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Contents A. Case study B. More information C. Editors' comments D. References E. CPD questions

Index

A. Case study
A 50-year-old pizzeria owner, who had cooked and worked in his restaurant for 20 years, presented with severe dermatitis on his fingers. He had had to give up work 6 weeks prior due to hyperkeratosis, swelling, and broken skin lesions. On questioning, he reported aggravation of pruritis as well as wheals and flares when working with various pizza toppings. He was unable to identify which were the main culprits. He had been treated previously with topical medications, including corticosteroid creams, lotions and ointments. These provided intermittent and temporary relief.

THOUGHT PROCESS:
What information is needed to determine the cause?
a. Does he have a family history of atopy?
b. Does he have a history of other types of adverse reactions?
c. Did he suffer from any type of skin reactions prior to the development of these skin reactions?
d. When does the dermatitis occur or worsen? Every day? At which specific time of day? After contact with something specific? Is it influenced by temperature changes?
e. Does the reaction occur outside the pizzeria at all?

DISCUSSION:
A detailed clinical and medical history was taken and established the following:
a. His father suffered from asthma, but there was no history of skin reactions or food-related allergy.
b and c. He had always suffered from allergic rhinitis until about 25 years of age, and then had developed mild asthma. He had never suffered from skin reactions before.
d and e. A mild dermatitis had started approximately 18 months before and worsened about 3 months before, when his skin had started breaking. The continued deterioration of his skin had resulted in his stopping work 6 weeks prior to his appointment. He linked the itching and symptoms to preparing the pizzas with their various toppings and baking them in the pizza oven. Approximately a year earlier, he had visited his family in Italy for 6 weeks and had noticed a marked improvement in his dermatitis. He thought that it had been approximately 2 weeks after returning to the pizzeria that skin symptoms had reoccurred. The dermatitis seemed to occur or worsen only when he was working at the pizzeria. He had particular difficulty when preparing his handmade pizzas. The dermatitis seemed to worsen daily but only in the evenings when he was working with pizzas. It did not appear to be influenced by heat, as he never experienced problems over weekends when braaing/barbequing at home.

THOUGHT PROCESS:
a. What elicits his and his father’s asthma? If food, is it related to the skin reaction?
b. What could be causing the skin reactions? It is likely to be contact with food or something else that he is exposed to while making the handmade pizzas: perhaps latex gloves, cooking equipment or utensils, or cleaning agents.
c. What changed in the pizzeria 18 months before when the symptoms started? And 3 months ago when they grew even worse? Could, for example, a new type of pizza, new equipment or a single new ingredient be possibilities?

DISCUSSION:
a. His father developed asthma to pollens and grasses. The patient’s asthma was caused by cat hairs, house dust mites and grasses. These agents had been confirmed by IgE tests, which he had had done when his asthma had initially appeared approximately 25 years before. His asthma and dermatitis did not appear to be related, as he never developed any skin irritation or symptoms when in contact with grasses or cats. His asthma, to his knowledge, was never worse at the restaurant either.
b. It was determined that contact with non-food substances was not a cause, as he did not use rubber gloves and had contact with the same equipment at home, where the contact did not cause aggravation of his dermatitis. He did not handle cleaning agents.
c. He could not think of anything specific that had changed 18 months or 3 months ago.

Therefore, his skin reaction seemed likely to be a result of contact with a food.

THOUGHT PROCESS:
Steps that can now be considered include:
a. Allergy tests
b. Food contact-symptom diary
c. Challenge through contact to specific foods

DISCUSSION:
a. Could be done specifically to screen for IgE-mediated reactions
b. Difficult to implement, as he was very busy in the pizzeria and would not have time to do this.
c. He had no idea which food might cause the reaction. Although practically there were too many foods to test for, conducting tests with the most common occupational food allergens might be of benefit; the range could be extended if required.

Skin prick tests and serum-specific IgE tests were performed to screen for the main food allergens (fx5). Results were mildly positive (class 2).

Most contact allergy reactions (especially reactions to chemicals) are cell-mediated and therefore require patch testing, but a fair number (especially reactions to food and protein) are IgE-mediated; therefore, an SPT or RAST test may be of value, despite a lack of sensitivity in identifying the actual contact allergy. The weak positive test result and the patient’s history made it relatively clear that food was aggravating the skin reaction.

On assessing the foods commonly worked with, it was decided to do patch testing for all the toppings used on the pizzas. Patch testing shows promise in diagnosing delayed, non-IgE or cell-mediated type food reactions. It is necessary to use an area of the body which is unaffected by skin lesions. In this case, the back was used. Also, all substances tested must be tested on the skin prior to patch testing to ensure that they are not natural irritants.

