Umbilical cord blood PBDEs concentrations are associated with placental DNA methylation

Zhao, Yan; Liu, Pengcheng; Junyong, Wang; Xiao, Xirong; Meng, Xiang−Zhou; Zhang, Yunhui

doi:10.1016/j.envint.2016.10.014

Cited by 41 publications

(19 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been identified in our previous study that global DNA hypomethylation is associated with high serum POP concentration (K. Li, unpublished data, 2017), which may be due to the upregulation of TET1 and TET2 methylcytosine dioxygenases. A recent population study showed that high level of BDE-66 exposure was associated with decreased DNA methylation and in utero PBDEs exposure ( 39 ); this study is similar to our observation that POP exposure decreased LINE1 methylation. Interestingly, LINE-1 can also participate in the regulation of telomere maintenance ( 47 ), of which mechanism is not well understood.…”

Section: Discussionsupporting

confidence: 92%

“…Previous evidence-based epidemiological studies have established the adverse effects of POPs on metabolic health, even at low-dose exposure levels. Bioaccumulation of POPs has been linked to many human diseases, including cardiovascular disease ( 36 ), metabolic disorders ( 8 ), developmental disorders ( 37 ), endocrine disorders ( 38 ), and epigenetic alterations ( 39 ). We observed that the POP exposure was highly associated with the occurrence of the type 2 diabetes, autoimmune disorders, abnormal pregnancy, and adverse fetal growth, which could be clustered to premature metabolic disorders.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Long-term Persistent Organic Pollutants Exposure Induced Telomere Dysfunction and Senescence-Associated Secretary Phenotype

Yuan

Liu

Wang

et al. 2018

The Journals of Gerontology: Series A

View full text Add to dashboard Cite

Environmentally persistent organic pollutant (POP) is the general term for refractory organic compounds that show long-range atmospheric transport, environmental persistence, and bioaccumulation. It has been reported that the accumulation of POPs could lead to cellular DNA damage and adverse effects of on metabolic health. To better understand the mechanism of the health risks associated with POPs, we conducted an evidence-based cohort investigation (n = 5,955) at the Jinghai e-waste disposal center in China from 2009 to 2016, where people endure serious POP exposure. And high levels of aging-related diseases, including hypertension, diabetes, autoimmune diseases, and reproductive disorders were identified associated with the POP exposure. In the subsequent molecular level study, an increased telomere dysfunction including telomere multiple telomere signals, telomere signal-free ends, telomere shortening and activation of alternative lengthening of telomeres were observed, which might result from the hypomethylated DNA modification induced telomeric repeat-containing RNA overexpression. Moreover, dysfunctional telomere-leaded senescence-associated secretory phenotype was confirmed, as the proinflammatory cytokines and immunosenescence hallmarks including interleukin-6, P16INK4a, and P14ARF were stimulated. Thus, we proposed that the dysfunctional telomere and elevated systemic chronic inflammation contribute to the aging-associated diseases, which were highly developed among the POP exposure individuals.

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Long-term Persistent Organic Pollutants Exposure Induced Telomere Dysfunction and Senescence-Associated Secretary Phenotype

Yuan

Liu

Wang

et al. 2018

The Journals of Gerontology: Series A

View full text Add to dashboard Cite

show abstract

“…Accumulating evidence indicates that prenatal POPs exposures result in adverse mental and physical development [158–161], visual recognition memory abnormity [162], neurodevelopmental delay [163], reproductive problems [164, 165], obesity [166], and immune diseases [167] in the later life of offspring. Moreover, such adverse health effects from prenatal exposure to POPs are associated with epigenetic dysregulation, for instance, DNA hypomethylation of repeat elements ( Alu ( Arthrobacter luteus ) and LINE-1 ) in fetal blood with exposure to DDT, DDE, and PBDEs [168]; hypomethylation of tumor necrosis factor alpha ( TNF-α ), IGF2 , and nuclear receptor subfamily 3 group C member 1 ( NR3C1 ) in core blood and placenta with exposure to PBDEs [169–171]; global and IGF2 hypomethylation in sperm cells and cord blood samples with exposure to PFOA [95, 172–174]; altered DNA methylation in the H19 , IGF2, and IGF2r genes with exposure to dioxin [175, 176]; hypermethylation of the Hoxa10 gene, hypomethylation in the Exon-4 of c-fos gene, and increased EZH gene expression with exposure to diethylstilbestrol [138, 177, 178]; and increased methylation in the Peg1 , Snrpn , Peg3, and ERβ genes with exposure to methoxychlor [151, 179]. In addition, certain POPs have been shown to promote epigenetic transgenerational inheritance of disease susceptibility [148, 180] (Table 2).…”

