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Thomas Sandstrom - One of the best experts on this subject based on the ideXlab platform.
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Combustion-derived nanoparticulate induces the adverse vascular effects of Diesel Exhaust
2020Co-Authors: Nicholas L. Mills, Mark R. Miller, Andrew J. Lucking, Jon Beveridge, Laura Flint, A. John, F. Boere, Paul H. B. Fokkens, Nicholas A. Boon, Thomas SandstromAbstract:Aim Exposure to road traffic and air pollution may be a trigger of acute myocardial infarction, but the individual pollutants responsible for this effect have not been established. We assess the role of combustion-derived-nanoparticles in mediating the adverse cardiovascular effects of air pollution. Methods To determine the in vivo effects of inhalation of Diesel Exhaust components, 16 healthy volunteers were exposed to (i) dilute Diesel Exhaust, (ii) pure carbon nanoparticulate, (iii) filtered Diesel Exhaust, or (iv) filtered air, in a randomized double blind cross-over study. Following each exposure, forearm blood flow was measured during intra-brachial bradykinin, acetylcholine, sodium nitroprusside, and verapamil infusions. Compared with filtered air, inhalation of Diesel Exhaust increased systolic blood pressure (145+4 vs. 133+3 mmHg, P , 0.05) and attenuated vasodilatation to bradykinin (P ¼ 0.005), acetylcholine (P ¼ 0.008), and sodium nitroprusside (P , 0.001). Exposure to pure carbon nanoparticulate or filtered Exhaust had no effect on endothelium-dependent or -independent vasodilatation. To determine the direct vascular effects of nanoparticulate, isolated rat aortic rings (n ¼ 6-9 per group) were assessed in vitro by wire myography and exposed to Diesel Exhaust particulate, pure carbon nanoparticulate and vehicle. Com- pared with vehicle, Diesel Exhaust particulate (but not pure carbon nanoparticulate) attenuated both acetylcholine (P , 0.001) and sodium-nitroprusside (P ¼ 0.019)-induced vasorelaxation. These effects were partially attributable to both soluble and insoluble components of the particulate. Conclusion Combustion-derived nanoparticulate appears to predominately mediate the adverse vascular effects of Diesel Exhaust inhalation. This provides a rationale for testing environmental health interventions targeted at reducing traffic-derived particulate emissions.
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Combustion-derived nanoparticulate induces the adverse vascular effects of Diesel Exhaust inhalation
European Heart Journal, 2011Co-Authors: Nicholas L. Mills, Thomas Sandstrom, Mark R. Miller, Andrew J. Lucking, Jon Beveridge, Laura Flint, Paul H. B. Fokkens, Nicholas A. Boon, A. John F. Boere, Anders BlombergAbstract:Aim Exposure to road traffic and air pollution may be a trigger of acute myocardial infarction, but the individual pollutants responsible for this effect have not been established. We assess the role of combustion-derived-nanoparticles in mediating the adverse cardiovascular effects of air pollution. Methods and results To determine the in vivo effects of inhalation of Diesel Exhaust components, 16 healthy volunteers were exposed to (i) dilute Diesel Exhaust, (ii) pure carbon nanoparticulate, (iii) filtered Diesel Exhaust, or (iv) filtered air, in a randomized double blind cross-over study. Following each exposure, forearm blood flow was measured during intra-brachial bradykinin, acetylcholine, sodium nitroprusside, and verapamil infusions. Compared with filtered air, inhalation of Diesel Exhaust increased systolic blood pressure (145 ± 4 vs. 133 ± 3 mmHg, P < 0.05) and attenuated vasodilatation to bradykinin ( P = 0.005), acetylcholine ( P = 0.008), and sodium nitroprusside ( P < 0.001). Exposure to pure carbon nanoparticulate or filtered Exhaust had no effect on endothelium-dependent or -independent vasodilatation. To determine the direct vascular effects of nanoparticulate, isolated rat aortic rings ( n = 6–9 per group) were assessed in vitro by wire myography and exposed to Diesel Exhaust particulate, pure carbon nanoparticulate and vehicle. Compared with vehicle, Diesel Exhaust particulate (but not pure carbon nanoparticulate) attenuated both acetylcholine ( P < 0.001) and sodium-nitroprusside ( P = 0.019)-induced vasorelaxation. These effects were partially attributable to both soluble and insoluble components of the particulate. Conclusion Combustion-derived nanoparticulate appears to predominately mediate the adverse vascular effects of Diesel Exhaust inhalation. This provides a rationale for testing environmental health interventions targeted at reducing traffic-derived particulate emissions.
