Occupational asthma caused by exposure to ash wood dust (Fraxinus americana)

A 63 year old man reported rhinitis and asthma, which occurred only at work where he was exposed to ash wood dust. Monitoring of peak expiratory flow rates (PEFR) and bronchial responsiveness to histamine when off work and at work showed increased variation of PEFR at work but no significant changes in nonspecific bronchial responsiveness assessed by the provocation concentration producing a 20% fall in FEV1 (PC20). Specific inhalation challenges were carried out in a special challenge room with ash wood dust. During the exposure for only 3 minutes, the mean concentration of particles was 3 mg-m3 and about 50% of particles had a diameter less than 10 mu. An immediate bronchospastic reaction was documented. Antibodies to a human serum albumin (HSA) ash wood conjugate were not significantly increased.     

Occupational asthma caused by palladium.

Occupational exposure to complex platinum salts is a well-known cause of occupational asthma. Although there is evidence that platinum refinery workers may also be sensitized to other precious metals, such as palladium or rhodium, no instances of occupational asthma due to an isolated sensitization to palladium have been reported. A case is reported of occupational rhinoconjunctivitis and asthma in a previously healthy worker exposed to the fumes of an electroplating bath containing palladium. There was no exposure to platinum. Sensitization to palladium was documented by skin-prick tests. The skin-prick test was positive with Pd(NH3)4Cl2, but not with (NH4)2PdCl4. Corresponding salts of platinum were all negative. A bronchial provocation test with Pd(NH3)4Cl2 (0.0001% for a total of 315 s, followed by 0.001% for a total of 210 s) led to an early decrease in forced expiratory volume in one second (-35%). A similar exposure (0.001% for a total of 16 min) in an unrelated asthmatic gave no reaction. This case shows that an isolated sensitization to palladium can occur and that respiratory exposure to palladium is a novel cause of metal-induced occupational asthma.     

Occupational asthma caused by white mushroom.

The commercial growing of white mushroom (Agaricus bisporus) is a frequent activity in certain Spain regions as La Rioja. We report two cases of white mushroom workers suffering from asthma caused by hypersensitivity to basidiocarp and spores of white mushroom.     

Occupational asthma caused by sewer flies

Insect emanations occasionally cause allergic asthma, which not infrequently is due to occupational exposures. This second report of asthma caused by sewer flies, Psychoda alternata, concerns a sewage plant worker who previously had developed immediate-type hypersensitivity to wax moths. Evidence for sewer fly allergy was derived from direct prick and intracutaneous skin tests, Prausnitz-Kustner testing, in vitro leukocyte histamine release, ELISA, and bronchial provocative challenge. The ELISA inhibition tests indicated little cross-reactivity between sewer fly and wax moth extract or midge hemoglobin, but direct skin testing suggested possible hypersensitivity to other families of the order Diptera.     

Occupational asthma caused by a coloring reagent

A case of occupational asthma associated with rhinitis and conjunctivitis occurred in a patient working in a textile factory and exposed to different coloring reagents is reported. Symptoms appeared in phases correlated with changes in the use of the coloring reagents. Prick tests were carried out with the different coloring reagents and were positive for the yellow color. The test was followed by a clear increase in bronchial hyperreactivity to methacholine. Some individual preventive measures, such as wearing a face mask, led to reduction then disappearence of the symptoms.     

Occupational asthma caused by chromium and nickel

We report the case of a 40-year-old woman who developed occupational asthma following exposure to chromium and nickel in the nickel-plating section of a metalworks company. Skin prick tests for specific antibodies proved positive for nickel chloride at a concentration of 1 mg/mL and negative for potassium dichromate. The specific bronchial provocation test confirmed the diagnosis of occupational asthma due to exposure to chromium and nickel. The patient presented a late positive reaction to nickel chloride (0.1 mg/mL) and an immediate positive reaction to a 10 mg/mL solution of potassium dichromate. These results indicate a dual response to nickel and chromium in this patient.     

Occupational asthma caused by chloramines in indoor swimming-pool air.

