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Cardiac Effects of Seasonal Ambient Particulate Matter and Ozone Co-exposure in Rats
Farraj, A., L. Walsh, N. Coates, F. Malik, J. Mcgee, D. Winsett, R. Duvall, K. Kovalcik, W. Cascio, M. Higuchi, AND M. Hazari. Cardiac Effects of Seasonal Ambient Particulate Matter and Ozone Co-exposure in Rats. Particle and Fibre Toxicology. BioMed Central Ltd, London, Uk, 12(1):12, (2015).
These findings collectively point to a marked effect of season on PM mass, size, composition, and contributing sources, with commensurate impact on cardiovascular responses. While there was variability in some responses, ambient particulate matter and O3 co-exposures during both seasons in this study caused more electrocardiographic and autonomic responses than exposure to either pollutant alone. Thus, these findings suggest that a multipollutant approach to health affects assessment should be considered. Moreover, seasonal variability in sources of anthropogenic emissions and evidence for winter elemental enrichment and smaller particle size suggests that PM size and composition may be as important as mass in determining health impacts from exposure. Future studies need to examine this possibility especially in light of the current US EPA National Ambient Air Quality Standards for PM, which are based on mass.
BackgroundThe potential for seasonal differences in the physicochemical characteristics of ambient particulate matter (PM) to modify interactive effects with gaseous pollutants has not been thoroughly examined. The purpose of this study was to compare cardiac responses in conscious hypertensive rats co-exposed to concentrated ambient particulates (CAPs} and ozone (03} in Durham, NC during the summer and winter, and to analyze responses based on particle mass and chemistry.MethodsRats were exposed once for 4 hrs by whole-body inhalation to fine CAPs alone (target concentration: 150 µg/m3), 03 (0.2 ppm) alone, CAPs plus 03,or filtered air during summer 2011 and winter 2012. Telemetered efectrocardiographic (ECG) data from implanted biosensors were analyzed for heart rate (HR), ECG parameters, heart ratevariability (HRV), and spontaneous arrhythmia. The sensitivity to triggering of arrhythmia was measured in a separate cohort one day after exposure using intravenously administered aconitine. PM elemental composition and organic and elemental carbon fractions were analyzed by high resolution inductively coupled plasma-mass spectrometry and thermo-optical pyrolytic vaporization, respectively. Particulate sources were inferred from elemental analysis using a chemical mass balance model.ResultsSeasonal differences in CAPs composition were most evident in particle mass concentrations (summer, 171 µg/m3; winter, 85 µg/m3 ), size (summer, 324 nm; winter, 125 nm), organic: elemental carbon ratios (summer, 16.6; winter, 9.7), and sulfate levels (summer, 49.1 µg/m3; winter, 16.8 µg/m3 ). Enrichment of metals in winter PM resulted in equivalent summer and winter metal exposure concentrations. Source apportionment analysis showed enrichment for anthropogenic and marine salt sourcesduring winter exposures compared to summer exposures, although only 4 % of the total PM mass was attributed to marine salt sources. Single pollutant cardiovascular effects with CAPS and O3 were present during both summer and winter exposures, with evidence for unique effects of co-exposures and associated changes In autonomictone.ConclusionsThese findings provide evidence for a pronounced effect of season on PM mass, size, composition, and contributing sources, and exposure-induced cardiovascular responses. Although there was inconsistency in biological responses, some cardiovascular responses were evident only in the co-exposure group during both seasons despite variability in PM physicochemical composition. These findings suggest that a single ambient PM metric alone is not sufficient to predict potential for interactive health effects with other air pollutants.
Record Details:Record Type: DOCUMENT (JOURNAL/PEER REVIEWED JOURNAL)
Organization:U.S. ENVIRONMENTAL PROTECTION AGENCY
OFFICE OF RESEARCH AND DEVELOPMENT
NATIONAL HEALTH AND ENVIRONMENTAL EFFECTS RESEARCH LABORATORY
ENVIRONMENTAL PUBLIC HEALTH DIVISION
CARDIOPULMONARY AND IMMUNOTOXICOLOGY BRANCH