Asbestosis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kim-Son H. Nguyen, M.D., M.P.A., Beth Israel Deaconess Medical Center, Harvard Medical School, Boston MA, Cafer Zorkun, M.D., Ph.D. [2]
Overview
Asbestosis is a chronic inflammatory medical condition affecting the parenchymal tissue of the lungs. It occurs after long-term, heavy exposure to asbestos, e.g. in mining, and is therefore regarded as an occupational lung disease. Sufferers have severe dyspnea (shortness of breath) and are at an increased risk regarding several different types of lung cancer.
As clear explanations are not always stressed in non-technical literature, care should be taken to distinguish between several forms of relevant diseases. According to the World Health Organisation (WHO), these may defined as; asbestosis (the subject of this article), lung cancer, and mesothelioma (generally a very rare form of cancer, but increasing in frequency as people exposed to asbestos age).
As a summary; Asbestosis is a chronic non-malignant pneumoconiosis caused by inhalation of asbestos fibers, characterized by slowly, progressive pulmonary fibrosis. Asbestos exposure is also associated with the development of benign pleural disease and malignancy.
Historical Perspective
- [Disease name] was first discovered by [scientist name], a [nationality + occupation], in [year] during/following [event].
- In [year], [gene] mutations were first identified in the pathogenesis of [disease name].
- In [year], the first [discovery] was developed by [scientist] to treat/diagnose [disease name].
Classification
- [Disease name] may be classified according to [classification method] into [number] subtypes/groups:
- [group1]
- [group2]
- [group3]
- Other variants of [disease name] include [disease subtype 1], [disease subtype 2], and [disease subtype 3].
Pathophysiology
- The pathogenesis of [disease name] is characterized by [feature1], [feature2], and [feature3].
- The [gene name] gene/Mutation in [gene name] has been associated with the development of [disease name], involving the [molecular pathway] pathway.
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Causes
- [Disease name] may be caused by either [cause1], [cause2], or [cause3].
- [Disease name] is caused by a mutation in the [gene1], [gene2], or [gene3] gene[s].
- There are no established causes for [disease name].
Differentiating [disease name] from other Diseases
- [Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as:
- [Differential dx1]
- [Differential dx2]
- [Differential dx3]
Epidemiology and Demographics
- The prevalence of [disease name] is approximately [number or range] per 100,000 individuals worldwide.
- In [year], the incidence of [disease name] was estimated to be [number or range] cases per 100,000 individuals in [location].
Age
- Patients of all age groups may develop [disease name].
- [Disease name] is more commonly observed among patients aged [age range] years old.
- [Disease name] is more commonly observed among [elderly patients/young patients/children].
Gender
- [Disease name] affects men and women equally.
- [Gender 1] are more commonly affected with [disease name] than [gender 2].
- The [gender 1] to [Gender 2] ratio is approximately [number > 1] to 1.
Race
- There is no racial predilection for [disease name].
- [Disease name] usually affects individuals of the [race 1] race.
- [Race 2] individuals are less likely to develop [disease name].
Risk Factors
- Common risk factors in the development of [disease name] are [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].
Natural History, Complications and Prognosis
- The majority of patients with [disease name] remain asymptomatic for [duration/years].
- Early clinical features include [manifestation 1], [manifestation 2], and [manifestation 3].
- If left untreated, [#%] of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
- Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
- Prognosis is generally [excellent/good/poor], and the [1/5/10year mortality/survival rate] of patients with [disease name] is approximately [#%].
Diagnosis
Diagnostic Criteria
- The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met:
- [criterion 1]
- [criterion 2]
- [criterion 3]
- [criterion 4]
Symptoms
- [Disease name] is usually asymptomatic.
- Symptoms of [disease name] may include the following:
- [symptom 1]
- [symptom 2]
- [symptom 3]
- [symptom 4]
- [symptom 5]
- [symptom 6]
Physical Examination
- Patients with [disease name] usually appear [general appearance].
