those from rodent urine, may contaminate animal cage bedding and other materials, and these allergens may become airborne through any type of disturbance. Additionally, allergens are carried on animal fur and dander and easily become airborne when the animal is handled.

Any factors that increase the concentration of allergens in the workplace also increase potential exposure. These factors include increased numbers of animals, decreased frequency of cage changing, increased manipulation of animals, and accumulation of dust. Cage washing and cleaning are associated with significantly increased environmental allergen concentration. Using a vacuum without a HEPA filter can result in allergens being expelled into the environment.

Pathobiology

Laboratory animals reared for use in research consist mainly of rodents. Those laboratory animals best studied regarding occupational allergy include mice, rats, guinea pigs, hamsters, and rabbits. In addition, frogs and monkeys that are laboratory reared may also cause occupational allergy.

Exposure to laboratory animals and associated materials may result in development of immediate-type IgE-mediated respiratory hypersensitivity. Immediate skin reactions including wheal and flare from skin contact (contact urticaria) may also occur.

The prevalence of allergy among lab animal handling workers is ~11–44%. About 4–22% of these workers develop asthma.1 Associations exist between the level of allergen exposure and the development of laboratory animal allergy.1,2 Evidence that exposure–response relationships exist had been reported with respect to rat allergy.2 Although many cases have been reported that developed more than 20 years after initial exposure, most laboratory animal allergies develop within the first few years of exposure. It has been suggested that of those who develop laboratory animal allergies, 30% do so within 1 year of employment.1 This percentage increases to 70% within 3 years of employment.

The intensity of allergen exposure may be a far greater determinant in the development of laboratory animal allergies compared to duration of exposure.3 Sensitized workers are more likely than nonsensitized workers to develop pulmonary symptoms3 and secondary hypersensitization to additional laboratory animals.4 These findings suggest that decreasing the level of exposure will limit sensitization. Due to a greater emphasis on workplace controls, the incidence of progression to occupational asthma secondary to laboratory animal allergy has decreased from a peak in the early 1980s.5

Allergy typically presents as rhinitis and conjunctivitis, which progresses into asthma in a minority of patients. Symptoms typically occur within 5–30 minutes after exposure. Asthma may occur immediately or may exhibit dual or delayed patterns. Skin reactions include contact urticaria from direct contact of the animal with exposed skin and a maculopapular pruritic rash on exposed skin in association with airborne exposure and respiratory symptoms.

The antigens responsible for laboratory animal allergy come from urine, dander, saliva, and serum. These antigens are typically small acidic glycoproteins with molecular weights of 15–30 000 kDa.6,7 For mice, rats, rabbits, and guinea pigs, urinary proteins and saliva are thought to cause the majority of hypersensitivity problems. The main allergen in mice is a urinary protein, possibly prealbumin,1 whereas the main allergens in rats are serum albumin, α2-urinary globulins, and prealbumin.3 Monkey dander has caused occupational asthma in researchers.8 The allergenic proteins share sequence homology with proteins from the Schistosoma parasite, which may explain why they can trigger an immune response.1

The presence of several general allergic symptoms and several historical indicators of atopy is moderately predictive of the new onset of laboratory animal allergy.1 IgE antibody is produced in response to allergen exposure. IgE antibodies bind allergen and this complex binds to mast cells. Absorption of the corresponding allergen triggers the release of histamine and other mediators from the sensitized mast cell. Other antigens, such as those derived from molds or mites, cause laboratory animal-related allergies and are found in the same settings. When evaluating a suspected case of LAA, these other allergens should also be considered as they may be the cause or symptoms, or the worker could be allergic to more than one source.

Several human leukocyte antigen (HLA) and the major histocompatibility complex (MHC) genes are associated with the laboratory animal allergy and sensitization.9 HLA class II molecules are involved in the presentation of allergen to the T cell. HLA-DR7 was found to be strongly associated with sensitization, respiratory symptoms at work, and sensitization with symptoms, while HLA-DR3 was found to be protective from sensitization.9

High levels of allergen-specific IgG have been associated with clinical efficacy in immunotherapy studies. Among workers with detectable mouse IgE, higher mouse IgG, and mouse IgG4 levels are associated with a decreased risk of mouse-related symptoms.10 IgG4 is postulated to block IgE-antigen binding complexes. Laboratory animal workers with high levels of IgG4 were found to have less circulating IgE-antigen binding complexes and the absence of pulmonary symptoms in the setting of the highest laboratory animal allergen exposures.11

Diagnosis

A clinical diagnosis of LAA can be made based on a careful medical and occupational history along with a physical examination. A detailed respiratory and dermatologic history will reveal symptoms of allergic disorders such as wheal and flare reaction to contact such as a rat’s tail wrapping around the hand. Respiratory symptoms may include rhinitis, conjunctivitis, sneezing spells, nasal congestion, cough, shortness of breath, and wheezing.

It is critical to document the fact that the symptoms are temporally associated with exposure to laboratory animal antigens and that they resolve when the individual is away from work. Objective evidence of temporality may be obtained by doing a physical examination or peak flow measurements prior to exposure and again at the end of the work shift. The finding of objective evidence of bronchoconstriction, such as wheezes or a decreased FEV1 and FVC, supports the diagnosis of occupational asthma.

Appropriate immunological testing for IgE antibodies to laboratory animal allergens are used to confirm a diagnosis. Skin prick testing with relevant allergens or RAST may be used to demonstrate IgE antibody. RAST to detect mouse- and rat-specific IgE are commercially available and have been developed for other animal allergens. Nonlaboratory animal antigens, such as house dust mite or molds, may be used to rule out disease from these animal-associated allergens or to establish coincidental allergies. Bronchial challenge testing with animal antigens can be used to confirm reversible airway constriction related to exposure.

Treatment

Avoidance of exposure to animal antigens should be the goal of treatment. Sensitized workers who have rhinitis should be counseled on their risk of developing secondary allergy, asthma, and the risk of eventual intolerance of exposure.

