Occupational lung disease (pneumoconioses)

Overview

Upper lobes are better ventilated than perfused (V/Q >1) so inhaled particles deposit there - explains upper zone predominance in inhalation diseases. Lower lobes are better perfused (V/Q <1) - explains lower zone predominance in systemic/drug/connective tissue disease.

🧠

CHARTS = upper zone fibrosis causes: Coal workers' pneumoconiosis, Histiocytosis/Hypersensitivity pneumonitis, Ankylosing spondylitis/ABPA, Radiation, Tuberculosis, Silicosis/Sarcoidosis.

ACID = lower zone fibrosis causes: Asbestosis, Connective tissue disease, Idiopathic pulmonary fibrosis, Drugs (methotrexate, nitrofurantoin, amiodarone).

Presentation

•Progressive exertional dyspnoea - cardinal symptom, insidious onset over years to decades
•Dry cough - persistent, non-productive
•Fine inspiratory crackles - basal in asbestosis; upper in CWP/silicosis
•Finger clubbing - particularly asbestosis
•Lifetime occupational history - single most important diagnostic tool; symptoms may emerge 20-40 years after exposure

Investigations

🥇 First-line

•Chest X-ray - upper zone nodular opacities (CWP/silicosis), eggshell hilar calcification (silicosis), pleural plaques and lower zone fibrosis (asbestosis)
•Spirometry - restrictive pattern (FEV1/FVC >0.7 with reduced FVC); reduced TLCO

🏆 Gold standard

•HRCT chest - defines distribution and extent of fibrosis, nodules, honeycombing, and pleural disease
🎯
Spirometry shows a RESTRICTIVE pattern in pneumoconiosis - this rules out COPD, asthma, and bronchiectasis (all obstructive). The key differentiator from IPF is the occupational history and upper zone predominance on imaging.

Management

•No disease-modifying treatment exists - management is supportive

🥇 First-line

•Cessation of dust exposure - cornerstone; slows but does not reverse progression
•Smoking cessation - especially critical in asbestosis (synergistic/multiplicative risk with asbestos for lung cancer)
•Annual influenza and pneumococcal vaccination; pulmonary rehabilitation

🥈 Second-line

•Long-term oxygen therapy (LTOT) - if SpO2 ≤92% at rest, cor pulmonale, or polycythaemia
•Silicotuberculosis - treat with standard anti-tuberculous therapy (prolonged course)

🥉 Third-line

•Lung transplantation - end-stage disease in suitable candidates

Complications

•Progressive massive fibrosis (PMF) - coalescence of nodules >1 cm; complicates silicosis and CWP; severe restrictive impairment
•Silicotuberculosis - silica impairs macrophage killing of Mycobacterium tuberculosis; screen all silicosis patients for TB
•Mesothelioma - almost exclusively asbestos (especially crocidolite); latency 20-40 years; median survival ~12 months
•Lung cancer - asbestos + smoking = ~50-fold increased risk (synergistic, not additive)
•Caplan syndrome - large pulmonary nodules in CWP/silicosis patients who also have rheumatoid arthritis
•Cor pulmonale - right heart failure from pulmonary hypertension; raised JVP, peripheral oedema, RV heave
📌
Asbestosis and mesothelioma are notifiable diseases - patients may be entitled to industrial injuries disablement benefit.

Comparison of the Three Major Pneumoconioses

Silicosis vs Coal Workers' Pneumoconiosis vs Asbestosis
FeatureSilicosisCoal workers' pneumoconiosis (CWP)Asbestosis
DustCrystalline silicaCoal dustAsbestos fibres
OccupationsMiners, quarry/pottery/granite workersCoal minersConstruction, dockyard, firefighters
CXR zoneUpper zone fibrosisUpper zone fibrosisLower zone fibrosis
Classic CXR findingUpper nodular opacities + eggshell hilar calcificationUpper nodular opacities (bilateral)Pleural plaques + basal fibrosis
Key complicationSilicotuberculosis; progressive massive fibrosisProgressive massive fibrosis (PMF)Mesothelioma; lung cancer (synergistic with smoking)
Finger clubbingLess commonLess commonParticularly associated