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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies were carried out in 4 groups of workers occupationally exposed to cadmium, tungsten, manganese and lead. All those groups were homogeneous, composed exclusively of men aged 35--45, of similar height, body weight, and duration of employment above 10 years. Following the same criteria, a group of forestry workers, unexposed to dust, was randomly selected. The smoking habit was similar in all groups. Several--days--clinical observation included a detailed interview (MRC questionnaire), physical and radiological examination and a wide range of functional tests of lungs. The results reveal clinical and physiopathological symptoms which might be indicative of emphysema. The results of some studies also indicate the possibility of intraparenchymatous fibrosis of lungs in the tungsten--exposed--workers. No clear effects upon the respiratory system were found.
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PMID:[Effect of metal dust on the respiratory system. II. Clinical examinations]. 44 67

The type of lung disease caused by metal compounds depends on the nature of the offending agent, its physicochemical form, the dose, exposure conditions and host factors. The fumes or gaseous forms of several metals, e.g. cadmium (Cd), manganese (Mn), mercury (Hg), nickel carbonyl (Nl(CO)4, zinc chloride (ZnCl2), vanadium pentoxide (V2O5), may lead to acute chemical pneumonitis and pulmonary oedema or to acute tracheobronchitis. Metal fume fever, which may follow the inhalation of metal fumes e.g. zinc (Zn), copper (Cu) and many others, is a poorly understood influenza-like reaction, accompanied by an acute self-limiting neutrophil alveolitis. Chronic obstructive lung disease may result from occupational exposure to mineral dusts, including probably some metallic dusts, or from jobs involving the working of metal compounds, such as welding. Exposure to cadmium may lead to emphysema. Bronchial asthma may be caused by complex platinum salts, nickel, chromium or cobalt, presumably on the basis of allergic sensitization. The cause of asthma in aluminium workers is unknown. It is remarkable that asthma induced by nickel (Ni) or chromium (Cr) is apparently infrequent, considering their potency and frequent involvement as dermal sensitizers. Metallic dusts deposited in the lung may give rise to pulmonary fibrosis and functional impairment, depending on the fibrogenic potential of the agent and on poorly understood host factors. Inhalation of iron compounds causes siderosis, a pneumoconiosis with little or no fibrosis. Hard metal lung disease is a fibrosis characterized by desquamative and giant cell interstitial pneumonitis and is probably caused by cobalt, since a similar disease has been observed in workers exposed to cobalt in the absence of tungsten carbide. Chronic beryllium disease is a fibrosis with sarcoid-like epitheloid granulomas and is presumably due to a cell-mediated immune response to beryllium. Such a mechanism may be responsible for the pulmonary fibrosis occasionally found in subjects exposed to other metals e.g. aluminium (Al), titanium (Ti), rare earths. The proportion of lung cancer attributable to occupation is around 15%, with exposure to metals being frequently incriminated. Underground mining of e.g. uranium or iron is associated with a high incidence of lung cancer, as a result of exposure to radon. At least some forms of arsenic, chromium and nickel are well established lung carcinogens in humans. There is also evidence for increased lung cancer mortality in cadmium workers and in iron or steel workers.
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PMID:Metal toxicity and the respiratory tract. 217 66

In order to examine the effect of cemented tungsten carbide dust on the animal lung, saline suspensions were intratracheally administered into the lungs of rats in a single dosage. About one-fifth of the animals died during the first three days. The acute response of the lungs was hemorrhagic edema with intense alveolar congestion. The animals killed at six months all presented pulmonary lesions of patchy fibrosis in the vicinity of the deposited dusts, occasionally associated with focal traction emphysema and bronchobronchiolar ectasia. At twelve months, two-third of the animals had neither fibrosis nor dust deposition, although the remaining animals showed pulmonary lesions similar to those seen in the six-months responders. Fibrosis of the lungs seemed to consist of collapsed alveoli with condensation of the preexistent reticulin fibers, but without noticeable collagenization. It is supposed that both the early toxic and the late fibrogenic effects of the carbide dust are attributable to the cytotoxic action of cobalt present in the dust particles. It is possible that recovery of the pulmonary lesions results from removal of the dusts from the lesions.
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PMID:Effects of cemented tungsten carbide dust on rat lungs following intratracheal injection of saline suspension. 738 1