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Rex Tingle - One of the best experts on this subject based on the ideXlab platform.
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occupational exposure to Crystalline Silica dust in the united states 1988 2003
Environmental Health Perspectives, 2005Co-Authors: Abdiaziz S Yassin, Francis Yebesi, Rex TingleAbstract:Silica is a mineral compound made up of one silicon atom and two oxygen atoms (SiO2). It has a melting point of 1,600°C and is a colorless, odorless, and noncombustible solid [American Conference of Governmental Industrial Hygienists (ACGIH) 2001]. Crystalline Silica is formed when Silica molecules are lined up in order and in crystal form. It is an abundant mineral in rock, sand, and soil. Quartz is a term often used to refer to Crystalline Silica dust. Crystalline Silica has been used in many industries such as blast furnaces, cement manufacturing, glass and concrete mixing product manufacture, ceramics, clay, glass and china pottery, electronic, foundry, sand-blasting and manufacturing abrasives, and many construction activities (Altindag et al. 2003; Flanagan et al. 2003; Irwin 2003; Rappaport et al. 2003). It is used as an abrasive agent in many industrial applications. Occupations having a high potential for exposure to Crystalline Silica dust (respirable quartz) are metal, coal, and nonmetal (except fuels) mining; foundry, stone clay, and glass production work; and agricultural, chemical production, highway repair, and tuck-pointing work [Akbar-Khanzadeh and Brillhart 2002; Occupational Safety and Health Administration (OSHA) 2004; Rappaport et al. 2003]. Silica dust is an inhalation hazard. Workers may be at risk of silicosis from exposure to Silica dust when high-velocity impact shatters the sand into smaller, respirable (< 0.5 to 5.0 μm in diameter) dust particles. Silicosis is a disease where scar tissue forms in the lungs and reduces the ability to extract oxygen from the air. Symptoms of silicosis can be acute, accelerated, or chronic. Acute silicosis may develop within weeks and up to 5 years after breathing large amounts of Crystalline Silica. Accelerated silicosis may develop shortly after exposure to high concentrations of respirable Crystalline Silica, whereas chronic silicosis occurs after ≥10 years of exposure to relatively low concentrations of Crystalline Silica [American Thoracic Society 1997; National Institute for Occupational Safety and Health (NIOSH) 2002]. Many workers in a wider range of industries are exposed to Silica, usually in the form of respirable quartz (OSHA 2001, 2003). OSHA has estimated that more than 2 million workers are exposed to Crystalline Silica dust in the general, maritime, and construction industries (OSHA 2003). More than 100,000 workers have high-risk exposure to airborne Silica dust through construction and mining operations (Akbar-Khanzadeh and Brillhart 2002; NIOSH 1991). There were an estimated 3,600–7,300 newly recognized silicosis cases per year in the United States from 1987 to 1996 (Rosenman et al. 2003). Between 1990 and 1996, 200–300 deaths per year are known to have occurred where silicosis was identified as a contributing cause on death certificates (Akbar-Khanzadeh and Brillhart 2002; OSHA 2003). The International Agency for Research on Cancer (IARC 1987, 1997) classified Crystalline Silica as a known human carcinogen. Exposure to Crystalline Silica has been associated with an increased risk of developing lung cancer (Engholm and Englund 1995; Knutsson et al. 2000; Hughes et al. 2001; Lynge et al. 1986; Robinson et al. 1995; Stern et al. 1995). Previous studies also documented an association between airborne Silica exposure and other health problems, including chronic obstructive pulmonary disease, rheumatoid arthritis, scleroderma, Sjogern’s syndrome, lupus, and renal disease (Goldsmith 1997; Hnizdo and Vallyathan 2003; Kane 1997; Parks et al. 2002). The current OSHA permissible exposure limit (PEL) for Crystalline Silica is based on a particle counting formula recommended by the ACGIH in the 1970s (ACGIH 1980; OSHA 1989, 1993). In 1986, the ACGIH revised the threshold limit value (TLV) of 0.1 mg/m3 for respirable quartz (ACGIH 1986). Currently, the NIOSH (1998) and the ACGIH (2001) both recommend an occupational exposure limit of 0.05 mg/m3 for respirable Crystalline Silica. OSHA recognized the need to revise the PEL to reflect current sampling and analytical methods, and the agency determined to address the significant risk of silicosis and other serious diseases associated with Silica through a special emphasis program (SEP) on silicosis (Dear 1996; Jeffress 1998; OSHA 2003). The purposes of this study were a) to summarize measurements of airborne (respirable) Crystalline Silica dust exposure levels among U.S. workers, b) to provide an update of the Stewart and Rice (1990) report on the airborne Silica exposure levels in high-risk industries and occupations with data for the time period 1988–2003, c) to estimate the number of workers potentially exposed to Silica in industries that OSHA inspected for high exposure levels, and d) to conduct time trend analyses on Silica dust exposure levels for time-weighted average (TWA) measurements.
