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← Respiratory indexChapter sections
Role and principlesAssessment and patient selectionBaseline assessmentInterventionsMedicines and treatment safetyTargets, monitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Occupational lung disease and workplace assessment

Respiratory · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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Time-critical presentation

Remove the person from an active exposure and use an ABCDE approach if there is acute bronchospasm, hypoxaemia, toxic inhalation, chemical pneumonitis or suspected asphyxiant exposure. Give emergency respiratory treatment according to the presentation and contact toxicology, emergency medicine and occupational-health expertise; do not send an unstable worker back to the workplace.

Role and principles

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.

Work-related lung disease is a causal framework rather than one diagnosis. It includes sensitiser-induced and irritant asthma, COPD from dust or fume exposure, hypersensitivity pneumonitis, pneumoconioses, asbestos-related pleural and malignant disease, infection, acute inhalational injury and occupational lung cancer. Smoking can interact with exposure but must not be used to dismiss occupational causation.

The decisive task is to connect a credible exposure with compatible disease and timing. Take a chronological work history from first job onward: employer and site, exact tasks, materials and trade names, visible dust or mist, ventilation, respiratory protection, spills or peaks, health surveillance, symptoms in coworkers, and symptom variation across shifts, weekends and holidays. Include hobbies, home renovation and environmental exposure.

Assessment is clinically and socially sensitive. A worker may fear lost income, immigration consequences or employer retaliation. Explain what will be recorded, obtain consent before contacting an employer, and involve a respiratory physician with occupational expertise early. Public-health or safeguarding obligations may sometimes override confidentiality, but disclosure should be proportionate and discussed whenever possible.

Assessment and patient selection

Sensitiser-induced occupational asthma

A latency period after starting exposure, work-related wheeze or chest tightness, associated rhinitis or conjunctivitis, and improvement away from work support sensitisation. Flour, isocyanates, wood dust, laboratory animals and enzymes are classic risks.

Irritant-induced asthma or inhalational injuryRed flag

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.

Pneumoconiosis and fibrotic disease

Progressive exertional breathlessness, dry cough, restrictive physiology and characteristic imaging after silica, coal or asbestos exposure may emerge many years after exposure ends. Silicosis also increases tuberculosis risk.

Hypersensitivity pneumonitis

Recurrent feverish episodes, cough and breathlessness hours after mouldy hay, birds, contaminated metalworking fluid or another antigen suggest inflammatory alveolitis; chronic exposure can produce irreversible fibrosis.

Occupational malignancyRed flag

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.

Work-aggravated respiratory disease

Pre-existing asthma, COPD or bronchiectasis worsens with cold, exertion, dust or nonspecific fumes at work without evidence that work caused the original disease. Workplace modification remains clinically important.

Baseline assessment

  1. 01
    Structured lifetime occupational history and exposure chronologyFirst step
    Why
    Establish plausible agents, dose pattern, latency and relation between symptoms and work.
    Interpretation and limitations
    Record task-level detail rather than job title alone. Improvement on holidays, affected colleagues, accidental peaks and inadequate controls strengthen causation but do not replace objective disease testing.
  2. 02
    Spirometry with bronchodilator reversibility
    Why
    Confirm variable airflow obstruction or identify a restrictive pattern requiring full physiology.
    Interpretation and limitations
    Normal spirometry does not exclude occupational asthma. Repeat when symptomatic and compare with previous health-surveillance records if the worker consents.
  3. 03
    Serial peak expiratory flow at work and away
    Why
    Objectively test whether airway calibre changes with occupational exposure.
    Interpretation and limitations
    Specialist-designed records generally require repeated readings across working and non-working periods with task and treatment diaries. Poor technique, treatment changes and insufficient time away can obscure a true pattern.
  4. 04
    FeNO, blood eosinophils and specific IgE where relevant
    Why
    Support eosinophilic airway inflammation or sensitisation to a recognised occupational allergen.

