Page 506 - Textbook of Pathology, 6th Edition

490 probably due to swallowing of coal dust containing
carcinogens. But bronchogenic carcinoma does not appear
to be more common in coal-miners than in other groups.

Silicosis

Historically, silicosis used to be called ‘knife grinders’ lung.
Silicosis is caused by prolonged inhalation of silicon dioxide,
commonly called silica. Silica constitutes about one-fourth
of earth’s crust. Therefore, a number of occupations engaged
in silceous rocks or sand and products manufactured from
them are at increased risk. These include miners (e.g. of
granite, sandstone, slate, coal, gold, tin and copper), quarry
workers, tunnellers, sandblasters, grinders, ceramic workers,
foundry workers and those involved in the manufacture of
abrasives containing silica. Peculiar to India are the occu-
pational exposure to pencil, slate and agate-grinding industry
carrying high risk of silicosis (agate = very hard stone
containing silica). According to an Indian Council of Medical
Figure 17.28 Histologic appearance of the lung in coal-workers’ Research report, it is estimated that about 3 million workers
pneumoconiosis. Coal macules composed of aggregates of dust-laden in India are at high potential risk of silica exposure employed
macrophages and collagens are seen surrounding respiratory in a variety of occupations including construction workers.
bronchioles. The alveoli and respiratory bronchioles surrounding the coal
macule are distended. An infrequent acute form of silicosis called accelerated silicosis
produces irregular fibrosis adjoining the alveoli which is
filled with lipoproteinaceous exudate and resembles alveolar
3. There is scanty inflammatory infiltrate of lymphocytes proteinosis (page 494). However, if not specified, silicosis
and plasma cells around the areas of massive scars. refers to the common chronic form of the disease characterised
4. The alveoli surrounding the scars are markedly by formation of small collagenous silicotic nodules.
dilated.
SECTION III
Progressive massive fibrosis probably has immuno- PATHOGENESIS. Silicosis appears after prolonged
logical pathogenetic basis as described above. exposure to silica dust, often a few decades. Besides, it
depends upon a number of other factors such as total dose,
RHEUMATOID PNEUMOCONIOSIS (CAPLAN’S duration of exposure, the type of silica inhaled and individual
SYNDROME). The development of rheumatoid arthritis host factors. The mechanisms involved in the formation of
in a few cases of coal-workers’ pneumoconiosis, silicosis silicotic nodules are not clearly understood. The following
or asbestosis is termed rheumatoid pneumoconiosis or sequence of events has been proposed and schematically
Caplan’s syndrome. illustrated in Fig. 17.26, B:
Grossly, the lungs have rounded, firm nodules with 1. Silica particles between 0.5 to 5 μm size on reaching the
central necrosis, cavitation or calcification. alveoli are taken by the macrophages which undergo
Histologically, the lung lesions are modified rheumatoid necrosis. New macrophages engulf the debris and thus a
nodules with central zone of dust-laden fibrinoid necrosis repetitive cycle of phagocytosis and necrosis is set up.
Systemic Pathology
enclosed by palisading fibroblasts and mononuclear cells. 2. Some silica-laden macrophages are carried to the respi-
The lung lesions in Caplan’s syndrome have immuno- ratory bronchioles, alveoli and in the interstitial tissue. Some
logical basis for their origin as evidenced by detection of of the silica dust is transported to the subpleural and
rheumatoid factor and antinuclear antibodies. interlobar lymphatics and into the regional lymph nodes. The
cellular aggregates containing silica become associated with
CLINICAL FEATURES. Simple coal-workers’ pneumo-
coniosis is the mild form of disease characterised by chronic lymphocytes, plasma cells, mast cells and fibroblasts.
cough with black expectoration. The radiological findings of 3. Silica dust is fibrogenic. Crystalline form, particularly
nodularities in the lungs appear after working for several quartz, is more fibrogenic than non-crystalline form of silica.
years in coal-mines. Progressive massive fibrosis is, however, 4. Simultaneously, there is activation of T and B lymphocytes.
a serious disabling condition manifested by progressive This results in increased serum levels of immunoglobulins
dyspnoea and chronic cough with jet-black sputum. (IgG and IgM), antinuclear antibodies, rheumatoid factor and
Recurrent bacterial infections may produce purulent sputum. circulating immune complexes as well as proliferation of T
More advanced cases develop pulmonary hypertension and cells.
right ventricular hypertrophy (cor pulmonale). The radio- 5. As noted above, silica is cytotoxic and kills the macro-
logical appearance may suggest tuberculosis or cancer. phages which engulf it. The released silica dust activates
Tuberculosis and rheumatoid arthritis are more common in viable macrophages leading to secretion of macrophage-
coal miners than the general population. Coal workers have derived growth factors such as interleukin-1 that favour
increased risk of developing carcinomas of the stomach, fibroblast proliferation and collagen synthesis.