The global incidence of asbestos-related lung diseases is expected to continue to rise. Although much attention is devoted to malignant diseases induced by asbestos, benign asbestos pleural diseases (pleural plaques, benign asbestos-related pleural effusion, diffuse pleural thickening, and rounded atelectasis) are common in clinical practice and often produce diagnostic difficulties. The authors describe the clinical features of benign asbestos-related pleural disease, before focusing on recent advances in radiology and on controversies surrounding the pathogenesis of asbestos-induced pleural injury. Advances in computed tomography have assisted the understanding and diagnosis of these diseases, and increasing evidence suggests radiologic appearances on computed tomography can predict impairment in pulmonary function tests. The pathogenesis of asbestos-induced pleural diseases has also been subject to extensive investigation. Asbestos fibers can provoke pleural inflammation from direct toxicity to mesothelial cells. Inhaled asbestos fibers can also elicit pleural injury indirectly via the release of growth factors and inflammatory cytokines from within the lung. Although progress has been made in the understanding of the mechanisms of asbestos pleural injury, many important questions remain unanswered. The role of genetic factors and possible environmental cofactors (eg, simian virus 40) in the pathogenesis of benign asbestos pleural diseases requires further research.
Abbreviations:CCT conventional computed tomography, DPT diffuse pleural thickening, HRCT high-resolution computed tomography
Asbestos consists of a family of naturally occurring hydrated silicate fibers [1•]. Asbestos fiber types may be subdivided into curly serpentine fibers and straight, needlelike amphiboles. Chrysotile is the only serpentine fiber in commercial use. Amphibole fibers include crocidolite (blue asbestos), amosite (brown asbestos), anthophyllite, tremolite, and actinolite. Although asbestos consumption in developed countries is strictly regulated, the use of chrysotile in developing economies continues to rise [2]. Also, the long latency between exposure and disease manifestation means that new cases will continue to present as a result of previous exposures. The majority of cases of benign asbestos-induced pleural diseases are the result of occupational exposure, particularly the mining, milling, and shipping of asbestos, and the use of asbestos products in construction and insulation. Environmental exposure probably accounts for low background rates of disease, although in certain areas asbestos is abundant in the environment and the local population is continuously exposed (eg, in areas of central and southeast Turkey, northwest Greece, and in Finland). Recent studies have addressed the nonmalignant pleural effects of environmental exposure in these regions [3-5].
Asbestos fibers have a natural, unexplained predilection to the pleura, where they may result in a diverse array of benign and malignant diseases. Benign asbestos pleural disease comprises pleural plaques, benign asbestos pleurisy, diffuse pleural thickening, and rounded atelectasis [6•]. These disorders are important because they are common and may result in abnormal lung function and symptoms. They may resemble other diseases of the pleura and may lead to diagnostic uncertainty. The diagnosis of asbestos-induced pleural diseases also has medicolegal implications. Furthermore, an increased knowledge of the pathogenesis of asbestos pleural disease may aid understanding of the mechanisms underlying other diseases that involve pleural inflammation/fibrosis. We describe the clinical features of benign asbestos-related pleural diseases before focusing on recent advances in radiology and controversies surrounding the pathogenesis of asbestos-induced pleural inflammation.