Imaging in Silicosis and Coal Worker Pneumoconiosis
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The word silicosis comes from the Greek word silex, meaning flint. It is perhaps the oldest known occupational disease; Hippocrates and Pliny referred to this disease. [1] Radiographic features of silicosis are seen in the images below.
Silica is a naturally occurring mineral that is mainly composed of silicon dioxide (SiO2). It exists in a crystalline and amorphous state. Quartz, cristobalite, and tridymite are the 3 most common forms of crystalline silica, which causes silicosis. Amorphous silica is not toxic. Quartz exists in alpha and beta forms, with alpha being more common than beta. Alpha quartz makes up 12% of the earth’s crust by weight, and it is a major component of igneous rocks, such as granite and pegmatite. It also occurs in sandstone, slate, and shale. Quartz is the most common form of inhaled silica.
Silicosis, asbestosis, and coal-workers’ pneumoconiosis (CWP) all belong to a group called pneumoconioses. The exact translation of this word is lung dust. These pulmonary diseases are characterized by nonneoplastic granulomatous and fibrotic changes in the lungs after the inhalation of inorganic substances, such as coal dust, asbestos, or crystalline silica. [2] Of these pneumoconioses, silicosis is the most common in the United States and most often occurs in people working in fields involving high exposure to dust. Such people include miners, construction workers, ceramics workers, tunnel drillers, sandblasters, quarry workers, and stone carvers. [3, 4]
Chronic silicosis is a diagnosis based on the patient’s history (ie, a history of probable exposure to silica dust combined with a proper temporal relationship of exposure to disease) and radiologic evaluation (ie, a chest radiograph demonstrating characteristic lesions). [5]
In 1980, the International Labour Office (ILO) International Classification of Radiographs of Pneumoconioses created standard radiographs that allowed for accurate diagnoses of pneumoconiosis and other interstitial lung diseases. This system uses a step-by-step method to describe the lesion. The shape, size, location, and abundance of opacities are considered. The radiographs are classified after they are compared with the standard radiographs, and all results are recorded in a systematic fashion.
However, this guideline has not been changed in more than 20 years, and although a digital version is being developed, no such classification exists for computed tomography (CT) scans at the present time. This lack creates a serious dilemma, because CT scanning is considered to be better than radiography as an imaging modality for diagnosing early signs of silicosis and CWP.
The chest radiograph is a relatively insensitive and nonspecific tool for diagnosing pneumoconiosis, because silicosis and CWP are virtually indistinguishable on radiologic studies. In addition, the results may cause underestimation or overestimation of the extent of disease. Moreover, normal chest radiographs do not rule out interstitial fibrosis. Consequently, without the proper history, occupational lung disease cannot be diagnosed on the basis of radiologic findings. [6] Even so, the ease of performing the study, combined with its cost-efficiency, makes radiography almost indispensable. [7, 8]
CT scanning is more sensitive and specific than chest radiography, and it is more useful in finding other lung diseases such as cancer, emphysema, and atelectasis, which may coexist in patients at risk for pneumoconiosis. [9, 10, 11] CT can depict nodules that chest radiography cannot, although HRCT is best for detecting nodules smaller than 3 mm. CT and HRCT scanning are useful in identifying large, confluent lesions that a chest radiograph may miss. HRCT can show fine parenchymal details, and it is the tool of choice for patients with normal chest radiographs and/or CT and for those with pulmonary lesions smaller than 1.5 mm. Emphysema is also best visualized on HRCT. The major downfall of CT and HRCT is the lack of standardization of technique and scoring. Therefore, for someone who may have silicosis or a borderline chest radiograph, chest CT should be done and supplemented with HRCT at several levels of the middle and upper lung. [9, 12, 13]
On chest radiographs and CT scans, the appearances of silicosis and CWP are almost identical. However, the nodules seem to be small on chest radiographs. (See the images below.)
Approximately 20 years of exposure is required to result in a positive chest radiograph. Chest radiography is about 80% sensitive, and the usual findings are multiple, small (< 1 cm) lung opacities. These opacities tend to occur in the upper and posterior regions of the lungs. They are usually round and well circumscribed. Their size and opacity vary little. These nodules are calcified in 10-20% of patients. With the progression of the disease, the nodules can merge to form large opacities. This change is indicative of progressive massive fibrosis (PMF), and it occurs more frequently in silicosis than in CWP. (See the image below.) [14]
The lesions must be at least 1 cm to be classified as PMF. Enlarged, calcified (eggshell calcification) lymph nodes are usually in the hila and mediastinum. PMF has a distinct appearance on chest radiography. PMF is usually symmetrical, but it may be unilateral. It appears as irregular, masslike or sausage-shaped opacities that are typically seen in the posterior upper lobes with associated hilar retraction. [9] These lesions are usually lenticular instead of round and therefore appear less dense than expected on frontal images.