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Occupational Exposure to Crystalline Silica Dust in the United States, 1988–2003
Environmental Health Perspectives, 2005Co-Authors: Abdiaziz S Yassin, Francis Yebesi, Rex TingleAbstract:Silica is a mineral compound made up of one silicon atom and two oxygen atoms (SiO2). It has a melting point of 1,600°C and is a colorless, odorless, and noncombustible solid [American Conference of Governmental Industrial Hygienists (ACGIH) 2001]. Crystalline Silica is formed when Silica molecules are lined up in order and in crystal form. It is an abundant mineral in rock, sand, and soil. Quartz is a term often used to refer to Crystalline Silica dust. Crystalline Silica has been used in many industries such as blast furnaces, cement manufacturing, glass and concrete mixing product manufacture, ceramics, clay, glass and china pottery, electronic, foundry, sand-blasting and manufacturing abrasives, and many construction activities (Altindag et al. 2003; Flanagan et al. 2003; Irwin 2003; Rappaport et al. 2003). It is used as an abrasive agent in many industrial applications. Occupations having a high potential for exposure to Crystalline Silica dust (respirable quartz) are metal, coal, and nonmetal (except fuels) mining; foundry, stone clay, and glass production work; and agricultural, chemical production, highway repair, and tuck-pointing work [Akbar-Khanzadeh and Brillhart 2002; Occupational Safety and Health Administration (OSHA) 2004; Rappaport et al. 2003]. Silica dust is an inhalation hazard. Workers may be at risk of silicosis from exposure to Silica dust when high-velocity impact shatters the sand into smaller, respirable (< 0.5 to 5.0 μm in diameter) dust particles. Silicosis is a disease where scar tissue forms in the lungs and reduces the ability to extract oxygen from the air. Symptoms of silicosis can be acute, accelerated, or chronic. Acute silicosis may develop within weeks and up to 5 years after breathing large amounts of Crystalline Silica. Accelerated silicosis may develop shortly after exposure to high concentrations of respirable Crystalline Silica, whereas chronic silicosis occurs after ≥10 years of exposure to relatively low concentrations of Crystalline Silica [American Thoracic Society 1997; National Institute for Occupational Safety and Health (NIOSH) 2002]. Many workers in a wider range of industries are exposed to Silica, usually in the form of respirable quartz (OSHA 2001, 2003). OSHA has estimated that more than 2 million workers are exposed to Crystalline Silica dust in the general, maritime, and construction industries (OSHA 2003). More than 100,000 workers have high-risk exposure to airborne Silica dust through construction and mining operations (Akbar-Khanzadeh and Brillhart 2002; NIOSH 1991). There were an estimated 3,600–7,300 newly recognized silicosis cases per year in the United States from 1987 to 1996 (Rosenman et al. 2003). Between 1990 and 1996, 200–300 deaths per year are known to have occurred where silicosis was identified as a contributing cause on death certificates (Akbar-Khanzadeh and Brillhart 2002; OSHA 2003). The International Agency for Research on Cancer (IARC 1987, 1997) classified Crystalline Silica as a known human carcinogen. Exposure to Crystalline Silica has been associated with an increased risk of developing lung cancer (Engholm and Englund 1995; Knutsson et al. 2000; Hughes et al. 2001; Lynge et al. 1986; Robinson et al. 1995; Stern et al. 1995). Previous studies also documented an association between airborne Silica exposure and other health problems, including chronic obstructive pulmonary disease, rheumatoid arthritis, scleroderma, Sjogern’s syndrome, lupus, and renal disease (Goldsmith 1997; Hnizdo and Vallyathan 2003; Kane 1997; Parks et al. 2002). The current OSHA permissible exposure limit (PEL) for Crystalline Silica is based on a particle counting formula recommended by the ACGIH in the 1970s (ACGIH 1980; OSHA 1989, 1993). In 1986, the ACGIH revised the threshold limit value (TLV) of 0.1 mg/m3 for respirable quartz (ACGIH 1986). Currently, the NIOSH (1998) and the ACGIH (2001) both recommend an occupational exposure limit of 0.05 mg/m3 for respirable Crystalline Silica. OSHA recognized the need to revise the PEL to reflect current sampling and analytical methods, and the agency determined to address the significant risk of silicosis and other serious diseases associated with Silica through a special emphasis program (SEP) on silicosis (Dear 1996; Jeffress 1998; OSHA 2003). The purposes of this study were a) to summarize measurements of airborne (respirable) Crystalline Silica dust exposure levels among U.S. workers, b) to provide an update of the Stewart and Rice (1990) report on the airborne Silica exposure levels in high-risk industries and occupations with data for the time period 1988–2003, c) to estimate the number of workers potentially exposed to Silica in industries that OSHA inspected for high exposure levels, and d) to conduct time trend analyses on Silica dust exposure levels for time-weighted average (TWA) measurements.
