Because the radiographic findings in silicosis early in its development are similar to those in a number of other diseases, it is essential to obtain an adequate history of exposure to make or suggest the diagnosis. Scattered small, round, nodular opacities are found in the upper and central portions of the lung as the initial roentgenographic change (Fig. 27-1). At first the opacities are discrete and small, on the order of 1 to 2 mm in diameter. At this stage, it is likely that an additive effect caused by overlapping nodules is necessary to make them visible. They are usually distributed symmetrically and widely, with a tendency to spare the lung bases. These opacities are usually clearly defined and uniform in density. They may be accompanied by small, irregular opacities, which are fewer in number than the round ones. The nodules gradually increase in size (Fig. 27-2). This may be termed “simple” or uncomplicated silicosis.

As the pulmonary nodules continue to increase in size, to 1 cm or more in diameter, they may coalesce and tend to become conglomerate (progressive massive fibrosis) (Fig. 27-3). The conglomeration and coalescence are usually accompanied by retraction toward the hilum, leaving the periphery
of the lung overinflated and relatively free of nodules (complicated silicosis). By the time this stage is reached there is often enough emphysema present to cause downward displacement of the diaphragm and a decrease in diaphragmatic motion with respiration. There can be considerable variation in the relative amounts of nodulation, hilar enlargement, and emphysema. Hilar node enlargement is common and may become apparent at any time during the development of the pulmonary abnormalities. The hilar nodes may undergo fibrosis and decrease in size by the time the nodular parenchymal lesions are large enough to be detected readily. Occasionally there is calcification in the silicotic pulmonary nodules. This is a manifestation of long-standing disease. In complicated silicosis, progressive massive fibrosis may ultimately cause migration of the conglomerate nodules toward the hila, and often slightly above them. Large, dense masses are then observed slightly above and lateral to the hilum. Although this process is bilateral, it is not always symmetrical. When it occurs, peripheral emphysema may become very severe. Very few nodules or pulmonary vessels are observed in this hyperlucent peripheral pulmonary tissue.

The hilar nodes are sometimes outlined because of the presence of a thin shell of calcium peripherally. This has been termed eggshell calcification, and when present it is very suggestive of silicosis. However, this type of calcification has also been described in patients with no exposure to silica or silicates and in patients with sarcoidosis, postradiation Hodgkin’s disease, blastomycosis, histoplasmosis, scleroderma, and amyloidosis (Fig. 27-4; see Fig. 27-6C). Rarely, an “eggshell” node may erode a bronchial wall and become a broncholith.

The diagnosis of silicosis can often be suspected on roentgen examination, but the clinical history is of great importance, because the diagnosis cannot accurately be made unless there is a history of enough exposure to silica-containing dust to produce it. Workers in “dusty” industries are often monitored at intervals by means of chest roentgenograms, and review of these serial films often leads to an accurate diagnosis. Extensive roentgen findings can be present without much alteration in pulmonary function, and the reverse is also true in some instances; therefore, there may be lack of correlation between roentgen appearance and pulmonary function.

Computed tomography (CT) has been correlated with plain films and pulmonary function tests in silicosis12,81. CT findings of silicosis and coal worker’s pneumoconiosis include micronodules (7 mm or less), macronodules (8 to 20 mm), congolmerate masses, and mediastinal adenopathy often with calcifications (Figs. 27-5 and 27-6)81. High-resolution computed tomography (HRCT) has been shown to be more sensitive than chest radiographs or conventional CT in the detection of micronodules in pneumoconiosis, and we routinely supplement our survey helical CT examination with HRCT slices in patients suspected of having occupational lung disease72,81. Parenchymal nodules in silicosis and coal worker’s pneumoconiosis on CT demonstrate an upper-lobe and posterior predilection12,81. In addition, a typical CT feature of silicosis and coal worker’s pneumoconiosis is the presence of subpleural nodules72,81. Subpleural nodules are seen in only a few other diseases (e.g., sarcoidosis). As disease extent becomes more severe, coalescence of nodules and conglomerate masses are appreciated on CT, as is the surrounding emphysema, fibrosis, and pleural tagging associated with these lesions. CT features of conglomerate masses include irregular margins, calcifications within the masses, bilaterality, and surrounding emphysema72,73,74,81. CT
can be particularly helpful in detecting cavitation within conglomerate masses, which should raise the suspicion for complicating tuberculosis72,81 (see Fig. 27-6).

Caplan’s syndrome is the combination of coal worker’s pneumoconiosis with rheumatoid arthritis63. Roentgen findings consist of rounded, peripheral nodules from 0.5 to 5.0 cm in diameter, which are clearly defined and may cavitate, on a background of nodular pneumoconiosis. This syndrome usually occurs in patients who have subcutaneous rheumatoid nodules but do not necessarily have arthritis. The pulmonary nodules may appear at intervals and often portend exacerbation of arthritis. They are similar to the necrobiotic nodules found in rheumatoid lung in patients without pneumoconiosis. This syndrome is uncommon, if not rare, in the United States but is evidently more common among coal miners in Wales.

