Asbestosis – Causes, Symptoms, Diagnosis, Treatment and Ongoing care



  • Slowly progressive lung disease caused by inhalation of dust from fibrous silicate asbestos used in insulation, cement, and other building and construction materials
  • Nodular interstitial fibrotic lung disease caused by cascade of inflammatory responses to inhaled asbestos fibers:
    • Pleural fibrosis, pleural plaques, and interstitial fibrosis develop.
    • Lung cancer risk is increased.
  • Synonym(s): Asbestos pneumoconiosis


  • In the US, an estimated 1.3 million people who work in maintenance and construction are at risk for exposure (1).
  • In a very large part of the world, data on mesothelioma are not available (2).
  • Predominant age: Middle age (40–75 years)
  • Predominant sex: Male > Female, owing to exposure pattern

Risk Factors

  • Professional exposures most common in construction workers; those who mine, mill, or remove asbestos; ship builders; textile workers; railroad workers.
  • Office workers, teachers, and students in buildings with asbestos in place have exposure significantly lower than those of construction workers.
  • Dose-response phenomenon: Higher amounts of asbestos exposure are associated with higher risk of asbestosis (3,4,5).
  • Cigarette smoking markedly increases risk of radiographic changes and eventual lung cancer risk:
    • Likely mechanism: Decreased clearance of asbestos fibers


  • Genetic polymorphisms have been implicated (6,7,8,9,10).
  • Familial mesothelioma has been reported (11).

General Prevention

  • In the US, asbestos is federally regulated by the Occupational Health and Safety Administration.
  • Primary responsibility of employers is to provide safe work environment (3,12,13,14,15)
  • Exposure control: Substitution of safer materials or adoption of control technologies
  • During high-exposure periods, such as building repair, use fit-tested personal respirators for workers.
  • To limit exposure to others in their household, those who work with asbestos should leave their clothing at work, if possible. Work clothes should be washed and stored separately from other clothing.


  • Asbestos fibers are inhaled. Macrophages engulf the fibers and release inflammatory mediators. Inflammatory mediators cause fibroblast proliferation, leading to fibrosis and remodeling of interstitial lung tissue, including intra-alveolar fibrosis and loss of alveolar capillary units (16).
  • Disease continues to slowly progress over the course of years, even if exposure is not ongoing (14,17,18).
  • Symptoms may be related to impaired gas exchange and/or a pattern of restrictive lung disease.

Commonly Associated Conditions

In addition to asbestosis, inhalation of asbestos is associated with several lung problems (11,18,19,20,21,22), including:

  • Benign plaques
  • Benign pleural effusions
  • Lung cancer
  • Malignant mesothelioma

Asbestos, Mesothelioma, Pleural disease, Asbestos fibers, Cancer, Lung cancer, Lung, progressive lung disease, interstitial fibrosis,



  • Credible history of exposure (usually occupational) to asbestos fibers (3,4,5,17,23,24):
    • Ask about intensity and duration of exposure.
    • Aircraft or electrical maintenance
    • Shipyard workers
    • Those exposed to cement or building materials
    • Asbestos mining
    • People exposed to asbestos when it is disrupted during building maintenance
    • Family members of those who work with asbestos
  • In addition to job type and activities and length of exposure, ask patients whether there was visible dust in air or on surfaces, visible dust in sputum, personal protective equipment used, and whether the workplace was cleaned during or after a shift (25).
  • Common symptoms include:
    • Dyspnea upon exertion
    • Nonproductive cough (26,27,28)
  • Delay from exposure to detection typically becomes clinically apparent 10–15 years after exposure.

Physical Exam

  • Insidious onset
  • Progressive dyspnea is the most common symptom.
  • Dry cough
  • Progressive exercise intolerance
  • Pleuritic chest pain
  • Inspiratory crackles (may be best heard laterally)
  • Wheeze with forced exhalation
  • Digital clubbing and cyanosis in advanced disease
  • Right-sided heart failure

Diagnostic Tests & Interpretation

Pulmonary function test:

  • Not diagnostically specific
  • Mainly restrictive pattern unless a smoker (29)
  • Decreased total lung capacity and vital capacity
  • Reduction in diffusing capacity to carbon monoxide (25)[B]
  • Useful for following level of impairment


No pathognomonic lab findings


  • Chest x-ray (CXR) (sensitivity 90%, specificity 93%):
    • Most common findings are bilateral pleural thickening and circumscribed calcified pleural plaques
    • Pleural plaques usually posterior-lateral, may also involve diaphragm (30)
    • As disease progresses, small, irregular, linear opacities with a fine reticular pattern are seen
    • Less common: Rounded atelectasis (Blesovsky syndrome) when fibrosis of visceral pleura extends into parenchyma (31)
  • Classification scheme available through International Labour Office (at
  • High-resolution computed tomography (CT) may increase sensitivity to near 100%:
    • Improves detection of interstitial fibrosis
    • May show honeycombing in later stages of the disease
  • Gallium scan with higher uptake even if the CXR and CT are normal

Pathological Findings

  • Lung biopsy or bronchoalveolar lavage (BAL) can reveal asbestos fibers or asbestos bodies (25):
    • May help diagnostically in cases with history of minimal exposure or with atypical clinical or radiographic features
    • Transbronchial biopsy is less reliable than BAL or open-lung biopsy in establishing diagnosis.
  • Pleural plaques are found in parietal pleura; made up of collagen bundles with rare inflammatory cells. Pleural thickening involves the visceral pleura (30).
  • Asbestos bodies may be seen with iron staining in intra-alveolar macrophages.

