Nemery B
Division of Pneumology, K. U. Leuven, Belgium.
Eur Respir J. 1990 Feb;3(2):202-19.
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.
金属化合物所致肺部疾病的类型取决于致病因子的性质、其物理化学形式、剂量、接触条件及宿主因素。几种金属的烟雾或气态形式,如镉(Cd)、锰(Mn)、汞(Hg)、羰基镍(Ni(CO)₄)、氯化锌(ZnCl₂)、五氧化二钒(V₂O₅),可能导致急性化学性肺炎和肺水肿或急性气管支气管炎。金属烟雾热可能在吸入金属烟雾后发生,如锌(Zn)、铜(Cu)等多种金属,这是一种了解甚少的类似流感的反应,伴有急性自限性中性粒细胞肺泡炎。职业接触矿物粉尘,可能包括一些金属粉尘,或从事涉及金属化合物加工的工作,如焊接,可能导致慢性阻塞性肺疾病。接触镉可能导致肺气肿。支气管哮喘可能由复杂的铂盐、镍、铬或钴引起,推测是基于过敏致敏。铝工人哮喘的病因不明。值得注意的是,考虑到镍(Ni)或铬(Cr)作为皮肤致敏剂的效力和频繁接触情况,由它们诱发的哮喘显然并不常见。沉积在肺部的金属粉尘可能导致肺纤维化和功能损害,这取决于该物质的致纤维化潜能以及尚不明确的宿主因素。吸入铁化合物会导致肺铁末沉着症,这是一种几乎没有或仅有轻微纤维化的尘肺病。硬金属肺病是一种以脱屑性和巨细胞间质性肺炎为特征的纤维化,可能由钴引起,因为在未接触碳化钨的钴接触工人中也观察到了类似疾病。慢性铍病是一种伴有类肉瘤样上皮样肉芽肿的纤维化,推测是由于对铍的细胞介导免疫反应所致。这种机制可能是接触其他金属(如铝(Al)、钛(Ti)、稀土)的个体偶尔出现肺纤维化的原因。职业性肺癌的比例约为15%,金属接触常被认为是病因。例如,铀或铁的地下开采因接触氡而与肺癌的高发病率相关。至少某些形式的砷、铬和镍是已被充分证实的人类肺癌致癌物。也有证据表明镉工人以及钢铁工人的肺癌死亡率增加。