American Association for Aerosol Research - Abstract Submission

AAAR 33rd Annual Conference
October 20 - October 24, 2014
Rosen Shingle Creek
Orlando, Florida, USA

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Linking Air Pollution and Health Effects: The Role of Semi-volatile Components of Ultrafine Ambient Particles

MICHAEL KLEINMAN, Andrew Keebaugh, David Herman, Vishal Verma, Payam Pakbin, Loyda Mendez, Constantinos Sioutas, University of California, Irvine

     Abstract Number: 97
     Working Group: Linking Aerosols with Public Health in a Changing World

Abstract
Air pollution exposure is associated with increased incidence of cardiovascular disease. Effects include increased daily mortality and hospital admissions. Urban airborne ultrafine PM contains semi-volatile organics (SVOCs) which have a high proportion of redox active compounds that can be bound to particles or can partition to the vapor phase after emission where they may be responsible for some of the observed exacerbation of PM-associated adverse cardiovascular health effects. Therefore, we hypothesized that the removal of SVOCs from an aerosol should decrease the ability of ultrafine PM to cause oxidative damage and reduce adverse cardiovascular effects including development of atherosclerotic plaque, induction of cardiac abnormalities measured by changes in electrocardiogram (ECG) waveform morphology and arrhythmias and losses of heart rate variability (HRV). Groups of genetically altered ApoE -/- mice (prone to developing atherosclerosis) were exposed to either purified air, quasi-ultrafine concentrated ambient particles (CAPs; under 0.18µm aerodynamic diameter), or to thermally denuded CAPs (deCAPs) from which SVOCs were removed from the particle core using a thermal denuder. The mice were exposed 5 hours/day, 4 days/week for 8 weeks in downtown Los Angeles, about 100m downwind of a major freeway. Implanted cardiac transducers monitored ECGs from the mice. The ECGs were analyzed to detect changes in HRV and abnormal waveforms including ischemia-related changes and arrhythmias. Histological and biochemical examination showed that CAPs exposed mice exhibited significantly more arterial atherosclerotic plaque than did deCAP or Air-exposed mice. They also exhibited progressive HRV losses that were accompanied by ischemia-related changes in ECG waveforms not seen in deCAPs or Air exposed mice. Losses of HRV and arrhythmias are common measures of myocardial dysfunction in humans associated with life-threatening cardiac events precipitated by atherosclerosis. Further investigation into the observed changes need be performed to explicate the mechanisms of the changes resulting from CAPs exposures.