The mechanical irritation of the long, stiff fibers when they become lodged in the lungs is believed to account, at least in part, for the fibrosis that results. There is circumstantial evidence to support a proposed autoimmune hypothesis
for the pathogenesis in this disease, as in silicosis. The silicates are more soluble than silica, so the fibrosis may be a response to the silicic acid and metallic ions released in solution. Bronchoalveolar lavage in pulmonary asbestosis reveals that first there is an alveolitis with an increase in alveolar macrophages, lymphocytes, and neutrophils. Fibroblast replication is accelerated, eventually leading to fibrosis, which is typical of asbestosis. The changes occur in the respiratory bronchioles and alveolar ducts, and the fibrosis is peribronchiolar in location. The cause of the pleural changes is not entirely clear. However, there is some evidence to show that the pleural reaction is at least in part caused by mechanical irritation by the fibers that penetrate the visceral pleura.

The disease does not develop unless there is a lengthy exposure, usually 10 years or more, to a fairly high concentration
of dust. When the pulmonary lesion is established, it progresses even though exposure is not continued. The clinical findings are those of progressive dyspnea which is often out of proportion to the amount of change noted on the chest films. There is often cyanosis and cough with sputum in which asbestos bodies can be detected. However, many patients with asbestos fibers in the lungs are asymptomatic. The incidence of tuberculosis is not as high as in silicosis. There is an increased incidence of carcinoma of the lung in patients with asbestosis. In patients with asbestos exposure who smoke, lung cancer is 70 times more likely than in nonsmokers who have no asbestos exposure. The lung tumors often develop in areas of fibrosis and are therefore extremely difficult to detect at an early stage. Insulation workers in building trades are six to seven times more likely to develop cancer of the lung or pleura than those not exposed to asbestos. This high incidence is found despite the relatively light and intermittent asbestos exposure in this group. Increased incidences of gastrointestinal cancer and of pleural and peritoneal mesothelioma have also been established. However, in one report of 36 cases of mesothelioma, 19 were not associated with asbestosis38. This is an unusual figure, however, because other reports indicate that only 11% to 16% of patients with malignant mesothelioma do not have a history of exposure to asbestos.

The fibrosis produced by the foreign material results in the appearance of small, irregular opacities, primarily in the lung bases as the earliest finding (see Figs. 27-8 and 27-9). As the number of these opacities increases, there may be an accentuation of interstitial markings extending into the perihilar regions and bases. Later there is an increase in the basal fibrotic changes, which usually appear stringy, irregular, and reticular. The cardiac borders assume a shaggy, poorly defined appearance as a result of a combination of interstitial fibrosis and small, irregular opacities. Increasing fibrosis may lead to large opacities, usually when interstitial fibrosis is extensive. This is not very common in asbestosis, however. The lung bases are usually involved, and in some instances the disease may involve the central and upper lungs as well. As a result of extensive basal disease, the outline of the diaphragm may become poorly defined. Cavitation and peripheral emphysema with central conglomeration (as seen in silicosis) does not occur.

HRCT is capable of detecting pulmonary parenchymal abnormalities in 96% of patients with clinical asbestosis1,2. Most CT findings, however, are not specific for asbestosis and can be seen in a variety of other lung diseases and in patients without exposure to asbestos11. CT findings that have been identified in patients with clinical asbestosis include dense fibrotic parenchymal bands, thickened interlobular septa and intralobular lines, thickened centrilobular core structures, architectural distortion of secondary pulmonary lobules, pleural-based nodular irregularities and subpleural dots, subpleural curvilinear lines, peripheral interstitial lines or reticulation, and honeycombing5,6,32,55,56,58,65 (see Fig. 27-9). Although changes of interstitial thickening and honeycombing on CT are not specific for pulmonary asbestosis and can be seen with any cause of interstitial fibrosis, their identification usually in conjunction with asbestos-related pleural plaques is strongly suggestive of asbestosis in a patient with a significant exposure history and an appropriate latency period before the onset of symptoms. The roles of CT and HRCT in the diagnosis of asbestosis remain controversial, however. There is little debate that CT is more sensitive for detection of pleural plaques and parenchymal changes of interstitial fibrosis than chest radiographs in patients exposed to asbestos,32,58 but the significance particularly of minimal or mild parenchymal abnormalities detected by HRCT is hotly contested. Standardization of HRCT criteria for diagnosis of asbestosis has not been established, and a lack of consensus among radiologists and pulmonologists as to the ultimate role of CT in establishing a diagnosis of asbestosis remains. Definitive diagnosis of asbestosis is still a pathologic determination requiring histologic evidence of peribronchiolar fibrosis in association with asbestos bodies in the lung.58