The first series of three workers who developed occupational asthma following exposure to airborne chloramines in indoor chlorinated swimming pools is reported. Health problems of swimmers in indoor pools have traditionally been attributed to the chlorine in the water. Chlorine reacts with bodily proteins to form chloramines; the most volatile and prevalent in the air above swimming pools is nitrogen trichloride. Two lifeguards and one swimming teacher with symptoms suggestive of occupational asthma kept 2-hourly measurements of peak expiratory flow at home and at work, analysed using the occupational asthma system (OASYS) plotter, and/or had specific bronchial challenge testing to nitrogen trichloride, or a workplace challenge. Air measurement in one of the pools showed the nitrogen trichloride levels to be 0.1-0.57 mg x m(-3), which was similar to other studies. Two workers had peak expiratory flow measurements showing occupational asthma (OASYS-2 scores 2.88 and 3.8), both had a positive specific challenge to nitrogen trichloride at 0.5 mg x m(-3) with negative challenges to chlorine released from sodium hypochlorite. The third worker had a positive workplace challenge. Swimming-pool asthma due to airborne nitrogen trichloride can occur in workers who do not enter the water because of this chloramine. The air above indoor swimming pools therefore needs to be assessed and managed as carefully as the water.     

Occupational asthma due to exposure to African cherry (Makore) wood dust

A 35-year-old man who had been a carpenter and a cabinet worker for over 15 years, was referred to our clinic with a 4-month history of cough, chest tightness and difficulty in breathing which occurred within minutes of exposure to African cherry wood (Makore). He developed a dual asthmatic reaction on specific challenge test with an extract of African cherry wood dust. Thus, the diagnosis of occupational asthma due to exposure to African cherry wood dust was confirmed by the specific challenge test. The mechanism of asthma due to African cherry wood dust exposure is not clear.     

Occupational rhinitis and asthma due to cedroarana (Cedrelinga catenaeformis Ducke) wood dust allergy.

We describe a case of occupational rhinitis and asthma in a 46-year-old carpenter who presented nasal and bronchial symptoms after cedrorana (Cedrelinga catenaeformis Ducke) wood dust exposure. Skin prick tests (SPT) with a battery of common allergens and different kinds of wood, were positive to cedrorana and grass pollen and negative to the other wood extracts. Nasal provocation and exposure challenge tests with Cedrorana wood dust also gave a positive reaction. IgE-immunoblotting showed two bands of 45 and 78 kDa respectively. This is the first reported case of occupational rhinitis and asthma due to Cedrorana wood dust where an IgE mediated mechanism has been found.     

Occupational asthma caused by stainless steel welding fumes: a clinical study.

The aim of the present study was to describe the cases of occupational asthma (OA) due to stainless steel welding fumes diagnosed at the Finnish Institute of Occupational Health during the period 1994-2003. OA was diagnosed according to patient history, lung function examinations and welding challenge tests with measurements of the forced expiratory volume in one second (FEV(1)) and peak expiratory flow (PEF) values. The present series comprised 34 patients, all male, with a mean age of 44.7 yrs (range 22-57), mainly working as welders. The mean duration of exposure was 22.4 yrs, and the mean duration of exposure before the onset of respiratory symptoms was 18 yrs. Dyspnoea was the most frequently reported work-related respiratory symptom. During the inhalation challenge tests, the mode of the asthmatic FEV(1)/PEF reaction was delayed in 16 (47%) patients, immediate in nine (26%) patients and dual (both immediate and delayed) in nine (26%) patients. In the follow-up assessment 6 months later, only six patients were considered able to continue performing welding tasks, whereas occupational injury pension was recommended for seven, and measures of vocational rehabilitation for 14 patients. In most cases, after the diagnosis of occupational asthma, the continuation of welding work was not possible.     

Occupational asthma induced by cephalosporins.

A 20-yr-old pharmaceutical worker who developed attacks of shortness of breath and wheezing 9 months after beginning work on a process in which cefadroxil powder was bottled or encapsulated will be described. Skin test with cefaxodril was negative. Baseline spirometry and methacholine inhalation test were normal. A controlled bronchial challenge test was carried out in a closed-circuit system with assessment of respirable dust concentration. Exposure to cefadroxil powder at a mean concentration of 10 mg x m(-3) for 10 min elicited an isolated immediate asthmatic response, but no response was observed to control challenge with lactose. Single-blind oral challenge test with amoxicillin up to 500 mg was well tolerated, whereas the oral challenge with cephalexin (25 mg) elicited an immediate asthmatic response. This patient had developed occupational asthma caused by inhalation of cefadroxil as confirmed by specific inhalation test. Since she tolerated oral amoxicillin, a synthetic penicillin with the side-chain identical to that of cefadroxil, it seems that she may be sensitized to the dihydrothiazine ring of cephalosporins.     

Occupational asthma caused by a hardener containing an aliphatic and a cycloaliphatic diamine.

