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Stephen Chapman

, Grace Robinson

, John Stradling

, Sophie West

, and John Wrightson

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date: 29 June 2022

Overview and causative mineral dusts

  • Pneumoconioses are non-neoplastic pulmonary diseases caused by the reaction of the lung to the inhalation of mainly mineral, but also organic, dusts (see Table 36.1)

  • Inhaled particles of dust size <5 micron reach the terminal airways and alveoli and settle on the epithelial lining. From here, they are slowly cleared by macrophages or alveolar cells. They may pass into the lymphatic system, be cleared via the airway, or remain in the alveolus

  • The dust particles can lead to an inflammatory reaction within the lung, depending on their physical and chemical properties

  • The inflammation causes characteristic alterations in pulmonary structure and radiological abnormalities

  • Of the diseases caused by inhalation of mineral dusts, many are becoming less common in the UK, due to improved protection of workers from dusts and decreasing levels of mining. Newer industrial nations may see increasing numbers of cases of pneumoconiosis

  • Organic dusts causing HP and extrinsic asthma are discussed on Pneumoconioses pp. [link][link] and Pneumoconioses pp. [link][link]. Asbestos-related diseases are discussed separately on Pneumoconioses p. [link].

Table 36.1 Causative mineral dusts

Mineral dust


Examples of exposure

Coal dust

  • Simple pneumoconiosis

  • Progressive massive fibrosis

  • Caplan’s syndrome

Coal mining, especially hard coal


  • Silicosis

  • Caplan’s syndrome

Foundry work, sandblasting, stone cutting, hard rock mining, ceramics


  • Asbestosis

  • Benign asbestos-related pleural disease

  • Mesothelioma

  • Lung cancer

  • Mining, milling, and fabrication

  • Installation and removal of insulation


  • Acute berylliosis

  • Beryllium granulomatosis

Mining, fabrication of electrical and electronic equipment, workers in nuclear and aerospace industry

Iron oxide



Barium sulphate



Tin oxide




Like silicosis (bauxite worker’s lung, Shaver’s disease)

Mining, firework, painting, and armament manufacture

Types of mineral dust exposure

Non-fibrous mineral dusts

  • Silica

  • Coal dust

  • Mixed mineral dusts containing quartz: slate, kaolin, talc, non-fibrous clays.

Fibrous mineral dusts

  • Asbestos

  • Other mineral fibres.

Metal dusts and fumes

  • Iron, aluminium, beryllium, cobalt

Chest disease in coal miners

It was recognized many years ago that coal miners had higher levels of respiratory disease than the general population. Coal miners can get any, or all, of:

  • Chronic bronchitis

  • COPD

  • Pneumoconiosis.

They may be eligible for compensation for all of these. It can be difficult to establish the independent effects of coal dust due to high smoking rates amongst miners. However, it is now thought that coal dust contributes to the COPD and bronchitis caused by smoking, because:

  • Miners have an increased prevalence of cough, sputum, and decreased FEV1 when compared with non-miners. The risk of cough increases with increasing dust exposure

  • FEV1 declines in proportion to the amount of dust exposure

  • In smokers, the response to dust is probably different to that of non-smokers, with worse disease at a given level of exposure.

In the past, TB has also been a major problem amongst miners and their families, relating to their socio-economic conditions.

SWORD is the Surveillance of Work-related and Occupational Respiratory Disease scheme run in the UK to monitor the numbers of patients with occupational lung diseases. Patients with a clinical diagnosis of an occupational lung disease are confidentially reported by respiratory or occupational health physicians.

Further information


Coal-worker’s pneumoconiosis

This is the condition caused by the deposition of coal dust within the lung and its associated inflammatory reaction.

There are two types:

  • Simple pneumoconiosis, which can progress to

  • Complicated pneumoconiosis, also known as progressive massive fibrosis (PMF).

These diseases are common amongst coal miners who work in poorly ventilated conditions. The risk of pneumoconiosis varies with different compositions of coal from different geographical areas, but the larger the amount of dust to which the miner is exposed, the greater the risk of developing pneumoconiosis. It is now rare for miners under the age of 50 to be diagnosed with pneumoconiosis in the UK.