Other chest radiograph and CT findings seen in patients with a history of asbestos exposure include pleural thickening, pleural plaques, and rounded atelectasis (see Figs. 27-10 and 27-11). The pleural changes related to asbestos exposure occur independently and are often observed when no parenchymal disease can be detected. The following pleural manifestations may occur alone or in combination with the others: diffuse pleural thickening, pleural plaque formation, calcification in pleural plaques, and pleural effusion. Diffuse pleural thickening, which may extend into the fissures, is a common roentgenographic finding; it is usually bilateral and is more likely to be associated with interstitial fibrosis than the combination of pleural plaques and interstitial fibrosis. Diffuse pleural thickening involves the visceral pleura and can be recognized as such only when it extends into the interlobar fissures, where there is no parietal pleura. It may encase the entire lung. In asymptomatic patients, the presence of bilateral pleural thickening has a high predictive value for previous asbestos exposure—about 80% when patients with known causes (other than asbestos) for pleural disease are excluded.

Parietal pleural plaques are often the only findings in asbestos-related pleural disease. The plaques vary in thickness from 1 to 10 mm. Because they often occur posterolaterally or anterolaterally in the midthorax, oblique films may be very useful in demonstrating them. However, oblique films also may be confusing and are more useful in demonstrating involvement of the major fissures in patients with diffuse pleural thickening. In problem cases CT is very useful, because it not only demonstrates the pleural plaques but also differentiates them from fat, which may cause confusion on plain films. Diaphragmatic plaques in the absence of calcification are more difficult to identify on CT, because the plane
of sectioning is no longer perpendicular to the plaque. Plaques appear early as thin, local areas of pleural thickening in the midthorax, and they are often overlooked until they enlarge and become thicker. Fissural (visceral pleura) pleural thickening is common in asbestos exposure, and its presence may indicate pulmonary asbestosis even when the chest x-ray is normal77. As indicated previously, asbestos-related pleural thickening is more easily detected on CT than on chest radiography, and extrapleural fat can readily be differentiated from thick pleura. HRCT has been shown to be more accurate than CT in detecting pleural changes. It can identify reduced lung function, indicative of restrictive lung disease, in patients with asbestos exposure and normal chest radiographs.87

Calcification also occurs in pleural plaques. It is noted most frequently over the diaphragm in the form of a thin, curvilinear opacity conforming to the upper surface of the diaphragm bilaterally and is virtually pathognomonic. Oblique and lateral projections are useful in its detection. Unilateral pleural calcification, particularly when it extends upward along the chest wall, usually indicates previous infection, not asbestos exposure.

Bilateral or unilateral pleural effusion can also occur, but the possibility of other causes must be excluded before effusion can be attributed to asbestosis. The effusion tends to be relatively small in amount (i.e., less than 500 mL), and it may be bloody or blood-tinged. It is often the earliest sign of asbestos-related disease and may be accompanied by pleural pain. In some instances, the effusion contributes to or causes diffuse pleural thickening. Multiple recurrences appear to be rare, but a single recurrence of fluid is observed in almost one third of patients.60

The relative incidence of pleural findings has been studied by McLoud and coworkers61. In a group of 1,373 exposed persons, 16.5% had pleural plaques and 13.5% had diffuse pleural thickening. In those with diffuse thickening, the radiographic findings appeared to indicate that it was caused by the residuals of effusion in 31.4%, represented confluent plaques in 25.4%, and was accompanied by pulmonary fibrosis in 10.3%. Malignancy and infection accounted for 25% of pleural thickening, and in 5% it was caused by obesity. As in silicosis, the diagnosis is based on correlation of the roentgen findings with the clinical findings, plus an accurate occupational history of exposure to asbestos61 (see Figs. 27-8 and 27-10).

Rounded atelectasis is another abnormality often found in patients with diffuse pleural thickening due to asbestos exposure, although not all cases involve asbestos-related pleural disease1,2,95. Rounded atelectasis can often be suspected on the chest radiograph by the presence of a rounded peripheral opacity, typically in the posterior lower aspect of the lungs in association with pleural thickening. Serial chest films over time may show that the opacity is preceded by a pleural effusion and develops as the effusion resolves to pleural fibrosis. CT is very helpful in establishing the diagnosis of rounded atelectasis. The CT findings include a rounded or lentiform opacity that is in contiguity with an area of diffuse pleural thickening (see Fig. 27-11). Associated volume loss in the adjacent lung and the characteristic “comet tail” of vessels and bronchi leading into the opacity are also characteristic1,2. The need for biopsy may be obviated if these CT criteria are met in the diagnosis of round atelectasis versus tumor.1,2,95