The Experts below are selected from a list of 17196 Experts worldwide ranked by ideXlab platform
Constantinos Sioutas - One of the best experts on this subject based on the ideXlab platform.
-
air pollution exposures and circulating biomarkers of effect in a susceptible population clues to potential Causal Component mixtures and mechanisms
Environmental Health Perspectives, 2009Co-Authors: Ralph J Delfino, Norbert Staimer, Thomas Tjoa, Daniel L Gillen, Andrea Polidori, Mohammad Arhami, Micheal T Kleinman, Nosratola D Vaziri, John C Longhurst, Constantinos SioutasAbstract:Ambient mass concentrations of particulate matter (PM) air pollution < 2.5 μm (PM2.5) and < 10 μm (PM10) in aerodynamic diameter have been associated with hospital admissions and mortality due to cardiovascular causes in time series studies (Pope and Dockery 2006). Mechanisms involving oxidative stress and inflammation have been proposed to explain these associations (Mills et al. 2007) (Figure 1). In addition, a growing toxicology literature suggests that ultrafine particles (UFP), < 0.1 μm in diameter, may have greater potential to induce oxidative stress and inflammation than larger particles that dominate PM2.5 and PM10 mass (Ntziachristos et al. 2007). This is likely because compared with larger particles, UFP have a higher airway deposition efficiency, magnitudes higher particle number (PN) concentration and surface area, and higher concentrations of organic Components shown to induce oxidative stress responses (Li et al. 2003). The ability of UFP to translocate systemically from pulmonary sites makes them particularly relevant to the cardiovascular effects of inhaled PM (Elder and Oberdorster 2006). Figure 1 Pathways from PM exposure to measured changes in systemic biomarkers and to hypothesized adverse cardiovascular health effects. The different source characteristics and particle-size fractions we measured represent different types and concentrations of ... We aimed to improve the characterization of PM exposure in order to yield clues to potentially important pollutant sources and Causal Component mixtures not otherwise evident with ambient PM2.5 and PM10 mass, which are regulated by the U.S. Environmental Protection Agency (Delfino et al. 2005) (Figure 1). For example, traffic (a common exposure source of redox active PM) increases spatial variability of UFP (Sioutas et al. 2005). Regional ambient data are thus likely to misrepresent personal exposure. In addition, ambient PM is made up of primary combustion aerosols, photochemically produced secondary organic aerosols, and mechanically generated crustal material. These particle types have different spatial and temporal variability. The organic Component mix and size distribution differs as well between these two classes of particulate organic matter, with primary aerosols being more common in UFP and secondary aerosols more common in the accumulation mode (~ 0.1–2.5 μm). To address these questions, we conducted a panel study with repeated measurements of biomarkers and exposures in 60 elderly individuals with a history of coronary artery disease (CAD), a population potentially susceptible to adverse effects of air pollution (von Klot et al. 2005). We investigated the relationship of intensive measurements of outdoor home air pollutants to changes in circulating bio-markers of inflammation, platelet activation, and antioxidant capacity (Figure 1). These bio-markers may be risk factors for cardiovascular diseases (Espinola-Klein et al. 2007; Pai et al. 2004). We investigated the relative strength of biomarker associations between various PM size fractions. We also investigated differences in associations between exposure markers of traffic-related primary PM compared with secondary PM. Results presented here add a second year of data from 31 subjects to data used in a previous analysis of 29 subjects (Delfino et al. 2008).
-
air pollution exposures and circulating biomarkers of effect in a susceptible population clues to potential Causal Component mixtures and mechanisms
Environmental Health Perspectives, 2009Co-Authors: Ralph J Delfino, Norbert Staimer, Thomas Tjoa, Daniel L Gillen, Andrea Polidori, Mohammad Arhami, Micheal T Kleinman, Nosratola D Vaziri, John C Longhurst, Constantinos SioutasAbstract:BackgroundMechanisms involving oxidative stress and inflammation have been proposed to explain associations of ambient air pollution with cardiovascular morbidity and mortality. Experimental eviden...
