Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/117697
DC FieldValueLanguage
dc.contributorDepartment of Civil and Environmental Engineeringen_US
dc.contributorResearch Institute for Sustainable Urban Developmenten_US
dc.creatorWang, Yen_US
dc.creatorXie, Jen_US
dc.creatorJin, Len_US
dc.creatorSun, Xen_US
dc.creatorZhang, Len_US
dc.creatorYang, Qen_US
dc.creatorLuo, Xen_US
dc.creatorLi, Jen_US
dc.creatorLi, Xen_US
dc.date.accessioned2026-02-27T04:02:54Z-
dc.date.available2026-02-27T04:02:54Z-
dc.identifier.issn0269-7491en_US
dc.identifier.urihttp://hdl.handle.net/10397/117697-
dc.language.isoenen_US
dc.publisherPergamon Pressen_US
dc.subjectEndotoxinsen_US
dc.subjectHealth risksen_US
dc.subjectIn vitro toxicityen_US
dc.subjectOxidative stressen_US
dc.subjectPM2.5en_US
dc.subjectToxic aerosol sourcesen_US
dc.titleBeyond mass concentration : the critical role of chemical and biological compositions and sources in PM₂.₅-induced toxicity in two Chinese megacitiesen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.volume385en_US
dc.identifier.doi10.1016/j.envpol.2025.127146en_US
dcterms.abstractStudies have established evidence between the chemical composition of PM<inf>2.5</inf> and its toxic effects, yet the toxicological contributions of biological components like endotoxins remain understudied. To address this gap, we developed an integrated assessment combining in vitro mixture-toxicity assays and source apportionment modeling. This approach quantifies the contributions of endotoxins, trace metals, and polycyclic aromatic hydrocarbons (PAHs) to PM<inf>2.5</inf>-induced intracellular oxidative stress and identifies source-specific toxicity patterns across six sites in Nanjing and Guangzhou, China. Our analysis revealed significant spatial gradients in PM<inf>2.5</inf>-induced toxicity correlated with anthropogenic activities. In Nanjing, suburban-industrial PM<inf>2.5</inf> exhibited double the toxicity of rural samples, while urban and semi-rural industrial sites in Guangzhou showed double the toxicity of the suburban area. These patterns suggest that reduced exposure to anthropogenic emissions corresponds to lower PM<inf>2.5</inf>-induced toxicity, highlighting anthropogenic contributions as key toxic drivers. Although endotoxins, trace metals, and PAHs constituted approximately 2.23 % of PM<inf>2.5</inf> mass, they accounted for 35.9–56.9 % of total reactive oxygen species (ROS) generation, with trace metals as the dominant contributor (31.6–46.7 %), followed by endotoxins (4.24–12.2 %) and PAHs (0.0218–0.135 %). Source apportionment revealed dominant regional toxic drivers: fugitive dust (23.2–24.6 %) and combustion (19.0–20.5 %) in Nanjing; while vehicle (19.8 %), industrial (18.4 %), combustion (18.5 %) and biological (20.0 %) emissions in Guangzhou. Notably, biological emissions contributed 10.3–20.0 % of total PM<inf>2.5</inf>-induced toxicity. These findings suggest that PM<inf>2.5</inf>-induced toxicity depends more on bioactive constituents than total mass concentration, emphasizing the need for toxicity-oriented air quality regulations, especially regarding bioaerosols, to supplement mass-based air quality standards.en_US
dcterms.accessRightsembargoed accessen_US
dcterms.bibliographicCitationEnvironmental pollution, 15 Nov. 2025, v. 385, 127146en_US
dcterms.isPartOfEnvironmental pollutionen_US
dcterms.issued2025-11-15-
dc.identifier.scopus2-s2.0-105017001473-
dc.identifier.pmid40983177-
dc.identifier.eissn1873-6424en_US
dc.identifier.artn127146en_US
dc.description.validate202602 bchyen_US
dc.description.oaNot applicableen_US
dc.identifier.SubFormIDG001046/2026-02-
dc.description.fundingSourceRGCen_US
dc.description.fundingTextThis study was supported by the Research Grants Council of Hong Kong (T24-508/22-N). We thank Prof. Jianzhen Yu and Dr. Wing Sze Chow from The Hong Kong University of Science and Technology for their kind help in analyzing the PAHs data.en_US
dc.description.pubStatusPublisheden_US
dc.date.embargo2027-11-15en_US
dc.description.oaCategoryGreen (AAM)en_US
Appears in Collections:Journal/Magazine Article
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Embargo End Date 2027-11-15
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