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Article: Indoor, outdoor, and personal exposure to PM2.5 and their bioreactivity among healthy residents of Hong Kong

TitleIndoor, outdoor, and personal exposure to PM2.5 and their bioreactivity among healthy residents of Hong Kong
Authors
KeywordsOrganic carbon
PAHs
Inflammation
Oxidative stress
Biomarkers
Issue Date2020
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/envres
Citation
Environmental Research, 2020, v. 188, p. article no. 109780 How to Cite?
AbstractDirect evidence about associations between fine particles (PM2.5) components and the corresponding PM2.5 bioreactivity at the individual level is limited. We conducted a panel study with repeated personal measurements involving 56 healthy residents in Hong Kong. Fractional exhaled nitric oxide (FeNO) levels were measured from these subjects. Out of 56 subjects, 27 (48.2%) participated in concurrent outdoor, indoor, and personal PM2.5 monitoring. Organic carbon (OC), elemental carbon (EC), particle bound-polycyclic aromatic hydrocarbons (PAHs), and phthalates were analyzed. Alteration in cell viability, lactic dehydrogenase (LDH), interleukin-6 (IL-6), and 8-isoprostane by 50 μg/mL PM2.5 extracts was determined in A549 cells in vitro. Moderate heterogeneities were shown in PM2.5 exposures and the corresponding PM2.5 bioreactivity across different sample types. Associations between the analyzed components and PM2.5 bioreactivity were assessed using the multiple regression models. Toxicological results revealed that indoor and personal exposure to OC as well as PAH compounds and their derivatives (e.g., Alkyl-PAHs, Oxy-PAHs) induced cell viability reduction and increase in levels of LDH, IL-6, and 8-isoprostane. Overall, OC in personal exposure played a dominant role in PM2.5-induced bioreactivity. Subsequently, we examined the associations of FeNO with IL-6 and 8-isoprostane levels using mixed-effects models. The results showed that per interquartile change in IL-6 and 8-isoprostane were associated with a 6.4% (p < 0.01) and 11.1% (p < 0.01) increase in FeNO levels, respectively. Our study explored the toxicological properties of chemical components in PM2.5 exposure, which suggested that residential indoors and personal OC and PAHs should be of great concern for human health. These findings indicated that further studies in inflammation and oxidative stress-related illnesses due to particle exposure would benefit from the assessment of in vitro PM2.5 bioreactivity.
Persistent Identifierhttp://hdl.handle.net/10722/284757
ISSN
2023 Impact Factor: 7.7
2023 SCImago Journal Rankings: 1.679
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChen, XC-
dc.contributor.authorChuang, HC-
dc.contributor.authorWard, TJ-
dc.contributor.authorTian, L-
dc.contributor.authorCao, JJ-
dc.contributor.authorHo, SSH-
dc.contributor.authorLau, NC-
dc.contributor.authorHsiao, TC-
dc.contributor.authorYim, SHL-
dc.contributor.authorHo, KF-
dc.date.accessioned2020-08-07T09:02:14Z-
dc.date.available2020-08-07T09:02:14Z-
dc.date.issued2020-
dc.identifier.citationEnvironmental Research, 2020, v. 188, p. article no. 109780-
dc.identifier.issn0013-9351-
dc.identifier.urihttp://hdl.handle.net/10722/284757-
dc.description.abstractDirect evidence about associations between fine particles (PM2.5) components and the corresponding PM2.5 bioreactivity at the individual level is limited. We conducted a panel study with repeated personal measurements involving 56 healthy residents in Hong Kong. Fractional exhaled nitric oxide (FeNO) levels were measured from these subjects. Out of 56 subjects, 27 (48.2%) participated in concurrent outdoor, indoor, and personal PM2.5 monitoring. Organic carbon (OC), elemental carbon (EC), particle bound-polycyclic aromatic hydrocarbons (PAHs), and phthalates were analyzed. Alteration in cell viability, lactic dehydrogenase (LDH), interleukin-6 (IL-6), and 8-isoprostane by 50 μg/mL PM2.5 extracts was determined in A549 cells in vitro. Moderate heterogeneities were shown in PM2.5 exposures and the corresponding PM2.5 bioreactivity across different sample types. Associations between the analyzed components and PM2.5 bioreactivity were assessed using the multiple regression models. Toxicological results revealed that indoor and personal exposure to OC as well as PAH compounds and their derivatives (e.g., Alkyl-PAHs, Oxy-PAHs) induced cell viability reduction and increase in levels of LDH, IL-6, and 8-isoprostane. Overall, OC in personal exposure played a dominant role in PM2.5-induced bioreactivity. Subsequently, we examined the associations of FeNO with IL-6 and 8-isoprostane levels using mixed-effects models. The results showed that per interquartile change in IL-6 and 8-isoprostane were associated with a 6.4% (p < 0.01) and 11.1% (p < 0.01) increase in FeNO levels, respectively. Our study explored the toxicological properties of chemical components in PM2.5 exposure, which suggested that residential indoors and personal OC and PAHs should be of great concern for human health. These findings indicated that further studies in inflammation and oxidative stress-related illnesses due to particle exposure would benefit from the assessment of in vitro PM2.5 bioreactivity.-
dc.languageeng-
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/envres-
dc.relation.ispartofEnvironmental Research-
dc.subjectOrganic carbon-
dc.subjectPAHs-
dc.subjectInflammation-
dc.subjectOxidative stress-
dc.subjectBiomarkers-
dc.titleIndoor, outdoor, and personal exposure to PM2.5 and their bioreactivity among healthy residents of Hong Kong-
dc.typeArticle-
dc.identifier.emailChen, XC: chenxcui@hku.hk-
dc.identifier.emailTian, L: linweit@hku.hk-
dc.identifier.authorityTian, L=rp01991-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.envres.2020.109780-
dc.identifier.pmid32554275-
dc.identifier.scopuseid_2-s2.0-85086414191-
dc.identifier.hkuros312380-
dc.identifier.volume188-
dc.identifier.spagearticle no. 109780-
dc.identifier.epagearticle no. 109780-
dc.identifier.isiWOS:000564651700015-
dc.publisher.placeUnited States-
dc.identifier.issnl0013-9351-

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