NIOSH
HAZARD REVIEW
Health
Effects of Occupational Exposure Department
of Health and Human Services DHHS
(NIOSH) Publication No. 2002-129 |
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Contents
2 Properties, Production, and Potential for Exposure
Appendix. Occupational Exposure Limits Tables
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Ordering Information To receive documents or more information about occupational safety and health topics, contact the National Institute for Occupational Safety and Health (NIOSH) at NIOSH Publications
Dissemination Telephone:
1-800-35-NIOSH (1-800-356-4674) or visit the NIOSH Web site at www.cdc.gov/niosh This document
is in the public domain and may be freely copied or reprinted. DHHS (NIOSH) Publication No. 2002-129 |
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Foreword Silicosis is the disease most associated with crystalline silica exposure; it is incurable but preventable. This debilitating and often fatal lung disease persists worldwide despite long-standing knowledge of its cause and methods for controlling it. This Hazard Review, Health Effects of Occupational Exposure to Respirable Crystalline Silica, describes published studies and literature on the health effects of occupational exposure to respirable crystalline silica among workers in the United States and many other countries. The review indicates a significant risk of chronic silicosis for workers exposed to respirable crystalline silica over a working lifetime at the current 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). In addition to the risk of silicosis, epidemiologic studies indicate that workers exposed to respirable crystalline silica have an increased risk of developing lung cancer, pulmonary tuberculosis, and airways diseases. The latest scientific information also indicates possible associations of occupational exposure to silica dust with various other adverse health effects. 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 as a time-weighted average (TWA) for up to a 10-hr workday during a 40-hr workweek. NIOSH also recommends substituting less hazardous materials for crystalline silica when feasible, using appropriate respiratory protection when source controls cannot keep exposures below the REL, and making medical examinations available to exposed workers.
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Abstract Occupational exposures to respirable crystalline silica are associated with the development of silicosis, lung cancer, pulmonary tuberculosis, and airways diseases. These exposures may also be related to the development of autoimmune disorders, chronic renal disease, and other adverse health effects. Recent epidemiologic studies demonstrate that workers have a significant risk of developing chronic silicosis when they are exposed to respirable crystalline silica over a working lifetime at the current 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). This NIOSH Hazard Review
Current sampling and analytical methods used to evaluate occupational exposure to respirable crystalline silica do not meet the accuracy criterion needed to quantify exposures at concentrations below the NIOSH REL of 0.05 mg/m3 as a time-weighted average (TWA) for up to a 10-hr workday during a 40-hr workweek. 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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Executive Summary 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 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
Although a large body of published literature describes the health effects of crystalline silica, some areas require further research. Many uncertainties exist, including
In addition, further information is needed about
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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Acknowledgments This Hazard Review was developed by the staff of the National Institute for Occupational Safety and Health (NIOSH). Paul A. Schulte, Director, Education and Information Division (EID), had overall responsibility for the document. Faye L. Rice (EID) was the principal author. The analytical methods section was prepared by Rosa Key-Schwartz, Ph.D.; David Bartley, Ph.D; Paul Baron, Ph.D; and Paul Schlecht. Michael Gressel and Alan Echt contributed material on control technology. The following NIOSH staff provided critical review and comments on this document and previous versions: Martin Abell; Heinz W. Ahlers, J.D.; Rochelle Althouse; Harlan Amandus, Ph.D.; Michael Attfield, Ph.D.; Nancy Bollinger, Ph.D.; Lorraine Cameron, Ph.D.; Robert Castellan, M.D.; Joseph Cocalis; Joseph Costello; Clayton Doak; Jerome Flesch; Bryan Hardin, Ph.D.; Kent Hatfield, Ph.D.; Frank Hearl; Paul Hewett, Ph.D.; Eva Hnizdo, Ph.D. (formerly of the National Centre for Occupational Health, South Africa); Michael Jacobsen, Ph.D. (visiting scientist); Kathleen Kreiss, M.D.; Kenneth Linch; Charles Lorberau; Tong-man Ong, Ph.D.; John Parker, M.D.; Larry Reed; Karl Sieber, Ph.D.; Rosemary Sokas, M.D.; Leslie Stayner, Ph.D.; Kyle Steenland, Ph.D.; Patricia Sullivan, Sc.D.; Marie Haring Sweeney, Ph.D.; Gregory Wagner, M.D.; William Wallace, Ph.D.; Joann Wess; Ralph Zumwalde. Editorial review and camera-copy production were provided by Vanessa L. Becks, Susan E. Feldmann, Joyce D. Godfrey, Anne C. Hamilton, Susan R. Kaelin, Laura A. Stroup, Kristina M. Wasmund, and Jane B. Weber. Dale Camper and Ronald Schuler performed literature searches, and the EID Library staff collected literature used in the development of the document. NIOSH also appreciates the comments of the following external reviewers: William
Beckett, M.D., M.P.H. Harvey Checkoway,
Ph.D. Gerald S.
Davis, M.D. Jeffrey
Gift, Ph.D. David Goldsmith,
Ph.D. Eva Hnizdo,
Ph.D. Janet Hughes,
Ph.D. Carol Jones,
Ph.D. William
Kojola Allen G.
Macneski Michelle
Schaper, Ph.D. Loretta
Schuman, Ph.D. James Sharpe David M.
Tucker John A.
Ulizio James L.
Weeks, Sc.D. References and information were submitted by William G.B. Graham, M.D., University of Vermont, College of Medicine. The author especially thanks David Goldsmith, Ph.D., for his major contribution and efforts on a previous draft. |
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