Objectives-To elucidate factors contributing to hard metal asthma, the entire workforce of a corporation producing hard metal tools (n = 703) was examined. Methods-The variables evaluated were the atopy reflected by immunoglobulin E (IgE) antibody against mite allergen, history of exposure to hard metal, smoking, concentration of airborne cobalt, specific IgE antibody reaction against cobalt, and the respiratory symptom of attacks of reversible dyspnoea with wheeze (asthmatic symptoms). Results-Univariate analysis showed that the prevalence ofthe asthmatic symptoms was significantly higher in formerly and currently exposed male workers than in non-exposed male workers. Positive IgE reaction against cobalt was found in seven men (2.0%), all of whom had asthmatic symptoms. Furthermore, it was found that atopy, positive IgE antibody against cobalt, and age of 40 or older were significantly correlated with asthmatic symptoms. Multilogistic analysis on the same factors and smoking in all of the workers showed that the age, experience of hard metal exposure, and atopy were significant risk factors associated with the asthmatic symptoms. Multilogistic analysis of data for currently exposed and nonexposed workers also showed that age and atopy were risk factors, and that the exposure to cobalt at the low concentration (at or below 50 ,g/in' ) but not at the higher concentration was a significant risk factor. Exposure to mist of coolants containing ionic cobalt, used during grinding, was not found to be any more hazardous in terms of onset of asthmatic symptoms than exposure to hard metal dust containing metallic cobalt. Conclusions-Accordingly, it is concluded that both environmental factors and individual susceptibility should be taken into consideration in efforts to reduce the prevalence of hard metal asthma. (Occup Environ Med 1996;53:188-193) Keywords: hard metal, asthma, cobalt Exposure to hard metal is known to cause interstitial pneumonia, pulmonary fibrosis, and asthma (hard metal asthma) among workers.1-4 Moreover, we have also found evidence of type I hypersensitivity mediated by specific immunoglobulin E (IgE) antibody against cobalt conjugated to human serum albumin (IgE-Co) in some cases of hard metal asthma.5Coates et al first reported the prevalence of occupational asthma (0 6%) at an American hard metal plant.3 We subsequently reported that the prevalence of hard metal asthma diagnosed by clinical and physiological findings was 5-6% at a Japanese hard metal plant.4 After that cross sectional study, the cumulative incidence of hard metal asthma found during a nine year prospective study (1981-9) was 3T6% (9/241) in newly recruited workers.6Studies of asthma at French hard metal plants,7 chest tightness at a Swedish hard metal plant,8 and work related wheeze at American hard metal corporations have also been compared with concentrations of airborne cobalt.9As well as hard metal asthma, there were reports of cases of asthma related to cobalt among diamond polishing workers in Belgium whose work ...
Objectives-To study individual effects on pulmonary function of exposure to hard metal including cobalt. Methods-All of the workers in a hard metal company (583 men and 120 women) were examined for smoking, respiratory symptoms, ventilatory function, occupational history of exposure to hard metal, and present exposure to airborne cobalt. The ventilatory function indices (forced vital capacity (FVC), forced expiratory volume in one second (FEV1), forced expiratory volume in one second per cent (FEV6%), peak expiratory flow (PEF), mid-maximal flow (MMF), forced expiratory flow at 50% vital capacity (Vso), forced expiratory flow at 25% vital capacity (425)) were standardised for height and age and expressed as a percentage of predicted values. Results-Two way analysis of variance of indices of ventilatory function showed that an interaction of hard metal exposure and smoking decreased %V50 for both men and women. Among the currently exposed men, those with asthmatic symptoms (defined as reversible dispnoea with wheeze) had significantly lower %FVC5 %FEV1%, %PEF5 %/MMF, %WV50 and %V25 than did workers without asthma. The ventilatory disfunction did not differ between exposed and nonexposed workers with asthmatic symptoms. Even among the men without asthmatic symptoms, %V50 was significantly lowered by the interaction of hard metal exposure and smoking. The multilinear regression analysis of indices of ventilatory function for all of the subjects on sex, smoking (Brinkman index), exposure to hard metal, and asthmatic symptoms showed that asthmatic symptoms and smoking had significant effects on all variables and that the decrease in %V25 was associated with hard metal exposure. In the currently exposed and non-exposed workers, multilinear regression analysis applying indices for cobalt exposure (mean cobalt concentration, duration of exposure, and cumulative dose) showed that not only asthmatic symptoms or smoking but also duration of exposure had significant decreasing effects on %FVC, %MMF, and %V2-5Conclusions--Occupational exposure to hard metal probably causes impairment of ventilatory fiction in a dose dependent manner.
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