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dc.contributor.authorRönkkö, TJ
dc.contributor.authorJalava, PI
dc.contributor.authorHappo, MS
dc.contributor.authorKasurinen, S
dc.contributor.authorSippula, O
dc.contributor.authorLeskinen, A
dc.contributor.authorKoponen, H
dc.contributor.authorKuuspalo, K
dc.contributor.authorRuusunen, J
dc.contributor.authorVäisänen, O
dc.contributor.authorHao, L
dc.contributor.authorRuuskanen, A
dc.contributor.authorOrasche, J
dc.contributor.authorFang, D
dc.contributor.authorZhang, L
dc.contributor.authorLehtinen, KEJ
dc.contributor.authorZhao, Y
dc.contributor.authorGu, C
dc.contributor.authorWang, Q
dc.contributor.authorJokiniemi, J
dc.contributor.authoret al.
dc.date.accessioned2018-06-13T10:41:48Z
dc.date.available2018-06-13T10:41:48Z
dc.date.issued2018
dc.identifier.urihttps://erepo.uef.fi/handle/123456789/6709
dc.description.abstractAmbient inhalable particulate matter (PM) is a serious health concern worldwide, but especially so in China where high PM concentrations affect huge populations. Atmospheric processes and emission sources cause spatial and temporal variations in PM concentration and chemical composition, but their influence on the toxicological characteristics of PM are still inadequately understood. In this study, we report an extensive chemical and toxicological characterization of size-segregated urban air inhalable PM collected in August and October 2013 from Nanjing, and assess the effects of atmospheric processes and likely emission sources. A549 human alveolar epithelial cells were exposed to day- and nighttime PM samples (25, 75, 150, 200, 300 μg/ml) followed by analyses of cytotoxicity, genotoxicity, cell cycle, and inflammatory response. PM10–2.5 and PM0.2 caused the greatest toxicological responses for different endpoints, illustrating that particles with differing size and chemical composition activate distinct toxicological pathways in A549 cells. PM10–2.5 displayed the greatest oxidative stress and genotoxic responses; both were higher for the August samples compared with October. In contrast, PM0.2 and PM2.5–1.0 samples displayed high cytotoxicity and substantially disrupted cell cycle; August samples were more cytotoxic whereas October samples displayed higher cell cycle disruption. Several components associated with combustion, traffic, and industrial emissions displayed strong correlations with these toxicological responses. The lower responses for PM1.0–0.2 compared to PM0.2 and PM2.5–1.0 indicate diminished toxicological effects likely due to aerosol aging and lower proportion of fresh emission particles rich in highly reactive chemical components in the PM1.0–0.2 fraction. Different emission sources and atmospheric processes caused variations in the chemical composition and toxicological responses between PM fractions, sampling campaigns, and day and night. The results indicate different toxicological pathways for coarse-mode particles compared to the smaller particle fractions with typically higher content of combustion-derived components. The variable responses inside PM fractions demonstrate that differences in chemical composition influence the induced toxicological responses.
dc.language.isoenglanti
dc.publisherElsevier BV
dc.relation.ispartofseriesSCIENCE OF THE TOTAL ENVIRONMENT
dc.relation.urihttp://dx.doi.org/10.1016/j.scitotenv.2018.05.260
dc.rightsCC BY 4.0
dc.subjectair pollution
dc.subjectcytotoxicity
dc.subjectgenotoxicity
dc.subjectinflammation
dc.subjectin vitro toxicology
dc.titleEmissions and atmospheric processes influence the chemical composition and toxicological properties of urban air particulate matter in Nanjing, China
dc.description.versionpublished version
dc.contributor.departmentYmpäristö- ja biotieteiden laitos / Toiminta
dc.contributor.departmentDepartment of Applied Physics, activities
uef.solecris.id55037037en
dc.type.publicationTieteelliset aikakauslehtiartikkelit
dc.relation.doi10.1016/j.scitotenv.2018.05.260
dc.description.reviewstatuspeerReviewed
dc.format.pagerange1290-1310
dc.relation.issn0048-9697
dc.relation.volume639
dc.rights.accesslevelopenAccess
dc.type.okmA1
uef.solecris.openaccessHybridijulkaisukanavassa ilmestynyt avoin julkaisu
dc.rights.copyright© Authors
dc.type.displayTypearticleen
dc.type.displayTypeartikkelifi
dc.rights.urlhttps://creativecommons.org/licenses/by/4.0/


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