FFS: Asbestosis

Asbestosis is a form of pneumoconiosis caused by inhalation of asbestos fibres, resulting in slowly progressive, diffuse pulmonary fibrosis. It is part of the broader group of interstitial lung diseases and arises from occupational exposure to asbestos, a group of naturally occurring silicate minerals.

Three major disease entities related to asbestos exposure:

Disease TypeExamples
AsbestosisChronic fibrotic lung disease
Pleural diseaseBenign effusion, pleural plaques, diffuse pleural thickening
Malignant diseasesSmall cell, squamous cell, adenocarcinoma, large cell carcinoma, mesothelioma

All forms of asbestos are carcinogenic. The most deadly is crocidolite (blue asbestos).

Clinical Presentations

  1. Exacerbation of fibrosis → acute respiratory distress
  2. Complications: lung cancer, mesothelioma
  3. Pneumonia (common in fibrotic lung disease)

Emergency considerations:

Assess need for a limitations of care plan

Look for reversible causes (e.g. pneumonia, acute heart failure, ACS)

Geology and Exposure

Types of Asbestos Fibres
TypeFormExampleNotes
SerpentineCoiledChrysotile (white)>90% of commercial use
AmphiboleStraight/rigidCrocidolite (blue), Amosite (brown), Tremolite, Actinolite, AnthophylliteCrocidolite = highest risk of mesothelioma

Asbestos fibres are microscopic and remain airborne for long periods, posing significant inhalation risks.

Asbestos Building Products
Product TypeRisk LevelExamples
FriableHigh (easily airborne)Loose fill insulation, sprayed coatings
BondedLower (fibres bound in cement)AC sheeting, “fibro”

Epidemiology

Risk is proportional to intensity, duration, fibre type, latency, and co-exposures (e.g. smoking).

Asbestos widely used in Australian buildings until late 1980s.

Total ban in Australia from 31 December 2003.

Pathology

Histological criteria:

  • Asbestos (ferruginous) bodies
  • Interstitial pulmonary fibrosis

Mechanism:

  • Direct toxicity from fibres
  • ROS and cytokine release
  • Fibroblast proliferation and collagen accumulation

Amphibole fibres more toxic than chrysotile due to deeper lung penetration and poor clearance.

Clinical Features
SystemFeatures
RespiratoryProgressive exertional dyspnoea, fine bibasilar crackles, clubbing
PleuralBenign effusions, plaques, diffuse thickening
CardiacCor pulmonale in advanced disease
ComplicationsRespiratory failure, lung cancer, mesothelioma

Latency: Symptoms may appear 20–30 years post-exposure.

Investigations

Imaging

ModalityFindings
CXRBasal reticular/nodular opacities, pleural plaques, “shaggy heart” sign
HRCTSubpleural linear opacities, parenchymal bands, honeycombing, plaques
Lung Function
  • Restrictive pattern: ↓ VC, ↓ TLC, ↓ DLCO
  • Early: exertional hypoxaemia
  • Advanced: resting hypoxaemia
Others
  • BAL: limited utility, may detect asbestos bodies
  • Biopsy: rarely needed
Differential Diagnosis of Pleural Effusions
Benign Effusion (BAPE)Malignant Effusion
Small, unilateral, exudativeOften associated with cancer spread
Resolves over weeks to monthsMay require biopsy/thoracoscopy
Associated pleural plaques, atelectasisIrregular septa, mediastinal involvement on CT
Malignant Disease
MalignancyNotes
Lung cancerRisk ↑ with smoking and amphibole exposure; multiplicative with smoking
Mesothelioma90% have confirmed asbestos exposure; most common = pleural mesothelioma

Latency for mesothelioma: ~24 years
Exposure history and fibre type crucial to risk.

Management

General Principles
  • No curative treatment
  • Focus on prevention, support, and complication management
Prevention
  • Cease exposure
  • Cease smoking
  • Vaccinate (influenza, pneumococcus)
Supportive
  • Oxygen therapy for hypoxaemia
  • Specialist respiratory follow-up

ED Management of Acute Respiratory Distress

StepApproach
OxygenationHigh-flow O₂; consider HFNO or CPAP
NIVCPAP preferred unless T2RF present
IntubationConsider if failing NIV; use restrictive ventilation strategy
Ventilation Strategy (Restrictive Pattern):
  • Low Vt (4–6 mL/kg IBW)
  • High frequency (18–25 bpm)
  • High I:E ratio (>1:1)
  • PEEP 10–20 cmH₂O
  • FiO₂ ≥ 0.6 initially, titrate to SpO₂ ≥ 88%
  • Permissive hypercapnia acceptable
  • Avoid fluid overload; use vasopressors if hypotensive

Appendix 1

asbestosis radiopaedia
Typical appearance of severe diffuse pulmonary fibrosis (Case courtesy of Dr Ian Bickle, Radiopaedia.org, rID- 50375)
asbestosis radiopaedia CT
Axial CT scan showing honeycombing of the lung in a patient with severe pulmonary fibrosis (Case courtesy of A. Prof Frank Gaillard, Radiopaedia.org, rID: 35820)

Appendix 2

asbestos locations

References

FOAMed

Resources

Fellowship Notes

Dr James Hayes LITFL Author Medical Educator

Educator, magister, munus exemplar, dicata in agro subitis medicina et discrimine cura | FFS |

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