Andrij Holian - One of the best experts on this subject based on the ideXlab platform.
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critical role of marco in Crystalline Silica induced pulmonary inflammation
Toxicological Sciences, 2009Co-Authors: Sheetal A Thakur, Celine A Beamer, Christopher T Migliaccio, Andrij HolianAbstract:Chronic exposure to Crystalline Silica can lead to the development of silicosis, an irreversible, inflammatory and fibrotic pulmonary disease. Although, previous studies established the macrophage receptor with collagenous structure (MARCO) as an important receptor for binding and uptake of Crystalline Silica particles in vitro, the role of MARCO in regulating the inflammatory response following Silica exposure in vivo remains unknown. Therefore, we determined the role of MARCO in Crystalline Silica–induced pulmonary pathology using C57Bl/6 wild-type (WT) and MARCO−/− mice. Increased numbers of MARCO+ pulmonary macrophages were observed following Crystalline Silica, but not phosphate-buffered saline and titanium dioxide (TiO2), instillation in WT mice, highlighting a specific role of MARCO in Silica-induced pathology. We hypothesized that MARCO−/− mice will exhibit diminished clearance of Silica leading to enhanced pulmonary inflammation and exacerbation of silicosis. Alveolar macrophages isolated from Crystalline Silica–exposed mice showed diminished particle uptake in vivo as compared with WT mice, indicating abnormalities in clearance mechanisms. Furthermore, MARCO−/− mice exposed to Crystalline Silica showed enhanced acute inflammation and lung injury marked by increases in early response cytokines and inflammatory cells compared with WT mice. Similarly, histological examination of MARCO−/− lungs at 3 months post–Crystalline Silica exposure showed increased chronic inflammation compared with WT; however, only a small difference was observed with respect to development of fibrosis as measured by hydroxyproline content. Altogether, these results demonstrate that MARCO is important for clearance of Crystalline Silica in vivo and that the absence of MARCO results in exacerbations in innate pulmonary immune responses.
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Critical Role of MARCO in Crystalline Silica–Induced Pulmonary Inflammation
Toxicological Sciences, 2009Co-Authors: Sheetal A Thakur, Celine A Beamer, Christopher T Migliaccio, Andrij HolianAbstract:Chronic exposure to Crystalline Silica can lead to the development of silicosis, an irreversible, inflammatory and fibrotic pulmonary disease. Although, previous studies established the macrophage receptor with collagenous structure (MARCO) as an important receptor for binding and uptake of Crystalline Silica particles in vitro, the role of MARCO in regulating the inflammatory response following Silica exposure in vivo remains unknown. Therefore, we determined the role of MARCO in Crystalline Silica–induced pulmonary pathology using C57Bl/6 wild-type (WT) and MARCO−/− mice. Increased numbers of MARCO+ pulmonary macrophages were observed following Crystalline Silica, but not phosphate-buffered saline and titanium dioxide (TiO2), instillation in WT mice, highlighting a specific role of MARCO in Silica-induced pathology. We hypothesized that MARCO−/− mice will exhibit diminished clearance of Silica leading to enhanced pulmonary inflammation and exacerbation of silicosis. Alveolar macrophages isolated from Crystalline Silica–exposed mice showed diminished particle uptake in vivo as compared with WT mice, indicating abnormalities in clearance mechanisms. Furthermore, MARCO−/− mice exposed to Crystalline Silica showed enhanced acute inflammation and lung injury marked by increases in early response cytokines and inflammatory cells compared with WT mice. Similarly, histological examination of MARCO−/− lungs at 3 months post–Crystalline Silica exposure showed increased chronic inflammation compared with WT; however, only a small difference was observed with respect to development of fibrosis as measured by hydroxyproline content. Altogether, these results demonstrate that MARCO is important for clearance of Crystalline Silica in vivo and that the absence of MARCO results in exacerbations in innate pulmonary immune responses.
Abdiaziz S Yassin - One of the best experts on this subject based on the ideXlab platform.
