Long-term Air Pollution Exposure and Acceleration of Atherosclerosis and Vascular Inflammation in an Animal Model

Sun, Qinghua

doi:10.1001/jama.294.23.3003

Cited by 754 publications

(552 citation statements)

References 35 publications

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“…Sun et al (27,28) used an apolipoprotein E knockout (ApoE -/-) mouse model to show that long-term exposure to low concentrations of PM 2.5 (particles smaller than 2.5 µm in diameter) altered vasomotor tone, and increased tissue-factor expression, vascular inflammation and atherosclerotic burden in these animals. Research at the Lovelace Respiratory Research Institute (New Mexico, USA) in ApoE -/-mice has shown vascular remodelling and altered atherosclerotic plaque composition following PM 10 exposure and diesel emission exposure (29)(30)(31).…”

Section: Méthodologie : Les Lapins Whlh (N=8) Exposés à 5 Mg De Partimentioning

confidence: 99%

Ultrastructural changes in atherosclerotic plaques following the instillation of airborne particulate matter into the lungs of rabbits

Tranfield

Eeden

Yatera

et al. 2010

Canadian Journal of Cardiology

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Section: Méthodologie : Les Lapins Whlh (N=8) Exposés à 5 Mg De Partimentioning

confidence: 99%

Ultrastructural changes in atherosclerotic plaques following the instillation of airborne particulate matter into the lungs of rabbits

Tranfield

Eeden

Yatera

et al. 2010

Canadian Journal of Cardiology

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“…A sudden surge in the level of PM has been linked to increased morbidity and mortality due to cardiorespiratory events, including asthma, chronic obstructive pulmonary disease (COPD), and atherosclerosis [1][2][3][4][5][6][7][8][9][10][11][12]. Both in vitro and in vivo studies of the health effects of ambient PM have identified the generation of oxidative stress as one of the major mechanisms by which air pollution particles exert adverse biological effects.…”

Section: Introductionmentioning

confidence: 99%

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Xia

Nel

2008

Free Radical Biology and Medicine

820

529

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Ambient particulate matter (PM) is an environmental factor that has been associated with increased respiratory morbidity and mortality. The major effect of ambient PM on the pulmonary system is the exacerbation of inflammation, especially in susceptible people. One of the mechanisms by which ambient PM exerts its proinflammatory effects is the generation of oxidative stress by its chemical compounds and metals. Cellular responses to PM-induced oxidative stress include activation of antioxidant defense, inflammation, and toxicity. The pro-inflammatory effect of PM in the lung is characterized by increased cytokine/chemokine production and adhesion molecule expression. Moreover, there is evidence that ambient PM can act as an adjuvant for allergic sensitization, which raises the possibility that long-term PM exposure may lead to increased prevalence of asthma. In addition to ambient PM, rapid expansion of nanotechnology has introduced the potential that engineered NP may also become airborne and may contribute to pulmonary diseases by novel mechanisms that could include oxidant injury. Currently, little is known about the potential adverse health effect of these particles. In this communication, the mechanisms by which particulate pollutants, including ambient PM and engineered NP, exert their adverse effects through the generation of oxidative stress and the impacts of oxidant injury in the respiratory tract will be reviewed. The importance of cellular antioxidant and detoxification pathways in protecting against particle-induced lung damage will also be discussed.

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“…Several potential mechanism have been postulated to cause the increase in atherotrombotic events, such as activation of inflammatory pathways, production of reactive oxygen species and alterations in vascular tone (Pope CA et al, 2004). There is another study showing that fine particulate exposure accelerates the development of atherosclerosis in animal model (Sun Q et al, 2005).…”

Section: Air Pollution and Cardiovascular Diseases (Cvd)mentioning

confidence: 99%

Particulate matter phagocytosis induces tissue factor in differentiating macrophages

Milano

Dongiovanni

Artoni

et al. 2015

J of Applied Toxicology

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Airborne exposure to particulate matter with diameter < 10 mcM (PM10) has been linked to an increased risk of thromboembolic events, but the mechanisms are not completely understood. The aim of this study was to evaluate the effect of PM10 phagocytosis on the release of procoagulant molecules in human differentiating macrophages, and that of PM10 inhalation in an experimental model in rats. Human monocytes were separated from the peripheral blood by the lymphoprep method, differentiated in vitro and treated with standard PM10 or vehicle. Sprague–Dawley rats were instilled intratracheally with PM10 or vehicle alone. The outcome was expression of proinflammatory genes and of tissue factor (TF). In human differentiating macrophages, PM10 exposure upregulated inflammatory genes, but most consistently induced TF mRNA and protein levels, but not TF protein inhibitor, resulting in increased TF membrane expression and a procoagulant phenotype. Differentiation towards the anti‐inflammatory M2 phenotype inhibited PM10‐mediated TF expression. TF induction required phagocytosis of PM10, whereas phagocytosis of inert particles was less effective. PM10 phagocytosis was associated with a gene expression profile consistent with intracellular retention of iron, inducing oxidative stress. Both PM10 and iron activated the stress kinases ERK1/2 pathway, involved in the induction of TF expression. In rats, alveolar exposure to PM10 was associated with pulmonary recruitment of inflammatory cells and resulted in local, but not systemic, induction of TF expression, which was sufficient to increase circulating TF levels. In conclusion, TF induction by differentiating lung macrophages, activated following phagocytosis, contributes to the increased risk of thromboembolic complications associated with PM10 exposure. Copyright © 2015 John Wiley & Sons, Ltd.

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Long-term Air Pollution Exposure and Acceleration of Atherosclerosis and Vascular Inflammation in an Animal Model

Abstract: In an apoE-/- mouse model, long-term exposure to low concentration of PM2.5 altered vasomotor tone, induced vascular inflammation, and potentiated atherosclerosis.

Cited by 754 publications

References 35 publications

Ultrastructural changes in atherosclerotic plaques following the instillation of airborne particulate matter into the lungs of rabbits

Ultrastructural changes in atherosclerotic plaques following the instillation of airborne particulate matter into the lungs of rabbits

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Particulate matter phagocytosis induces tissue factor in differentiating macrophages

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