Airborne particulate matter and mitochondrial damage: a cross-sectional study

Background 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 individua...
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Autor*in:	Hou, Lifang [verfasserIn] Zhu, Zhong-Zheng Zhang, Xiao Nordio, Francesco Bonzini, Matteo Schwartz, Joel Hoxha, Mirjam Dioni, Laura Marinelli, Barbara Pegoraro, Valeria Apostoli, Pietro Bertazzi, Pier Alberto Baccarelli, Andrea

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2010

Schlagwörter:	Reactive Oxygen Species Coarse Particle Metal Component Dynamic Reaction Cell Foundry Worker

Anmerkung:	© Hou et al; licensee BioMed Central Ltd. 2010

Übergeordnetes Werk:	Enthalten in: Environmental health - London : BioMed Central, 2002, 9(2010), 1 vom: 09. Aug.
Übergeordnetes Werk:	volume:9 ; year:2010 ; number:1 ; day:09 ; month:08

Links:	Volltext

DOI / URN:	10.1186/1476-069X-9-48

Katalog-ID:	SPR028722930

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024	7		\|a 10.1186/1476-069X-9-48 \|2 doi
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100	1		\|a Hou, Lifang \|e verfasserin \|4 aut
245	1	0	\|a Airborne particulate matter and mitochondrial damage: a cross-sectional study
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520			\|a Background 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 $ 1^{st} $ (time 1) and $ 4^{th} $ day (time 2) of the same work week. Individual exposures to $ PM_{10} $, $ PM_{1} $, coarse particles ($ PM_{10} $-$ PM_{1} $) and airborne metal components of $ PM_{10} $ (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 $ 4^{th} $ day (mean = 1.31; 95%CI = 1.22 to 1.40) than on the $ 1^{st} $ 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 $ 4^{th} $ ($ PM_{10} $: β = 0.06, 95%CI = -0.06 to 0.17; $ PM_{1} $: β = 0.08, 95%CI = -0.08 to 0.23; coarse: β = 0.06, 95%CI = -0.06 to 0.17) or the $ 1^{st} $ day ($ PM_{10} $: β = 0.18, 95%CI = 0.09 to 0.26; $ PM_{1} $: 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.
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700	1		\|a Pegoraro, Valeria \|4 aut
700	1		\|a Apostoli, Pietro \|4 aut
700	1		\|a Bertazzi, Pier Alberto \|4 aut
700	1		\|a Baccarelli, Andrea \|4 aut
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allfields	10.1186/1476-069X-9-48 doi (DE-627)SPR028722930 (SPR)1476-069X-9-48-e DE-627 ger DE-627 rakwb eng Hou, Lifang verfasserin aut Airborne particulate matter and mitochondrial damage: a cross-sectional study 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Hou et al; licensee BioMed Central Ltd. 2010 Background 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 $ 1^{st} $ (time 1) and $ 4^{th} $ day (time 2) of the same work week. Individual exposures to $ PM_{10} $, $ PM_{1} $, coarse particles ($ PM_{10} $-$ PM_{1} $) and airborne metal components of $ PM_{10} $ (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 $ 4^{th} $ day (mean = 1.31; 95%CI = 1.22 to 1.40) than on the $ 1^{st} $ 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 $ 4^{th} $ ($ PM_{10} $: β = 0.06, 95%CI = -0.06 to 0.17; $ PM_{1} $: β = 0.08, 95%CI = -0.08 to 0.23; coarse: β = 0.06, 95%CI = -0.06 to 0.17) or the $ 1^{st} $ day ($ PM_{10} $: β = 0.18, 95%CI = 0.09 to 0.26; $ PM_{1} $: 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. Reactive Oxygen Species (dpeaa)DE-He213 Coarse Particle (dpeaa)DE-He213 Metal Component (dpeaa)DE-He213 Dynamic Reaction Cell (dpeaa)DE-He213 Foundry Worker (dpeaa)DE-He213 Zhu, Zhong-Zheng aut Zhang, Xiao aut Nordio, Francesco aut Bonzini, Matteo aut Schwartz, Joel aut Hoxha, Mirjam aut Dioni, Laura aut Marinelli, Barbara aut Pegoraro, Valeria aut Apostoli, Pietro aut Bertazzi, Pier Alberto aut Baccarelli, Andrea aut Enthalten in Environmental health London : BioMed Central, 2002 9(2010), 1 vom: 09. Aug. (DE-627)355849550 (DE-600)2092232-2 1476-069X nnns volume:9 year:2010 number:1 day:09 month:08 https://dx.doi.org/10.1186/1476-069X-9-48 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2010 1 09 08