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Contribution of Endothelin 1 to the Vascular Effects of Diesel Exhaust Inhalation in Humans
Hypertension, 2009Co-Authors: Jeremy P. Langrish, Anders Blomberg, Thomas Sandstrom, Nicholas L. Mills, Magnus Lundbäck, Neil R. Johnston, David J. Webb, David E. NewbyAbstract:Diesel Exhaust inhalation impairs vascular function, and, although the underlying mechanism remains unclear, endothelin (ET) 1 and NO are potential mediators. The aim of this study was to identify whether Diesel Exhaust inhalation affects the vascular actions of ET-1 in humans. In a randomized, double-blind crossover study, 13 healthy male volunteers were exposed to either filtered air or dilute Diesel Exhaust (331±13 μg/m 3 ). Plasma concentrations of ET-1 and big-ET-1 were determined at baseline and throughout the 24-hour study period. Bilateral forearm blood flow was measured 2 hours after the exposure during infusion of either ET-1 (5 pmol/min) or the ET A receptor antagonist, BQ-123 (10 nmol/min) alone and in combination with the ET B receptor antagonist, BQ-788 (1 nmol/min). Diesel Exhaust exposure had no effect on plasma ET-1 and big-ET-1 concentrations ( P >0.05 for both) or 24-hour mean blood pressure or heart rate ( P >0.05 for all). ET-1 infusion increased plasma ET-1 concentrations by 58% ( P P P P >0.05). Diesel Exhaust inhalation increases vascular sensitivity to ET-1 and reduces vasodilatation to ET A receptor antagonism despite unchanged plasma ET-1 concentrations. Given the tonic interaction between the ET and NO systems, we conclude that Diesel Exhaust inhalation alters vascular reactivity to ET-1 probably through its effects on NO bioavailability.
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ischemic and thrombotic effects of dilute Diesel Exhaust inhalation in men with coronary heart disease
The New England Journal of Medicine, 2007Co-Authors: Nicholas L. Mills, Thomas Sandstrom, Nicholas A. Boon, Hakan Tornqvist, Manuel Gonzalez, Simon D Robinson, K Donaldson, Stefan Soderberg, Elen Vink, Anders BlombergAbstract:A b s t r ac t During both exposure sessions, the heart rate increased with exercise (P<0.001); the increase was similar during exposure to Diesel Exhaust and exposure to filtered air (P = 0.67). Exercise-induced ST-segment depression was present in all patients, but there was a greater increase in the ischemic burden during exposure to Diesel Exhaust (−22±4 vs. −8±6 millivolt seconds, P<0.001). Exposure to Diesel Exhaust did not ag- gravate preexisting vasomotor dysfunction, but it did reduce the acute release of en- dothelial tissue plasminogen activator (P = 0.009; 35% decrease in the area under the curve). Conclusions Brief exposure to dilute Diesel Exhaust promotes myocardial ischemia and inhibits endogenous fibrinolytic capacity in men with stable coronary heart disease. Our find- ings point to ischemic and thrombotic mechanisms that may explain in part the ob- servation that exposure to combustion-derived air pollution is associated with adverse cardiovascular events. (ClinicalTrials.gov number, NCT00437138.)