An otherwise healthy 44-yr-old man experienced a serious attack of bronchial obstruction after working with resins and hardeners, releasing fumes of a mixture of an alipathic and a cycloaliphatic diamine hardener. Eight hours after deliberate challenge with the hardener a large increase of airway resistance was found. Seventy-two hours after challenge, eosinophilia in the bronchoalveolar lavage (BAL) fluid together with a decrease of peripheral eosinophils was seen. After cessation of contact with this hardener, no more acute episodes occurred, although maintenance treatment with a topical corticosteroid and a beta 2-agonist remained necessary. A BAL performed 1 yr later showed a normal cell distribution. The results suggest that these aliphatic and cycloaliphatic diamine hardeners may be occupational hazards. Eosinophil inflammation may play a causal role.     

Occupational asthma caused by formalin in a hospital milieu. Apropos of 3 cases

Three cases of formalin-induced occupational asthma observed in 2 hospital nurses and 1 hospital medical secretary are reported. The characteristics of this type of occupational asthma which seems to be infrequent, probably because it is often undiagnosed, are described. The prognosis is often severe, even after discontinuation of exposure to the risk. These patients are eligible to disability pensions as compensation for occupational disease.     

Occupational asthma caused by isocyanates: patterns of asthmatic reactions to increasing day-to-day doses.

Inhalation challenges to isocyanates are conducted in specialized centers to confirm occupational asthma. The pattern of asthmatic reactions due to consecutively increasing daily doses of isocyanates is unknown. We conducted a study involving 24 subjects who had undergone specific inhalation challenges to isocyanates (toluene diisocyanate [TDI], n = 8; hexamethylene diisocyanate [HDI], n = 10; and methylene diisocyanate [MDI], n = 6) on three or more consecutive days. Challenge tests were given through a closed-circuit apparatus (n = 12) or in small cubicles (n = 12), allowing assessment of the total inhaled dose (concentration x duration). The pattern of asthmatic reactions was described. In addition, dose-response curves were analyzed and tested for their linear and quadratic trends. Four patterns of response were observed: (1) linear (n = 10); (2) minimal effect followed by a brisk change (n = 7); (3) significant change followed by tachyphylaxis or a plateau (n = 4); (4) biphasic (i.e., significant change followed by a reduction in the effect and significant change on the last day of exposure [n = 3]). Subjects with a linear dose-response pattern had been exposed to isocyanates at work for a significantly shorter interval (7.2 +/- 6.7 yr) than subjects with a nonlinear pattern (20.0 +/- 13.1 yr). An analysis of variance covering a 3-d period for all subjects showed a significant linear model for the response (p < 0.0001); there was no quadratic trend. However, when the analysis was done on subjects with four or more days of challenge (n = 10), we found both linear and quadratic significant components. This analysis shows that the most common pattern of asthmatic reactions to inhaled isocyanates generated on consecutive days is linear; however, other patterns are also observed. In some individuals, particularly those in whom more days of challenge are required, we observed in addition to a strong linear component a quadratic component manifested by a brisk change on the last day of exposure.     

Occupational asthma caused by pyrazolone derivative used in silver halide photographic paper

Occupational asthma has been documented in workers exposed to a wide variety of chemical compounds. Reactive dyes have been described as causing occupational asthma in textile industry workers. We report a case of occupational asthma resulting from exposure to pyrazolone dye used in silver halide photographic paper. There is a need for both further surveys of workers exposed to other reactive dyes and careful preventive measures in the handling of such compounds.     

Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust

Eight asthmatic patients who had no history of asthma before starting work in a hard-metal plant and eight control subjects (three atopic, three nonatopic asthmatic, and two normal volunteers) without a history of exposure to hard metal dust were subjected to provocation tests, skin tests, radioallergosorbent tests (RAST) and Farr test with cobalt. Four of the eight patients were atopic, and seven showed bronchial hyperresponsiveness to methacholine (BHR). Patch and intradermal skin tests with cobalt chloride (CoCl2) could not discriminate the patients from control subjects. All patients had positive reactions to CoCl2 in the provocation tests; two developed immediate asthmatic reaction (IAR), four late asthmatic reaction (LAR), and two dual asthmatic reaction (DAR), while the control subjects showed no reaction. Evidence of specific IgE antibodies to cobalt-conjugated human serum albumin (Co-HSA) was presented by four patients (RAST score greater than 2) based on comparison of serum samples from 60 asthmatic patients and 25 asymptomatic workers in the same plant. Positive serum samples selectively bound 57Co, and the test was blocked by nonlabled cobalt sulfate (CoSO4). These findings suggest the development of hard metal-induced asthma from cobalt sensitivity.