Differential Diagnosis

Other pneumoconioses:

  • Idiopathic pulmonary fibrosis
  • Hypersensitivity pneumonitis
  • Sarcoidosis
  • Other pneumoconiosis, including mixed exposures



First Line

  • No specific pharmacologic treatment
  • Oxygen
  • Bronchodilators for pulmonary toilet

Second Line

  • Antibiotics for respiratory infections
  • Diuretics if cor pulmonale develops

Additional Treatment

General Measures

  • As of now, there is no effective treatment to reverse the course of the disease.
  • Clinical approach is directed at amelioration of symptoms, elimination of progression, and reduction of risk of associated disorders.
  • Withdrawal from exposure (30)[B]:
    • Workers with no symptoms and only radiographic changes may make an informed choice to continue employment using maximum environmental and personal protection.
  • Smoking cessation:
    • Cigarette smokers have more radiographic signs of disease and have a significantly increased risk for lung cancer.
  • Pneumococcal and influenza vaccines (28)[B]
  • Chest physiotherapy as needed
  • Home oxygen as needed

Issues for Referral

All new cases must be reported to health authorities.

Ongoing Care

Follow World Health Organization (WHO) recommendations for regular health screening of exposed workers (32):

  • CXR film at baseline
  • For workers with <10 years since 1st exposure: CXR every 3–5 years
  • >10 years: CXR every 1–2 years
  • >20 years: CXR annually
  • All workers: Annual respiratory symptom questionnaire, physical exam, and spirometry (alternatively can be done on CXR schedule)

Follow-Up Recommendations

Patient Monitoring

  • CXR
  • Occasional pulmonary function tests
  • Prompt treatment of infections


High-calorie, high-protein with advanced disease

Patient Education

  • Smoking cessation counseling as needed
  • In the US, asbestos has been federally regulated by the Occupational Health and Safety Administration since 1972:
  • Printed patient information available from National Cancer Institute:
  • Agency for Toxic Substances and Disease Registry:


  • Severity depends on duration and intensity of exposure.
  • Lung disease is irreversible.
  • Increased risk for lung cancer (synergistic increase with cigarette smoking) and mesothelioma (25)[B]


  • Mesothelioma:
    • Related to dose, time elapsed from exposure (usually 25–40 years after exposure)
    • Risk is higher with exposure to amphibole fibers rather than chrysotile fibers.
    • Pleural effusion in 80–95% (31)[B]
    • Insidious but progressive. Median survival for mesothelioma is 8–18 months (33)[B].
  • Lung cancer risk is associated with asbestos exposure, whether asbestosis is present or not; synergistically increased risk in asbestos workers who smoke (13).
  • Gastrointestinal cancer risk may also be increased with asbestos exposure.


1. American Thoracic Society. Diagnosis and initial management of nonmalignant diseases related to asbestos. Am J Respir Crit Care Med. 2004;170:691–715.

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2. Bianchi C, Bianchi T. Malignant mesothelioma: global incidence and relationship with asbestos. Ind Health. 2007;45:379–87.

3. Lin RT, Takahashi K, Karjalainen A et al. Ecological association between asbestos-related diseases and historical asbestos consumption: an international analysis. Lancet. 2007;369:844–9.

4. Bhattacharya K, Dopp E, Kakkar P et al. Biomarkers in risk assessment of asbestos exposure. Mutat Res. 2005;579:6–21.

5. Chow S, Campbell C, Sandrini A et al. Exhaled breath condensate biomarkers in asbestos-related lung disorders. Respir Med. 2009.

6. Horská A, Kazimírová A, Barancoková M et al. Genetic predisposition and health effect of occupational exposure to asbestos. Neuro Endocrinol Lett. 2006;27(Suppl 2):100–3.

7. Franko A, Dolzan V, Arnerić N et al. The Influence of Genetic Polymorphisms of GSTP1 on the Development of Asbestosis. J Occup Environ Med. 2008;50:7–12.

8. Helmig S, Belwe A, Schneider J. Association of Transforming Growth Factor beta1 Gene Polymorphisms and Asbestos-Induced Fibrosis and Tumors. J Investig Med. 2009.

9. Franko A, Dodic-Fikfak M, Arnerić N et al. Manganese and extracellular superoxide dismutase polymorphisms and risk for asbestosis. J Biomed Biotechnol. 2009;2009:493083.

