Occupational lung disease: silicosis, asbestos and hypersensitivity pneumonitis

Why occupational lung disease matters in Australian general practice

Occupational lung disease — lung injury caused by inhaled workplace dusts, fumes, vapours, fibres, or biological antigens — is underdiagnosed in Australian general practice. The key reason is that a detailed occupational history is not routinely taken. A question as simple as “tell me about all the jobs you’ve ever worked in and what you were exposed to” has the potential to change the diagnosis, the management, and the medico-legal pathway.

Australia is currently managing two major occupational respiratory crises. First, a silicosis epidemic among workers who cut engineered stone (artificial stone kitchen benchtops) — with some developing severe, progressive lung fibrosis within five years of exposure. Second, an ongoing burden of asbestos-related disease from the decades when Australia had one of the highest per-capita asbestos uses in the world. The engineered stone ban came into effect on 1 July 2024 — the first worldwide.

The consequence for general practice is twofold. Clinicians are seeing the downstream effects of past exposures presenting as slowly progressive breathlessness, and are encountering workers from previously exposed industries who need surveillance and early-disease detection. A respiratory presentation without an occupational history is an incomplete assessment.

Taking that history, arranging HRCT chest imaging, referring to respiratory medicine and occupational physician, and supporting a workers compensation claim are the four practical GP contributions that change outcomes in occupational lung disease.

A. Core clinical — the AU general-practice framework

Taking an occupational history

The occupational history is the foundation of diagnosis. For every patient with respiratory symptoms, establish:

• Chronological job history — every job from leaving school to the present day; do not assume the current job is the relevant one
• Specific exposures at each job — silica dust (stone cutting, mining, sandblasting, pottery, dental ceramics), asbestos (construction, demolition, plumbing, electrical, shipyards, automotive brakes), coal dust (mining), cotton or flour dust (textile and bakery workers), animal proteins (farmers, veterinarians, laboratory workers), chemical sensitisers (isocyanates in spray-painters, persulfates in hairdressers)
• Personal protective equipment (PPE) — was it provided and consistently used?
• Duration and intensity — years exposed; dusty environment vs occasional exposure
• Hobbies and home exposures — DIY renovation (pre-2004 materials may contain asbestos), bird-keeping, home composting, indoor mould

Document this history verbatim. It becomes medico-legal evidence if a compensation claim proceeds.

Symptoms to identify

• Progressive exertional breathlessness — cardinal symptom of most occupational interstitial lung diseases
• Persistent cough — non-productive in silicosis and asbestosis; may be productive in occupational bronchitis
• Chest tightness and wheeze — especially if worse at work and better on weekends or holidays (occupational asthma)
• Flu-like episodes 4–8 hours after specific exposures — hypersensitivity pneumonitis
• Pleuritic chest pain or recurrent pleural effusion — asbestos-related effusion or mesothelioma
• Weight loss, haemoptysis — mesothelioma or lung cancer
• Asymptomatic — many patients with early occupational interstitial lung disease have no symptoms; disease is found on surveillance imaging

Examination

• Respiratory rate, oxygen saturation
• Fine bibasal inspiratory crackles (pulmonary fibrosis — asbestosis, fibrotic hypersensitivity pneumonitis)
• Wheeze and expiratory flow reduction (occupational asthma, COPD component)
• Clubbing (advanced asbestosis, mesothelioma)
• Signs of right heart failure (cor pulmonale from advanced disease)
• Lymphadenopathy or pleural effusion

Investigations

Per Therapeutic Guidelines — Respiratory and TSANZ guidance:

• Spirometry ± lung volumes ± DLCO — obstructive pattern (occupational asthma, COPD), restrictive pattern (silicosis, asbestosis, hypersensitivity pneumonitis), reduced DLCO (gas exchange impairment)
• Chest X-ray — pleural plaques, fibrosis, nodules, masses; less sensitive than HRCT for early disease
• HRCT chest — gold standard for interstitial lung disease pattern recognition; upper-zone centrilobular nodules (silicosis), lower-zone fibrosis and pleural plaques (asbestos), ground-glass with mosaic attenuation (hypersensitivity pneumonitis)
• Bloods — ANA, ANCA, RF, anti-CCP (autoimmune ILD exclusion or overlap), specific IgG precipitins for avian or thermophilic actinomycetes antigens (hypersensitivity pneumonitis), HIV, FBC
• TST or IGRA — tuberculosis (TB) screening in silicosis patients given substantially increased reactivation risk
• ECG, echocardiogram — pulmonary hypertension or cor pulmonale

Spirometry, lung volumes, DLCO, chest X-ray, HRCT, autoimmune bloods, and TST/IGRA are all Medicare-rebatable.