After 48 hours, all tests were negative except for a positive reaction to the spice mix which the patient added to the ground/ mince meat when preparing the Mexicana pizza. It was necessary to ascertain which specific spice was causing the occupational dermatitis. The patient mentioned then that he had changed his supplier for the spice mix around 2 years before. The ingredients of the mix were compared with the ingredients of the mix before the change in supplier, and 3 differences in the form of new spices were identified. Specific IgE and patch testing were done on each of the 3 new spices in the mix, and only paprika was positive.

After removing all paprika from all dishes in the pizzeria, the dermatitis started improving and had virtually disappeared by 3 months. A contact sensitivity to paprika was diagnosed.

He returned 2 months later, concerned that his asthma had become a major problem, specifically while he was working with food in the restaurant kitchen; the asthma seemed to be progressively worsening.

POSSIBLE REASONS FOR DETERIORATION:
a. He could be reacting to a hidden source of paprika (or a cross-reactive food).
b. He could be reacting to another unidentified food allergen.
c. He could be demonstrating a reaction to a non-food allergen such as house dust mites, storage mites, lupine seed flour or cockroaches in the restaurant.

DISCUSSION:
a. Paprika was an unlikely cause for his asthma, as he had never experienced worsening of his asthma over the 18 months when paprika had formed part of the spice mix prior to the confirmation of his allergy to it.
b. This is a possibility. Whether he was being exposed to a new allergen in his working environment needed to be explored. Generally, serum-specific IgE tests (fx5) had been mildly positive, so further specific IgE tests for common food allergens were carried out.
c. The restaurant had never experienced problems with cockroach infestation. The floors were tiled, and there were no carpeted areas, making house dust mites an unlikely culprit. Hygiene and regular cleaning were characteristic of the restaurant. Nonetheless, specific IgE tests were done to investigate possible reactions to the non-food allergens mentioned above.

Results of the specific RAST test revealed negative reactions to dairy, fish, soya, peanut and shellfish. Storage mites, cockroach and lupine seed flour were also negative. Wheat and house dust mites produced positive IgE. The patient had originally demonstrated allergy to house dust mites, but his asthma had worsened only recently, so this was an unlikely cause. The wheat results were Class 3, which could indicate sensitisation but not necessarily clinical reaction. The sensitivity of these tests in detecting occupational allergy is, however, low, and the results would always need to be confirmed with other tests.

The patient was questioned about anything that might have changed in the kitchen in the previous 2 months. He had become far more aware of the possible link between his symptoms and surroundings, and on questioning said that the major change was that he had been making the pizza bases for the last 2 months, as the person usually responsible for the preparation had been in a car accident. He had never previously done this, and ever since filling in he had become very tight-chested and his asthma had markedly worsened.

Pulmonary function tests suggested occupational asthma, and on examination of the pizza preparation method, the use of fine wheat flour before and after flattening of the dough was considered a possible cause, similar to causes seen in Baker’s Asthma. He soon started using ready-made pizza bases which did not require preparation in his kitchen; a key part of the change was that the raw bases did not need to be rolled out on dry flour prior to filling with toppings. The change eliminated the presence of flour dust from his restaurant, and his symptoms improved slowly over time. Occupational asthma to wheat flour was diagnosed.

TIP for Allergy Advisor users: Allergy Advisor contains a very useful function to explore occupational reactions. If you choose the “Assessment” tab from the main window, and you click on “Specific Occupations”, it will open up a function that allows you to select an occupational category or an individual occupation. Once a category or specific occupation is selected, all the substances that can be in the immediate environment (and could therefore be a cause of an adverse reaction) of this occupation will be shown.

B. More information:
Occupation allergies affect a broad range of industries. A wide variety of substances, both food-derived and non-food may be considered as sensitising agents. Continued exposure of workers to these can lead to hypersensitivity reactions.

Non-food agents which may induce immunologic (allergic) reactions include honey bees, grain storage mites, antibiotics, chemicals in hair products, latex-containing supplies, metal salts and even rubber boots.

Food proteins are far more likely to induce sensitisation, and it is for this reason that the focus of this review is on the food industry. The most common allergens from farm to fork will be explored.

We often forget the various stages involved in bringing food to our tables. Workers in food manufacturing and preparation are constantly exposed to potent food-derived allergens.

