Document xj2GzKxXeKnYe4eDpqMq7mqQg

Topics in Radiology / Diagnostic Radiology Harold G. Jacobson, MD, Section Editor E. Robert Heitzman, MD, Section Coordinator Radiology of Asbestos Disease Lawrence R. Goodman, MD ALTHOUGH the hazards of asbestos exposure were first reported in the early 1900s, the full extent of its effects is still being evaluated. Per sons with occupational exposure to asbestos have a higher incidence of pulmonary fibrosis (asbestosis), vari ous pleural disorders (plaque, thick ening, and effusion), and neoplasms (lung, pleura, and gastrointestinal). In recent years, attention has turned to asbestos as an environmental pol lutant. Household contacts of asbes tos workers, persons living near asbestos plants, and urban dwellers frequently have asbestos fibers in the lungs at autopsy. The chest roentgenogram often offers the first evidence of asbestos exposure, because a history of asbes tos exposure is difficult to obtain or is not sought. Therefore, it is important for both the radiologist and clinician to understand both the radiological findings of asbestos exposure and the significance of each change. The final diagnosis of asbestosis (pulmonary fibrosis) rests on a com bination of pulmonary lesions on the roentgenogram, bibasilar rales, and reduced lung function in a patient with the appropriate exposure histo ry. Microscopic verification is usually not obtained.1,1 The diagnosis of asbestos-related pleural disease relies more heavily on the radiological changes (see below). Roentgenograms demonstrating the typical lateral pleural changes in the absence of old trauma or empyema have a 0.81 correlation with prior exposure to asbestos.' A rough correlation exists between the degree of asbestos exposure and the type of disease produced. Pulmo nary fibrosis (asbestosis) and malig nant neoplasms of the lung and gas- From the Department of Diagnostic Radiology, Hahnemann Medical College and Hospital, Phliadel* '-.-MV... . ,, Reprint request! to the Department of Dfagnoatlo Radiology, Hahnemann Medical College and Hoaplf'.. tel. 230 N Breed St, Philadelphia. PA 19t02 (Dr F Goodman). trointestinal tract are most likely to develop in those individuals with the heaviest exposure. Those persons with mild to moderate exposure are more likely to contract benign or malignant pleural disease. These rela tionships are complex and depend on the type of fiber, pattern of exposure, and time since initial exposure. Usu ally, a 15- to 20-year latency period occurs between the initial exposure and the first radiological or clinical evidence of disease. Cigarette smok ing potentiates both the fibrogenic and carcinogenic effects of asbestos.1 For both epidemiologic studies and the individual patient, good-quality 120-kV posteroanterior and lateral roentgenograms usually provide the necessary radiological information. Oblique roentgenograms may accen tuate questionable pleural changes. Although computed tomography (CT) will demonstrate lesser degrees of fibrosis, pleural plaques, and pleural calcification, routine use of it hardly seems justified. The major value of CT appears to be in distinguishing focal plaques (benign) from intraparenchymal nodules (presumably can cer) and determining whether large lesions are lung masses, solid pleural lesions (presumably mesotheliomas), or focal pleural fluid collections. In patients with proven lung cancer and mesothelioma, CT is a valuable aid in determining the extent of the lesion both for planning of treatment and determining prognosis. Asbestosis (Pulmonary Fibroala) The radiological changes of pulmo nary fibrosis may precede, be associ ated with, or follow the onset of pulmonary symptoms. Unlike most other pneumoconioses (with the ex ception of talcosis), the predominant radiological lesions involve the lower half of the lungs. These are usually small, irregular, poorly defined linear opacities. Pinpoint opacities, thick ened septal lines, gross linear strand ing, and honeycombing are less fre- Fig 1.