Interventions

01First consultationBuild the exposure–disease hypothesisFirst stepNew or worsening respiratory symptoms in anyone currently or previously employed.+
  1. 1Stabilise acute illness, document oxygenation and ask whether symptoms began during a specific exposure, spill, fire or confined-space event.
  2. 2Create a lifetime job and task chronology, including materials, processes, controls, personal protective equipment, coworkers and symptom variation away from work.
  3. 3Confirm the respiratory phenotype with spirometry and appropriate imaging rather than diagnosing from exposure alone.
  4. 4Explain uncertainty, employment implications and the value of early specialist occupational-respiratory referral.
02Possible occupational asthmaPreserve diagnostic opportunity safelyVariable airway symptoms with a credible workplace sensitiser or irritant pattern.+
  1. 1

Medicines and treatment safety

Controls airway inflammation while exposure causation and workplace protection are addressed.

Inhaled corticosteroid-containing asthma treatment

Use 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.

Reduces additive respiratory and cancer risk and slows avoidable loss of lung function.

Smoking-cessation pharmacotherapy

Offer 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.

Treats acute hypoxaemia from bronchospasm, inhalational injury or advanced occupational lung disease.

Controlled oxygen for acute hypoxaemia

Titrate to the BTS target range for the clinical context; use a lower target when hypercapnic respiratory failure is a recognised risk.

Document device and target, obtain blood gases when indicated and escalate ventilatory support promptly. Long-term oxygen requires formal assessment, not an acute prescription carried forward.

Targets, monitoring and follow-up

  • Track symptoms, rescue inhaler use, attacks and spirometry against specific tasks, exposure changes, weekends and holidays.
  • For suspected occupational asthma, review serial peak-flow quality early so an unusable record is not collected for weeks.
  • For fibrotic occupational disease, trend FVC, gas transfer, exertional saturation, imaging and functional status through specialist follow-up.
  • Confirm that workplace controls or redeployment actually reduce exposure; respiratory protective equipment alone may fail through fit, maintenance or task mismatch.
  • Revisit mental health, income, benefits, work identity and family impact because diagnostic and exposure decisions can cause substantial harm.
  • Safety-net haemoptysis, weight loss, progressive breathlessness, syncope, fever or acute post-exposure symptoms for urgent reassessment.

Special situations

The job title is not the exposure

Two bakers, welders or healthcare workers may encounter entirely different agents. Ask what is mixed, cut, sprayed, heated, cleaned or aerosolised and request safety data sheets through occupational health.

Timing can be delayed

Sensitiser-induced asthma may worsen late in a shift or overnight, so a worker who feels better while physically at work can still have a convincing occupational pattern.

Removal can erase evidence

Peak-flow variation and bronchial hyperresponsiveness may lessen after exposure stops. Preserve diagnostic testing promptly, while never continuing exposure when it is unsafe.

Pleural plaques are a marker

They support previous asbestos exposure but are usually not the cause of severe breathlessness. Look for diffuse pleural thickening, asbestosis, malignancy or another cardiorespiratory diagnosis.

Control hierarchy matters

Eliminating or substituting the hazard and controlling it at source are more reliable than depending on behaviour or a mask after contamination reaches the breathing zone.

Common pitfalls

  1. 01

    Asking only for the current occupation and missing exposure decades earlier.

  2. 02

    Using one normal spirometry result to exclude occupational asthma.

  3. 03

    Treating a positive specific-IgE result as proof of occupational causation.

  4. 04

    Advising immediate resignation before objective assessment and specialist workplace planning.

  5. 05

    Contacting an employer without consent when there is no overriding safety duty.

  6. 06

    Assuming smoking fully explains COPD, cancer or fibrosis despite substantial occupational exposure.

  7. 07

    Confusing the clinician’s role with the employer’s RIDDOR reporting responsibility.

Practice

Two practice questions

Your practice draft is saved in this browser.

