Silica (crystalline, respirable) - OEHHA

FINAL February 2005
Various attempts have been made to estimate the changes in silica levels in workplaces over time
(e.g., Seixas et al., 1997 for diatomaceous earth facilities in California; Verma et al., 1989 for
Ontario hard rock miners). However, although some conversion factors have been proposed,
correlation between dust particle number in earlier studies, when dust concentrations were
higher, and dust particle weight in the later studies, when the dust concentrations have been
lowered, is imprecise so it is difficult to compare the earlier silica measurements with the more
recent ones.
IV. Effects of Human Exposures
Inhalation of crystalline silica initially causes respiratory irritation and an inflammatory reaction
in the lungs (e.g., Vallyathan et al., 1995). Acute exposures to high concentrations cause cough,
shortness of breath, and pulmonary alveolar lipoproteinosis (acute silicosis). After chronic but
lower workplace exposures to silica for six to sixteen years, the small airways become obstructed
as measured by pulmonary function tests (e.g., decreased FEV1) in granite quarry workers (no
measurement of silica levels reported; Chia et al., 1992). In a report on the hazards of exposure
to crystalline silica, the American Thoracic Society (1997) stated: “Studies from many different
work environments suggest that exposure to working environments contaminated by silica at
dust levels that appear not to cause roentgenographically visible simple silicosis can cause
chronic airflow limitation and/or mucus hypersecretion and/or pathologic emphysema.” Hnizdo
and Vallyathan (2003) also concluded that “chronic levels of silica dust that do not cause
disabling silicosis may cause the development of chronic bronchitis, emphysema, and/or small
airways disease that can lead to airflow obstruction, even in the absence of radiological
silicosis.” Fibrotic lesions associated with crystalline silica have also been found at autopsy in
the lungs of granite workers who lacked radiological evidence of silicosis (Craighead and
Vallyathan, 1980).
Silicosis results from chronic exposure; it is characterized by the presence of histologically
unique silicotic nodules and by fibrotic scarring of the lung. The histological progression of
silicosis has been described as: (1) granuloma composed of histiocytic cells, collagen, and
lymphocytes; (2) cellular fibrotic nodule with irregular collagen at the center and circular
collagen at the periphery; (3) more mature nodule with acellular and avascular center; and
(4) late mature nodule composed of dust and collagen including a calcified center (Green and
Vallyathan, 1996). Lung diseases other than cancer associated with silica exposure include
silicosis, tuberculosis/silicotuberculosis, chronic bronchitis, small airways disease, and
emphysema (Oxman et al., 1993; Park et al., 2002; Hnizdo and Vallyathan, 2003; Balmes et al.,
2003). Silica exposure has been implicated in autoimmune diseases (rheumatoid arthritis,
scleroderma, systemic lupus erythematosus) in gold miners and granite workers (Steenland and
Goldsmith, 1995; Parks et al., 1999) and in the causation of kidney disease in some occupations
(Goldsmith and Goldsmith, 1993; Stratta et al., 2001), possibly by an immune mechanism.
At the cellular level, silica particles are engulfed in the lung by alveolar macrophages (AM).
According to the generally assumed pathological model, the AM subsequently release various
growth factors and reactive oxygen species (ROS; superoxide anion, hydrogen peroxide,
hydroxyl radical) (Lapp and Castranova, 1993; Mossman and Churg, 1998; Ding et al., 2002).
ROS and some growth factors (e.g., activator protein-1, platelet activating factor) are
inflammatory and attract neutrophils to the site of inflammation, while other factors (fibronectin,
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