Occupational allergic airbone contact dermatitis and delayed bronchial asthma from epoxy resin revealed by bronchial provocation test

ARTICLE

Epoxy resins (ER) belong to the list of common causes of occupational allergic contact dermatitis [1, 2]. Only a few cases of immediate type allergy to ER compounds have been reported [3] although both diglycidyl ether of bisphenol A (DGEBA) (Fig. 1) ER [4, 5] and organic acid anhydride epoxy hardeners [6] are potential causes of contact urticaria and bronchial asthma. In a recent occupational asthma textbook DGEBA was not mentioned among the causes of occupational asthma [7]. Here we report a patient with both occupational asthma and contact dermatitis from DGEBA.

Case report and methods

A 26-year-old non-atopic concrete worker had worked for 10 years in the same precast concrete factory, when he was accidentally exposed to a 2-component epoxy resin. He was filling concrete cracks with a two-component epoxy resin product when the resin product accidentally splashed on his clothes, right lower arm and left thigh. The patient continued to use the same ER contaminated working clothes for the next two working days. Erythema developed on the exposed lower arm and thigh, and within two weeks an eczematous reaction developed on the exposed skin, indicating active sensitization [8, 9]. Further exposure to ER products at work resulted in relapsing contact dermatitis.

Patch testing was performed, according to the suggestions of ICDRG, two months after the accident, revealing allergy to DGEBA (1% pet, 3⁺) and diaminodiphenylmethane (DDM). DDM was the hardener used in the ER system. Good protective clothing enabled the patient to continue his work although he suffered from relapsing contact dermatitis which gradually worsened.

Five years later, the patient started to have respiratory symptoms related to work, and two years after this, the diagnosis of bronchial asthma was established. After one further year, the patient came for investigations suspected of having occupational asthma. Prick tests with standard environmental allergens were negative, total IgE was normal 62 kU/l. Spirometry was normal. Forced expiratory volume in 1 second (FEV₁) was 3.88, 91% of predicted, without significant response in the bronchodilation test. A mild bronchial hyperreactivity was recorded in a histamine provocation test. A bronchial provocation test with the epoxy resin without the hardener was performed as previously described [10, 11]. PEF was followed up with a Wright peak flow meter (Clement Clarke M286, Ferraris Medical) [11]. The patient spread the ER (DGEBA according to the material safety data sheet) he used at work on a plate continuously for 30 minutes. 8 hours after the epoxy provocation the PEF value had dropped 22% and wheezing rales were heard. Inhalation of a beta₂-sympathomimetic temporarily relieved the symptoms but the lowest peak flow value (36%) was recorded 17h after the provocation, reflecting a delayed type of bronchial asthma. This 36% drop of the PEF value was considered diagnostic for occupational DGEBA induced asthma. The control provocation test with lactose powder was negative.

A scratch test with DGEBA [3, 12] was negative. On re-patch testing, the patient was revealed to have a 3⁺ allergic patch test reaction to DGEBA (1% pet) in the standard series, a 2⁺ allergic patch test reaction to diaminodiphenyl methane (DDM, 0.5% pet) in a plastic and glue series, and a 2⁺ allergic patch test reaction to 2,2-bis[4-(2-hydroxy-3-methacryloxypropoxy)phenyl]-propane (BIS-GMA; 2% pet, Chemotechnique Diagnostics, Malmö, Sweden) in a dental screening series [13]. The BIS-GMA reaction probably reflected cross-reactivity between epoxy acrylates and DGEBA [14].

The bronchial provocation test also provoked an undesired strong allergic contact dermatitis reaction of the exposed skin, namely the face, neck, the auricles and the hands (Fig. 2) indicating airborne allergic contact dermatitis from DGEBA [1]. Erythema of the face had already started 3.5 h after the ER provocation.

The patient was advised to change to a job where no further ER exposure would occur. In a follow-up control 10 months later the patient's skin was symptomless. He was still on asthma medication but had no more bronchial hyperreactivity.

Discussion

Few cases of immediate allergy from DGEBA have been reported. In 1974, a patch test with an epoxy resin was reported to induce generalized urticaria and an asthmatic reaction [15]. Suhonen [16] reported two patients who in a patch test showed immediate urticarial reactions, probably due to an impure DGEBA epoxy resin used in a ski pole factory. Kanerva et al. [3] described two patients with both immediate and delayed allergy to DGEBA epoxy resin [3]. In these patients the specific IgE-mediated immediate sensitization from DGEBA with a MW of 340 was revealed [3]. According to the history, exposure, and sensitization to DGEBA it was concluded that those two patients had occupational asthma from DGEBA although bronchial provocation tests with DGEBA could not be performed [3]. In the present patient we performed the bronchial provocation test but were not able to make determinations of specific IgE to DGEBA. Lambourn and coworkers reported occupational asthma from an epoxy resin hardening agent, EPO 60 [17], but the causative agent was considered to be a polyamine hardening system. Recently, Sasseville [18] reported a patient who presented with contact urticaria while working in an aircraft factory. On patch testing, at the 30-min reading, he had urticarial reactions both to epoxy resin (1% pet), and to two reactive epoxy diluents, phenylglycidyl ether (0.25% pet) and cresylglycidyl ether (0.25% pet). No delayed reactions were seen. Similarly, Miyamoto and Okumura [19] reported on contact urticaria confirmed by a 15-minute open test and a 15-minute closed patch test for epoxy resin at 1% in petrolatum. We recently had a patient with contact urticaria from DGEBA (to be reported). In addition, contact urticaria and asthma can be caused by amine epoxy hardeners [1, 20, 21]. Another epoxy compound, triglycidyl isocyanurate has caused occupational asthma [22]. The epoxy hardeners phthalic anhydrides are well known causes of bronchial asthma and contact urticaria [1, 7, 23], but were not used in the present patient's workplace.

The provocation test was performed in a provocation chamber in which exposure was both to the respiratory tract and the skin. This resulted in an asthma reaction and a strong allergic airborne skin reaction (Fig. 2). In our experience, skin reactions are rare from bronchial provocation but it would be desirable to use direct bronchial provocation with mask to avoid skin exposure [24].

Our patient's primary sensitization occurred after a single accidental exposure to DGEBA [9]. Very little is known about the mechanisms of respiratory sensitization. Our patient continued to work with exposure to ER even after the diagnosis of occupational allergic contact dermatitis to ER had been established. There is a risk of developing occupational asthma from continuous exposure [1, 3] but it is not clear whether this risk is increased compared with patients who do not have a delayed contact allergy to the corresponding chemical. Interestingly, our patient's occupational asthma could be classified as a type IV allergic reaction: he had allergic patch test reactions to DGEBA and a delayed asthma reaction but no signs of IgE-mediated allergy. Symptoms of respiratory disease associated with type IV allergy have occasionally been reported [25].

Article accepted on 10/5/00

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