Symptomatic care may include antihistamines or corticosteroids for upper tract symptoms and bronchodilators, corticosteroids, and theophylline for asthma. Cromolyn may prevent asthma from allergen exposure. Long-acting bronchodilators may be tried as preventive therapy. Immunotherapy is not likely to be helpful for most sensitized individuals who remain in an environment where regular exposure occurs.12,13

Medical surveillance

Recent literature supports the notion that atopy predisposes to laboratory animal allergy and is an important risk factor to assess in medical surveillance.1,14 One review reports a statistically significant odd ratio of 3 : 2 for the development of laboratory animal allergies in atopic individuals compared to nonatopic individuals.1 Conversely, it has been suggested that HLA-B16 may confer a protective effect against the development of LAA.15 Other theoretical protective factors include early childhood exposure to dogs, which is reported in mouse to modulate the immune system against allergic disease development.16

Skin prick testing and RAST have been suggested as surveillance methods that may prove useful in detecting preclinical allergy to laboratory animals; however, these would only be useful in the setting of significant ongoing exposure and cannot be recommended for routine use. Respiratory history may be used to document early symptoms of laboratory animal allergy. If nasal symptoms are detected early and further exposure is eliminated, subsequent progression to asthma or development of secondary allergies may be prevented.

Prevention

Containment of the source protein is the cornerstone of animal allergy prevention measures. A comprehensive program including education for engineering controls and administrative controls, use of personal protective equipment, and medical surveillance can prevent the development of laboratory animal allergy.17 Efforts should be made to limit airborne dust, such as by housing and transporting animals in filter-top cages or separately ventilated cages. For shaving animals, a wet prep can be used if it does not lower their body temperature too far or a shaver with an attached HEPA-filtered vacuum can be used. Room vacuums should have HEPA-filtered exhaust. Engineering controls such as negative pressure rooms, construction of clean corridors, provision of high ventilation rates with limited recirculation of air, use of downdraft (ceiling to floor) ventilation, use of robots or mechanical systems for cage cleaning and washing, and installation of HEPA filters are helpful.

Airborne antigen levels have been found to be related to litter type and stock density. In one study, significant reduction in rat allergen concentrations were achieved by replacing wood-based (sawdust) contact litter with noncontact absorbent pads.5 The concentration of airborne animal allergen is dependent on the activities in the contaminated areas. For example, rate allergen concentrations in air have been found to be 10–100 times higher during animal handling or disturbance of bedding than at quiet times.2

Because allergens from laboratory animals adhere to all types of particulate matter, contamination of facilities occurs easily, as evidenced by the presence of antigen in all types of dust. Therefore, a reservoir of allergens exists outside the immediate animal housing areas.12 Removal of animals from work areas will not eliminate exposure. In homes where pets are removed, it takes 4–6 months before allergen levels are at clinically insignificant levels.

Personal protective equipment can be used to supplement engineering and hygiene controls. Gloves and laboratory coats should be worn routinely for animal handling. Respiratory protection should be required in situations when engineering controls are not adequate to prevent exposure because of the high incidence of LAA. Requiring the use of hairnets reduces the transfer of laboratory animal allergens from an employee’s workplace to home.18 Protective equipment should be confined to the animal facility. Workers should remove protective equipment and wash their hands before leaving to perform other activities or go to common areas such as the cafeteria.

Many animal-allergic workers also have household pets, which may complicate treatment. Whenever possible, pets in the home should be removed. It is possible that cromolyn or combined treatment with inhaled corticosteroids and long-acting bronchodilators may prevent asthma exacerbations.

References

  1. 1. Bush RK, Stave GM. Laboratory animal allergy: an update. ILAR J 2003; 44(1):28–51.
  2. 2. Hollander A, Heederick D, Doekes G. Respiratory allergy to rats: exposure–response relationships in laboratory animal workers. Am J Resp Crit Care Med 1997; 155:562–7.
  3. 3. Nieuwenhuijsen MJ, Putcha V, Gordon S, et al. Exposure–response relations among laboratory animal workers exposed to rats. Occup Environ Med 2003; 60(2):104–8.
  4. 4. Goodno LE, Stave GM. Primary and secondary allergies to laboratory animals. J Occup Environ Med 2002; 44(12):1143–52.
  5. 5. Folletti I, Forcina A, Marabini A, et al. Have the prevalence and incidence of occupational asthma and rhinitis because of laboratory animals declined in the last 25 years? Allergy 2008; 63(7):834–41.
  6. 6. Gordon S, Tee RD, Lowson D, et al. Reduction of airborne allergenic urinary proteins from laboratory rats. Br J Ind Med 1992; 49:416–22.
  7. 7. Heederik D, Doekes G, Nieuwenhuijsen MJ. Exposure assessment of high molecular weight sensitisers: contribution to occupational epidemiology and disease prevention. Occup Environ Med 1999; 56(11):735–41.
  8. 8. Petry RW, Voss MJ, Kroutil LA, et al. Monkey dander asthma. Allergy Clin Immunol 1985; 75:268–71.
  9. 9. Jeal H, Draper A, Jones M, et al. HLA associations with occupational sensitization to rat lipocalin allergens: a model for other animal allergies? J Allergy Clin Immunol 2003; 111(4):795–9.
  10. 10. Matsui EC, Diette GB, Krop EJ, et al. Mouse allergen-specific immunoglobulin G4 and risk of mouse skin test sensitivity. Clin Exp Allergy 2006; 36(8):1097–103.
  11. 11. Jones M, Jeal H, Schofield S, et al. Rat-specific IgG and IgG4 antibodies associated with inhibition of IgE-allergen complex binding in laboratory animal workers. Occup Environ Med 2014; 71(9):619–23.
  12. 12. Eggleston PA, Wood KA. Management of allergies to animals. Allergy Proc 1992; 13:289–92.
  13. 13. Bush RK. Assessment and treatment of laboratory animal allergy. ILAR J 2001; 42(1):55–64.
  14. 14. Hollander A, Doekes G, Heederik D. Cat and dog allergy and total IgE as risk factors of laboratory animal allergy. J Allergy Clin Immunol 1996; 98:545–54.
  15. 15. Sjostedt L, Willers S, Orbaek P. Human leukocyte antigens in occupational allergy: a possible protective effect of HLA-B16 in laboratory animal allergy. Am J Indust Med 1996; 30:415–20.
  16. 16. Fujimura KE, Demoor T, Rauch M, et al. House dust exposure mediates gut microbiome Lactobacillus enrichment and airway immune defense against allergens and virus infection. Proc Natl Acad Sci USA 2014; 111(2):805–10.
  17. 17. Stave GM, Darcey DJ. Prevention of laboratory animal allergy in the United States: a national survey. J Occup Environ Med 2012; 54(5):558–63.
  18. 18. Krop EJ, Doekes G, Stone MJ, et al. Spreading of occupational allergens: laboratory animal allergens on hair-covering caps and in mattress dust of laboratory animal workers. Occup Environ Med 2007; 64(4):267–72.