Little is known about occupational diseases resulting from antigen exposure. But in occupational exposure to food allergens, routes of exposure appear to be primarily either skin contact or inhalation, depending on the type of agent and the area of the industry.¹

Commonly affected occupations and problem allergens
Occupational allergens may be classified as high- or low-molecular-weight compounds with molecular weights of greater than 2kDa and less than 1kDa, respectively. High-molecular-weight allergens tend to cause reactions through IgE-mediated mechanisms. Low-molecular-weight allergens need to be conjugated to a carrier protein to be allergenic. They cause disease largely through unknown mechanisms, although non-IgE-mediated and cell-dependent immunologic mechanisms may play a role. Allergic occupational reactions are more likely to develop due to exposure to high-molecular-weight proteins.^2,3,4

The most commonly affected occupations, and the allergens involved, are the following:

1. The ever-increasing demand for fish and shellfish has resulted in burgeoning processing and production of seafood. Occupational asthma, rhinitis, hypersensitivity pneumonitis and even anaphylaxis have been described in the seafood processing industry, particularly in oyster, prawn, fish and snow crab workers. Reactions occur due to aerosols generated from cutting, scrubbing, cleaning, cooking, boiling and drying the seafood. The arthropods, particularly in the class Crustacea, have been more commonly implicated as an exposure risk; however, the specific allergens have yet to be identified.2,3,5,6,7

2. Baker’s Asthma is one of the most common forms of IgE-mediated occupational asthma worldwide. Bakers experience a spectrum of allergy that ranges from rhinitis to conjunctivitis to asthma to dermatitis. Bakers are exposed to a variety of grains and have been reported to react to wheat, rye, barley, buckwheat and soybean flours through inhalation. Following sensitisation and re-exposure to the flour, workers may demonstrate both immediate and late-type reactions. Cross-reactivity may occur among wheat, rye, barley and oat flour; i.e.. if you are sensitised to one, you may develop sensitivity to another. Occupational dermatitis usually results from continued exposure to wet, sticky dough, additives and flavourings. Flour itself can induce contact urticaria.2,3,8,9, 0,11

3. Enzymes derived from the fungus Aspergillus (a-amylase, cellulose, hemicellulase and glycoprotein) are frequently used in the food industry, particularly in the baking industry, to improve the quality of bread, decrease baking time and enhance yeast fermentation. Sensitisations to these various enzymes have been demonstrated in many cases of Baker’s Asthma, and reactivity has been shown in the absence of reaction to the cereal allergen.2

4. Exposure to soybean dust has been associated with asthma from soybean unloading by harbour labourers, farmers and other workers. The main allergen is considered to be the soy bean hull. This differs from typical soya allergy through ingestion, as it may be possible to tolerate ingested soybean hull despite reacting to it when it is inhaled. 2,12,13,14,15

5. Workers in the coffee industry handling green coffee beans may develop asthma, rhinitis and dermatitis. The nature of the allergen in green coffee beans and dust has not been elucidated. In a study, similar allergens could not be identified in roasted coffee, and no similar reactions to it were found to have been reported. In 1996, however, a case was reported of confirmed occupational asthma to both green coffee beans and roasted coffee beans in a 34-year-old-man employed in a company producing coffee. He initially reacted only to the green coffee beans but became sensitised to the roasted coffee beans as well. This indicates that there are similar allergens in roasted coffee beans, but in lower concentrations than in green coffee beans.2,16,16

6. Mushroom Worker’s Lung has been linked to a variety of antigens derived from microorganisms and mushroom spores. Mushroom spores in particular may cause hypersensitivity pneumonitis. Most commercial mushrooms (Agaricus sp.) are harvested before sporulation; however, if picking occurs before this stage, workers may be exposed to high spore levels. Occupational asthma has also been reported in mushroom growers, packers and soup processors. Recently, several new allergens have been described, particularly those from mushroom species originating in the Far East (Hypsizigus marmoreus/bunashimeji).Importation of exotic mushrooms, including oyster and shiitake, is common in EU countries, and some of the exotic species of mushrooms are cultivated locally. The increased movement of commercial product and labour markets worldwide may contribute to an increase in clinical cases of mushroom hypersensitivity pneumonitis.1,3,18,19,20,21

7. Various spices may elicit occupational skin disease, including allergic contact dermatitis. In a study conducted on 1000 patients in Denmark (1996), spices as causative agents included garlic, cinnamon, ginger and clove. The affected occupations were found to be chefs and other food service workers. It is therefore important to remember that although occupational allergic contact dermatitis from spices is relatively rare, it needs to be considered as a possibility in individuals who have hand dermatitis and work with spices.22 The development of rhinitis and asthma after