10. Neri M, Ugolini D, Dianzani I et al. Genetic susceptibility to malignant pleural mesothelioma and other asbestos-associated diseases. Mutat Res. 2008;659:126–36.

11. You B, Blandin S, Gérinière L et al. [Family mesotheliomas: genetic interaction with environmental carcinogenic exposure?] Bull Cancer. 2007;94:705–10.

12. Mueller TB. Tomorrow’s causation standards for yesterday’s wonder material: Reiter v. Acands, Inc. and Maryland’s changing asbestos litigation. J Contemp Health Law Policy. 2009;25:437–61.

13. Dement J, Welch L, Haile E et al. Mortality among sheet metal workers participating in a medical screening program. Am J Ind Med. 2009.

14. Centers for Disease Control and Prevention (CDC). Asbestosis-related years of potential life lost before age 65 years—United States, 1968–2005. MMWR Morb Mortal Wkly Rep. 2008;57:1321–5.

15. Gehanno JF, Takahashi K, Darmoni S et al. Citation classics in occupational medicine journals. Scand J Work Environ Health. 2007;33:245–51.

16. Tercelj M, Salobir B, Simcic S et al. Chitotriosidase activity in sarcoidosis and some other pulmonary diseases. Scand J Clin Lab Invest. 2009;1–4.

17. Kurumatani N, Kumagai S. Mapping the risk of mesothelioma due to neighborhood asbestos exposure. Am J Respir Crit Care Med. 2008.

18. Mastrangelo G, Ballarin MN, Bellini E et al. Asbestos exposure and benign asbestos diseases in 772 formerly exposed workers: Dose-response relationships. Am J Ind Med. 2009.

19. Wagner GR. The fallout from asbestos. Lancet. 2007;369:973–4.

20. Wagner JC. The discovery of the association between blue asbestos and mesotheliomas and the aftermath. Br J Ind Med. 1991;48:399–403.

21. Wagner GR. Asbestosis and silicosis. Lancet. 1997;349:1311–5.

22. Toyokuni S. Mechanisms of asbestos-induced carcinogenesis. Nagoya J Med Sci. 2009;71:1–10.

23. Hansell A. Airborne environmental exposure to asbestos. Am J Respir Crit Care Med. 2008;178:556–7.

24. Banks DE, Shi R, McLarty J et al. American College of Chest Physicians consensus statement on the respiratory health effects of asbestos. Results of a Delphi study. Chest. 2009;135:1619–27.

25. Costabel U, Uzaslan E, Guzman J. Bronchoalveolar lavage in drug-induced lung disease. Clin Chest Med. 2004;25:25–35.

26. Reid A, Berry G, de Klerk N et al. Age and sex differences in malignant mesothelioma after residential exposure to blue asbestos (crocidolite). Chest. 2007;131:376–82.

27. Wilson D, Takahashi K, Pan G et al. Respiratory symptoms among residents of a heavy-industry province in China: prevalence and risk factors. Respir Med. 2008.

28. O’Reilly KM, Mclaughlin AM, Beckett WS et al. Asbestos-related lung disease. Am Fam Physician. 2007;75:683–8.

29. Abejie BA, Wang X, Kales SN, Christiani DC, et al. Patterns of pulmonary dysfunction in asbestos workers: a cross-sectional study. J Occup Med Toxicol. 2010;5:12.

30. Huggins JT, Sahn SA. Causes and management of pleural fibrosis. Respirology. 2004;9:441–7.

31. Cugell DW, Kamp DW. Asbestos and the pleura: a review. Chest. 2004;125:1103–17.

32. Welch LS, Haile E. Asbestos-related disease among sheet metal workers 1986–2004: Radiographic changes over time. Am J Ind Med. 2009.

33. Martino D, Pass HI. Integration of multimodality approaches in the management of malignant pleural mesothelioma. Clin Lung Cancer. 2004;5:290–8.

Additional Reading

Antonescu-Turcu AL, Schapira RM, et al. Parenchymal and airway diseases caused by asbestos. Curr Opin Pulm Med. 2010;16:155–61

35. Brody AR, et al. Asbestos and lung disease. Am J Respir Cell Mol Biol. 2010;42:131–2.

36. Kamp DW, et al. Asbestos-induced lung diseases: an update. Transl Res. 2009;153:143–52.



  • 501 Asbestosis
  • 515 Postinflammatory pulmonary fibrosis


  • 22607003 Asbestosis (disorder)
  • 51615001 fibrosis of lung (disorder)

Clinical Pearls

  • Associations between asbestos and all histologic subtypes of lung cancer have been observed.
  • Higher amounts of asbestos exposure are associated with higher risk of asbestosis.
  • Smoking cessation is particularly important because cigarette smokers have more radiographic signs of asbestosis and are at a synergistically increased risk for lung cancer.
  • For those who work with asbestos, to limit exposure to others in their household, clothing should be left at work, if possible, or should be washed and stored separately from other clothing.

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