Shortly after the end of the First World War, while doing research to find a material able to replace diamond in metal-drawing nozzles, Karl Schoeter patented in Berlin a sintering process (pressurization plus heating at 1,500°C) of a mixture of fine tungsten carbide (WC) powder with 10% of cobalt to produce “hard metal”. The main characteristics of this sinter are the extreme hardness, only slightly inferior to that of diamond, and the maintenance of its mechanical properties at high temperatures; these characteristics make it suitable for use in drawing metal, for welded inserts, and for high-speed tools for machining of metals, stone, wood and materials with high resistance to wear or to heat, in the mechanical, aeronautical and ballistic fields. The use of hard metal is continually expanding all over the world. In 1927 Krupp extended the use of hard metal into the cutting tools field, calling it “Widia” (wie Diamant—like diamond), a name still in use today.
Sintering remains the basis of all hard metal production: techniques are improved by the introduction of other metallic carbides—titanium carbide (TiC) and tantalum carbide (TaC)—and by treatment of hard metal parts for mobile cutting inserts with one or more layers of titanium nitride or aluminium oxide and of other very hard compounds applied with chemical vapour deposition (CVD) or physical vapour deposition (PVD). The fixed inserts welded to the tools cannot be plated, but are repeatedly sharpened by a diamond grinding wheel (figures 1 and 2).
Figure 1. (A) Examples of some hard metal drawing mobile inserts, plated with golden-yellow tungsten nitride; (B) insert welded to the tool and working in steel drawing.
The hard metal sinter is formed by particles of metallic carbides incorporated in a matrix formed by cobalt, which melts during sintering, interacting and occupying the interstices. Cobalt is therefore the structure gluing material, which assumes metal-ceramic characteristics (figures 3, 4, and 5).
Figure 4. Microstructure of a WC + TiC + TaC + Co sintering. Along with WC prismatic particles, globular particles formed by a solid solution of TiC + TaC are observed. The light matrix is formed by Co (1,500x).
The sintering process uses very fine metallic carbide powders (average diameters from 1 to 9μm) and cobalt powders (average diameter from 1 to 4μm) which are mixed, treated with paraffin solution, die-pressed, de-waxed at low temperature, pre-sintered at 700 to 750°C and sintered at 1,500°C (Brookes 1992).
When sintering is done with inadequate methods, improper techniques and poor industrial hygiene, the powders can pollute the atmosphere of the work environment: workers are therefore exposed to the risk of inhalation of metallic carbide powders and cobalt powders. Along with the primary process there are other activities which can expose the workers to the risk of aerosol inhalation of hard metal. Sharpening of fixed inserts welded to tools is normally carried out by dry diamond grinding or, more frequently, cooled with liquids of different kinds, producing powders or mists formed by very small drops containing metallic particles. Particles of hard metal are also used in the production of a high-resistance layer on steel surfaces subjected to wear, applied through methods (plasma coating process and others) based on the combination of a powder spray with an electric arc or a controlled explosion of a gas mixture at high temperature. The electric arc or the explosive flow of the gas determines the fusion of the metallic particles and their impact on the surface being plated.
First observations on “hard metal diseases” were described in Germany in the 1940s. They reported a diffuse, progressive pulmonary fibrosis, called Hartmetallungenfibrose. During the next 20 years parallel cases were observed and described in all industrial countries. The workers affected were in the majority of cases in charge of the sintering. From 1970 to the present, several studies indicate that the pathology to the breathing apparatus is caused by the inhalation of hard metal particles. It affects only susceptible subjects, and consists of the following symptoms:
- acute: rhinitis, asthma
- subacute: fibrosant alveolitis
- chronic: diffuse and progressive interstitial fibrosis.
It affects not only workers in charge of sintering, but anyone inhaling aerosol containing hard metal and particularly cobalt. It is mainly and perhaps exclusively caused by cobalt.
The definition of hard metal disease now includes a group of pathologies of the breathing apparatus, different from each other in clinical gravity and prognosis, but having in common a variable individual reactivity to the aetiological factor, cobalt.
