BASICS
DESCRIPTION
- Pneumoconiosis caused by inhalation of asbestos fibers often through environmental or occupational exposure.
- Characterized by slowly progressive pulmonary fibrosis
- Clinical presentation exists along a spectrum ranging from asymptomatic to severe pulmonary disease requiring palliative care.
- Associated with an increased risk of pulmonary malignancy
- Synonym(s): asbestos pneumoconiosis
EPIDEMIOLOGY
- The physical properties of asbestos made it popular for use in a variety of commercial industries beginning in the early 1900s.
- Widespread use led to occupational and environmental exposure for millions of people around the globe.
- In the United States, an estimated 1.3 million people who work in maintenance and construction are at risk for exposure to asbestos (1).
ETIOLOGY AND PATHOPHYSIOLOGY
- Asbestos refers to naturally occurring silicate fibers.
- Exposure occurs when environments and materials containing asbestos fibers are disturbed and released into the air.
- Inhalation of asbestos fibers is thought to result in asbestosis when (2):
- Inhaled particles are retained within the pulmonary system.
- Activation of various immune mediators occurs to address retained fibers and results in inflammation.
- Ongoing inflammation leads to breakdown of normal cellular structure(s).
- Fibroblast proliferation and remodeling ultimately result in fibrosis.
- The disease can continue to progress even if exposure is not ongoing.
- Latency period from initial exposure to symptom development can range from 10 to 40 years (1).
- The effects of asbestos inhalation are dependent on cumulative dose, time since exposure, and the type of asbestos fibers inhaled (2).
- Symptoms may be related to impaired gas exchange and/or a pattern of restrictive lung disease.
Genetics
- Genetic polymorphisms have been implicated.
- Familial mesothelioma has been reported.
RISK FACTORS
- High-risk industries and occupations for asbestos exposure include but are not limited to the following:
- Automobile repair
- Aviation
- Construction
- Maintenance
- Manufacturing
- Mill work and mining
- Plumbing
- Shipbuilding and maintenance
- Rail transportation employees
- High-risk environmental exposures can be seen with the following:
- Routine exposure to family members in high-risk occupations
- Residing in highly industrialized areas
- Repeated exposure to structures with asbestos-containing materials undergoing demolition or maintenance
- Asbestosis increases lung cancer risk and, with smoking, has an additive effect (3).
GENERAL PREVENTION
- In the United States, asbestos is federally regulated by the Occupational Health and Safety Administration.
- Primary responsibility of employers is to provide safe work environment.
- 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.
COMMONLY ASSOCIATED CONDITIONS
In addition to asbestosis, inhalation of asbestos is associated with other lung-related disorders, including the following:
- Benign pleural plaques
- Benign pleural effusions
- Lung cancer
- Malignant mesothelioma
DIAGNOSIS
HISTORY
- Obtain a thorough history of any respiratory symptoms. The most common symptoms include the following:
- Shortness of breath
- Dry cough
- Chest pain or tightness
- Risk of asbestos exposure should be assessed with occupational history (3)[C].
- If there is a history of exposure to asbestos:
- Establish the specific occupation(s), which resulted in the exposure.
- Duration of exposure
- Intensity of exposure
- Inquire about personal or family history of underlying respiratory disorders because these may predispose the patient to development of asbestos-related lung disease.
- Obtain a smoking history.
PHYSICAL EXAM
- Unexplained weight loss
- Dry cough
- Exercise intolerance
- Basilar inspiratory crackles
- Digital clubbing
- Hypoxemia in moderate to severe cases
- In advanced cases, signs of cor pulmonale may be present.
DIFFERENTIAL DIAGNOSIS
- Idiopathic pulmonary fibrosis
- Hypersensitivity pneumonitis
- Sarcoidosis
- Other pneumoconiosis, including mixed exposures
DIAGNOSTIC TESTS & INTERPRETATION
Initial Tests (lab, imaging)
Labs: generally nonspecific, no pathognomonic lab findings
- Pulmonary function tests: not diagnostic but may demonstrate the following:
- Reduced lung volumes
- Decreased diffusing capacity of lung for carbon monoxide (DLCO)
- Restrictive pattern unless associated with smoking history
- 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
- 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
- Classification scheme available through International Labour Office (www.ilo.org)
- 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 lung scan: Use remains experimental because degree of gallium uptake does not correlate with findings on CXR, pulmonary function tests, or BAL.
Test Interpretation
- Lung biopsy or bronchoalveolar lavage (BAL) can reveal asbestos fibers or asbestos bodies:
- 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.
- Asbestos bodies may be seen with iron staining in intra-alveolar macrophages.
TREATMENT
GENERAL MEASURES
- No curative treatment for asbestosis
- Clinical approach should focus on prevention and symptom relief.
- Preventive measures
- Avoidance of further asbestos exposure
- Smoking cessation (3)[A]
- Pneumococcal and influenza vaccines (3)[C]
- Management of comorbid respiratory disease
- Symptom relief
- Management of comorbid respiratory conditions
- Supplemental oxygen if hypoxemia is present
MEDICATION
First Line
- No specific pharmacologic treatment
- Oxygen
- Bronchodilators for pulmonary toilet
Second Line
- Antibiotics for respiratory infections
- Diuretics if cor pulmonale develops
ISSUES FOR REFERRAL
All new cases must be reported to health authorities.
ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
Patient Monitoring
- Ongoing surveillance for persons with significant exposure history or current exposure with CXR and pulmonary function testing every 3 to 5 years (3)[C]
- Prompt treatment of infections
DIET
High calorie, high protein with advanced disease
PATIENT EDUCATION
- Smoking cessation counseling, as needed
- In the United States, asbestos has been federally regulated by the Occupational Health and Safety Administration since 1972 (www.osha.gov).
- Printed patient information available from the National Cancer Institute (www.cancer.gov/cancertopics/factsheet/Risk/asbestos)
- Agency for Toxic Substances and Disease Registry (www.atsdr.cdc.gov)
PROGNOSIS
- Lung disease is irreversible.
- Symptoms range from asymptomatic to severe requiring palliation.
- Increased risk for lung cancer (synergistic increase with cigarette smoking) and mesothelioma
COMPLICATIONS
- Mesothelioma:
- Related to dose; time elapsed from exposure (usually 25 to 40 years after exposure)
- Pleural effusion seen in 80-95% of cases
- Insidious but progressive; median survival for mesothelioma is 8 to 18 months
- Prognosis is dependent on the histologic type of mesothelioma (epithelioid > mixed > sarcomatoid).
- Lung cancer risk is associated with asbestos exposure, whether asbestosis is present or not; synergistically increased risk in asbestos workers who smoke.
REFERENCES
11 Centers for Disease Control and Prevention. Asbestosis-related years of potential life lost before age 65 years-United States, 1968-2005. MMWR Morb Mortal Wkly Rep. 2008;57(49):1321-1325.22 Kamp DW. Asbestos-induced lung diseases: an update. Transl Res. 2009;153(4):143-152.33 O'Reilly KM, McLaughlin AM, Beckett WS, et al. Asbestos-related lung disease. Am Fam Physician. 2007;75(5):683-688.
ADDITIONAL READING
- Abejie BA, Wang X, Kales SN, et al. Patterns of pulmonary dysfunction in asbestos workers: a cross-sectional study. J Occup Med Toxicol. 2010;5:12.
- Antonescu-Turcu AL, Schapira RM. Parenchymal and airway diseases caused by asbestos. Curr Opin Pulm Med. 2010;16(2):155-161.
- 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(6):1619-1627.
- Brody AR. Asbestos and lung disease. Am J Respir Cell Mol Biol. 2010;42(2):131-132.
- Deng Q, Wang X, Wang M, et al. Exposure-response relationship between chrysotile exposure and mortality from lung cancer and asbestosis. Occup Environ Med. 2012;69(2):81-86.
- Helmig S, Belwe A, Schneider J. Association of transforming growth factor beta1 gene polymorphisms and asbestos-induced fibrosis and tumors. J Investig Med. 2009;57(5):655-661.
- Husain AN, Colby T, Ordonez N, et al. Guidelines for pathologic diagnosis of malignant mesothelioma: 2012 update of the consensus statement from the International Mesothelioma Interest Group. Arch Pathol Lab Med. 2013;137(5):647-667.
- Markowitz SB, Levin SM, Miller A, et al. Asbestos, asbestosis, smoking, and lung cancer. New findings from the North American insulator cohort. Am J Respir Crit Care Med. 2013;188(1):90-96.
- Park EK, Takahashi K, Jiang Y, et al. Elimination of asbestos use and asbestos-related diseases: an unfinished story. Cancer Sci. 2012;103(10):1751-1755.
- Prazakova S, Thomas PS, Sandrini A, et al. Asbestos and the lung in the 21st century: an update. Clin Respir J. 2014;8(1):1-10.
- Toyokuni S. Mechanisms of asbestos-induced carcinogenesis. Nagoya J Med Sci. 2009;71(1-2):1-10.
- Wang X, Yano E, Qiu H, et al. A 37-year observation of mortality in Chinese chrysotile asbestos workers. Thorax. 2012;67(2):106-110.
CODES
ICD10
- J61 Pneumoconiosis due to asbestos and other mineral fibers
- J84.10 Pulmonary fibrosis, unspecified
- J92.0 Pleural plaque with presence of asbestos
ICD9
- 501 Asbestosis
- 515 Postinflammatory pulmonary fibrosis
- 511.0 Pleurisy without mention of effusion or current tuberculosis
SNOMED
- Asbestosis (disorder)
- Fibrosis of lung (disorder)
- Asbestos-induced pleural plaque (disorder)
CLINICAL PEARLS
- The increased latency period from initial exposure to asbestos to onset of symptoms can span many years.
- Symptoms range from asymptomatic to severe disease requiring palliative care.
- There is no cure for asbestosis and treatment is aimed at prevention and symptom management.
- Smoking cessation is particularly important because they are at a synergistically increased risk for lung cancer.
- Those who work with asbestos should limit exposure to others in their household; clothing should either be left at work or be washed and stored separately from other clothing.
- Ongoing surveillance for persons with significant exposure history or current exposure with asbestos
- CXR and pulmonary function testing every 3 to 5 years