Synonyms

Asbestos-related pleural fibrosis; Fibrous pleural plaque; Hyaline pleural plaques

Definition

Pleural plaques are focal, benign tumorlike lesions that arise from the epithelial lining of the thoracic cavity in response to chronic injury. They almost always occur in the setting of asbestos exposure but may also be seen in other pneumoconioses. Pleural plaques are the most common manifestation of asbestos inhalation and are an indicator of asbestos exposure according to the American Thoracic Society (2003). The specificity of pleural plaques as a marker for asbestos exposure is 80–90%. Plaques take years to develop and are rarely seen within 20 years after the first exposure; incidence increases with time from first exposure.

The process of pleural plaque formation is not itself malignant. However plaque formation implies a certain level of asbestos exposure, as the threshold for disease has been reached. Determining the absolute amount and type of dust to which a person has been exposed and the amount and type of exposure needed to produce pleural plaques has proven to be difficult. Therefore pleural plaques serve as a surrogate for the amount of asbestos exposure, which may be higher than what the occupational history might suggest.

Diagnosing pleural plaques and other nonmalignant asbestos-related disease is important, because it implies of a lifelong elevated risk of malignancy, most commonly lung cancer and mesothelioma. The presence of pleural plaques also closely correlates to the presence of parenchymal disease (interstitial fibrosis, or asbestosis). Patients with pleural plaques have asbestos fibers in their lung tissue, and asbestos bodies are seen in their bronchoalveolar lavage (BAL) fluid.

Although pleural plaques have been thought to be asymptomatic markers of asbestos exposure, dyspnea on exertion and reduced functional vital capacity have both been reported in association with plaques, independent of parenchymal disease detectable by radiography. This may be due to decreased lung compliance or subclinical parenchymal lung disease. Most people with pleural plaques alone, however, have well-preserved lung function.

Asbestos is a general commercial term, rather than a mineralogic term, for a variety of hydrated magnesium silicates. The various types of asbestos have great tensile strength and are resistant to acid and heat, but share a common tendency to break apart into fibers when crushed. More than 90% of commercially used asbestos is the serpentine mineral, chrysotile. The remaining forms are amphibole minerals. All types of asbestos have been shown to be connected to the development of pleural plaques.

The pathogenesis of pleural plaques begins with the inhalation of dust particles like asbestos. These particles are able to be carried deep into the lung alveoli and often deposit at airway bifurcations along the way. Fibers reach the visceral pleura via direct penetration, via migration into the interstitium with subsequent transportation to the visceral pleural by macrophages, or both. Some small fibers enter the pleural space where they are resorbed by lymphatic flow which occurs exclusively across the parietal pleural surface. The parietal surface has unique features that enable fluid turnover, most notably the presence of lymphatic stomata between mesothelial cells (see also “Pleura, Anatomy and Histology of”). Within the parietal pleura, the foreign fibers are phagocytosed by macrophages which become activated and release factors that stimulate fibroblasts. After decades of low-grade submesothelial activity, the fibroblasts will have formed a pleural plaque.

The major determinants of the degree of pleural plaque fibrosis are time from asbestos exposure and degree of asbestos exposure. The duration of asbestos exposure has not been shown to be significant. Compared to other benign asbestos-related entities, the formation of pleural plaques requires the least amount of asbestos exposure. More is required for diffuse pleural thickening and still more for asbestosis of the lung parenchyma.

Conventional chest plain film is sensitive and appropriate for screening modality for pleural plaques. The borders of pleural plaque lesions are sharp, often serrated or foliate, when seen face on. High-resolution computed tomography (HRCT) is not practical for screening because of the separation between sections, higher radiation exposure, and lack of access to technology in certain areas. It is useful as a secondary study for identifying abnormalities that resemble plaques.

Clinical Features

  • Incidence

    Pleural plaques are found most frequently in urban populations, where occupational asbestos exposure is prevalent. The incidence of pleural plaques in Western countries is 1–6.8% among men 30 years or more in age. In the United States, chest films of 2.3% of males show pleural plaques consistent with asbestos exposure (stable from the 1970s to 1990s). In France, HRCT imaging of 46.9% of asbestos-exposed workers over the age of 50 showed pleural plaques (screening study).

  • Age

    Older adults are affected due to the amount of elapsed time necessary for pleural plaque formation. The prevalence of pleural plaques increases after age 30 in men and after age 50 in women.

  • Sex

    Men are affected more often than women primarily due to occupational asbestos exposure. However, passive environmental exposure can occur, for example, when asbestos is brought into the home on clothing, and may cause disease.