More recent epidemiological and experimental information agree on the causal role of cobalt for acute symptoms in the upper respiratory tract (rhinitis, asthma) and for subacute and chronic symptoms in the bronchial parenchyma (fibrosing alveolitis and chronic interstitial fibrosis).
The pathogenic mechanism is based on the induction by Co of a hypersensitive immunoreaction: in fact, only some of the subjects present pathologies after short exposures to relatively low concentration, or even after longer and more intense exposures. Co concentrations in biological samples (blood, urine, skin) are not significantly different in those who have the pathology and those who do not; there is no correlation of dose and response at the tissue level; specific antibodies have been individuated (immunoglobins IgE and IgG) against a Co-albumin compound in asthmatics, and the Co patch test is positive in the subjects with alveolitis or fibrosis; the cytological aspects of the giant-cellular alveolitis are compatible with immunoreaction, and acute or subacute symptoms tend to regress when the subjects are removed from exposure to Co (Parkes 1994).
The immunological basis of hypersensitivity to Co has not yet been satisfactorily explained; it is not possible, therefore, to identify a reliable marker of individual susceptibility.
Identical pathologies to those found in the subjects exposed to hard metals were also observed in diamond cutters, who use disks formed by microdiamonds cemented with Co and who therefore inhale only Co and diamond particles.
It is not yet fully demonstrated that pure Co (all other inhaled particles excluded) is capable alone of producing the pathologies and above all the diffused interstitial fibrosis: the particles inhaled with Co could have a synergistic as well as modulating effect. Experimental studies seem to demonstrate that the biological reactivity to a mixture of Co particles and of tungsten is stronger than that caused by Co alone, and significant pathologies are not to be observed in the workers in charge of the production of pure Co powder (Science of the Total Environment 1994).
Clinical symptoms of hard metal disease, which, on the basis of current aetiopathogenic knowledge should be more precisely called “cobalt disease”, are, as mentioned before, acute, subacute and chronic.
Acute symptoms include a specific respiratory irritation (rhinitis, laryngo-tracheitis, pulmonary oedema) caused by exposure to high concentrations of Co powder or Co smoke; they are observable only in exceptional cases. Asthma is observed more frequently. It appears in 5 to 10% of the workers exposed to cobalt concentrations of 0.05 mg/m3, the current US threshold limit value (TLV). Symptoms of thoracic constriction with dyspnoea and cough tend to appear at the end of the work shift or during the night. The diagnosis of occupational allergic bronchial asthma due to cobalt can be suspected on the basis of case history criteria, but it is confirmed by a specific bronchial stimulation test which determines the appearance of an immediate, delayed or dual bronchospastic response. Even respiratory capacity tests carried out at the beginning and at the end of the work shift can help the diagnosis. Asthmatic symptoms due to cobalt tend to disappear when the subject is removed from exposure, but, similarly to all other forms of occupational allergic asthma, symptoms can become chronic and irreversible when the exposure continues for a long time (years), despite the presence of respiratory disturbances. Highly bronchoreactive subjects can present non-allergic aetiological asthmatic symptoms, with a non-specific response to inhalation of cobalt and other irritating powders. In a high percentage of cases with allergic bronchial asthma, specific reaction towards a human Co-seroalbumin compound was found in the IgE serum. The radiological finding does not vary: only in rare cases can mixed forms of asthma plus alveolitis with radiological alteration specifically caused by alveolitis be found. Bronchodilator therapy, along with an immediate end of the work exposure, leads to complete recovery for cases that are of recent onset, not yet chronic.
Subacute and chronic symptoms include fibrosant alveolitis and chronic diffuse and progressive interstitial fibrosis (DIPF). The clinical experience seems to indicate that the transition from alveolitis to interstitial fibrosis is a process which evolves gradually and slowly in time: one can find cases of pure initial alveolitis reversible with withdrawal from the exposure plus corticosteroid therapy; or cases with an already present fibrosis component, which can improve but not reach complete recovery by removing the subject from exposure, even with additional therapy; and finally, cases in which the predominant situation is that of an irreversible DIPF. The occurrence of such cases is low in the exposed workers, very much lower than the percentage of allergic asthma cases.
