title: Is atherosclerotic disease associated with organic components of ambient fine particles?
abstract: Heart disease is a major killer in western societies; coronary artery disease and atherosclerosis are important contributors to this mortality. Atherosclerosis in mice with a deleted apoE gene (apoE-/-) is accelerated by exposure to ambient ultrafine particles (UFP) which are particles smaller than 180 nm in diameter. UFP contain organic components that are pro-oxidant and may cause or aggravate heart disease. Could removal of these organic constituents mitigate adverse cardiovascular effects? ApoE-/- mice were exposed to concentrated UFP (CAP), CAP from which organic constituents were removed by thermal denuding (deCAP) or purified air (controls) for 5 hr/day, 4 days/week for 8 weeks. Heart rate (HR), heart rate variability (HRV), biomarkers of oxidative stress and the sizes of arterial plaques were measured. Adverse effects were seen in CAP-exposed mice (increased size of arterial plaque, increased oxidative stress and decreased HRV, compared to controls). Adverse effects were not observed in deCAP-exposed mice. Removal of organic constituents from ambient particles resulted in significant reduction of toxic cardiovascular effects of air pollution exposure.
authors.affiliation: Occupational and Environmental Medicine Division, Department of Medicine, School of Medicine, University of California, Irvine (UCI), Irvine, CA, USA.
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Keebaugh
authors.affiliation: Department of Civil and Environmental Engineering, Viterbi School of Engineering, University of Southern California, Los Angeles, CA, USA.
authors.forename: Constantinos
authors.initials: C
authors.lastname: Sioutas
authors.affiliation: Department of Civil and Environmental Engineering, Viterbi School of Engineering, University of Southern California, Los Angeles, CA, USA.
authors.forename: Payam
authors.initials: P
authors.lastname: Pakbin
authors.affiliation: Department of Civil and Environmental Engineering, College of Engineering, University of Wisconsin, Madison, Madison WI, USA.
authors.forename: James J
authors.initials: JJ
authors.lastname: Schauer
authors.affiliation: School of Science and Technology, Universidad del Este, Carolina, PR, USA.
authors.forename: Loyda B
authors.initials: LB
authors.lastname: Mendez
authors.affiliation: Occupational and Environmental Medicine Division, Department of Medicine, School of Medicine, University of California, Irvine (UCI), Irvine, CA, USA. Electronic address: mtkleinm@uci.edu.
authors.forename: Michael T
authors.initials: MT
authors.lastname: Kleinman
mesh_terms: D000393:Air Pollutants / Q000633:toxicity*; D000397:Air Pollution; D000818:Animals; D001057:Apolipoproteins E; D050197:Atherosclerosis / Q000139:chemically induced*; D019570:Inhalation Exposure; D051379:Mice; D018384:Oxidative Stress; D052638:Particulate Matter / Q000633:toxicity*
chemical_list: D000393:Air Pollutants; D001057:Apolipoproteins E; D052638:Particulate Matter
keywords: Ambient PM; atherosclerosis; cardiovascular disease; heart rate variability