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Maternal smoking during pregnancy induces persistent epigenetic changes into adolescence, independent of postnatal smoke exposure and is associated with cardiometabolic risk
Citation
Rauschert, S and Melton, PE and Burdge, G and Craig, JM and Godfrey, KM and Holbrook, JD and Lillycrop, K and Mori, TA and Beilin, LJ and Oddy, WH and Pennell, C and Huang, R-C, Maternal smoking during pregnancy induces persistent epigenetic changes into adolescence, independent of postnatal smoke exposure and is associated with cardiometabolic risk, Frontiers in Genetics, 10 Article 770. ISSN 1664-8021 (2019) [Refereed Article]
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Copyright Statement
Copyright 2019 Rauschert, Melton, Burdge, Craig, Godfrey, Holbrook, Lillycrop, Mori, Beilin, Oddy, Pennell and Huang. Licensed under Creative Commons Attribution 4.0 International (CC BY 4.0) https://creativecommons.org/licenses/by/4.0/
DOI: doi:10.3389/fgene.2019.00770
Abstract
Materials and Methods: DNA methylation was measured using the Illumina HumanMethylation450K BeadChip in whole blood from 995 participants attending the 17-year follow-up of the Raine Study. Linear mixed effects models were used to identify differential methylated CpGs, adjusting for parental smoking during pregnancy, and paternal, passive, and adolescent smoke exposure. Additional models examined the association between DNA methylation and paternal, adolescent, and passive smoking over the life course. Offspring CpGs identified were analyzed against cardiometabolic risk factors (blood pressure, triacylglycerols (TG), high-density lipoproteins cholesterol (HDLC), and body mass index).
Results: We identified 23 CpGs (genome-wide p level: 1.06 × 10−7) that were associated with maternal smoking during pregnancy, including associated genes AHRR (cancer development), FTO (obesity), CNTNAP2 (developmental processes), CYP1A1 (detoxification), MYO1G (cell signalling), and FRMD4A (nicotine dependence). A sensitivity analysis showed a dose-dependent relationship between maternal smoking and offspring methylation. These results changed little following adjustment for paternal, passive, or offspring smoking, and there were no CpGs identified that associated with these variables. Two of the 23 identified CpGs [cg00253568 (FTO) and cg00213123 (CYP1A1)] were associated with either TG (male and female), diastolic blood pressure (female only), or HDL-C (male only), after Bonferroni correction.
Discussion: This study demonstrates a critical timing of cigarette smoke exposure over the life course for establishing persistent changes in DNA methylation into adolescence in a dose-dependent manner. There were significant associations between offspring CpG methylation and adolescent cardiovascular risk factors, namely, TG, HDL-C, and diastolic blood pressure. Future studies on current smoking habits and DNA methylation should consider the importance of maternal smoking during pregnancy and explore how the persistent DNA methylation effects of in utero smoke exposure increase cardiometabolic risk.
Item Details
| Item Type: | Refereed Article |
|---|---|
| Keywords: | DNA methylation, maternal smoking during pregnancy, epigenetics, Raine Study, cardiometabolic health, adolescence |
| Research Division: | Biological Sciences |
| Research Group: | Genetics |
| Research Field: | Epigenetics (incl. Genome Methylation and Epigenomics) |
| Objective Division: | Health |
| Objective Group: | Specific Population Health (excl. Indigenous Health) |
| Objective Field: | Child Health |
| UTAS Author: | Oddy, WH (Professor Wendy Oddy) |
| ID Code: | 135280 |
| Year Published: | 2019 |
| Deposited By: | Menzies Institute for Medical Research |
| Deposited On: | 2019-10-10 |
| Last Modified: | 2019-11-11 |
| Downloads: | 4 View Download Statistics |
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