Ambient air pollution exposure during the late gestational period is linked with lower placental iodine load in a Belgian birth cohort

Neven, Kristof Y.; Wang, Congrong; Janssen, Bram G.; Roels, Harry; Vanpoucke, Charlotte; Ruttens, Ann; Nawrot, Tim S.

doi:10.1016/j.envint.2020.106334

Cited by 16 publications

(8 citation statements)

References 55 publications

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“…Our study has several strengths. We used a validated, high-resolution spatial–temporal interpolation method to assess daily PM 2.5 exposures during pregnancy, which has been used in several studies [ 5 , 66 , 67 ] and was validated for gestational exposures and accumulation of nanoparticles in placental tissue [ 67 ]. To determine the MT-ND4L 10550A>G SNP, we used Droplet Digital PCR allowing the detection of low-level mutations by partitioning the PCR mixture into approximately 20,000 droplets, causing it to have superior sensitivity and accuracy compared to other methods [ 68 ].…”

Section: Discussionmentioning

confidence: 99%

In utero particulate matter exposure in association with newborn mitochondrial ND4L10550A>G heteroplasmy and its role in overweight during early childhood

et al. 2022

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Background Mitochondria play an important role in the energy metabolism and are susceptible to environmental pollution. Prenatal air pollution exposure has been linked with childhood obesity. Placental mtDNA mutations have been associated with prenatal particulate matter exposure and MT-ND4L10550A>G heteroplasmy has been associated with BMI in adults. Therefore, we hypothesized that in utero PM2.5 exposure is associated with cord blood MT-ND4L10550A>G heteroplasmy and early life growth. In addition, the role of cord blood MT-ND4L10550A>G heteroplasmy in overweight during early childhood is investigated. Methods This study included 386 mother-newborn pairs. Outdoor PM2.5 concentrations were determined at the maternal residential address. Cord blood MT-ND4L10550A>G heteroplasmy was determined using Droplet Digital PCR. Associations were explored using logistic regression models and distributed lag linear models. Mediation analysis was performed to quantify the effects of prenatal PM2.5 exposure on childhood overweight mediated by cord blood MT-ND4L10550A>G heteroplasmy. Results Prenatal PM2.5 exposure was positively associated with childhood overweight during the whole pregnancy (OR = 2.33; 95% CI: 1.20 to 4.51; p = 0.01), which was mainly driven by the second trimester. In addition, prenatal PM2.5 exposure was associated with cord blood MT-ND4L10550A>G heteroplasmy from gestational week 9 – 13. The largest effect was observed in week 10, where a 5 µg/m3 increment in PM2.5 was linked with cord blood MT-ND4L10550A>G heteroplasmy (OR = 0.93; 95% CI: 0.87 to 0.99). Cord blood MT-ND4L10550A>G heteroplasmy was also linked with childhood overweight (OR = 3.04; 95% CI: 1.15 to 7.50; p = 0.02). The effect of prenatal PM2.5 exposure on childhood overweight was mainly direct (total effect OR = 1.18; 95% CI: 0.99 to 1.36; natural direct effect OR = 1.20; 95% CI: 1.01 to 1.36)) and was not mediated by cord blood MT-ND4L10550A>G heteroplasmy. Conclusions Cord blood MT-ND4L10550A>G heteroplasmy was linked with childhood overweight. In addition, in utero exposure to PM2.5 during the first trimester of pregnancy was associated with cord blood MT-ND4L10550A>G heteroplasmy in newborns. Our analysis did not reveal any mediation of cord blood MT-ND4L10550A>G heteroplasmy in the association between PM2.5 exposure and childhood overweight.

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Section: Discussionmentioning

confidence: 99%

In utero particulate matter exposure in association with newborn mitochondrial ND4L10550A>G heteroplasmy and its role in overweight during early childhood

et al. 2022

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“…Obviously, iodine deficiency might promote these deleterious effects and thus deregulate transcription and thyroid hormone-induced epigenetic effects on target genes [ 109 ]. The urgency of this issue is the coincidence of the still prevailing inadequate iodine supply and continuously increasing exposure of humans to TDCs [ 6 , 22 , 110 , 111 , 112 ].…”

Section: Resultsmentioning

confidence: 99%

Iodine Deficiency, Maternal Hypothyroxinemia and Endocrine Disrupters Affecting Fetal Brain Development: A Scoping Review

Großklaus

Liesenkötter

Doubek³

et al. 2023

Nutrients

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This scoping review critically discusses the publications of the last 30 years on the impact of mild to moderate iodine deficiency and the additional impact of endocrine disrupters during pregnancy on embryonal/fetal brain development. An asymptomatic mild to moderate iodine deficiency and/or isolated maternal hypothyroxinemia might affect the development of the embryonal/fetal brain. There is sufficient evidence underlining the importance of an adequate iodine supply for all women of childbearing age in order to prevent negative mental and social consequences for their children. An additional threat to the thyroid hormone system is the ubiquitous exposure to endocrine disrupters, which might exacerbate the effects of iodine deficiency in pregnant women on the neurocognitive development of their offspring. Ensuring adequate iodine intake is therefore essential not only for healthy fetal and neonatal development in general, but it might also extenuate the effects of endocrine disruptors. Individual iodine supplementation of women of childbearing age living in areas with mild to moderate iodine deficiency is mandatory as long as worldwide universal salt iodization does not guarantee an adequate iodine supply. There is an urgent need for detailed strategies to identify and reduce exposure to endocrine disrupters according to the “precautional principle”.

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“…Our study has several strengths. To assess the daily air pollution exposures during the entire pregnancy, we used a validated, high-resolution spatial–temporal interpolation method that has been used in multiple studies. − We used whole mitochondrial genome sequencing to analyze the entire mitochondrial genome. As the mean coverage was 19,627×, base calls were made with a high degree of confidence.…”

Section: Discussionmentioning

confidence: 99%

In Utero Exposure to Air Pollutants and Mitochondrial Heteroplasmy in Neonates

Cosemans

Wang

Martens

et al. 2022

Environ. Sci. Technol.

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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 (PM 2.5 ) and NO 2 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 PM 2.5 and NO 2 concentrations were determined by a highresolution 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 NO 2 exposure and cord-blood mtDNA heteroplasmy. A 5 μg/m 3 increment in NO 2 was linked with MT-D-Loop 16311T>C heteroplasmy from gestational weeks 17−25. MT-CYTB 14766C>T was negatively associated with NO 2 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 PM 2.5 exposure. This is the first study to show that prenatal NO 2 exposure is associated with cord-blood mitochondrial mutations and suggests two critical windows of exposure in mid-to-late pregnancy.

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Ambient air pollution exposure during the late gestational period is linked with lower placental iodine load in a Belgian birth cohort

Cited by 16 publications

References 55 publications

In utero particulate matter exposure in association with newborn mitochondrial ND4L10550A>G heteroplasmy and its role in overweight during early childhood

In utero particulate matter exposure in association with newborn mitochondrial ND4L10550A>G heteroplasmy and its role in overweight during early childhood

Iodine Deficiency, Maternal Hypothyroxinemia and Endocrine Disrupters Affecting Fetal Brain Development: A Scoping Review

In Utero Exposure to Air Pollutants and Mitochondrial Heteroplasmy in Neonates

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