American Association for Aerosol Research - Abstract Submission

AAAR 37th Annual Conference
October 14 - October 18, 2019
Oregon Convention Center
Portland, Oregon, USA

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New Approach for Source Apportionment of Toxicity by Atmospheric Organic Aerosols

AKIHIRO FUSHIMI, Daisuke Nakajima, Akiko Furuyama, Go Suzuki, Tomohiro Ito, Kei Sato, Yuji Fujitani, Yoshinori Kondo, Akinori Takami, National Institute for Environmental Studies, Japan

     Abstract Number: 228
     Working Group: From Aerosol Dosimetry and Toxicology to Health

Abstract
Fine particulate matter (PM2.5) in the atmosphere is of high priority for air quality management efforts due to observed associations with adverse effects on human health. To examine countermeasures against PM2.5 emission, origins of PM2.5 should be elucidated. On the other hand, toxicity per PM mass can remarkably differ among emission sources or atmospheres in different places. Therefore, it is better to understand source contributions not only to PM2.5 mass but also to PM2.5 toxicity. In this study, we have proposed a new approach to estimate source contributions to various kinds of toxicities by atmospheric organic aerosols (OA), using chemical mass balance model and toxicity data. To see how this approach works, we performed the following studies.

First, we chose four kinds of sources (i.e. secondary organic aerosols: SOA, automobiles, open burning of biomass, and cooking) as possible important OA sources for source apportionment. Then we conducted source testing and collected PM2.5 samples from these sources. We also collected ambient PM2.5 samples in different places (e.g. Ryogoku, Tokyo as an urban site; northern foot of Mt. Fuji as a forest site; and Hedo, Okinawa as a remote site in summer) for evaluating our approach. The chemical composition (i.e. elemental carbon, organic carbon: OC, ionic species, elements, and organic compounds) of the PM2.5 samples were measured. Cytotoxicity and cellular responses to the samples, including oxidative stress (measured with gene expression of heme oxygenase-1 and reporter gene assay for Nrf2), DNA-damage (measured with umu test), inflammation (measured with gene expression of interleukin-8), and aryl hydrocarbon receptor agonist activity, were also quantified.

We have done the chemical analysis and the in-vitro bioassays for some source and ambient samples. All kinds of cellular responses per OC of diesel exhaust particle samples were 3–10 times or larger than the biogenic SOA samples. Among the above-mentioned ambient PM2.5 samples collected, the urban site samples had the largest cellular responses per OC followed by the forest site samples. The remote site samples consistently showed the weakest cellular responses. In the presentation, we will show the additional results.