Dust reduction measures in coal mines around the globe have drastically reduced the incidence of coal dust-induced disease. The spectrum of lung findings in coal workers is wide, varying
from (1) asymptomatic anthracosis to (2) simple coal workers' pneumoconiosis (CWP) with little to no pulmonary dysfunction to (3) complicated CWP, or progressive massive fibrosis
(PMF), in which lung function is compromised.[61] It should be noted that PMF is a generic term that applies to a confluent, fibrosing reaction in the lung that can be a complication of any
pneumoconiosis, although it is more common in CWP and silicosis.
The pathogenesis of complicated CWP, particularly what causes the lesions of simple CWP to progress to PMF, is incompletely understood. Contaminating silica in the coal dust can favor
progressive disease. In most cases, carbon dust itself is the major culprit, and studies have shown that complicated lesions contain considerably more dust than simple lesions do.
Morphology.
Anthracosisis the most innocuous coal-induced pulmonary lesion in coal miners and is commonly seen in all urban dwellers and tobacco smokers. Inhaled carbon pigment is engulfed by
alveolar or interstitial macrophages, which then accumulate in the connective tissue along the lymphatics, including the pleural lymphatics, or in organized lymphoid tissue along the
bronchi or in the lung hilus. At autopsy, linear streaks and aggregates of anthracotic pigment readily identify pulmonary lymphatics and mark the pulmonary lymph nodes.
Simple CWPis characterized by coal macules(1 to 2 mm in diameter) and the somewhat larger coal nodules. The coal macule consists of carbon-laden macrophages; the nodule also
contains small amounts of a delicate network of collagen fibers. Although these lesions are scattered throughout the lung, the upper lobes and upper zones of the lower lobes are more
heavily involved. They are located primarily adjacent to respiratory bronchioles, the site of initial dust accumulation. In due course, dilation
of adjacent alveoli occurs, a condition sometimes referred to as centrilobular emphysema.
Complicated CWP (PMF)occurs on a background of simple CWP and generally requires many years to develop. It is characterized by intensely blackened scars larger than 2 cm,
sometimes up to 10 cm in greatest diameter. They are usually multiple ( Fig. 15-18 ). Microscopically, the lesions consist of dense collagen and pigment. The center of the lesion is often
necrotic, resulting most likely from local ischemia.
Clinical Course.
CWP is usually a benign disease that causes little decrement in lung function. Even mild forms of complicated CWP fail to demonstrate abnormalities of lung function. In a minority of
cases (fewer than 10%), PMF develops, leading to increasing pulmonary dysfunction, pulmonary hypertension, and cor pulmonale. Once PMF develops, it may become progressive even if
further exposure to dust is prevented. Unlike silicosis (discussed later), there is no convincing evidence that coal dust increases susceptibility to tuberculosis. There is some evidence that
exposure to coal dust increases the incidence of chronic bronchitis and emphysema,
Figure 15-18Progressive massive fibrosis superimposed on coal workers' pneumoconiosis. The large, blackened scars are located principally in the upper lobe. Note the extensions of
scars into surrounding parenchyma and retraction of adjacent pleura. (Courtesy of Dr. Werner Laquer, Dr. Jerome Kleinerman, and the National Institute of Occupational Safety and
Health, Morgantown, WV.)
Figure 15-19Advanced silicosis seen on transection of lung. Scarring has contracted the upper lobe into a small dark mass (arrow). Note the dense pleural thickening. (Courtesy of Dr.
John Godleski, Brigham and Women's Hospital, Boston, MA.)
Figure 15-20Several coalescent collagenous silicotic nodules. (Courtesy of Dr. John Godleski, Brigham and Women's Hospital, Boston, MA.)
Figure 15-21High-power detail of an asbestos body, revealing the typical beading and knobbed ends (arrow).
Figure 15-22Asbestos exposure evidenced by severe, discrete, characteristic fibrocalcific plaques on the pleural surface of the diaphragm. (Courtesy of Dr. John Godleski, Brigham and
Women's Hospital, Boston, MA.)
TABLE 15-7-- Examples of Drug-Induced Pulmonary Disease