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Improved conditions and the progressive contraction of the coal industry in the UK have led to a considerable reduction in the number of cases of pneumoconiosis. The disease is caused by dust particles approximately 2-5 μm in diameter that are retained in the small airways and alveoli of the lung. The incidence of the disease is related to total dust exposure, which is highest at the coal face, particularly if ventilation and dust suppression are poor. Two very different syndromes result from the inhalation of coal.

Simple pneumoconiosis

This simply reflects the deposition of coal dust in the lung. It produces fine micronodular shadowing on the chest X-ray and is by far the most common type of pneumoconiosis. It is graded on the chest X-ray appearance according to standard categories set by the International Labour Office (see below). Considerable dispute remains about the effects of simple pneumoconiosis on respiratory function and symptoms. In many cases the symptoms are due to COPD related to cigarette smoking, but this is not always the case. Changes to UK workers' compensation legislation means that coal miners who develop COPD may be compensated for their disability regardless of their chest X-ray appearance.

Categories of simple pneumoconiosis are as follows:
small round opacities definitely present but few in number
small round opacities numerous but normal lung markings still visible
small round opacities very numerous and normal lung markings partly or totally obscured.
Simple pneumoconiosis may lead to the development of progressive massive fibrosis (PMF) (see below). PMF virtually never occurs on a background of category 1 simple pneumoconiosis but occurs in about 7% of those with category 2 and in 30% of those with category 3. Miners with category 1 pneumoconiosis are unlikely to receive compensation unless they also have evidence of COPD. Those with more extensive radiographic changes may be compensated solely on the basis of their X-ray appearances.

Progressive massive fibrosis

In PMF, patients develop round fibrotic masses several centimetres in diameter, almost invariably in the upper lobes and sometimes having necrotic central cavities. The pathogenesis of PMF is still not understood, though it seems clear that some fibrogenic promoting factor is present in individuals developing the disease. At one time this was thought to be M. tuberculosis, but it is more probably due to immune complexes, analogous to the development of large fibrotic nodules in coal miners with rheumatoid arthritis (Caplan's syndrome). Rheumatoid factor and antinuclear antibodies are both often present in the serum of patients with PMF, and also in those suffering from asbestosis or silicosis. Pathologically there is apical destruction and disruption of the lung, resulting in emphysema and airway damage. Lung function tests show a mixed restrictive and obstructive ventilatory defect with loss of lung volume, irreversible airflow limitation and reduced gas transfer.

The patient with PMF suffers considerable effort dyspnoea, usually with a cough. The sputum may be black. The disease can progress (or even develop) after exposure to coal dust has ceased and may lead to respiratory failure.