MITES

Common names: Dust mites, storage mites, red spider mites, citrus red mites

Occupational setting

Occupational illness from exposure to mites may occur in a variety of settings. Workplaces associated with mite-related illnesses include warehouses, barns, poultry houses, greenhouses, flower farms, fruit orchards, livestock farms, grain storage facilities, bakeries, and animal housing facilities.

Exposure (route)

Occupational allergy to mites results from inhalation exposure or skin contact. Because mites are tiny creatures, entire animals can be airborne and readily inhaled. In addition, skin exposure to mite-infested materials may result in contact allergy, occupational dermatitis, or contact urticaria.

Pathobiology

Mites are a class of arthropods. Storage mites are wingless, translucent, microscopic invertebrates. Dust mites, or pyroglyphid mites, are more abundant than nonpyroglyphid or storage mites. In optimal conditions, mites can self-multiply at rates of four- to 10-fold weekly.1

Various mite species are ubiquitous in our environment. Dust mites infest organic particles in dusts such as mattress, bedding, pillow, carpet, or floor dust. Storage mites infest stored food and vegetable products as well as hay and straw. Red spider mites, Tetranychus species, parasitize flowers such as carnations in greenhouse cultivation as well as in open fields. Mites, especially storage types, thrive in damp environments. The major species in infestations vary by season.

Inhalation of mites or their by-products may result in immediate-type IgE-mediated respiratory hypersensitivity. Mites as well as their feces are allergenic.2 Mites that have been implicated in occupational allergy include storage mites, grain mites, dust mites, red spider mites, citrus red mites, fowl mites, and hay itch mites. Spider silks have also been implicated as workplace allergens. Exposure to antigens from these arachnids may cause rhinoconjunctivitis and asthma upon exposure in sensitized individuals. With Dermatophagoides pteronyssinus, late-phase asthma (occurring hours after exposure) is associated with a Th17 inflammatory response mediated by IL-17.3 Acute hypersensitivity reactions to house dust mites and storage mites are orchestrated by a Th2-mediated inflammatory response that stimulates B-cells to produce IgE antibodies.4 Contact allergy has been reported with two-spotted spider mites and red spider mites.5 Case reports have described occupational allergy to cheese mites (Blomia kulagini), chorizo mites (Euroglyphus maynei), and salty ham mites (Tyrophagus putrescens).6

Storage mites contain the most important antigens that have been related to asthma and allergic rhinoconjunctivitis among grain farmers.7 A strong association between storage mite allergy and house dust allergy has been noted in areas or occupations with high exposure to both.8 In one survey, >80% of patients thought to be at risk of occupational exposure had storage mite allergy. Bakers appear to be excluded from this risk as recent research indicates that cosensitization to storage mites is less likely to exist among bakers who are allergic to wheat flour.9

In one study, D. pteronyssinus was the most allergically potent of four mite species evaluated. The Dermatophagoides genus provides the major allergens of house dust. Up to three-quarters of serum IgE to mites are directed against antigen P1, which is associated with fecal particles.2 Cross-reactivity may occur between several species of house dust mite. There may also be shared antigens among storage mite species.

Diagnosis

Medical history may reveal symptoms of nasal and ocular itching, rhinorrhea, sneezing, shortness of breath, wheezing, and dry or productive cough.7 Mite-induced skin disorders include contact urticaria and dermatitis. These symptoms in association with exposure to mite-infested material suggest the diagnosis of allergy. Immunological testing may provide supportive evidence for IgE-mediated hypersensitivity, or, in the case of contact dermatitis, delayed-type allergy.

Skin prick test materials are available for house dust mite (Dermatophagoides farinae and D. pteronyssinus), storage mite (Acarus siro, Tyrophagus putrescentiae, Glycyphagus domesticus, and Lepidoglyphus destructor), and northern fowl mite. Skin prick testing may be the most sensitive immunologic test in confirming a diagnosis of occupational mite allergy. Skin patch testing (Finn Chamber, urticaria-inducing open test, and acute eczema-inducing open test) is used to detect allergic contact dermatitis or overlapping contact cutaneous syndrome to red spider mite.10 Specific IgE can be measured by RAST for house dust mites, storage mites, and northern fowl mites. ELISA and EAST have been used to document citrus mite and red spider mite allergy, respectively. Correlation between skin prick testing with RAST and skin prick/RAST testing with symptoms is variable. Conjunctival provocation can be used to substantiate rhinoconjunctivitis from specific allergens. Bronchial challenge with mite antigen may cause immediate, dual type, or delayed reactions.7 Methacholine challenge, documenting bronchial hyperreactivity, may be useful but must be conducted by a clinician with expertise in the procedure.

Treatment

Avoidance of further exposure to allergen will prevent symptoms of mite allergy. Since changing vocations is often difficult, medical management of symptoms may be tried, such as conventional therapies including antihistamines and inhaled beta agonists. Immunotherapy has been used with some success. Pretreatment with cromolyn sodium can prevent the occurrence of asthma from exposure to mite allergens.3 Because of the abundance of various mites in the environment, attempts to avoid exposure must extend to nonoccupational settings.

Medical surveillance

Respiratory symptoms can be assessed periodically in mite-exposed workers. Skin prick testing and RAST have no proven utility in surveillance for occupational arachnid allergy but may be considered on an experimental basis.

Prevention

Approximately 30% of allergic farm workers have symptoms consistent of allergy, hay fever, or respiratory problems to spider mites, and the intensity of symptoms is associated with high levels of total and mite allergen-specific IgE.11,12 This finding suggests that atopic individuals may be at increased risk of mite allergy. Also, sensitization to house dust mites may indicate increased susceptibility to spider mite allergy.11,12 Preventive measures should be aimed at reducing the mite population in the workplace. Intensification in such fields as poultry husbandry may have actually increased the concentration of mites in some workplaces.13 Open field cultivation may be associated with a lower prevalence of clinical spider mite allergy than greenhouse environments because of ventilation.14,15 To decrease mite populations, decreasing reservoirs, decreasing humidity, and using miticides may be helpful. HEPA filters on air ducts and vacuum cleaners can be used. Once the population has been minimized through housekeeping measures and other types of dust control, secondary means of preventing exposure can be undertaken. Secondary exposure control should aim at minimizing the opportunities for mites and related dusts to become airborne.