Section: Prenatal Environmental Pollution and Epigenetic Dysregulationmentioning

confidence: 99%

Prenatal epigenetics diets play protective roles against environmental pollution

Chen

Tollefsbol

2019

Clin Epigenet

View full text Add to dashboard Cite

It is thought that germ cells and preimplantation embryos during development are most susceptible to endogenous and exogenous environmental factors because the epigenome in those cells is undergoing dramatic elimination and reconstruction. Exposure to environmental factors such as nutrition, climate, stress, pathogens, toxins, and even social behavior during gametogenesis and early embryogenesis has been shown to influence disease susceptibility in the offspring. Early-life epigenetic modifications, which determine the expression of genetic information stored in the genome, are viewed as one of the general mechanisms linking prenatal exposure and phenotypic changes later in life. From atmospheric pollution, endocrine-disrupting chemicals to heavy metals, research increasingly suggests that environmental pollutions have already produced significant consequences on human health. Moreover, mounting evidence now links such pollution to relevant modification in the epigenome. The epigenetics diet, referring to a class of bioactive dietary compounds such as isothiocyanates in broccoli, genistein in soybean, resveratrol in grape, epigallocatechin-3-gallate in green tea, and ascorbic acid in fruits, has been shown to modify the epigenome leading to beneficial health outcomes. This review will primarily focus on the causes and consequences of prenatal environment pollution exposure on the epigenome, and the potential protective role of the epigenetics diet, which could play a central role in neutralizing epigenomic aberrations against environmental pollutions.

show abstract

“…Therefore, changes in DNA methylation in the placenta may be one of the potential mechanisms that explain the impact of POPs on human fetal outcomes [ 16 ]. Existing studies of POPs and placental DNA methylation were based on candidate gene-based approaches [ 17 – 20 ]. Two studies among 109 pregnant women from the CHECK (Children’s Health and Environmental Chemicals in Korea) cohort reported associations of β-hexachlorocyclohexane (β-HCH) with decreased methylation in LINE-1 (a surrogate marker of global methylation) and p , p ′-dichlorodiphenyltrichloroethane ( p , p ′-DDT) with increased methylation of IGF2 (implicated in placental and fetal growth) [ 17 ] and MCT8 among boys [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

“…P,p ′-dichlorodiphenyldichloroethylene ( p,p ′-DDE) and polybrominated diphenyl ether-47 (PBDE 47) were significantly associated with increased methylation in DIO3 among female infants [ 18 ]. Higher PBDE 66 in cord blood was associated with decreased placental methylation in LINE-1 and higher PBDEs 153 and 209 with decreased placental methylation of IGF2 among Chinese [ 20 ] while others did not find any associations [ 19 ]. Most studies have investigated individual POPs, although pregnant women are exposed to a mixture of chemicals [ 1 ].…”

Section: Introductionmentioning

confidence: 99%

Concentrations of persistent organic pollutants in maternal plasma and epigenome-wide placental DNA methylation

et al. 2020

View full text Add to dashboard Cite

Background Prenatal maternal plasma persistent organic pollutant (POP) concentrations have been associated with neonatal outcomes. However, the underlying mechanisms remain unknown. Placental epigenetic mechanisms may be involved, but no prior epigenome-wide studies have investigated the impact of maternal POPs on placental DNA methylation. We studied the association between maternal plasma POP concentration in early pregnancy and epigenome-wide placental DNA methylation among 260 pregnant women from the NICHD Fetal Growth Studies. Results Our analysis focused on POPs with more than 80% plasma concentrations above the limit of quantification, including 3 organochlorine pesticides (hexachlorobenzene, trans-nonachlor, p,p’ -dichlorodiphenyldichloroethylene), 1 polybrominated diphenyl ether (PBDE 47), 3 polychlorinated biphenyls (138/158, 153, 180), and 6 poly- and perfluorinated alkyl substances (PFASs) (perfluorodecanoic acid, perfluorohexanesulfonic acid, perfluorononanoic acid, perfluorooctanesulfonic acid, perfluoroundecanoic acid (PFUnDA)). Using 5% false discovery rate, POPs were associated with a total of 214 differentially methylated CpG sites (nominal p values ranging from 2.61 × 10 −21 to 2.11 × 10 −7 ). Out of the 214 CpG sites, 24 (11%) were significantly correlated with placental expression of 21 genes. Notably, higher PFUnDA was associated with increased methylation at 3 CpG sites (cg13996963, cg12089439, cg18145877) annotated to TUSC3 , and increased methylation at those 3 CpG sites was correlated with decreased expression of TUSC3 in the placenta. Increased methylation at cg18145877 ( TUSC3 ) and decreased expression of TUSC3 were correlated with shorter birth length. Out of the 214 CpG sites, methylation at 44 CpG sites was correlated ( p value < 0.10) with at least one neonatal anthropometry measure (i.e., birth weight, birth length, and head circumference). Seven CpG sites mediated ( p value < 0.05) the association between PBDE 47 and neonatal anthropometry measures. Genes annotating the top differentially methylated CpG sites were enriched in pathways related to differentiation of embryonic cells (PBDE 47) and in pathways related to brain size and brain morphology (PFASs). Conclusions DNA methylation changes in the placenta were significantly associated with maternal plasma POPs concentration. The findings suggest that placental DNA methylation and gene expression mechanism may be involved in the prenatal toxicity of POPs and their association with neonatal anthropometry measures.

show abstract

Umbilical cord blood PBDEs concentrations are associated with placental DNA methylation

Cited by 41 publications

References 49 publications

Long-term Persistent Organic Pollutants Exposure Induced Telomere Dysfunction and Senescence-Associated Secretary Phenotype

Long-term Persistent Organic Pollutants Exposure Induced Telomere Dysfunction and Senescence-Associated Secretary Phenotype

Prenatal epigenetics diets play protective roles against environmental pollution

Concentrations of persistent organic pollutants in maternal plasma and epigenome-wide placental DNA methylation

Contact Info

Product

Resources

About