Asbestosis
The term pneumoconiosis dates to Zenker’s 1866 description of pulmonary disease processes related to the inhalation of dusts [1]. As some dust, including asbestos fibers, may be found in the lungs of virtually all adults from the general population, pneumoconiosis now refers to the accumulation of excessive amounts of dust in the parenchyma of the lung and the pathologic response to its presence [2]. Asbestosis, the form of pneumoconiosis related to excessive amounts of asbestos fibers in the substance of the lung, is the prototype of diseases caused by inhalation of mineral fibers. Asbestos is a commercial, legal, and regulatory term, rather than a strictly mineralogical one, that encompasses a group of naturally occurring fibrous silicates whose differing physicochemical attributes confer a spectrum of pathologic properties upon their inhalation and deposition into the lung. Much has been learned from experimental models about the pathogenesis of asbestos-induced lung injury, which is reviewed in detail in Chap. 10. The reader is directed to Chap. 3 for a discussion of asbestos bodies, the histologic emblem of asbestos exposure, and a requisite component of the pathologic diagnosis of asbestosis. Chapter 11 discusses the methodology and results of quantitative tissue analysis for asbestosis, other asbestos-related diseases, as well as normal and disease control populations. The present chapter describes the morphologic features of asbestosis and relates them to the clinical and radiographic features of the disease.