Educating workers about the risk of allergy to mites is important in preventing the illness. Workers who are aware of the risks are better prepared to prevent exposure. Home-related exposures should be assessed in workers with occupational allergic symptoms to mites.

References

  1. 1. Wraith DG, Cunningham AM, Seymour WM. The role and allergenic importance of storage mites in house dust and other environments. Clin Allergy 1979; 9:545–62.
  2. 2. Tovey ER, Chapman MD, Platt Mills TXE. Mite faeces are a major source of house dust allergens. Nature 1981; 289:592–3.
  3. 3. Bajoriuniene I, Malakauskas K, Lavinskiene S, et al. Th17 response to Dermatophagoides pteronyssinus is related to late-phase airway and systemic inflammation in allergic asthma. Int Immunopharmacol 2013; 17(4):1020–7.
  4. 4. Yu SJ, Liao EC, Tsai JJ. House dust mite allergy: environment evaluation and disease prevention. Asia Pac Allergy 2014; 4(4):241–52.
  5. 5. Wirtz RA. Occupational allergies to arthropods – documentation and prevention. Bull Entomol Soc Am 1980; 26:356–60.
  6. 6. Armentia A, Fernandez A, Perez-Santos C, et al. Occupational allergy to mites in salty ham, chorizo, and cheese. Allergol et Immunopathol 1994; 22:152–4.
  7. 7. Armentia A, Tapias J, Bowber D, et al. Sensitization to the storage mite Lepidoglyphus destructor in wheat flour respiratory allergy. Ann Allergy 1992; 68:398–406.
  8. 8. Morales M, Iraola V, Leonor JR, et al. Different sensitization to storage mites depending on the co-exposure to house dust mites. Ann Allergy Asthma Immunol 2015; 114(1):36–42.
  9. 9. Droste J, Myny K, Van Sprundel M, et al. Allergic sensitization, symptoms, and lung function among bakery workers as compared with a nonexposed work population. Occup Environ Med 2003; 45(6):648–55.
  10. 10. Astarita C, Di Martino P, Scala G, et al. Contact allergy: another occupational risk to Tetranychus urticae. J Allergy Clin Immunol 1996; 98:732–8.
  11. 11. Gargano D, Romano C, Manguso F, et al. Relationship between total and allergen-specific IgE serum levels and presence of symptoms in farm workers sensitized to Tetranychus urticae. Allergy 2002; 57(11):1044–7.
  12. 12. Jeebhay MF, Baatjies R, Chang YS, et al. Risk factors for allergy due to the two-spotted spider mite (Tetranychus urticae) among table grape farm workers. Int Arch Allergy Immunol 2007; 144(2):143–9.
  13. 13. Rimac D, Macan J, Varnai VM, et al. Exposure to poultry dust and health effects in poultry workers: impact of mould and mite allergens. Int Arch Occup Environ Health 2010; 83(1):9–19.
  14. 14. Burches E, Pelaez A, Morales C, et al. Occupational allergy due to spider mites: Tetranychus urticae (Koch) and Panonychus citri (Koch). Clin Exp Allergy 1996; 26:1262–7.
  15. 15. Kronqvist M, Johansson E, Kolmodin-Hedman B, et al. IgE-sensitization to predatory mites and respiratory symptoms in Swedish greenhouse workers. Allergy 2005; 60(4):521–6.

PLANTS

Common names: Poison ivy (Toxicodendron radicans), eastern poison oak (Toxicodendron quercifolium), western poison oak (Toxicodendron diversilobum), poison sumac (Toxicodendron vernix), coffee beans, tobacco, psyllium, tea leaves, ipecac, colophony, others (natural rubber latex is covered in Chapter 29)

Occupational setting

Plant allergies may result from exposure in agricultural settings such as outdoor farming areas. In addition, facilities that process plant materials may provide a setting for the development of occupational allergy. Tobacco and garlic farmers, coffee bean processors, tea blenders, plant-leasing farm workers, plant wholesalers, woodwork teachers, spice processors, paper and rubber workers, florists, gardeners, and beekeepers may have exposure to plant-derived antigens. Exposure to plant products occurs in the pharmaceutical industry and in healthcare settings. For example, ispaghula husks (psyllium) and senna pods are used as bulk laxatives. In addition to these settings, occupations where workers may be exposed to natural vegetation also provide an opportunity for plant-derived antigen exposure. Examples of outdoor occupations where workers may be exposed to poison ivy or poison oak include forest rangers (and other forest workers), surveyors, and utility company field workers.

Exposure (route)

Plant allergy results from dermal or respiratory exposure. For those substances that cause skin allergy, exposure occurs via direct contact of the plant material with exposed skin. Alternatively, contamination of objects such as clothing and tools with antigen such as that from rhus plants (of the family Anacardiaceae) may result in exposure when these objects come into contact with skin. Inhalation of plant-derived allergens is necessary for the development of respiratory sensitization to plants.

Pathobiology

The plant kingdom contains organisms with a vast array of characteristics, and many plants have sensitizing capabilities. The plants considered here are ones that have been documented to be capable of inducing occupational allergy. Included are tobacco, tea, poison oak and ivy, colophony from Pinus species, ispaghula, senna, ipecacuanha, natural rubber latex, and others. Many other plants have been implicated in occupational allergy including spathe flower, saffron, compositae species (sesquiterpene lactone allergen: e.g., chicory, camomile), weeping fig, Christmas cactus, carnation, umbrella tree, mugwort, alstroemeria, and narcissus.1–4 Cross-sensitization to other flowering plants is common.5,6

Exposure to plant materials may cause skin or respiratory allergy. There may be some overlap of respiratory allergy and skin symptoms; for example, contact or generalized urticaria can occur along with respiratory symptoms in IgE-mediated disorders.

Contact dermatitis is caused by a delayed IgG-mediated hypersensitivity. It is manifested by an itchy, red, raised skin rash that results from repeated contact with an allergen. Once allergy has developed, contact dermatitis occurs one to several days after exposure. Repeated allergen exposure may cause a chronic dermatitis characterized by thickening and lichenification of the skin. Occupational contact dermatitis typically involves the hands and other exposed skin such as arms and face.