Alveolitis is easy to study today in its cytological components through broncho-alveolar lavage (BAL); it is characterized by a large increase of the total cell number, mainly formed by macrophages, with numerous multinuclear giant cells and the typical aspect of foreign-body giant cells containing at times cytoplasmic cells (figure 6); even an absolute or relative increase of lymphocytes is frequent, with a decreased CD4/CD8 ratio, associated with a large increase of eosinophiles and mast cells. Rarely, alveolitis is mainly lymphocytic, with CD4/CD8 ratio inverted, as it occurs in the pneumopathies due to hypersensitivity.
Figure 6. Cytological BAL in a macrophagic mono-nuclear giant-cellular alveolitis case caused by hard metal. Between the mononuclear macrophages and the lymphocyte, a giant foreign-body type of cell (400x) is observed.
Subjects with alveolitis report dyspnoea linked with fatigue, loss of weight and dry cough. Crepitation is present in the lower lung with functional alteration of a restrictive kind and diffused round or irregular radiological opacity. The patch test for cobalt is positive in the majority of cases. In the susceptible subjects, alveolitis is revealed after a relatively short period of workplace exposure, of one or a few years. In its initial phases this form is reversible up to complete recovery with the simple removal from exposure, with better results if this is combined with cortisone therapy.
The development of diffuse interstitial fibrosis aggravates the clinical symptoms with a worsening of the dyspnoea, which appears even after minimal strain and then even at rest, with worsening of the restrictive ventilatory impairment which is linked to a reduction of the capillary-alveolar diffusion, and with appearance of radiographic opacities of a linear type and of honeycombing (figure 7). The histological situation is that of a fibrosing alveolitis of a “mural type”.
Figure 7. Thoracic radiograph of a subject affected by interstitial fibrosis caused by hard metal. Linear and diffused opacity and honeycombing aspects are observed.
The evolution is rapidly progressive; therapies are ineffective and the prognosis doubtful. One of the cases diagnosed by the author eventually required a lung transplant.
The occupational diagnosis is based on case history, BAL cytological pattern and cobalt patch test.
Prevention of hard metal disease, or, more precisely, of cobalt disease, is now mainly technical: protecting the workers through the elimination of powder, smokes or mists with adequate ventilation of the work areas. In fact, the lack of knowledge about the factors which determine individual hypersensitivity to cobalt makes the identification of susceptible people impossible, and the maximum effort must be made to reduce the atmospheric concentrations.
The number of people at risk is underestimated because many sharpening activities are carried out in small industries or by craftspeople. In such workplaces, the US TLV of 0.05 mg/m3 is frequently exceeded. There is also some question as to the adequacy of the TLV for protecting workers against cobalt disease since dose-effect relationships for disease mechanisms involving hypersensitivity are not completely understood.
Routine surveillance must be accurate enough to identify cobalt pathologies in their earliest stages. An annual questionnaire aimed mainly at temporary symptoms must be administered, along with a medical examination that includes pulmonary function testing and other appropriate medical examinations. Since it has been demonstrated that there is a good correlation between cobalt concentrations in the work environment and the urinary excretion of the metal, it is appropriate to carry out semi-annual measurement of cobalt in urine (CoU) on samples taken at the end of the work week. When the exposure is at the level of the TLV, the biological exposure index (BEI) is estimated to be equal to 30μg Co/litre urine.
Pre-exposure medical examinations for the presence of pre-existing respiratory disease and bronchial hypersensitivity can be useful in the counselling and placement of workers. Metacholine tests are a useful indicator of non-specific bronchial hyperreactivity and may be useful in some settings.
International standardization of environmental and medical surveillance methods for workers exposed to cobalt is highly recommended.