Benign Asbestos Pleural Diseases

Stephen J. Chapman, BMBCh, MRCP, William O.C. Cookson, MD, DPhil, FRCP, FRS, A. William Musk, MD, FRACP, Y.C. Gary Lee, MBChB, PhD, FRACP

Disclosures

Curr Opin Pulm Med. 2003;9(4) 

In This Article

Clinical Aspects of Benign Asbestos Pleural Disease

Circumscribed pleural plaques are the most common manifestation of asbestos exposure and comprise discrete areas of white or yellow thickening on the parietal pleura (see the review by Rudd[7]). They are frequently bilateral and symmetric, and occur particularly on the posterolateral chest wall between the fifth and eighth ribs, over the mediastinal pleura, and on the dome of the diaphragm. Histologic examination reveals plaques to be acellular, with a "basket-weave" pattern of hyalinized collagen strands. They are covered by a single layer of normal mesothelial cells on the pleural surface.

Pleural plaques typically develop 20 to 30 years after exposure, and their incidence increases with longer duration of exposure. They are found in as many as 50% of asbestos-exposed workers, but may also occur after low-dose exposures. The total surface area of pleural plaques measured via CT does not appear to be related to cumulative asbestos exposure.[8]

Assessment of pulmonary function in patients with pleural plaques has yielded conflicting results, and studies are complicated by variations in the degree of exposure, the presence of other asbestos-related diseases, and confounding factors such as smoking. Although some studies have demonstrated evidence of small airway obstruction in subjects with asbestos exposure and pleural plaques, this is presumed to be the result of underlying asbestosis (and peribronchial fibrosis) not detected by plain radiographs.[9] This effect has been demonstrated recently in nonsmoking female Chinese subjects with heavy asbestos exposure.[10] The majority of studies demonstrated no significant association between pleural plaques and lung function abnormalities.[8,11**,12] The extent of pleural plaques and thickening also did not predict arterial oxygen desaturation in subjects with asbestosis.[13]

Some epidemiologic studies suggest an increased risk of coronary heart disease after asbestos exposure, which is independent of age and smoking status.[14,15] A recent study demonstrated a significantly higher prevalence of pleural plaques on chest radiographs in patients referred for coronary angiography than in patients with lung cancer.[16] It is unclear whether this apparent association of pleural plaques with coronary heart disease is a result of confounding factors. Mukherjee et al.[14] also described a significant relation between angina and the presence of asbestos-induced pleuropulmonary abnormalities.

Benign asbestos effusions are a relatively early manifestation of asbestos pleural disease[17] and can occur within 10 years of exposure. They are typically small and unilateral, and may be asymptomatic or associated with pain, fever, and dyspnea. They usually resolve spontaneously over a few months, although some may recur. The risk of development of benign asbestos pleural effusions is considered to be dose dependent.[18] There has been no demonstration of a threshold dose, and they can occasionally occur after minimal exposure.

The diagnosis of benign asbestos-related pleural effusion is one of exclusion of other specific causes in a patient with past asbestos exposure. The pleural effusion is an exudate, often bloodstained, with no characteristics on pleural fluid analysis. This often creates diagnostic difficulty in asbestos-exposed individuals, especially because pleural fluid in patients with mesothelioma may be false negative for malignant cells.[19] The diagnosis of benign asbestos-related pleural effusion depends on a history of asbestos exposure and the exclusion of other causes.[20] Benign asbestos pleurisy may precede the development of diffuse pleural thickening (DPT).

Diffuse pleural thickening consists of extensive fibrosis of the visceral pleura with areas of adhesion with the parietal pleura and consequent obliteration of the pleural space (see the review by Rudd[7]). Unlike pleural plaques, its margins are ill defined and it frequently involves the costophrenic angles, apices, and interlobar fissures. DPT has been known to follow benign asbestos-related pleural effusion, and it has been suggested that benign asbestos-related pleural effusion is a necessary precursor of DPT.

It has variable radiologic definitions. On conventional chest radiography it may be defined as a smooth, uninterrupted pleural opacity extending over at least a quarter of the chest wall, often with obliteration of the costophrenic angles.[21] DPT has been defined arbitrarily on CT as a pleural density extending more than 8 cm craniocaudally, 5 cm laterally, and is more than 3 mm thick.[22]

Diffuse pleural thickening most commonly follows extensive asbestos exposure, although not inevitably.[23] Exertional breathlessness and chest pain (which can be chronic and severe) are relatively common symptoms of DPT.[14,24] DPT is usually progressive and may lead to significant restrictive pulmonary function impairment, especially if the costophrenic angle is obliterated.[9,11**,12] This occurs as a result of reduced inspiratory excursion of the lower chest wall and diaphragm.[25] Rarely, hypercapnic respiratory failure can develop, and this has been treated successfully with home noninvasive ventilation.[26] Surgical decortication is generally ineffective in providing clinical or functional improvement.

Rounded atelectasis (also known as folded lung, Blesovsky syndrome, or shrinking pleuritis with atelectasis) develops as contracting visceral pleural fibrosis ensnares and then rolls into the underlying lung.[27,28] This results in the distinctive radiologic appearance of a rounded or oval pleural-based mass of 2.5 to 5 cm in diameter, with bands of contracted and atelectatic lung radiating out in a whirling fashion. CT is often diagnostic, demonstrating a "comet tail" of vessels and bronchi converging toward the lesion, adjacent thickened pleura, and volume loss in the affected lobe. An atypical appearance may require biopsy to exclude malignant disease. Rounded atelectasis is typically asymptomatic, although some patients experience breathlessness or dry cough. Serious complications (eg, obstructive pneumonia and local pulmonary artery thrombosis[29]) may be rarely associated. In most cases rounded atelectasis is stable or slowly progressive, and no specific treatment is required. Surgical decortication designed to improve symptoms often results in reduced lung volumes[30] and is not generally recommended.

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