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Diesel Exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis
Circulation, 2005Co-Authors: Nicholas L. Mills, Anders Blomberg, Nicholas A. Boon, Hakan Tornqvist, Manuel Gonzalez, Simon D Robinson, William Macnee, K Donaldson, Kareen Darnley, Thomas SandstromAbstract:Background—Although the mechanisms are unknown, it has been suggested that transient exposure to traffic-derived air pollution may be a trigger for acute myocardial infarction. The study aim was to investigate the effects of Diesel Exhaust inhalation on vascular and endothelial function in humans. Methods and Results—In a double-blind, randomized, cross-over study, 30 healthy men were exposed to diluted Diesel Exhaust (300 g/m 3 particulate concentration) or air for 1 hour during intermittent exercise. Bilateral forearm blood flow and inflammatory factors were measured before and during unilateral intrabrachial bradykinin (100 to 1000 pmol/min), acetylcholine (5 to 20 g/min), sodium nitroprusside (2 to 8 g/min), and verapamil (10 to 100 g/min) infusions 2 and 6 hours after exposure. There were no differences in resting forearm blood flow or inflammatory markers after exposure to Diesel Exhaust or air. Although there was a dose-dependent increase in blood flow with each vasodilator (P0.0001 for all), this response was attenuated with bradykinin (P0.05), acetylcholine (P0.05), and sodium nitroprusside (P0.001) infusions 2 hours after exposure to Diesel Exhaust, which persisted at 6 hours. Bradykinin caused a dose-dependent increase in plasma tissue plasminogen activator (P0.0001) that was suppressed 6 hours after exposure to Diesel (P0.001; area under the curve decreased by 34%). Conclusions—At levels encountered in an urban environment, inhalation of dilute Diesel Exhaust impairs 2 important and complementary aspects of vascular function in humans: the regulation of vascular tone and endogenous fibrinolysis. These important findings provide a potential mechanism that links air pollution to the pathogenesis of atherothrombosis and acute myocardial infarction. (Circulation. 2005;112:3930-3936.)
Anders Blomberg - One of the best experts on this subject based on the ideXlab platform.
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Combustion-derived nanoparticulate induces the adverse vascular effects of Diesel Exhaust inhalation
European Heart Journal, 2011Co-Authors: Nicholas L. Mills, Thomas Sandstrom, Mark R. Miller, Andrew J. Lucking, Jon Beveridge, Laura Flint, Paul H. B. Fokkens, Nicholas A. Boon, A. John F. Boere, Anders BlombergAbstract:Aim Exposure to road traffic and air pollution may be a trigger of acute myocardial infarction, but the individual pollutants responsible for this effect have not been established. We assess the role of combustion-derived-nanoparticles in mediating the adverse cardiovascular effects of air pollution. Methods and results To determine the in vivo effects of inhalation of Diesel Exhaust components, 16 healthy volunteers were exposed to (i) dilute Diesel Exhaust, (ii) pure carbon nanoparticulate, (iii) filtered Diesel Exhaust, or (iv) filtered air, in a randomized double blind cross-over study. Following each exposure, forearm blood flow was measured during intra-brachial bradykinin, acetylcholine, sodium nitroprusside, and verapamil infusions. Compared with filtered air, inhalation of Diesel Exhaust increased systolic blood pressure (145 ± 4 vs. 133 ± 3 mmHg, P < 0.05) and attenuated vasodilatation to bradykinin ( P = 0.005), acetylcholine ( P = 0.008), and sodium nitroprusside ( P < 0.001). Exposure to pure carbon nanoparticulate or filtered Exhaust had no effect on endothelium-dependent or -independent vasodilatation. To determine the direct vascular effects of nanoparticulate, isolated rat aortic rings ( n = 6–9 per group) were assessed in vitro by wire myography and exposed to Diesel Exhaust particulate, pure carbon nanoparticulate and vehicle. Compared with vehicle, Diesel Exhaust particulate (but not pure carbon nanoparticulate) attenuated both acetylcholine ( P < 0.001) and sodium-nitroprusside ( P = 0.019)-induced vasorelaxation. These effects were partially attributable to both soluble and insoluble components of the particulate. Conclusion Combustion-derived nanoparticulate appears to predominately mediate the adverse vascular effects of Diesel Exhaust inhalation. This provides a rationale for testing environmental health interventions targeted at reducing traffic-derived particulate emissions.
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Contribution of Endothelin 1 to the Vascular Effects of Diesel Exhaust Inhalation in Humans
Hypertension, 2009Co-Authors: Jeremy P. Langrish, Anders Blomberg, Thomas Sandstrom, Nicholas L. Mills, Magnus Lundbäck, Neil R. Johnston, David J. Webb, David E. NewbyAbstract:Diesel Exhaust inhalation impairs vascular function, and, although the underlying mechanism remains unclear, endothelin (ET) 1 and NO are potential mediators. The aim of this study was to identify whether Diesel Exhaust inhalation affects the vascular actions of ET-1 in humans. In a randomized, double-blind crossover study, 13 healthy male volunteers were exposed to either filtered air or dilute Diesel Exhaust (331±13 μg/m 3 ). Plasma concentrations of ET-1 and big-ET-1 were determined at baseline and throughout the 24-hour study period. Bilateral forearm blood flow was measured 2 hours after the exposure during infusion of either ET-1 (5 pmol/min) or the ET A receptor antagonist, BQ-123 (10 nmol/min) alone and in combination with the ET B receptor antagonist, BQ-788 (1 nmol/min). Diesel Exhaust exposure had no effect on plasma ET-1 and big-ET-1 concentrations ( P >0.05 for both) or 24-hour mean blood pressure or heart rate ( P >0.05 for all). ET-1 infusion increased plasma ET-1 concentrations by 58% ( P P P P >0.05). Diesel Exhaust inhalation increases vascular sensitivity to ET-1 and reduces vasodilatation to ET A receptor antagonism despite unchanged plasma ET-1 concentrations. Given the tonic interaction between the ET and NO systems, we conclude that Diesel Exhaust inhalation alters vascular reactivity to ET-1 probably through its effects on NO bioavailability.