Ralph J Delfino - One of the best experts on this subject based on the ideXlab platform.
-
air pollution exposures and circulating biomarkers of effect in a susceptible population clues to potential Causal Component mixtures and mechanisms
Environmental Health Perspectives, 2009Co-Authors: Ralph J Delfino, Norbert Staimer, Thomas Tjoa, Daniel L Gillen, Andrea Polidori, Mohammad Arhami, Micheal T Kleinman, Nosratola D Vaziri, John C Longhurst, Constantinos SioutasAbstract:Ambient mass concentrations of particulate matter (PM) air pollution < 2.5 μm (PM2.5) and < 10 μm (PM10) in aerodynamic diameter have been associated with hospital admissions and mortality due to cardiovascular causes in time series studies (Pope and Dockery 2006). Mechanisms involving oxidative stress and inflammation have been proposed to explain these associations (Mills et al. 2007) (Figure 1). In addition, a growing toxicology literature suggests that ultrafine particles (UFP), < 0.1 μm in diameter, may have greater potential to induce oxidative stress and inflammation than larger particles that dominate PM2.5 and PM10 mass (Ntziachristos et al. 2007). This is likely because compared with larger particles, UFP have a higher airway deposition efficiency, magnitudes higher particle number (PN) concentration and surface area, and higher concentrations of organic Components shown to induce oxidative stress responses (Li et al. 2003). The ability of UFP to translocate systemically from pulmonary sites makes them particularly relevant to the cardiovascular effects of inhaled PM (Elder and Oberdorster 2006). Figure 1 Pathways from PM exposure to measured changes in systemic biomarkers and to hypothesized adverse cardiovascular health effects. The different source characteristics and particle-size fractions we measured represent different types and concentrations of ... We aimed to improve the characterization of PM exposure in order to yield clues to potentially important pollutant sources and Causal Component mixtures not otherwise evident with ambient PM2.5 and PM10 mass, which are regulated by the U.S. Environmental Protection Agency (Delfino et al. 2005) (Figure 1). For example, traffic (a common exposure source of redox active PM) increases spatial variability of UFP (Sioutas et al. 2005). Regional ambient data are thus likely to misrepresent personal exposure. In addition, ambient PM is made up of primary combustion aerosols, photochemically produced secondary organic aerosols, and mechanically generated crustal material. These particle types have different spatial and temporal variability. The organic Component mix and size distribution differs as well between these two classes of particulate organic matter, with primary aerosols being more common in UFP and secondary aerosols more common in the accumulation mode (~ 0.1–2.5 μm). To address these questions, we conducted a panel study with repeated measurements of biomarkers and exposures in 60 elderly individuals with a history of coronary artery disease (CAD), a population potentially susceptible to adverse effects of air pollution (von Klot et al. 2005). We investigated the relationship of intensive measurements of outdoor home air pollutants to changes in circulating bio-markers of inflammation, platelet activation, and antioxidant capacity (Figure 1). These bio-markers may be risk factors for cardiovascular diseases (Espinola-Klein et al. 2007; Pai et al. 2004). We investigated the relative strength of biomarker associations between various PM size fractions. We also investigated differences in associations between exposure markers of traffic-related primary PM compared with secondary PM. Results presented here add a second year of data from 31 subjects to data used in a previous analysis of 29 subjects (Delfino et al. 2008).
-
air pollution exposures and circulating biomarkers of effect in a susceptible population clues to potential Causal Component mixtures and mechanisms
Environmental Health Perspectives, 2009Co-Authors: Ralph J Delfino, Norbert Staimer, Thomas Tjoa, Daniel L Gillen, Andrea Polidori, Mohammad Arhami, Micheal T Kleinman, Nosratola D Vaziri, John C Longhurst, Constantinos SioutasAbstract:BackgroundMechanisms involving oxidative stress and inflammation have been proposed to explain associations of ambient air pollution with cardiovascular morbidity and mortality. Experimental eviden...
