Respiratory diseases in hard metal workers: an occupational hygiene study in a factory (original) (raw)

Respiratory health of cobalt production workers

American Journal of Industrial Medicine, 2003

BackgroundCobalt production workers are exposed to metallic cobalt and nickel and their compounds and to different irritant gases. The aim of our study was to determine whether long‐term exposure is associated with an increased occurrence of respiratory symptoms and findings or diseases, other than asthma, which is a known hazard, among cobalt processing workers.MethodsThe study population was comprised of 110 current and former cobalt workers who had worked more than 10 years in a cobalt plant. The reference group consisted of 140 unexposed workers. All the participants were men. The analysis was based on exposure history, pulmonary function, chest X‐ray findings, and symptom questionnaires.ResultsSymptoms of asthma based on questionnaire responses were statistically more prevalent among the exposed workers. The respiratory flow rates MEF25 and MEF50, which refer to smaller airways, were significantly lower among the smoking exposed workers than among the smoking unexposed workers....

Evaluation of workers exposed to dust containing hard metals and aluminum oxide

American Journal of Industrial Medicine, 1998

Background Fourteen workers exposed to hard metals and aluminum oxide were evaluated. Methods Six heavily exposed workers underwent bronchoscopy and bronchoalveolar lavage, and five workers underwent transbronchial biopsy. Results Microchemical analysis of transbronchial biopsies showed a high lung burden of exogenous particles, especially metals related to their hard metals exposure. Lung tissue and cellular changes, which were associated with exposure to hard metal and aluminum oxide, corresponded well with the microanalytic test results. Conclusions Three workers had at biopsy diffuse interstitial inflammatory changes: two of them were asymptomatic with normal chest X-ray films, and one had clinically evident disease with severe giant cell inflammation. Two other workers showed focal inflammation. The worker showing clinical disease and one asymptomatic worker with interstitial inflammatory changes had elevated bronchoalveolar lavage fluid-eosinophilia counts. These two were father (with clinical disease) and son (asymptomatic). Am.

Metal-induced asthma and chest X-ray changes in welders

International Journal of Occupational Medicine and Environmental Health, 2012

The aim of this study was to evaluate the coexisting factors and usefulness of diagnostic methods in metal-induced asthma in Polish welders. Materials and Methods: Examination of 50 welders occupationally exposed to metals and with suspicion of metal-induced asthma (group A), 100 welders occupationally exposed to metals but without suspicion of metal-induced asthma (group B), and two control groups (10 patients with atopic asthma and 10 healthy subjects) was carried out. Questionnaire survey, clinical examination, skin prick tests to common aeroallergens and metal salts, rest spirometry tests, X-ray, metacholine challenge and a single-blind, placebo controlled specific inhalation challenge tests with metals (or work-like conditions challenge tests) were performed. Results: In group A-in 9 cases we obtained positive results of specific inhalation challenge tests with metals (in 3 cases with nickel, in 4 cases with chromium, in 1 case with cobalt and in 1 case with manganese). Nine cases of metal-induced occupational asthma were recognized. In group B-only in one case we obtained positive results of work-like conditions challenge test (clinical and spirometry changes, eosinophil influx in induced sputum), which confirmed the diagnosis of occupational asthma. In most of examined welders (62%), pulmonary changes in chest X-ray images were noted. The statistical analysis revealed that working as a welder for more than 10 years is the coexisting factor of presence of chest X-ray changes (p-or q-type nodular changes or interstitial changes). Positive results of skin prick tests with metal salts were the coexisting factors of occupational asthma due to metals among examined group of welders. Conclusions: Specific inhalation challenge plays the key role in diagnostics of metal-induced asthma in welders. Pulmonary changes in chest X-ray were found in a significant percentage of examined welders.

