Associations of cadmium, bisphenol A and polychlorinated biphenyl co-exposure in utero with placental gene expression and neonatal outcomes

Xu, Xijin; Chiung, Yin Mei; Lu, Fangfang; Qiu, Shaoshan; Ji, Minhui; Huo, Xia

doi:10.1016/j.reprotox.2015.02.004

Cited by 60 publications

(47 citation statements)

References 48 publications

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“…The potential health ramifications of these expression changes in the placenta, however, are not clear, and this study did not account for potential sex differences. Another recent study showed that KISS1 mRNA expression in the placenta was positively correlated to exposure of pregnant women to cadmium, BPA, and polychlorinated biphenyls (88). Elevated concentrations of leptin and leptin receptor were also positively associated with BPA concentrations.…”

Section: Environmental Chemicalsmentioning

confidence: 93%

“…A decrease in DNA methylation was evident in AluYb8 for boys exposed to the highest total effective xenoestrogen burden, but no differences were detected in girls. Animal model and human studies, which did not explore for sex differences, suggest that EDCs can affect imprinted genes in the placenta (78,79), other gene transcripts and pathways (80,81), DNA methylation patterns (82), miRNAs (83), and placental structure. This latter study showed that BPA exposure of fetal mice reduced the labyrinth region and increased metrial gland size, resulted in thinning of intervillous spaces, and degenerative changes in trophoblastic giant cells and the spongiotrophoblast layer (84).…”

Section: Environmental Chemicalsmentioning

confidence: 99%

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Sex-Specific Placental Responses in Fetal Development

2015

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The placenta is an ephemeral but critical organ for the survival of all eutherian mammals and marsupials. It is the primary messenger system between the mother and fetus, where communicational signals, nutrients, waste, gases, and extrinsic factors are exchanged. Although the placenta may buffer the fetus from various environmental insults, placental dysfunction might also contribute to detrimental developmental origins of adult health and disease effects. The placenta of one sex over the other might possess greater ability to respond and buffer against environmental insults. Given the potential role of the placenta in effecting the lifetime health of the offspring, it is not surprising that there has been a resurging interest in this organ, including the Human Placental Project launched by the National Institutes of Child Health and Human Development. In this review, we will compare embryological development of the laboratory mouse and human chorioallantoic placentae. Next, evidence that various species, including humans, exhibit normal sex-dependent structural and functional placental differences will be examined followed by how in utero environmental changes (nutritional state, stress, and exposure to environmental chemicals) might interact with fetal sex to affect this organ. Recent data also suggest that paternal state impacts placental function in a sex-dependent manner. The research to date linking placental maladaptive responses and later developmental origins of adult health and disease effects will be explored. Finally, we will focus on how sex chromosomes and epimutations may contribute to sex-dependent differences in placental function, the unanswered questions, and future directions that warrant further consideration.

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Section: Environmental Chemicalsmentioning

confidence: 93%

Section: Environmental Chemicalsmentioning

confidence: 99%

Sex-Specific Placental Responses in Fetal Development

2015

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“…At the same level as the sex hormones, also affecting the overall development of the foetus, endocrine-disrupting chemicals (EDC) have been highlighted as the main effectors altering placental and foetal performance in a deleterious way. EDC has been shown to alter gene transcription, signaling pathways (Tan et al 2013, Xu et al 2015, DNA methylation patterns (Nahar et al 2015), miRNAs (Avissar-Whiting et al 2010) and placental structure (Tachibana et al 2007). However, a sex-dependent placental response is still not strongly supported by the literature.…”