B. Silicosis — Australia’s current epidemic

Epidemiology

Safe Work Australia defines respirable crystalline silica as a confirmed human carcinogen. Engineered stone products contain up to 90–95% crystalline silica — compared with less than 10% in natural granite. Workers cutting, grinding, or polishing engineered stone benchtops were exposed to silica concentrations far exceeding safe levels. Many worked without adequate respiratory protection or respiratory surveillance.

The workplace exposure standard for respirable silica was reduced from 0.1 mg/m³ to 0.05 mg/m³ on 1 July 2020. Australia became the first country to ban the use, supply, manufacture, and import of engineered stone from 1 July 2024 — a landmark public health decision.

Approximately 600 cases of silicosis were identified in the engineered stone cohort in Queensland and Victoria between 2017 and 2023; national surveillance continues. Other silica-exposed industries remain: mining, tunnelling, quarrying, sandblasting, foundry work, pottery, and dental ceramics production.

Disease forms

• Acute silicosis — heavy short-term exposure; rare; rapidly progressive alveolar proteinosis-like pattern; high mortality
• Accelerated silicosis — the engineered stone form; 5–10 years of exposure; rapid progression; often in young workers
• Chronic silicosis — longer latency (10–30+ years); slower progression; classic nodular pattern on HRCT
• Progressive massive fibrosis (PMF) — conglomerate fibrotic masses; silicotic conglomerate upper-zone; poor prognosis
• Silico-tuberculosis — silicosis increases TB reactivation risk three to eightfold; LTBI screening and treatment are non-negotiable in all silicosis patients; refer to guidelines on LTBI
• Autoimmune complications — Caplan syndrome (silicosis plus rheumatoid nodules), scleroderma, ANCA vasculitis (Erasmus syndrome)

HRCT findings

• Centrilobular nodules — upper-zone predominance; may be diffuse in severe disease
• Eggshell calcified hilar lymphadenopathy — pathognomonic of silicosis (also sarcoidosis)
• Conglomerate masses (PMF) — large fibrotic masses replacing upper-lobe architecture
• Ground-glass opacity — acute or accelerated forms

Management

• Remove from silica exposure — the non-negotiable cornerstone of management; initiate a workers compensation claim
• No specific approved drug therapy for established silicosis progression; pirfenidone and nintedanib (antifibrotics) are being trialled in PMF in specialist tertiary settings
• TB and LTBI treatment — isoniazid preventive therapy for positive IGRA or TST
• Vaccinate — influenza, pneumococcal Prevenar 20, COVID-19, RSV (per ATAGI for chronic lung disease)
• Pulmonary rehabilitation — improve exercise tolerance and quality of life
• Lung transplant — for end-stage disease in eligible patients; long waitlists in Australia
• Notification — silicosis is notifiable in Victoria (since 2019) and Queensland; other states evolving

C. Asbestos-related disease, hypersensitivity pneumonitis, and occupational asthma

Asbestos-related disease

Australia had one of the highest per-capita asbestos uses globally until the chrysotile ban took effect on 31 December 2003 (amphibole types banned earlier). The long latency — 20–50 years from exposure to mesothelioma, 10–30 years to asbestosis — means new cases continue to be diagnosed from 1960s–1990s exposures.

The spectrum of asbestos-related disease:

• Pleural plaques — bilateral calcified pleural plaques; benign markers of past asbestos exposure; no malignant transformation per se
• Asbestosis — interstitial lung fibrosis from heavy asbestos exposure; bilateral lower-zone fibrosis and honeycombing in advanced cases; restrictive spirometry and reduced DLCO; no effective disease-modifying treatment; supportive care
• Pleural thickening — diffuse restrictive pathology
• Benign asbestos pleural effusion — may precede malignant disease
• Lung cancer — asbestos exposure multiplies the risk; asbestos combined with cigarette smoking is synergistic and multiplicative (approximately 50 times the risk of non-smoking, non-asbestos-exposed individuals); smoking cessation is critical
• Mesothelioma — pleural most common; peritoneal; universally fatal; median survival 12–21 months; treatment has improved with nivolumab plus ipilimumab immunotherapy combination (CheckMate-743 trial, first-line for unresectable) and cisplatin-pemetrexed chemotherapy

People at risk: miners (Wittenoom WA, Baryulgil NSW), construction and demolition workers, plumbers, electricians, shipyard and navy workers, automotive workers (brake linings), household renovators (pre-1990 materials). Family members who washed work clothes were exposed paraoccupationally.