Micheal T Kleinman - One of the best experts on this subject based on the ideXlab platform.
-
air pollution exposures and circulating biomarkers of effect in a susceptible population clues to potential Causal Component mixtures and mechanisms
Environmental Health Perspectives, 2009Co-Authors: Ralph J Delfino, Norbert Staimer, Thomas Tjoa, Daniel L Gillen, Andrea Polidori, Mohammad Arhami, Micheal T Kleinman, Nosratola D Vaziri, John C Longhurst, Constantinos SioutasAbstract:Ambient mass concentrations of particulate matter (PM) air pollution < 2.5 μm (PM2.5) and < 10 μm (PM10) in aerodynamic diameter have been associated with hospital admissions and mortality due to cardiovascular causes in time series studies (Pope and Dockery 2006). Mechanisms involving oxidative stress and inflammation have been proposed to explain these associations (Mills et al. 2007) (Figure 1). In addition, a growing toxicology literature suggests that ultrafine particles (UFP), < 0.1 μm in diameter, may have greater potential to induce oxidative stress and inflammation than larger particles that dominate PM2.5 and PM10 mass (Ntziachristos et al. 2007). This is likely because compared with larger particles, UFP have a higher airway deposition efficiency, magnitudes higher particle number (PN) concentration and surface area, and higher concentrations of organic Components shown to induce oxidative stress responses (Li et al. 2003). The ability of UFP to translocate systemically from pulmonary sites makes them particularly relevant to the cardiovascular effects of inhaled PM (Elder and Oberdorster 2006). Figure 1 Pathways from PM exposure to measured changes in systemic biomarkers and to hypothesized adverse cardiovascular health effects. The different source characteristics and particle-size fractions we measured represent different types and concentrations of ... We aimed to improve the characterization of PM exposure in order to yield clues to potentially important pollutant sources and Causal Component mixtures not otherwise evident with ambient PM2.5 and PM10 mass, which are regulated by the U.S. Environmental Protection Agency (Delfino et al. 2005) (Figure 1). For example, traffic (a common exposure source of redox active PM) increases spatial variability of UFP (Sioutas et al. 2005). Regional ambient data are thus likely to misrepresent personal exposure. In addition, ambient PM is made up of primary combustion aerosols, photochemically produced secondary organic aerosols, and mechanically generated crustal material. These particle types have different spatial and temporal variability. The organic Component mix and size distribution differs as well between these two classes of particulate organic matter, with primary aerosols being more common in UFP and secondary aerosols more common in the accumulation mode (~ 0.1–2.5 μm). To address these questions, we conducted a panel study with repeated measurements of biomarkers and exposures in 60 elderly individuals with a history of coronary artery disease (CAD), a population potentially susceptible to adverse effects of air pollution (von Klot et al. 2005). We investigated the relationship of intensive measurements of outdoor home air pollutants to changes in circulating bio-markers of inflammation, platelet activation, and antioxidant capacity (Figure 1). These bio-markers may be risk factors for cardiovascular diseases (Espinola-Klein et al. 2007; Pai et al. 2004). We investigated the relative strength of biomarker associations between various PM size fractions. We also investigated differences in associations between exposure markers of traffic-related primary PM compared with secondary PM. Results presented here add a second year of data from 31 subjects to data used in a previous analysis of 29 subjects (Delfino et al. 2008).
-
air pollution exposures and circulating biomarkers of effect in a susceptible population clues to potential Causal Component mixtures and mechanisms
Environmental Health Perspectives, 2009Co-Authors: Ralph J Delfino, Norbert Staimer, Thomas Tjoa, Daniel L Gillen, Andrea Polidori, Mohammad Arhami, Micheal T Kleinman, Nosratola D Vaziri, John C Longhurst, Constantinos SioutasAbstract:BackgroundMechanisms involving oxidative stress and inflammation have been proposed to explain associations of ambient air pollution with cardiovascular morbidity and mortality. Experimental eviden...
