Etiology and Pathogenesis
The disease is based on the accumulation of coal dust and the development of sclerosis. The severity of fibrosis directly depends on the type of coal inhaled:
- Anthracite dust causes the most severe sclerosis.
- Bituminous coal dust leads to less pronounced changes.
- Charcoal practically does not cause sclerotic processes.
There is an ongoing scientific debate regarding the role of silicon dioxide ($SiO_2$). Some researchers suggest that fibrosis is exclusively caused by quartz impurities in coal seams. Other specialists note that coal dust possesses its own sclerosing properties, although they are markedly weaker than those of pure silica dust.
Macroscopic Changes and Morphology
Initial manifestations of the disease are recorded predominantly in the lower parts of the lungs, but as it progresses, the pigment distributes evenly across all lobes, giving the organ a characteristic gray-black color.
With marked diffuse tissue proliferation, the lungs lose their airiness and become dense. In pathological anatomy, this condition is referred to as slate induration (or anthracotic induration). Under a microscope, dust particles are found both freely in the tissue and inside numerous macrophages. Connective tissue proliferates in the interalveolar septa, as well as around blood vessels and the bronchial tree, forming small anthracotic foci and large nodules.
Clinical Course and Severe Forms: "Black Phthisis"
Pure anthracosis has a much longer and more benign course than silicosis because macrophages effectively clear coal particles via the bronchi and the lymphatic system. However, if the dust contains a high amount of silicon dioxide, mixed forms develop — anthracosilicosis (or silicoanthracosis) with massive sclerosis.
Advanced manifestations of the disease are historically termed "black phthisis". This form is characterized by the following features:
- formation of round or irregular cavities in the lungs with crumbling black walls;
- accumulation of black masses within disintegrating areas;
- clinical presentations with hemoptysis, mimicking tuberculosis;
- adhesion of altered lymph nodes to the trachea and bronchi with the risk of coal contents rupturing into the airways.
Associated Complications
Massive involvement of the lung tissue inevitably entails a number of severe consequences:
- Marked pulmonary emphysema.
- Chronic bronchitis and recurrent focal pneumonia.
- Tissue necrosis and softening due to impaired blood circulation and dust accumulation.
- Rupture of lymph node contents into the bronchial lumen, which can lead to aspiration, abscess, or gangrene.
- Development of cor pulmonale (right ventricular hypertrophy) against the background of severe pulmonary pneumosclerosis.