Asbestosis

Asbestosis is long term inflammation and scarring of the lungs due to asbestos fibres. Symptoms may include shortness of breath, cough, wheezing, and chest tightness. Complications may include lung cancer, mesothelioma, and pulmonary heart disease.Figure A shows the location of the lungs, airways, pleura, and diaphragm in the body. Figure B shows lungs with asbestos-related diseases, including pleural plaque, lung cancer, asbestosis, plaque on the diaphragm, and mesothelioma.'Extensive fibrosis of pleura and lung parenchyma.''The arrow points to an uncoated segment of asbestos fiber in this ferruginous body.''Severe pleural fibrosis with focal calcification.''The black arrows point to ferrugionous bodies that are located at the periphery of a focus of non-small cell lung carcinoma, NOS.'61 yr old working industrially with asbestos for decades. Asbestosis is long term inflammation and scarring of the lungs due to asbestos fibres. Symptoms may include shortness of breath, cough, wheezing, and chest tightness. Complications may include lung cancer, mesothelioma, and pulmonary heart disease. Asbestosis is caused by breathing in asbestos fibers. Generally it requires a relatively large exposure over a long period of time. Such levels of exposure typically only occur in those who work with the material. All types of asbestos fibers are associated with an increased risk. It is generally recommended that currently existing asbestos be left undisturbed. Diagnosis is based upon a history of exposure together with medical imaging. Asbestosis is a type of interstitial pulmonary fibrosis. There is no specific treatment. Recommendations may include influenza vaccination, pneumococcal vaccination, oxygen therapy, and stopping smoking. Asbestosis affected about 157,000 people and resulted in 3,600 deaths in 2015. Asbestos use has been banned in a number of countries in an effort to prevent disease. The signs and symptoms of asbestosis typically manifest after a significant amount of time has passed following asbestos exposure, often several decades under current conditions in the US. The primary symptom of asbestosis is generally the slow onset of shortness of breath, especially with physical activity. Clinically advanced cases of asbestosis may lead to respiratory failure. When a physician listens with a stethoscope to the lungs of a person with asbestosis, they may hear inspiratory crackles. 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 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 a low amount of oxygen in the blood of the arteries. The cause of asbestosis is the inhalation of microscopic asbestos mineral fibers suspended in the air. In the 1930s, E. R. A. Merewether found that greater exposure resulted in greater risk. Asbestosis is the scarring of lung tissue (beginning around terminal bronchioles and alveolar ducts and extending into the alveolar walls) resulting from the inhalation of asbestos fibers. There are two types of fibers: amphibole (thin and straight) and serpentine (curly). All forms of asbestos fibers are 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 lungs' local immune system and provoke an inflammatory reaction dominated by lung macrophages that respond to chemotactic factors activated by the fibers. This inflammatory reaction can be described as chronic rather than acute, with a slow ongoing progression of the immune system attempting 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, some macrophages are killed and others release inflammatory chemical signals, attracting further lung macrophages and fibrolastic cells that synthesize fibrous scar tissue, which eventually becomes diffuse and can progress in heavily exposed individuals. This tissue can be seen microscopically soon after exposure in animal models. Some asbestos fibers become layered by an iron-containing proteinaceous material (ferruginous body) in cases of heavy exposure where about 10% of the fibers become coated. Most inhaled asbestos fibers remain uncoated. About 20% of the inhaled fibers are transported by cytoskeletal components of the alveolar epithelium to the interstitial compartment of the lung where they interact with macrophages and mesenchymal cells. The cytokines, transforming growth factor beta and tumor necrosis factor alpha, appear to play major roles in the development of scarring inasmuch as the process can be blocked in animal models by preventing the expression of the growth factors. The result is fibrosis in the interstitial space, thus asbestosis. This fibrotic scarring 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. This can result in shortness of breath, a common symptom exhibited by individuals with asbestosis. According to the American Thoracic Society (ATS), the general diagnostic criteria for asbestosis are: 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.