Nosratola D Vaziri - One of the best experts on this subject based on the ideXlab platform.
-
air pollution exposures and circulating biomarkers of effect in a susceptible population clues to potential Causal Component mixtures and mechanisms
Environmental Health Perspectives, 2009Co-Authors: Ralph J Delfino, Norbert Staimer, Thomas Tjoa, Daniel L Gillen, Andrea Polidori, Mohammad Arhami, Micheal T Kleinman, Nosratola D Vaziri, John C Longhurst, Constantinos SioutasAbstract:Ambient mass concentrations of particulate matter (PM) air pollution < 2.5 μm (PM2.5) and < 10 μm (PM10) in aerodynamic diameter have been associated with hospital admissions and mortality due to cardiovascular causes in time series studies (Pope and Dockery 2006). Mechanisms involving oxidative stress and inflammation have been proposed to explain these associations (Mills et al. 2007) (Figure 1). In addition, a growing toxicology literature suggests that ultrafine particles (UFP), < 0.1 μm in diameter, may have greater potential to induce oxidative stress and inflammation than larger particles that dominate PM2.5 and PM10 mass (Ntziachristos et al. 2007). This is likely because compared with larger particles, UFP have a higher airway deposition efficiency, magnitudes higher particle number (PN) concentration and surface area, and higher concentrations of organic Components shown to induce oxidative stress responses (Li et al. 2003). The ability of UFP to translocate systemically from pulmonary sites makes them particularly relevant to the cardiovascular effects of inhaled PM (Elder and Oberdorster 2006). Figure 1 Pathways from PM exposure to measured changes in systemic biomarkers and to hypothesized adverse cardiovascular health effects. The different source characteristics and particle-size fractions we measured represent different types and concentrations of ... We aimed to improve the characterization of PM exposure in order to yield clues to potentially important pollutant sources and Causal Component mixtures not otherwise evident with ambient PM2.5 and PM10 mass, which are regulated by the U.S. Environmental Protection Agency (Delfino et al. 2005) (Figure 1). For example, traffic (a common exposure source of redox active PM) increases spatial variability of UFP (Sioutas et al. 2005). Regional ambient data are thus likely to misrepresent personal exposure. In addition, ambient PM is made up of primary combustion aerosols, photochemically produced secondary organic aerosols, and mechanically generated crustal material. These particle types have different spatial and temporal variability. The organic Component mix and size distribution differs as well between these two classes of particulate organic matter, with primary aerosols being more common in UFP and secondary aerosols more common in the accumulation mode (~ 0.1–2.5 μm). To address these questions, we conducted a panel study with repeated measurements of biomarkers and exposures in 60 elderly individuals with a history of coronary artery disease (CAD), a population potentially susceptible to adverse effects of air pollution (von Klot et al. 2005). We investigated the relationship of intensive measurements of outdoor home air pollutants to changes in circulating bio-markers of inflammation, platelet activation, and antioxidant capacity (Figure 1). These bio-markers may be risk factors for cardiovascular diseases (Espinola-Klein et al. 2007; Pai et al. 2004). We investigated the relative strength of biomarker associations between various PM size fractions. We also investigated differences in associations between exposure markers of traffic-related primary PM compared with secondary PM. Results presented here add a second year of data from 31 subjects to data used in a previous analysis of 29 subjects (Delfino et al. 2008).
-
air pollution exposures and circulating biomarkers of effect in a susceptible population clues to potential Causal Component mixtures and mechanisms
Environmental Health Perspectives, 2009Co-Authors: Ralph J Delfino, Norbert Staimer, Thomas Tjoa, Daniel L Gillen, Andrea Polidori, Mohammad Arhami, Micheal T Kleinman, Nosratola D Vaziri, John C Longhurst, Constantinos SioutasAbstract:BackgroundMechanisms involving oxidative stress and inflammation have been proposed to explain associations of ambient air pollution with cardiovascular morbidity and mortality. Experimental eviden...