spelling	10.1186/1476-069X-9-48 doi (DE-627)SPR028722930 (SPR)1476-069X-9-48-e DE-627 ger DE-627 rakwb eng Hou, Lifang verfasserin aut Airborne particulate matter and mitochondrial damage: a cross-sectional study 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Hou et al; licensee BioMed Central Ltd. 2010 Background 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 $ 1^{st} $ (time 1) and $ 4^{th} $ day (time 2) of the same work week. Individual exposures to $ PM_{10} $, $ PM_{1} $, coarse particles ($ PM_{10} $-$ PM_{1} $) and airborne metal components of $ PM_{10} $ (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 $ 4^{th} $ day (mean = 1.31; 95%CI = 1.22 to 1.40) than on the $ 1^{st} $ 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 $ 4^{th} $ ($ PM_{10} $: β = 0.06, 95%CI = -0.06 to 0.17; $ PM_{1} $: β = 0.08, 95%CI = -0.08 to 0.23; coarse: β = 0.06, 95%CI = -0.06 to 0.17) or the $ 1^{st} $ day ($ PM_{10} $: β = 0.18, 95%CI = 0.09 to 0.26; $ PM_{1} $: 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. Reactive Oxygen Species (dpeaa)DE-He213 Coarse Particle (dpeaa)DE-He213 Metal Component (dpeaa)DE-He213 Dynamic Reaction Cell (dpeaa)DE-He213 Foundry Worker (dpeaa)DE-He213 Zhu, Zhong-Zheng aut Zhang, Xiao aut Nordio, Francesco aut Bonzini, Matteo aut Schwartz, Joel aut Hoxha, Mirjam aut Dioni, Laura aut Marinelli, Barbara aut Pegoraro, Valeria aut Apostoli, Pietro aut Bertazzi, Pier Alberto aut Baccarelli, Andrea aut Enthalten in Environmental health London : BioMed Central, 2002 9(2010), 1 vom: 09. Aug. (DE-627)355849550 (DE-600)2092232-2 1476-069X nnns volume:9 year:2010 number:1 day:09 month:08 https://dx.doi.org/10.1186/1476-069X-9-48 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2010 1 09 08
allfields_unstemmed	10.1186/1476-069X-9-48 doi (DE-627)SPR028722930 (SPR)1476-069X-9-48-e DE-627 ger DE-627 rakwb eng Hou, Lifang verfasserin aut Airborne particulate matter and mitochondrial damage: a cross-sectional study 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Hou et al; licensee BioMed Central Ltd. 2010 Background 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 $ 1^{st} $ (time 1) and $ 4^{th} $ day (time 2) of the same work week. Individual exposures to $ PM_{10} $, $ PM_{1} $, coarse particles ($ PM_{10} $-$ PM_{1} $) and airborne metal components of $ PM_{10} $ (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 $ 4^{th} $ day (mean = 1.31; 95%CI = 1.22 to 1.40) than on the $ 1^{st} $ 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 $ 4^{th} $ ($ PM_{10} $: β = 0.06, 95%CI = -0.06 to 0.17; $ PM_{1} $: β = 0.08, 95%CI = -0.08 to 0.23; coarse: β = 0.06, 95%CI = -0.06 to 0.17) or the $ 1^{st} $ day ($ PM_{10} $: β = 0.18, 95%CI = 0.09 to 0.26; $ PM_{1} $: 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. Reactive Oxygen Species (dpeaa)DE-He213 Coarse Particle (dpeaa)DE-He213 Metal Component (dpeaa)DE-He213 Dynamic Reaction Cell (dpeaa)DE-He213 Foundry Worker (dpeaa)DE-He213 Zhu, Zhong-Zheng aut Zhang, Xiao aut Nordio, Francesco aut Bonzini, Matteo aut Schwartz, Joel aut Hoxha, Mirjam aut Dioni, Laura aut Marinelli, Barbara aut Pegoraro, Valeria aut Apostoli, Pietro aut Bertazzi, Pier Alberto aut Baccarelli, Andrea aut Enthalten in Environmental health London : BioMed Central, 2002 9(2010), 1 vom: 09. Aug. (DE-627)355849550 (DE-600)2092232-2 1476-069X nnns volume:9 year:2010 number:1 day:09 month:08 https://dx.doi.org/10.1186/1476-069X-9-48 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2010 1 09 08
