Levels of select PCB and PBDE congeners in human postmortem brain reveal possible environmental involvement in 15q11‐q13 duplication autism spectrum disorder
Open accessAbstract
Persistent organic pollutants (POPs), including polychlorinated biphenyls (PCBs) and polybrominated diphenylethers (PBDEs) that bioaccumulate in lipid‐rich tissues are of concern as developmental neurotoxicants. Epigenetic mechanisms such as DNA methylation act at the interface of genetic and environmental factors implicated in autism‐spectrum disorders. The relationship between POP levels and DNA methylation patterns in individuals with and without neurodevelopmental disorders has not been previously investigated. In this study, a total of 107 human frozen postmortem brain samples were analyzed for eight PCBs and seven PBDEs by GC‐micro electron capture detector and GC/MS using negative chemical ionization. Human brain samples were grouped as neurotypical controls ( n = 43), neurodevelopmental disorders with known genetic basis ( n = 32, including Down, Rett, Prader‐Willi, Angelman, and 15q11‐q13 duplication syndromes), and autism of unknown etiology ( n = 32). Unexpectedly, PCB 95 was significantly higher in the genetic neurodevelopmental group, but not idiopathic autism, as compared to neurotypical controls. Interestingly, samples with detectable PCB 95 levels were almost exclusively those with maternal 15q11‐q13 duplication (Dup15q) or deletion in Prader‐Willi syndrome. When sorted by birth year, Dup15q samples represented five out of six of genetic neurodevelopmental samples born after the 1976 PCB ban exhibiting detectable PCB 95 levels. Dup15q was the strongest predictor of PCB 95 exposure over age, gender, or year of birth. Dup15q brain showed lower levels of repetitive DNA methylation measured by LINE‐1 pyrosequencing, but methylation levels were confounded by year of birth. These results demonstrate a novel paradigm by which specific POPs may predispose to genetic copy number variation of 15q11‐q13. Environ. Mol. Mutagen., 2012. © 2012 Wiley Periodicals, Inc.
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PCB 95, but not other PCBs or PBDEs, are significantly higher in postmortem brains of children with a syndromic form of autism, compared with neurotypical controls.
“This possibility is supported by a recent report that PCB 95, but not other PCBs or PBDEs, are significantly higher in postmortem brains of children with a syndromic form of autism, compared with neurotypical controls (Mitchell et al., 2012).”
From The Environmental Neurotoxicant PCB 95 Promotes Synaptogenesis via Ryanodine Receptor-Dependent miR132 Upregulation (2014) · cites this paper as Mitchell et al., 2012
The Results (Comprehensive analysis of POP levels; page unavailable) report significantly higher PCB 95 in the combined genetic neurodevelopmental-disorder group than in neurotypical controls; Dup15q was a strong predictor in the subgroup analysis. The paper does not establish that this comparison was specifically between children with syndromic autism and controls. It also reports significantly lower BDE 153, though not higher levels of other PBDEs. (LLM, conf=0.88)
Experimental — accuracy not yet measured15q duplication was the strongest predictor of PCB 95 exposure and these individuals also exhibited DNA hypomethylation of the LINE-1 element.
“15q duplication was the strongest predictor of PCB 95 exposure and these individuals also exhibited DNA hypomethylation of the LINE-1 element [ 40 ].”
From DNA methylation: a mechanism linking environmental chemical exposures to risk of autism spectrum disorders? (2016) · cites this paper as [40]
Of the eight PCB congeners examined, the only environmental chemical that varied significantly between groups was the NDL congener PCB 95.
“Of the eight PCB congeners examined, the only environmental chemical that varied significantly between groups was the NDL congener PCB 95.”
From DNA methylation: a mechanism linking environmental chemical exposures to risk of autism spectrum disorders? (2016) · cites this paper as [40]
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“This possibility is supported by a recent report that PCB 95, but not other PCBs or PBDEs, are significantly higher in postmortem brains of children with a syndromic form of autism, compared with neurotypical controls (Mitchell et al., 2012).”
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- Authors
- Mitchell, M. M., Woods, R., Chi, L., Schmidt, R. J., Pessah, I. N., Kostyniak, P. J., & LaSalle, J. M.
- Affiliations
- University of California, Davis (US)
- University at Buffalo, State University of New York (US)
- Corresponding author
- LaSalle, Janine M.
- Venue
- Environmental and Molecular Mutagenesis
- Publisher
- Wiley
- Published
- 2012-08-29
- Volume
- 53
- Issue
- 8
- Pages
- 589-598
- ISSN
- 0893-6692 (ISSN-L)
- 1098-2280
- PMC
- PMC3739306
- OpenAlex
- W1994103322
- Cited by
- 164
- References
- 71
- Citations by year
- 2026: 9 · 2025: 9 · 2024: 8 · 2023: 8 · 2022: 16 · 2021: 17 · 2020: 12 · 2019: 9 · 2018: 11 · 2017: 14 · 2016: 12 · 2015: 12 · 2014: 14 · 2013: 10 · 2012: 3
- FWCI
- 8.61
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Environmental and Molecular Mutagenesis (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Environmental Health Sciences (R01ES015171, R01ES017425, R01ES021707, R01ES0210707, T32ES002321, P01ES011269, R01ES014901)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD041462, K12HD051958)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Keywords
- polychlorinated biphenyls, polybrominated diphenyl ethers, persistent organic pollutants, autism spectrum disorder, Prader-Willi syndrome, neurodevelopmental disorders, DNA methylation, LINE-1 methylation, PCB 95, developmental neurotoxicity, copy number variation, maternal exposure, postmortem brain
- MeSH terms
- Adolescent, Adult, Brain, Child, Child Development Disorders, Pervasive, Child, Preschool, Chromosomes, Human, Pair 15, Female, Humans, Male, Middle Aged, Polychlorinated Biphenyls, Prader-Willi Syndrome, DNA Methylation, Epigenesis, Genetic, Halogenated Diphenyl Ethers, Young Adult, DNA Copy Number Variations
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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