Dimorphic placental stress: A repercussion of interaction between endocrine disrupting chemicals (EDCs) and fetal sex

Sood, Surbhi; Shekhar, Sudhanshu; Santosh, Winkins

doi:10.1016/j.mehy.2017.01.002

Cited by 24 publications

(14 citation statements)

References 38 publications

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“…Exposure to environmental agents may lead to epigenetic reprogramming, including changes in non-coding RNAs signatures, which can contribute to the induction of developmental changes or lead to disease progression and/or pathophysiology state (Miguel et al 2020). Until now, most studies have focused on chemical exposures including cadmium (Brooks and Fry 2017), phthalates (LaRocca et al 2016), arsenic, and endocrine disrupting chemicals (Sood et al 2017) in association with placental miRNAs. Indeed, miRNAs are considered guardians of cellular homeostasis, regulating several processes including stress responses.…”

Section: Discussionmentioning

confidence: 99%

Environmental pollutants and essential elements as regulators of miR-30b, miR-223 and Let-7a microRNAs expression in maternal sera from the NEHO cohort

Longo

Drago²,

Longo³

et al. 2022

Preprint

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Background: Birth cohorts of women living in highly industrialized areas provide an ideal setting for studying the correlation between environmental exposure and health. Objectives: To evaluate serum microRNA expression in response to environmental contaminants in 68 healthy pregnant women from the NEHO birth cohort. Methods: Serum contaminants were determined by GC-MS/MS and ICP-MS/MS. Serum microRNA expression was determined by qPCR. Associations between miRNA dCTs and single serum element levels were tested by linear regression models, while whole mixture effect was studied by WQS regression analysis. Results: In separate regression models, a positive association was found between miR-223 dCT and concentrations of Se and Zn, while a negative association between miR-30b and Hg levels was observed. Similar regression models were also conducted using tertiles of each chemical as independent variables. In this setting, the Let-7a dCT was decreased in the comparison between medium and low tertiles of Se. The highest tertiles of Zn and p,p-DDE showed a significant association with increasing levels of miR-223 dCT with respect to the lower tertile; moreover, miR-30b dCT was reduced in the comparison between high and low tertiles of Hg. The observed data were confirmed by fold-change analysis. A WQS analysis built on tertiles of contaminant distribution revealed a significant mixture effect on the expression of the analyzed miRNAs. The inverse association between Let-7a dCT and the WQS index was dominated by Zn, Se, Cu, Hg and HCB. Moreover, miR-223 dCT was positively associated with the WQS index, where p,p-DDE, Zn and Se showed the greatest contributions to the association. Conversely, the reduction of miR-30b dCT was mainly driven by Hg and Se. Discussion: This study allowed us to characterize the role of prolonged exposure to environmental contaminants influencing the expression of circulating miRNAs in the serum of women in the last trimester of pregnancy.

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Section: Discussionmentioning

confidence: 99%

Environmental pollutants and essential elements as regulators of miR-30b, miR-223 and Let-7a microRNAs expression in maternal sera from the NEHO cohort

Longo

Drago²,

Longo³

et al. 2022

Preprint

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“…S2 presents a simplified version) and were included in the models if they changed the effect estimates > 10% for at least one outcome [ 25 ]. Since the mechanism of action of endocrine disrupting chemicals may be sex-specific and influenced by folic acid, we tested for statistical interaction of bisphenol urine concentrations with fetal sex and folic acid supplement use [ 26 , 27 ]. We did not find statistically significant interactions ( p -values> 0.10) and no further stratified analyses were performed.…”