allfieldsGer	10.1186/1476-069X-9-48 doi (DE-627)SPR028722930 (SPR)1476-069X-9-48-e DE-627 ger DE-627 rakwb eng Hou, Lifang verfasserin aut Airborne particulate matter and mitochondrial damage: a cross-sectional study 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Hou et al; licensee BioMed Central Ltd. 2010 Background 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 $ 1^{st} $ (time 1) and $ 4^{th} $ day (time 2) of the same work week. Individual exposures to $ PM_{10} $, $ PM_{1} $, coarse particles ($ PM_{10} $-$ PM_{1} $) and airborne metal components of $ PM_{10} $ (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 $ 4^{th} $ day (mean = 1.31; 95%CI = 1.22 to 1.40) than on the $ 1^{st} $ 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 $ 4^{th} $ ($ PM_{10} $: β = 0.06, 95%CI = -0.06 to 0.17; $ PM_{1} $: β = 0.08, 95%CI = -0.08 to 0.23; coarse: β = 0.06, 95%CI = -0.06 to 0.17) or the $ 1^{st} $ day ($ PM_{10} $: β = 0.18, 95%CI = 0.09 to 0.26; $ PM_{1} $: 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. Reactive Oxygen Species (dpeaa)DE-He213 Coarse Particle (dpeaa)DE-He213 Metal Component (dpeaa)DE-He213 Dynamic Reaction Cell (dpeaa)DE-He213 Foundry Worker (dpeaa)DE-He213 Zhu, Zhong-Zheng aut Zhang, Xiao aut Nordio, Francesco aut Bonzini, Matteo aut Schwartz, Joel aut Hoxha, Mirjam aut Dioni, Laura aut Marinelli, Barbara aut Pegoraro, Valeria aut Apostoli, Pietro aut Bertazzi, Pier Alberto aut Baccarelli, Andrea aut Enthalten in Environmental health London : BioMed Central, 2002 9(2010), 1 vom: 09. Aug. (DE-627)355849550 (DE-600)2092232-2 1476-069X nnns volume:9 year:2010 number:1 day:09 month:08 https://dx.doi.org/10.1186/1476-069X-9-48 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2010 1 09 08
allfieldsSound	10.1186/1476-069X-9-48 doi (DE-627)SPR028722930 (SPR)1476-069X-9-48-e DE-627 ger DE-627 rakwb eng Hou, Lifang verfasserin aut Airborne particulate matter and mitochondrial damage: a cross-sectional study 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Hou et al; licensee BioMed Central Ltd. 2010 Background 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 $ 1^{st} $ (time 1) and $ 4^{th} $ day (time 2) of the same work week. Individual exposures to $ PM_{10} $, $ PM_{1} $, coarse particles ($ PM_{10} $-$ PM_{1} $) and airborne metal components of $ PM_{10} $ (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 $ 4^{th} $ day (mean = 1.31; 95%CI = 1.22 to 1.40) than on the $ 1^{st} $ 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 $ 4^{th} $ ($ PM_{10} $: β = 0.06, 95%CI = -0.06 to 0.17; $ PM_{1} $: β = 0.08, 95%CI = -0.08 to 0.23; coarse: β = 0.06, 95%CI = -0.06 to 0.17) or the $ 1^{st} $ day ($ PM_{10} $: β = 0.18, 95%CI = 0.09 to 0.26; $ PM_{1} $: 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. Reactive Oxygen Species (dpeaa)DE-He213 Coarse Particle (dpeaa)DE-He213 Metal Component (dpeaa)DE-He213 Dynamic Reaction Cell (dpeaa)DE-He213 Foundry Worker (dpeaa)DE-He213 Zhu, Zhong-Zheng aut Zhang, Xiao aut Nordio, Francesco aut Bonzini, Matteo aut Schwartz, Joel aut Hoxha, Mirjam aut Dioni, Laura aut Marinelli, Barbara aut Pegoraro, Valeria aut Apostoli, Pietro aut Bertazzi, Pier Alberto aut Baccarelli, Andrea aut Enthalten in Environmental health London : BioMed Central, 2002 9(2010), 1 vom: 09. Aug. (DE-627)355849550 (DE-600)2092232-2 1476-069X nnns volume:9 year:2010 number:1 day:09 month:08 https://dx.doi.org/10.1186/1476-069X-9-48 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2010 1 09 08
language	English
source	Enthalten in Environmental health 9(2010), 1 vom: 09. Aug. volume:9 year:2010 number:1 day:09 month:08
sourceStr	Enthalten in Environmental health 9(2010), 1 vom: 09. Aug. volume:9 year:2010 number:1 day:09 month:08
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Reactive Oxygen Species Coarse Particle Metal Component Dynamic Reaction Cell Foundry Worker
isfreeaccess_bool	true
container_title	Environmental health