--In this postaroanterlor film of right hemithorax, reticular nodular Interstitial infil trate Is present throughout lupga (asbestosis) in this patient with emphysema. Observe mild pleural thickening along lateral chest wall and minor fissure. Small calcified plaque Is noted as well (black arrow). Spheroid, pleural-based mass (while arrow) waa nof present on previous films, proving at surgery to be adenocarcinoma involving lung, pleura, and chest wall. quent (Figs 1 and 2, left). (Their severity is scored on a 12-point scale adopted by the International Labor Office.) Lung volumes tend to be normal or diminished. Associated obstructive lung disease is more likely caused by smoking than by asbestos. Conglomerate masses (progressive massive fibrosis), a well-known com plication of silicosis and coal workers pneumoconiosis, are extremely rare in asbestosis. When it does occur in asbestosis, it tends to be in the lower lobes, the area of predominant pulmo nary fibrosis. Therefore, any focal lung density appearing in a patient with exposure to asbestos should sug gest a carcinoma rather than a con glomerate mass.1,4 A recently recognized entity that may mimic lung cancer or the rare Section Coordinator*: Thomas C. Beneventano, MO (Caaa of the Month); Juan A. del Ragato, MO (Tharapautlc Radiology); Jack Edeikeo. MO (Diagnostic Radiology); Barry B. Gokfbarg, MO (Ultrasonography); E. Robert Heitzman, MO (Diagnoatlc Radiol ogy); Stanley S. Slegeiman, MO (Computed Tomography); Edward B. Sliberated, MO (Nuclear Radiology). 844 JAMA, Feb 4, 1933--Vol 249, No. 5 DPMC-12754 Radiology In Asbestos Disease--Goodman LAM 019131 I[ Fig 2.--Left, In this posteroanterior roentgenogram of chest, considerable dense, linear, interstitial thickening is noted in lower half of right lung (asbestosls). Costophrenic angle is blunted and pleura is thickened to level of posterior segment ol third rib. On left side, upper lobe nodule as well as homogeneous opacification of lung base is present. Differential diagnosis included loculated effusion, mesothelioma, and lung cancer. Right, Computed tomographic scan through lung base demonstrates large, left lower lobe lung mass (M), bilateral pleural thickening, and calcification (arrows) (oat cell carcinoma, left lower lobe). lower lobe progressive massive fibro sis is the pulmonary pseudotumor (rounded atelectasis). This is usually a swirl of atelectatic parenchyma adjacent to thickened pleura. Tomo grams or oblique films may demon strate a "tail" to the medial aspect of the mass, and CT may show clearly the atelectatic nature of the lesion. Thus, one can often distinguish between round atelectasis and a tumor.11 \ Lung Cancer Asbestos and cigarette smoking are cocarcinogens. Lung cancer is 70 times more likely to develop in a smoking asbestos worker than in a nonsmoker without asbestos expo sure. The malignant neoplasms are most frequently peripheral and at the bases of the lungs as opposed to the more frequent upper lobe predomi nance. The tumor frequently arises in a background of interstitial fibrosis or pleural disease, making detection of a small neoplasm difficult (Fig 1). Any change identified on serial films should be viewed with great suspi cion, because fibrosis and plaques often take years to demonstrate radiological progression. Tomograms or CT may be helpful in distinguish ing overlapping shadows, a lung nod ule, or a pleural mass11 (Fig 2). Benign Pleural Disease Pleural disease may take several guises. Asymptomatic, focal, bilateral pleural thickening along the midlat eral thoracic wall are characteristic of pleural plaque due to moderate asbestos exposure. Plaques may also be discerned along the mediastinal pleura, the pericardium, and the dia phragm. They tend to spare the lung apexes and costophrenic angles. The majority are not calcified, and most are noted in the absence of pulmonary fibrosis. When calcification occurs, it is in the parietal pleura in a charac teristic distribution along the surface of the diaphragm and the lateral chest wall (Figs 1 and 3). Plaques do not undergo malignant degeneration, but are an indicator of significant asbestos exposure. When these char acteristic plaques are present, the vast majority of patients have a his tory of asbestos exposure.' Asbestos workers with pleural plaques, but no fibrosis, have a 2'^-fold increase in lung cancer.11 Diffuse pleural thickening with involvement from the apex to the base may also be due to asbestos exposure. Unlike pleural plaques, this radiological appearance may be ob served in a variety of diseases (Fig 2, left). Pleural effusions are frequently harbingers of pleural or pulmonary malignant neoplasms. Any patient with a notable asbestos history and at least ten years since