8. Chefs and food service professionals may be at high risk for developing occupational asthma or dermatitis through inhalation of odours or skin contact with foods, respectively. Occupational asthma was described in a butcher who reacted to several aromatic herbs, including rosemary, bay leaf, thyme and garlic, after contact but not ingestion. RAST showed that garlic was the most potent allergen. 28

9. Vegetables have been implicated as occupational allergens. Greengrocers are of course particularly susceptible. Occupational dermatitis after handling broccoli has been described in a few cases. A case report, on a 29-year-old greengrocer’s son described oral allergy syndrome, rhinoconjunctivitis, urticaria, nausea and facial angiooedema as reactions to raw and cooked chicory. Exposure through inhalation, ingestion and contact precipitated reactions.34,35

There have been many reports of adverse reactions in adults handling or peeling raw potatoes. Most reports were of housewives and workers in the potato industry. Symptoms reported include rhinoconjunctivitis, asthma, contact urticaria, atopic dermatitis, angioedema and immediate finger itching upon handling raw potato.3,38,39,40,41,42

10. Fruits have also been described as occupational allergens. In 2004, a case of a 29-year-old woman complaining of dermatitis on her hands was described. She had no other clinical presentation, and her dermatitis appeared after contact with various types of melons. Strangely, she was able to tolerate all melon when ingested. A kitchen assistant noted an increase in pruritis on his hands after handling apple, orange, peach, pear, potato, garlic and onion. Wheals would appear after contact with melon. Specific

IgE tests were found to be positive to birch pollen and profilin, suggesting that he had been sensitised previously to these and had developed contact dermatitis due to continued contact with cross-reactive foods, namely melon, apple and peach.45,46

11. An unusual cause of occupational asthma is honey. A 42-year-old woman who was employed as a quality control worker in a company that produced breakfast cereal had occupational asthma after sensitisation to inhaled honey.47

12. Inhalation of egg particles from the spraying of egg and water solution as a glaze on rolls was reported to lead to occupational asthma in 8 out of 13 workers (usually bakers). Respiratory sensitivity to inhaled egg does not appear to be related to atopy, and powdered egg may be a more potent allergen than aerolised egg.21

13. A rare case was reported of a homemaker who experienced rhinoconjunctivitis, asthma and contact urticaria when trimming raw green beans or inhaling vapour from boiling green beans. She was able to eat and touch cooked green beans without any reaction.48

14. Peanut dust may cause anaphylaxis if inhaled by sensitive individuals working invarious food and catering industries.49

Occupational reactions to foods
Common symptoms seen in the food industry include occupational asthma, rhinitis, conjunctivitis, dermatitis and hypersensitivity pneumonitis. The 3 primary categories of occupational reactions to food allergens/antigens, whether IgE or non-IgE mediated, are considered occupational asthma, hypersensitivity pneumonitis and occupational dermatitis. All of these conditions would have a profound effect on the health of affected farmers, food processors or food preparers even after removal of the offending food.^1,3

1. Occupational asthma
Occupational asthma (OA) is considered the most common occupational respiratory disease (affecting 2 to 20% of all asthmatics). In about 1 in 10 cases, new or recurrent asthma in adulthood will be caused by work. Two types have been described. One is irritant-induced asthma (Reactive Airways Dysfunction Syndrome) caused by a single high-intensity exposure to an irritant substance. It has no latency period and is not immunologically mediated. The other, more common type is immunologically mediated occupational asthma. It results from sensitisation to a substance and thus has a latency period of varying length, depending on the specific agent and the amount and duration of exposure. It may be preceded by nasal and ocular allergy symptoms.^2,3,50

2. Hypersensitivity pneumonitis
Also known as extrinsic allergic alveolitis, hypersensitivity pneumonitis affects the food industry generally and remains an important disease in mushroom workers. It has a significant morbidity, and early diagnosis and removal from exposure to the antigen are critically important in its management.^1,3,18

3. Occupational dermatitis & contact urticaria
Occupational skin disease may represent up to 15% of all occupational diseases. There is both irritant and allergic contact dermatitis. Irritant contact dermatitis is a non-immunologic inflammatory skin disorder that can occur without previous exposure to sensitise an individual. The duration of exposure and the amount of agent are important. In contrast, allergic contact dermatitis may present as an urticaria reaction or as a delayed hypersensitivity reaction. It presents as an eczematous skin reaction to an agent to which there has been previous sensitisation, and clinically there may be pruritis, erythema, oedema and papulovesiclar eruption. Most reactions are irritant (80%) rather than allergic (20%) and result from continuous exposure to various agents through handling or occasionally through ingestion of food products, particularly in the food processing and food service industries. An affected worker may have both irritant and allergic contact dermatitis.^1,3,51