authorswithroles_txt_mv	Hou, Lifang @@aut@@ Zhu, Zhong-Zheng @@aut@@ Zhang, Xiao @@aut@@ Nordio, Francesco @@aut@@ Bonzini, Matteo @@aut@@ Schwartz, Joel @@aut@@ Hoxha, Mirjam @@aut@@ Dioni, Laura @@aut@@ Marinelli, Barbara @@aut@@ Pegoraro, Valeria @@aut@@ Apostoli, Pietro @@aut@@ Bertazzi, Pier Alberto @@aut@@ Baccarelli, Andrea @@aut@@
publishDateDaySort_date	2010-08-09T00:00:00Z
hierarchy_top_id	355849550
id	SPR028722930
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR028722930</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230520005145.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s2010 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/1476-069X-9-48</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR028722930</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)1476-069X-9-48-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Hou, Lifang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Airborne particulate matter and mitochondrial damage: a cross-sectional study</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2010</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© Hou et al; licensee BioMed Central Ltd. 2010</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background 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 $ 1^{st} $ (time 1) and $ 4^{th} $ day (time 2) of the same work week. Individual exposures to $ PM_{10} $, $ PM_{1} $, coarse particles ($ PM_{10} $-$ PM_{1} $) and airborne metal components of $ PM_{10} $ (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 $ 4^{th} $ day (mean = 1.31; 95%CI = 1.22 to 1.40) than on the $ 1^{st} $ 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 $ 4^{th} $ ($ PM_{10} $: β = 0.06, 95%CI = -0.06 to 0.17; $ PM_{1} $: β = 0.08, 95%CI = -0.08 to 0.23; coarse: β = 0.06, 95%CI = -0.06 to 0.17) or the $ 1^{st} $ day ($ PM_{10} $: β = 0.18, 95%CI = 0.09 to 0.26; $ PM_{1} $: 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. 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author	Hou, Lifang
spellingShingle	Hou, Lifang misc Reactive Oxygen Species misc Coarse Particle misc Metal Component misc Dynamic Reaction Cell misc Foundry Worker Airborne particulate matter and mitochondrial damage: a cross-sectional study
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topic_title	Airborne particulate matter and mitochondrial damage: a cross-sectional study Reactive Oxygen Species (dpeaa)DE-He213 Coarse Particle (dpeaa)DE-He213 Metal Component (dpeaa)DE-He213 Dynamic Reaction Cell (dpeaa)DE-He213 Foundry Worker (dpeaa)DE-He213
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title	Airborne particulate matter and mitochondrial damage: a cross-sectional study
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title_full	Airborne particulate matter and mitochondrial damage: a cross-sectional study
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author_browse	Hou, Lifang Zhu, Zhong-Zheng Zhang, Xiao Nordio, Francesco Bonzini, Matteo Schwartz, Joel Hoxha, Mirjam Dioni, Laura Marinelli, Barbara Pegoraro, Valeria Apostoli, Pietro Bertazzi, Pier Alberto Baccarelli, Andrea
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title_sort	airborne particulate matter and mitochondrial damage: a cross-sectional study
title_auth	Airborne particulate matter and mitochondrial damage: a cross-sectional study
abstract	Background 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 $ 1^{st} $ (time 1) and $ 4^{th} $ day (time 2) of the same work week. Individual exposures to $ PM_{10} $, $ PM_{1} $, coarse particles ($ PM_{10} $-$ PM_{1} $) and airborne metal components of $ PM_{10} $ (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 $ 4^{th} $ day (mean = 1.31; 95%CI = 1.22 to 1.40) than on the $ 1^{st} $ 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 $ 4^{th} $ ($ PM_{10} $: β = 0.06, 95%CI = -0.06 to 0.17; $ PM_{1} $: β = 0.08, 95%CI = -0.08 to 0.23; coarse: β = 0.06, 95%CI = -0.06 to 0.17) or the $ 1^{st} $ day ($ PM_{10} $: β = 0.18, 95%CI = 0.09 to 0.26; $ PM_{1} $: 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. © Hou et al; licensee BioMed Central Ltd. 2010
