Effects of Subchronic Exposures to Concentrated Ambient Particles (CAPs) in Mice: V. CAPs Exacerbate Aortic Plaque Development in Hyperlipidemic Mice

Chen, Lung Chi; Nadziejko, Christine

doi:10.1080/08958370590912815

Cited by 154 publications

(70 citation statements)

References 30 publications

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“…The present results confirm a previous report from our laboratory showing that exposure to ambient particulate matter (PM 10 ) accelerates the progression of atherosclerosis over the surface of the aorta and into the aortic wall of Watanabe rabbits (45), and a recent study from another laboratory in Apo-E mice supports this notion (7). They extend these novel findings by showing that circulating monocytes are recruited into the plaques to a greater degree in the PM 10 -exposed animals than in the control animals.…”

Section: Discussionsupporting

confidence: 82%

“…5). These molecules are known to promote monocyte adhesion to endothelium and migration into atherosclerotic plaques (2,7,21,37,44) via a mechanism that involves ligation of Mac-1 (CD11b/CD18 or ␣ M ␤ 2 ) and CD49d/CD29 (VLA-4) on the monocyte surface to ICAM-1 and VCAM-1 on the endothelial cells, respectively. Proinflammatory mediators responsible for endothelial activation may originate either from the lung or from circulating leukocytes such as monocytes.…”

Section: Discussionmentioning

confidence: 99%

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Particulate matter air pollution exposure promotes recruitment of monocytes into atherosclerotic plaques

Yatera

Hsieh²,

Hogg³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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demiologic studies have shown an association between exposure to ambient particulate air pollution Ͻ10 m in diameter (PM10) and increased cardiovascular morbidity and mortality. We previously showed that PM10 exposure causes progression of atherosclerosis in coronary arteries. We postulate that the recruitment of monocytes from the circulation into atherosclerotic lesions is a key step in this PM10-induced acceleration of atherosclerosis. The study objective was to quantify the recruitment of circulating monocytes into vessel walls and the progression of atherosclerotic plaques induced by exposure to PM10. Female Watanabe heritable hyperlipidemic rabbits, which naturally develop systemic atherosclerosis, were exposed to PM10 (EHC-93) or vehicle by intratracheal instillation twice a week for 4 wk. Monocytes, labeled with 5-bromo-2Ј-deoxyuridine (BrdU) in donors, were transfused to recipient rabbits as whole blood, and the recruitment of BrdU-labeled cells into vessel walls and plaques in recipients was measured by quantitative histological methodology. Exposure to PM10 caused progression of atherosclerotic lesions in thoracic and abdominal aorta. It also decreased circulating monocyte counts, decreased circulating monocytes expressing high levels of CD31 (platelet endothelial cell adhesion molecule-1) and CD49d (very late antigen-4 ␣-chain), and increased expression of CD54 (ICAM-1) and CD106 (VCAM-1) in plaques. Exposure to PM10 increased the number of BrdU-labeled monocytes adherent to endothelium over plaques and increased the migration of BrdU-labeled monocytes into plaques and smooth muscle underneath plaques. We conclude that exposure to ambient air pollution particles promotes the recruitment of circulating monocytes into atherosclerotic plaques and speculate that this is a critically important step in the PM10-induced progression of atherosclerosis. atherosclerosis; adhesion molecules EPIDEMIOLOGIC STUDIES have associated exposure to ambient particulate air pollution Ͻ10 m in diameter (PM 10

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Particulate matter air pollution exposure promotes recruitment of monocytes into atherosclerotic plaques

Yatera

Hsieh²,

Hogg³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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“…The first subchronic study, conducted in Tuxedo, NY, in spring/summer 2003, consisted of 5-6 months of daily exposures (5 days/week, 6 hr/day) in ApoE −/-mice. Results of this large study were reported in a special issue of Inhalation Toxicology Hwang et al, 2005;Chen and Hwang, 2005;Chen and Nadziejko, 2005;Gunnison and Chen, 2005;Veronesi et al, 2005;Lippmann et al, 2005aLippmann et al, , 2005b. However, none of these papers evaluated the potential influence of CAPs composition on longterm biological responses.…”

Section: Toxicological Studiesmentioning

confidence: 99%

Long-term particulate matter exposure: Attributing health effects to individual PM components