Occupational contact urticaria is an important manifestation of occupational skin disease in the food industry. The rash is associated with a specific occupational exposure. Risk factors include a breakdown in the skin barrier and a history of atopy. There is very little data available; however, cooks, bakers, caterers and food handlers are at increased risk. Potential allergens include apple, bean, beer, caraway seed, carrot, egg, fish, garlic, kiwi fruit, lettuce, meat (beef, chicken, lamb, liver, pork, and turkey), milk, peach, potato, rice, shellfish, spices, strawberries, cereal flours and flour enzymes.^3,52,53,54

Although not considered a common symptom to occupational food allergens, mild occupational rhinitis may be triggered by exposure to cooking odours.¹

Diagnosis and laboratory tests
Diagnosis requires establishment of a causal relationship between an exposure at work and the resultant disease. It is necessary to rule out the existence of the disorder prior to employment in the current position. In addition, an agent known to cause the occupational disease must be identified and isolated from the workplace. In the case of occupational asthma, diagnosis may be relatively straightforward; however, problems are likely to occur in diagnosing patients with pre-existing asthma or in those with unusual exposures, especially if these are to low-molecular-weight agents.^3,50

There is no definitive diagnostic test when it comes to occupational allergy. A clear and detailed clinical history and physical examination is essential in all cases. Skin prick tests and serum-specific IgE tests may be useful for screening or monitoring in high risk industries, but positive responses do not necessarily correlate with disease or predict who will develop occupational asthma, dermatitis or rhinitis. Demonstration of antibodies will merely confirm that there was exposure.^1,3

If hypersensitivity to a food allergen is suspected, inhalation challenges rather than the traditional ingested food challenges are performed to diagnose occupational asthma. Inhalation challenge testing should be performed only in a controlled setting with adequate resources to handle medical emergencies. Repeated bronchial hyper-responsiveness data showing improvement following removal from the workplace has good positive predictive value, helpful for excluding pre-existing abnormalities. The negative predictive value, however, is poor, as airway hyper-responsiveness may take a long time to improve. The absence of improvement does not rule out occupational asthma as a diagnosis. A normal hyper-responsiveness challenge within 24 hours of a symptomatic episode would make a diagnosis of occupational asthma unlikely. Asthma symptoms or peak flows that improve outside the workplace may help suggest occupational asthma.^1,3,55,56,57

The use of patch testing with suspected agents can help distinguish between irritant and allergic responses in occupational dermatitis. Allergic contact dermatitis would be confirmed by positive tests, as there is no specific test for irritant contact dermatitis. It is also helpful to look for delayed reactions and to determine whether any irritant reactions have cleared. Something to bear in mind when doing patch testing is that foods and spices may act as irritants. The sensitivity and specificity of patch testing is about 70%.^1,3,58

Nasal challenges for diagnosing occupational rhinitis are not widely used, as they are time-consuming and the methods are not standardised.^1,3

The CAST test has also been used in the diagnosis of occupational allergens. It may be useful in instances in which other in vitro or in vivo diagnostic tests are not reliable, as well as in non-IgE-mediated immediate hypersensitivity reactions.⁵⁹

In the case of hypersensitivity pneumonitis, serum IgE will not usually be elevated. Specific IgG antibody to a putative agent by immunoprecipitation may be highly suggestive of disease, although there may be false positives.³

In most cases of occupational disease, elimination of followed by re-exposure to a suspected allergen should lead to improvement or removal of symptoms, with the subsequent return of reactions confirming the diagnosis more precisely.

Prevention and treatment
The best treatment of allergic occupational disease is elimination of the cause. The reduction of exposure levels is the only way to significantly reduce or remove symptoms.^1,3

In the case of occupational asthma, symptoms may be slow to resolve or remain unchanged long after removal of the patient from the workplace. Correct management of occupational asthma must be based on a good knowledge of the natural history of the disease and of its prognostic factors. Management may, however, prove difficult, as there are often important employment and social issues to be taken into account.^1,3,50,60

Longitudinal studies have demonstrated that improvement of symptoms, especially airway hyper-responsiveness, may be prolonged after cessation of exposure. Severity of asthma at diagnosis is the best predictor of clinical symptoms and functional impairment at follow-up. The molecular weight of the causal agent does not seem to be a prognostic factor. Airway inflammation is associated with the persistence of symptoms after cessation of exposure. Further studies are needed to investigate the prognostic value of sputum eosinophils and neutrophils, and to determine whether some specific agents are associated with a better prognosis than others.^50,60

As the number of individuals employed in the food industry grows, and the globalisation of the industry increases the range of exposures, it is essential for health professionals and employers alike to be aware of new and unusual occupational reactions.

