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In Utero Exposure to Air Pollutants and Mitochondrial Heteroplasmy in Neonates

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posted on 2022-12-14, 17:03 authored by Charlotte Cosemans, Congrong Wang, Dries S. Martens, Bram G. Janssen, Charlotte Vanpoucke, Wouter Lefebvre, Karen Smeets, Tim S. Nawrot, Michelle Plusquin
Mitochondria are sensitive to oxidative stress, which can be caused by traffic-related air pollution. Placental mitochondrial DNA (mtDNA) mutations have been previously linked with air pollution. However, the relationship between prenatal air pollution and cord-blood mtDNA mutations has been poorly understood. Therefore, we hypothesized that prenatal particulate matter (PM2.5) and NO2 exposures are associated with cord-blood mtDNA heteroplasmy. As part of the ENVIRONAGE cohort, 200 mother–newborn pairs were recruited. Cord-blood mitochondrial single-nucleotide polymorphisms were identified by whole mitochondrial genome sequencing, and heteroplasmy levels were evaluated based on the variant allele frequency (VAF). Outdoor PM2.5 and NO2 concentrations were determined by a high-resolution spatial–temporal interpolation method based on the maternal residential address. Distributed lag linear models were used to determine sensitive time windows for the association between NO2 exposure and cord-blood mtDNA heteroplasmy. A 5 μg/m3 increment in NO2 was linked with MT-D-Loop16311T>C heteroplasmy from gestational weeks 17–25. MT-CYTB14766C>T was negatively associated with NO2 exposure in mid pregnancy, from weeks 14–17, and positively associated in late pregnancy, from weeks 31–36. No significant associations were observed with prenatal PM2.5 exposure. This is the first study to show that prenatal NO2 exposure is associated with cord-blood mitochondrial mutations and suggests two critical windows of exposure in mid-to-late pregnancy.

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