Comparison of Smoking-Related DNA Methylation Between Newborns from Prenatal Exposure and Adults from Personal Smoking

Sikdar, Sinjini; Joehanes, Roby; Joubert, Bonnie R.; Xu, Cheng‐Jian; Vives-Usano, Marta; Rezwan, Faisal I.; Felix, Janine F.; Ward, James M.; Guan, Weihua; Richmond, Rebecca C; Brody, Jennifer A.; Küpers, Leanne K.; Baïz, Nour; Håberg, Siri E.; Smith, Jennifer A.; Reese, Sarah E.; Aslibekyan, Stella; Hoyo, Cathrine; Dhingra, Radhika; Markunas, Christina A.; Xu, Tao; Reynolds, Lindsay M.; Just, Allan C.; Mandaviya, Pooja R.; Ghantous, Akram; Bennett, Brian D.; Wang, Tianyuan; Consortium, The BIOS; Bakulski, Kelly M.; Melén, Erik; Zhao, Shanshan; Jin, Jianping; Herceg, Zdenko; Meurs, Joyce van; Taylor, Jack A.; Baccarelli, Andrea A.; Murphy, Susan K.; Liu, Yongmei; Munthe‐Kaas, Monica Cheng; Deary, Ian J.; Nystad, Wenche; Waldenberger, Mélanie; Annesi‐Maesano, Isabella; Conneely, Karen N.; Jaddoe, Vincent W. V.; Arnett, Donna K.; Snieder, Harold; Kardia, Sharon L.R.; Relton, Caroline; Ong, Ken K.; Ewart, Susan; Moreno-Macías, Hortensia; Romieu, Isabelle; Sotoodehnia, Nona; Fornage, Myriam; Motsinger‐Reif, Alison A.; Koppelman, Gerard H.; Bustamante, Mariona; Levy, Daniel; London, Stephanie J.

doi:10.2217/epi-2019-0066

Cited by 68 publications

(81 citation statements)

References 44 publications

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“…Conversely, as an indication of the long-term and strong effects of active smoking, we did find enrichment for child CpGs associated with maternal smoking in pregnancy among CpGs described for current smoking in other studies. Indeed, it has been described a remarkable overlap between the blood methylation signatures detected in adult smokers and in newborns of smoker mothers [74].…”

Section: Discussionmentioning

confidence: 99%

In utero and childhood exposure to tobacco smoke and multi-layer molecular signatures in children

Vives-Usano

Hernández-Ferrer

Maitre

et al. 2020

BMC Med

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Background: The adverse health effects of early life exposure to tobacco smoking have been widely reported. In spite of this, the underlying molecular mechanisms of in utero and postnatal exposure to tobacco smoke are only partially understood. Here, we aimed to identify multi-layer molecular signatures associated with exposure to tobacco smoke in these two exposure windows. Methods: We investigated the associations of maternal smoking during pregnancy and childhood secondhand smoke (SHS) exposure with molecular features measured in 1203 European children (mean age 8.1 years) from the Human Early Life Exposome (HELIX) project. Molecular features, covering 4 layers, included blood DNA methylation and gene and miRNA transcription, plasma proteins, and sera and urinary metabolites. Results: Maternal smoking during pregnancy was associated with DNA methylation changes at 18 loci in child blood. DNA methylation at 5 of these loci was related to expression of the nearby genes. However, the expression of these genes themselves was only weakly associated with maternal smoking. Conversely, childhood SHS was not associated with blood DNA methylation or transcription patterns, but with reduced levels of several serum metabolites and with increased plasma PAI1 (plasminogen activator inhibitor-1), a protein that inhibits fibrinolysis. Some of the in utero and childhood smoking-related molecular marks showed dose-response trends, with stronger effects with higher dose or longer duration of the exposure.

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Section: Discussionmentioning

confidence: 99%

In utero and childhood exposure to tobacco smoke and multi-layer molecular signatures in children

Vives-Usano

Hernández-Ferrer

Maitre

et al. 2020

BMC Med

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“…A study of the Danish National Birth Cohort (608 cases vs 626 control) identified the UACA gene at the cg12157761 associated with the offspring of women with gestational diabetes mellitus [21]. In addition, a meta-analysis showed that newborn blood DNA CpG cg01244124 located in UACA was negatively associated with sustained maternal smoking during pregnancy [22]. Though the gene UACA in responding to different CpGs among the various studies, the results of these two studies were not contradictive with our findings, in that diabetes mellitus and smoking were the classic risk factor of CVD and may induce DNA methylation alteration at specific site to result in the outcome of CVD.…”

