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Occupational asthma and IgE‐mediated contact dermatitis from sapele wood

A 35-year-old man had a medical history of atopic disease, with rhinitis, asthma and flexural dermatitis since childhood. He had worked as a carpenter since he was 18 years old. After 1 year in this work, he reported more severe relapsing episodes of asthma, rhinitis, conjunctivitis and widespread dermatitis but not urticarial lesions. He improved only on weekends and holidays. Every time he returned to work, he experienced a worsening of symptoms and these were so severe that he occasionally required systemic corticosteroids. He was first referred to our Department of Dermatology (Hospital de Cabuenes) when he was 35 years old. Dermatological examination showed disseminated erythematous, excoriated, lichenified plaques, more severe in exposed areas of the face, neck and forearms. Patch tests were performed, according to the recommendations of the International Contact Dermatitis Research Group, with the European standard series, resins, glues, plastics and acrylates all of which were negative. Also, the patient was patch tested to the sawdust of the various woods that he used in his work (iroko, oak, maple, beech, pine, cherry, sapele and chestnut), both ‘as is’ and at 10% in pet., and all of these tests were also negative. Prick tests were then performed. The positive control was histamine 10mg/ml and saline 0.9% the negative control. We considered a prick testpositive if the diameter of the wheal was at least 3mm larger than the negative control. Positive prick tests (Leti, Barcelona, Spain) were obtained with latex (diameter wheal 20mm) and Dermatophagoides pteronyssinus (diameter wheal 15mm). Negative prick tests were obtained with other common aeroallergens (other mites, molds, pollens and animal allergens) and with all the previously mentioned wood extracts. Intradermal testing was also negative for these woods. Total serum immunoglobulin E (IgE) was more than 2000 kU/l, and we detected high levels of allergenspecific IgE antibodies to latex (more than 100 kU/l) by radioallergosorbent test (RAST) (UniCAP System, Pharmacia, Uppsala, Sweden). RAST to woods was not performed. Immunoblotting was performed according to the method described by Towbin et al. (1). Several IgE-specific bands were detected to latex and a different molecular weight (60kDa) band was detected to sapele but not to the other 7 woods. We concluded that the worsening of both his asthma and his dermatitis was IgE-mediated and occupational, caused by airborne contact with sapele wood.We found no latex sources in his working environment, but he recognized recreational exposure as he reported swelling of the lips when blowing up balloons. The patient was informed and he gave up working as a carpenter, after which he experienced a great improvement in both cutaneous and respiratory symptoms. Discussion