Hard metal pneumoconiosis

Granulomatous pulmonary foci with lymphoid fol-Hcles, round folHcular groups of histiocytes, and a patchy infiltration of eosinophils and much well advanced fibrous tissue had developed in a 33-year-old male who had worked as a precision grinder, grinding a hard metal compound (stellite) with a silicone carbide wheel and without any exhaust ventilation (Joseph 1968). The chemical analysis of the lung biopsy showed only titanium, but no tungsten or cobalt. 

Electron microscopy of a lung biopsy of a 49-years old white man who had spent 12 years in the manufacturing area revealed markedly altered alveolar lining cells and basement membranes (Coates and Watson 1971). Normal appearing type I pneu-mocytes were absent. 

Unusual cannibalistic multinucleated giant cells in air spaces as seen in giant cell interstitial pneumonia occurred in four of five cases exposed to cemented tungsten carbides and cobalt for 5 to 19 years (Auchincloss et al. 1992). By electron microscopy, the multinucleate giant cells in three patients who had restrictive ventilatory defects comprised both type II pneumocytes and multinucleate macrophages (Davison et al. 1983). 

Urinary cobalt concentrations were exceeded in workers exposed to hard metal dust, and the coefficient of correlation between the cobalt concentrations in the air and in the workers urine was 0.753 (Linnainmaa and Kiilunen 1997). 

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Cobalt (Co) Inhalation exposure "hard metal" pneumoconiosis Alloy in metals - but also associated with vitamin Bq2... 

Inhalation. Respiratory irritation. Hard metal pneumoconiosis. 

Cobalt is an essential nutrient at low levels ( 40mgday ). In industrial settings, inhalation of high concentrations of cobalt compounds has led to hard-metal pneumoconiosis, which may result in interstitial fibrosis. Workers with this condition typically develop hypersensitivity to cobalt compounds (symptoms include coughing and wheezing). A few workers have developed skin hypersensitivity after dermal contact with cobalt and its compounds. Cobalt can cause cardiomyopathy and (if inhaled as a dust) interstitial lung disease. 

In these patients, no relationship between Ta concentration and hard-metal pneumoconiosis was demonstrated (Sabbioni et al. 1994). 

Della Torre F, Cassani M, Segale M, Scarpazza G, PiETRA R and Sabbioni E (1990) Trace metal lung diseases a new fatal case of hard metal pneumoconiosis. Respiration 57 248-253. 

It has been proven that chelators, such as calcium-EDTA or penicillamine, are not efficient [38]. BAL (2,3-dimercaptopropanol-l) can be used to treat rabbits that absorbed high quantities of sodium tungstate but the LD50 does not increase very much (84 mg/kg instead of 71 mg/kg) [20]. Hard-metal pneumoconiosis is generally treated with corticoids, although their real efficiency has not been proven. 

The toxicity of cobalt and cobalt-nickel alloys in experimental hard metal pneumoconiosis is well documented. Metallic cobalt powder instilled in-tratracheally in the lungs of rats had an acute irritant action and lead to severe alterations in capillaries (Harding 1950, Schiller 1958,1961). The solubility of cobalt in plasma is some 500 times greater than in saline, but a fairly large (10 ml) intraperito-neal dose of plasma saturated with cobalt was without evident effects on the rat (Harding 1950). 

CHRONIC HEALTH RISKS (Molybdenum and insoluble molybdenum and insoluble compounds) based upon animal experiments, accumulation of molybdenum dust in the lungs, spleen, and heart, showed a decrease of DNA and RNA in the kidneys, spleen, and liver exposure to molybdenum dust from alloys or carbides caused "hard-metal lung disease" in humans. (Soluble molybdenum compounds) repeated exposure to soluble molybdenum compounds, based on animals data, suggests an association with the gout can cause anemia in animals exposure to molybdenum trioxide (M0O3), over a period of 3-7 years, has caused pneumoconiosis in workers. 

Chronic fibrotic occupational lung diseases include asbestosis (see p 121), silicosis, coal workers pneumoconiosis, and a few other less common fibrotic lung diseases associated with occupational exposures to such substances as beryllium and hard metal (cobalt-tungsten carbide). These conditions occur after years of exposure and with long latency, although patients may present for evaluation after an acute exposure. Referral for follow-up surveillance is appropriate if exposure is anticipated to be long term. 

Auerbach O, Garfinkel VA, Joubert L (1984) Histologic type of lung cancer and asbestos exposure. Cancer 54 3017-3021 Bar-Ziv J, Goldberg GM (1974) Simple siliceous pneumoconiosis in Negev bedouins. Arch Environ Health 29 121-126 Bech AO, Kipling MD, Heather JC (1962) Hard metal disease. Br J Indust Med 19 239-252... 

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