- Physical examination may be remarkable for:
- [finding 1]
- [finding 2]
- [finding 3]
- [finding 4]
- [finding 5]
- [finding 6]
Laboratory Findings
- There are no specific laboratory findings associated with [disease name].
- A [positive/negative] [test name] is diagnostic of [disease name].
- An [elevated/reduced] concentration of [serum/blood/urinary/CSF/other] [lab test] is diagnostic of [disease name].
- Other laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].
Imaging Findings
- There are no [imaging study] findings associated with [disease name].
- [Imaging study 1] is the imaging modality of choice for [disease name].
- On [imaging study 1], [disease name] is characterized by [finding 1], [finding 2], and [finding 3].
- [Imaging study 2] may demonstrate [finding 1], [finding 2], and [finding 3].
Other Diagnostic Studies
- [Disease name] may also be diagnosed using [diagnostic study name].
- Findings on [diagnostic study name] include [finding 1], [finding 2], and [finding 3].
Treatment
Medical Therapy
- There is no treatment for [disease name]; the mainstay of therapy is supportive care.
- The mainstay of therapy for [disease name] is [medical therapy 1] and [medical therapy 2].
- [Medical therapy 1] acts by [mechanism of action 1].
- Response to [medical therapy 1] can be monitored with [test/physical finding/imaging] every [frequency/duration].
Surgery
- Surgery is the mainstay of therapy for [disease name].
- [Surgical procedure] in conjunction with [chemotherapy/radiation] is the most common approach to the treatment of [disease name].
- [Surgical procedure] can only be performed for patients with [disease stage] [disease name].
Prevention
- There are no primary preventive measures available for [disease name].
- Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
- Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].
References
Historical Perspective
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Kim-Son H. Nguyen, M.D., M.P.A., Beth Israel Deaconess Medical Center, Harvard Medical School, Boston MA, Cafer Zorkun, M.D., Ph.D. [2]
Overview
Historical Perspective
Legal Issues
The first lawsuits against asbestos manufacturers were in 1929. Since then, many lawsuits have been filed against asbestos manufacturers and employers, for neglecting to implement safety measures after the link between asbestos, asbestosis and mesothelioma became known (some reports seem to place this as early as 1898. The liability resulting from the sheer number of lawsuits and people affected has reached billions of dollars. The amounts and method of allocating compensation have been the source of many court cases, and government attempts at resolution of existing and future cases.
References
Classification
Pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kim-Son H. Nguyen, M.D., M.P.A., Beth Israel Deaconess Medical Center, Harvard Medical School, Boston MA, Cafer Zorkun, M.D., Ph.D. [2]
Overview
Pathophysiology
Asbestosis is the scarring of lung tissue (around terminal bronchioles and alveolar ducts) resulting from the inhalation of asbestos fibers.[1] There are two types of fibers, amphibole (thin and straight) and serpentine (curved). The former are primarily responsible for human disease as they are able to penetrate deeply into the lungs. When such fibers reach the alveoli (air sacs) in the lung, where oxygen is transferred into the blood, the foreign bodies (asbestos fibers) cause the activation of the lung’s local immune system and provoke an inflammatory reaction. This inflammatory reaction can be described as chronic rather than acute, with a slow ongoing progression of the immune system in an attempt to eliminate the foreign fibres. Macrophages phagocytose (ingest) the fibers and stimulate fibroblasts to deposit connective tissue. Due to the asbestos fibres’ natural resistance to digestion, the macrophage will die off, releasing certain cytokines and attracting further lung macrophages and fibrolastic cells to lay down fibrous tissue, which eventually forms a fibrous mass. The result is interstitial fibrosis. The fibrotic scar tissue causes alveolar walls to thicken, which reduces elasticity and gas diffusion, reducing oxygen transfer to the blood as well as the removal of carbon dioxide.
Asbestos presents as a restrictive lung disease. The total lung capacity (TLC) may be reduced through alveolar wall thickening. In the more severe cases, the drastic reduction in lung function due to the stiffening of the lungs and reduced TLC may induce right-sided heart failure (cor pulmonale).[2][3]
More than 50% of people affected with asbestos develop plaques in the parietal pleura, in the space between the chest wall and lungs. Clinically, patients present with dry inspiratory crackles, clubbing of the fingers, and a diffuse fibrotic pattern in the lower lung lobes (where asbestosis is most prevalent).