Section: Discussionmentioning

confidence: 99%

Genome-wide analysis of DNA methylation and risk of cardiovascular disease in a Chinese population

Gao

Pang

Chen

et al. 2021

BMC Cardiovasc Disord

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Background Systemic studies of association of genome-wide DNA methylated sites with cardiovascular disease (CVD) in prospective cohorts are lacking. Our aim was to identify DNA methylation sites associated with the risk of CVD and further investigate their potential predictive value in CVD development for high-risk subjects. Methods We performed an epigenome-wide association study (EWAS) to identify CpGs related to CVD development in a Chinese population.We adopted a nested case–control design based on data from China PEACE Million Persons Project. A total of 83 cases who developed CVD events during follow-up and 83 controls who were matched with cases by age, sex, BMI, ethnicity, medications treatment and behavior risk factors were included in the discovery stage. Genome-wide DNA methylation from whole blood was detected using Infinium Human Methylation EPIC Beadchip (850 K). For significant CpGs [FDR(false discovery rate) < 0.005], we further validated in an independent cohort including 38 cases and 38 controls. Results In discovery set, we identified 8 significant CpGs (FDR < 0.005) associated with the risk of CVD after adjustment for cell components, demographic and cardiac risk factors and the first 5 principal components. Two of these identified CpGs (cg06901278 and cg09306458 in UACA) were replicated in another independent set (p < 0.05). Enrichment analysis in 787 individual genes from 1036 CpGs in discovery set revealed a significant enrichment for anatomical structure homeostasis as well as regulation of vesicle-mediated transport. Receiver operating characteristic (ROC) analysis showed that the model combined 8 CVD-related CpGs with baseline characteristics showed much better predictive effect for CVD occurrence compared with the model with baseline characteristics only [AUC (area under the curve) = 0.967, 95% CI (0.942 − 0.991); AUC = 0.621, 95% CI (0.536 − 0.706); p = 9.716E-15]. Conclusions Our study identified the novel CpGs associated with CVD development and revealed their additional predictive power in the risk of CVD for high-risk subjects.

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“…Maternal smoking during pregnancy is associated with many adverse consequences on the offspring, including early respiratory illness, reduced pulmonary function, reduced birthweight, sudden infant death syndrome, and neurobehavioral disorders. 9,10 It has been well documented that smoking during pregnancy is associated with several adverse obstetric outcomes. [11][12][13] There is evidence that several tobacco metabolites can cross the placental barrier and cause both perinatal and postnatal health consequences; however, the causal relationship between exposure to smoking and increase in human cellular injury is not yet clearly understood.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Plasma Asymmetric Dimethylarginine Levels and Abdominal Aortic Intima-Media Thickness in Infants of Smoker Mothers

et al. 2020

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Objective Smoking during pregnancy has harmful effects on the fetus and infant. Although some studies suggest that exposure to fetal–maternal smoking adversely affects both fetal growth and cardiovascular development, the mechanisms and biochemical consequences of smoking in pregnancy and newborns are not yet fully understood. We aimed to investigate whether maternal smoking during pregnancy causes fetal cardiovascular effect by measuring serum asymmetric dimethylarginine (ADMA) level and abdominal aortic intima-media thickness (aIMT). Study Design This prospective study was conducted in newborns of smoking mothers and never-smoker control mothers during their pregnancies. The babies were evaluated echocardiographically on the first day following birth. In two-dimensional mode, abdominal aIMT measurements were performed. ADMA was measured in umbilical cord blood at birth. Results There were 25 mothers in the study group and 25 mothers in the control group. Serum ADMA levels were 0.459 ± 0.119 μmol/L in the study group and 0.374 ± 0.1127 μmol/L in the control group (p = 0.034). The aIMT value in the study group was 0.84 ± 0.026 mm and the aIMT value in the control group was 0.63 ± 0.011 mm (p = 0.005). Conclusion We found that both the serum ADMA and the aIMT significantly increased in the group with newborns of smoker mothers compared with the group of the newborns of never-smoker mothers. It may also be suggested that exposure to fetal–maternal smoking adversely affects cardiovascular development. Key Points

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Comparison of Smoking-Related DNA Methylation Between Newborns from Prenatal Exposure and Adults from Personal Smoking

Cited by 68 publications

References 44 publications

In utero and childhood exposure to tobacco smoke and multi-layer molecular signatures in children

In utero and childhood exposure to tobacco smoke and multi-layer molecular signatures in children

Genome-wide analysis of DNA methylation and risk of cardiovascular disease in a Chinese population

Evaluation of Plasma Asymmetric Dimethylarginine Levels and Abdominal Aortic Intima-Media Thickness in Infants of Smoker Mothers

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