Wyzga

Rohr

2015

Journal of the Air & Waste Management Association

122

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While most in the scientific community are of the opinion that the composition of fine particulate matter (PM 2.5 ) is an important driver of resultant health effects, there is still some degree of uncertainty regarding those components considered to be most harmful. Reviews of the subject from several perspectives have been published, but to our knowledge a comprehensive review of the epidemiological and toxicological literature related to long-term exposure to PM 2.5 components does not exist. We reviewed published epidemiological studies that were of a cohort design, included at least one PM component as well as PM 2.5 mass, and included quantitative analysis to relate health outcomes to individual components. Toxicological studies were included if they were ≥5 months in duration and either included at least one PM component as well as PM mass or focused on a specific PM or emissions type. Overall, we find that epidemiological and toxicological evidence for long-term effects of PM components is limited, in contrast to the short-term literature, which is more plentiful. Epidemiological literature suggests that a number of components are associated with health effects, and that no component is unequivocally not so associated. Toxicological studies that can more easily identify potentially causal components are generally limited to long-term studies using concentrated ambient particles (CAPs), of which few long-term studies exist. Epidemiological study designs that utilize existing monitoring data routinely collected by the U.S. Environmental Protection Agency would be valuable additions to the literature, as would novel toxicological studies that incorporate innovative designs to separate components or groups of components, such as denuders, filtration, or other approaches. From a policy perspective, it is important to more comprehensively investigate this issue so that if particular constituents are determined to be more potent in inducing health effects, their sources can be controlled.Implications: Understanding the components of PM 2.5 that are most harmful to human health is a critical policy issue. This review examined the epidemiological and toxicological literature related to long-term exposure to PM components and found that, unlike the literature on short-term health effects, there is insufficient information to make clear inferences about causal components. There is a need for further research in this area to exploit existing PM monitoring data in epidemiological studies and to design experimental studies that are able to tease out the effects of multiple constituents.

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“…Animal studies demonstrate a link between chronic PM exposure and the development of atherosclerosis via systemic inflammation [11,12]. Human studies show that the effects appear to be mediated by the inflammatory cytokines IL-6, TNF-ά, and Creactive protein (CRP).…”

Section: Cardiovascular Mechanismsmentioning

confidence: 99%

Clearing the Air: A Review of the Effects of Particulate Matter Air Pollution on Human Health

2011

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The World Health Organization estimates that particulate matter (PM) air pollution contributes to approximately 800,000 premature deaths each year, ranking it the 13th leading cause of mortality worldwide. However, many studies show that the relationship is deeper and far more complicated than originally thought. PM is a portion of air pollution that is made up of extremely small particles and liquid droplets containing acids, organic chemicals, metals, and soil or dust particles. PM is categorized by size and continues to be the fraction of air pollution that is most reliably associated with human disease. PM is thought to contribute to cardiovascular and cerebrovascular disease by the mechanisms of systemic inflammation, direct and indirect coagulation activation, and direct translocation into systemic circulation. The data demonstrating PM's effect on the cardiovascular system are strong. Populations subjected to long-term exposure to PM have a significantly higher cardiovascular incident and mortality rate. Short-term acute exposures subtly increase the rate of cardiovascular events within days of a pollution spike. The data are not as strong for PM's effects on cerebrovascular disease, though some data and similar mechanisms suggest a lesser result with smaller amplitude. Respiratory diseases are also exacerbated by exposure to PM. PM causes respiratory morbidity and mortality by creating oxidative stress and inflammation that leads to pulmonary anatomic and physiologic remodeling. The literature shows PM causes worsening respiratory symptoms, more frequent medication use, decreased lung function, recurrent health care utilization, and increased mortality. PM exposure has been shown to have a small but significant adverse effect on cardiovascular, respiratory, and to a lesser extent, cerebrovascular disease. These consistent results are shown by multiple studies with varying populations, protocols, and regions. The data demonstrate a dose-dependent relationship between PM and human disease, and that removal from a PM-rich environment decreases the prevalence of these diseases. While further study is needed to elucidate the effects of composition, chemistry, and the PM effect on susceptible populations, the preponderance of data shows that PM exposure causes a small but significant increase in human morbidity and mortality. Most sources agree on certain "common sense" recommendations, although there are lonely limited data to support them. Indoor PM exposure can be reduced by the usage of air conditioning and particulate filters, decreasing indoor combustion for heating and cooking, and smoking cessation. Susceptible populations, such as the elderly or asthmatics, may benefit from limiting their outdoor activity during peak traffic periods or poor air quality days. These simple changes may benefit individual patients in both short-term symptomatic control and long-term cardiovascular and respiratory complications.

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Effects of Subchronic Exposures to Concentrated Ambient Particles (CAPs) in Mice: V. CAPs Exacerbate Aortic Plaque Development in Hyperlipidemic Mice

Cited by 154 publications

References 30 publications

Particulate matter air pollution exposure promotes recruitment of monocytes into atherosclerotic plaques

Particulate matter air pollution exposure promotes recruitment of monocytes into atherosclerotic plaques

Long-term particulate matter exposure: Attributing health effects to individual PM components

Clearing the Air: A Review of the Effects of Particulate Matter Air Pollution on Human Health

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