Silicosis and coal-worker pneumoconiosis — Rapid

Synopsis

Recognise silica and coal-dust pneumoconiosis, identify accelerated disease and tuberculosis, stop hazardous exposure and provide specialist, occupational and statutory support.

Pneumoconiosis describes diffuse lung disease caused by retained inhaled mineral dust; silicosis and coal-worker pneumoconiosis are important UK occupational examples.
Respirable crystalline silica arises from stone, rock, sand and clay, with high-risk tasks including cutting engineered stone, dry grinding, tunnelling, quarrying and sandblasting.
Silicosis may be chronic after long latency, accelerated after intense exposure over fewer years, or acute after very high exposure.
Chronic simple silicosis classically produces upper-lobe small nodules and sometimes eggshell nodal calcification; progressive massive fibrosis forms large conglomerate opacities.
Coal-mine dust can cause simple coal-worker pneumoconiosis, progressive massive fibrosis and COPD; smoking is an additional but not necessary cause of airflow obstruction.
Silica exposure and silicosis increase tuberculosis risk, so fever, weight loss, night sweats, haemoptysis or radiological change demands microbiological assessment.
No drug removes deposited dust or reliably reverses established fibrosis; prevention and cessation of harmful exposure are fundamental.
A disposable paper mask is not a substitute for elimination, wet cutting, extraction, enclosure and correctly selected respiratory protective equipment within a lawful control system.
Diagnosis requires a credible task-based exposure history, compatible imaging and exclusion of mimics such as sarcoidosis, infection, malignancy and other ILDs.
Specialist documentation supports occupational-health action and possible Industrial Injuries Disablement Benefit, but clinical diagnosis does not guarantee statutory eligibility.

Key red flags

Accelerated or acute silicosis

High-intensity exposure, particularly dry engineered-stone processing or sandblasting, is followed within a shorter latency by rapidly worsening cough, breathlessness, diffuse opacity or alveolar-filling disease.

Tuberculosis complication

Fever, night sweats, weight loss, haemoptysis, cavitation or new focal change in silica-exposed disease requires urgent TB sampling, infection-control assessment and specialist notification pathways.

Malignancy or alternative disease

An enlarging asymmetric mass, nodal change, haemoptysis or systemic decline needs cancer and infection evaluation rather than automatic attribution to progressive massive fibrosis.

Investigation priorities

Task-based occupational historyFirst step

Estimate dust type, intensity, duration, latency and current exposure.

Management branches

DiagnosisLink the radiology to the real task

Nodular or fibrotic lung disease appears in a person with possible mineral-dust exposure.

Assess respiratory stability and infectious red flags, then build a detailed exposure chronology covering materials, processes, visible dust and controls across every job and hobby.
Obtain chest imaging, full pulmonary function and exercise oxygenation; ask thoracic radiology to distinguish small-opacity disease, progressive massive fibrosis, emphysema and suspicious focal lesions.
Evaluate tuberculosis, sarcoidosis, fungal infection, malignancy and other ILD according to symptoms and imaging before confirming pneumoconiosis at specialist review.
Document diagnosis, impairment and exposure evidence separately, explaining uncertainty and the plan for occupational-health and statutory support.

Key medicines

Controlled oxygenFor acute hypoxaemia target 94–98% in most adults or 88–92% if at risk of hypercapnic respiratory failure, pending blood gases and an individual prescription.Oxygen does not remove mineral dust or halt fibrosis. Long-term and ambulatory use requires formal assessment; increasing need should prompt investigation for tuberculosis, infection, malignancy, embolism or pulmonary hypertension.

Inhaled bronchodilator for coexisting obstructive diseaseSelect the inhaler and licensed dose from objective COPD or asthma assessment, inhaler technique, current NICE guidance and the local formulary; there is no pneumoconiosis-specific bronchodilator regimen.Do not infer COPD from breathlessness alone or expect bronchodilation to reverse fibrosis. Review technique, adherence, cardiovascular and antimuscarinic adverse effects and exacerbation history; avoid inhaled corticosteroid without the appropriate indication.

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