Classification: Coal is a rock, which was created about 50 billion years ago by plants covered with sand and similar materials. The covering materials induced strong pressures and high temperatures. The water of the plants was removed, and with increasing pressure coal was created with increasing
content of C. Two different types of coal can be distinguished: a) brown coal, which has a higher content of water and SO2, and b) hard coal, which was formed under higher pressures, and which has a smaller content of water. Hard coal is usually mined, and the miners are exposed to silica included
in the coal. Brown coal is usually found in open pits. Anthracite is richest in carbon and the hardest variety of coal rocks.
Synonyms/Trade Names: Anthracite Particles,
Coal Facings, Coal-Milled, Coal-Slag Milled, Sea Coal.
Lung function is normal insimple CWP; it shows decreased diffusion capacity and increased pO2 during exercise in complicated CWP.
Bronchoalveolar Lavage: Black particles and dust-laden macrophages can be detected in the lavage fluid.
Natural Sources: Coal is mined world-wide.
Key Hazards: Fibrogenic.
Involved Organs: Lung.
Exposure/Epidemiology: Exposure of coal dust may occur during mining and processing. Simple coal worker pneumoconiosis (CWP) is radiographically seen in 12% of all miners and in 50% of anthracite miners having more than 20 years of exposure. Bituminous coal miners have a lower prevalence.
Thresholds: In Germany, MAK 6 mg/m3.
Etiology/Pathophysiology: The pathogenesis of the lung fibrosis is not clearly understood. The following hypotheses are under discussion: a) The fibrosis is a reaction of the lung tissue to the coal contaminated by silica; b) The clearance of the conducting airways is insufficient due to the excessive
amount of the dust; c) The fibrosis is of immunologic nature, and a result of tissue damage; d) The fibrosis is an abnormal reaction of the lung tissue to an infection with mycobacterium tuberculosis. Only dust particles of less than 5 ?m in diameter can penetrate to the peripheral bronchioles
and alveoli. If the clearing processes are overwhelmed, the pure coal dust is retained, and primary lesions containing coal dust, macrophages, and fibroblasts are induced. Fibrogenic substances are released, if free silica are included in the dust.
Lung Diseases: Coal dust induces the so called coal worker pneumoconiosis (CWP, black lung disease): Natural sources of coal dust may be associated with severe fibrosis, although the development of massive fibrosis in coal miner’s lung
is still an open question (depending on silica?). Coal dust is less toxic to macrophages compared to quartz particles. Coal miners have an increased risk of tuberculosis, a normal risk of lung cancer, and a slightly increased risk of stomach cancer. A
higher risk of lung cancer associated with polycyclic aromatic hydrocarbons has been reported in persons working in coal gasifying processes and coke production. Two forms of CWP can be distinguished a) a simple form and b) a complicated form.
Clinical Presentation: The patients produce black sputum, often without any additional symptoms. In some cases symptoms of progressive massive fibrosis have been reported (dyspnea, cough, cor pulmonale).
Radiology: Chest radiographs show small irregular opacities, or, less often, small rounded opacities measuring 1–5 mm in diameter (pinhead type). The lower zones are more frequently involved than the upper ones. Calcification of the lymph
nodes (simple form of CWP) is seen in 10% of the anthracite miners. The size of the anthracotic nodes ranges from 1 cm to several centimeters in diameter. Calcification may be seen in advanced stages, eggshell calcification is not common.
There is a close correlation between the findings of chest radiographs and the degree of pneumoconiosis. Abnormal findings on chest radiographs are a thickened pleura, parenchymal calcifications, and marked emphysema.
Gross: The alterations of lung parenchyma seen in coal miners can be subdivided into a simple and a complicated pneumoconiosis, and are similar to those seen in graphite lung or carbon lung. The lungs show multiple solid nodules of black color
in simple pneumoconiosis. The size of the nodules is 2–5 mm in maximum diameter. Complicated pneumoconiosis is characterized by massive hard black lesions measuring several centimeters in maximum diameter. The nodules are usually localized
in the upper lobes. Reactive pleural fibrosis and adhesions as well as involvement of the proximal localized intrapulmonary lymph nodes is common. The emphysematous changes may develop in a honeycomb lung.
Histology: Simple coal pneumoconiosis is characterized by four different findings: a) natural sources of black dust particles in the distant air ways including the respiratory bronchioles;
b) absent fibrosis and absent inflammatory infiltrates;
c) emphysematous changes of the surrounding alveoli (proximal acinar emphysema);
d) clear-cut boundaries of the lesions with the adjacent healthy lung parenchyma. Complicated pneumoconiosis shows large amounts of collagenous fibers intermingled with dust particles.
Mild interstitial mononuclear inflammatory infiltrates are usually present as well as areas with liquefuctive necrosis. The small and larger arteries, veins and bronchi are also involved, and their lumens may be occluded due to severe fibrotic
changes. Caseous epithelioid granulomas are signs of additional tuberculous infection.
Prognosis: Poor in complicated CWP, and fair in simple CWP.
Caplan’s Syndrome: Caplan’s syndrome (association of rheumatoid arthritis with coal pneumoconiosis and progression into severe fibrosis) was estimated in 2–3% in coal miners; for further information see under the heading silica.
Silicosis: Silicosis is often seen in coal miners; compare to silica.
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