Editorials

Respiratory Diseases from Hard Metal or Cobalt Exposure: Solving the Enigma

Mono-component adsorption of Co²⁺ ions from simulated industrial water was investigated by using cow bone (CB), cow bone char (CBC), and activated cow bone carbon (ACBC) adsorbents synthesized from raw cow bone as the precursor. The resulting prepared adsorbent materials were then characterized using analytical methods such as: zeta potential measurements, BET surface area, FTIR, SEM, EDS, and XRD analysis. For all synthesized adsorbents, the main compositions were mesopores with the presence of CC, PO₃²⁻, CO₃² and O-H bonds signifying hydroxyapatite nature of the adsorbents. The isoelectric point (pH_IEP) of ACBC was obtained to be 3.59 (lowest among the prepared adsorbents) thereby signifying that ACBC's electrostatic force of attraction was relatively higher between the Co²⁺ and its surface. The study showed that the pseudo second-order kinetic model had the best correlation for all the adsorption kinetic experimental data for each prepared adsorbent, inferring that the rate-controlling step during the Co²⁺ ions adsorption onto the prepared adsorbents is chemisorption. The Sips isotherm model excellently predicted the adsorption data for the adsorption of Co²⁺ ions on the CB adsorbents while the Langmuir isotherm best fitted the equilibrium data of the CBC, and ACBC prepared adsorbents with excellent correlation coefficients, while maximum adsorption capacities, q_max, were obtained to be 52.50, 58.80, and 64.50 mg g⁻¹ for CB, CBC, and ACBC respectively. The study of the thermodynamic properties of the adsorption of Co²⁺ showed the process was endothermic, non-spontaneous and endogenic for the ACBC adsorbent, while being exothermic for the CB, and CBC adsorbents in addition to having physisorption properties.

Chronic inhalation of hard metal particles can produce an interstitial lung disease (hard metal disease). Recent studies on rats and on isolated alveolar and peritoneal macrophages have demonstrated that this disorder can be explained by an interaction between cobalt metal (Co) and tungsten carbide (WC) particles, which represent the main constituents of hard metal. The exact mechanism of this interaction is still undefined. The present study was undertaken to assess in vitro whether a similar interaction also occurs between cobalt and other metallic carbide particles which may also be incorporated in hard metals depending on the desired applications. When tested separately, Co and metallic carbide particles did not affect the cell integrity. In contrast, TiC, NbC and Cr₃C₂ exerted a synergistic effect with Co (interactive carbides) while TaC, Mo₂C and SiC did not (non-interactive carbides). The interaction did not simply result from an increased cobalt bioavailability since cobalt uptake by the macrophages was increased 4–7-fold in the presence of interactive as well as non-interactive carbides. The interactive effect appeared dependent on the size of the carbide particles, which suggests that a physicochemical reaction taking place at the interface between certain carbides and cobalt particles may be responsible for the toxicity of the Co-carbide mixture. Other non-carbide particles (Fe, diamond, crystalline silica) did not produce a similar interaction with cobalt. This observation may contribute to the better delineation of the pathogenesis of hard metal disease.

The occurence of interstitial lung disease similar to hard metal lung disease in diamond polishers who had been exposed to cobalt (in the absence of tungsten carbide) through the use of polishing disks containing microdiamonds sintered with cobalt, led us to experimentally test the hypothesis that cobalt has pro-oxidant activity in lung tissue. Several experiments were carried out in which we measured indices of oxidant stress, mainly changes in the oxidation state of glutathione and in the activity of the pentose phosphate pathway, upon exposure of hamster pulmonary tissue to CoCl₂ in vivo by intratracheal instillation, or in vitro by incubating lung slices. These experiments indicated that cobalt ions are capable of causing thiol oxidation in lung tissue as an early manifestation of oxidant stress, but more studies are needed to establish the relevance of this mechanism in the causation of lung disease in subjects exposed to cobalt-containing dusts.

Eight hard metal workers exposed to cobalt containing dust (four producers of stone-cutting cobalt-diamond wheels and four grinders of hard metal tools) and affected by interstitial lung fibrosis have been examined. A close relationship between cobalt exposure and clinical findings was observed in six patients who were still working. The clinical picture ranged from minor symptoms to manifestations resembling those of hypersensitivity pneumonitis, with fever, weightloss, non-productive cough and dyspnea. A restrictive impairment of the ventilatory function was prevalent. The chest roentgenogram of one patient showed a diffuse reticular nodular pattern, while the others presented a mild reticular accentuation of the interstitium. In five patients, bioptic specimens of the lung parenchima showed interstitial collagenic fibrosis with inflammatory cells infiltrating the alveolar septa. An increased number of lymphocytes and polymorphs was reported in the bronchoalveolar lavage (BAL) fluid from seven patients. Giant multinucleated cells were present in the BAL of four subjects while an inversion of the helper-suppressor ratio was evident in those patients who were still exposed to cobalt when BAL was performed. In this study, the causal role of metallic cobalt inhalation in the etiology of the lung disease is examined and discussed.

Cobalt is an essential oligoelement which enters in the composition of vitamin B₁₂. For the general population, food and beverages represent the main source of cobalt exposure. Traces of cobalt are also present in cement and various household products. In industry, the potential for exposure to cobalt is particularly important during the production of cobalt powder, the production, processing and use of hard metals, the polishing of diamonds with cobalt containing disks and the processing of cobalt alloys. Except in the production of cobalt powders, these activities involve exposure not only to cobalt but also to other substances such as tungsten carbide, iron and diamond which may modulate the biological reactivity of cobalt. Cobalt salts are used for the preparation of enamels and pigments. Cobalt is mainly absorbed from the pulmonary and the gastrointestinal tracts. Absorption through the skin can occur but is low. Concomitant exposure to tungsten carbide increases the pulmonary absorption rate of cobalt metal. Cobalt is not a cumulative toxin and is mainly excreted in urine and to a lesser extent via faeces. Cobalt in blood and urine mainly reflects recent exposure. In the past, outbreaks of cardiomyopathy occurred among heavy consumers of cobalt fortified beer. It is likely that poor nutrition and ethanol had played a synergistic role. Toxic manifestations, however, have mainly been reported following inhalation of cobalt containing dusts in industry. The two main target organs are the skin and the respiratory tract. Cobalt itself may cause allergic dermatitis, rhinitis and asthma. Specific IgE against a complex of cobalt with albumin can sometimes be shown and a bronchial provocation test with a cobalt salt may be positive. Inhalation of cobalt containing dust has also lead to pathologic reactions in the lung parenchyma. The lesions, called ‘hard metal disease’, have ranged from intense alveolitis resembling desquamative or giant-cell interstitial pneumonitis to end-stage pulmonary fibrosis. Epidemiological and experimental data suggest that parenchymal lesions are rarely if ever induced by pure cobalt dust alone, but require the concomitant exposure to other compounds such as tungsten carbide. At the present time, there is inadequate evidence to indicate whether cobalt alone can increase the risk of lung cancer in workers. Concomitant exposure to cobalt and other substances such as in hard metal industry might increase the risk of lung cancer, but this requires confirmation.

Several clinical and experimental findings point to cobalt as the only sensitizer and causal agent of hard metal asthma. The clinical features have been clearly defined by bronchial provocation tests, with a prevalence of late phase responses. Epidemiology is still insufficient to configure prevalence and incidence rates for cobalt asthma. IgE and IgG antibodies with cobalt specificity have been demonstrated, but T-lymphocytes and eosinophyls involvement seem to be important in the mechanism of an allergic inflammation in the airways. Such an immunological pathogenesis links cobalt asthma with other manifestation of hard metal disease.