Mohammad Arhami - One of the best experts on this subject based on the ideXlab platform.
-
air pollution exposures and circulating biomarkers of effect in a susceptible population clues to potential Causal Component mixtures and mechanisms
Environmental Health Perspectives, 2009Co-Authors: Ralph J Delfino, Norbert Staimer, Thomas Tjoa, Daniel L Gillen, Andrea Polidori, Mohammad Arhami, Micheal T Kleinman, Nosratola D Vaziri, John C Longhurst, Constantinos SioutasAbstract:Ambient mass concentrations of particulate matter (PM) air pollution < 2.5 μm (PM2.5) and < 10 μm (PM10) in aerodynamic diameter have been associated with hospital admissions and mortality due to cardiovascular causes in time series studies (Pope and Dockery 2006). Mechanisms involving oxidative stress and inflammation have been proposed to explain these associations (Mills et al. 2007) (Figure 1). In addition, a growing toxicology literature suggests that ultrafine particles (UFP), < 0.1 μm in diameter, may have greater potential to induce oxidative stress and inflammation than larger particles that dominate PM2.5 and PM10 mass (Ntziachristos et al. 2007). This is likely because compared with larger particles, UFP have a higher airway deposition efficiency, magnitudes higher particle number (PN) concentration and surface area, and higher concentrations of organic Components shown to induce oxidative stress responses (Li et al. 2003). The ability of UFP to translocate systemically from pulmonary sites makes them particularly relevant to the cardiovascular effects of inhaled PM (Elder and Oberdorster 2006). Figure 1 Pathways from PM exposure to measured changes in systemic biomarkers and to hypothesized adverse cardiovascular health effects. The different source characteristics and particle-size fractions we measured represent different types and concentrations of ... We aimed to improve the characterization of PM exposure in order to yield clues to potentially important pollutant sources and Causal Component mixtures not otherwise evident with ambient PM2.5 and PM10 mass, which are regulated by the U.S. Environmental Protection Agency (Delfino et al. 2005) (Figure 1). For example, traffic (a common exposure source of redox active PM) increases spatial variability of UFP (Sioutas et al. 2005). Regional ambient data are thus likely to misrepresent personal exposure. In addition, ambient PM is made up of primary combustion aerosols, photochemically produced secondary organic aerosols, and mechanically generated crustal material. These particle types have different spatial and temporal variability. The organic Component mix and size distribution differs as well between these two classes of particulate organic matter, with primary aerosols being more common in UFP and secondary aerosols more common in the accumulation mode (~ 0.1–2.5 μm). To address these questions, we conducted a panel study with repeated measurements of biomarkers and exposures in 60 elderly individuals with a history of coronary artery disease (CAD), a population potentially susceptible to adverse effects of air pollution (von Klot et al. 2005). We investigated the relationship of intensive measurements of outdoor home air pollutants to changes in circulating bio-markers of inflammation, platelet activation, and antioxidant capacity (Figure 1). These bio-markers may be risk factors for cardiovascular diseases (Espinola-Klein et al. 2007; Pai et al. 2004). We investigated the relative strength of biomarker associations between various PM size fractions. We also investigated differences in associations between exposure markers of traffic-related primary PM compared with secondary PM. Results presented here add a second year of data from 31 subjects to data used in a previous analysis of 29 subjects (Delfino et al. 2008).
-
air pollution exposures and circulating biomarkers of effect in a susceptible population clues to potential Causal Component mixtures and mechanisms
Environmental Health Perspectives, 2009Co-Authors: Ralph J Delfino, Norbert Staimer, Thomas Tjoa, Daniel L Gillen, Andrea Polidori, Mohammad Arhami, Micheal T Kleinman, Nosratola D Vaziri, John C Longhurst, Constantinos SioutasAbstract:BackgroundMechanisms involving oxidative stress and inflammation have been proposed to explain associations of ambient air pollution with cardiovascular morbidity and mortality. Experimental eviden...