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occupational exposure to Crystalline Silica dust in the united states 1988 2003
Environmental Health Perspectives, 2005Co-Authors: Abdiaziz S Yassin, Francis Yebesi, Rex TingleAbstract:Silica is a mineral compound made up of one silicon atom and two oxygen atoms (SiO2). It has a melting point of 1,600°C and is a colorless, odorless, and noncombustible solid [American Conference of Governmental Industrial Hygienists (ACGIH) 2001]. Crystalline Silica is formed when Silica molecules are lined up in order and in crystal form. It is an abundant mineral in rock, sand, and soil. Quartz is a term often used to refer to Crystalline Silica dust. Crystalline Silica has been used in many industries such as blast furnaces, cement manufacturing, glass and concrete mixing product manufacture, ceramics, clay, glass and china pottery, electronic, foundry, sand-blasting and manufacturing abrasives, and many construction activities (Altindag et al. 2003; Flanagan et al. 2003; Irwin 2003; Rappaport et al. 2003). It is used as an abrasive agent in many industrial applications. Occupations having a high potential for exposure to Crystalline Silica dust (respirable quartz) are metal, coal, and nonmetal (except fuels) mining; foundry, stone clay, and glass production work; and agricultural, chemical production, highway repair, and tuck-pointing work [Akbar-Khanzadeh and Brillhart 2002; Occupational Safety and Health Administration (OSHA) 2004; Rappaport et al. 2003]. Silica dust is an inhalation hazard. Workers may be at risk of silicosis from exposure to Silica dust when high-velocity impact shatters the sand into smaller, respirable (< 0.5 to 5.0 μm in diameter) dust particles. Silicosis is a disease where scar tissue forms in the lungs and reduces the ability to extract oxygen from the air. Symptoms of silicosis can be acute, accelerated, or chronic. Acute silicosis may develop within weeks and up to 5 years after breathing large amounts of Crystalline Silica. Accelerated silicosis may develop shortly after exposure to high concentrations of respirable Crystalline Silica, whereas chronic silicosis occurs after ≥10 years of exposure to relatively low concentrations of Crystalline Silica [American Thoracic Society 1997; National Institute for Occupational Safety and Health (NIOSH) 2002]. Many workers in a wider range of industries are exposed to Silica, usually in the form of respirable quartz (OSHA 2001, 2003). OSHA has estimated that more than 2 million workers are exposed to Crystalline Silica dust in the general, maritime, and construction industries (OSHA 2003). More than 100,000 workers have high-risk exposure to airborne Silica dust through construction and mining operations (Akbar-Khanzadeh and Brillhart 2002; NIOSH 1991). There were an estimated 3,600–7,300 newly recognized silicosis cases per year in the United States from 1987 to 1996 (Rosenman et al. 2003). Between 1990 and 1996, 200–300 deaths per year are known to have occurred where silicosis was identified as a contributing cause on death certificates (Akbar-Khanzadeh and Brillhart 2002; OSHA 2003). The International Agency for Research on Cancer (IARC 1987, 1997) classified Crystalline Silica as a known human carcinogen. Exposure to Crystalline Silica has been associated with an increased risk of developing lung cancer (Engholm and Englund 1995; Knutsson et al. 2000; Hughes et al. 2001; Lynge et al. 1986; Robinson et al. 1995; Stern et al. 1995). Previous studies also documented an association between airborne Silica exposure and other health problems, including chronic obstructive pulmonary disease, rheumatoid arthritis, scleroderma, Sjogern’s syndrome, lupus, and renal disease (Goldsmith 1997; Hnizdo and Vallyathan 2003; Kane 1997; Parks et al. 2002). The current OSHA permissible exposure limit (PEL) for Crystalline Silica is based on a particle counting formula recommended by the ACGIH in the 1970s (ACGIH 1980; OSHA 1989, 1993). In 1986, the ACGIH revised the threshold limit value (TLV) of 0.1 mg/m3 for respirable quartz (ACGIH 1986). Currently, the NIOSH (1998) and the ACGIH (2001) both recommend an occupational exposure limit of 0.05 mg/m3 for respirable Crystalline Silica. OSHA recognized the need to revise the PEL to reflect current sampling and analytical methods, and the agency determined to address the significant risk of silicosis and other serious diseases associated with Silica through a special emphasis program (SEP) on silicosis (Dear 1996; Jeffress 1998; OSHA 2003). The purposes of this study were a) to summarize measurements of airborne (respirable) Crystalline Silica dust exposure levels among U.S. workers, b) to provide an update of the Stewart and Rice (1990) report on the airborne Silica exposure levels in high-risk industries and occupations with data for the time period 1988–2003, c) to estimate the number of workers potentially exposed to Silica in industries that OSHA inspected for high exposure levels, and d) to conduct time trend analyses on Silica dust exposure levels for time-weighted average (TWA) measurements.