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ischemic and thrombotic effects of dilute Diesel Exhaust inhalation in men with coronary heart disease
The New England Journal of Medicine, 2007Co-Authors: Nicholas L. Mills, Thomas Sandstrom, Nicholas A. Boon, Hakan Tornqvist, Manuel Gonzalez, Simon D Robinson, K Donaldson, Stefan Soderberg, Elen Vink, Anders BlombergAbstract:A b s t r ac t During both exposure sessions, the heart rate increased with exercise (P<0.001); the increase was similar during exposure to Diesel Exhaust and exposure to filtered air (P = 0.67). Exercise-induced ST-segment depression was present in all patients, but there was a greater increase in the ischemic burden during exposure to Diesel Exhaust (−22±4 vs. −8±6 millivolt seconds, P<0.001). Exposure to Diesel Exhaust did not ag- gravate preexisting vasomotor dysfunction, but it did reduce the acute release of en- dothelial tissue plasminogen activator (P = 0.009; 35% decrease in the area under the curve). Conclusions Brief exposure to dilute Diesel Exhaust promotes myocardial ischemia and inhibits endogenous fibrinolytic capacity in men with stable coronary heart disease. Our find- ings point to ischemic and thrombotic mechanisms that may explain in part the ob- servation that exposure to combustion-derived air pollution is associated with adverse cardiovascular events. (ClinicalTrials.gov number, NCT00437138.)
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Diesel Exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis
Circulation, 2005Co-Authors: Nicholas L. Mills, Anders Blomberg, Nicholas A. Boon, Hakan Tornqvist, Manuel Gonzalez, Simon D Robinson, William Macnee, K Donaldson, Kareen Darnley, Thomas SandstromAbstract:Background—Although the mechanisms are unknown, it has been suggested that transient exposure to traffic-derived air pollution may be a trigger for acute myocardial infarction. The study aim was to investigate the effects of Diesel Exhaust inhalation on vascular and endothelial function in humans. Methods and Results—In a double-blind, randomized, cross-over study, 30 healthy men were exposed to diluted Diesel Exhaust (300 g/m 3 particulate concentration) or air for 1 hour during intermittent exercise. Bilateral forearm blood flow and inflammatory factors were measured before and during unilateral intrabrachial bradykinin (100 to 1000 pmol/min), acetylcholine (5 to 20 g/min), sodium nitroprusside (2 to 8 g/min), and verapamil (10 to 100 g/min) infusions 2 and 6 hours after exposure. There were no differences in resting forearm blood flow or inflammatory markers after exposure to Diesel Exhaust or air. Although there was a dose-dependent increase in blood flow with each vasodilator (P0.0001 for all), this response was attenuated with bradykinin (P0.05), acetylcholine (P0.05), and sodium nitroprusside (P0.001) infusions 2 hours after exposure to Diesel Exhaust, which persisted at 6 hours. Bradykinin caused a dose-dependent increase in plasma tissue plasminogen activator (P0.0001) that was suppressed 6 hours after exposure to Diesel (P0.001; area under the curve decreased by 34%). Conclusions—At levels encountered in an urban environment, inhalation of dilute Diesel Exhaust impairs 2 important and complementary aspects of vascular function in humans: the regulation of vascular tone and endogenous fibrinolysis. These important findings provide a potential mechanism that links air pollution to the pathogenesis of atherothrombosis and acute myocardial infarction. (Circulation. 2005;112:3930-3936.)
