Pneumoconioses

The cause of the pneumoconioses is the inhalation of the mineral or metal. National Institute for Occupational Safety and Health: pneumoconioses Opens in new window Sensitisation to beryllium may occur after skin exposure.

Silica

Silica is the element silicon (Si) combined with oxygen (SiO₂). Crystalline silica (quartz) is fibrogenic. When silica is heated (as occurs either when in contact with molten metal in a foundry or naturally from geological processes), it is transformed into tridymite and cristobalite. In animal models, both these forms of silica are fibrogenic. Amorphous silica (diatomaceous earth) is a non-crystalline form (e.g., silica around the skeleton of a marine fossil), and is generally thought to be less fibrogenic. However, when amorphous silica is heated (calcined) during processing it is converted to crystalline silica. National Institute for Occupational Safety and Health: silica Opens in new window
Exposure to silica occurs in mining and quarrying; foundries; toilet bowl, sink, and ceramic manufacture; engineered countertop manufacturing and installation; abrasive blasting; and cement cutting in construction. Silica use as an abrasive material is banned in Europe, but not in the US.
Artificial stone silicosis (e.g., used in kitchen benchtop production) appears to differ from silicosis associated with other occupational settings, having a shorter latency and rapid progression.[11]

Coal

Coal is predominantly the element carbon, with oxygen, hydrogen, and a trace of sulfur. Anthracite has the highest percentage of carbon (>91%), with the carbon content of bituminous coal ranging from 75% to 91%, and lignite <75%.
Coal exposure occurs in underground coal mines; exposures to workers are significantly less in open-pit mines. Some coal miners may also be exposed to the overburden around the coal, and therefore will be exposed to silica (e.g., coal miners who do drilling, roof bolting, or pinning, and operators of continuous mining machines, or motormen who may be exposed to silica used for traction for coal cars). Coal mining has been identified as a risk for both silicosis and coal workers' pneumoconiosis.[19][20]

Beryllium

Beryllium ore, beryl, is beryllium aluminium cyclosilicate or bertrandite, or beryllium silicate hydroxide. In a beryllium smelter, metallic beryllium is separated and combined with various metals to form different alloys, or formed into beryllium oxide for use in ceramics. During this processing, or while annealing, grinding, cutting, or welding machining of beryllium alloys, dusts and fumes containing beryllium are produced. National Institute for Occupational Safety and Health: beryllium Opens in new window
Beryllium exposure occurs in the manufacture of master alloy (98% copper and 2% beryllium) used in electronic circuitry and the manufacture of heat-resistant ceramics, dental prostheses, metal products, and nuclear weapons.[13] Historically, exposure occurred in the manufacture of fluorescent light bulbs and atomic bomb triggers.
The risk of developing chronic beryllium disease is highly dependent on the presence of a genetic polymorphism in the HLA-DP gene.[18][21]

Silicosis

Silica particles of 5 microns or less gain access to the alveoli and are ingested by macrophages, causing lysosomal damage and activation of the inflammasome. The downstream effects of this include increased cellular apoptosis and subsequent lung fibrosis, mediated by interleukin-1 (IL-1), tumour necrosis factor (TNF) alpha, and free radicals. Silica nodules are often observed in the upper lobes of the lungs, with progression into the lower lobes associated with more severe disease. Silica is believed to be a more potent inducer of oxidative stress than coal.[22]

Coal workers' pneumoconiosis

Coal, like silica, has an activation and lytic effect on alveolar macrophages. Macrophages and other alveolar cells secrete pro-inflammatory molecules such as IL-1, interleukin-6, and TNF alpha, which serve as chemoattractants and mediate further tissue damage. Coal dust particles engulfed in macrophages accumulate in the upper lobes of the lungs in the form of macules or lesions. Lesions are initially fairly small (<10 mm in diameter); however, during prolonged exposure, larger lesions form due to fibroblast activation and subsequent collagen deposition. Lung fibrosis eventually ensues.[22] Freshly fractured coal, or coal of a higher rank (e.g., anthracite), has more free radicals and causes more severe oxidative stress.

Beryllium sensitisation and chronic beryllium disease

Beryllium has a different pathophysiology than the other minerals and metals that cause pneumoconiosis. Beryllium does not have a clear exposure response, with increased disease with longer duration of exposure. This exposure changes the T cell receptor peptide binding so that they react differently with other antigens. The likelihood of this interaction occurring is related to the presence of polymorphisms of the HLA system. The presence of glutamic acid at position 69 of the B1 chain of the HLA-DPB molecule is the polymorphism with the largest risk for beryllium sensitisation and disease.[18][21]

Types of pneumoconiosis

The pneumoconioses are chronic lung diseases caused by exposure to a mineral dust or metal. The major diseases in this category include:

Asbestosis
Silicosis
Coal workers' pneumoconiosis (black lung disease)
Chronic beryllium disease.

There are many other causes of pneumoconiosis. Many are less common, and are benign, with chest x-ray changes but without respiratory impairment. Examples include:

Aluminosis
Baritosis
Graphite pneumoconiosis
Oil shale pneumoconiosis
Siderosis
Stannosis
Talcosis.

Acute silicosis is a rare condition and presents as alveolar proteinosis, with radiographic findings of perihilar filling of the alveoli. Acute beryllium disease is also a rare condition and presents as a chemical pneumonitis, with radiographic findings of pulmonary oedema.

Pathophysiology

Classification

Types of pneumoconiosis