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Occupational Exposure to Crystalline Silica Dust in the United States, 1988–2003
Environmental Health Perspectives, 2005Co-Authors: Abdiaziz S Yassin, Francis Yebesi, Rex TingleAbstract:Silica is a mineral compound made up of one silicon atom and two oxygen atoms (SiO2). It has a melting point of 1,600°C and is a colorless, odorless, and noncombustible solid [American Conference of Governmental Industrial Hygienists (ACGIH) 2001]. Crystalline Silica is formed when Silica molecules are lined up in order and in crystal form. It is an abundant mineral in rock, sand, and soil. Quartz is a term often used to refer to Crystalline Silica dust. Crystalline Silica has been used in many industries such as blast furnaces, cement manufacturing, glass and concrete mixing product manufacture, ceramics, clay, glass and china pottery, electronic, foundry, sand-blasting and manufacturing abrasives, and many construction activities (Altindag et al. 2003; Flanagan et al. 2003; Irwin 2003; Rappaport et al. 2003). It is used as an abrasive agent in many industrial applications. Occupations having a high potential for exposure to Crystalline Silica dust (respirable quartz) are metal, coal, and nonmetal (except fuels) mining; foundry, stone clay, and glass production work; and agricultural, chemical production, highway repair, and tuck-pointing work [Akbar-Khanzadeh and Brillhart 2002; Occupational Safety and Health Administration (OSHA) 2004; Rappaport et al. 2003]. Silica dust is an inhalation hazard. Workers may be at risk of silicosis from exposure to Silica dust when high-velocity impact shatters the sand into smaller, respirable (< 0.5 to 5.0 μm in diameter) dust particles. Silicosis is a disease where scar tissue forms in the lungs and reduces the ability to extract oxygen from the air. Symptoms of silicosis can be acute, accelerated, or chronic. Acute silicosis may develop within weeks and up to 5 years after breathing large amounts of Crystalline Silica. Accelerated silicosis may develop shortly after exposure to high concentrations of respirable Crystalline Silica, whereas chronic silicosis occurs after ≥10 years of exposure to relatively low concentrations of Crystalline Silica [American Thoracic Society 1997; National Institute for Occupational Safety and Health (NIOSH) 2002]. Many workers in a wider range of industries are exposed to Silica, usually in the form of respirable quartz (OSHA 2001, 2003). OSHA has estimated that more than 2 million workers are exposed to Crystalline Silica dust in the general, maritime, and construction industries (OSHA 2003). More than 100,000 workers have high-risk exposure to airborne Silica dust through construction and mining operations (Akbar-Khanzadeh and Brillhart 2002; NIOSH 1991). There were an estimated 3,600–7,300 newly recognized silicosis cases per year in the United States from 1987 to 1996 (Rosenman et al. 2003). Between 1990 and 1996, 200–300 deaths per year are known to have occurred where silicosis was identified as a contributing cause on death certificates (Akbar-Khanzadeh and Brillhart 2002; OSHA 2003). The International Agency for Research on Cancer (IARC 1987, 1997) classified Crystalline Silica as a known human carcinogen. Exposure to Crystalline Silica has been associated with an increased risk of developing lung cancer (Engholm and Englund 1995; Knutsson et al. 2000; Hughes et al. 2001; Lynge et al. 1986; Robinson et al. 1995; Stern et al. 1995). Previous studies also documented an association between airborne Silica exposure and other health problems, including chronic obstructive pulmonary disease, rheumatoid arthritis, scleroderma, Sjogern’s syndrome, lupus, and renal disease (Goldsmith 1997; Hnizdo and Vallyathan 2003; Kane 1997; Parks et al. 2002). The current OSHA permissible exposure limit (PEL) for Crystalline Silica is based on a particle counting formula recommended by the ACGIH in the 1970s (ACGIH 1980; OSHA 1989, 1993). In 1986, the ACGIH revised the threshold limit value (TLV) of 0.1 mg/m3 for respirable quartz (ACGIH 1986). Currently, the NIOSH (1998) and the ACGIH (2001) both recommend an occupational exposure limit of 0.05 mg/m3 for respirable Crystalline Silica. OSHA recognized the need to revise the PEL to reflect current sampling and analytical methods, and the agency determined to address the significant risk of silicosis and other serious diseases associated with Silica through a special emphasis program (SEP) on silicosis (Dear 1996; Jeffress 1998; OSHA 2003). The purposes of this study were a) to summarize measurements of airborne (respirable) Crystalline Silica dust exposure levels among U.S. workers, b) to provide an update of the Stewart and Rice (1990) report on the airborne Silica exposure levels in high-risk industries and occupations with data for the time period 1988–2003, c) to estimate the number of workers potentially exposed to Silica in industries that OSHA inspected for high exposure levels, and d) to conduct time trend analyses on Silica dust exposure levels for time-weighted average (TWA) measurements.
