Coal workers' pneumoconiosis and silicosis

Lesion

Inhaled coal or silica dust is eaten by macrophages. Coal gives black spots and nodules; silica gives hard, whorled scars and a higher TB risk.

Updated Nov 12, 2026

Key points

Anthracosis: harmless carbon pigment in macrophages along lymphatics and nodes (city dwellers, smokers).
Simple coal workers' pneumoconiosis: coal macules and small nodules near respiratory bronchioles, upper zones, with centrilobular emphysema.
Progressive massive fibrosis: black scars of a centimetre or more, often with necrotic centres; arises in a minority.
Silicosis: whorled collagen nodules in upper zones and hilar nodes; eggshell calcification of nodes; birefringent particles under polarised light.
Silica activates the NLRP3 inflammasome (IL-1, IL-18) and impairs macrophage killing of mycobacteria: higher tuberculosis risk, and a higher lung cancer risk.
Exposures: mining, quarrying, sandblasting (including stressed denim), stone cutting and carving, foundries, concrete demolition.

What it is

Pneumoconioses are lung reactions to inhaled mineral dust, mostly at work. Particles of about one to five micrometres reach the small airways and are taken up by alveolar macrophages, which release inflammatory and fibrogenic mediators. Coal dust usually causes little harm; silica, the commonest occupational lung disease in the world, causes progressive nodular fibrosis that continues after exposure ends.

Structure

Coal macule: aggregates of carbon-laden macrophages around respiratory bronchioles with a fine collagen network; adjacent alveoli dilate.
Progressive massive fibrosis: dense collagen and abundant black pigment, central necrosis from ischaemia.
Silicotic nodule: central whorled, hyalinised collagen with a peripheral rim of dust-laden macrophages; nodules coalesce into hard scars and may cavitate.
Hilar nodes: fibrosis and thin rims of calcification (eggshell); pleural fibrosis.

Step by step

Fine particles escape mucociliary clearance and deposit in respiratory bronchioles and alveoli.
Alveolar macrophages phagocytose the particles.
Crystalline silica (quartz) damages phagolysosomes and activates the inflammasome; IL-1 and IL-18 recruit more cells.
Activated macrophages release TGF-β and growth factors that stimulate fibroblasts to make collagen.
Nodules form around the dust and coalesce; the disease can keep progressing without further exposure.
Coal dust is less fibrogenic, but contaminating silica and heavy burdens drive progressive massive fibrosis.

Coal vs silica vs asbestos

Feature	Coal	Silica	Asbestos
Where in the lung	Upper zones	Upper zones, hilar nodes	Lower lobes, subpleural
Hallmark lesion	Coal macule, progressive massive fibrosis	Whorled collagen nodule, eggshell nodes	Diffuse fibrosis with asbestos bodies, pleural plaques
Tuberculosis risk	Not increased	Increased	Not notably increased
Cancer risk	Not increased without smoking	Increased lung cancer	Lung carcinoma and mesothelioma

Markers

Polarised light: weakly birefringent silica

Clinical notes

Silicosis is usually chronic (10 to 30 years) but can be accelerated or, after intense exposure, acute with alveolar proteinosis-like filling.
Chest film: fine upper-zone nodules; dyspnoea appears late, when massive fibrosis develops.
Patients with silicosis need screening for tuberculosis, a relevant point in Latin American mining regions.
Coal workers may also develop emphysema and chronic bronchitis independent of smoking.

Test yourself

Think of the answer, then tap the question to see it.

What is the hallmark histologic lesion of silicosis?

A silicotic nodule: central whorled hyalinised collagen surrounded by a zone of dust-laden macrophages, with weakly birefringent particles under polarised light.

Why does silicosis increase the risk of tuberculosis?

Crystalline silica impairs the ability of alveolar macrophages to kill phagocytosed mycobacteria.

What is progressive massive fibrosis?

Large black or grey scars of a centimetre or more that form on a background of simple coal or silica pneumoconiosis, impairing lung function.

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Connections

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Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Sources: Interstitial Lung Diseases (MedlinePlus, US National Library of Medicine, 2025); Tuberculosis (MedlinePlus, US National Library of Medicine, 2025).

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Representative model, for educational purposes only.