Question 1 of 2
0 correct
RespiratoryOriginal SBA

Work-related wheeze in a spray painter

A vehicle spray painter has six months of wheeze that improves on holidays. Spirometry is normal today and they fear losing their job. What is the best next step?

Choose one answer, then submit
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Sources and review status5 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • BTS Clinical Statement on Occupational AsthmaValid BTS statement covering exposure history, objective diagnosis, workplace management and prognosis.
  • HSE work-related lung disease overviewOfficial Great Britain regulator overview of pneumoconiosis, silicosis and hypersensitivity pneumonitis.
  • HSE health surveillance overviewCurrent statutory and occupational-health surveillance context.
  • HSE reportable occupational diseasesCurrent RIDDOR disease and responsible-person framework.
  • HSE silicosis causes and risk controlsExposure, complications, health surveillance and control principles.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom

Exposure limits, statutory duties, prescribed-disease benefits and reporting rules vary by jurisdiction and change; verify current HSE, local occupational-health and benefits guidance before making an occupational-health determination.

Key points

  • 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.
Interpretation and limitations
A positive IgE result shows sensitisation, not necessarily occupational asthma; a negative result does not exclude low-molecular-weight sensitisers such as isocyanates.
  • 05
    Chest radiograph and high-resolution CT
    Why
    Identify pneumoconiosis, pleural plaques, fibrosis, hypersensitivity pneumonitis or malignancy.
    Interpretation and limitations
    Imaging pattern and distribution must be integrated with exposure and physiology. Pleural plaques mark asbestos exposure but do not by themselves explain breathlessness.
  • 06
    Full pulmonary function tests and exercise oxygen assessment
    Why
    Quantify restriction, gas-transfer impairment and functional consequence.
    Interpretation and limitations
    Falling TLCO or exertional desaturation may precede severe resting abnormality; compare serial results and account for haemoglobin and smoking status.
  • 07
    Targeted microbiology and autoimmune testing
    Why
    Find mimics or complications such as tuberculosis in silicosis or connective-tissue disease causing fibrosis.
    Interpretation and limitations
    Order tests from the differential, not as a blanket panel. Haemoptysis, systemic illness or epidemiological TB risk warrants prompt infection assessment.
    • Treat current asthma according to the joint BTS/NICE/SIGN pathway while checking severity and attack risk.
  • 2Refer early to a clinician experienced in occupational asthma; arrange serial peak-flow assessment while still exposed only if clinically safe.
  • 3With consent, involve occupational health to reduce or suspend exposure using substitution, engineering controls or temporary redeployment.
  • 4After objective assessment, agree a durable exposure plan, document work advice and review lung function and socioeconomic impact.
    • 03Dust or fibrotic diseaseDefine exposure and complicationsRestrictive physiology, impaired gas transfer, fibrosis or pleural disease with a relevant historical exposure.+
    1. 1Obtain chest imaging and full physiology, then refer to respiratory or ILD expertise for multidisciplinary interpretation.
    2. 2Stop continuing hazardous exposure and smoking, assess vaccination and pulmonary-rehabilitation needs, and manage hypoxaemia according to BTS criteria.
    3. 3Screen selectively for complications such as tuberculosis with silicosis or malignancy with asbestos exposure, guided by symptoms and national pathways.
    4. 4Discuss occupational-health documentation, benefits advice and legal/reporting routes without implying that a clinical opinion alone establishes compensation.
    04Workplace actionCommunicate without causing avoidable harmA credible workplace cause or aggravating exposure has been identified.+
    1. 1Ask what the patient wants shared, explain confidentiality, and record consent for communication with occupational health or the employer.
    2. 2Describe functional restrictions and exposure risk rather than demanding dismissal; seek competent occupational-medicine input for adjustments.
    3. 3Clarify that RIDDOR duties normally fall to the responsible employer or self-employed person after a confirmed linked diagnosis.
    4. 4EscalationSafety-net deterioration, arrange clinical follow-up and escalate a continuing serious hazard through appropriate HSE or public-health channels when necessary.
    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.