abstractGer	Background 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 $ 1^{st} $ (time 1) and $ 4^{th} $ day (time 2) of the same work week. Individual exposures to $ PM_{10} $, $ PM_{1} $, coarse particles ($ PM_{10} $-$ PM_{1} $) and airborne metal components of $ PM_{10} $ (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 $ 4^{th} $ day (mean = 1.31; 95%CI = 1.22 to 1.40) than on the $ 1^{st} $ 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 $ 4^{th} $ ($ PM_{10} $: β = 0.06, 95%CI = -0.06 to 0.17; $ PM_{1} $: β = 0.08, 95%CI = -0.08 to 0.23; coarse: β = 0.06, 95%CI = -0.06 to 0.17) or the $ 1^{st} $ day ($ PM_{10} $: β = 0.18, 95%CI = 0.09 to 0.26; $ PM_{1} $: 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. © Hou et al; licensee BioMed Central Ltd. 2010
abstract_unstemmed	Background 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 $ 1^{st} $ (time 1) and $ 4^{th} $ day (time 2) of the same work week. Individual exposures to $ PM_{10} $, $ PM_{1} $, coarse particles ($ PM_{10} $-$ PM_{1} $) and airborne metal components of $ PM_{10} $ (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 $ 4^{th} $ day (mean = 1.31; 95%CI = 1.22 to 1.40) than on the $ 1^{st} $ 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 $ 4^{th} $ ($ PM_{10} $: β = 0.06, 95%CI = -0.06 to 0.17; $ PM_{1} $: β = 0.08, 95%CI = -0.08 to 0.23; coarse: β = 0.06, 95%CI = -0.06 to 0.17) or the $ 1^{st} $ day ($ PM_{10} $: β = 0.18, 95%CI = 0.09 to 0.26; $ PM_{1} $: 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. © Hou et al; licensee BioMed Central Ltd. 2010
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title_short	Airborne particulate matter and mitochondrial damage: a cross-sectional study
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fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR028722930</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230520005145.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s2010 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/1476-069X-9-48</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR028722930</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)1476-069X-9-48-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Hou, Lifang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Airborne particulate matter and mitochondrial damage: a cross-sectional study</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2010</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© Hou et al; licensee BioMed Central Ltd. 2010</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background 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 $ 1^{st} $ (time 1) and $ 4^{th} $ day (time 2) of the same work week. Individual exposures to $ PM_{10} $, $ PM_{1} $, coarse particles ($ PM_{10} $-$ PM_{1} $) and airborne metal components of $ PM_{10} $ (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 $ 4^{th} $ day (mean = 1.31; 95%CI = 1.22 to 1.40) than on the $ 1^{st} $ 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 $ 4^{th} $ ($ PM_{10} $: β = 0.06, 95%CI = -0.06 to 0.17; $ PM_{1} $: β = 0.08, 95%CI = -0.08 to 0.23; coarse: β = 0.06, 95%CI = -0.06 to 0.17) or the $ 1^{st} $ day ($ PM_{10} $: β = 0.18, 95%CI = 0.09 to 0.26; $ PM_{1} $: 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. 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Airborne particulate matter and mitochondrial damage: a cross-sectional study

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