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

Lifang Hou, Xiao Zhang, Laura Dioni, Francesco Barretta, Chang Dou, Yinan Zheng, Mirjam Hoxha, Pier Alberto Bertazzi, Joel Schwartz, Shanshan Wu, Sheng Wang, Andrea A. Baccarelli

Research output: Contribution to journalArticle

48 Citations (Scopus)

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 PM2.5 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.

Original languageEnglish
Article number17
JournalParticle and Fibre Toxicology
Volume10
Issue number1
DOIs
Publication statusPublished - Apr 29 2013

Fingerprint

Particulate Matter
Mitochondrial DNA
China
Truck drivers
Blood
Motor Vehicles
Mitochondria
Oxidative stress
Beijing
Air Pollution
Air pollution
Real-Time Polymerase Chain Reaction
Oxidative Stress
Carbon
Air
Association reactions
Monitoring

Keywords

  • China
  • Mitochondrial DNA
  • Mitochondrial DNA copy number
  • Particulate matter
  • Traffic pollution

ASJC Scopus subject areas

  • Health, Toxicology and Mutagenesis
  • Toxicology

Cite this

Inhalable particulate matter and mitochondrial DNA copy number in highly exposed individuals in Beijing, China : A repeated-measure study. / Hou, Lifang; Zhang, Xiao; Dioni, Laura; Barretta, Francesco; Dou, Chang; Zheng, Yinan; Hoxha, Mirjam; Bertazzi, Pier Alberto; Schwartz, Joel; Wu, Shanshan; Wang, Sheng; Baccarelli, Andrea A.

In: Particle and Fibre Toxicology, Vol. 10, No. 1, 17, 29.04.2013.

Research output: Contribution to journalArticle

Hou, Lifang ; Zhang, Xiao ; Dioni, Laura ; Barretta, Francesco ; Dou, Chang ; Zheng, Yinan ; Hoxha, Mirjam ; Bertazzi, Pier Alberto ; Schwartz, Joel ; Wu, Shanshan ; Wang, Sheng ; Baccarelli, Andrea A. / Inhalable particulate matter and mitochondrial DNA copy number in highly exposed individuals in Beijing, China : A repeated-measure study. In: Particle and Fibre Toxicology. 2013 ; Vol. 10, No. 1.
@article{24406b83a2ad4e92ac277fffcef3cee8,
title = "Inhalable particulate matter and mitochondrial DNA copy number in highly exposed individuals in Beijing, China: A repeated-measure study",
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 PM2.5 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.",
keywords = "China, Mitochondrial DNA, Mitochondrial DNA copy number, Particulate matter, Traffic pollution",
author = "Lifang Hou and Xiao Zhang and Laura Dioni and Francesco Barretta and Chang Dou and Yinan Zheng and Mirjam Hoxha and Bertazzi, {Pier Alberto} and Joel Schwartz and Shanshan Wu and Sheng Wang and Baccarelli, {Andrea A.}",
year = "2013",
month = "4",
day = "29",
doi = "10.1186/1743-8977-10-17",
language = "English",
volume = "10",
journal = "Particle and Fibre Toxicology",
issn = "1743-8977",
publisher = "BioMed Central",
number = "1",

}

TY - JOUR

T1 - Inhalable particulate matter and mitochondrial DNA copy number in highly exposed individuals in Beijing, China

T2 - A repeated-measure study

AU - Hou, Lifang

AU - Zhang, Xiao

AU - Dioni, Laura

AU - Barretta, Francesco

AU - Dou, Chang

AU - Zheng, Yinan

AU - Hoxha, Mirjam

AU - Bertazzi, Pier Alberto

AU - Schwartz, Joel

AU - Wu, Shanshan

AU - Wang, Sheng

AU - Baccarelli, Andrea A.

PY - 2013/4/29

Y1 - 2013/4/29

N2 - 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 PM2.5 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.

AB - 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 PM2.5 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.

KW - China

KW - Mitochondrial DNA

KW - Mitochondrial DNA copy number

KW - Particulate matter

KW - Traffic pollution

UR - http://www.scopus.com/inward/record.url?scp=84876795487&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84876795487&partnerID=8YFLogxK

U2 - 10.1186/1743-8977-10-17

DO - 10.1186/1743-8977-10-17

M3 - Article

C2 - 23628000

AN - SCOPUS:84876795487

VL - 10

JO - Particle and Fibre Toxicology

JF - Particle and Fibre Toxicology

SN - 1743-8977

IS - 1

M1 - 17

ER -