Asbestos-related
- Naturally occurring mineral, processed in Australia for 100+ years.
- Banned in 2003.
- Long lag-time between exposure and disease development (20+ years).
- Can cause various lung pathologies from benign plaques to malignant melanomas:
- Two main types of asbestos fibres
- Serpentine asbestos fibres (white asbestos, chrysotile): Wispy, flexible & relatively long (up to 2cm)→ less easily inhaled to the periphery of the lung. Not as fibrogenic
- Amphibole asbestos fibres (brown/blue asbestos, crocidolite): Penetrate more deeply into the lung and are more resistant to breakdown within the lung
- Exposure to amphiboles have a greater risk of developing asbestos related lung disease.
- Straight fibres up to 50mm long and 1-2μm wide
- Most likely to cause asbestosis and mesothelioma as it is readily trapped in the lung
- Must take a detailed occupational history as workers can get exposed to asbestos under many different settings
- There are now strict precautions (introduced in 1970s) but there is a long lag period between exposure and symptoms so we are still seeing disease.
THERE ARE SEVERAL DIFFERENT DISEASES RELATED TO ASBESTOS EXPOSURE
1. Asbestosis
- Pneumoconiosis with diffuse parenchymal lung fibrosis
- Type of interstitial lung disease
- Spirometry shows restrictive picture; DLCO is reduced.
- Develops as a result of heavy prolonged exposure
- Lag period of 10-25 years
- Disease progress usually slowly progressive, but may occasionally be rapidly progressive.
- Symptoms similar to interstitial lung diseases such as IPF
- Cough, dyspnoea, crackles, clubbing, restrictive ventilatory defect, ↓ gas diffusion
- CXR: Bilateral reticulonodular shadowing
- Fibrosis first shows around respiratory bronchioles at lung bases then becomes more diffuse
- Asbestos bodies (look like dumbbells)
- ↑ risk of lung cancer
2. Pleural plaques:
- 50% of people exposed to asbestos will develop pleural plaques.
- These are benign and have no impact on lung function. Follow-up is not required.
- Often visible on CXR – dense white lines on pleura of the chest wall, diaphragm, pericardium & mediastinum
- Don’t give rise to any impairment of lung function or disability
3. Asbestos related pleurisy and pleural effusions
- Pleural fluid is an exudate (protein rich) which is often bloodstained
- Sometimes get ↑ ESR (inflammation)
- Other causes of pleural effusion need to be excluded (empyema, haemothorax, transudate)
- Biopsy shows inflammation and fibrosis (without any specific diagnostic features)
- Usually spontaneous resolution but recurrent episodes affecting both sides may occur and may → pleural thickening
4. Pleural thickening
- Usually as a consequence of BAPE (benign asbestos-related pleural effusion)
- Localised or diffuse thickening and fibrosis of the pleura
- History of recurrent episodes of acute pleurisy
- Thickening is usually worst at the lung bases with obliteration/blunting of the costophrenic angles
- Can initially be unilateral but usually becomes bilateral
- When extensive → SOB, restrictive lung defects
5. Asbestos related lung cancer
- Also related to asbestos WITH smoking
- Distribution of cell type, investigation and treatment of asbestos related lung cancer is the same as normal lung cancer
6. Mesothelioma
- Malignant tumour of the pleura
- Highly aggressive malignancy
- median survival 12 months from diagnosis
- 5-10% of all exposed to asbestos will get this.
- Lag period can be as short as a few months after exposure (but average is 20-40 years)
- Presenting symptoms:
- Pain, dyspnoea, weight loss, lethargy, features of unilateral pleural effusion on CXR.
- As the tumour progresses, it encases the lung and may involve the pericardium and peritoneum and give rise to blood borne metastases
- Tumour also has a tendency to spread along needle biopsy tracks → cutaneous nodules (so give local radiotherapy at site of biopsy)
- Definitive histological diagnosis (via open thoracotomy or VATS) is essential given the medicolegal consequences
- Prognosis is poor
- No effective treatment and management focuses on palliation of symptoms (high dose opiates) and support
| Exposure | CXR | Lung function | Symptoms | Outcome | |
| Asbestos bodies | Light | Normal | Normal | None | Evidence of asbestos exposure only |
| Pleural plaques | Light | Pleural thickening (parietal) and calcification | Mild restrictive defect | Rare – maybe mild Exertional dyspnoea | No other sequelae |
| Effusion | First 2 decades following exposure | Effusion | Restrictive | Pleuritic pain, dyspnoea | Often recurrent |
| Bilateral diffuse pleural thickening | Light/moderate | Bilateral diffuse thickening of pleural (>5mm thick and extending > than ¼ of chest wall) | Restrictive | Effort dyspnoea | May progress in absence of further exposure |
| Mesothelioma | Light (interval of 20-40 yrs from exposure to disease) | Pleural effusion, usually unilateral | Restrictive | Pleuritic pain, increasing dyspnoea, malignancy symptoms | Median survival is 2 years |
| Asbestosis | Heavy (interval of 5-10 yrs from exposure to disease) | Diffuse bilateral streaky shadows, honeycomb lung | Severe restrictive and reduced gas transfer | Progressive dyspnoea | Poor, progression in some cases even after exposure stops |
| Asbestos-related carcinoma of the bronchus | Features of asbestosis, bilateral diffuse pleural thickening or bilateral pleural plaques plus those of bronchial carcinoma | ||||