Cases reported "Bronchial Hyperreactivity"

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1/15. Irritant-induced asthma: clinical and functional aspects.

    We report on three patients who experienced persistent asthma symptoms after repetitive irritant exposure which took place over a period from several days to months. Airway inflammation was assessed by induction of sputum and functional follow-up information was obtained from serial lung function tests. All patients had bronchial hyperresponsiveness to methacholine at the time of diagnosis. However, induced sputum samples did not show increased differential count of eosinophils. Treatment with inhaled corticosteroids was started in all of the patients and two of them were removed from work. In the two patients who left the workplace, methacholine inhalation test became negative when symptoms disappeared, whereas the patient who continued working had persistent asthma symptoms and a deterioration of bronchial hyperresponsiveness.
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2/15. Occupational asthma and rhinitis caused by multiple herbal agents in a pharmacist.

    BACKGROUND: Herb agents have been widely used for centuries in the Orient and they have been cultivated throughout asia. There have been a few cases of occupational allergy caused by herb materials. We report a case of occupational asthma and rhinitis caused by six herb materials in a pharmacist working at a pharmacy. OBJECTIVE: We sought the role of immediate hypersensitivity in herbal agent-induced asthma in a pharmacist. methods AND RESULTS: The patient had strong positive responses on skin prick test to extracts of six herb materials: Chunkung (Cnidii rhizoma), Banha (pinellia ternata), Sanyak (dioscorea radix), Kangwhal (Ostericum koreanum), Danggui (angelica radix), and Kunkang (Zingiberis rhizoma). Bronchoprovocation tests showed an early asthmatic response to Danggui extract. serum specific IgE antibodies to Chunkung, Banha, and Sanyak were detected by ELISA with no specific IgE bindings to Kangwhal, Danggui, and Kunkang extracts. Twelve percent sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and IgE immunoblotting revealed one IgE binding component (60 kD) within Chunkung extract, two (10, 25 kD) in Banha, and four (33, 34, 65, 98 kD) in Sanyak. Basophil histamine release test revealed that Danggui extract could release a greater amount of histamine from basophils in the patient than in a healthy control. CONCLUSIONS: Chunkung, Banha, and Sanyak may induce IgE-mediated bronchoconstriction in an exposed worker, and Danggui can cause bronchoconstriction by direct histamine-releasing effect from mast cells in a sensitized patient.
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3/15. Occupational asthma caused by exposure to cyanoacrylate.

    BACKGROUND: Exposure to acrylates may give rise to rhinitis and asthma in both industrial and domestic environments. The mechanisms underlying these respiratory conditions caused by acrylates remain largely unknown. methods: We studied two assembly operators exposed to cyanoacrylate glue who developed rhinitis and asthma symptoms. The causal relationship of these symptoms to cyanoacrylate glue exposure was investigated by serial peak expiratory flow (PEF) monitoring at work and off work. Moreover, inhalation testing was performed by asking the patients to mimic exposure at work with the cyanoacrylate glue in a 7-m3 challenge chamber. RESULTS: Serial PEF monitoring at work and away from work was consistent with occupational asthma in both patients. The methacholine inhalation test was negative in patient 1 (off work) and showed bronchial hyperresponsiveness in patient 2. After 20-min exposure to cyanoacrylate, the patients had late and progressive asthmatic reactions, respectively, and the methacholine test became positive in patient 1. Induced-sputum samples obtained 3 and 24 h after the cyanoacrylate challenge showed a marked increase in sputum eosinophils. CONCLUSION: Exposure to cyanoacrylate in these patients provoked not only variable airflow limitation and bronchial hyperresponsiveness, but also pronounced eosinophilia in sputum.
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4/15. Dentist's occupational asthma, rhinoconjunctivitis, and allergic contact dermatitis from methacrylates.

    BACKGROUND: Allergic contact dermatitis (ACD) caused by (meth)acrylates (MA) is common in dental personnel. MAs have also caused asthma and rhinoconjunctivitis, but asthma, rhinoconjunctivitis and ACD caused by MAs in the same patient appears to be very rare. methods: Occupational asthma and rhinoconjunctivitis were diagnosed in a dentist according to patient history, PEF monitoring, and a work-simulated bronchial provocation test. ACD was diagnosed by skin-patch testing with MAs with the occlusive Finn Chamber-technique. RESULTS: The patient's skin-prick test reactions to common environmental allergens and MAs were negative. The total IgE was not elevated. Occupational asthma was diagnosed by a specific inhalation challenge test in which the patient handled liquid dental MAs for 30 min causing a delayed 23% reduction in FEV1. The provocation test also resulted in rhinoconjunctivitis. On patch testing, positive reactions were provoked by several MAs including 2-hydroxyethyl methacrylate (2-HEMA) to which the patient was occupationally exposed. The patient has not been able to continue her work with dental MAs. CONCLUSIONS: A case of occupational asthma, rhinoconjunctivitis and ACD caused by dental acrylate compounds is presented. patients with respiratory hypersensitivity from MAs have to stop working with MAs, whereas patients with ACD from MAs need to avoid direct contact with MAs, but can often continue in their present job if they use no-touch techniques.
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5/15. Reactive airways dysfunction syndrome following metal fume fever.