Toxicodendron (Rhus) dermatitis from poison ivy, poison oak, and poison sumac may occur in outdoor workers. Rhus rash occurs within 48 hours after exposure in sensitized individuals. It is characterized by intense itching followed by inflammation and grouped vesicles resulting from contact with plant oil. No spread of the dermatitis occurs after the oil has been removed; however, new patches may occur because of the delayed nature of this disorder. Attacks usually last 2–3 weeks, with patches becoming crusted and dry. The antigen involved in Rhus dermatitis is pentadecylcatechol, a component of the oleoresin urushiol.7

Colophony is a resin that is derived from Pinus and other species of trees. Rosin may be obtained from living trees or may be a by-product of paper pulp manufacturing.8 It is used as a resin in solder. Colophony is an important cause of contact allergy, especially hand eczema. Positive patch test results are frequent.

Propolis, a sticky, resinous material collected by bees from the bud scales of plants and trees, is a well-known cause of allergic eczematous contact dermatitis in beekeepers.9 The major allergens in propolis seem to come from poplar species, including 1,1-dimethylallyl caffeic acid ester from poplar bud extracts.

In one case report, a saxophonist developed cheilitis due to a musical reed. In this patient, a skin prick test to cane reed scraping was positive, indicating an IgE-mediated dermatitis. Contact skin allergy to reed has been noted in other types of musicians, as well as workers who handle the reed Arundo donax.10

Although reports of cutaneous reactions are rare, olive oil has been reported to cause contact allergy, including cases of hand eczema in an aromatherapy masseuse,11 and occupational asthma in an olive oil mill worker.12 The sensitizers in olive oil are largely unknown, but thaumatin-like proteins, which are found in plants and in pollen, are thought to play a role in sensitization.12 Coffee bean dust may cause occupational contact dermatitis. Dandelion, a member of the daisy family, has been reported to cause allergic contact dermatitis in gardeners.13 Cross-reactivity between dandelions and other allergenic Compositae may occur.

Occupational asthma has been found to occur from tea leaves, ficus, ispaghula, senna, green tobacco, green coffee beans, baby’s breath (Gypsophila), and many other plants. These hypersensitivities are in general of the Type I IgE-mediated type.

Asthma from inhalation exposure to green tobacco leaf has been documented in tobacco workers. In one study, green tobacco leaf asthma was found to result from an immediate, IgE-mediated hypersensitivity, as evidenced by positive RAST, nasal and bronchial provocation, and histamine release assay.14 Because this illness is related to green tobacco exposure, it is postulated that the antigen degrades in the curing process. Other allergens found in association with tobacco plants—for example, microfungi—may also cause asthma. Asthma associated with green tobacco is a distinct entity from green tobacco sickness. Green tobacco sickness is a form of nicotine poisoning resulting from dermal absorption during the handling of wet plant leaves.

Respiratory sensitization (IgE mediated) from green coffee beans may result in upper respiratory symptoms as well as asthma. As with tobacco, the processing of coffee beans destroys some antigen, although roasted coffee allergy also occurs. An estimated 10% of exposed workers develop allergy, a small proportion of who also develop asthma. Immediate- and delayed-type allergy may coexist in coffee bean-sensitized workers.15

Inhalation allergy to pharmaceutical products such as psyllium (from ispaghula husks) and senna pods seems to cause asthma less frequently than other respiratory allergies. One cross-sectional study found a prevalence of asthma of 3.2% in a population of whom 7.6% were allergic to ispaghula.16 Anaphylaxis and eczema have also been reported following ispaghula husk exposure.

Descriptions in the literature of respiratory allergy and asthma from plants are varied and may be documented in only an article or two for each plant. For example, a few studies have described mushroom workers’ lung, a hypersensitivity pneumonitis that may result from mushroom spores or microorganisms.17,18 Farm workers who harvest garlic bulbs and spice factory workers have been shown to have garlic allergy. Pectin has been found to cause IgG4-mediated occupational asthma in a candy maker.19 Pectin is a large-molecular-weight product of fruits and fruit rinds that contains methyl-esterified galacturonan, galactan, and araban. Tea leaf allergy typically occurs at facilities where tea leaves are mixed together or blended, generating a fine dust.

Diagnosis

Medical and occupational history coupled with physical examination may be used to make a presumptive diagnosis of contact dermatitis from plants. The presence of an itchy, red skin rash occurring hours or days after contact with allergenic material should lead to a suspicion of allergic dermatitis. Acute eruptions are usually vesicular and edematous. Rhus contact occurs in a linear fashion, such as from brushing against twigs or leaves. Rashes associated with these plants are usually linear.

Patch skin testing should usually be done to confirm a diagnosis of allergic contact dermatitis when the causative agent is in question or if the consequences of the diagnosis may affect decisions about the risk of further exposure. Usually, the allergen is applied to the skin for 24–48 hours, after which a delayed rash appears in positive cases. Care must be taken to distinguish between irritant and allergic causes. Other allergenic exposures such as insects and mites should be considered in appropriate settings. Castor bean allergy may complicate the diagnosis of green coffee bean allergy; onion or pollen allergy may be comorbid in garlic allergic patients.20

Respiratory sensitization to plants results in similar symptoms to those found with other inhalant allergens. These symptoms, which must be temporally associated with exposure, include rhinitis, conjunctivitis, nasal congestion, cough, wheezing, and shortness of breath.

Skin prick tests and RAST, among other immunological studies, may be used to confirm plant allergies of the immediate, respiratory type. Pulmonary function testing is also helpful in diagnosing inhalant allergy. Bronchial provocation has been used to demonstrate coffee bean, garlic, and tea leaf allergy, among others. Significant differences have been documented in peak expiratory flow rates between tobacco workers and unexposed controls.21 Coffee bean-exposed workers may have a higher than average incidence of chronic respiratory problems.

Treatment

For allergic contact dermatitis, treatment with local topical corticosteroid creams or ointments is recommended. For more extensive and severe cases, systemic steroids should be used. For Rhus dermatitis, standard steroid protocols usually begin with 40–60 mg of prednisone orally in a single daily dose with a 3-week taper.7 Calamine lotion may ease the symptoms. Local antihistamine and anesthetic ointments should be avoided because of the possibility of contact sensitization.

Allergic respiratory disorders from plant exposure may be treated with conventional allergy therapies. These include antihistamines, bronchodilators, and steroids. Avoidance of exposure is the only definitive treatment.

