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

Abstract

Doc number: 17

Abstract

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 PM₁₀ 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 PM₁₀ (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 PM₁₀ (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 PM₁₀ 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.