Silica (crystalline, respirable) - OEHHA

FINAL February 2005
alveolar macrophage-derived growth factor) stimulate fibroblasts to proliferate and to make
collagen. Since silica particles cannot be digested by the macrophage, the inflammatory process
becomes chronic (frustrated phagocytosis). An increased silica burden leads to more foci of
inflammation, nodule formation, and fibrosis. The internal process can continue after external
exposure ends. Silica particles also enter into alveolar Type I epithelial cells (Churg, 1996),
which can lead to cell death of Type I cells and to hypertrophy and proliferation of Type II
epithelial cells to replace the Type I cells. The epithelial repair process is associated with a
subsequent increase in collagen formation.
The initial diagnosis of silicosis is often based on chest radiographs. Recent papers have used
the 1980 classification by the International Labor Organization (ILO, 1980) to identify and
classify silicosis into categories and subcategories of seriousness by comparison of patient
radiographs with ILO-supplied reference radiographs taken at various stages of silicosis (Table
1):
Table 1. International Labor Organization categorization of silicosis (ILO, 1980).
ILO Category Qualitative Description
0/0 No small (up to 1 cm) silicotic opacities (nodules) are present
0/1 Probably no nodules, but some areas of radiograph are suspect
[possible silicosis]
1/0 Small silicotic nodules are most likely present, but not certainly
[probable silicosis]
1/1 Small silicotic nodules are definitely present
1/2 Small silicotic nodules are definitely present; other areas of the
radiograph may indicate more advanced lesions including large
opacities (> 1 cm), pleural thickening, etc.
2/1, 2/2, 2/3, 3/2, 3/3 More advanced stages of silicosis/increasing certainty of the presence
of lung abnormalities
Some reports (e.g., Kreiss and Zhen, 1996; Hughes et al., 1998) use 1/0 (probable) as the basis of
classification of silicosis, since many cases of silicosis are not detected by chest radiographs, yet
silicotic nodules and other lesions are found at autopsy (Craighead and Vallayathan, 1980;
Hnizdo et al., 1993). Other reports (e.g., Hnizdo and Sluis-Cremer, 1993) use the definite 1/1 as
the lowest category indicating silicosis. Some disease is missed by radiography and is
determined only by autopsy (Hnizdo et al., 1993). The ILO criteria are intended as an
epidemiologic classification and comparison tool, not as a diagnostic classification on an
individual basis. In occupational medicine practice, a group of tests is used to clinically
diagnose silica-related lung disease including physical examination, X-rays, and high resolution
computed tomography (CT) scans of the lung (e.g., Begin et al., 1991; Olivetti et al., 1993).
A. Environmental silicosis
Several studies have reported "environmental silicosis", cases where the silicosis occurs in the
absence of an industry usually associated with the disease (reviewed by USEPA, 1996). In one
of the stronger examples, Saiyed et al. (1991) investigated non-occupational pneumoconiosis in
Ladakh, India, high in the western Himalayas where there are no mines or industries. Among
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