Pathology and Mineralogy of the Pneumoconioses

Abstract

Pneumoconioses represent the spectrum of lung diseases caused by inhalation of respirable particulate matter small enough (typically <5-µm diameter) to reach the terminal airways and alveoli. Pneumoconioses primarily occur in occupational settings where workers perform demanding and skilled manual labor including mining, construction, stone fabrication, farming, plumbing, electronics manufacturing, shipyards, and more. Most pneumoconioses develop after decades of exposure, though shorter latencies can occur from more intense particulate matter exposures. In this review, we summarize the industrial exposures, pathologic findings, and mineralogic features of various well-characterized pneumoconioses including silicosis, silicatosis, mixed-dust pneumoconiosis, coal workers' pneumoconiosis, asbestosis, chronic beryllium disease, aluminosis, hard metal pneumoconiosis, and some less severe pneumoconioses. We also review a general framework for the diagnostic work-up of pneumoconioses for pulmonologists including obtaining a detailed occupational and environmental exposure history. Many pneumoconioses are irreversible and develop due to excessive cumulative respirable dust inhalation. Accurate diagnosis permits interventions to minimize ongoing fibrogenic dust exposure. A consistent occupational exposure history coupled with typical chest imaging findings is usually sufficient to make a clinical diagnosis without the need for tissue sampling. Lung biopsy may be required when exposure history, imaging, and testing are inconsistent, there are unusual or new exposures, or there is a need to obtain tissue for another indication such as suspected malignancy. Close collaboration and information-sharing with the pathologist prior to biopsy is of great importance for diagnosis, as many occupational lung diseases are missed due to insufficient communication. The pathologist has a broad range of analytic techniques including bright-field microscopy, polarized light microscopy, and special histologic stains that may confirm the diagnosis. Advanced techniques for particle characterization such as scanning electron microscopy/energy dispersive spectroscopy may be available in some centers.

Fig. 1

Mature silicotic nodule. The center of the nodule (arrow) is composed of hyalinized, whorled collagen surrounded by concentric rings of collagen. The periphery of the lesion demonstrates dust-laden histiocytes. There is alveolar proteinosis noted (star). The inset shows abundant weakly birefringent silica and strongly birefringent silicate particles under polarized light microscopy. Strands of collagen are also evident as fibrillar birefringence.

Fig. 2

Silica-type progressive massive fibrosis (PMF). (A) Silica-type PMF, greater than 1-cm diameter, in a contemporary miner comprised of fused, mature silicotic nodules. The surrounding lung parenchyma shows silicotic nodules (stars), bridging fibrosis (arrows), and mild scar emphysema (arrowheads) adjacent to areas of fibrosis. (B) Silica-type PMF again comprised of fused silicotic nodules. A majority of the silicotic nodules within this PMF lesion and in the parenchyma are immature. There is also severe interstitial fibrosis (arrows).

Fig. 3

Mineral dust–related alveolar proteinosis (MDAP) or silicoproteinosis. (A) Low-power view of airspaces filled with pink, slightly granular material (arrows) with artifactual cracks from shrinkage (arrowheads). (B) High-power view of MDAP in a coal miner with extensive silica exposure highlights the granularity of the lipoproteinaceous material.

Fig. 4

Talcosis. Lung biopsy from an intravenous drug user presenting with large pulmonary masses and interstitial fibrosis. A section of parenchyma shows small fibrotic nodular lesions in the interstitium adjacent to small pulmonary vessels. Strongly birefringent particles are seen throughout the nodules, along with occasional macrophage giant cells (arrows). The particles are platelike and substantially larger (up to 30 μm in maximum dimension) than would be expected in distal lung tissue from inhalation. The large particle size, location of particles adjacent to small pulmonary vessels, and history of intravenous drug use were diagnostic of talcosis. X-ray spectroscopy may be used to confirm the presence of talc but is not required for diagnosis.