Sheetal A Thakur - One of the best experts on this subject based on the ideXlab platform.
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critical role of marco in Crystalline Silica induced pulmonary inflammation
Toxicological Sciences, 2009Co-Authors: Sheetal A Thakur, Celine A Beamer, Christopher T Migliaccio, Andrij HolianAbstract:Chronic exposure to Crystalline Silica can lead to the development of silicosis, an irreversible, inflammatory and fibrotic pulmonary disease. Although, previous studies established the macrophage receptor with collagenous structure (MARCO) as an important receptor for binding and uptake of Crystalline Silica particles in vitro, the role of MARCO in regulating the inflammatory response following Silica exposure in vivo remains unknown. Therefore, we determined the role of MARCO in Crystalline Silica–induced pulmonary pathology using C57Bl/6 wild-type (WT) and MARCO−/− mice. Increased numbers of MARCO+ pulmonary macrophages were observed following Crystalline Silica, but not phosphate-buffered saline and titanium dioxide (TiO2), instillation in WT mice, highlighting a specific role of MARCO in Silica-induced pathology. We hypothesized that MARCO−/− mice will exhibit diminished clearance of Silica leading to enhanced pulmonary inflammation and exacerbation of silicosis. Alveolar macrophages isolated from Crystalline Silica–exposed mice showed diminished particle uptake in vivo as compared with WT mice, indicating abnormalities in clearance mechanisms. Furthermore, MARCO−/− mice exposed to Crystalline Silica showed enhanced acute inflammation and lung injury marked by increases in early response cytokines and inflammatory cells compared with WT mice. Similarly, histological examination of MARCO−/− lungs at 3 months post–Crystalline Silica exposure showed increased chronic inflammation compared with WT; however, only a small difference was observed with respect to development of fibrosis as measured by hydroxyproline content. Altogether, these results demonstrate that MARCO is important for clearance of Crystalline Silica in vivo and that the absence of MARCO results in exacerbations in innate pulmonary immune responses.
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Critical Role of MARCO in Crystalline Silica–Induced Pulmonary Inflammation
Toxicological Sciences, 2009Co-Authors: Sheetal A Thakur, Celine A Beamer, Christopher T Migliaccio, Andrij HolianAbstract:Chronic exposure to Crystalline Silica can lead to the development of silicosis, an irreversible, inflammatory and fibrotic pulmonary disease. Although, previous studies established the macrophage receptor with collagenous structure (MARCO) as an important receptor for binding and uptake of Crystalline Silica particles in vitro, the role of MARCO in regulating the inflammatory response following Silica exposure in vivo remains unknown. Therefore, we determined the role of MARCO in Crystalline Silica–induced pulmonary pathology using C57Bl/6 wild-type (WT) and MARCO−/− mice. Increased numbers of MARCO+ pulmonary macrophages were observed following Crystalline Silica, but not phosphate-buffered saline and titanium dioxide (TiO2), instillation in WT mice, highlighting a specific role of MARCO in Silica-induced pathology. We hypothesized that MARCO−/− mice will exhibit diminished clearance of Silica leading to enhanced pulmonary inflammation and exacerbation of silicosis. Alveolar macrophages isolated from Crystalline Silica–exposed mice showed diminished particle uptake in vivo as compared with WT mice, indicating abnormalities in clearance mechanisms. Furthermore, MARCO−/− mice exposed to Crystalline Silica showed enhanced acute inflammation and lung injury marked by increases in early response cytokines and inflammatory cells compared with WT mice. Similarly, histological examination of MARCO−/− lungs at 3 months post–Crystalline Silica exposure showed increased chronic inflammation compared with WT; however, only a small difference was observed with respect to development of fibrosis as measured by hydroxyproline content. Altogether, these results demonstrate that MARCO is important for clearance of Crystalline Silica in vivo and that the absence of MARCO results in exacerbations in innate pulmonary immune responses.
Francis Yebesi - One of the best experts on this subject based on the ideXlab platform.
