Placental Mitochondrial DNA Content and Particulate Air Pollution during in Utero Life

Abstract

Background: Studies emphasize the importance of particulate matter (PM) in the formation of reactive oxygen species and inflammation. We hypothesized that these processes can influence mitochondrial function of the placenta and fetus.Objective: We investigated the influence of PM10 exposure during pregnancy on the mitochondrial DNA content (mtDNA content) of the placenta and umbilical cord blood.Methods: DNA was extracted from placental tissue (n = 174) and umbilical cord leukocytes (n = 176). Relative mtDNA copy numbers (i.e., mtDNA content) were determined by real-time polymerase chain reaction. Multiple regression models were used to link mtDNA content and in utero exposure to PM10 over various time windows during pregnancy.Results: In multivariate-adjusted analysis, a 10-µg/m³ increase in PM10 exposure during the last month of pregnancy was associated with a 16.1% decrease [95% confidence interval (CI): –25.2, –6.0%, p = 0.003] in placental mtDNA content. The corresponding effect size for average PM10 exposure during the third trimester was 17.4% (95% CI: –31.8, –0.1%, p = 0.05). Furthermore, we found that each doubling in residential distance to major roads was associated with an increase in placental mtDNA content of 4.0% (95% CI: 0.4, 7.8%, p = 0.03). No association was found between cord blood mtDNA content and PM10 exposure.Conclusions: Prenatal PM10 exposure was associated with placental mitochondrial alterations, which may both reflect and intensify oxidative stress production. The potential health consequences of decreased placental mtDNA content in early life must be further elucidated.

Placental mitochondrial methylation and exposure to airborne particulate matter in the early life environment: An ENVIRONAGE birth cohort study

“…It is noteworthy to mention that we observed an inverse correlation between placental mtDNA methylation and mtDNA content in contrast to a positive correlation observed in blood leukocytes. 22 Previous investigations have shown that mtDNA content is variable and fluctuates during aging, 31,32 under the influence of different environmental factors, 33 and the tissue investigated, 11,31,34 as well as different effects from recent versus long-term exposures. Nevertheless, we found similar results when we compared placental mtDNA content between mothers who continued smoking vs. non-smoking pregnant mothers (i.e., lower mtDNA content in smokers; relative difference of ¡21.98%, 95% CI: ¡41.10 to ¡0.86%, P D 0.01).…”

“…10 Changes in fetal mtDNA content may represent a biological effect along the path linking air pollution to effects on the fetus, such as birth weight. Previously, we showed a lower mtDNA content in placental tissue in association with in utero exposure to PM 10 (PM with aerodynamic diameter 10 mm), 11 which reflects signs of mitophagy and mitochondrial death.…”

Decrease in Respiratory Function and Electron Transport Chain Induced by Airborne Particulate Matter (PM10) Exposure in Lung Mitochondria

“…PM 10 exposure increase in the last pregnancy month is associated with decrease in mtDNA content (Janssen et al 2012), and as a result, a decrease On the other hand, we recognize that an important number of studies showed that PM collected from different cities, including Ohio (Xu et al 2011), Washington, D.C. (Mutlu et al 2011), and Boston (Golomb et al 2012) in United States, Paris, (Ferecatu et al 2010), and Milan (Gualtieri et al 2009), among others, shares some mitochondrial disturbances. However, we cannot discard the fact that some of the mitochondrial effects observed in this work could be attributed partially to the specific-PM 10 composition collected from Mexico City.…”

The Maternal Thyroid Gland as A Sentinel Organ for A Development: Signs of The Possible Harm of Air Pollution in Development

“…These variations may be attributed to PM exposure during the gestation can increase the activity of glucocorticoid (Thomson et al 2013) suppressing the release of TSH (Wilber and Utiger 1969). Also, the antiinflammatory actions of glucocorticoids can induce the response of a systemic oxidative stress (Janssen et al 2012) and elevate the placental protein-bound 3-nitrotyrosine (Saenen et al 2016). Alternatively, PM2.5 can enter the lungs and blood circulation, where they may prompt the release of oxidative stress resulting in several neurodevelopment complications (Grahame et al, 2014).…”