Investigation: HRCT chest, spirometry and DLCO, pleural fluid cytology and biopsy for suspected mesothelioma. Refer to the Asbestos Diseases Foundation of Australia for patient support resources.

Hypersensitivity pneumonitis

Hypersensitivity pneumonitis (HP) — also called extrinsic allergic alveolitis — is an immune-mediated interstitial lung disease caused by repeated inhalation of organic antigens.

Common Australian causes:

• Farmer’s lung — thermophilic actinomycetes in mouldy hay or grain; seasonal farming workers
• Bird-fancier’s / pigeon-breeder’s lung — avian serum proteins; pigeon racers, budgerigar and cockatoo owners
• Hot tub lung — Mycobacterium avium complex aerosol from inadequately maintained spa pools
• Chemical HP — isocyanates (spray-painters), anhydrides, nitrofurantoin (drug-induced)
• Domestic mould — damp homes; common and underrecognised

Clinical forms:

• Acute — flu-like episode 4–8 hours after exposure; fever, cough, breathlessness; resolves within days of antigen avoidance
• Subacute — weeks to months of progressive breathlessness and weight loss
• Fibrotic chronic HP — mimics idiopathic pulmonary fibrosis; upper-lobe or diffuse fibrosis; traction bronchiectasis on HRCT; mosaic attenuation and air trapping distinguish from IPF

Management: identify and avoid the causative antigen (definitive treatment); prednisolone for symptomatic or progressive disease; antifibrotics (nintedanib) for fibrotic chronic HP (PBS Authority under specialist supervision); refer to Lung Foundation Australia for patient resources.

Occupational asthma

Occupational asthma is new-onset asthma, or significantly worsened pre-existing asthma, caused by a workplace exposure.

Sensitiser-induced occupational asthma develops after an initial sensitisation period (weeks to months) with no symptoms, then asthma after each subsequent exposure. Common sensitisers and occupations: bakers (flour, amylase enzymes), spray-painters (isocyanates), hairdressers (persulfate bleaches), laboratory animal workers (animal proteins), healthcare workers (latex, glutaraldehyde), farmers (grain dust).

Irritant-induced asthma (RADS) follows a single high-level chemical exposure — chlorine gas, ammonia, acid aerosols — causing persistent airway hyperresponsiveness without a sensitisation phase.

Diagnosis: peak-flow diary comparing work days and non-work days (at least two weeks of readings); spirometry and reversibility; bronchial provocation testing if needed; specific IgE or skin prick testing to occupational antigens. Refer to specialist respiratory and occupational physician.

Management per Australian Asthma Handbook: inhaled corticosteroids plus bronchodilators (same as standard asthma); for sensitiser-induced cases, permanent removal from exposure gives the best chance of symptom resolution or substantial improvement; ongoing exposure leads to permanent disease. Workers compensation applies.

D. Australian operations

Workers compensation and Dust Diseases Authorities

Occupational lung disease claims are managed through state and territory workers compensation schemes. For asbestos-related disease, silicosis, and coal workers’ pneumoconiosis, dedicated Dust Diseases Authorities provide statutory compensation:

• NSW icare Dust Diseases Care — one of the most comprehensive schemes; covers current and former workers with asbestos, silica, or coal dust disease; benefits include medical expenses, weekly compensation, lump-sum payments, and case management
• Victoria WorkSafe — covers occupational disease including silicosis and asbestos-related disease
• Queensland WorkCover — workers compensation and employer reporting obligations
• Other states and territories — equivalent WorkCover or WorkSafe agencies

The GP’s role in this pathway: provide an initial medical certificate linking the diagnosis to occupational exposure; coordinate specialist assessments (respiratory physician, occupational physician); gather serial lung function measurements and imaging; provide ongoing medical evidence for claim management.

Common law negligence claims are also available in most states and may yield additional compensation beyond statutory schemes. An asbestos and dust disease specialist solicitor can advise.

MBS items

Per MBS Online:

• GP attendance — items 23, 36, 44, 45
• GPCCMP — items 965/967 for chronic disease management plan and allied health referrals (post 1 July 2025)
• Spirometry + DLCO — Medicare-rebatable; lung function laboratory referral
• HRCT chest — Medicare-rebatable
• TST / IGRA — Medicare-rebatable
• Autoimmune bloods, IgG precipitins — Medicare-rebatable
• Pulmonary rehabilitation — items 81100 series

PBS

• Pirfenidone (Esbriet) and nintedanib (Ofev) — PBS Authority Required for IPF; off-label under specialist oversight for fibrotic HP and silicotic PMF in selected cases
• Mesothelioma pharmacotherapy — nivolumab plus ipilimumab (CheckMate-743 regimen) PBS Section 100; cisplatin-pemetrexed chemotherapy PBS-listed; specialist oncology
• Standard asthma medications — PBS general schedule for occupational asthma

Lung Cancer Screening Program 2025

High-risk patients with asbestos or silica exposure who are also long-term smokers may qualify for the Lung Cancer Screening Program from 2025 — eligibility criteria include age 50–70, ≥30 pack-year history, current smoker or quit within 10 years. Low-dose CT is the screening modality.

