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dc.contributor.authorHou, Lifang
dc.contributor.authorZhu, Zhong-Zheng
dc.contributor.authorNordio, Francesco
dc.contributor.authorBonzini, Matteo
dc.contributor.authorHoxha, Mirjam
dc.contributor.authorDioni, Laura
dc.contributor.authorMarinelli, Barbara
dc.contributor.authorPegoraro, Valeria
dc.contributor.authorApostoli, Pietro
dc.contributor.authorBertazzi, Pier Alberto
dc.contributor.authorZhang, Xiao
dc.contributor.authorSchwartz, Joel David
dc.contributor.authorBaccarelli, Andrea
dc.date.accessioned2011-04-22T15:27:14Z
dc.date.issued2010
dc.identifier.citationHou, Lifang, Zhong-Zheng Zhu, Xiao Zhang, Francesco Nordio, Matteo Bonzini, Joel Schwartz, Mirjam Hoxha, and et al. 2010. Airborne particulate matter and mitochondrial damage: A cross-sectional study. Environmental Health 9: 48.en_US
dc.identifier.issn1476-069Xen_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:4872804
dc.description.abstractBackground: Oxidative stress generation is a primary mechanism mediating the effects of Particulate Matter (PM) on human health. Although mitochondria are both the major intracellular source and target of oxidative stress, the effect of PM on mitochondria has never been evaluated in exposed individuals. Methods: In 63 male healthy steel workers from Brescia, Italy, studied between April and May 2006, we evaluated whether exposure to PM was associated with increased mitochondrial DNA copy number (MtDNAcn), an established marker of mitochondria damage and malfunctioning. Relative MtDNAcn (RMtDNAcn) was determined by real-time PCR in blood DNA obtained on the 1st (time 1) and 4th day (time 2) of the same work week. Individual exposures to PM10, PM1, coarse particles (PM10-PM1) and airborne metal components of PM10 (chromium, lead, arsenic, nickel, manganese) were estimated based on measurements in the 11 work areas and time spent by the study subjects in each area. Results: RMtDNAcn was higher on the 4th day (mean = 1.31; 95%CI = 1.22 to 1.40) than on the 1st day of the work week (mean = 1.09; 95%CI = 1.00 to 1.17). PM exposure was positively associated with RMtDNAcn on either the 4th (PM10: β = 0.06, 95%CI = -0.06 to 0.17; PM1: β = 0.08, 95%CI = -0.08 to 0.23; coarse: β = 0.06, 95%CI = -0.06 to 0.17) or the 1st day (PM10: β = 0.18, 95%CI = 0.09 to 0.26; PM1: β = 0.23, 95%CI = 0.11 to 0.35; coarse: β = 0.17, 95%CI = 0.09 to 0.26). Metal concentrations were not associated with RMtDNAcn. Conclusions: PM exposure is associated with damaged mitochondria, as reflected in increased MtDNAcn. Damaged mitochondria may intensify oxidative-stress production and effects.en_US
dc.language.isoen_USen_US
dc.publisherBioMed Centralen_US
dc.relation.isversionofdoi://10.1186/1476-069X-9-48en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2928195/pdf/en_US
dash.licenseLAA
dc.titleAirborne Particulate Matter and Mitochondrial Damage: A Cross-Sectional Studyen_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalEnvironmental Healthen_US
dash.depositing.authorSchwartz, Joel David
dc.date.available2011-04-22T15:27:14Z
dash.affiliation.otherHMS^Medicine-Brigham and Women's Hospitalen_US
dash.affiliation.otherSPH^Exposure Epidemiology and Risk Programen_US
dash.affiliation.otherSPH^Exposure Epidemiology and Risk Programen_US
dc.identifier.doi10.1186/1476-069X-9-48*
dash.authorsorderedfalse
dash.contributor.affiliatedSchwartz, Joel
dash.contributor.affiliatedBaccarelli, Andrea


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