Scientific Meeting of the Contact Group "Respiratory Physiopathology" of the "National Fund for Scientific Research" of June 3, 1989 at the Catholic University of Leuven Invited Lectures on: Inhalation pathology Metal toxicity and the respiratory tract

This article is a review of the human pulmonary disorders which may result from exposure to inhaled metals. Since carbon and silicon are not metals, this review does not cover coal workers' pneumoconiosis, silicosis, asbestos-related diseases, or pneumoconioses caused by other silicates. The type of lung disease caused by metal compounds depends on the nature of the offending agent, its physico-chemical form, the dose, exposure conditions and host factors. The fumes or gaseous forms of several metals (e.g. Cd, Mn, Hg, Ni(C0) 4 , ZnCI , vp~ may lead to acute chemical pneumonitis and pufmonary oedema or to acute tracheo-bronchitis. Metal fume fever, which may follow the inhalation of metal fumes (e.g. Zn, Cu and many others) is still a poorly understood influenza-like reaction, accompanied by an acute self-limited neutrophil alveolitis. Chronic obstructive lung disease may result from occupational exposure to mineral dusiS, including probably some metallic dusts, or from jobs involving the working of metal compounds such as welding. Exposure to cadmium has been demonstrated to be capable of leading 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 Ni or Cr is apparently infrequent, considering their p<)tency and frequent involvements as dermal sensitizers. Metallic dusts deposited in the lung may give rise to more or less marked pulmonary fibrosis and functional impairment, depending on the ubrogenic potential of the agent and on poorly understood host factors. Inhalation of iron compounds causes siderosis, a pneumoconiosis with liule 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 wilh sarcoid-like epitheloid granulomas and is presumably due to a cellmediated immune response to beryWum. Such a mechanism may be responsible for pulmonary fibrosis occasionally found in subjects exposed to other metals (AI, 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 expos·ure 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 mortaJity in cadmium workers and in iron or steel workers. (Full paper to be published in Eur. Respir. J).