The term pneumoconiosis refers to a group of chronic fibrosing lung diseases caused by the inhalation and retention of inorganic mineral dusts. It remains an important occupational lung disease, historically common in miners, construction workers, and shipbuilders.

🔎 About

Industrial fibrosing lung disease due to chronic inhalation of dusts such as coal, silica, and asbestos.
Characterised by progressive fibrosis, restrictive lung physiology, and increased malignancy risk.
Represents one of the main occupational interstitial lung diseases.

🧪 Aetiology

Coal dust → Coal Workers’ Pneumoconiosis (CWP, "black lung").
Silica → Silicosis (mining, sandblasting, stone cutting).
Asbestos fibres → Asbestosis (shipbuilding, insulation, construction).

🧬 Pathophysiology

Dust particles inhaled → engulfed by alveolar macrophages.
Persistent dust burden triggers chronic inflammation, cytokine release (TNF-α, IL-1), and fibroblast activation.
Results in progressive interstitial fibrosis and loss of alveolar architecture.
Upper vs lower lobe predominance depends on dust type (coal/silica → upper lobes, asbestos → lower lobes).

👩‍⚕️ Clinical Features

Progressive exertional breathlessness.
Chronic cough ± sputum (black sputum in CWP).
Clubbing of fingers (especially in asbestosis).
Pleuritic chest pain (with asbestos pleural plaques).
Advanced disease → hypoxaemia, cor pulmonale, respiratory failure.

🧾 Types

CWP – simple vs progressive massive fibrosis (PMF).
Silicosis – nodular upper lobe disease, “eggshell” hilar node calcification.
Asbestosis – lower lobe fibrosis + pleural plaques; associated with lung cancer & mesothelioma.

🧪 Investigations

Chest X-ray: Small nodules (CWP/silicosis), pleural plaques (asbestos), large upper lobe masses (PMF).
HRCT: Defines distribution, honeycombing, and nodularity.
Pulmonary function tests: Restrictive pattern with reduced TLCO; mixed defects if COPD coexists.
Sputum culture: Exclude secondary TB in silicosis/CWP.

⚠️ Complications

Progressive massive fibrosis (CWP, silicosis).
Tuberculosis (especially silicosis).
Rheumatoid overlap (Caplan’s syndrome in CWP).
Mesothelioma and bronchogenic carcinoma (asbestos).
Pulmonary hypertension & cor pulmonale.

💊 Management

Prevention: Dust control, PPE, occupational health surveillance.
Smoking cessation: Critical to reduce COPD and cancer risk.
Symptomatic treatment: Bronchodilators, inhaled therapy if coexistent airway disease.
Oxygen therapy: For hypoxaemia.
Pulmonary rehabilitation: Improves exercise tolerance & quality of life.
Vaccination: Flu and pneumococcal vaccines recommended.
Advanced disease: Consider transplantation; palliative care support.

📊 Comparison of Pneumoconioses

Feature	CWP 🪨	Silicosis 💎	Asbestosis 🪵
Aetiology	Coal dust (miners)	Silica dust (stone, mining)	Asbestos (construction, shipbuilding)
Radiology	Upper lobe nodules ± PMF	Upper lobe nodules + “eggshell” hilar nodes	Lower lobe reticulation, pleural plaques
Complications	PMF, Caplan’s syndrome, TB	TB, progressive fibrosis, lung cancer	Mesothelioma, bronchogenic carcinoma
Prognosis	Simple CWP benign; PMF disabling	Often progressive despite exposure cessation	Poor due to malignancy risk

📚 Teaching Commentary

🩺 Think of these as occupational lung “siblings”:

CWP: Black sputum, upper lobe nodules, rheumatoid overlap (Caplan’s).
Silicosis: Classic “eggshell” calcification + TB risk.
Asbestosis: Lower lobe fibrosis + pleural plaques, with dual cancer risk (mesothelioma + lung carcinoma).

💡 Exam pearl: Upper lobe nodules → think coal or silica. Lower lobe + pleural disease → think asbestos.

📖 References

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Pneumoconiosis