Coalworker's pneumoconiosis

Black lung disease, also known as coal workers' pneumoconiosis (CWP), is caused by long exposure to coal dust. It is a common affliction of coal miners and others who work with coal, similar to both silicosis from inhaling silica dust, and to the long term effects of tobacco smoking. Inhaled coal dust progressively builds up in the lungs and is unable to be removed by the body, leading to inflammation, fibrosis, and in the worst case necrosis.

Full blown coal workers' pneumoconiosis develops after the initial, milder form of the disease known as anthracosis (anthrac - coal, carbon). This is often asymptomatic and is found to at least some extent in all urban dwellers^[1] due to air pollution. Prolonged exposure to large amounts of carbon dust results in progression to the more serious forms of the disease, simple coal workers' pneumoconiosis and complicated coal workers' pneumoconiosis.

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Pathogenesis

Coal dust that enters the lungs can neither be destroyed nor removed by the body. The particles are engulfed by resident alveolar or interstitial macrophages and remain in the lungs, residing in the connective tissue or pulmonary lymph nodes. Aggregations of carbon-laden macrophages can be visualised under a microscope as granular, black areas. In serious cases, the lung may grossly appear black. These aggregations can cause inflammation and fibrosis, as well as the formation of nodular lesions within the lungs. The centres of dense lesions may become necrotic due to ischaemia, leading to large cavities within the lung

Appearance

Simple CWP is marked by the presence of 1-2mm nodular aggregations of anthracotic macrophages, supported by a fine collagen network, within the lungs. Those 1-2mm in diameter are known as coal macules, with larger aggregations known as coal nodules. These structures occur most frequently around the initial site of coal dust accumulation - the upper regions of the lungs around respiratory bronchioles^[1].

Continued exposure to coal dust following the development of simple CWP may result in its progression to complicated CWP, which generally requires a number of years to develop. Large, black, fibrotic scars 2-10cm in diameter are present, with accompanying decreased lung function. The lung itself appears blackened. A minority of these cases progresses to progressive massive fibrosis (PMF), the most serious form of CWP.

Symptoms

Both CWP and mild complicated CWP are often unsymptomatic or only affect lung function slightly. Shortness of breath and pain may be felt. However, progression to PMF is marked by lung dysfunction, pulmonary hypertension, and cor pulmonale.

See also

• Caplan syndrome

References