Occupational asthma due to manual metal-arc welding of special stainless steels.

Occupational asthma (OA) can be induced by fumes of manual metal-arc welding on stainless steel. In recent years, the use of special stainless steels (SSS) with high chromium content has increased. This study presents two cases of OA caused by manual metal-arc welding on SSS. In both cases, the diagnosis of OA was based on respiratory symptoms, occupational exposure and positive findings in the specific challenge tests. In the first case, a 46-yr-old welder had experienced severe dyspnoea while welding SSS (SMO steel), but not in other situations. Challenge tests with both mild steel and stainless steel using a common electrode were negative. Welding SSS with a special electrode caused a delayed 37% drop in forced expiratory volume in one second (FEV1). In the second case, a 34-yr-old male had started to experience dyspnoea during the past few years, while welding especially SSS (Duplex steel). The workplace peak expiratory flow monitoring was suggestive of OA. Challenge tests with both mild steel and stainless steel using a common electrode did not cause bronchial obstruction. Welding SSS with a special electrode caused a delayed 31% drop in FEV1. In conclusion, exposure to manual metal-arc welding fumes of special stainless steel should be considered as a new cause of occupational asthma.     

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 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 due to fumes of galvanized metal

Two solderers exposed to fumes of galvanized metal reported a history of shortness of breath and fever which occurred during the evening and night of days spent at work. Specific inhalation challenges performed by asking subjects to do soldering on galvanized iron revealed a late bronchospastic reaction. One subject also demonstrated a significant increase in oral temperature and peripheral neutrophils. Environmental measurements revealed the presence of zinc after soldering on galvanized metal. This contaminant was not present after a control exposure while soldering on iron. Although metal fume fever has been described in workers exposed to fumes of galvanized metal, this is the first account of occupational asthma due to this agent.     

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 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 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 Ipe (Tabebuia spp) dust.

BACKGROUND: Ipe is a resistant hardwood that contains naphtoquinones. It is easily found and frequently used in South and Central America. Naphtoquinones are skin sensitizers. OBJECTIVE: To describe a case of occupational asthma related to Ipe wood dust. METHODS: The patient was submitted to a clinical evaluation consisting of a respiratory symptom questionnaire, occupational history, serial measurements of lung function by spirometry, skin prick tests, patch tests, specific IgE and specific bronchial provocation tests to Ipe dust. RESULTS: Serial lung function measurements showed sustained regression of obstruction following removal from exposure. Skin prick tests, but not patch tests, were positive to Ipe, and a specific bronchial challenge showed a late asthmatic reaction. Specific IgE search was negative. CONCLUSIONS: Exposure to Ipe wood dust can lead to occupational asthma. The underlying mechanism should be investigated.     

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: a case of Baker's asthma.

Asthma is one of the most prominent respiratory diseases worldwide. It is defined by airflow limitation and/or airway hyperresponsiveness and can be exacerbated by a number of environmental allergens. When allergic asthma exacerbations are attributed to stimuli in a particular work environment, then occupational asthma must be considered. Incidence estimates vary, but in 1999 the Surveillance of Work-Related and Occupational Respiratory Disease in the United Kingdom estimated 4293 incident cases of occupational respiratory disease, an increase of 1427 cases over the previous year. Occupational asthma represented 26% of these cases. Baker's asthma is one of the most frequently reported types of occupational asthma in several countries. Diagniostic steps include thorough history, careful exam, and demonstration of functional reversible airflow obstruction. Treatment modalities used for occupational asthma are similar to those used in the management of other forms of asthma, with particular attention to reducing the level of exposure to the inciting allergen.     

Occupational asthma: a practical approach.

Although evaluation of possible occupational asthma may be complex, it can be pursued systematically by first assessing whether asthma is present, and then determining whether asthma is caused or triggered by the workplace or by alternative or confounding nonoccupational explanations. A detailed history is of great importance in raising suspicion of occupational asthma, but studies have shown that even detailed histories obtained by experienced specialists can lead to inaccurate conclusions about the presence or absence of occupational asthma. Consequently, objective measurements should be performed to establish the diagnosis of occupational asthma whenever possible. If the patient is still working in the workplace, work-related changes in spirometry or peak flow measurements can confirm the diagnosis. For occupational asthma from some airborne sensitizers, immediate-type skin testing or in vitro tests for specific IgE may establish sensitization. However, there is evidence that for some isocyanates, in vitro tests for specific IgG serum antibody levels correlate better with documented bronchospasm from isocyanate exposure, even though the IgG antibody is not thought to be pathogenic. Controlled, specific inhalation tests may be valuable, but they should be performed only under experienced medical supervision. Intervention should be focused on reducing or avoiding harmful workplace exposures so that permanent lung impairment and need for chronic medical treatment are avoided. Assessment of permanent impairment/disability from occupational asthma optimally should be determined 2 years after the removal from occupational exposure, when improvement has been shown to plateau and the patient will likely have reached maximal medical improvement.     

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 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 hypersensitivity pneumonitis in a smelter exposed to zinc fumes.

A smelter exposed to zinc fumes reported severe recurrent episodes of cough, dyspnea and fever. Bronchoalveolar lavage showed a marked increase in lymphocytes count with predominance of CD8 T-lymphocytes. Presence of zinc in alveolar macrophages was assessed by analytic transmission electron microscopy. This is the first case of recurrent bronchoalveolitis related to zinc exposure in which the clinical picture and BAL results indicate a probable hypersensitivity pneumonitis.     

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.     

Meningitis caused by streptococci other than Streptococcus pneumoniae: a retrospective clinical study.

We reviewed the medical records of 26 patients (median age 62 years, range 5-76 years) admitted to our institution during 1978-98 with acute bacterial meningitis (ABM) caused by streptococci other than Streptococcus pneumoniae (comprising 1.9% of all patients with ABM). 19 cases were community-acquired and 7 were nosocomial. 73% had comorbid or predisposing conditions and 73% had an identifiable extracerebral focus; only in 2 patients no comorbid disease, primary focus or predisposing condition was present. Five patients had cerebral abscesses, and 5 had endocarditis. Beta-haemolytic streptococci were grown in 14 cases (serotype A: 4, B: 5, C: 1, G: 4) and were predominant among patients with endocarditis, whereas alpha- or non-haemolytic strains grew in 12 cases (S. mitis: 4, S. constellatus: 2, E. faecalis: 2, S. bovis: 1, unspecified: 3) and were predominant in patients with a brain abscess. Staphylococcus aureus grew together with a streptococcus in 2 cases. Blood culture was positive in 9 cases (35%). Neurologic complications occurred in 11 patients (42%) and extraneurologic complications in 18 patients (69%). Adverse outcomes occurred in 10 patients (38%), including 3 patients who died. Occurrence of seizures at any time of disease was significantly associated with an adverse outcome; no other clinical or paraclinical features appeared to affect outcome.