Airborne particulate matter and mitochondrial damage: a cross-sectional study

Environmental Health

Research

Pier Alberto Bertazzi¹  Valeria Pegoraro¹  Mirjam Hoxha¹  Barbara Marinelli¹  Laura Dioni¹  Francesco Nordio²  Zhong-Zheng Zhu³  Andrea Baccarelli⁴  Matteo Bonzini⁵  Pietro Apostoli⁶  Xiao Zhang⁷  Lifang Hou⁸  Joel Schwartz⁹ 

[1] Center of Molecular and Genetic Epidemiology, Department of Environmental and Occupational Health, University of Milan and IRCCS Maggiore Policlinico Hospital, Mangiagalli and Regina Elena Foundation, Milan, Italy;Center of Molecular and Genetic Epidemiology, Department of Environmental and Occupational Health, University of Milan and IRCCS Maggiore Policlinico Hospital, Mangiagalli and Regina Elena Foundation, Milan, Italy;Department of Clinical Medicine, Nephrology and Health Sciences, University of Parma Medical School, Parma, Italy;Center of Molecular and Genetic Epidemiology, Department of Environmental and Occupational Health, University of Milan and IRCCS Maggiore Policlinico Hospital, Mangiagalli and Regina Elena Foundation, Milan, Italy;Department of Oncology, No.3 People's Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China;Center of Molecular and Genetic Epidemiology, Department of Environmental and Occupational Health, University of Milan and IRCCS Maggiore Policlinico Hospital, Mangiagalli and Regina Elena Foundation, Milan, Italy;Exposure, Epidemiology and Risk Program, Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA;Department of Clinical and Biological Sciences, University of Insubria, Varese, Italy;Department of Experimental and Applied Medicine, Occupational Medicine and Industrial Hygiene, University of Brescia, Brescia, Italy;Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA;Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA;Robert H. Lurie Comprehensive Cancer Center Feinberg, School of Medicine, Northwestern University, Chicago, Illinois, USA;Exposure, Epidemiology and Risk Program, Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA;

关键词: Reactive Oxygen Species;    Coarse Particle;    Metal Component;    Dynamic Reaction Cell;    Foundry Worker;   

DOI  :  10.1186/1476-069X-9-48

 received in 2009-12-21, accepted in 2010-08-09,  发布年份 2010

来源: Springer

【 摘 要 】

BackgroundOxidative 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.MethodsIn 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.ResultsRMtDNAcn 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: β = 0.06, 95%CI = -0.06 to 0.17; PM1: β = 0.08, 95%CI = -0.08 to 0.23; coarse: β = 0.06, 95%CI = -0.06 to 0.17) or the 1st day (PM10: β = 0.18, 95%CI = 0.09 to 0.26; PM1: 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.ConclusionsPM exposure is associated with damaged mitochondria, as reflected in increased MtDNAcn. Damaged mitochondria may intensify oxidative-stress production and effects.

【 授权许可】

CC BY   
© Hou et al; licensee BioMed Central Ltd. 2010