title: Airborne particulate matter and mitochondrial damage: a cross-sectional study.
abstract: 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: beta = 0.06, 95%CI = -0.06 to 0.17; PM1: beta = 0.08, 95%CI = -0.08 to 0.23; coarse: beta = 0.06, 95%CI = -0.06 to 0.17) or the 1st day (PM10: beta = 0.18, 95%CI = 0.09 to 0.26; PM1: beta = 0.23, 95%CI = 0.11 to 0.35; coarse: beta = 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.
authors.affiliation: Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA. l-hou@northwestern.edu
authors.forename: Lifang
authors.initials: L
authors.lastname: Hou
authors.forename: Zhong-Zheng
authors.initials: ZZ
authors.lastname: Zhu
authors.forename: Xiao
authors.initials: X
authors.lastname: Zhang
authors.forename: Francesco
authors.initials: F
authors.lastname: Nordio
authors.forename: Matteo
authors.initials: M
authors.lastname: Bonzini
authors.forename: Joel
authors.initials: J
authors.lastname: Schwartz
authors.forename: Mirjam
authors.initials: M
authors.lastname: Hoxha
authors.forename: Laura
authors.initials: L
authors.lastname: Dioni
authors.forename: Barbara
authors.initials: B
authors.lastname: Marinelli
authors.forename: Valeria
authors.initials: V
authors.lastname: Pegoraro
authors.forename: Pietro
authors.initials: P
authors.lastname: Apostoli
authors.forename: Pier Alberto
authors.initials: PA
authors.lastname: Bertazzi
authors.forename: Andrea
authors.initials: A
authors.lastname: Baccarelli
mesh_terms: D000393:Air Pollutants / Q000009:adverse effects* / Q000032:analysis; D003430:Cross-Sectional Studies; D004249:DNA Damage; D004272:DNA, Mitochondrial / Q000187:drug effects*; D006801:Humans; D007558:Italy; D008297:Male; D008928:Mitochondria / Q000187:drug effects*; D016273:Occupational Exposure; D018384:Oxidative Stress / Q000187:drug effects; D052638:Particulate Matter
chemical_list: D000393:Air Pollutants; D004272:DNA, Mitochondrial; D052638:Particulate Matter