Section: Response To Sex Hormones and Endocrine Disruptorsmentioning

confidence: 99%

Early sex-dependent differences in response to environmental stress

et al. 2018

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Developmental plasticity enables the appearance of long-term effects in offspring caused by exposure to environmental stressors during embryonic and foetal life. These long-term effects can be traced to pre-and post-implantation development, and in both cases, the effects are usually sex specific. During preimplantation development, male and female embryos exhibit an extensive transcriptional dimorphism mainly driven by incomplete X chromosome inactivation. These early developmental stages are crucial for the establishment of epigenetic marks that will be conserved throughout development, making it a particularly susceptible period for the appearance of long-term epigenetic-based phenotypes. Later in development, gonadal formation generates hormonal differences between the sexes, and male and female placentae exhibit different responses to environmental stressors. The maternal environment, including hormones and environmental insults during pregnancy, contributes to sex-specific placental development that controls genetic and epigenetic programming during foetal development, regulating sex-specific differences, including sex-specific epigenetic responses to environmental hazards, leading to long-term effects. This review summarizes several human and animal studies examining sex-specific responses to environmental stressors during both the periconception period (caused by differences in sex chromosome dosage) and placental development (caused by both sex chromosomes and hormones). The identification of relevant sex-dependent trajectories caused by sex chromosomes and/or sex hormones is essential to define diagnostic markers and prevention/intervention protocols.Reproduction (2018) 155 R39-R51

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“…Although the placenta may act as a partial barrier to Cd being transferred to the fetus, it is likely that at least some Cd accumulates in the placenta 26. There it can act as a barrier to the transfer of micronutrients, particularly zinc, by induction of metallothionein production,3 and this could restrict fetal growth directly.…”

Section: Commentsmentioning

confidence: 99%

“…(1) Although we were able to account for many possible confounders in our analyses, there are likely to be others that were unable to adjust for. These include the effects of other environmental pollutants, such as polychlorinated biphenols 26. (2) There were a large number of values for B‐Cd below the limit of detection, making the use of the measurement as a continuous variable in linear models less robust.…”

Section: Commentsmentioning

confidence: 99%

Moderate Prenatal Cadmium Exposure and Adverse Birth Outcomes: a Role for Sex‐Specific Differences?

Taylor

Golding

Emond

2016

Paediatric Perinatal Epid

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Background/AimStudies on the effects of moderate prenatal exposure to cadmium (Cd) on birth outcomes have been contradictory and it has been suggested that effects may be partly masked by sex‐specific effects. Our aim was to examine the association of Cd exposure in a large group of pregnant women with birth outcomes in the whole group of participants and by sex.MethodsPregnant women were enrolled in the Avon Longitudinal Study of Parents and Children (ALSPAC). Whole blood samples for singleton pregnancies with a live birth were analysed for Cd (n = 4191). Data collected on the infants included anthropometric variables and gestational age at delivery. Data were analysed using SPSS v18.ResultsThere were adverse associations of maternal blood Cd level with birthweight (unstandardized B coefficient −62.7 g, 95% CI −107.0, −18.4) and crown–heel length (−0.28 cm, 95% CI −0.48, −0.07) in adjusted regression models. On stratification by sex, maternal blood Cd level was adversely associated with birthweight (−87.1 g, 95% CI −144.8, −29.4), head circumference (−0.22 cm, 95% CI −0.39, −0.04), and crown–heel length (−0.44 cm, 95% CI −0.71, −0.18) in girls but not in boys in adjusted regression models.ConclusionIn these pregnant women with moderate prenatal Cd exposure there evidence of adverse associations with birth anthropometry variables in the whole group. However, there was evidence of associations with anthropometric variables in girls that were not evident in boys. Sex‐specific effects require further investigation in large cohorts as a possible contributor to the lack of associations generally found in mixed‐sex studies.

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Associations of cadmium, bisphenol A and polychlorinated biphenyl co-exposure in utero with placental gene expression and neonatal outcomes

Cited by 60 publications

References 48 publications

Sex-Specific Placental Responses in Fetal Development

Sex-Specific Placental Responses in Fetal Development

Early sex-dependent differences in response to environmental stress

Moderate Prenatal Cadmium Exposure and Adverse Birth Outcomes: a Role for Sex‐Specific Differences?

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