Reviewers: Elliot Weisenberg, M.D. (see Reviewers page)
Revised: 26 September 2011, last major update September 2011
Copyright: (c) 2003-2011, PathologyOutlines.com, Inc.
● Similar to other pneumoconiosis
● Initial injury is at bifurcations of small airways and ducts; macrophages ingest fibers, release chemotactic factors and fibrogenic mediators, causing interstitial fibrosis similar to other fibrosing lung diseases such as UIP
● Begins around respiratory bronchioles and alveolar ducts, extends distally; eventually causes honeycomb lungs
● Begins in lower lobes and subpleurally (in contrast to coal workers pneumoconiosisP and silicosis), progresses to middle and upper lobes
● Visceral pleura becomes fibrotic, may bind lung to chest wall; may have associated Caplan syndrome
● Symptoms: usually begin after 10 years of exposure, initially shortness of breath with exertion and later at rest; may progress to heart failure
● Pleural plaques: well circumscribed plaques of dense collagen, often with calcium; on parietal pleura and dome of diaphragm; do not contain asbestos bodies, but rare if no asbestos history; may induce pleural effusions, usually no symptoms
● Asbestos fiber detection: H&E, Prussian blue, incineration and EM
● Early: interstitial pneumonia with desquamative features, hyperplastic alveolar cells with intracytoplasmic Mallory’s hyaline tissue
● Later: diffuse interstitial fibrosis with honeycombing (silicosis is nodular), asbestos bodies (golden brown, fusiform or beaded rods with translucent center; asbestos fibers coated with iron-containing proteinaceous material); iron from phagocyte ferritin
● Asbestos fibers may have oxalate crystal deposition (Hum Pathol 2003;34:737)
● Ferruginous bodies: inorganic particulates coated with phagocyte ferritin
End of Lung-nontumor > Pneumoconiosis > Asbestosis
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