Mitochondrial oxidative DNA damage and exposure to particulate air pollution in mother-newborn pairs

Environmental Health

Research

Charlotte Vanpoucke¹  Bram G. Janssen²  Tim S. Nawrot³  Valentina Bollati⁴  Lotte Grevendonk⁴  Mirjam Hoxha⁴  Wouter Lefebvre⁵ 

[1] Belgian Interregional Environment Agency, Brussels, Belgium;Centre for Environmental Sciences, Hasselt University, Hasselt, Belgium;Centre for Environmental Sciences, Hasselt University, Hasselt, Belgium;Department of Public Health & Primary Care, Occupational and Environmental Medicine, Leuven University, Leuven, Belgium;EPIGET-Epidemiology, Epigenetics and Toxicology Lab-Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy;Flemish Institute for Technological Research (VITO), Mol, Belgium;

关键词: 8-OHdG;    Foetal development;    Mitochondrial function;    Oxidative damage;    Particulate matter;   

DOI  :  10.1186/s12940-016-0095-2

 received in 2015-08-11, accepted in 2016-01-10,  发布年份 2016

来源: Springer

【 摘 要 】

BackgroundStudies emphasize the importance of particulate matter (PM) in the formation of reactive oxygen species and inflammation. We hypothesized that PM exposure during different time windows in pregnancy influences mitochondrial 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels, which is an established biomarker for oxidative stress, in both maternal and foetal blood.MethodsWe investigated maternal (n = 224) and cord blood (n = 293) from mother-newborn pairs that were enrolled in the ENVIRONAGE birth cohort. We determined mitochondrial 8-OHdG by quantitative polymerase chain reaction (qPCR). Multivariable regression models were used to assess the association between mitochondrial 8-OHdG with PM10 and PM2.5 exposure over various time windows during pregnancy.ResultsIn multivariable analysis, PM10 exposure during the entire pregnancy was positively associated with levels of mitochondrial 8-OHdG in maternal blood. For an IQR increment in PM10 exposure an increase of 18.3 % (95 % confidence interval (CI): 5.6 to 33.4 %, p = 0.004) in 8-OHdG was observed. PM10 exposure during the last trimester of pregnancy was positively associated with levels of 8-OHdG (28.1, 95 % CI: 8.6 to 51.2 %, p = 0.004, for an IQR increment in PM10). In a similar way, PM2.5 exposure was significantly associated with an increase of mitochondrial 8-OHdG levels in maternal blood during the entire pregnancy (13.9, 95 % CI: 0.4 to 29.4 %, p = 0.04 for an IQR increment in PM2.5 exposure) and third trimester of pregnancy (28.1, 95 % CI: 3.6 to 58.4 %, p = 0.02 for an IQR increment in PM2.5 exposure). In umbilical cord blood, 8-OHdG levels were significantly associated with PM10 exposure during first and second trimester of pregnancy with respectively an increase of 23.0 % (95 % CI: 5.9 to 42.8 %, p = 0.007) and 16.6 % (95 % CI: 1.8 to 33.5 %, p = 0.03) for an IQR increment in PM10 exposure.ConclusionsWe found PM-associated increased mitochondrial oxidative DNA damage during pregnancy in both mothers and their newborns. Accordingly, our study showed that particulate air pollution exposure in early life plays a role in increasing systemic oxidative stress, at the level of the mitochondria, both in mother and foetus.

【 授权许可】

CC BY   
© Grevendonk et al. 2016