Simple pneumoconiosis

Coal dust is inhaled into the alveolus and is engulfed by macrophages, forming a black stellate lesion, the coal macule. This causes cytokine release and subsequent inflammatory cell recruitment, leading to fibroblast activation. These coal macules are found throughout the lung, especially in the upper zones of the upper and lower lobes and often associated with surrounding bronchiolar dilatation. They are not palpable. Regional lymph nodes also become blackened. In time, larger nodules develop, containing reticulin and collagen between the macrophages, and associated bronchiolar dilatation leading to focal emphysema is seen.


occurs on this background but with aggregation of the fibrotic nodules to form larger lesions 2–10cm diameter. Macroscopically, these look like large black scars, extending from the lung parenchyma to the chest wall. The central area of these nodules may be necrotic, and the outer rim is firm and collagenous. It is not understood what causes the progression of small nodules to PMF, although continued exposure to coal dust in the presence of simple pneumoconiosis makes this development more likely.

Clinical features

Simple pneumoconiosis

is usually asymptomatic, with no associated clinical signs. This is a relatively benign disease.


is usually associated with cough, productive of mucoid or blackened sputum, and breathlessness, particularly on exertion, and may, in time, lead to the development of cor pulmonale. Examination is unremarkable, with no clubbing and no crepitations audible (the presence of crepitations suggests a different diagnosis).


  • CXR In simple pneumoconiosis, there is nodular shadowing, with nodules of varying size, up to 10mm, particularly in the upper and middle zones. Pneumoconiosis can be graded according to the number of different sized nodules: p = <1.5mm, q = 1.5–3mm, and r = 3–10mm. Nodule numbers increase with increasing dust inhalation and usually stop forming when the miner has left the work environment. PMF is diagnosed when one or more opacities of >1cm diameter are present, on the background of simple pneumoconiosis. These lesions are often located in the upper lobes and enlarge, becoming increasingly radiodense and clearly demarcated with time. They may distort the adjacent lung and cause emphysema. The lesions continue to progress out of the work environment

  • HRCT of simple pneumoconiosis shows parenchymal nodules 1–10mm in size, with upper zone predominance. In PMF, nodules of >1cm are seen, with irregular borders and associated parenchymal distortion and emphysema. Larger lesions may have cavitation and necrosis. They may also have areas of calcification

  • PFTs Simple pneumoconiosis: FEV1 and FVC are normal, although TLCO may be slightly decreased. PMF: signs of airway obstruction due to emphysema, and restriction due to loss of lung volumes. TLCO is reduced.


Minimization of dust exposure with improved mine ventilation, respirator provision, and monitoring of dust levels. Miners have CXR every 4y and are moved to less dusty work, if they show signs of pneumoconiosis, to prevent the development of PMF. Miners with signs of coal-worker’s pneumoconiosis are entitled to industrial injury benefits from British Coal (see Pneumoconioses p. [link]). No increased risk of lung cancer with pneumoconiosis or PMF.

Caplan’s syndrome

Miners with seropositive RA or positive serum RhF can develop large well-defined nodules. These occur on a background of simple pneumoconiosis and in those with a relatively low coal dust exposure. They may be multiple and may cavitate. They cause no significant functional impairment and have no malignant potential.


This is a chronic nodular, densely fibrosing pneumoconiosis, caused by the prolonged inhalation of silica particles.

  • Long lag time of decades between exposure and clinical disease

  • Insidious onset, progressive

  • Larger radiological opacities than those seen in coal-worker’s pneumoconiosis and more rapid progression

  • The pattern of disease depends on the level and duration of the silicone dust exposure.

Silica is present mostly as crystalline quartz, which is mined and quarried, and used in industries such as ceramics, brick making, and stone masonry. It is becoming less prevalent in Western societies, due to changes in silica working conditions.