Notification requirements

• Silicosis — notifiable in Victoria (since 2019) and Queensland; national standards evolving
• Mesothelioma — mandatory cancer registry reporting in all states and territories
• Asbestos-related disease — state Dust Diseases Authority registration for compensation-relevant cases
• Occupational asthma — may be reportable under state OH&S regulations as a notifiable incident

E. Special populations

Young workers — engineered stone cohort

Workers who cut engineered stone from the mid-2010s onwards are a specific surveillance population. Many are young (20s–40s) with severely progressive disease. If a patient in this age group worked in stone benchtop fabrication or installation and reports progressive breathlessness or cough, arrange HRCT chest promptly rather than waiting for spirometry abnormality — early disease may be identifiable before symptoms or lung function decline.

Aboriginal and Torres Strait Islander peoples

Historical employment in mining (particularly WA and NT) places some Aboriginal and Torres Strait Islander communities at risk for silicosis and asbestos-related disease. Culturally safe access to specialist respiratory care and workers compensation support via Aboriginal Medical Services and Indigenous-specific health services reduces barriers. Tuberculosis prevalence is higher in some remote communities — TB screening in silicosis patients from these communities requires particular attention.

Women in occupationally exposed roles

Historically occupational lung disease has been seen as predominantly male, but women work in hairdressing (persulfate HP), healthcare (latex), cleaning (chemical irritants), food processing, and laboratory animal work — all with significant sensitiser exposures. A gendered history that assumes women haven’t had relevant occupational exposures will miss diagnoses.

Older adults

People who worked in heavily asbestos-exposed trades through the 1960s–1990s are now aged 60–80+. New-onset progressive breathlessness, a recurrent pleural effusion, or unexplained weight loss in this cohort should always prompt an asbestos history and appropriate imaging (HRCT, PET in mesothelioma workup).

When to escalate

Refer to respiratory physician when:

• HRCT shows interstitial lung pattern, pleural plaques, or pulmonary nodules consistent with occupational exposure
• Spirometry or DLCO is impaired
• Diagnosis is uncertain — pattern of disease on imaging or clinical course needs specialist characterisation
• Treatment decisions for HP (corticosteroids, antifibrotics) or mesothelioma need specialist input
• Lung transplant assessment for end-stage disease
• Siica or coal exposure with positive TST or IGRA — specialist TB service for LTBI treatment

Refer to occupational physician when:

• Workers compensation assessment is needed
• Fitness for work or return-to-work decisions need independent medical opinion
• Causation needs to be established for a legal claim

Refer urgently when: suspected mesothelioma (rapidly evolving pleural effusion, weight loss, chest pain), acute silicosis (rapidly progressive hypoxia in a stone worker), or suspected primary lung cancer in an asbestos-exposed heavy smoker with new pulmonary mass.

What this article is and is not

This is general health information drawn from Australian clinical resources — Therapeutic Guidelines — Respiratory, TSANZ, Lung Foundation Australia, Safe Work Australia, RACGP, and NPS MedicineWise. It is not personal medical advice and does not create a doctor–patient relationship. Decisions about investigation, diagnosis, treatment, and medico-legal pathways are made with your own GP, respiratory physician, occupational physician, and legal advisers as appropriate.

For Australian consumer resources: Lung Foundation Australia, Asbestos Diseases Foundation of Australia, HealthDirect, Better Health Channel.

---

Sources cited

1. Lung Foundation Australia — Occupational lung disease
2. Thoracic Society of Australia and New Zealand (TSANZ)
3. Safe Work Australia — Engineered stone ban and silica WES
4. Therapeutic Guidelines — Respiratory / occupational
5. RACGP
6. NPS MedicineWise
7. icare NSW — Dust Diseases Care
8. Asbestos Diseases Foundation of Australia
9. HealthDirect Australia
10. Better Health Channel
11. Australian Asthma Handbook 2025
12. PBS — antifibrotics; mesothelioma immunotherapy
13. MBS Online