In general;
- Asbestos is a useful product because of its thermal, electric and sound-insulating qualities, and has been used in many settings for these reasons.
- Asbestos refers to a group of naturally-occurring fibers composed of hydrated magnesium silicates.
- World production and consumption peaked in the mid-1970s around 5.0 million tons, and has fallen thereafter to about 2.5 million tons today. Use has fallen in Europe and America, but has risen in countries with rapidly growing economies.
- As many as 8 million persons living in the U.S. have been occupationally exposed in the last 50 years.
- Asbestosis is a fibrotic interstitial lung disease.
- The asbestos fibers are inhaled into the pulmonary tree.
- The fibers tend to deposit at the level of the respiratory bronchiole and alveolar duct bifurcans. Most are removed by mucociliary clearance, but some are taken up by alveolar macrophages and alveolar cells.
- Alveolar macrophages accumulate and inflammation develops, and there is movement of other inflammatory cells into the lung.
- Various mediators including proteases, cytokines, growth factors and reactive oxygen species are released by inflammatory cells in response to the fibers. As alveolar and interstitial macrophages, neutrophils, lymphocytes, and eosinophils accumulate, normal alveolar cells are lost.
- The asbestos fibers probably have a direct toxic effect on the lung as well.
- Fibroblast proliferation and collagen accumulation eventually develop resulting in pulmonary fibrosis.
- Onset of fibrosis occurs 15-30 years after first exposure.
References
- ↑ Asbestosis: A Medical Dictionary, Bibliography, And Annotated Research Guide, Icon Health Publications, ISBN 0-597-84339-2
- ↑ Asbestos content of lung tissue and carcinoma of the lung: a clinicopathologic correlation and mineral fiber analysis of 234 cases, Victor L. Roggli and Linda L. Sanders, Ann. Hyg., Apr 2000; 44: 109 – 117.
- ↑ An Expert System for the Evaluation of Historical Asbestos Exposure as Diagnostic Criterion in Asbestos-related Diseases, Alex Burdorf and Paul Swuste, Ann. Hyg., Jan 1999; 43: 57 – 66.
Causes
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
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Causes
References
Differentiating Asbestosis from other Disorders

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kim-Son H. Nguyen, M.D., M.P.A., Beth Israel Deaconess Medical Center, Harvard Medical School, Boston MA, Cafer Zorkun, M.D., Ph.D. [2]
Overview
Differential Diagnosis
- Pleural disease is common in patients with asbestos exposure, occurring in up to 50%, but does not necessarily indicate asbestosis. Pleural disease includes circumscribed pleural plaques, with or without calcification, or diffuse pleural thickening, including blunting of the costrophrenic angle, and rarely rounded atelectasis secondary to pleural adhesions.
- The plaques are most commonly on the parietal pleura, particularly adjacent to ribs, most commonly along the 6th-9th ribs and along the diagphragm. They are typically absent from the apices and costrophrenic angle. Calcification is found on CXR in 20%, on CT scanning in 50%, and at post in 80%.
- Parenchymal fibrosis from asbestos exposure can occur with or without pleural plaques
- Pleural disease is not common in other causes of interstitial lung diseases
References
Epidemiology and Demographics
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Please help WikiDoc by adding content here. It’s easy! Click here to learn about editing.
Epidemiology and Demographics
References
Natural History, Complications and Prognosis
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kim-Son H. Nguyen, M.D., M.P.A., Beth Israel Deaconess Medical Center, Harvard Medical School, Boston MA, Cafer Zorkun, M.D., Ph.D. [2]
Overview
Natural History
Complications
Prognosis
People with extensive occupational exposure to the mining, manufacturing, handling or removal of asbestos are at risk of developing asbestosis.[1] There is also an increased risk of lung cancer and mesothelioma. Asbestosis and lung cancer require prolonged exposure to asbestos. However, cases of mesothelioma have been documented with even 1-3 months of exposure,[2][3] and only indirect exposure (through air ventilation system.) Most cases of asbestosis do not present until 5-10 years after exposure to the material.