Prevention

Atopy may be a risk factor in green coffee bean allergy.22 Protecting workers from skin and respiratory exposure can prevent occupational plant allergies. Engineering controls and personal protective equipment as well as sound work practices may be helpful. Persons with latex allergy of the immediate type should be removed from exposure because of the risk of serious reactions. Substitute gloves are available.

Use of mechanical blending processes with extraction ventilation rather than hand mixing reduces personnel exposure to tea leaf dust. Wearing cotton glove liners reduces contact with skin sensitizers and therefore prevents allergy. Personal protective equipment to prevent inhalation and skin exposure to airborne materials, such as respirators and barrier clothing, should also be considered.

References

  1. 1. Pirson F, Detry B, Pilette C. Occupational rhinoconjunctivitis and asthma caused by chicory and oral allergy syndrome associated with bet v 1-related protein. J Investig Allergol Clin Immunol 2009; 19(4):306–10.
  2. 2. Rudzki E, Rapiejko P, Rebandel P. Occupational contact dermatitis, with asthma and rhinitis, from camomile in a cosmetician also with contact urticaria from both camomile and lime flowers. Contact Dermatitis 2003; 49(3):162.
  3. 3. Sánchez-Fernández C, González-Gutiérrez ML, Esteban-López MI, et al. Occupational asthma caused by carnation (Dianthus caryophyllus) with simultaneous IgE-mediated sensitization to Tetranychus urticae. Allergy 2004; 59(1):114–5.
  4. 4. Grob M, Wuthrich B. Occupational allergy to the umbrella tree (Schefflera). Allergy 1998; 53:1008–9.
  5. 5. deJong NW, Vermeulen AM, Gerth van Wijk R, et al. Occupational allergy caused by flowers. Allergy 1998; 53:204–9.
  6. 6. Akpinar-Elci M, Elci OC, Odabasi A. Work-related asthma-like symptoms among florists. Chest 2004; 125(6):2336–9.
  7. 7. Ellenhorn MJ, Barceloux DG. Medical Toxicology. New York: Elsevier, 1988:1299–304.
  8. 8. Downs AM, Sansom JE. Colophony allergy: a review. Contact Dermatitis 1999; 41(6):305–10.
  9. 9. de Groot AC. Propolis: a review of properties, applications, chemical composition, contact allergy, and other adverse effects. Dermatitis 2013; 24(6):263–82.
  10. 10. Ruiz-Hornillos FJ, Alonso E, Zapatero L, et al. Clarinetist’s cheilitis caused by immediate-type allergy to cane reed. Contact Dermatitis 2007; 56(4):243–5.
  11. 11. Williams JD, Tate BJ. Occupational allergic contact dermatitis from olive oil. Contact Dermatitis 2006; 55(4):251–2.
  12. 12. Palomares O, Alcántara M, Quiralte J, et al. Airway disease and thaumatin-like protein in an olive-oil mill worker. N Engl J Med 2008; 358(12):1306–8.
  13. 13. Lovell CR, Rowan M. Dandelion dermatitis. Contact Dermatitis 1991; 25:185–8.
  14. 14. Gleich GJ, Welsh PW, Yunginger JW, et al. Allergy to tobacco: an occupational hazard. N Engl J Med 1980; 302(11):617–9.
  15. 15. Treudler R, Tebbe B, Orfanos CE. Coexistence of type I and type IV sensitization in occupational coffee allergy. Contact Dermatitis 1997; 36:109.
  16. 16. Marks GB, Salome SM, Woodcock AJ. Asthma and allergy associated with occupational exposure to ispaghula and senna products in a pharmaceutical work force. Am Rev Resp Dis 1991; R4:1065–9.
  17. 17. Vereda A, Quirce S, Fernández-Nieto M, et al. Occupational asthma due to spores of Pleurotus ostreatus. Allergy 2007; 62(2):211–2.
  18. 18. Foti C, Nettis E, Damiani E, et al. Occupational respiratory allergy due to Boletus edulis powder. Ann Allergy Asthma Immunol 2008; 101(5):552–3.
  19. 19. Kraut A, Peng Z, Becker NB, et al. Christmas candy maker’s asthma. IgG5-mediated pectin allergy. Chest 1992; 102:1605–7.
  20. 20. Anibarro B, Fontela JL, De La Hoz F. Occupational asthma induced by garlic dust. J Allergy Clin Immunol 1997; 100:734–8.
  21. 21. O’Holleran MT. Byssinoses and tobacco related asthma. In: Bardana EJ Jr., Montanaro A, O’Holleran MT, eds., Occupational Asthma. Philadelphia: Hanley & Belfus, 1992:77–85.
  22. 22. Larese F, Fiorito A, Casasola F, et al. Sensitization to green coffee beans and work-related allergic symptoms in coffee workers. Am J Ind Med 1998; 34:623–7.

SHELLFISH AND OTHER MARINE INVERTEBRATES

Common names: Crustacean, crab, lobster, shellfish, prawn

Occupational setting

Food processing facilities that handle prawns, lobster, crabs, and other shellfish are a potential source of exposure to crustacean-derived allergens. Oyster farming may also cause exposure to invertebrate allergens. Because of the diversity of sea animals associated with occupational and nonoccupational allergy, any setting where marine animals are handled may pose risks from exposure. Exposure to horseshoe crab-derived antigen may occur in laboratory settings where assays for bacterial endotoxins are performed. The snow crab industry has high prevalence of sensitization (18.4%) and occupational asthma (15.8%) among workers in Canadian processing plants.1 In one study of 107 employees of one snow crab processing plant, 26% reported experiencing asthma-like symptoms over the course of one processing season.2 The rates of sensitization are associated with cumulative and dose exposure.

Exposure (route)

Inhalation of allergenic components of shellfish may result in respiratory sensitization. Allergens become airborne in food processing facilities by aerosolization or by being carried along with steam and water vapor. Dust from the processing of dried products may also cause inhalant allergy.

Pathobiology

Shellfish, such as mollusks and crustaceans, are aquatic invertebrate animals with a shell or exoskeleton. Crustaceans such as crabs and lobsters are arthropods. A variety of other marine invertebrates may cause illnesses similar to those seen with shellfish.

Allergy to marine invertebrates typically results from an IgE-mediated immediate hypersensitivity. As with other IgE-mediated respiratory allergies, these disorders are manifested by watery, itchy eyes and nose and sneezing; less frequently, they produce cough and wheezing, with shortness of breath.

