UC Irvine

Introduction: Chronic exposure to particulate matter (PM) has been associated with increased risks for several cardiovascular (CV) diseases which can culminate in higher morbidity and mortality. This research will test the effects of particle chemistry on the mouse electrocardiogram (ECG) by investigating adverse cardiac outcomes following exposures 1) during different seasons (winter/summer), and 2) to whole concentrated ambient particle (CAPs; containing organic species) or denuded CAPs (DeCAPs; PM thermally stripped of organic species) with/without the addition of ozone (O3), a ubiquitous environmental pollutant.

Methods: A Versatile Aerosol Concentration Enrichment System (VACES) was used to concentrated PM atmospheres. Hyperlipidemic mice (apoE-/-) were exposed via whole body inhalation chambers for 5 hrs./day, 4 days/wk. All ECG parameters were acquired from freely moving, conscious mice and assessed at the same time every evening. An aerosol mass spectrometer (AMS) provided single-particle size and chemical composition as well as cumulative size-classified mass concentrations in real-time for non-refractory sub-micron aerosol particles. The oxidative potential of different types of PM was analyzed using the antioxidant enzymes glutathione peroxidase (GPx) and glutathione reductase (GR).

Results: Electrocardiogram (ECG) anomalies were exacerbated during periods with high ambient O3 levels suggesting that increased atmospheric interaction with O3 and other atmospheric pollutants generates more biologically active PM. CAPs exposure was found to be more cardiotoxic than DeCAPs exposure. Adding O3 to either CAPs or DeCAPs failed to elicit more severe adverse health effects compared to single pollutant exposures. Particles containing semi-volatile organic compounds (SVOCs) produced dissimilar inhibitory responses in GPx and GR suggesting that oxidative stress could be altered via GSH accumulation. Levels of enzymatic impairment were similar in response to PM+O3 mixtures regardless of PM-bound SVOCs present suggesting that O3 is reacting with a more stable PM-bound constituents.

Conclusion: This report describes how inhaled ambient PM is linked to alterations in cardiac electrophysiology and provides useful insight into particle characterization and cardiac dysfunction in relation to specific PM fractions and/or PM+O3 mixtures. Information about particle oxidative stress would be a valued addition to air quality legislation which currently relies on particle size as a main toxicological risk factor.