C. Comments by our editors

Prof Janice M. Joneja Ph. D., RDN This excellent review of allergic diseases triggered by food allergens encountered not by the usual route of eating and digestion, but through contact and inhalation, highlights the increasing realisation that foods contain powerful allergens; allergens that are not only constituents of the food itself, but may also be introduced during the manufacturing process. Primary sensitisation to ingested foods in adulthood is unusual; infancy is the time when allergy to foods first appears, and the majority of children outgrow their early food allergies as their immune systems and digestive tracts mature. The exception is oral allergy syndrome, which arises in adults after previous allergic sensitisation to inhaled pollens. The fact that the route of sensitisation to food allergens in adulthood is primarily via the skin and respiratory tract emphasises the unique function of the immune system of the digestive tract in its processing of such powerful allergens without a subsequent allergic response. In the vast majority of cases allergic sensitization to food allergens via the respiratory tract and skin does not lead to food allergy when the same food is consumed. This might indicate that either the specific allergens that trigger the allergic reaction in the respiratory tract and skin differ from those that induce food allergy, or that the GALT in the digestive tract is highly proficient in filtering out the allergen and preventing an immunological response even when allergen-specific IgE is already in the system. We are beginning to have a clear picture of the immunological mechanisms that are responsible for production of allergen-specific antibody, but it is reviews such as this that bring to our attention that we still have a long way to go in understanding exactly what processes are involved in the clinical expression of allergy – the symptoms – and how these differ in one organ system as compared to another.

Dr. Harris Steinman M.B.Ch.B. Prof. Joneja summarises this review perfectly.

