The Effect of Urban Air Pollution on Inflammation, Oxidative Stress, Coagulation, and Autonomic Dysfunction in Young Adults

Chuang, Kai Jen; Chan, Chang-Chuan; Su, Ta-Chen; Lee, Chung Te; Tang, Chin-Sheng

doi:10.1164/rccm.200611-1627oc

Cited by 598 publications

(423 citation statements)

References 49 publications

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“…Our results are largely consistent with recent repeated measures studies showing associa tions between ambient air pollution and bio markers of systemic inflammation in healthy young adults (Chuang et al 2007) and sus ceptible subjects with CAD (Dubowsky et al 2006;Rückerl et al 2006Rückerl et al , 2007a2007b;Yue et al 2007). We extended these previous find ings with data from intensive home exposure assessments and modeling that provided clues to potentially causal pollutant components.…”

Section: Discussionsupporting

confidence: 92%

Air Pollution Exposures and Circulating Biomarkers of Effect in a Susceptible Population: Clues to Potential Causal Component mixtures and mechanisms

Delfino¹,

Staimer²,

Tjoa³

et al. 2009

Environ Health Perspect

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Section: Discussionsupporting

confidence: 92%

Air Pollution Exposures and Circulating Biomarkers of Effect in a Susceptible Population: Clues to Potential Causal Component mixtures and mechanisms

Delfino¹,

Staimer²,

Tjoa³

et al. 2009

Environ Health Perspect

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“…54 Several studies have demonstrated an association between PM exposure and plasma PAI-1 levels in humans and in mice. 51,55 In this study, we detected only a slight increase of circulating PAI-1 but a 3-fold increase of the lung PAI-1 level after PM 2.5 exposure, indicating that the dose of PM 2.5 exposure (100 g/mouse) used in our studies is not sufficient to trigger systemic coagulation responses, but potent enough to induce localized lung pathologic changes. Although there was no significant difference in plasma PAI-1 levels between Sirt1 Ϫ/Ϫ and Sirt1 ϩ/ϩ littermates, lung PAI-1 level was higher in Sirt1 Ϫ/Ϫ mice after PM 2.5 treatment, indicating that Sirt1 deletion may lead to abnormal lung PAI-1 expression.…”

Section: Sirt1 Controls Lung Inflammation and Coagulation 2427mentioning

confidence: 53%

Sirt1 protects against thrombomodulin down-regulation and lung coagulation after particulate matter exposure

Liu

Liang

et al. 2012

Blood

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Exposure to ambient particulate matter (PM) air pollution has been reported to trigger inflammation and thrombosis. However, molecular mechanisms underlying the modulation of coagulation pathways in PM-induced thrombosis remain largely unknown. We report here that Sirt1, a member of class III histone deacetylase, controls lung inflammation and coagulation after PM exposure. Sirt1 knock-out mice exhibited aggravated lung vascular leakage and inflammation after PM exposure, which was correlated with increased NF-B acetylation and activation. Furthermore, Sirt1 knock-out mice were highly susceptible to PM-induced lung coagulation as demonstrated by increased fibrin formation. The increased fibrin formation was associated with reduced tissue factor pathway inhibitor (TFPI) expression and increased plasminogen activator inhibitor-1 (PAI-1) activity in the lungs, thus favoring elevated coagulation and disrupted fibrinolysis responses. Thrombomodulin (TM), a central player of the anticoagulant protein C system, is regulated by Kruppel-like factor 2 (KLF2) at the transcriptional level. IntroductionExposure to ambient particulate matter (PM) air pollution has been associated with impaired pulmonary function and increased cardiovascular disease-related mortality including inflammation and thrombosis. 1-5 Acute exposure to increased ambient fine particulate matter Ͻ 2.5 m in diameter (PM 2.5 ) was estimated to cause the premature deaths of tens of thousands of people each year in the United States. 6 Urban particulate matter (UPM) PM 2.5, one of the major air pollutants closely monitored by the US Environmental Protection Agency (EPA), is a complex mixture of substances that are directly emitted into the air from dust, soot, smoke, and combustion. 6 To protect public health, the EPA issued the current 24-hour PM 2.5 standard at 35 g/m 3 . 6 Despite the enormous health problems caused by PM 2.5 exposure, there have been few studies performed to explore the molecular mechanisms of PM 2.5 -induced lung vascular dysfunction. PM 2.5 can reach deep in the lung to the small airway and alveoli, 6 and directly cause lung inflammation and injury. [7][8][9][10][11][12][13] The pulmonary complications may lead to detrimental effects on other organs, particularly cardiovascular dysfunction such as systemic microvascular dysfunction and thrombosis. 1,2,4,5,13 A recent study demonstrated that short-term UPM exposure triggered the activation of primary hemostasis in healthy mice, with no substantial secondary hemostasis activation, leading to arterial but not venous thrombosis. 5 Whereas another study showed that short-term UPM exposure may cause activation of coagulation responses and fibrin formation in the lung. 14 Tissue factor pathway inhibitor (TFPI) and plasminogen activator inhibitor-1 (PAI-1) play important roles in coagulation and fibrinolysis cascades, respectively. TFPI is an inhibitor of tissue factor (TF)-mediated coagulation responses. 15 PAI-1, on the other hand, is a major regulator of fibrinolysis, which functions by in...

