ArticleMetabolism: clinical and experimental2010
In utero tobacco exposure epigenetically modifies placental CYP1A1 expression.
Article in Metabolism: clinical and experimental, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
94 citing papers in PubMed, 2 syntheses or guidelines pooled it, 188 citations in OpenAlex.
- The role of epigenetics in respiratory health in urban populations in low and middle-income countries.Global health, epidemiology and genomics · 2019Pooled it
- Environmental Epigenetic Changes, as Risk Factors for the Development of Diseases in Children: A Systematic Review.Annals of global health · 2018Pooled it
- Vitamin C supplementation improves placental function and alters placental gene expression in smokers.Scientific reports · 2024Trial
- Trial
- Differences in gene expression between first and third trimester human placenta: a microarray study.PloS one · 2012Trial
- Nicotine Exposure During Gestation: From Placental Dysfunction to Long-Term Neurobehavioral Outcomes.Birth defects research · 2026Review
- Early-life exposures and risk of multiple gynecological diseases: evidence from a large community-based study of 272,706 women.BMC women's health · 2026Observational
- The Developmental Origins of Asthma and COPD.Annual review of physiology · 2026Review
- Prenatal cannabis smoke exposure alters placental development in a murine model of pregnancy.PloS one · 2026Article
- Maternal DNA methylation signatures of gestational diabetes across all stages of pregnancy.Journal of translational medicine · 2025Article
- Examination of DNA Methylation Patterns in Children Born Premature with Prenatal Tobacco Smoke Exposure.Toxics · 2025Article
- Placental Polycyclic Aromatic Hydrocarbon (PAH) Levels Are Associated with Spontaneous Preterm Birth.International journal of molecular sciences · 2025Article
- Machine learning-enhanced surface-enhanced spectroscopic detection of polycyclic aromatic hydrocarbons in the human placenta.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Environmental exposures influence multigenerational epigenetic transmission.Clinical epigenetics · 2024Review
- Early-life exposure to cigarette smoke primes lung function and DNA methylation changes atAmerican journal of physiology. Lung cellular and molecular physiology · 2023Article
- Preterm Birth, Developmental Smoke/Nicotine Exposure, and Life-Long Pulmonary Sequelae.Children (Basel, Switzerland) · 2023Review
- Nrf2Frontiers in genetics · 2023Article
- Article
- Developmental origins of adult diseases.Medical review (2021) · 2022Review
- Methylation in the Promoter Region of the Dopamine TransporterInternational journal of environmental research and public health · 2022Article
34 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The metabolic pathways used by higher-eukaryotic organisms to deal with potentially carcinogenic xenobiotic compounds from tobacco smoke have been well characterized. Carcinogenic compounds such as polycyclic aromatic hydrocarbons are metabolized sequentially in 2 phases: in phase I, CYP1A1 catalyzes conversion into harmful hydrophilic DNA adducts, whereas in phase II, GSTT1 enables excretion via conjugation into polar electrophiles. In an effort to understand susceptibility to in utero tobacco exposure, we previously characterized known metabolic functional polymorphisms and demonstrated that although deletion of fetal GSTT1 significantly modified birth weight in smokers, no polymorphism fully accounted for fetal growth restriction. Because smoking up-regulates CYP1A1 expression, we hypothesized that nonallelic (epigenetic) dysregulation of placental CYP1A1 expression via alterations in DNA methylation (meCpG) may further modify fetal growth. In the present article, we compared placental expression of multiple CYP family members among gravidae and observed significantly increased CYP1A1 expression among smokers relative to controls (4.4-fold, P < .05). To fully characterize CYP1A1 meCpG status, bisulfite modification and sequencing of the entire proximal 1-kilobase promoter (containing 59 CpG sites) were performed. CpG sites immediately proximal to the 5′-xenobiotic response element transcription factor binding element were significantly hypomethylated among smokers (55.6% vs 45.9% meCpG, P = .027), a finding that uniquely correlated with placental gene expression (r = 0.737, P = .007). Thus, in utero tobacco exposure significantly increases placental CYP1A1 expression in association with differential methylation at a critical xenobiotic response element.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.