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A. Seaton

and P. Reid



This chapter has been extensively re-written.

Acknowledgement—the excellent figures from the chapter previously written by Dr A. Seaton have been retained, and his section on ‘other pneumoconioses’ has been little altered.

Updated on 30 May 2013. The previous version of this content can be found here.
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date: 29 April 2017

Pneumoconiosis describes the pathological reaction of the lung to inhaled dust, which is most frequently, but not necessarily, one of fibrosis, and most often, but not exclusively, related to exposures occurring at work. It may be more formally defined as a permanent alteration of lung structure due to the inhalation of mineral dust and the tissue reactions of the lung to its presence, excluding bronchitis and emphysema. Lung damage occurs when respirable dusts reach the acinus in sufficient quantity to overwhelm the normal phagoctyic and clearance mechanisms. The causes of pneumconiosis are many and varied, but many epidemiological studies have shown an exposure–response relationship between the total mass of respirable dust to which workers have been exposed and their risks of developing disease. These form the basis of regulations specifying limits to permitted levels of exposure. Workers, whose exposure results in pneumoconiosis, may be entitled to compensation in some countries.

Coal-worker’s pneumoconiosis

Caused by inhalation of coal-mine dust. Now uncommon in the United Kingdom and other Western countries, but in China the disease is widespread, and in India it affects about 1–2% of the workforce. The presence of simple coal workers pneumoconiosis, which causes no respiratory symptoms or physical signs, is heralded by the development of coal macules in a centriacinar and interlobular distribution, which may be detected by chest radiography as they become more profuse. Complicated pneumoconiosis is characterized by the appearance of progressive massive fibrosis (PMF), which may be diagnosed when any radiographic lesion exceeds 1 cm in diameter. PMF often progresses, causing mixed airflow obstruction and restriction, and—when severe—leads to respiratory failure, cor pulmonale, and death.


Caused by inhalation of crystalline silicon dioxide, usually in the form of quartz. Crystalline silica is highly fibrogenic, causing fibrous pleural adhesions, enlarged lymph nodes that contain fibrotic nodules and often calcify, and grey nodules throughout the lung with a typical whorled appearance when cut across. The clinical presentation ranges from acute silicosis, which is very rare, but leads to death within months, to slowly progressive lung fibrosis, to asymptomatic radiological abnormalities. The progression of silicosis may be complicated by tuberculosis, lung cancer, chronic obstructive pulmonary disease, and rarely by connective tissue disease and renal damage.


Exposure to asbestos fibres can cause a range of respiratory conditions, including benign pleural plaques, acute effusion, diffuse fibrosis of the visceral pleura, asbestosis, and mesothelioma (see Chapter 18.19.3). Asbestosis occurs only in people working regularly with asbestos over several years and not in those with occasional or incidental exposure. Disease is usually progressive, with radiological appearance identical to idiopathic pulmonary fibrosis, i.e. predominantly basal and peripheral irregular linear shadowing, progressing to honeycombing. The risk of lung carcinoma is related to asbestos exposure, interacting multiplicatively with smoking.

Other causes of pneumoconiosis include talc, kaolin, Fuller’s earth, mica, fibrous erionite, berylliosis.

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