Apr . 01, 2024 10:01 Back to list

Diffuse Parenchymal Lung Diseases Associated With Known Etiologic Agents

Coal Worker's Pneumoconiosis

Individuals who have worked as part of the coal mining process and have been exposed to large amounts of coal dust are at risk for development of CWP. In comparison with silica, coal dust is a less fibrogenic material, and the tissue reaction is much less marked for equivalent amounts of dust deposited in the lungs. In addition to its role in the development of CWP, coal mining also appears to be associated with an increased risk of chronic obstructive pulmonary disease, including anatomic evidence of emphysema that is most commonly centrilobular in distribution.

Tissue reaction to inhaled coal dust is much less than that to silica.4

The pathologic hallmark of CWP is the coal macule, which is a focal collection of coal dust surrounded by relatively little cellular infiltration or fibrosis (Fig. 10.3). The initial lesions tend to be distributed primarily around respiratory bronchioles. Small associated regions of emphysema, termed focal emphysema, may be seen.

As with silicosis, the disease is often separated into simple and complicated forms. In simple CWP the chest radiograph consists of relatively small and discrete densities that usually are more nodular than linear. In this phase of the disease, patients have few symptoms, and pulmonary function usually is relatively preserved. In later stages of the disease, to which only a small minority of individuals progress, chest radiographic findings and clinical symptoms are more pronounced. With extensive disease and coalescent opacities on chest radiographs, patients are said to have complicated CWP, also called progressive massive fibrosis. Pulmonary function may show restrictive disease, obstructive disease, or a mixed pattern, depending upon the relative amounts of fibrosis, airways disease, and emphysema.

Why complicated disease develops in some patients with CWP is not clear. At one time, it was speculated that patients with progressive massive fibrosis had also been exposed to toxic amounts of silica and that the simultaneous silica exposure was responsible for most of the fibrotic process. However, although some patients do have a mixed form of pneumoconiosis from both coal dust and silica exposure, progressive massive fibrosis can result from coal dust in the absence of concomitant exposure to silica. Whether genetic polymorphisms may help to explain the different clinical responses to inhalational exposures is currently unknown.

Symptoms and pulmonary function changes in coal worker's pneumoconiosis (CWP) are related to the extent of fibrosis and coexistent chronic obstructive pulmonary disease (COPD), if present.

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