The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.
Prenatal environmental exposures, epigenetics, and disease
Open accessAbstract
This review summarizes recent evidence that prenatal exposure to diverse environmental chemicals dysregulates the fetal epigenome, with potential consequences for subsequent developmental disorders and disease manifesting in childhood, over the lifecourse, or even transgenerationally. The primordial germ cells, embryo, and fetus are highly susceptible to epigenetic dysregulation by environmental chemicals, which can thereby exert multiple adverse effects. The data reviewed here on environmental contaminants have potential implications for risk assessment although more data are needed on individual susceptibility to epigenetic alterations and their persistence before this information can be used in formal risk assessments. The findings discussed indicate that identification of environmental chemicals that dysregulate the prenatal epigenome should be a priority in health research and disease prevention.
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Cites
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Environmental epigenomics and disease susceptibility
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Linking DNA methylation and histone modification: patterns and paradigms
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“Two examples include coordinated epigenetic modifications of chromatin by DNA methylation and posttranslational covalent modifications of histone proteins [4,11,12] and micro-RNA-induced suppression of gene expression during development [13].”
Transposable elements: targets for early nutritional effects on epigenetic gene regulation
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“The fact that CpG sites were altered in tissues derived from the ectodermal, endodermal, and mesodermal lineages indicates that methylation profiles were changed early in embryonic development [7,18,37].”
Stability and flexibility of epigenetic gene regulation in mammalian development
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“As noted, imprinted genes do not undergo genome-wide demethylation before implantation but maintain their methylation patterns throughout this period of reprogramming, allowing for the inheritance of parental-specific monoallelic expression in somatic tissues throughout adulthood [20].”
InfluentialDevelopmental plasticity and human health
Bateson, P., Barker, D., Clutton-Brock, T., Deb, D., D'Udine, B., Foley, R. A., Gluckman, P., Godfrey, K., Kirkwood, T., Lahr, M. M., et al. (2004) · Nature · doi:10.1038/nature02725 · Cited by 1,742
Glucose tolerance in adults after prenatal exposure to famine
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Decrease in anogenital distance among male infants with prenatal phthalate exposure
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Cited by
Delcuve, G. P., Khan, D. H., & Davie, J. R. (2012) · Clinical Epigenetics · doi:10.1186/1868-7083-4-5 · Cited by 505
Perera, F. P. (2017) · Environmental Health Perspectives · doi:10.1289/ehp299 · Cited by 426
Self-citationReproductive and developmental effects of phthalate diesters in females
Kay, V. R., Chambers, C., & Foster, W. G. (2013) · Critical Reviews in Toxicology · doi:10.3109/10408444.2013.766149 · Cited by 396
Gabory, A., Roseboom, T. J., Moore, T., Moore, L. G., & Junien, C. (2013) · Biology of Sex Differences · doi:10.1186/2042-6410-4-5 · Cited by 344
Cortessis, V. K., Thomas, D. C., Levine, A. J., Breton, C. V., Mack, T. M., Siegmund, K. D., Haile, R. W., & Laird, P. W. (2012) · Human Genetics · doi:10.1007/s00439-012-1189-8 · Cited by 319
Metadata
- Authors
- Perera, F., & Herbstman, J.
- Venue
- Reproductive Toxicology
- Publisher
- Elsevier BV
- Published
- 2011-04
- Volume
- 31
- Issue
- 3
- Pages
- 363-373
- ISSN
- 0890-6238 (ISSN-L)
- OpenAlex
- W2101526557
- Cited by
- 641
- References
- 28
- FWCI
- 14.69
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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