Lably
Skip to content

Black lung disease

Human disease caused by long-term exposure to coal dust

  • 12 min read
  • 6 chapters

Related on Lably

Through Lung, Air pollution and Lymph node

Black lung disease develops after the initial, milder form of the disease known as anthracosis (from the Greek ἄνθραξ, or ánthrax – coal, carbon). This is often asymptomatic and is found to at least some extent in all urban dwellers due to air pollution. Prolonged exposure to large amounts of coal dust can result in more serious forms of the disease, simple coal workers' pneumoconiosis and complicated coal workers' pneumoconiosis (or progressive massive fibrosis, PMF). More commonly, workers exposed to coal dust develop industrial bronchitis, clinically defined as chronic bronchitis (i.e. a productive cough for three months per year for at least two years) associated with workplace dust exposure. The incidence of industrial bronchitis varies with age, job, exposure, and smoking. In non-smokers (who are less prone to develop bronchitis than smokers), studies of coal miners have shown a 16% to 17% incidence of industrial bronchitis.

In 2013, BLD resulted in 25,000 deaths globally—down from 29,000 deaths in 1990. In the US, a 2018 study by the National Institute of Occupational Safety and Health shows a resurgence among veteran coalminers, recording the highest rate of BLD in roughly two decades.

Pathogenesis

Coal dust is not as fibrogenic as silica dust. Most coal dust that enters healthy lungs is removed by mucociliary clearance and the cough reflex. Coal dust that is not removed by these mechanisms can neither be destroyed nor removed by the body. The particles are engulfed by resident alveolar macrophages 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 development of inflammation and fibrosis in BLD. 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 BLD is marked by the presence of 1–2 mm (0.039–0.079 in) 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 BLD and has a surrounding area of enlargement of the airspace, known as focal emphysema. Focal emphysema extends into progressive centrilobular emphysema. Less commonly a variant of panacinar emphysema develops.

Continued exposure to coal dust following the development of simple BLD may progress to complicated BLD with progressive massive fibrosis (PMF), wherein large masses of dense fibrosis develop, usually in the upper lung zones, measuring greater than 1 cm (0.39 in) in diameter, with accompanying decreased lung function. These cases generally require a number of years to develop. Grossly, the lung itself appears blackened. Pathologically, these consist of fibrosis with haphazardly-arranged collagen and many pigment-laden macrophages and abundant free pigment. Radiographically, BLD can appear strikingly similar to silicosis. In simple BLD, small rounded nodules predominate, tending to first appear in the upper lung zones. The nodules may coalesce and form large opacities (>1 cm), characterizing complicated BLD, or PMF.

Sign in to keep reading

5 more chapters are free with a Lably account.

More in Health