However, a later 2018 study by the National Institute of Occupational Safety and Health shows a resurgence, recording the highest rate of CWP in roughly two decades. Pathogenesis
Coal dust is not as fibrogenic as silica dust. 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. Coal dust provides a sufficient stimulus for the macrophage to release various products, including enzymes, cytokines, oxygen radicals, and fibroblast growth factors, which are important in the inflammation and fibrosis of CWP. Aggregations of carbon-laden macrophages can be visualized 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 centers of dense lesions may become necrotic due to ischemia, leading to large cavities within the lung. Appearance
Simple CWP is marked by the presence of 1–2 mm nodular aggregations of anthracotic macrophages, supported by a fine collagen network, within the lungs. Those 1–2 mm 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. The coal macule is the basic pathological feature of CWP and has a surrounding area of enlargement of the airspace, known as focal emphysema.
Intravascular papillary endothelial hyperplasia is a rare, benign tumor. It may mimic an angiosarcoma, with lesions that are red or purplish 5-mm to 5-cm papules and deep nodules on the head, neck, or upper extremities. : 592

Pathology
Histopathology Images
See also
List of cutaneous conditions

References


== External links ==