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D. References
1. Metcalfe D, Sampson, H, Simon R. Food Allergy: Adverse reactions to foods and food additives, Third edition. Blackwell publishing 2003. Chapter 21 p270-295
2. Lachowsky F, Lopez M. Occupational allergens. Current Allergy and Asthma reports 2001, 1: 587-593
3. Aresery M, Lehrer SB. Occupational reactions to food. Current Allergy and Asthma reports 2002, 2: 78-86
4. Milton DK, Solomon GM, Rosiello RA, Herrick RF. Risk and incidence of asthma attributable to occupational exposure among HMO members. Am J Ind Med 1998, 33(1):1-10
5. Cartier A, Malo Jl, Forest F et al. Occupational asthma in snow crab processing workers. J Allergy Clin Immunol 1984, 74: 261-269
6. Rodriguez J, Reano M, Vives R et al. Occupational allergy caused by fish inhalation. Allergy 1997, 52: 866-869
7. Jeebhay MF, Robins TG, Lehrer SB, Lopata AL. Occupational seafood allergy-a review. Occup Environ Med 2001
8. Baur X, Posch A. Characterised allergens causing baker’s asthma. Allergy 1998, 53: 562-566
9. Sandiford CP, Tee RD, Newman-Taylor AJ. Identification of cross reacting wheat, rye, barley and soya flour allergens using sera from individuals with wheat-induced asthma. Clin Exp Allergy 1995, 25: 340-349
10. Weiss W, Vogelmeier C, Gorg A. Electrophoretic characterisation of wheat grain allergens from different cultivars involved in baker’s asthma. Electrophoresis 1993, 14: 805-816
11. Quirce S, Polo F, Figueredo E et al. Occupational asthma caused by soybean flour in bakers-differences with soybean-induced epidemic asthma. Clinical and Experimental Allergy 2000, 30: 839-846
12. Anto JM, Sunyer J, Rodriguez-Roisin R et al. Community outbreaks of asthma associated with inhalation of soy bean dust. Toxicoepidemiological Committee. N Engl J Med 1989, 320: 1097-1102
13. Bourgeois. Asthma severe par inhalation de poussiere de soja. Rev Fr Allergol 1984, 24: 210-211
14. Swanson MC, Li JTC, Wentz-Murtha PE et al. Source of the aeroallergen of soybean dust: a low molecular mass glycopeptide from the soybean tela. J Allergy Clin Immunol 1991, 87:783-788
15. Gonzales R, Zapatero L, Caravaca F, Carreira J. Identification of soybean proteins responsible for respiratory allergies. Int Arch Allergy Appl Immunol 1991, 95: 53-57
16. Lehrer SB, Karr M, Salvaggio JE: Extraction and analysis of coffee bean allergens. Clin Allergy 1978, 8: 217-226
17. Lemiera C, Malo JL, McCants M, Lehrer S. Occupational asthma caused by roasted coffee: Immunologic evidence that roasted coffee contains the same antigens as green coffee but in lower concentration. J Allergy Clin Immunol Aug 1996, 98 (2): 464-466
18. Moore JE, Convery RP, Millar BC, et al. Hypersensitivity pneumonitis associated with mushroom worker's lung: an update on the clinical significance of the importation of exotic mushroom varieties. Int Arch Allergy Immunol. 2005 Jan; 136 (1):98-102. Epub 2005 Jan 11
19. Tanaka H, Sugawara H, Saikai T et al. Mushroom worker’s lung caused by spores of Hypsizigus marmoreus (Bunashimeji): elevated serum surfactant protein D levels. Chest 2000, 118: 1506-1509
20. Symington IS, Kerr JW, Mclean D. Type 1 allergy in mushroom soup processors. Clin Allergy 1981, 11: 43-47
21. Carol O’Neill. Occupational respiratory diseases resulting from exposure to eggs, honey, spices and mushrooms. Allergy Proc Mar-Apr 1990, 11 (2): 69-70
22. Kanerva L, Estlander T, Jolanki R. Occupational allergic contact dermatitis from spices. Contact Dermatitis 1996, 35: 157-162
23. Sastro J, Olmo M, Novalvos A et al. Occupational asthma due to different spices. Case report. Allergy 1996, 51: 117-120
24. Foti C, Carino M, Cassano N et al. Occupational contact urticaria from paprika. Contact Dermatitis 1997, 37: 135
25. Occupational protein contact dermatitis from coriander. Contact Dermatitis 2001, 45: 345-355
26. Irigoyen JA, Fabuel AT, Lizana FM. Occupational rhinoconjunctivitis from white pepper. Case report. J Invest Allergol Clin Immunol 2003; Vol 13 (3): 213-215
27. Garcia-Gonzalez JJ, Bartolome-Zavala B etal. Occupational rhinoconjunctivitis and food allergy because of aniseed sensitization. Case report. Annals of allergy, asthma & immunology 2002, 88: 18-522
28. Lemiere C, Cartier A, Lehrer SB et al. Occupational asthma caused by aromatic herbs. Case report. Allergy 1996, 51: 647-649
29. Cronin E. Dermatitis of the hands in caterers. Contact Dermatitis 1987, 17: 265-269
30. Lybarger JA, Gallagher JS, Pulver DW et al. Occupational asthma unduced by inhalation and ingestion of garlic. J Allergy Clin Immunol 1982; 69: 448-54
31. Falleroni AE, Zeiss CR, Levitz D. Occupational asthma secondary to inhalation of garlic dust. J Allergy Clin Immunol 1981, 68: 156-160
32. Seuri M, Taivanen A, Ruoppi P et al. Three cases of occupational asthma and rhinitis caused by garlic. Clin Experimental Allergy 1993, 23: 1011-1014
33. Monteseirin J, Perez-Formoso JL, Sanchez-Hernandez MC et al. Occupational contact dermatitis to dill. Allergy 2002, 57: 865-866
34. Sanchez-Guerrero IM, Escudero AI. Occupational contact dermatitis to broccoli. Allergy 1998, 53: 621-628
35. Cadot P, Kochuyt AM, Deman R, Stevens EAM. Inhalation and ingestive immediate-type allergy caused by chicory. Clin Experim Allergy 1996, 26: 940-944
36. Quirce S, Madero WF et al. Occupational asthma due to inhalation of cauliflower and cabbage vapours. Allergy 2005, 60: 969-974
37. Quirce S, Diet Gomez ML, Hinjosa M, Cuevas, et al. Housewives with raw potato-induced bronchial asthma. Allergy 1989;44:532-536
38. Nater JP, Zwartz JA. Atopic allergic reactions due to raw potato. J Allergy 1967 Oct;40(4):202-6
39. Jeannet-Peter N, Piletta-Zanin PA, Hauser C. Facial dermatitis, contact urticaria, rhinoconjunctivitis, and asthma induced by potato. Am J Contact Dermat 1999 Mar;10(1):40-2
40. Larko O, Lindstedt G, Lundberg PA, Mobacken H. Biochemical and clinical studies in a case of contact urticaria to potato. Contact Dermatitis 1983 Mar;9(2):108-14
41. Gomez Torrijos E, Galindo PA, Borja J, Feo F, Garcia Rodriguez R, Mur P. Allergic contact urticaria from raw Potato. J Investig Allergol Clin Immunol 2001;11(2):129
42. Peter JN, et al. Contact urticaria from potatoes. Contact Dermatitis 1999;10(1):40-42
43. Taylor SL, Bush RK, Selner JC, Nordlee JA, Wiener MB, Holden K, Koepke JW, Busse WW. Sensitivity to sulfited foods among sulfite-sensitive subjects with asthma. J Allergy Clin Immunol 1988;81(6):1159-67
44. Steinman HA, Le Roux M, Potter PC. The incidence of Sulfite sensitivity in South African asthmatic children. SAMJ 1993;83:387-390
45. Occupational protein contact dermatitis from fruits. Contact Dermatitis 2000, 43: 43
46. Garcia S, Lombardero M et al. Occupational protein contact dermatitis due to melon. Allergy 2004, 59: 558-559
47. Johnson A, Dittrick M, Chan-Yeung M. Occupational asthma caused by honey. Allergy 1999, 54: 189-190
48. Igea JM, Fernandez M, Quirce S. Green bean hypersensitivity: An occupational allergy in a homemaker. J Allergy Clin Immunol July 1994, 94 (1)
49. Rayman RB. Peanut allergy in-flight. Aviat Space Environ Med 2002 May;73(5):501-2.
50. Cullinan P.Clinical aspects of occupational asthma. Panminerva Med. 2004 Jun;46(2):111-20
51. Beltrani VS. Occupational dermatoses. Ann Allergy Asthma Immunol 1999, 83 (6 pt 2): 607-613
52. Reitschel RL, Fowler JF: Contact urticaria. In Fischer’s Contact Dermatitis Edition 4. Edited by Reitschel RL, Fowler JF. Baltimore: Williams & Wilkins. 1995: 778-807
53. Taylor JS, Leow YH, Fischer AA. Contact urticaria. In Occupational skin diseases Edition 3. Edited by Adams RM. Philadelphia: WB Saunders, 1999: 111-134
54. Lushniak BD. Occupational skin diseases [review]. Prim Care 2000, 27: 895-916
55. Malo JL, Trudeau C, Ghezzo H et al. Do subjects investigated for occupational asthma through serial peak expiratory flow measurements falsify their results? J Allergy Clin Immunol, 1995, 96 (5 pt 1): 601-607
56. Banks DE, Wang ML. Occupational asthma: “ the big picture” Occup Med 2000, 15: 335-358
57. Talini D, Benvenuti A, Carrara M. Diagnosis of flour-induced occupational asthma in a cross-sectional study. Respiratory medicine 2002, 96: 236-243
58. Nethercott JR. Practical problems in the use of patch testing in the evaluation of patients with contact dermatitis. Curr Probl Dermatol 1990, 2L4
59. de Weck AL, Sanz ML. Cellular allergen stimulation test (CAST) 2003, A review. J Investig Allergol Clin Immunol. 2004; 14 (4):253-73
60. Ameille J, Descatha A. Outcome of occupational asthma. Curr Opinion Allergy Clin Immunol 2005 Apr;5(2):125-8

