Inhalable particulate matter and mitochondrial DNA copy number in highly exposed individuals in Beijing, China: a repeated-measure study

BACKGROUND: Mitochondria are both a sensitive target and a primary source of oxidative stress, a key pathway of air particulate matter (PM)-associated diseases. Mitochondrial DNA copy number (MtDNAcn) is a marker of mitochondrial damage and malfunctioning. We evaluated whether ambient PM exposure affects MtDNAcn in a highly-exposed population in Beijing, China. METHODS: The Beijing Truck Driver Air Pollution Study was conducted shortly before the 2008 Beijing Olympic Games (June 15-July 27, 2008) and included 60 truck drivers and 60 office workers. Personal PM(2.5) and elemental carbon (EC, a tracer of traffic particles) were measured during work hours using portable monitors. Post-work blood samples were obtained on two different days. Ambient PM(10) was averaged from 27 monitoring stations in Beijing. Blood MtDNAcn was determined by real-time PCR and examined in association with particle levels using mixed-effect models. RESULTS: In all participants combined, MtDNAcn was negatively associated with personal EC level measured during work hours (β=−0.059, 95% CI: -0.011; -0.0006, p=0.03); and 5-day (β=−0.017, 95% CI: -0.029;-0.005, p=0.01) and 8-day average ambient PM(10) (β=−0.008, 95% CI: -0.043; -0.008, p=0.004) after adjusting for possible confounding factors, including study groups. MtDNAcn was also negatively associated among office workers with EC (β=−0.012, 95% CI: -0.022;-0.002, p=0.02) and 8-day average ambient PM(10) (β=−0.030, 95% CI: -0.051;-0.008, p=0.007). CONCLUSIONS: We observed decreased blood MtDNAcn in association with increased exposure to EC during work hours and recent ambient PM(10) exposure. Our results suggest that MtDNAcn may be influenced by particle exposures. Further studies are required to determine the roles of MtDNAcn in the etiology of particle-related diseases.