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“…Based on these results, it would appear that air pollution may determine short-term hypercoagulability, which in turn contributes to the increase in atherothrombotic cardiovascular events observed in the presence of high ambient concentrations of pollutants. The influence of ambient air pollution on inflammation, oxidative stress, blood coagulation and autonomic function was also investigated in 76 young healthy adults from Taiwan by Chuang et al [66], who found that increases in PM 10 , PM 2.5 , sulfate, nitrate and O 3 were associated with increases in C-reactive protein, 8-hydroxy-2¢-deoxyguanosine (an oxidative stress marker), fibrinogen, plasminogen activator inhibitor-1 and decreased heart rate variability. The same author had previously found that urban air pollution increased plasma fibrinogen and plasminogen activator inhibitor-1 in patients with, or at risk of, cardiovascular disease [67].…”

Section: Potential Mechanismsmentioning

confidence: 99%

Short‐term effects of air pollution on cardiovascular diseases: outcomes and mechanisms

Franchini¹,

Mannucci

2007

Journal of Thrombosis and Haemostasis

123

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Summary. The effects of air pollution on health have been intensively studied in recent years. Acute exposure to environmental pollutants such as particulate and gaseous matters (carbon monoxide, nitrogen oxides, sulphur dioxide and ozone) was associated with an increased rate of events and mortality because of cardiovascular diseases. These effects were investigated in short‐term studies, which related day‐to‐day variations in air pollution to disease, and in long‐term studies, which have followed cohorts of exposed individuals over time. The evidence from the literature on the short‐term cardiovascular effects of air pollutants is discussed from clinical and mechanistic points of view.

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The Effect of Urban Air Pollution on Inflammation, Oxidative Stress, Coagulation, and Autonomic Dysfunction in Young Adults

Abstract: Urban air pollution is associated with inflammation, oxidative stress, blood coagulation and autonomic dysfunction simultaneously in healthy young humans, with sulfate and O(3) as two major traffic-related pollutants contributing to such effects.

Cited by 598 publications

References 49 publications

Air Pollution Exposures and Circulating Biomarkers of Effect in a Susceptible Population: Clues to Potential Causal Component mixtures and mechanisms

Air Pollution Exposures and Circulating Biomarkers of Effect in a Susceptible Population: Clues to Potential Causal Component mixtures and mechanisms

Sirt1 protects against thrombomodulin down-regulation and lung coagulation after particulate matter exposure

Short‐term effects of air pollution on cardiovascular diseases: outcomes and mechanisms

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