Synopsis
Recognise when work has caused or aggravated respiratory disease, establish exposure–response evidence without jeopardising employment prematurely, and coordinate early specialist, occupational-health and workplace action.
- Ask every patient with new asthma, cough, breathlessness or interstitial disease what they do now, what they previously did, and which dusts, fumes, vapours, aerosols, animals or biological materials they encounter.
- A pattern that improves on rest days or holidays and worsens during particular tasks is a diagnostic clue, but delayed reactions mean symptoms need not begin during the shift.
- Occupational asthma is new asthma caused by work; work-aggravated asthma is pre-existing or coincidental asthma worsened by workplace conditions. The distinction affects prognosis and workplace control.
- Objective testing should begin while the worker is still exposed when it is safe: serial peak-flow records at and away from work are much more useful than one clinic spirometry result.
- Silica, asbestos, coal, welding fume, wood dust, flour, isocyanates, laboratory animals, metalworking fluid and farming bioaerosols cause different airway, interstitial, malignant and infectious risks.
- Exposure control is treatment. Substitution, enclosure, local exhaust ventilation and process change take precedence over relying only on respiratory protective equipment.
- Do not advise resignation at the first consultation. Early specialist assessment, occupational-health liaison and carefully consented communication can protect both lung function and livelihood.
- The clinician diagnoses and documents; the employer or other responsible person usually holds the RIDDOR reporting duty. Explain this distinction and seek occupational-medicine advice when uncertain.
- Long latency matters: pneumoconiosis, asbestos-related disease and occupational cancer may present decades after retirement, so a lifetime job chronology is required.
- Ask whether colleagues have similar symptoms and whether health surveillance exists; clustering can identify an uncontrolled workplace hazard.
Key red flags
Symptoms begin after a high-level irritant exposure or repeated intense peaks, sometimes without a sensitisation latency. Acute hypoxaemia, bronchospasm or radiographic infiltrates require emergency assessment.
Haemoptysis, weight loss, persistent chest pain, unilateral effusion or radiographic mass after asbestos, silica, diesel exhaust, welding or wood-dust exposure needs urgent cancer-pathway investigation.
Investigation priorities
Establish plausible agents, dose pattern, latency and relation between symptoms and work.
Management branches
New or worsening respiratory symptoms in anyone currently or previously employed.
- Stabilise acute illness, document oxygenation and ask whether symptoms began during a specific exposure, spill, fire or confined-space event.
- Create a lifetime job and task chronology, including materials, processes, controls, personal protective equipment, coworkers and symptom variation away from work.
- Confirm the respiratory phenotype with spirometry and appropriate imaging rather than diagnosing from exposure alone.
- Explain uncertainty, employment implications and the value of early specialist occupational-respiratory referral.
Key medicines
Inhaled corticosteroid-containing asthma treatmentUse the current joint BTS/NICE/SIGN step appropriate to symptoms, attacks and objective response; verify the device and regimen in the current BNF.Medication does not make continued sensitiser exposure safe. Check technique, adherence, voice effects and oral candidiasis, and do not let symptom improvement delay occupational referral.
Smoking-cessation pharmacotherapyOffer an evidence-based licensed option with behavioural support, selected and prescribed using the current NICE tobacco guidance and BNF.Match treatment to pregnancy, renal function, mental-health history, interactions and patient preference. Smoking history must never be used to discount an occupational contribution.