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September 11, 2003 4:36 AM
Health Effects of Occupational Exposure to Respirable Crystalline Silica

Occupational exposures to respirable crystalline silica occur in a variety of industries and occupations because of its extremely common natural occurrence and the wide uses of materials and products that contain it. At least 1.7 million U.S. workers are potentially exposed to respirable crystalline silica [NIOSH 1991], and many are exposed to concentrations that exceed limits defined by current regulations and standards.

Silicosis, usually a nodular pulmonary fibrosis, is the disease most associated with exposure to respirable crystalline silica. Although the reported mortality associated with silicosis has declined over the past several decades, many silicosis associated deaths still occur (nearly 300 deaths were reported each year during the period 1992-1995) [NIOSH 1996a; Althouse 1998]. In addition, the number of silicosis associated deaths among persons aged 15 to 44 has not declined substantially [CDC 1998a,b]. An unknown number of workers also continue to die from silica-related diseases such as pulmonary tuberculosis (TB), lung cancer, and scleroderma. The number of cases of silicosis and silica-related diseases in the United States today is unknown.

Symptoms of acute silicosis, another form of silicosis, may develop shortly after exposure to high concentrations of respirable crystalline silica. Epidemiologic studies focus on chronic silicosis, which develops years after exposure to relatively low concentrations of respirable crystalline silica. Epidemiologic studies have found that chronic silicosis may develop or progress even after occupational exposure has ceased [Hessel et al. 1988; Hnizdo and Sluis-Cremer 1993; Hnizdo and Murray 1998; Ng et al. 1987; Kreiss and Zhen 1996; Miller et al. 1998]. Over a 40- or 45-year working lifetime, workers have a significant chance (at least 1 in 100) of developing radiographic silicosis when exposed to respirable crystalline silica at the Occupational Safety and Health Administration (OSHA) permissible exposure limit (PEL), the Mine Safety and Health Administration (MSHA) PEL, or the National Institute for Occupational Safety and Health (NIOSH) recommended exposure limit (REL).* 

Silicosis may be complicated by severe mycobacterial or fungal infections. About half of these are caused by Mycobacterium tuberculosis and result in TB. Epidemiologic studies have firmly established that silicosis is a risk factor for developing TB.

*See appendix for the OSHA and MSHA PELs. The NIOSH REL is 0.05 mg/m3 
as a time-weighted average (TWA) for up to a 10-hr workday during a 40-hr workweek.

The carcinogenicity of crystalline silica in humans has been strongly debated in the scientific community. In 1996, the International Agency for Research on Cancer (IARC) reviewed the published experimental and epidemiologic studies of cancer in animals and workers exposed to respirable crystalline silica and concluded that there was sufficient evidence in humans for the carcinogenicity of inhaled crystalline silica in the form of quartz or cristobalite from occupational sources [IARC 1997]. In the same year, directors of the American Thoracic Society (ATS) adopted an official statement that described the adverse health effects of exposure to crystalline silica, including lung cancer [ATS 1997]. The ATS found that “the available data support the conclusion that silicosis produces increased risk for bronchogenic carcinoma.”

However, the ATS noted that less information was available for lung cancer risks among silicotics who had never smoked and for silica-exposed workers who did not have silicosis. They also stated that it was less clear whether silica exposure was associated with lung cancer in the absence of silicosis. NIOSH has reviewed the studies considered by IARC and ATS, and NIOSH concurs with the conclusions of IARC [1997] and the ATS [1997]. These conclusions agree with NIOSH testimony to OSHA, in which NIOSH recommended that crystalline silica be considered a potential occupational carcinogen [54 Fed. Reg.* 2521 (1989)]. Further research is needed to determine the exposure-response relationship between lung cancer in nonsmokers and occupational silica dust exposure and to determine why lung cancer risks appear to be higher in workers with silicosis. The cellular mechanisms for development of lung cancer after crystalline silica exposure have been explored in many experimental studies and are not yet fully understood.

