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|Classification and external resources|
|Classification and external resources|
Asbestosis is a chronic inflammatory and fibrotic medical condition affecting the parenchymal tissue of the lungs caused by the inhalation and retention of asbestos fibers. It usually occurs after high intensity and/or long-term exposure to asbestos (particularly in those individuals working on the production or end-use of products containing asbestos) and is therefore regarded as an occupational lung disease. People with extensive occupational exposure to the mining, manufacturing, handling, or removal of asbestos are at risk of developing asbestosis. Sufferers may experience severe dyspnea (shortness of breath) and are at an increased risk for certain malignancies, including lung cancer but especially mesothelioma. Asbestosis specifically refers to interstitial (parenchymal) fibrosis from asbestos, and not pleural fibrosis or plaquing.
The signs and symptoms of asbestosis do not manifest until after an appreciable latency (time since first exposure), often several decades under current conditions in the US. The primary symptom of asbestosis is generally the slow onset of dyspnea, especially on exertion. Clinically advanced cases of asbestosis may lead to respiratory failure. On auscultation of the lungs, the physician may hear inspiratory rales.
The characteristic pulmonary function finding in asbestosis is a restrictive ventilatory defect. This manifests as a reduction in lung volumes, particularly the vital capacity (VC) and total lung capacity (TLC). The TLC may be reduced through alveolar wall thickening; however this is not always the case. Large airway function, as reflected by FEV1/FVC, is generally well preserved. 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). In addition to a restrictive defect, asbestosis may produce reduction in diffusion capacity and arterial hypoxemia.
Asbestosis is the scarring of lung tissue (around terminal bronchioles and alveolar ducts) resulting from the inhalation of asbestos fibers. 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 fibers. Macrophages phagocytose (ingest) the fibers and stimulate fibroblasts to deposit connective tissue. Due to the asbestos fibers' natural resistance to digestion, the macrophage dies off, releasing cytokines and attracting further lung macrophages and fibrolastic cells to lay down fibrous tissue, which eventually forms a fibrous mass. This mass can be seen microscopically, with the asbestos fiber layered by an iron-containing proteinaceous material (psammoma body). 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.
The abnormal chest x-ray and its interpretation remain the most important factors in establishing the presence of pulmonary fibrosis. The findings usually appear as small, irregular parenchymal opacities, primarily in the lung bases. Using the ILO Classification system, "s", "t", and/or "u" opacities predominate. CT or high-resolution CT (HRCT) are more sensitive than plain radiography at detecting pulmonary fibrosis (as well as any underlying pleural changes). More than 50% of people affected with asbestosis develop plaques in the parietal pleura, the space between the chest wall and lungs. Once apparent, the radiographic findings in asbestosis may slowly progress or remain static, even in the absence of further asbestos exposure. Rapid progression suggests an alternative diagnosis.
Asbestosis resembles many other diffuse interstitial lung diseases, including other pneumoconioses. The differential diagnosis includes Idiopathic Pulmonary Fibrosis (IPF), Hypersensitivity pneumonitis, sarcoidosis, and others. The presence of pleural plaquing may provide supportive evidence of causation by asbestos. Although lung biopsy is usually not necessary, the presence of asbestos bodies in association with pulmonary fibrosis establishes the diagnosis. Conversely, interstitial pulmonary fibrosis in the absence of asbestos bodies is most likely not asbestosis. Asbestos bodies in the absence of fibrosis indicate exposure, not disease.
There is no curative treatment for asbestosis. Oxygen therapy at home is often necessary to relieve the shortness of breath and correct underlying hypoxia. Supportive treatment of symptoms includes respiratory physiotherapy to remove secretions from the lungs by postural drainage, chest percussion, and vibration. Nebulized medications may be prescribed in order to loosen secretions or treat underlying Chronic Obstructive Pulmonary Disease. Immunization against pneumococcal pneumonia and annual influenza vaccination is administered due to increased sensitivity to the diseases. Patients are at increased risk for certain malignancies. If the patient smokes, cessation reduces further damage. Periodic PFTs, chest x-rays, and clinical evaluations, including cancer screening/evaluations, are given to detect additional hazards.
The death of English textile worker Nellie Kershaw in 1924 from pulmonary asbestosis was the first case to be described in medical literature, and the first published account of disease attributed to occupational asbestos exposure. However, her former employers (Turner Brothers Asbestos) denied that asbestosis even existed because the medical condition was not officially recognised at the time. As a result, they accepted no liability for her injuries and paid no compensation, either to Kershaw during her final illness or to her bereaved family after she had died. Even so, the findings of the inquest into her death were highly influential insofar as they led to a parliamentary enquiry by the British Government. The enquiry formally acknowledged the existence of asbestosis, recognised that it was hazardous to health and concluded that it was irrefutably linked to the prolonged inhalation of asbestos dust. Having established the existence of asbestosis on a medical and judicial basis, the report resulted in the first Asbestos Industry Regulations being published in 1931, which came into effect on 1 March 1932.
The first lawsuits against asbestos manufacturers occurred 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 in modern times). 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.
Some notable persons have died from lung fibrosis associated with asbestos include:
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