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occupational exposure to Crystalline Silica dust in the united states 1988 2003
Environmental Health Perspectives, 2005Co-Authors: Abdiaziz S Yassin, Francis Yebesi, Rex TingleAbstract:Silica is a mineral compound made up of one silicon atom and two oxygen atoms (SiO2). It has a melting point of 1,600°C and is a colorless, odorless, and noncombustible solid [American Conference of Governmental Industrial Hygienists (ACGIH) 2001]. Crystalline Silica is formed when Silica molecules are lined up in order and in crystal form. It is an abundant mineral in rock, sand, and soil. Quartz is a term often used to refer to Crystalline Silica dust. Crystalline Silica has been used in many industries such as blast furnaces, cement manufacturing, glass and concrete mixing product manufacture, ceramics, clay, glass and china pottery, electronic, foundry, sand-blasting and manufacturing abrasives, and many construction activities (Altindag et al. 2003; Flanagan et al. 2003; Irwin 2003; Rappaport et al. 2003). It is used as an abrasive agent in many industrial applications. Occupations having a high potential for exposure to Crystalline Silica dust (respirable quartz) are metal, coal, and nonmetal (except fuels) mining; foundry, stone clay, and glass production work; and agricultural, chemical production, highway repair, and tuck-pointing work [Akbar-Khanzadeh and Brillhart 2002; Occupational Safety and Health Administration (OSHA) 2004; Rappaport et al. 2003]. Silica dust is an inhalation hazard. Workers may be at risk of silicosis from exposure to Silica dust when high-velocity impact shatters the sand into smaller, respirable (< 0.5 to 5.0 μm in diameter) dust particles. Silicosis is a disease where scar tissue forms in the lungs and reduces the ability to extract oxygen from the air. Symptoms of silicosis can be acute, accelerated, or chronic. Acute silicosis may develop within weeks and up to 5 years after breathing large amounts of Crystalline Silica. Accelerated silicosis may develop shortly after exposure to high concentrations of respirable Crystalline Silica, whereas chronic silicosis occurs after ≥10 years of exposure to relatively low concentrations of Crystalline Silica [American Thoracic Society 1997; National Institute for Occupational Safety and Health (NIOSH) 2002]. Many workers in a wider range of industries are exposed to Silica, usually in the form of respirable quartz (OSHA 2001, 2003). OSHA has estimated that more than 2 million workers are exposed to Crystalline Silica dust in the general, maritime, and construction industries (OSHA 2003). More than 100,000 workers have high-risk exposure to airborne Silica dust through construction and mining operations (Akbar-Khanzadeh and Brillhart 2002; NIOSH 1991). There were an estimated 3,600–7,300 newly recognized silicosis cases per year in the United States from 1987 to 1996 (Rosenman et al. 2003). Between 1990 and 1996, 200–300 deaths per year are known to have occurred where silicosis was identified as a contributing cause on death certificates (Akbar-Khanzadeh and Brillhart 2002; OSHA 2003). The International Agency for Research on Cancer (IARC 1987, 1997) classified Crystalline Silica as a known human carcinogen. Exposure to Crystalline Silica has been associated with an increased risk of developing lung cancer (Engholm and Englund 1995; Knutsson et al. 2000; Hughes et al. 2001; Lynge et al. 1986; Robinson et al. 1995; Stern et al. 1995). Previous studies also documented an association between airborne Silica exposure and other health problems, including chronic obstructive pulmonary disease, rheumatoid arthritis, scleroderma, Sjogern’s syndrome, lupus, and renal disease (Goldsmith 1997; Hnizdo and Vallyathan 2003; Kane 1997; Parks et al. 2002). The current OSHA permissible exposure limit (PEL) for Crystalline Silica is based on a particle counting formula recommended by the ACGIH in the 1970s (ACGIH 1980; OSHA 1989, 1993). In 1986, the ACGIH revised the threshold limit value (TLV) of 0.1 mg/m3 for respirable quartz (ACGIH 1986). Currently, the NIOSH (1998) and the ACGIH (2001) both recommend an occupational exposure limit of 0.05 mg/m3 for respirable Crystalline Silica. OSHA recognized the need to revise the PEL to reflect current sampling and analytical methods, and the agency determined to address the significant risk of silicosis and other serious diseases associated with Silica through a special emphasis program (SEP) on silicosis (Dear 1996; Jeffress 1998; OSHA 2003). The purposes of this study were a) to summarize measurements of airborne (respirable) Crystalline Silica dust exposure levels among U.S. workers, b) to provide an update of the Stewart and Rice (1990) report on the airborne Silica exposure levels in high-risk industries and occupations with data for the time period 1988–2003, c) to estimate the number of workers potentially exposed to Silica in industries that OSHA inspected for high exposure levels, and d) to conduct time trend analyses on Silica dust exposure levels for time-weighted average (TWA) measurements.