Statistically significant excesses of mortality from stomach or gastric cancer have been reported in various occupational groups exposed to crystalline silica. However, no conclusion about an association has been reached because most studies did not adjust for the effects of confounding factors or assess an exposure-response relationship for crystalline silica. The same problem exists for the infrequent reports of statistically significant numbers of excess deaths or cases of other nonlung cancers in silica-exposed workers.

Occupational exposure to respirable crystalline silica is associated with chronic obstructive pulmonary disease, including bronchitis and emphysema. The results of some epidemiologic studies suggest that these diseases may be less frequent or absent in nonsmokers. Exposure to respirable crystalline silica is not associated with asthma.

*Federal Register. See Fed. Reg. in references.

Significant increases in mortality from nonmalignant respiratory disease (a broad category that can include silicosis and other pneumoconioses, chronic bronchitis, emphysema, asthma, and other related respiratory conditions) have been reported for silica-exposed workers [Checkoway et al. 1997, 1993; Chen et al. 1992; Cherry et al. 1998; Brown et al. 1986; Costello and Graham 1988; Costello et al. 1995; Costello 1983; Steenland and Brown 1995b; Steenland and Beaumont 1986; Thomas and Stewart 1987; Thomas 1990] and silicotics [Goldsmith et al. 1995; Brown et al. 1997; Rosenman et al. 1995].

Many case reports have been published about autoimmune diseases or autoimmune-related diseases in workers exposed to crystalline silica or workers with silicosis. In addition, several recent epidemiologic studies reported statistically significant numbers of excess cases or deaths from known autoimmune diseases or immunologic disorders (scleroderma, systemic lupus erythematosus, rheumatoid arthritis, sarcoidosis), chronic renal disease, and subclinical renal changes. The pathogenesis of autoimmune and renal diseases in silica-exposed workers is not clear.

Various other health effects (such as hepatic or hepatosplenic silicosis, extrapulmonary deposition of silica particles, liver granulomas, hepatic porphyria, cutaneous silica granulomas, pulmonary alveolar proteinosis, podoconiosis, and dental abrasion) have been reported in studies of silica-exposed workers, but these effects have not been studied in depth with epidemiologic methods.

This Hazard Review also provides an abbreviated review of experimental research studies conducted to identify the molecular mechanisms responsible for the development of silicosis and lung cancer. The results of these studies indicate the need for

additional long-term carcinogenesis studies in animals to determine dose-response relationships and 
in vivo and in vitro studies to develop effective cellular and molecular models of carcinogenesis. 
Although a large body of published literature describes the health effects of crystalline silica, some areas require further research. Many uncertainties exist, including

mechanisms and the influence of particle characteristics on development of disease; 
toxicity and pathogenicity of nonquartz crystalline silica, silica substitutes, and dust mixtures; 
translocation of particles from the lung; and 
dose/exposure-response relationships in animals and in humans. 
In addition, further information is needed about

methods for reducing dust exposures in a wide variety of industries and the feasibility of implementing such methods, 
methods for effectively communicating to workers the dangers of inhaling silica dust and the importance of using appropriate control technologies and other protective measures, and 
exposure sampling and analytical methods that will allow quantification of crystalline silica at low airborne concentrations (currently these techniques do not meet the accuracy criterion needed to quantify exposures at concentrations below the NIOSH REL). 
Until improved sampling and analytical methods are developed for respirable crystalline silica, NIOSH will continue to recommend an exposure limit of 0.05 mg/m3 to reduce the risk of developing silicosis, lung cancer, and other adverse health effects. NIOSH also recommends minimizing the risk of illness that remains for workers exposed at the REL by substituting less hazardous materials for crystalline silica when feasible, by using appropriate respiratory protection when source controls cannot keep exposures below the NIOSH REL, and by making medical examinations available to exposed workers.

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