Section: Methodsmentioning

confidence: 99%

Maternal bisphenol urine concentrations, fetal growth and adverse birth outcomes: A population-based prospective cohort

et al. 2021

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Background Exposure to bisphenols may affect fetal growth and development. The trimester-specific effects of bisphenols on repeated measures of fetal growth remain unknown. Our objective was to assess the associations of maternal bisphenol urine concentrations with fetal growth measures and birth outcomes and identify potential critical exposure periods. Methods In a population-based prospective cohort study among 1379 pregnant women, we measured maternal bisphenol A, S and F urine concentrations in the first, second and third trimester. Fetal head circumference, length and weight were measured in the second and third trimester by ultrasound and at birth. Results An interquartile range increase in maternal pregnancy-averaged bisphenol S concentrations was associated with larger fetal head circumference (difference 0.18 (95% confidence interval (CI) 0.01 to 0.34) standard deviation scores (SDS), p-value< 0.05) across pregnancy. When focusing on specific critical exposure periods, any detection of first trimester bisphenol S was associated with larger second and third trimester fetal head circumference (difference 0.15 (95% CI 0.05 to 0.26) and 0.12 (95% CI 0.02 to 0.23) SDS, respectively) and fetal weight (difference 0.12 (95% CI 0.02 to 0.22) and 0.16 (95% CI 0.06 to 0.26) SDS, respectively). The other bisphenols were not consistently associated with fetal growth outcomes. Any detection of bisphenol S and bisphenol F in first trimester was also associated with a lower risk of being born small size for gestational age (Odds Ratio 0.56 (95% CI 0.38 to 0.74) and 0.55 (95% CI 0.36 to 0.85), respectively). Bisphenols were not associated with risk of preterm birth. Conclusions Higher maternal bisphenol S urine concentrations, especially in the first trimester, seem to be related with larger fetal head circumference, higher weight and a lower risk of being small size for gestational age at birth.

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“…Until now, most studies focused on chemical exposures including cadmium [57], phthalates [58], arsenic [59], and endocrine disrupting chemicals [60] in association with placental miRNAs. Moreover, multiple studies confirm a role for miRNAs in the response to air pollution exposure in adults [61–63].…”

Section: Air Pollution-induced Placental Epigenetic Alterationsmentioning

confidence: 99%

Air pollution-induced placental alterations: an interplay of oxidative stress, epigenetics, and the aging phenotype?

et al. 2019

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According to the "Developmental Origins of Health and Disease" (DOHaD) concept, the early-life environment is a critical period for fetal programming. Given the epidemiological evidence that air pollution exposure during pregnancy adversely affects newborn outcomes such as birth weight and preterm birth, there is a need to pay attention to underlying modes of action to better understand not only these air pollution-induced early health effects but also its later-life consequences. In this review, we give an overview of air pollution-induced placental molecular alterations observed in the ENVIRONAGE birth cohort and evaluate the existing evidence. In general, we showed that prenatal exposure to air pollution is associated with nitrosative stress and epigenetic alterations in the placenta. Adversely affected CpG targets were involved in cellular processes including DNA repair, circadian rhythm, and energy metabolism. For miRNA expression, specific air pollution exposure windows were associated with altered miR-20a, miR-21, miR-146a, and miR-222 expression. Early-life aging markers including telomere length and mitochondrial DNA content are associated with air pollution exposure during pregnancy. Previously, we proposed the air pollution-induced telomere-mitochondrial aging hypothesis with a direct link between telomeres and mitochondria. Here, we extend this view with a potential co-interaction of different biological mechanisms on the level of placental oxidative stress, epigenetics, aging, and energy metabolism. Investigating the placenta is an opportunity for future research as it may help to understand the fundamental biology underpinning the DOHaD concept through the interactions between the underlying modes of action, prenatal environment, and disease risk in later life. To prevent lasting consequences from early-life exposures of air pollution, policy makers should get a basic understanding of biomolecular consequences and transgenerational risks.

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Dimorphic placental stress: A repercussion of interaction between endocrine disrupting chemicals (EDCs) and fetal sex

Cited by 24 publications

References 38 publications

Environmental pollutants and essential elements as regulators of miR-30b, miR-223 and Let-7a microRNAs expression in maternal sera from the NEHO cohort

Environmental pollutants and essential elements as regulators of miR-30b, miR-223 and Let-7a microRNAs expression in maternal sera from the NEHO cohort

Maternal bisphenol urine concentrations, fetal growth and adverse birth outcomes: A population-based prospective cohort

Air pollution-induced placental alterations: an interplay of oxidative stress, epigenetics, and the aging phenotype?

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