Asbestos exposure may result in asbestosis (pulmonary fibrosis) and in lung cancer in patients with asbestosis.
Pleural findings include plaques, calcified plaques, diffuse thickening, effusion, and mesothelioma. The type of asbestos (crocidolite or chrysotile), the duration of exposure, the amount of exposure, and the year the patient was first exposed are related to the type and severity of the asbestos-related condition.
Asbestosis is defined as a pneumoconiosis with interstitial fibrosis of the pulmonary parenchyma in which asbestos bodies or fibers may be demonstrated. Generally, a large cumulative exposure is necessary for the development of asbestosis, with moderate-to-high levels over several years. Such exposures occurred early in the twentieth century in the weaving industry and later in the ship building and insulation trades in the 1940's and 1950's. In the United States, such high exposures have ceased since the mid 1970's.
Considering the latency period, the occurrence of asbestosis should have decreased in the 1990's. The latency is generally 20 years. A small percentage of asbestos-exposed workers may have clinical features consistent with asbestosis yet have non-asbestos interstitial lung disease. Dyspnea is the most common symptom. End-inspiratory fine crackles are heard in more than 60 percent of patients. Finger clubbing, cyanosis, and cor pulmonale are late findings. The chest roentgenogram shows small linear irregular opacities at the lung bases. Honeycombing is seen late. The physiologic findings indicate a decreased vital capacity with no evidence of major airflow obstruction except in smokers. The diffusing capacity is the physiologic hallmark of the disorder and is decreased in virtually all patients with asbestosis. Asbestosis remains static in most patients but progresses in a small percentage of individuals depending fiber type, cumulative exposure, level of exposure, and duration of exposure.
Asbestos-related lung cancer was described in patients with asbestosis in 1935 and was confirmed epidemiologically in 1955. Cigarette smoking is an important factor in asbestos-related lung cancer and acts in a multiplicative synergistic manner; the two combined exposures cause a higher occurrence of cancer than the two exposures separately. Asbestos-related lung cancer is rare among non-smokers. The cancerous lesions may occur centrally or peripherally. Small cell, squamous cell, and adeno-carcinoma occur with equal frequency.
Pleural effects are the most common asbestos-related findings. Unlike asbestosis, pleural plaques may occur in individuals with peripheral exposure such as working in a shipyard for one or two years during World War II, living next to an asbestos mine, or employment as an electrician, welder, or plumber. Pleural plaques generally have a latency period of 20 years and occur in as many as 60% of shipyard workers. Generally single or even multiple plaques are not a cause of symptoms or clinically significant physiologic abnormalities. The chest roentgenogram is distinctive and shows plaques along the lateral pleural surfaces, diaphragmatic surfaces, or along the mediastinal or pericardial surfaces.
Plaques may calcify approximately 30 years after first exposure. Benign asbestos effusion, unlike other asbestos conditions, can occur within the first 10 years of exposure. Approximately 50% of patients with this condition are asymptomatic, but occasionally, a fibrothorax may develop necessitating surgical decortication. Diffuse pleural thickening or blunted costophrenic angles may be the result of a prior effusion and may be associated with volume limitation.
Mesothelioma usually results from crocidolite asbestos exposure and occurs 30 to 40 years after first exposure. Chest pain and effusion develop in 90% of these patients. Long-term survivors have been reported; however, the prognosis remains dismal despite triple therapy including surgery, radiation, and chemotherapy.
From: Environmental and Occupational Lung Diseases
Gary R. Epler, M.D