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health effects of Diesel Exhaust emissions
European Respiratory Journal, 2001Co-Authors: A Sydbom, Anders Blomberg, Sam Parnia, Nikolai Stenfors, Thomas Sandstrom, S E DahlenAbstract:Epidemiological studies have demonstrated an association between different levels of air pollution and various health outcomes including mortality, exacerbation of asthma, chronic bronchitis, respiratory tract infections, ischaemic heart disease and stroke. Of the motor vehicle generated air pollutants, Diesel Exhaust particles account for a highly significant percentage of the particles emitted in many towns and cities. This review is therefore focused on the health effects of Diesel Exhaust, and especially the particular matter components. Acute effects of Diesel Exhaust exposure include irritation of the nose and eyes, lung function changes, respiratory changes, headache, fatigue and nausea. Chronic exposures are associated with cough, sputum production and lung function decrements. In addition to symptoms, exposure studies in healthy humans have documented a number of profound inflammatory changes in the airways, notably, before changes in pulmonary function can be detected. It is likely that such effects may be even more detrimental in asthmatics and other subjects with compromised pulmonary function. There are also observations supporting the hypothesis that Diesel Exhaust is one important factor contributing to the allergy pandemic. For example, in many experimental systems, Diesel Exhaust particles can be shown to act as adjuvants to allergen and hence increase the sensitization response. Much of the research on adverse effects of Diesel Exhaust, both in vivo and in vitro, has however been conducted in animals. Questions remain concerning the relevance of exposure levels and whether findings in such models can be extrapolated into humans. It is therefore imperative to further assess acute and chronic effects of Diesel Exhaust in mechanistic studies with careful consideration of exposure levels. Whenever possible and ethically justified, studies should be carried out in humans.
Nicholas L. Mills - One of the best experts on this subject based on the ideXlab platform.
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Combustion-derived nanoparticulate induces the adverse vascular effects of Diesel Exhaust
2020Co-Authors: Nicholas L. Mills, Mark R. Miller, Andrew J. Lucking, Jon Beveridge, Laura Flint, A. John, F. Boere, Paul H. B. Fokkens, Nicholas A. Boon, Thomas SandstromAbstract:Aim Exposure to road traffic and air pollution may be a trigger of acute myocardial infarction, but the individual pollutants responsible for this effect have not been established. We assess the role of combustion-derived-nanoparticles in mediating the adverse cardiovascular effects of air pollution. Methods To determine the in vivo effects of inhalation of Diesel Exhaust components, 16 healthy volunteers were exposed to (i) dilute Diesel Exhaust, (ii) pure carbon nanoparticulate, (iii) filtered Diesel Exhaust, or (iv) filtered air, in a randomized double blind cross-over study. Following each exposure, forearm blood flow was measured during intra-brachial bradykinin, acetylcholine, sodium nitroprusside, and verapamil infusions. Compared with filtered air, inhalation of Diesel Exhaust increased systolic blood pressure (145+4 vs. 133+3 mmHg, P , 0.05) and attenuated vasodilatation to bradykinin (P ¼ 0.005), acetylcholine (P ¼ 0.008), and sodium nitroprusside (P , 0.001). Exposure to pure carbon nanoparticulate or filtered Exhaust had no effect on endothelium-dependent or -independent vasodilatation. To determine the direct vascular effects of nanoparticulate, isolated rat aortic rings (n ¼ 6-9 per group) were assessed in vitro by wire myography and exposed to Diesel Exhaust particulate, pure carbon nanoparticulate and vehicle. Com- pared with vehicle, Diesel Exhaust particulate (but not pure carbon nanoparticulate) attenuated both acetylcholine (P , 0.001) and sodium-nitroprusside (P ¼ 0.019)-induced vasorelaxation. These effects were partially attributable to both soluble and insoluble components of the particulate. Conclusion Combustion-derived nanoparticulate appears to predominately mediate the adverse vascular effects of Diesel Exhaust inhalation. This provides a rationale for testing environmental health interventions targeted at reducing traffic-derived particulate emissions.