Quartz and cristobalite forms of crystalline silica cause silicosis. When they accumulate within the airways, lymphocytes and alveolar macrophages engulf the particles and are removed into the lymphatic system. Any remaining silica dust causes focal aggregations of macrophages, which are, in time, converted into fibrosing nodules, the silicotic nodule. Silica dust can cause surfactant secretion from the alveolus due to local irritation. This leads to further macrophage recruitment. Large nodules are formed by the aggregation of smaller nodules.

Different types of silicosis

There are four types, and the distinction is often not clear.

  • Acute silicosis is caused by intense exposure to fine dusts such as those produced by sandblasting. It may become apparent in workers within a few months to a year of starting work. Rapid deterioration over 1–2y, with treatment being ineffective. Rare now, due to regulation of silica levels in the workplace

    • Clinically Dry cough, SOB, and a feeling of tightness on breathing deeply. Rapid deterioration over a few weeks. Fine crepitations are heard over the lower zones bilaterally. Respiratory failure

    • CXR Patchy bilateral lower airspace consolidation, which may look like pulmonary oedema

    • Pathology Irregular fibrosis adjacent to alveolar spaces filled with a lipoproteinaceous exudate, similar to that found in alveolar proteinosis

  • Subacute silicosis This is the classic picture of silicosis, which is now quite rare. Dry cough, gradual onset of SOB

    • CXR Upper and mid-zone nodules are present, measuring between 3 and 5mm diameter. Initially indistinct but become clearer with time. Nodules coalesce and calcify and can progress to PMF where the centre may cavitate. Associated calcified hilar lymphadenopathy (eggshell calcification) and possible pleural thickening. Nodules continue to develop with continued exposure but, due to long lag time, will also develop when patient stops being exposed. In some cases with heavy exposure to silica, patients may develop progressive upper zone fibrosis with sparse nodularity

    • PFTs Slow decline, including in TLCO, with mild restrictive pattern, unless the silicosis has caused emphysema when obstructive or mixed picture is seen

    • Pathology Dust particles within the alveoli are phagocytosed by macrophages. They are removed to the lymphatics where they lodge and cause diffuse inflammatory change. Layers of collagen are deposited around the dust particle. Nodules are found within the 2° pulmonary lobule where they cause fibrosis

  • Chronic silicosis occurs with lower dust concentrations than those seen in active silicosis; appears 10–30y after first exposure

    • CXR A few upper and mid-zone nodules occur, which become calcified after 10y or so. There is no associated parenchymal distortion. There may be associated hilar lymphadenopathy.

If there is further silica exposure, this disease may progress, with coalescence of nodules.

  • Silicotuberculosis Increased likelihood of active TB infection in people with silicosis, most likely due to the reactivation of quiescent lesions. Silica within the lung is thought to affect the efficacy of the macrophage at clearing Mycobacterium tuberculosis. TB can be difficult to diagnose, due to multiple pre-existing CXR nodules. Cavitation may occur. Haemoptysis, fever, worsening respiratory function, and new soft CXR opacities should prompt sputum examination and BAL. Confirmed TB should be treated with the usual three- or four-drug regime. NTM infection is also more common.


Prevention of silicosis by monitoring and minimizing dust levels with adequate ventilation. Masks can be useful for short-term use if the high levels of dust are transiently unavoidable. Silicosis diagnosed with: history of silica exposure (with amount of exposure and latency taken into account), compatible imaging, and lack of another diagnosis which would fit history and imaging better. Lung biopsy is usually not necessary if these three conditions are met, only if alternative diagnosis being considered. Prescribe bronchodilators if airflow limitation, O2 if respiratory failure; consider lung transplant if severe. Disability benefits available from the Department for Work and Pensions (see Pneumoconioses p. [link]). Small increased risk of lung cancer with silicosis and associated PMF.


Beryllium is a light, strong industrial metal. It is mined and often used as an alloy in the manufacture of fluorescent tubes for lighting and televisions, radiological equipment, in atomic reactors, and in heat-resistant ceramics. Cases of berylliosis are now rare, as beryllium levels have been tightly regulated to avoid sensitization. However, due to the long latent period between exposure and granuloma formation, as well as accidental beryllium exposure, cases are still occurring. There are two types of disease.