- Malignancy is associated with asbestos exposure:
- Mesothelioma
- Mesotheiloma is an insidious neoplasm arising from the mesothelial surfaces of the pleural and peritoneal cavities or pericardium. 80% are pleural.
- The tumor forms on the visceral and parietal pleura in discrete plaques and nodules, and can grow to several centimeters with minimal lung penetration. Adjacent structures including the pericardium, chest wall, and diaphragm are commonly involved. Local lymph nodes may be involved, and distant hematogenous metastases in the liver, lung, bone and adrenals may develop.
- Asbestos exposure is the only known risk factor for mesothelioma, involved in >70% of cases. Lifetime risk of mesothelioma among asbestos workers is 8-13%.
- Annual U.S. incidence is 2200 cases per year. It is increasingly common in non-Western countries where there is increasing asbestos exposure.
- Tobacco use does not increase risk
- Patients present with increasing dyspnea, often in the 5th-7th decades of life.
- CXR usually initially shows a large unilateral pleural effusion. Chest CT more clearly shows extent of disease.
- Video-assisted thorascopy or open biopsy are often required to make the diagnosis.
- Median survival is 6-18 months and is ‘’not particularly amenable to treatment.’’ Death is from respiratory failure, or due to complications of invasion of involved organs.
- Lung cancer
- Lung cancer is more common in patients with asbestosis
- In one study, asbestos exposure increased relative risk of lung cancer 6-fold
- Tobacco use increases risk of developing lung cancer in a multiplicative fashion
- Cigarette smoking alone increased relative risk of lung cancer 11-fold.
- Cigarette smoking and asbestos exposure increased relative risk of cancer 59-fold
- Furthermore, a dose-response curve exists for cigarettes
- The risk of asbestos workers dying of lung cancer increases 9-fold if they smoked 1-20 cigarettes a day, and 16-fold if they smoke >20 cigarettes a day
- Other cancers
- Risk may be increased for gastrointestinal, larynx, oropharynx, and kidney and other cancers. Associations have been noted in some studies.
- Mesothelioma
References
- ↑ Becklake MR. Asbestos-related diseases of the lung and other organs: Their epidemiology and implications for clinical practice. Am Rev Respir Dis 1976;114:187-227
- ↑ Occupational Characteristics of Cases with Asbestos-related Diseases in The Netherlands, ALEX BURDORF, MOHSSINE DAHHAN, and PAUL SWUSTE, Ann. Hyg., Aug 2003; 47: 485 – 492.
- ↑ HYGIENE STANDARDS FOR AIRBORNE AMOSITE ASBESTOS DUST: BRITISH OCCUPATIONAL HYGIENE SOCIETY COMMITTEE ON HYGIENE STANDARDS, Committee on hygiene standards:, J. Glover, J. M. Barnes, D. Turner, S. A. Roach, D. E. Hickish, Sub-committee on asbestos:, J. C. Gilson, C. G. Addingley, G. Berry, S. Holmes, R. Hunt, H. C. Lewinsohn, S. G. Luxon, W. J. Smither, and S. A. Roach, Ann. Hyg., April 1973; 16: 1 – 5.
Diagnosis
Diagnosis
History and Symptoms | Physical Examination | Laboratory Findings | Chest X Ray | CT | MRI | Other Imaging Findings | Other Diagnostic Studies
Treatment
Treatment
Medical Therapy | Surgery | Primary prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
Related Chapters
Related Chapters
- Pneumoconiosis
- Coalworker’s pneumoconiosis (also known as “black lung”) – coa] dust
- Silicosis (also known as “grinhelloders’ disease”) – silica dust
- Bauxite fibrosis – bauxite dust
- Berylliosis – beryllium dust
- Siderosis – iron dust
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