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Combustion-derived nanoparticulate induces the adverse vascular effects of Diesel Exhaust inhalation
European Heart Journal, 2011Co-Authors: Nicholas L. Mills, Thomas Sandstrom, Mark R. Miller, Andrew J. Lucking, Jon Beveridge, Laura Flint, Paul H. B. Fokkens, Nicholas A. Boon, A. John F. Boere, Anders BlombergAbstract:Aim Exposure to road traffic and air pollution may be a trigger of acute myocardial infarction, but the individual pollutants responsible for this effect have not been established. We assess the role of combustion-derived-nanoparticles in mediating the adverse cardiovascular effects of air pollution. Methods and results To determine the in vivo effects of inhalation of Diesel Exhaust components, 16 healthy volunteers were exposed to (i) dilute Diesel Exhaust, (ii) pure carbon nanoparticulate, (iii) filtered Diesel Exhaust, or (iv) filtered air, in a randomized double blind cross-over study. Following each exposure, forearm blood flow was measured during intra-brachial bradykinin, acetylcholine, sodium nitroprusside, and verapamil infusions. Compared with filtered air, inhalation of Diesel Exhaust increased systolic blood pressure (145 ± 4 vs. 133 ± 3 mmHg, P < 0.05) and attenuated vasodilatation to bradykinin ( P = 0.005), acetylcholine ( P = 0.008), and sodium nitroprusside ( P < 0.001). Exposure to pure carbon nanoparticulate or filtered Exhaust had no effect on endothelium-dependent or -independent vasodilatation. To determine the direct vascular effects of nanoparticulate, isolated rat aortic rings ( n = 6–9 per group) were assessed in vitro by wire myography and exposed to Diesel Exhaust particulate, pure carbon nanoparticulate and vehicle. Compared with vehicle, Diesel Exhaust particulate (but not pure carbon nanoparticulate) attenuated both acetylcholine ( P < 0.001) and sodium-nitroprusside ( P = 0.019)-induced vasorelaxation. These effects were partially attributable to both soluble and insoluble components of the particulate. Conclusion Combustion-derived nanoparticulate appears to predominately mediate the adverse vascular effects of Diesel Exhaust inhalation. This provides a rationale for testing environmental health interventions targeted at reducing traffic-derived particulate emissions.
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Contribution of Endothelin 1 to the Vascular Effects of Diesel Exhaust Inhalation in Humans
Hypertension, 2009Co-Authors: Jeremy P. Langrish, Anders Blomberg, Thomas Sandstrom, Nicholas L. Mills, Magnus Lundbäck, Neil R. Johnston, David J. Webb, David E. NewbyAbstract:Diesel Exhaust inhalation impairs vascular function, and, although the underlying mechanism remains unclear, endothelin (ET) 1 and NO are potential mediators. The aim of this study was to identify whether Diesel Exhaust inhalation affects the vascular actions of ET-1 in humans. In a randomized, double-blind crossover study, 13 healthy male volunteers were exposed to either filtered air or dilute Diesel Exhaust (331±13 μg/m 3 ). Plasma concentrations of ET-1 and big-ET-1 were determined at baseline and throughout the 24-hour study period. Bilateral forearm blood flow was measured 2 hours after the exposure during infusion of either ET-1 (5 pmol/min) or the ET A receptor antagonist, BQ-123 (10 nmol/min) alone and in combination with the ET B receptor antagonist, BQ-788 (1 nmol/min). Diesel Exhaust exposure had no effect on plasma ET-1 and big-ET-1 concentrations ( P >0.05 for both) or 24-hour mean blood pressure or heart rate ( P >0.05 for all). ET-1 infusion increased plasma ET-1 concentrations by 58% ( P P P P >0.05). Diesel Exhaust inhalation increases vascular sensitivity to ET-1 and reduces vasodilatation to ET A receptor antagonism despite unchanged plasma ET-1 concentrations. Given the tonic interaction between the ET and NO systems, we conclude that Diesel Exhaust inhalation alters vascular reactivity to ET-1 probably through its effects on NO bioavailability.
