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Relation of DNA Methylation of 5′-CpG Island of ACSL3 to Transplacental Exposure to Airborne Polycyclic Aromatic Hydrocarbons and Childhood Asthma
Open accessAbstract
In a longitudinal cohort of approximately 700 children in New York City, the prevalence of asthma (>25%) is among the highest in the US. This high risk may in part be caused by transplacental exposure to traffic-related polycyclic aromatic hydrocarbons (PAHs) but biomarkers informative of PAH-asthma relationships is lacking. We here hypothesized that epigenetic marks associated with transplacental PAH exposure and/or childhood asthma risk could be identified in fetal tissues. Mothers completed personal prenatal air monitoring for PAH exposure determination. Methylation sensitive restriction fingerprinting was used to analyze umbilical cord white blood cell (UCWBC) DNA of 20 cohort children. Over 30 DNA sequences were identified whose methylation status was dependent on the level of maternal PAH exposure. Six sequences were found to be homologous to known genes having one or more 5'-CpG island(s) (5'-CGI). Of these, acyl-CoA synthetase long-chain family member 3 (ACSL3) exhibited the highest concordance between the extent of methylation of its 5'-CGI in UCWBCs and the level of gene expression in matched fetal placental tissues in the initial 20 cohort children. ACSL3 was therefore chosen for further investigation in a larger sample of 56 cohort children. Methylation of the ACSL3 5'-CGI was found to be significantly associated with maternal airborne PAH exposure exceeding 2.41 ng/m(3) (OR = 13.8; p<0.001; sensitivity = 75%; specificity = 82%) and with a parental report of asthma symptoms in children prior to age 5 (OR = 3.9; p<0.05). Thus, if validated, methylated ACSL3 5'CGI in UCWBC DNA may be a surrogate endpoint for transplacental PAH exposure and/or a potential biomarker for environmentally-related asthma. This exploratory report provides a new blueprint for the discovery of epigenetic biomarkers relevant to other exposure assessments and/or investigations of exposure-disease relationships in birth cohorts. The results support the emerging theory of early origins of later life disease development.
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Dolinoy, D. C., Huang, D., & Jirtle, R. L. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0703739104 · Cited by 1,369 · cited 1×
“The best studied mechanisms underpinning the latter scenario is the induction of aberrant DNA methylation of regulatory sequences in susceptible genes by environmental toxicants during critical developmental periods, leading to inappropriate gene expression and disease pathogenesis in later life [12–16].”
BackgroundHo, S.-M., Tang, W.-Y., Belmonte de Frausto, J., & Prins, G. S. (2006) · Cancer Research · doi:10.1158/0008-5472.can-06-0516 · Cited by 796
Self-citationPerera, F. P., Rauh, V., Tsai, W.-Y., Kinney, P., Camann, D., Barr, D., Bernert, T., Garfinkel, R., Tu, Y.-H., Diaz, D., et al. (2003) · Environmental Health Perspectives · doi:10.1289/ehp.5742 · Cited by 625
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Alegría-Torres, J. A., Baccarelli, A., & Bollati, V. (2011) · Epigenomics · doi:10.2217/epi.11.22 · Cited by 587
The biodiversity hypothesis and allergic disease: world allergy organization position statement
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Metadata
- Authors
- Perera, F., Tang, W.-Y., Herbstman, J., Tang, D., Levin, L., Miller, R., & Ho, S.-M.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2009-02-16
- Volume
- 4
- Issue
- 2
- Pages
- e4488
- ISSN
- 1932-6203 (ISSN-L)
- OpenAlex
- W1965691847
- Cited by
- 396
- References
- 3
- FWCI
- 14.88
- Type
- journal article
- Language
- en
- Open access
- gold
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- Perera, F., Tang, W.-Y., Herbstman, J., Tang, D., Levin, L., Miller, R., & Ho, S.-M. (2009). Relation of DNA Methylation of 5′-CpG Island of ACSL3 to Transplacental Exposure to Airborne Polycyclic Aromatic Hydrocarbons and Childhood Asthma. PLoS ONE. https://doi.org/10.1371/journal.pone.0004488
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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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