Abstract
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.Electronic supplementary materialThe online version of this article (doi:10.1186/s12940-016-0095-2) contains supplementary material, which is available to authorized users.
Highlights
Studies emphasize the importance of particulate matter (PM) in the formation of reactive oxygen species and inflammation
We explored whether assisted reproductive technologies may alter the association between PM exposure and cord or maternal 8-OHdG levels
To explore the functional significance of the association between mitochondrial 8-OHdG with exposure to PM, we evaluated the association between mitochondrial DNA (mtDNA) content, a measure of altered mitochondrial function, and 8-OHdG levels in maternal and cord blood
Summary
Studies 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. Among the different types of ROS-induced DNA damage, the oxidation of guanine and the formation of 8-hydroxy-2′-deoxyguanosine (8-OHdG) is the most common one [7]. Oxidative DNA damage can be repaired by means of 8-OHdG removal from the nuclear, and the mitochondrial genome, representing a steady-state level of oxidative stress within a cell [8]. High and continuous exposure to PM-induced ROS in mitochondria are likely to cause oxidative mtDNA damage as reflected by increased amounts of mitochondrial 8OHdG levels. Several studies demonstrated an association between nuclear 8-OHdG levels and PM exposure [12,13,14,15,16] but whether exposure to PM during gestation influences mitochondrial 8-OHdG both in mothers and newborns is not known
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