The Pneumoconioses

Chapter 8 The Pneumoconioses

Many respiratory disorders can be occupationally induced. The most important of these are the pneumoconioses. A pneumoconiosis is a diagnosable disease produced by the inhalation of dust (i.e., particulate matter in the solid phase, excluding living organisms). Mineral dust can be classified as fibrogenic, such as asbestos and silica, or inert, such as iron, tin, or barium. The metal dusts include beryllium and cobalt, which are associated with granulomatous pneumonitis and giant cell pneumonitis, respectively (Table 8-1). Most pneumoconioses produce diffuse opacities on the chest radiograph that are similar to those seen in other interstitial lung disorders.

Table 8-1 Dust Diseases

Agent Examples Disorders
Mineral dusts Asbestos
Metal dusts Iron
“Inert dust” pneumoconioses
Metal dusts Beryllium
Granulomatous pneumonitis
Giant cell pneumonitis
Biologic dusts Spores
Bird droppings
Hypersensitivity pneumonitis (allergic alveolitis)


The International Labour Organization (ILO) classification of the radiographic appearances of the pneumoconioses is a standardized, internationally accepted system used to codify the radiographic changes in the pneumoconioses in a reproducible manner (Box 8-1). The advantage of the system is that it provides graphic and morphometric terms to describe diffuse lung patterns. The classification includes conventions of small, rounded (nodules) and small, irregular (linear and reticular) opacities (Fig. 8-1). The small, rounded opacities are classified according to the approximate diameter of the predominant opacity: p (up to 1.5 mm in diameter), q (1.5 to 3 mm in diameter), and r (3 to 10 mm in diameter). Small, irregular opacities are classified on the basis of thickness and appearance: s (fine, up to 1.5 mm thick), t (medium, 1.5 to 3 mm thick), and u (coarse or blotchy, 3 to 10 mm thick).

The ILO scheme also quantifies the radiographic severity, or profusion, on a 12-point scale. There are four basic categories: 0, normal; 1, slight; 2, moderate; and 3, advanced. The distribution and extent of opacities are recorded in six zones. The convention for large opacities describes the conglomerate masses identified in some of the pneumoconioses. The 1980 ILO classification also includes detailed categorization of pleural thickening that is quantified and classified as diffuse or circumscribed (i.e., plaque).


General Description

Silicosis (Box 8-2) is a fibrotic disease of the lungs caused by inhalation of dust containing free crystalline silica or silicon dioxide. It is the predominant constituent of the earth’s crust. Silica dust may be encountered in almost any mining, quarrying, or tunneling operation. Occupations at risk therefore include the mining of heavy metals, such as gold, tin, copper, silver, nickel, and uranium, and to a lesser extent, coal mining; the pottery industry; sandblasting; foundry work; and stone masonry. Silicosis is usually a chronic, slowly progressive disease that occurs with a latency period of at least 20 years.

Simple Silicosis

Simple silicosis (Box 8-3) has no symptoms and is not associated with any significant changes in pulmonary function.

Computed Tomography Findings

Because silicosis and coal worker’s pneumoconiosis exhibit a nodular pattern, conventional computed tomography (CT) and high-resolution CT (HRCT) should be used. CT clearly depicts the characteristic nodules in patients with simple silicosis, and it is more sensitive in the detection of these nodules than conventional radiographs (see Fig. 8-2B). Conventional 10-mm CT is preferred because the thin sections in HRCT may lead to underestimation of the prevalence of nodules, and it is often difficult to differentiate small nodules from normal pulmonary vessels. However, conventional scans should be supplemented with thin-section HRCT to depict fine parenchymal detail. These scans can be limited and performed at preselected levels. The study should include at least three slices through the upper lung zones, where nodules of silicosis predominate.

Complicated Silicosis

Radiographic Findings

On the chest radiograph, the opacities of complicated silicosis appear in the middle zone or in the periphery of the lung in the upper lobes (Fig. 8-4A). They tend to migrate to the hilum, leaving overinflated emphysematous lung tissue in the surrounding lung, particularly at the bases. The more extensive the progressive massive fibrosis, the less the apparent the nodularity in the remaining lungs.

As conglomeration develops, the lungs gradually lose volume, and cavitation of the masses may result from ischemic necrosis. In this setting, tuberculosis or infection with atypical mycobacteria may supervene. Superimposed tuberculosis may be difficult to detect radiographically; findings such as cavitation of conglomerate masses, pleural reaction at the apices, or other rapid radiographic changes are suggestive (Fig. 8-5). The diagnosis of supervening tuberculosis, however, is bacteriologic rather than radiologic.

Accelerated Silicosis and Acute Silicosis

Acute Silicosis

Acute silicosis or silicoproteinosis (see Box 8-5) usually occurs as a consequence of exposure to large quantities of fine particulate silica in enclosed spaces over a period of a few weeks. Pathologically, the alveoli are filled with an eosinophilic and lipid-rich exudate, which is periodic acid–Schiff (PAS) stain positive. The disease rapidly progresses, and death is caused by respiratory failure.

The radiographic appearance of acute silicosis is quite different from that of classic simple silicosis. Acute silicosis has a pattern of diffuse consolidation or airspace disease with a perihilar distribution and air bronchograms. Radiographic and pathologic findings are similar to those in alveolar proteinosis. Mycobacterial infection is quite prevalent (25%), and one half of the cases are caused by atypical organisms.

Caplan’s Syndrome

Silicosis is associated with increased prevalence of several connective tissue diseases, including progressive systemic sclerosis, rheumatoid arthritis, Caplan’s syndrome, and systemic lupus erythematosus. Caplan’s syndrome (Box 8-6) consists of large, necrobiotic nodules (i.e., rheumatoid nodules) superimposed on a background of simple silicosis or coal worker’s pneumoconiosis (Fig. 8-7). It is a manifestation of rheumatoid lung disease, and it is seen more commonly in coal worker’s pneumoconiosis than in silicosis. The nodules are 0.5 to 5 cm in diameter, and they may cavitate and calcify. Although they most often develop concomitantly with the joint disease, their formation may precede the onset of arthritis by months or years.


Coal worker’s pneumoconiosis is a compensable occupational disease in the United States. This disease is particularly common in underground miners. In studies of coal worker’s pneumoconiosis in this population, prevalences between 9% and 27% have been reported.

Simple Coal Worker’s Pneumoconiosis

Causes and Pathology

Simple coal worker’s pneumoconiosis (Box 8-7) results from the retention of coal dust alone. Pathologically, the hallmark of coal worker’s pneumoconiosis is the coal macule. It consists of aggregations of dust around dilated respiratory bronchioles. Fibrosis is minimal. Simple coal worker’s pneumoconiosis is not associated with any significant functional impairment, and workers are usually asymptomatic.

Computed Tomography Findings

The CT findings for simple coal worker’s pneumoconiosis include parenchymal and subpleural micronodules (<7 mm in diameter) (Fig. 8-8). The nodules show an upper-zone and right-sided predominance. When they occur in the subpleural zones, they may become confluent, forming pseudoplaques, which consist of subpleural focal linear areas of increased attenuation that are less than 7 mm wide. Larger nodules that are between 7 and 20 mm in diameter can be seen scattered on a background of micronodules.

Feb 28, 2016 | Posted by in RESPIRATORY IMAGING | Comments Off on The Pneumoconioses

Full access? Get Clinical Tree

Get Clinical Tree app for offline access