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Chapter 8

Ultrafine Particles and Atherosclerosis

Air Pollution has been associated with significant adverse health effects leading to increased cardiovascular morbidity and mortality. Epidemiological studies support the association of exposure to air particulate matter with atherosclerosis, to the extent that PM exposure can be regarded as a cardiovascular risk factor. Experimental animal work has demonstrated that this association is likely causal. The proatherogenic potential of ambient particles appears to depend on their ability to elicit systemic prooxidative and proinflammatory effects. Particle size and chemical composition seem to be important in determining their prooxidative properties. We have reported that ultrafine particles (>0.18 ┬Ám) enhance early atherosclerosis, partly due to their high content in redox cycling chemicals and their ability to synergize with known mediators in the activation of proatherogenic molecular pathways. These effects take place in parallel with increased evidence of phase 2 enzymes expression, via the electrophile-sensitive transcription factor, p45-NFE2 related transcription factor 2 (Nrf2). Exposure to ultrafine particles also results in alterations of the plasma HDL antiinflammatory function that could be indicative of systemic proatherogenic effects. This article reviews the epidemiological, clinical and experimental animal evidence that support the association of particulate matter, especially in the ultrafine size range, with systemic oxidative stress and atherosclerosis

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Print publication date
03 Dec 2010
Copyright year
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From the book series:
Issues in Toxicology