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 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.