Sjögren I, Hillerdal G, Andersson A, Zetterström O
Thorax. 1980 Sep;35(9):653-9. doi: 10.1136/thx.35.9.653.
Four patients were found to react to occupational exposure to grinding of hard metal (tungsten carbide). Three of the patients had symptoms and signs compatible with an allergic alveolitis, the symptoms disappearing and the chest radiograph clearing when they were absent from work for a few months. Re-exposure to the offending agent led to new signs and symptoms. The first patient was re-exposed twice and each time reacted a little more seriously. After the last episode her chest radiograph has not cleared completely, in contrast to the first two times. The fourth patient had more typical occupational asthma. All the cases occurred in the part of the factory where air concentrations of cobalt were the lowest. The cobalt there is dissolved in the coolant necessary for grinding the hard metal. It occurs mainly in the ionised form, which is known to react with proteins and therefore presumably acts as a hapten. Protective measures, including choosing a coolant with minimal ability to dissolve cobalt and an effective exhaust system, should minimise the risk of this occupational disease in the future.
发现有4名患者对硬质金属(碳化钨)磨削的职业暴露产生反应。其中3名患者的症状和体征符合过敏性肺泡炎,当他们离开工作岗位几个月后,症状消失,胸部X光片恢复正常。再次接触致病因子会导致新的症状和体征出现。第一名患者被再次暴露了两次,每次反应都更严重一些。与前两次不同,最后一次发作后她的胸部X光片没有完全恢复正常。第四名患者患有更典型的职业性哮喘。所有病例都发生在工厂中钴空气浓度最低的区域。那里的钴溶解在磨削硬质金属所需的冷却液中。它主要以离子形式存在,已知其能与蛋白质发生反应,因此大概起半抗原的作用。包括选择钴溶解能力最小的冷却液和有效的排气系统在内的防护措施,应能在未来将这种职业病的风险降至最低。