initial exposure should be presumed to have a malig nant neoplasm until proved other wise. However, effusions may be benign in nature. Epler et ai4 have recently shown that benign effusion was the most common asbestosrelated abnormality during the first twenty years after exposure. Mesothelioma Mesothelioma is approximately three to five times more frequent in asbestos workers than in nonasbestos workers. Because it is a relatively rare tumor, however, its incidence is considerably less than lung cancer. Exposure to asbestos is often mild to moderate, and frequently a 30- to 40-year latency period ensues be tween initial exposure and develop ment of the mesothelioma.11 Mesotheliomas may arise from any mesothelial surface, but the vast majority are located in the pleura or pericardium. Symptoms include the insidious onset of pain, dyspnea, and weight loss. The most frequent radio logical manifestation is that of pleu ral effusion. The effusion is often large and may obscure the pleural JAMA, Feb 4, 1983--Vol 249, No. 5 Radiology in Asbestos Disease--Goodman 645 DPMC-12755 LAM 019132 Fig 3.--Posteroanterior chest roentgenogram shows lobular pleural plaques along each lateral chest wall (arrows). Lung apexes and costophrenic angles are spared. Calcitied pleural plaque is noted on left diaphragm (arrowhead). Little or no interstitial fibrosis is present (asbestosispleural plaques). Fig 4.--In this posteroanterior roentgenogram of chest, large right pleural effusion obscures extensive malignant mesothelioma. Lateral portion of right third rib (upper arrows) is destroyed, and upper segment of trachea is deviated to left. Two nodules observed over left upper lobe represent calcified pieural plaques en face. Diaphragmatic, mediastinal pleura and lateral pleural calcifications are also present (lower arrows). ..umor. Large effusions may cause the mediastinum to shift to the contralat eral side or mediastinal pleural involvement may "freeze" the medi astinum and prevent mediastinal shift (Fig 4). When the mesothelioma is visible, it usually appears as a lobular mass between the lung and the chest wall. It may be localized in a small area or may encase a large portion of the lung. The volume of the involved hemithorax may be diminished. Sec ondary invasion of the chest wall, lung invasion, or lung metastasis are frequently observed late in the course of the disease (Fig 4). Computed tomographic examination frequently discloses the tumor to be more exten sive than initially appreciated. Me diastinal invasion and contralateral or subdiaphragmatic spread are fre quently demonstrated by CT exami nation. Nonoccupatlonal Lung Disease Concern for the effects of asbestos on the general population arises from multiple sources. Families of asbestos workers have a higher incidence of asbestos-related lung disease. The air in most urban areas contains small numbers of asbestos particles. Autop sies of adults in urban centers fre quently show asbestos bodies in the lung, although at a much lower con centration than in asbestos workers.' The disease-producing potential of inhalation of asbestos in a low con centration in the general population is still unknown. It has been sug gested that the lateral pleural thick ening occasionally observed in nonas bestos workers may be related to low levels of asbestos exposure.' References 1. Preger L: Asbestos-Related Disease. New York, Grune &. Stratton Inc, 197R. 2. Becklake MG: Asbestos-related diseases of the lung and other organs: Their epidemology and implications for clinical practice. Am Rev Rcspir Dis 1976;114:187-227. 3. Albelda SM, Epstein DM, Gefter WB, et al: Pleural thickening: Its significance and relation ship to asbestos dust exposure. Am Rev Respir Dis 1982;126:621-624. 4. Souter CA, Simon G, Turner-Warwick M: The radiology of asbestos-induced disease of the lungs. Br J Dis Chest 1974;68:235-252. 5. Mintzer RA, Cugell DW: The association of asbestos-induced pleural disease and rounded atelectasis. Chest 1982;81:457-460. 6. Epler GR, McLoud TC, Gaensler EA: Preva lence and incidence of benign asbestos pleural effusion in a working population. JAMA 1982; 247:617-622. 7. Ochs CW, Smith JP: Chronic pleural thick ening: Some observations on cause and patho genesis. Military Med 1976;141:77-81. 646 JAMA. Feb 4, 1983--Vol 249, No. 5 Radiology in Asbestos Disease--Goodman DPMC-12756 LAM 019133