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ischemic and thrombotic effects of dilute Diesel Exhaust inhalation in men with coronary heart disease
The New England Journal of Medicine, 2007Co-Authors: Nicholas L. Mills, Thomas Sandstrom, Nicholas A. Boon, Hakan Tornqvist, Manuel Gonzalez, Simon D Robinson, K Donaldson, Stefan Soderberg, Elen Vink, Anders BlombergAbstract:A b s t r ac t During both exposure sessions, the heart rate increased with exercise (P<0.001); the increase was similar during exposure to Diesel Exhaust and exposure to filtered air (P = 0.67). Exercise-induced ST-segment depression was present in all patients, but there was a greater increase in the ischemic burden during exposure to Diesel Exhaust (−22±4 vs. −8±6 millivolt seconds, P<0.001). Exposure to Diesel Exhaust did not ag- gravate preexisting vasomotor dysfunction, but it did reduce the acute release of en- dothelial tissue plasminogen activator (P = 0.009; 35% decrease in the area under the curve). Conclusions Brief exposure to dilute Diesel Exhaust promotes myocardial ischemia and inhibits endogenous fibrinolytic capacity in men with stable coronary heart disease. Our find- ings point to ischemic and thrombotic mechanisms that may explain in part the ob- servation that exposure to combustion-derived air pollution is associated with adverse cardiovascular events. (ClinicalTrials.gov number, NCT00437138.)
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persistent endothelial dysfunction in humans after Diesel Exhaust inhalation
American Journal of Respiratory and Critical Care Medicine, 2007Co-Authors: Hakan Tornqvist, Mark R. Miller, Nicholas L. Mills, Manuel Gonzalez, Simon D Robinson, Ian L Megson, William Macnee, K Donaldson, Stefan Soderberg, David E. NewbyAbstract:Rationale: Exposure to combustion-derived air pollution is associated with an early (1–2 h) and sustained (24 h) rise in cardiovascular morbidity and mortality. We have previously demonstrated that inhalation of Diesel Exhaust causes an immediate (within 2 h) impairment of vascular and endothelial function in humans.Objectives: To investigate the vascular and systemic effects of Diesel Exhaust in humans 24 hours after inhalation.Methods: Fifteen healthy men were exposed to Diesel Exhaust (particulate concentration, 300 μg/m3) or filtered air for 1 hour in a double-blind, randomized, crossover study. Twenty-four hours after exposure, bilateral forearm blood flow, and inflammatory and fibrinolytic markers were measured before and during unilateral intrabrachial bradykinin (100–1,000 pmol/min), acetylcholine (5–20 μg/min), sodium nitroprusside (2–8 μg/min), and verapamil (10–100 μg/min) infusions.Measurements and Main Results: Resting forearm blood flow, blood pressure, and basal fibrinolytic markers were si...
T. Sandström - One of the best experts on this subject based on the ideXlab platform.
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Efficiency of automotive cabin air filters to reduce acute health effects of Diesel Exhaust in human subjects.
Occupational and environmental medicine, 1999Co-Authors: B. Rudell, P. Hörstedt, U Wass, J O Levin, Y Ostberg, Ulf Rannug, Anna Lena Sunesson, Roger Lindahl, T. SandströmAbstract:OBJECTIVES: To evaluate the efficiency of different automotive cabin air filters to prevent penetration of components of Diesel Exhaust and thereby reduce biomedical effects in human subjects. Filtered air and unfiltered diluted Diesel Exhaust (DDE) were used as negative and positive controls, respectively, and were compared with exposure to DDE filtered with four different filter systems. METHODS: 32 Healthy non-smoking subjects (age 21-53) participated in the study. Each subject was exposed six times for 1 hour in a specially designed exposure chamber: once to air, once to unfiltered DDE, and once to DDE filtered with the four different cabin air filters. Particle concentrations during exposure to unfiltered DDE were kept at 300 micrograms/m3. Two of the filters were particle filters. The other two were particle filters combined with active charcoal filters that might reduce certain gaseous components. Subjective symptoms were recorded and nasal airway lavage (NAL), acoustic rhinometry, and lung function measurements were performed. RESULTS: The two particle filters decreased the concentrations of Diesel Exhaust particles by about half, but did not reduce the intensity of symptoms induced by Exhaust. The combination of active charcoal filters and a particle filter significantly reduced the symptoms and discomfort caused by the Diesel Exhaust. The most noticable differences in efficacy between the filters were found in the reduction of detection of an unpleasant smell from the Diesel Exhaust. In this respect even the two charcoal filter combinations differed significantly. The efficacy to reduce symptoms may depend on the abilities of the filters investigated to reduce certain hydrocarbons. No acute effects on NAL, rhinometry, and lung function variables were found. CONCLUSIONS: This study has shown that the use of active charcoal filters, and a particle filter, clearly reduced the intensity of symptoms induced by Diesel Exhaust. Complementary studies on vehicle cabin air filters may result in further diminishing the biomedical effects of Diesel Exhaust in subjects exposed in traffic and workplaces.
