ArticlePloS one2014
Prenatal polycyclic aromatic hydrocarbon, adiposity, peroxisome proliferator-activated receptor (PPAR) γ methylation in offspring, grand-offspring mice.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 84 citations in OpenAlex.
- Relationship Between Polycyclic Aromatic Hydrocarbons and Cardiovascular Diseases: A Systematic Review.Frontiers in public health · 2021Pooled it
- Is breast cancer a result of epigenetic responses to traffic-related air pollution? A review of the latest evidence.Epigenomics · 2019Pooled it
- Prenatal Internal Exposure to Polycyclic Aromatic Hydrocarbons, Maternal Genetic Susceptibility, and Child Growth Trajectories: Evidence from a Prospective Cohort Study.Environmental science & technology · 2026Article
- Prenatal polycyclic aromatic hydrocarbons exposure and child growth and adiposity: A longitudinal study.Environmental research · 2025Article
- An evaluation of in utero polycyclic aromatic hydrocarbon exposure on the neonatal meconium microbiome.Environmental research · 2024Article
- Environmental Obesogens and Their Perturbations in Lipid Metabolism.Environment & health (Washington, D.C.) · 2024Review
- Cohort Profile: The Mothers and Newborns (MN) Cohort of the Columbia Center for Children's Environmental Health.International journal of epidemiology · 2024Article
- Association of mixed polycyclic aromatic hydrocarbons exposure with hearing loss and the mediating role of blood cell markers of inflammation in U.S. adults.Frontiers in public health · 2024Article
- Prenatal exposures to mixtures of endocrine disrupting chemicals and sex-specific associations with children's BMI and overweight at 5.5 years of age in the SELMA study.Environment international · 2023Article
- Prenatal airborne polycyclic aromatic hydrocarbon exposure, altered regulation of peroxisome proliferator-activated receptor gamma (Ppar)γ, and links with mammary cancer.Environmental research · 2023Article
- Inherited Epigenetic Hallmarks of Childhood Obesity Derived from Prenatal Exposure to Obesogens.International journal of environmental research and public health · 2023Review
- Chronic Exposure to Low-Molecular-Weight Polycyclic Aromatic Hydrocarbons Promotes Lipid Accumulation and Metabolic Inflammation.Biomolecules · 2023Article
- Recent progress in epigenetics of obesity.Diabetology & metabolic syndrome · 2022Review
- The Role of Persistent Organic Pollutants in Obesity: A Review of Laboratory and Epidemiological Studies.Toxics · 2022Review
- Increased PPARD Expression May Play a Protective Role in Human Lung Adenocarcinoma and Squamous Cell Carcinoma.PPAR research · 2022Article
- Obesogens in Children-An Uncharted Territory.Metabolites · 2021Review
- Epigenetic Mechanisms of Endocrine-Disrupting Chemicals in Obesity.Biomedicines · 2021Review
- Ambient air pollution and endocrinologic disorders in childhood.Annals of pediatric endocrinology & metabolism · 2021Article
- Prenatal polycyclic aromatic hydrocarbons, altered ERα pathway-related methylation and expression, and mammary epithelial cell proliferation in offspring and grandoffspring adult mice.Environmental research · 2021Article
- Polycyclic Aromatic Hydrocarbons and Mammary Cancer Risk: Does Obesity Matter too?Journal of cancer immunology · 2021Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
rationaleGreater levels of prenatal exposure to polycyclic aromatic hydrocarbon (PAH) have been associated with childhood obesity in epidemiological studies. However, the underlying mechanisms are unclear.
objectivesWe hypothesized that prenatal PAH over-exposure during gestation would lead to weight gain and increased fat mass in offspring and grand-offspring mice. Further, we hypothesized that altered adipose gene expression and DNA methylation in genes important to adipocyte differentiation would be affected. MATERIALS AND
methodsPregnant dams were exposed to a nebulized PAH mixture versus negative control aerosol 5 days a week, for 3 weeks. Body weight was recorded from postnatal day (PND) 21 through PND60. Body composition, adipose cell size, gene expression of peroxisome proliferator-activated receptor (PPAR) γ, CCAAT/enhancer-binding proteins (C/EBP) α, cyclooxygenase (Cox)-2, fatty acid synthase (FAS) and adiponectin, and DNA methylation of PPAR γ, were assayed in both the offspring and grand-offspring adipose tissue.
findingsOffspring of dams exposed to greater PAH during gestation had increased weight, fat mass, as well as higher gene expression of PPAR γ, C/EBP α, Cox2, FAS and adiponectin and lower DNA methylation of PPAR γ. Similar differences in phenotype and DNA methylation extended through the grand-offspring mice.
conclusionsGreater prenatal PAH exposure was associated with increased weight, fat mass, adipose gene expression and epigenetic changes in progeny.
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What OpenQuestion holds
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.