Clinical findings among hard metal workers

Occupational and Environmental Medicine, 1992

In 1940, the first report appeared describing a pulmonary disorder associated with occupational exposures in the cemented tungsten carbide industry. The disease, known as "hard metal disease," has subsequently been characterised in detail and comprises a wide range of clinical signs and symptoms. In this report, clinical findings in a group of 41 hard metal workers employed until recently are described. A high prevalence ofrespiratory symptoms was found. Thirteen workers (31%) had abnormal chest radiographs indicative of interstitial lung disease. Fifty per cent of these had been employed in hard metal manufacturing for less than 10 years. Abnormalities of pulmonary function were also frequent and included a restrictive pattern of impairment and decrease in diffusing capacity (27%). Associations were found between diffusing capacity, chest radiographic abnormalities and right ventricular ejection fraction at exercise indicating cardiopulmonary effects. The findings show the continuous need to control excessive occupational exposures to prevent hard metal disease, the history of which now enters its sixth decade. During the first decades of this century, a metallurgical process was developed for the production of hard metals. These are typically alloys of tungsten carbide, titanium carbide, and cobalt. Occasionally,

Decreased ventilatory function in hard metal workers

Occupational and Environmental Medicine, 1996

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 %V2-5 Conclusions-Occupational exposure to hard metal probably causes impairment of ventilatory fiction in a dose dependent manner.

Experimental research into the pathogenesis of cobalt/hard metal lung disease

European Respiratory Journal, 1996

In recent years clinical, epidemiological and experimental evidence has accumulated indicating that cobalt metal particles, when inhaled in association with other agents such as metallic carbides (hard metals) or diamond dust, may produce an interstitial lung disease termed "hard metal disease" or "cobalt lung". This article summarizes the progress accomplished in our two laboratories to understand the pathogenesis of this disease. Gaps and weaknesses in our current knowledge have also been highlighted in order to suggest potential avenues for further research. Whilst animal models have proved useful for the demonstration of the toxic synergy between cobalt and carbides (e.g. tungsten carbide), most animal models have remained descriptive and have not provided information on the mechanism for this synergy. In particular, the bizarre multinucleated giant cells which are an important hallmark of the human disease, have not been reproduced consistently in experimental animals. Since cobalt is a known sensitizer, there may also be a need to develop experimental models to test the possible involvement of immunological mechanisms in the pathogenesis of the interstitial disease. In vitro systems including macrophage cell cultures and physico-chemical tests have been useful to investigate the mechanism underlying the toxic synergy.

Lung Function Changes in Workers Exposed to Cobalt Compounds

American Journal of Respiratory and Critical Care Medicine, 2004

The objective of the study was to examine the influence of cobalt exposure on lung function changes in workers from a cobaltproducing plant in a health monitoring program implemented between 1988 and 2001. A total of 122 male workers with at least 4 (median ϭ 6) lung function tests (FEV 1 and FVC) during the followup period were assessed longitudinally. Cobalt exposure significantly decreased over the follow-up period, as reflected by the measurements in air and urine. The possible association of spirometric changes with cobalt exposure was examined by a random coefficients model, taking into account other potential influential variables, such as smoking, age, previous respiratory illness, exposure to other lung toxicants, or the presence of glutamate in position 69 in the HLA-DP ␤-chain, an HLA polymorphism possibly associated with hard-metalinduced lung diseases. The main finding of the follow-up study was that cobalt exposure contributed to a decline in FEV 1 over time, and only in association with smoking. No influence of glutamate in position 69 in the HLA-DP ␤-chain polymorphism was detected. Although the amplitude of the additional FEV 1 decrement associated with smoking exposure was relatively small (Ͻ 20%) compared with the expected decline in a non-cobalt-exposed smoker, the results indicate that further efforts to reduce cobalt exposure and to encourage workers to quit smoking are still warranted.

Effect of hard metal dust on ventilatory function

Occupational and Environmental Medicine, 1986

The effect of hard metal dust generated in shaping on ventilatory function has been studied, in particular, the relation between levels of exposure to cobalt and changes in ventilatory function. In 15 healthy young men a significant decrease in FVC occurred after a six hour exposure to hard metal dust containing cobalt at a mean concentration of 38 pg/m3 (range 14-76 pg/m3). No dose-effect relation could be discerned between the decrease in FVC and the hard metal concentration or the cobalt concentration. All the subjects complained of irritation of the airways. On the