Epidemiological study of hard metal asthma.

Abstract

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 ...

Characterization of exposures among cemented tungsten carbide workers. Part I: Size-fractionated exposures to airborne cobalt and tungsten particles

“…If occupational asthma is caused by exposure to particles with aerodynamic sizes capable of depositing in the tracheobronchial, bronchial, and alveolar regions of the lung and with chemical composition that contains cobalt (alone or in the presence of tungsten carbide), then our air-monitoring results in conjunction with in vitro dissolution test results may help to explain why cases of occupational asthma are observed among workers who handle pre-sintered hard metal powders and grind and manipulate sintered CTC parts (Davison et al, 1983;Sprince et al 1988;Meyer-Bisch et al, 1989;Shirakawa et al, 1989;Kusaka et al, 1996) and among diamond polishers whose only exposure is to cobalt (Gheysens et al, 1985). Consistent with these studies, we observed exposures to cobalt in all work areas spanning powder production to handling finished product parts.…”

“…Inhalation of dusts generated during the production of CTC is associated with the development of occupational asthma, hard metal lung disease (HMD), and lung cancer. Workplace studies have identified cases of occupational asthma among CTC workers exposed to both cobalt and tungsten (Davison et al, 1983;Sprince et al 1988;Meyer-Bisch et al, 1989;Shirakawa et al, 1989;Kusaka et al, 1996) and diamond polishers exposed to cobalt alone (Gheysens et al, 1985). Cases of HMD have been reported among workers in all phases of CTC production (Bech et al, 1962;Coates and Watson, 1971;Sjo¨gren et al, 1980;Davison et al, 1983;Sprince et al, 1984Sprince et al, , 1988Meyer-Bisch et al, 1989;Cugell et al, 1990;Figueroa et al, 1992;Fischbein et al, 1992), which may be due to exposures to tungsten carbide particles in association with cobalt particles (Lasfargues et al, 1992(Lasfargues et al, , 1995Lison and Lauwerys, 1990, 1994, 1995Lison et al, , 1996.…”

Mechanisms of immunosensitization to metals (IUPAC Technical Report)

“…Type I hypersensitivity mediated by IgE is suggested. More recently, 2.0 % of 700 workers producing hard metal tools had cobalt-specific IgE antibodies and symptoms of asthma [42]. However, the same investigators subjected eight patients with hard metal asthma to bronchial provocation challenge with NiSO 4 [43].…”

Oxidative Damage Modeling by Biomonitoring of Exposure to Metals for Manual Metal Arc Welders

“…Cadmium, chromium, lead, nickel, magnesium, and other metals are commonly detectable in welding exposure; stainless steel welding mostly contain chromium fume (6,7). Metals can induce different diseases such as chronic obstructive pulmonary disease (8), bronchitis (9), metal fume fever (10), cancer (11), and dermatitis (12). Exposure to fumes increases the risk of lung cancer.…”