Many marine species have allergenic components. Occupational allergy has been reported from exposure to marine sponge,3 clam,4 abalone,5 brine shrimp, and daphnia. Sea squirt-induced asthma has been associated with oyster farming.6 Limulus amoebocyte lysate (LAL), a horseshoe crab-derived product, used in a laboratory assay, has been reported to cause occupational allergy.7 Cross-reactivity between shrimp, crab, lobster, scallops, and crayfish antigens has been documented.8,9

Diagnosis

The presence of respiratory allergic symptoms in temporal association with exposure to marine animal products suggests the diagnosis of occupational allergy. A thorough history, including qualitative assessment of exposure and the relationship of symptoms to exposure, is critical. Physical examination may support the diagnosis of occupational allergy if mucosal change or wheezing is found. Resolution of symptoms upon removal from the workplace can provide sufficient evidence for a working diagnosis.

Immunological studies such as skin prick testing may be employed. RAST is available for crab, shrimp, chironomids, lobster,4 and sea squirt. Skin prick testing has been used with horseshoe crab7 and others. Bronchial provocation may be used to demonstrate asthma in the presence of the suspected allergen. One case study demonstrated this principal by confirming sensitization to octopus in a chef working in a seafood restaurant.10

Treatment

There is no specific treatment for marine animal allergy. Definitive treatment involves removal of the patient from exposure to the allergen. Conventional allergy therapies such as antihistamines and bronchodilators may be used. Immunotherapy has been used in treating sea squirt asthma with reported success.6

Medical surveillance

Surveillance methods should be directed toward detecting respiratory symptoms. History and pulmonary function testing may be useful.

Prevention

Inhalation of dusts and vapors containing marine animal allergen should be avoided. Engineering and administrative controls can help prevent personnel exposure. Personal protective equipment including respirators may be useful.

References

  1. 1. Gautrin D, Cartier A, Howse D, et al. Occupational asthma and allergy in snow crab processing in Newfoundland and Labrador. Occup Environ Med 2010; 67(1):17–23. doi:10.1136/oem.2008.039578. Epub 2009 Sep 6.
  2. 2. Ortega HG, Daroowalla F, Petsonk EL, et al. Respiratory symptoms among crab processing workers in Alaska: epidemiological and environmental assessment. Am J Ind Med 2001; 39(6):598–607.
  3. 3. Baldo BA, Krils S, Taylor KM. IgE mediated acute asthma following inhalation of a powdered marine sponge. Clin Allergy 1982; 12:171–86.
  4. 4. Desjardins A, Malo JL, L’Archevêque J, et al. Occupational IgE-mediated sensitization and asthma caused by clam and shrimp. J Allergy Clin Immunol 1995; 96(5 Pt 1):608–17.
  5. 5. Masuda K, Tashima S, Katoh N, et al. Anaphylaxis to abalone that was diagnosed by prick test of abalone extracts and immunoblotting for serum immunoglobulin E. Int J Dermatol 2012; 51(3):359–60.
  6. 6. Montanaro A. Asthma in the food industry. In: Bardana EJ Jr., Montanaro A, O’Hollaren MT, eds., Occupational Asthma. Philadelphia: Hanley & Belfus, 1992:125–30.
  7. 7. Ebner C, Kraft D, Prasch F, et al. Type I allergy induced by limulus amoebocyte lysate (LAL). Clin Exp Allergy 1992; 22:417–9.
  8. 8. Lopata AL, Jeebhay MF. Airborne seafood allergens as a cause of occupational allergy and asthma. Curr Allergy Asthma Rep 2013; 13(3):288–97.
  9. 9. Rosado A, Tejedor MA, Benito C, et al. Occupational asthma caused by octopus particles. Allergy 2009; 64(7):1101–2.
  10. 10. Goetz DW, Whisman BA. Occupational asthma in a seafood restaurant worker: cross-reactivity of shrimp and scallops. Ann Allergy Asthma Immunol 2000; 85(6 Pt 1):461–6.

WHEAT FLOUR AND EGG

Common names for disease: Bakers’ asthma, wheat flour asthma, egg allergy

Occupational setting

Baker’s asthma has been associated with occupational wheat flour exposure in bakers since the 1700s. Other settings in which occupational grain dust allergy occurs include flour mill work, grain handling (including loading, unloading, and storage operations), pastry factories, cereal factories, and animal feed facilities. Confectionary and baking industry workers also have exposure to egg products.

Exposure (route)

Flour and grain dust and powdered egg readily become airborne. Inhalation exposure may result in occupational allergic disorders, including asthma. Extrinsic allergic alveolitis may result from egg allergy.1

Pathobiology

Wheat flour is a grass product that contains albumin, globulin, gliadin, and glutenin proteins. Contaminants of and additives to flour are considered separately in the section on “Grain Dust.” Egg proteins such as ovalbumin are allergenic.1

Repeated inhalation of wheat flour may result in IgE-mediated, immediate-type allergic respiratory disorders in susceptible individuals. These allergic disorders, which may become manifest after months or years of exposure, occur in 10–30% of workers and include rhinoconjunctivitis and asthma.2 Asthma is typically immediate but may also be delayed. Although >40 wheat antigens have been documented, many of which produce disease; albumin in wheat flour is most closely linked to bakers’ asthma.2 Many wheat antigens are insoluble and therefore of questionable significance in bakers’ asthma, but the strongest IgE response is associated with water-soluble albumins and globulins with in the 12–17 kD range.3

In baker’s asthma, individual strongly react to wheat thioredoxin-hB (Triticum aestivum allergen 25 (Tri a 25)), a class of wheat allergens. Other allergens associated with flour dust, including egg, molds, fungi, insects, storage mites, pollens, and bacteria, may also cause asthma in flour dust workers. Workers who are skin tested with combinations of flour and related allergens rather than wheat flour alone have been shown to have a high prevalence of positivity.4 In addition, cross-reactivity has been reported among wheat, rye, and barley.5

The risk of development of wheat flour allergy is related to the intensity and duration of exposure. Working conditions important to the development of allergy include dust concentration, ventilation, lack of engineering controls on machinery, and varying levels of allergen.6, 7 Rhinitis and conjunctivitis typically precede the development of asthma. The incidence of bakers’ asthma increases with longer duration of wheat flour exposure.8 Exposure to wheat flour at levels of 1–2 mg/m3 results in a significant risk of allergy development.9 Individuals with atopic characteristics are at increased risk.