Fig. 5

Mixed-dust pneumoconiosis. Lung section from an autopsied coal miner showing a ~4 mm fibrotic nodule (arrow) with central necrosis and whorling of the surrounding hyalinized collagen fibers, indicative of a silicotic nodule. The periphery of the lesion is composed of black dust, fibroblasts/fibrocytes, and irregularly arranged collagen fibers. Higher magnification showed black dust consistent with the bituminous coal mine dust, but there were also fine particles more consistent with combustion products such as from smoking or diesel emissions. Examination with polarized light microscopy (inset) revealed a heavy burden of small, weakly birefringent particles (consistent with silica), and lesser numbers of larger particles with strong birefringence (consistent with silicates). Note: This pathology is common to a wide variety of occupations with sufficient silica exposure to produce some of its characteristic pathologic features. The worker in this case was a coal miner, so this mixed-dust lesion might be best classified as coal workers’ pneumoconiosis, with coal and silicotic nodules. The diagnosis of mixed-dust pneumoconiosis on its own is best reserved for workers with a complex exposure history and/or multiple relevant jobs.

Fig. 6

Coal macules and nodules. (A) Classic coal macule from a coal miner with dust-laden macrophages in a reticulin stroma in the wall of a respiratory bronchiole, and with associated centrilobular emphysema (arrowheads). The small pulmonary artery (star) supplying this terminal region appears normal, as does the parenchyma further away from the macule. (B) Several coal nodules are shown in the lung parenchyma of a coal miner. Coal nodules are generally larger than macules, have more collagen, and are palpable to the touch. Smaller nodules are shown in the walls of respiratory bronchioles and have more pink collagen than the macule in A. Several nodules adjacent to larger airways and blood vessels coalesce to form the large centrally placed nodule (arrow); and this tendency to coalesce and agglomerate is considered the major factor in development of progressive massive fibrosis lesions.

Fig. 7

Coal-type progressive massive fibrosis (PMF). (A) PMF lesion in a traditional coal miner. PMF, by definition, must have a long-axis diameter greater than 1 cm. The truncated lesion shown is substantially larger than 1 cm and appears to further extend beyond the resection margins. There is also an area of necrosis with cavitation (star), vascular changes (arrow), and extension into the lung parenchyma. (B) Intense black pigmentation with characteristic features of anthracite coal is shown under high-power view.

Fig. 8

Asbestos bodies. (A) Characteristic appearance of asbestos bodies in a tissue section from a patient with asbestosis. The orange-brown color comes from a beaded iron coating laid down on the asbestos fiber by alveolar macrophages. The translucent asbestos fibers may be visible (black arrows). X-ray spectroscopic studies have shown that asbestos bodies always form on amphibole asbestos fibers, which are thin and straight. (B) Scanning electron micrograph of two asbestos bodies extracted from lung tissue by bleach digestion. The beading results from attempts by alveolar macrophages to phagocytose particles many times their size.

Fig. 9

Chronic beryllium disease (CBD). The classic histologic appearance of CBD resembles sarcoidosis. There are coalescing, well-formed, nonnecrotizing granulomas surrounded by collagen. The inset demonstrates the presence of Schaumann bodies (arrows), which are calcium and protein inclusions within the giant cells of the compact granuloma. Patients with chronic beryllium disease may develop interstitial fibrosis, and over time, the only hint to CBD is the collection of Schaumann bodies within the interstitium. Schaumann bodies are not pathognomonic of CBD and may be see in other granulomatous conditions.

Fig. 10

Aluminosis. Exposure to aluminum fumes in this aluminum arc welder’s lung imparts a gray-tan appearance to the dust-laden macrophages within the interstitium. Early in disease, centrilobular macules are evident, as in this image. Although the bronchiole is not identifiable, the centrilobular location can be deduced by the presence of a small pulmonary artery (star). Two lymphoid aggregates (arrows) accompany the nodular collection of aluminum-laden histiocytes.

Fig. 11

Hard metal pneumoconiosis. Lung biopsy from a machinist exposed to tungsten carbide dust illustrates the classic appearance of GIP. GIP is typified by airspace multinucleated giant cells and a centrilobular chronic interstitial inflammatory infiltrate. Lymphoid aggregates, some with germinal center formation, are evident (stars). Multinucleated giant cells are seen throughout (arrows) and shown on high-power view (inset).

Fig. 12

Siderosis (welder’s lung). (A) Characteristic parenchymal lesion in the lung of a steel welder showing a macular lesion at the junction of a terminal bronchiole and the respiratory bronchioles. The lesion shows some pink collagen but the overall fibrosis is mild. Airspaces adjacent to the macule are enlarged and characteristic of mild centrilobular emphysema. (B) The macule is similar to those in coal miners (►Fig. 6A); however, Perls Prussian blue stain for iron is strongly positive, confirming the diagnosis of siderosis.