TY - JOUR
T1 - Airborne particulate matter and mitochondrial damage
T2 - A cross-sectional study
AU - Hou, Lifang
AU - Zhu, Zhong Zheng
AU - Zhang, Xiao
AU - Nordio, Francesco
AU - Bonzini, Matteo
AU - Schwartz, Joel
AU - Hoxha, Mirjam
AU - Dioni, Laura
AU - Marinelli, Barbara
AU - Pegoraro, Valeria
AU - Apostoli, Pietro
AU - Bertazzi, Pier Alberto
AU - Baccarelli, Andrea
N1 - Funding Information:
This work was supported by research grants from the CARIPLO Foundation (2007-5469); the National Institute of Environmental Health Sciences (ES015172-01); and the Italian Ministry of Scientific Research - Research Programs of National Interest (PRIN 2007-2S2HT8).
PY - 2010
Y1 - 2010
N2 - 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 1st (time 1) and 4th day (time 2) of the same work week. Individual exposures to PM10, PM1, coarse particles (PM10-PM 1) 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: = 0.06, 95%CI = -0.06 to 0.17; PM1: = 0.08, 95%CI = -0.08 to 0.23; coarse: = 0.06, 95%CI = -0.06 to 0.17) or the 1st day (PM10: = 0.18, 95%CI = 0.09 to 0.26; PM1: = 0.23, 95%CI = 0.11 to 0.35; coarse: = 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.
AB - 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 1st (time 1) and 4th day (time 2) of the same work week. Individual exposures to PM10, PM1, coarse particles (PM10-PM 1) 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: = 0.06, 95%CI = -0.06 to 0.17; PM1: = 0.08, 95%CI = -0.08 to 0.23; coarse: = 0.06, 95%CI = -0.06 to 0.17) or the 1st day (PM10: = 0.18, 95%CI = 0.09 to 0.26; PM1: = 0.23, 95%CI = 0.11 to 0.35; coarse: = 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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U2 - 10.1186/1476-069X-9-48
DO - 10.1186/1476-069X-9-48
M3 - Article
C2 - 20696069
AN - SCOPUS:77955283436
SN - 1476-069X
VL - 9
JO - Environmental Health: A Global Access Science Source
JF - Environmental Health: A Global Access Science Source
IS - 1
M1 - 48
ER -