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Occupational Exposure to Crystalline Silica Dust in the United States, 1988–2003
Environmental Health Perspectives, 2005Co-Authors: Abdiaziz S Yassin, Francis Yebesi, Rex TingleAbstract:Silica is a mineral compound made up of one silicon atom and two oxygen atoms (SiO2). It has a melting point of 1,600°C and is a colorless, odorless, and noncombustible solid [American Conference of Governmental Industrial Hygienists (ACGIH) 2001]. Crystalline Silica is formed when Silica molecules are lined up in order and in crystal form. It is an abundant mineral in rock, sand, and soil. Quartz is a term often used to refer to Crystalline Silica dust. Crystalline Silica has been used in many industries such as blast furnaces, cement manufacturing, glass and concrete mixing product manufacture, ceramics, clay, glass and china pottery, electronic, foundry, sand-blasting and manufacturing abrasives, and many construction activities (Altindag et al. 2003; Flanagan et al. 2003; Irwin 2003; Rappaport et al. 2003). It is used as an abrasive agent in many industrial applications. Occupations having a high potential for exposure to Crystalline Silica dust (respirable quartz) are metal, coal, and nonmetal (except fuels) mining; foundry, stone clay, and glass production work; and agricultural, chemical production, highway repair, and tuck-pointing work [Akbar-Khanzadeh and Brillhart 2002; Occupational Safety and Health Administration (OSHA) 2004; Rappaport et al. 2003]. Silica dust is an inhalation hazard. Workers may be at risk of silicosis from exposure to Silica dust when high-velocity impact shatters the sand into smaller, respirable (< 0.5 to 5.0 μm in diameter) dust particles. Silicosis is a disease where scar tissue forms in the lungs and reduces the ability to extract oxygen from the air. Symptoms of silicosis can be acute, accelerated, or chronic. Acute silicosis may develop within weeks and up to 5 years after breathing large amounts of Crystalline Silica. Accelerated silicosis may develop shortly after exposure to high concentrations of respirable Crystalline Silica, whereas chronic silicosis occurs after ≥10 years of exposure to relatively low concentrations of Crystalline Silica [American Thoracic Society 1997; National Institute for Occupational Safety and Health (NIOSH) 2002]. Many workers in a wider range of industries are exposed to Silica, usually in the form of respirable quartz (OSHA 2001, 2003). OSHA has estimated that more than 2 million workers are exposed to Crystalline Silica dust in the general, maritime, and construction industries (OSHA 2003). More than 100,000 workers have high-risk exposure to airborne Silica dust through construction and mining operations (Akbar-Khanzadeh and Brillhart 2002; NIOSH 1991). There were an estimated 3,600–7,300 newly recognized silicosis cases per year in the United States from 1987 to 1996 (Rosenman et al. 2003). Between 1990 and 1996, 200–300 deaths per year are known to have occurred where silicosis was identified as a contributing cause on death certificates (Akbar-Khanzadeh and Brillhart 2002; OSHA 2003). The International Agency for Research on Cancer (IARC 1987, 1997) classified Crystalline Silica as a known human carcinogen. Exposure to Crystalline Silica has been associated with an increased risk of developing lung cancer (Engholm and Englund 1995; Knutsson et al. 2000; Hughes et al. 2001; Lynge et al. 1986; Robinson et al. 1995; Stern et al. 1995). Previous studies also documented an association between airborne Silica exposure and other health problems, including chronic obstructive pulmonary disease, rheumatoid arthritis, scleroderma, Sjogern’s syndrome, lupus, and renal disease (Goldsmith 1997; Hnizdo and Vallyathan 2003; Kane 1997; Parks et al. 2002). The current OSHA permissible exposure limit (PEL) for Crystalline Silica is based on a particle counting formula recommended by the ACGIH in the 1970s (ACGIH 1980; OSHA 1989, 1993). In 1986, the ACGIH revised the threshold limit value (TLV) of 0.1 mg/m3 for respirable quartz (ACGIH 1986). Currently, the NIOSH (1998) and the ACGIH (2001) both recommend an occupational exposure limit of 0.05 mg/m3 for respirable Crystalline Silica. OSHA recognized the need to revise the PEL to reflect current sampling and analytical methods, and the agency determined to address the significant risk of silicosis and other serious diseases associated with Silica through a special emphasis program (SEP) on silicosis (Dear 1996; Jeffress 1998; OSHA 2003). The purposes of this study were a) to summarize measurements of airborne (respirable) Crystalline Silica dust exposure levels among U.S. workers, b) to provide an update of the Stewart and Rice (1990) report on the airborne Silica exposure levels in high-risk industries and occupations with data for the time period 1988–2003, c) to estimate the number of workers potentially exposed to Silica in industries that OSHA inspected for high exposure levels, and d) to conduct time trend analyses on Silica dust exposure levels for time-weighted average (TWA) measurements.