E. CPD Questions (For South African dietitians only. Australian dietitians: where you have relevant learning goals, CPD hours related to this resource can be included in your APD log.)

2. Exposure to which proteins are more likely to lead to allergic occupational reactions?
a. Low-molecular-weight
b. High-molecular-weight
c. Neither of the above
d. Both of the above

3. Baker’s Asthma may occur due to cross-reactivity between:
a. Wheat, rye, barley and oat flour
b. Wheat, rice, corn and rye flour
c. Wheat, rye, soya and barley flour
d. Wheat, buckwheat, oat and sago flour

4. True or false: Allergy to garlic has been reported to cause dermatitis, asthma and rhinitis.
a. True
b. False

5. True or false: Irritant-induced asthma has a latency period and is immunologically mediated.
a. True
b. False

6. Risk factors for occupational contact urticaria include:
a. Smoking and a history of atopy
b. Rhinitis and a history of atopy
c. Asthma, smoking and continual hand washing
d. A breakdown in skin barrier and a history of atopy
e. None of the above

7. How can patch testing with suspected agents be helpful in diagnosing occupational dermatitis?
a. A patch test will confirm both irritant and allergic contact dermatitis.
b . A patch test is able to confirm irritant contact dermatitis but not allergic contact dermatitis.
c . Allergic contact dermatitis will be confirmed, but not irritant contact dermatitis.
d . A patch test cannot confirm either allergic or irritant contact dermatitis.

8. True or false: In the case of occupational asthma, symptoms may resolve completely after removal from the workplace.
a. True
b. False

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Occupational allergy
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