Diagnosis

Bakers’ asthma may be diagnosed through a thorough history and physical examination, along with demonstration of reversible airway obstruction in association with flour dust exposure. Rhinitis, conjunctivitis, cough, wheezing, and shortness of breath are typical. Symptoms develop after varying periods of exposure; rhinitis usually precedes asthma. Once sensitized, workers become ill within minutes to hours after starting the workday and are generally well during weekends and holidays. Late responses often occur, typically 4–8 hours after exposure; antecedent rhinorrhea, congestion, and sneezing are typical. Atopic individuals are at higher risk of developing disease.

Workplace physical examination and serial peak flow testing may be useful in documenting reactive airways. Diagnostic tests include prick skin testing with commercially available wheat flour standardized extract, specific IgE RAST, leukocyte histamine release, and inhalation challenge with wheat flour extract. In a study of 71 symptomatic bakers with high IgE concentrations and positive skin prick test, 37 subjects were found to have a positive bronchial challenge test.5 Those with positive prick tests are more likely to have reactive airways. Bakers may have hypersensitivity to other flour-associated antigens; therefore, care must be taken not to miss multiple hypersensitivities. In one study, five patients with wheat flour hypersensitivity also had allergy to alpha-amylase or cellulose.10 Nasal provocation has been used to reproduce symptoms from egg allergy.1 Nasal challenge test has been validated for use in flour allergic subjects through the measurement of increases in eosinophil and basophil numbers, albumin/total protein ratio, eosinophil cationic protein, and tryptase levels.5, 11

Treatment

Definitive treatment of wheat flour-related allergic disorders and asthma requires prevention of further exposure. Since changing occupations is often not possible, affected workers often rely on palliative therapy with careful monitoring. Cromolyn sodium or combined long-acting beta agonist and corticosteroid pretreatment, along with short-acting beta agonist treatment of symptoms may allow patients to continue with work. Respirator use may reduce work-related symptoms. Allergen-specific immunotherapy (SIT) with wheat flour extract injections has been shown to produce a decrease in hyperresponsiveness to methacholine, skin sensitivity, and specific IgE to wheat flour as well as subjective improvement in symptoms.12 When considering SIT, all potential hypersensitivities such as enzymes, mites, and multiple grains should be investigated and ruled out prior to therapy.

Medical surveillance

Surveillance for bakers’ asthma should include a periodic detailed respiratory history that may be supplemented by pulmonary function testing. Although the relationship of positive skin prick tests to the development of asthma is not known, consideration should be given to the use of skin prick tests as a marker of exposure. An increase in the prevalence of positive skin tests among bakers from 9% initially to >30% by the fifth year has been documented.13 Some of these workers reverted to negative within 12 months.

Prevention

The demonstration of exposure–response relationships in bakers’ asthma indicates that preventive efforts are worthwhile. Measurements of inhalable flour dust particulate from personal sampling have a strong correlation to levels of wheat and rye exposure.7

Avoiding inhalation exposure to dusts can prevent occupational allergy in flour workers. Implementation of engineering controls can help to ensure proper dust containment and exhaust ventilation and is associated with a twofold reduction decrease in alpha-amylase exposures.7 Administrative controls include starting mixers at slow speeds until the addition of wet ingredients is completed, the elimination of dry sweeping and flour dusting, the application of mixer lids, formal training, and supervision.6,7,14 An 80% reduction of flour dust was observed with a combination of these controls.14

As with any inhalation exposure, respirator use will decrease the dose of antigen received. The use of dust/mist respirators, half face masks for short-term activities, and PAPR for individuals with facial hair for long-term activities is recommended.6

References

  1. 1. Valero A, Lluch M, Amat P, et al. Occupational egg allergy in confectionary workers. Allergy 1996; 51:588–92.
  2. 2. O’Holleran MT. Baker’s asthma and reactions secondary to soybean and grain dust. In: Bardana EJ Jr., Montanaro A, O’Holleran MT, eds., Occupational Asthma. Philadelphia: Hanley & Belfus, 1992:107–16.
  3. 3. Brant A. Baker’s asthma. Curr Opin Allergy Clin Immunol 2007; 7(2):152–5.
  4. 4. Quirce S, Fernández-Nieto M, Escudero C, et al. Bronchial responsiveness to bakery-derived allergens is strongly dependent on specific skin sensitivity. Allergy 2006; 61(10):1202–8.
  5. 5. van Kampen V, Rabstein S, Sander I, et al. Prediction of challenge test results by flour-specific IgE and skin prick test in symptomatic bakers. Allergy 2008; 63(7):897–902.
  6. 6. Patouchas D, Sampsonas F, Papantrinopoulou D, et al. Determinants of specific sensitization in flour allergens in workers in bakeries with use of skin prick tests. Eur Rev Med Pharmacol Sci 2009; 13(6):407–11.
  7. 7. Baatjies R, Jeebhay MF. Sensitisation to cereal flour allergens is a major determinant of elevated exhaled nitric oxide in bakers. Occup Environ Med 2013; 70(5):310–6.
  8. 8. Cullinan P, Cook A, Nieuwenhuijsen MJ, et al. Allergen and dust exposure as determinants of work-related symptoms and sensitization in a cohort of flour-exposed workers: a case–control analysis. Ann Occup Hyg 2001; 45(2):97–103.
  9. 9. Baur X, Chen Z, Liebers V. Exposure–response relationships of occupational inhalative allergens. Clin Exp Allergy 1998; 28(5):537–44.
  10. 10. Quirce S, Cuevas M, Díez-Gómez M, et al. Respiratory allergy to Aspergillus-derived enzymes in bakers’ asthma. J Allergy Clin Immunol 1992; 90(6 Pt 1):970–8.
  11. 11. Gorski P, Krakowiak A, Pazdrak K, et al. Nasal challenge test in the diagnosis of allergic respiratory diseases in subjects occupationally exposed to a high molecular allergen (flour). Occup Med 1998; 48:91–7.
  12. 12. Quirce S, Diaz-Perales A. Diagnosis and management of grain-induced asthma. Allergy Asthma Immunol Res 2013; 5(6):348–56.
  13. 13. Herxheimer H. The skin sensitivity to flour of bakers’ apprentices. Acta Allergol 1973; 28:42.
  14. 14. Baatjies R, Meijster T, Heederik D, et al. Effectiveness of interventions to reduce flour dust exposures in supermarket bakeries in South Africa. Occup Environ Med 2014; 71(12):811–8.

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