Maternal smoking, passive tobacco smoke, and neural tube defects

Suarez, Lucina; Ramadhani, Tunu A.; Felkner, Marilyn; Canfield, Mark A.; Brender, Jean D.; Romitti, Paul A.; Sun, Lin

doi:10.1002/bdra.20743

Cited by 33 publications

(43 citation statements)

References 33 publications

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“…Environmental factors such as exposure to alcohol, cigarette smoke, numerous drugs and chemicals, microbial infection, and lack of nutrients ( e.g. , trace elements and folate) have been implicated in the etiology of numerous developmental anomalies [21,24,50–53]. A potential molecular mechanism underlying many of these environmental insults is aberrant methylation of susceptible genes which results in the altered expression of genes indispensable for normal embryogenesis.…”

Section: Discussionmentioning

confidence: 99%

Alcohol modulates expression of DNA methyltranferases and methyl CpG-/CpG domain-binding proteins in murine embryonic fibroblasts

Mukhopadhyay

Rezzoug

Kaikaus

et al. 2013

Reproductive Toxicology

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Fetal alcohol syndrome (FAS), presenting with a constellation of neuro-/psychological, craniofacial and cardiac abnormalities, occurs frequently in offspring of women who consume alcohol during pregnancy, with a prevalence of 1–3 per 1000 livebirths. The present study was designed to test the hypothesis that alcohol alters global DNA methylation, and modulates expression of the DNA methyltransferases (DNMTs) and various methyl CpG-binding proteins. Murine embryonic fibroblasts (MEFs), utilized as an in vitro embryonic model system, demonstrated ~5% reduction in global DNA methylation following exposure to 200 mM ethanol. In addition, ethanol induced degradation of DNA methyltransferases (DNMT-1, DNMT-3a, and DNMT-3b), as well as the methyl CpG-binding proteins (MeCP-2, MBD-2 and MBD-3), in MEF cells by the proteasomal pathway. Such degradation could be completely rescued by pretreatment of MEF cells with the proteasomal inhibitor, MG-132. These data support a potential epigenetic molecular mechanism underlying the pathogenesis of FAS during mammalian development.

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Section: Discussionmentioning

confidence: 99%

Alcohol modulates expression of DNA methyltranferases and methyl CpG-/CpG domain-binding proteins in murine embryonic fibroblasts

Mukhopadhyay

Rezzoug

Kaikaus

et al. 2013

Reproductive Toxicology

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“…Individuals exposed to secondhand smoke are subjected to a majority of the same constituents as those contained in mainstream smoke, although the pattern and amounts of exposure differ [Windham et al, 2000]. Studies of secondhand smoke exposure and birth defects have identified increased risks of neural tube defects, cleft lip with/without palate, and anorectal atresia [Miller et al, 2009; Li et al, 2010; Suarez et al, 2011]. …”

Section: Discussionmentioning

confidence: 99%

Analysis of selected maternal exposures and non‐syndromic atrioventricular septal defects in the National Birth Defects Prevention Study, 1997–2005.

Patel

Burns

Botto

et al. 2012

American J of Med Genetics Pt A

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Although the descriptive epidemiology of atrioventricular septal defects (AVSDs), a group of serious congenital heart defects (CHDs), has been recently reported, non-genetic risk factors have not been consistently identified. Using data (1997–2005) from the National Birth Defects Prevention Study, an ongoing multisite population-based case–control study, the association between selected non-genetic factors and non-syndromic AVSDs was examined. Data on periconceptional exposures to such factors were collected by telephone interview from 187 mothers of AVSD case infants and 6,703 mothers of unaffected infants. Adjusted odds ratios (aORs) and 95% confidence intervals (CIs) were estimated from logistic regression models. Mothers who reported cigarette smoking during the periconceptional period were more likely to have infants with AVSDs compared with non-smokers, independent of maternal age, periconceptional alcohol consumption, infant gestational age, family history of CHDs, and study site (aOR 1.5, 95% CI 1.1–2.4). The association was strongest in mothers who smoked more than 25 cigarettes/day. In addition, mothers with periconceptional passive smoke exposure were more likely to have infants with AVSDs than unexposed mothers, independent of maternal age, active periconceptional smoking, infant gestational age, and family history of CHDs (aOR 1.4, 95% CI 1.0–2.0). No associations were observed between AVSDs and maternal history of a urinary tract infection or pelvic inflammatory disease, maternal use of a wide variety of medications, maternal occupational exposure, parental drug use, or maternal alcohol consumption. If the results of this preliminary study can be replicated, minimizing maternal active and passive smoke exposure may decrease the incidence of AVSDs.

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“…These include medical conditions such as maternal diabetes 16 or maternal obesity, 17 while environmental exposures such as cigarette smoke, mycotoxins or use of anti-epileptic drugs may have teratogenic effects. [18][19][20] Maternal dietary factors leading to a high dietary glycemic index or a high glycemic load are associated with increased risk of an NTD affected pregnancy, 21 as are sub-optimal levels of folate and vitamin B 12 . 22,23 Particular attention has been paid to the role of folate onecarbon metabolism, especially owing to the finding that maternal supplementation with folic acid reduces the risk of NTDs.…”

Section: O N O T D I S T R I B U T Ementioning

confidence: 99%

The emerging role of epigenetic mechanisms in the etiology of neural tube defects

Greene¹,

Stanier²,

Moore

2011

Epigenetics

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The molecular requirements for neural tube closure are complex. This is illustrated by the occurrence of neural tube defects (NTDs) in many genetic mouse mutants, which implicate a variety of genes, pathways and cellular functions. NTDs are also prevalent birth defects in humans, affecting around 1 per 1000 pregnancies worldwide. In humans the causation is thought to involve the interplay of fetal genes and the effect of environmental factors. Recent studies on the aetiology of human NTDs, as well as analysis of mouse models, have raised the question of the possible involvement of epigenetic factors in determining susceptibility. A consideration of potential causative factors in human NTDs must now include both alterations in the regulation of gene expression, through mutation of promoter or regulatory elements, and the additional analysis of epigenetic regulation. Alterations in the epigenetic status can be directly modified by various environmental insults or maternal dietary factors.

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Maternal smoking, passive tobacco smoke, and neural tube defects

Abstract: Results suggest that maternal exposure to passive smoke is associated with NTDs. Women who plan on becoming pregnant should minimize their exposure to passive smoke and refrain from smoking.

Cited by 33 publications

References 33 publications

Alcohol modulates expression of DNA methyltranferases and methyl CpG-/CpG domain-binding proteins in murine embryonic fibroblasts

Alcohol modulates expression of DNA methyltranferases and methyl CpG-/CpG domain-binding proteins in murine embryonic fibroblasts

Analysis of selected maternal exposures and non‐syndromic atrioventricular septal defects in the National Birth Defects Prevention Study, 1997–2005.

The emerging role of epigenetic mechanisms in the etiology of neural tube defects

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