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Effects on symptoms and lung function in humans experimentally exposed to Diesel Exhaust.
Occupational and environmental medicine, 1996Co-Authors: B. Rudell, M. L. Ledin, U. Hammarström, N. Stjernberg, B Lundbäck, T. SandströmAbstract:OBJECTIVES: Diesel Exhaust is a common air pollutant made up of several gases, hydrocarbons, and particles. An experimental study was carried out which was designed to evaluate if a particle trap on the tail pipe of an idling Diesel engine would reduce effects on symptoms and lung function caused by the Diesel Exhaust, compared with exposure to unfiltered Exhaust.\n\nMETHODS: Twelve healthy non-smoking volunteers (aged 20-37) were investigated in an exposure chamber for one hour during light work on a bicycle ergometer at 75 W. Each subject underwent three separate double blind exposures in a randomised sequence: to air and to Diesel Exhaust with the particle trap at the tail pipe and to unfiltered Diesel Exhaust. Symptoms were recorded according to the Borg scale before, every 10 minutes during, and 30 minutes after the exposure. Lung function was measured with a computerised whole body plethysmograph.\n\nRESULTS: The ceramic wall flow particle trap reduced the number of particles by 46%, whereas other compounds were relatively constant. It was shown that the most prominent symptoms during exposure to Diesel Exhaust were irritation of the eyes and nose and an unpleasant smell increasing during exposure. Both airway resistance (R(aw)) and specific airway resistance (SR(aw)) increased significantly during the exposures to Diesel Exhaust. Despite the 46% reduction in particle numbers by the trap effects on symptoms and lung function were not significantly attenuated.\n\nCONCLUSION: Exposure to Diesel Exhaust caused symptoms and bronchoconstriction which were not significantly reduced by a particle trap.
Robert A. Cary - One of the best experts on this subject based on the ideXlab platform.
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Elemental carbon-based method for occupational monitoring of particulate Diesel Exhaust: methodology and exposure issues
Analyst, 1996Co-Authors: M. Eileen Birch, Robert A. CaryAbstract:Diesel Exhaust has been classified a probable human carcinogen, and the National Institute for Occupational Safety and Health (NIOSH) has recommended that employers reduce workers' exposures. Because Diesel Exhaust is a chemically complex mixture containing thousands of compounds, some measure of exposure must be selected. Previously used methods involving gravimetry or analysis of the soluble organic fraction of Diesel soot lack adequate sensitivity and selectivity for low-level determination of particulate Diesel Exhaust; a new analytical approach was therefore needed. In this paper, results of investigation of a thermal–optical technique for the analysis of the carbonaceous fraction of particulate Diesel Exhaust are discussed. With this technique, speciation of organic and elemental carbon is accomplished through temperature and atmosphere control and by an optical feature that corrects for pyrolytically generated carbon, or ‘char,’ which is formed during the analysis of some materials. The thermal–optical method was selected because the instrument has desirable design features not present in other carbon analysers. Although various carbon types are determined by the method, elemental carbon is the superior marker of Diesel particulate matter because elemental carbon constitutes a large fraction of the particulate mass, it can be quantified at low levels and its only significant source in most workplaces is the Diesel engine. Exposure-related issues and sampling methods for particulate Diesel Exhaust also are discussed.
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elemental carbon based method for monitoring occupational exposures to particulate Diesel Exhaust
Aerosol Science and Technology, 1996Co-Authors: M. Eileen Birch, Robert A. CaryAbstract:ABSTRACT Diesel Exhaust has been classified a probable human carcinogen, and the National Institute for Occupational Safety and Health (NIOSH) has recommended that employers reduce workers' exposures. Because Diesel Exhaust is a chemically complex mixture containing thousands of compounds, some measure of exposure must be selected. Previously used methods involving gravimetry or analysis of the soluble organic fraction of Diesel soot lack adequate sensitivity and selectivity for low-level determination of particulate Diesel Exhaust; a new analytical approach was therefore needed. In this paper, results of investigation of a thermal-optical technique for analysis of the carbonaceous fraction of particulate Diesel Exhaust are reported. With this technique, speciation of organic and elemental carbon is accomplished through temperature and atmosphere control, and by an optical feature that corrects for pyrolytically generated carbon, or “char,” which is formed during the analysis of some materials. The therma...