PMF has an angel’s-wing appearance on chest radiographs. They are large lesions kept apart from the pleura by aerated lung. Sequential imaging shows that these lesions tend to migrate toward the hila, leaving behind peripheral areas of emphysema. The emphysema and lung volume loss help distinguish unilateral PMF from lung cancer. Cavitation may be a complication, with ischemic necrosis or concomitant tuberculous infection. Punctate, linear, or massive calcifications of the PMF lesions may be noted. [15]
On CT scans, these diseases appear as small, discrete nodules that have a predilection for the posterior portions of the upper lobes. The size of the nodules should be well correlated on CT scans and on chest radiographs.
On CT, PMF typically appears as irregular, lens-shaped, bilateral, large (>10 mm) attenuations in the posterior portions of the upper lobes. These lesions are often well circumscribed, calcified, and surrounded by cicatricial emphysema. Thickening of the adjacent extrapleural fat is common. Masses larger than 4 cm in diameter may exhibit central necrosis. Cavitation is infrequent. If necrosis or cavitation is seen in PMF, mycobacterial infection should always be considered. Pulmonary massive fibrosis can be misdiagnosed as bronchogenic carcinoma when pathognomonic characteristics, such as bilateral lens-shaped attenuations, well-defined borders, irregular calcifications, and lung nodularity, are missing. [16, 12, 13]
The typical appearance of pneumoconiosis on HRCT is branching and nonbranching centrilobular nodules that represent bronchiolar lesions. These lesions can be divided into 2 patterns: (1) ill-defined, fine, branching lines or nodules and (2) well-defined, discrete nodules. If present, interstitial fibrosis manifests as traction bronchiectasis, honeycombing, or large attenuations. [15, 17] HRCT scans of CWP appear below.
On HRCT, lesions classified as p in the ILO criteria appear as small, branching structures or a group of small dots. They are usually associated with centrilobular emphysema. Lesions designated as q or r appear as either discrete, well-circumscribed, round nodules or as irregularly shaped, contracted nodules. Fusion of the small nodules can produce a large confluent lesion. [9]
On HRCT, silicoproteinosis appears as a ground-glass or alveolar pattern; no nodules are observed.
CWP appears as focal emphysema and nodularity of the posterior portions of the upper lobes. Nodules smaller than 7 mm are micronodules, those 7-20 mm are macronodules, and those larger than 20 mm are PMF. According to the ILO criteria, round nodules smaller than 1.5 mm are p, those 1.3-3 mm are q, and those 3-10 mm are r. Lesions of CWP also become cavitated and calcified.
On HRCT, CWP with p lesion appears as small, branching lines or ill-defined, punctate attenuations. In some cases, small areas of low attenuation with a central dot can be seen. These areas are thought to represent either irregular fibrosis surrounding respiratory bronchioles or dust macules on dilated respiratory bronchioles. Lesions classified as q and r types are well-circumscribed, round, or contracted nodules. [15]
Subpleural micronodules can be seen on HRCT. These lesions can coalesce into large pseudoplaques in CWP.
The appearance of PMF is similar to that of silicosis.
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Andrzej R Jedynak, MD, MS Clinical Assistant Professor, Department of Radiology, State University of New York Downstate Medical Center
Andrzej R Jedynak, MD, MS is a member of the following medical societies: American College of Radiology, American Medical Association, Radiological Society of North America
Disclosure: Nothing to disclose.
Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, New York Academy of Medicine, American Academy of Dermatology, American College of Physicians, Sigma Xi
Disclosure: Nothing to disclose.
Bernard D Coombs, MB, ChB, PhD Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.
Kavita Garg, MD Professor, Department of Radiology, University of Colorado School of Medicine
Kavita Garg, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, Radiological Society of North America, Society of Thoracic Radiology
Disclosure: Nothing to disclose.
Judith K Amorosa, MD, FACR Clinical Professor of Radiology and Vice Chair for Faculty Development and Medical Education, Rutgers Robert Wood Johnson Medical School
Judith K Amorosa, MD, FACR is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, Association of University Radiologists, Radiological Society of North America, Society of Thoracic Radiology
Disclosure: Nothing to disclose.
Corey D Eber, MD, MS Assistant Professor of Radiology, University of Medicine and Dentistry of New Jersey; Vice-Chairman, Department of Radiology, University Hospital
Disclosure: Nothing to disclose.
Imaging in Silicosis and Coal Worker Pneumoconiosis
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