  • Acute beryllium disease is an acute alveolitis due to the direct effects of high-dose inhaled beryllium fumes. There is subsequent widespread airway oedema and pulmonary oedema, which causes dyspnoea, cyanosis, and widespread inspiratory crepitations. CXR shows pulmonary oedema. It may be self-limiting if mild but, if severe, is usually fatal. Corticosteroids may prevent progression, but the patient is often left with residual pulmonary impairment

  • Subacute and chronic berylliosis is a delayed hypersensitivity-type reaction due to beryllium, occurring a long time after beryllium exposure in a minority of individuals. It can be clinically indistinguishable from sarcoidosis. It has also been seen in the wives of beryllium workers and those who live near beryllium refineries. Inhalation of beryllium or the exposure of beryllium to a skin abrasion causes initial sensitization in 2–19% of exposed individuals. Only low levels of exposure are required for this. There is a T-cell-mediated immune response, with the production of numerous inflammatory cytokines, which cause granulomatous inflammation. Following a long latent period, which may be months to 10y plus after exposure, non-caseating granulomatous tissue reactions occur in the lungs or on the skin. There is a genetic predisposition to the response to beryllium exposure, and it is HLA-mediated (HLA-DPB1(Glu69)). HLA status could be used to identify workers at high risk of berylliosis (but is not routinely used at present).

Clinical features of chronic berylliosis

  • Symptoms Dry cough, dyspnoea, fever, malaise, night sweats. Macular skin lesions, which do not spontaneously resolve

  • Signs No clubbing or crepitations in early disease, but both occur with established fibrosis. Hepato/splenomegaly and macular skin lesions. Do not get uveitis or erythema nodosum.


  • CXR Fine reticulonodular appearance throughout both lungs. Finer nodules than those seen in sarcoidosis. Progression to interstitial fibrosis, with irregular linear opacities diffusely or favouring upper lobes. Hilar lymphadenopathy can occur, but always in association with ILD

  • HRCT Subpleural micronodular change, thickened interlobular septae, traction bronchiectasis, and honeycombing. There may be ground-glass shadowing

  • BAL High levels of T-lymphocytes

  • PFTs Restrictive defect, with decreased kCO

  • Pathology Non-caseating granulomata. Endobronchial and transbronchial biopsies may be adequate, taken from area of abnormal lung on CT. May be indistinguishable from sarcoidosis. May develop irregular fibrosis with bulla and cyst formation

  • Beryllium lymphocyte proliferation test (BeLPT) assesses whether patient is sensitized to beryllium. This blood test has become the standard industry test to see which beryllium workers are sensitized and therefore part of the diagnostic work-up. Can also be performed on BAL fluid to increase diagnostic accuracy. False negative rate, so borderline and negative tests generally repeated.

It can be difficult to distinguish berylliosis from sarcoidosis.


Corticosteroids are given to try and prevent disease progression. Continue indefinitely on the lowest dose which maintains symptom control, as few patients gain complete resolution of symptoms, CXR, or PFTs. Other immunosuppressants have been tried, but evidence limited. Annual screening of beryllium-exposed workers with CXR. If they develop breathlessness or skin rashes, this may be an indication to start oral steroids to delay progression to interstitial fibrosis. Avoid further beryllium exposure once evidence of berylliosis occurs and possibly when evidence of sensitization.


Progressive disease, although those with very low exposure who develop CXR changes may find they resolve. Associated delayed skin sensitivity (anergy) to tuberculin. Granulomata do not spontaneously resolve although can be excised if causing problems such as troublesome lesions on the skin. Interstitial fibrosis occurs in the lungs, which is progressive and leads to cyanosis and death. Other complications include pneumothorax, hypercalcaemia, hypercalciuria, and nephrocalcinosis.

Differential diagnosis

  • Sarcoidosis

  • TB.

In clinic

  • Ask patients with suspected sarcoidosis about possible exposure to beryllium

  • Monitor PFTs and CXR to assess disease response or progression.