Asbestosis is a disease of the lung that causes a diffuse and fibrosing interstitial damage. The term was first coined by the British pathologist, Dr. Cooke, in the early 1930s to refer to his postmortem findings in the lungs of asbestos textile workers in Britain. Today, it is widely recognized that asbestosis is indeed a direct result from the duration and intensity of one’s exposure to any of the asbestiform fiber types.
The disease starts to manifest around at least 10 years after moderate to severe exposure to asbestos. Physiologic studies of the lung reveal that asbestosis follows a restrictive pattern, causing noted decrease in both lung volumes and diffusing capacity. Evidence of peribronchiolar fibrosis causing mild airflow obstruction may also be seen. Reactive oxygen species are generated by transition metals found on the surface of fibers cause oxidative injury in the parenchyma of the lung. This also contributes to much of the fibrosis seen in the lung parenchyma. Cells engaged in phagocytosis also effect fibrosis.
A simple chest radiograph can detect much of the lesions caused by asbestos exposure. Past exposure is characteristically seen as thickenings or calcifications in the parietal pleura, along the lower lung fields, diaphragm, and heart border. These thickenings or calcifications are termed as pleural plaques. Benign pleural effusions that are usually serous or bloody exudates may also be seen. These effusions may progress slowly or resolve spontaneously. As asbestosis progresses, the pleural plaques that were first noted on the lower lung fields will slowly spread into the middle and upper lung fields. This causes the characteristic ground glass appearance of the lungs on chest radiographs.
The management of patients diagnosed with asbestosis mainly center around supportive care. Therapy does not reverse the fibrosis. As with other interstitial lung diseases, the major goals for the treatment of asbestosis include the permanent removal of the offending agent, in this case, removal of the asbestos containing products or taking oneself away from where the source is found, early identification of the symptoms of asbestosis, early and correct diagnosis and prompt institution of treatment to aggressively suppress the acute and chronic inflammatory processes that are in place. All these are done to help reduce and prevent further lung damage.
Glucocorticoids remain as the mainstay of therapy in the suppression of alveolitis found in the different forms of interstitial lung diseases, including asbestosis. A starting dose of prednisone 0.5-1 mg/kg patient’s body weight in a once daily dosing is recommended. This dosage is given for a period of 4 to 12 weeks, and at which time the patient is reevaluated. If the patient’s condition is found to be stable or have even improved, this dose is tapered to 0.25 to 0.5 mg/kg. This level is maintained for 4 to 12 more weeks. Rapid tapering of glucocorticoids should be avoided to avoid recurrence of the inflammatory processes. A second agent such as the immunosuppressant agents cyclophosphamide or azathioprine can be added if patient’s condition continues to decline when on glucocorticoids alone. Lung transplantation may be considered after maximal medical treatment fails to bring improvement.
Asbestosis is an inevitable disease brought about by continual exposure to asbestos containing products. Meticulous precautionary methods should be employed, especially people in high-risk occupations in order to minimize the level of exposure.