Asbestos is a family of crystalline hydrated silicates with a fibrous geometry. On the basis of epidemiologic studies, occupational exposure to asbestos is linked to (1) parenchymal interstitial fibrosis (asbestosis); (2) localized fibrous plaques, or, rarely, diffuse fibrosis in the pleura; (3) pleural effusions; (4) lung carcinoma; (5) malignant pleural and peritoneal mesothelioma; and (6) laryngeal carcinoma. An increased incidence of asbestos-related cancers in family members of asbestos workers has alerted the general public to the potential hazards of asbestos in the environment.
As with silica crystals, once phagocytosed by macrophages, asbestos fibers activate the inflammasome and damage phagolysosomal membranes, stimulating the release of proinflammatory factors and fibrogenic mediators. In addition to cellular and fibrotic lung reactions, asbestos probably also functions as both a tumor initiator and a promoter. Some of the oncogenic effects of asbestos on the mesothelium are mediated by reactive free radicals generated by asbestos fibers, which preferentially localize in the distal lung close to the mesothelial layer. However, potentially toxic chemicals adsorbed onto the asbestos fibers also undoubtedly contribute to the pathogenicity of the fibers. For example, the adsorption of carcinogens in tobacco smoke onto asbestos fibers may be the basis for the remarkable synergy between tobacco smoking and the development of lung carcinoma in asbestos workers.
Fig. 13.19 High-powerdetailofanasbestosbody,revealingthetypicalbeadingandknobbedends(arrow).
MORPHOLOGYAsbestosisismarkedbydiffuse pulmonary interstitial fibrosis,characterizedbythepresenceofasbestos bodies, whichareseenasgoldenbrown,fusiformorbeadedrodswithatranslucentcenter.Theyconsistofasbestosfiberscoatedwithaniron-containingproteinaceousmaterial(
Fig.13.19 ).Asbestosbodiesapparentlyareformedwhenmacrophagesattempttophagocytoseasbestosfibers;theiron“crust”isderivedfromphagocyteferritin.
IncontrastwithCWPandsilicosis,asbestosisbeginsinthelowerlobesandsubpleurally,spreadingtothemiddleandupperlobesofthelungsasthefibrosisprogresses.Contractionofthefibroustissuedistortsthenormalarchitecture,creatingenlargedairspacesenclosedwithinthickfibrouswalls;eventually,theaffectedregionsbecomehoneycombed.Simultaneously,fibrosisdevelopsinthevisceralpleura,causingadhesionsbetweenthelungsandthechestwall.Thescarringmaytrapandnarrowpulmonaryarteriesandarterioles,causingpulmonaryhypertensionandcorpulmonale.
Fig.13.20 ),oftencontainingcalcium.Theydevelopmostfrequentlyontheanteriorandposterolateralaspectsoftheparietal pleura andoverthedomesofthediaphragm.Uncommonly,asbestosexposureinducespleuraleffusionordiffusepleuralfibrosis.
The clinical findings in asbestosis are indistinguishable from those of any other chronic interstitial lung disease. Progressively worsening dyspnea appears 10 to 20 years after exposure. It is usually accompanied by a cough and production of sputum. The disease may remain static or progress to congestive heart failure, cor pulmonale, and death. Pleural plaques are usually asymptomatic and are detected on radiographs as circumscribed densities.