    Metal fume fever (MFF) is an acute response to the inhalation of heavy metals used in industry. The patient typically experiences symptoms of cough, fever, chills, malaise, and myalgia that are self-limited and of short duration. Wheezing may occur and pulmonary function may be acutely impaired with a decrease in lung volumes and diffusing capacity of carbon monoxide. Nevertheless, respiratory function quickly returns to normal, and persistent pulmonary insufficiency is unusual. Irritant-induced asthma is a non-immunogenic form of airway injury that may be associated with industrial inhalation exposure. In this situation, the direct toxic effect on the airways causes persistent airway inflammation and bronchial hyperreactivity. The two conditions are considered distinct entities, but we report a previously healthy worker who had classic MFF and was left with irritant-induced asthma or reactive airways dysfunction syndrome (RADS).
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6/15. Glucoamylase: another fungal enzyme associated with baker's asthma.

    BACKGROUND: Aspergillus-derived enzymes are widely used as dough additives in the baking industry. These enzymes may give rise to immunoglobulin (Ig)E-mediated sensitization and occupational asthma. Glucoamylase (or amyloglucosidase) is an important industrial enzyme obtained from aspergillus niger and used to provide fermentable sugars for yeast to improve loaf volume and texture. OBJECTIVE: The aim of our study was to investigate the potential allergenic role of glucoamylase in baker's asthma. methods: We report four subjects with work-related allergic respiratory symptoms who were exposed to glucoamylase and other starch-cleaving enzymes used as baking additives. The causative role of glucoamylase in work-related asthma was investigated by immunologic tests and specific inhalation challenges (SIC). Glucoamylase allergenic components were characterized by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting. RESULTS: Skin prick tests to glucoamylase (10 mg/mL) gave a positive response in all patients. Further, a positive skin prick test to alpha-amylase was obtained in the four patients and to hemicellulase in two of them. SIC to glucoamylase elicited isolated early asthmatic responses in the three patients tested, and SIC to alpha-amylase elicited early asthmatic responses in two patients and a dual asthmatic response in another patient. immunoblotting with glucoamylase showed several IgE-binding bands with molecular masses between 33 and 96 kD. IgE-inhibition assays showed scarce to moderate allergenic cross-reactivity between glucoamylase and alpha-amylase. CONCLUSIONS: These bakers had developed IgE-mediated occupational asthma to glucoamylase and alpha-amylase. Fungal glucoamylase is widely used as a baking additive and this enzyme may give rise to allergic respiratory reactions among exposed workers.
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7/15. Bronchial asthma due to sensitization to chloramine T.

    Chloramine T, an organic, highly reactive derivative of chlorine with potent bactericidal properties, is used as a disinfectant in the food industry. Described as an occupational sensitizer in 1945 for the first time, it produces late or dual asthma, occasionally accompanied by fever and leukocytosis, which is mediated by IgE. We present the case of a male dairy worker who, after 4 years of exposure to the product, developed rhinitis and asthma. skin tests with chloramine T were positive at a concentration of 10 mg/ml, while all other allergens tested negative. RAST detected specific IgE at 12 PRU and bronchial provocation induced immediate and late bronchoconstriction.
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8/15. Occupational asthma due to piperazine citrate.

    BACKGROUND: Piperazine is a secondary heterocyclic amine that may give rise to occupational asthma of uncertain mechanism. methods: We report on a 42-year-old woman, a process operator in a chemical factory, who developed work-related symptoms of rhinitis and asthma upon exposure to piperazine citrate. She remained symptom free during holidays and days off work. RESULTS: Skin prick test with piperazine citrate was positive. Specific inhalation challenge with piperazine citrate at a concentration of 5 mg/m3 for 30 minutes elicited an isolated late asthmatic response. Airway hyperresponsiveness to methacholine significantly increased 3 hours after the piperazine challenge, preceding the late asthmatic response. CONCLUSION: This patient had developed occupational asthma caused by piperazine, as confirmed by the specific inhalation challenge test, possibly due to an immunological mechanism.
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9/15. Occupational asthma due to heated polypropylene.

    A 35 year-old nonatopic woman was referred to the hospital for possible work-related asthma. She had worked as an operator, at a plant producing polypropylene bags, for the previous four yrs. Her main complaint was a productive cough with dyspnoea and wheezing, as well as rhinitis over the past 3 yrs. She had been absent from work for 6 months on maternity leave, and had improved greatly. She was on a beta 2-adrenergic agent and had to take it at least four times daily. Baseline spirometry whilst at work showed marked airflow obstruction (forced expiratory volume in one second (FEV1) of 43% predicted (pred). After two months away from work FEV1 improved to 89% pred; provocative concentration of histamine causing a 25% fall in FEV1 (PC20) was 3.6 mg.ml-1 (mild airway hyperresponsiveness). return to work resulted in a marked deterioration in FEV1, and serial peak expiratory flow (PEFR) values. PC20 was 0.11 mg.ml-1 (severe airway hyperresponsiveness) one week after she had returned to work. Specific inhalation challenges with polypropylene heated to 250 degrees C resulted in a late asthmatic reaction. As formaldehyde is one of the degradation products of heating polypropylene, we exposed her to it for up to 2 h, but we elicited no bronchospastic reaction. We conclude that heated polypropylene should be listed as one of the agents that causes occupational asthma.
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10/15. Occupational asthma caused by pectin inhalation during the manufacture of jam.

    We report a case of pectin-induced occupational asthma in a 35-year-old man. His job involved mixing powdered pectin into a fruit puree during the manufacture of jam. Within minutes of adding pectin, he developed coryza, rhinorrhea, coughing, and wheezing. His symptoms cleared during weekends while away from work and improved with the use of a protective face mask at work. Peak flow rates were significantly lower while at work compared with those at home, and a prick skin test with the pectin powder was positive. We conclude that pectin should be added to the list of the substances known to induce occupational asthma.
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