Pneumoconiosis
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- 作者：David Fishwick
- 关键词：coal ; complicated ; COPD ; dust ; lung ; occupation ; pneumoconiosis ; silica ; simple
- 刊名：Medicine
- 出版年：2008
- 出版时间：May 2008
- 年：2008
- 卷：36
- 期：5
- 页码：258-260
- 全文大小：69 K
文摘
The term ‘pneumoconiosis’ is used to describe pulmonary diseases associated with dust inhalation, and is normally used in the context of coal-worker’s pneumoconiosis, but many other dusts can cause the disease (for example, tin, barium, zirconium). This article focuses on the major causes of pneumoconiosis in the UK (coal-worker’s pneumoconiosis and silicosis). The site of damage within the lung is a function of both the size and the toxicity of the inhaled particle. Generally, particles with a median diameter of 0.5–10 μm can penetrate the alveoli, and those that are toxic to host cells (particularly macrophages) can cause permanent harm. Many mechanisms are likely to be particle specific; in general, however, release of pro-inflammatory cytokines (initially from alveolar macrophages) causes fibroblast formation and eventual fibrosis. The propensity of different types of particles to cause fibrosis varies widely; for example, silica dust is highly fibrogenic, whereas iron dust is not. Coal workers pneumoconiosis (CWP) is due directly to the effects of both coal and stone dust, and may be simple or complicated. Often regarded as a historic disease, new cases continue to occur. Most cases remain at simple level, when radiographic abnormalities are not associated with significant symptoms or reduction in lung function. Complicated CWP is caused by progression to fibrosis and in severe cases confluent fibrotic masses are seen, predominantly in the upper lobes. Silicosis, the pneumoconiosis caused by inhaled crystalline silica, also has both simple and complex forms, and again new cases continue to arise. The potential relationship between silica exposure and COPD continues to attract attention.