OCCUPATIONAL EXPOSURES AND PULMONARY DISEASE
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In addition to exposures to asbestos that may occur during the production of asbestos products (from mining to manufacturing), common occupational asbestos exposures occur in shipbuilding and other construction trades (e.g., pipefitting, boilermaking) and in the manufacture of safety garments and friction materials (e.g., brake and clutch linings). Along with worker exposure in these areas, bystander exposure (e.g., spouses) can be responsible for some asbestos-related lung diseases.
A range of respiratory diseases has been associated with asbestos exposure. Pleural plaques indicate that asbestos exposure has occurred, but they are typically not symptomatic. Interstitial lung disease, often referred to as asbestosis, is pathologically and radiologically similar to idiopathic pulmonary fibrosis; it is typically accompanied by a restrictive ventilatory defect with reduced diffusing capacity of the lung for carbon monoxide (DLCO) on pulmonary function testing. Asbestosis, which is directly related to the intensity and duration of exposure, usually develops at least 10 years after exposure, and no specific therapy is available.
Benign pleural effusions can also occur from asbestos exposure. Lung cancer is clearly associated with asbestos exposure but does not typically present for at least 15 years after initial exposure. The lung cancer risk increases multiplicatively with cigarette smoking. In addition, mesotheliomas (both pleural and peritoneal) are strongly associated with asbestos exposure, but they are not related to smoking. Relatively brief asbestos exposures may lead to mesotheliomas, which typically do not develop for decades after the initial exposure. Biopsy of pleural tissue, typically by thoracoscopic surgery, is required for diagnosing mesothelioma.
Silicosis results from exposure to free silica (crystalline quartz), which occurs in mining, stone cutting, sand blasting, abrasive industries (e.g., glass and cement manufacturing), foundry work, and quarrying. Heavy exposures over relatively brief time periods (as little as 10 months) can cause acute silicosis—which is pathologically similar to pulmonary alveolar proteinosis and associated with a characteristic chest CT pattern known as “crazy paving.” Acute silicosis can be severe and progressive; whole lung lavage may be of some therapeutic benefit.
Longer-term exposures can result in simple silicosis, with small rounded opacities in the upper lobes of the lungs. Calcification of hilar lymph nodes can give a characteristic “eggshell” appearance on radiographic studies. Progressive nodular fibrosis can result in masses >1 cm in diameter in complicated silicosis. When such masses become very large, the term progressive massive fibrosis is used to describe the condition. Due to impaired cell-mediated immunity, silicosis pts are at increased risk of tuberculosis, atypical mycobacterial infections, and fungal infections. Silica may also be a lung carcinogen.
Coal Worker’s Pneumoconiosis (CWP)
Occupational exposure to coal dust predisposes to coal worker’s CWP, which is less common among coal workers in the western United States due to a lower risk from the bituminous coal found in that region. Simple CWP is defined radiologically by small nodular opacities and is not typically symptomatic. The development of larger nodules (>1 cm in diameter), usually in the upper lobes, characterizes complicated CWP. Complicated CWP is often symptomatic and is associated with reduced pulmonary function and increased mortality. In addition to CWP, coal dust exposure can cause COPD.
Beryllium exposure may occur in the manufacturing of alloys, ceramics, and electronic devices. Although acute beryllium exposure can rarely produce acute pneumonitis, a chronic granulomatous disease very similar to sarcoidosis is much more common. Radiologically, chronic beryllium disease, like sarcoidosis, is characterized by pulmonary nodules along septal lines. As in sarcoidosis, either a restrictive or obstructive ventilatory pattern with reduced diffusing capacity (DLCO) on pulmonary function testing can be seen. Bronchoscopy with transbronchial biopsy is typically required to diagnose chronic beryllium disease. The most effective way to distinguish chronic beryllium disease from sarcoidosis is to assess for delayed hypersensitivity to beryllium by performing a lymphocyte proliferation test using blood or bronchoalveolar lavage lymphocytes. Removal from further beryllium exposure is required, and corticosteroids may be beneficial.