  • Site

    Pleural plaques are lesions of the parietal pleura and have a predilection for the lower lung zones. They are almost always bilateral in the context of asbestos exposure, but are not necessarily symmetric. Pleural plaques are found in characteristic locations: over the central tendons (domes) of the diaphragm and beneath the inferior posterolateral ribs. They are generally absent from the costophrenic angles and the lung apices. Pleural plaques rarely involve the visceral pleura. They can occasionally be found in fissures between lung lobes.

  • Treatment

    Pleural plaques do not require treatment as they are generally asymptomatic and pose no risk of malignant degeneration. Patients diagnosed with pleural plaques should be informed of the risk of malignancy, especially the interaction between smoking and asbestos exposure. Guidelines for further screening studies are provided by the American Thoracic Society (2003).

  • Outcome

    Pleural plaques do not progress or transform from benignancy to malignancy. Mortality in patients with pleural plaques is primarily related to the development of malignancy. The majority of patients with pleural plaques alone do not develop cancer.

Macroscopy

Pleural plaques can be diagnosed on radiology or histologic examination. Grossly pleural plaques are firm, tan-white, slightly raised, and flat or nodular lesions of the parietal pleura. They are localized to the lower lung zones and bilateral in the context of asbestos exposure. Pleural plaques may be calcified as seen by radiography in 10–15% of cases by plain films and in 15–20% of cases by CT (Fig. 1).

Pleural Plaques, Fig. 1
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HRCT demonstrates pleural thickening with calcification (red arrows) in the posterior recess of the right lung base and in the left hemithorax, consistent with prior asbestos exposure. This 80-year-old previous smoker also had squamous cell carcinoma of the lung (green arrows)

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Microscopy

Pleural plaques are well-circumscribed proliferations of dense, mature collagen (Fig. 2). Fibers are arranged in an open (basket-weave) pattern (Fig. 3). The collagen is covered by a monolayer of flat to cuboidal benign mesothelial cells. Mesothelial cell proliferation is not a feature of pleural plaques. Pleural plaques show a paucity of vessels and are relatively acellular. They contain minimal inflammation and are sharply demarcated from the surrounding subpleural tissue. Central calcifications are common (Fig. 4). Asbestos bodies are not seen within or adjacent to the lesions, but may be seen in corresponding lung tissue or BAL fluid, as above.

Pleural Plaques, Fig. 2
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Low power H&E stain demonstrates a well-circumscribed proliferation of dense, mature collagen. There is a paucity of vessels. The lesion is relatively acellular

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Pleural Plaques, Fig. 3
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Medium power H&E shows fibers arranged in an open (basket-weave) pattern. Asbestos bodies are not seen within the lesion or in the adjacent soft tissue

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Pleural Plaques, Fig. 4
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Low power H&E shows central calcification within the pleural plaque, seen commonly

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Immunophenotype

The histologic diagnosis of pleural plaques does not require immunohistochemical staining. D2-40 and cytokeratin stains may be useful for differentiating a possible population of overlying spindled mesothelial cells from the fibroblast population forming the pleural plaque.

Molecular Features

Pleural plaques are benign proliferations of polyclonal fibroblasts with no known molecular alterations. However asbestos is thought to play a role in lung cancer carcinogenesis, encompassing transfection of DNA into cells and unregulation of proto-oncogenes. These mechanisms are beyond the scope of discussion for pleural plaques.

Differential Diagnosis

Tumorlike conditions of the pleura are rare and must be distinguished from extrapleural, pleural, and peripheral lung tumors. Radiographic features are helpful; for example, pulmonary-based tumors form an acute angle with the chest wall. The most common pleural tumors are metastases, which are usually nodular and have associated pleural effusions. Benign and malignant mesothelial proliferations must be excluded. Benign and malignant “solitary fibrous tumor” can occur in the pleura. Circumscribed fibrous pleural scars may occur after trauma or infection, as seen in tuberculosis (see also “Localized Pleural Fibrosis”). However scars will be unilateral and can be located anywhere, not just the lower lung zone. Diffuse pleural thickening (see also “Asbestos-Induced Pleural Disease”) arises from the visceral pleural, is ill defined, and affects pulmonary function more than plaques do. Pleural plaques and diffuse pleural thickening both may be seen in the same hemithorax and can even attach to form contiguous lesions. Fat pads can occur in the midthoracic wall, between the fourth and eighth ribs. These can be distinguished from pleural plaques on HRCT.