2002
DOI: 10.1289/ehp.5646
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Personal PM2.5 Exposure and Markers of Oxidative Stress in Blood

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Cited by 208 publications
(102 citation statements)
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References 32 publications
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“…30 The third (and most plausible hypothesis) is predicated on the premise that airborne particulates enter the bloodstream where they may then interact with tissue components to promote the observed pathologic effects 30,31 ; the latter is supported by emerging evidence suggesting that inhaled inert gold nanoparticles not only enter the bloodstream of healthy adult volunteers, but are detected in the urine within minutes after exposure, providing a proof of concept that inhaled nanoparticles get filtered and excreted by the kidney. 31 These three hypotheses provide contextual background to evaluate the experimental and clinical findings describing the extrapulmonary effect of particulate matter air pollution, where it has been reported that exposure to elevated levels of PM 2.5 is associated with increased inflammatory mediators (including TNF-a, IL-6, and plasminogen activator inhibitor-1), oxidative stress, [32][33][34] increased atherosclerotic plaque area, and exaggerated vasoconstrictor responses to phenylephrine and serotonin. 35 Evidence suggests that increased PM 2.5 concentrations are associated with significant decrease in flow-mediated dilatation, 36,37 increases in systolic BP and pulse pressure, [38][39][40] and disturbances in the hypothalamic-pituitary-adrenal axis.…”
Section: Discussionmentioning
confidence: 99%
“…30 The third (and most plausible hypothesis) is predicated on the premise that airborne particulates enter the bloodstream where they may then interact with tissue components to promote the observed pathologic effects 30,31 ; the latter is supported by emerging evidence suggesting that inhaled inert gold nanoparticles not only enter the bloodstream of healthy adult volunteers, but are detected in the urine within minutes after exposure, providing a proof of concept that inhaled nanoparticles get filtered and excreted by the kidney. 31 These three hypotheses provide contextual background to evaluate the experimental and clinical findings describing the extrapulmonary effect of particulate matter air pollution, where it has been reported that exposure to elevated levels of PM 2.5 is associated with increased inflammatory mediators (including TNF-a, IL-6, and plasminogen activator inhibitor-1), oxidative stress, [32][33][34] increased atherosclerotic plaque area, and exaggerated vasoconstrictor responses to phenylephrine and serotonin. 35 Evidence suggests that increased PM 2.5 concentrations are associated with significant decrease in flow-mediated dilatation, 36,37 increases in systolic BP and pulse pressure, [38][39][40] and disturbances in the hypothalamic-pituitary-adrenal axis.…”
Section: Discussionmentioning
confidence: 99%
“…Contrariando esses achados, um estudo na Dinamarca em 50 universitários com idade entre 20-33 anos encontrou associações positivas entre exposição pessoal ao material particulado (particulate matter) ≤ 2,5 µm (PM 2,5 ) e concentração de GV e hemoglobina apenas em estudantes do sexo feminino 27 . A diferença entre os nossos achados e os desse estudo pode ser decorrente da nossa impossibilidade de medir partículas ultrafinas, apesar de, como um estudo na Guatemala descobriu, haver associação entre exposição à poluição do ar interna resultante da queima de combustíveis de biomassa e elevação na concentração de hemoglobina 28 .…”
Section: Discussionunclassified
“…3a) (Hristov 2011). Several studies have found that PM 2.5 may deposit in the lungs, causing oxidative stress and possibly leading to increased morbidity (Riva et al 2011;Sorensen et al 2003). However, the toxicity of PM 2.5 seems to largely depend on the specific composition (Schlesinger 2007).…”
Section: The Soil Microbiome and The N-cyclementioning
confidence: 99%