Prenatal Exposures to Persistent and Non‐Persistent Organic Compounds and Effects on Immune System Development
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Abstract: Immune system development, particularly in the prenatal period, has far‐reaching consequences for health during early childhood, as well as throughout life. Environmental disturbance of the complex balances of Th1 and Th2 response mechanisms can alter that normal development. Dysregulation of this process or an aberrant trajectory or timing of events can result in atopy, asthma, a compromised ability to ward off infection, or other auto‐immune disease. A wide range of chemical, physical and biological agents appear to be capable of disrupting immune development. This MiniReview briefly reviews developmental milestones of the immune system in the prenatal period and early life, and then presents examples of environmentally induced alterations in immune markers. The first example involves a birth cohort study linked to an extensive programme of air pollution monitoring; the analysis shows prenatal ambient polycyclic aromatic hydrocarbons (PAH) and fine particle (PM2.5) exposures to be associated with altered lymphocyte immunophenotypic distributions in cord blood and possible changes in cord serum immunoglobulin E levels. The second example is a study of prenatal‐polychlorinated biphenyl (PCB) exposures and the foetal development of the thymus, the organ responsible for lymphocyte maturation. Mothers with higher serum concentrations of PCBs gave birth to neonates having smaller indices of thymus size. Finally, this report underscores the tight connection between development of the immune system and that of the central nervous system, and the plausibility that disruption of critical events in immune development may play a role in neurobehavioural disorders.
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Collectively, DDT, PCBs, and PBDEs have shown adverse endocrine, immune, and neurodevelopmental effects in humans.
“Collectively, these agents have shown adverse endocrine, immune, and neurodevelopmental effects in humans [209].”
From The contribution of environmental exposure to the etiology of autism spectrum disorder (2019) · cites this paper as [209]
Other mechanisms of these organic pollutants include neurotoxicity and immunotoxicity.
“Other pathophysiological mechanisms of these organic pollutants include neurotoxicity or immunotoxicity.”
From Environmental Chemical Exposures and Autism Spectrum Disorders: A Review of the Epidemiological Evidence (2014) · cites this paper as [147]
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- Authors
- Hertz‐Picciotto, I., Park, H., Dostal, M., Kocan, A., Trnovec, T., & Sram, R.
- Affiliations
- University of California, Davis (US)
- Slovak Medical University (SK)
- Corresponding author
- Hertz‐Picciotto, Irva
- Venue
- Basic & Clinical Pharmacology & Toxicology
- Publisher
- Wiley
- Published
- 2008-01-22
- Volume
- 102
- Issue
- 2
- Pages
- 146-154
- ISSN
- 1742-7835 (ISSN-L)
- 1742-7843
- OpenAlex
- W2146912985
- Cited by
- 253
- References
- 88
- Citations by year
- 2026: 9 · 2025: 8 · 2024: 12 · 2023: 7 · 2022: 7 · 2021: 17 · 2020: 9 · 2019: 11 · 2018: 17 · 2017: 16 · 2016: 9 · 2015: 16 · 2014: 10 · 2013: 21 · 2012: 18
- FWCI
- 1.59
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Basic & Clinical Pharmacology & Toxicology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Environmental Protection Agency (R-829388)
- United States Agency for International Development
- Health Effects Institute
- Ministry of Environment
- National Institutes of Health (ES11269, R01-CA96525)
- National Cancer Institute (R01 CA96525, R01CA096525)
- National Institute of Environmental Health Sciences (1 P01-ES11269, P01ES011269, R829388, ES11269)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Keywords
- prenatal exposure, persistent organic pollutants, immune system development, Th1/Th2 balance, polycyclic aromatic hydrocarbons, PM2.5, air pollution, polychlorinated biphenyls, thymus development, cord blood lymphocytes, immunoglobulin E, atopy, asthma, neurobehavioral disorders
- MeSH terms
- Air Pollution, Animals, Autistic Disorder, Environmental Pollutants, Female, Humans, Hypersensitivity, Immune System, Maternal-Fetal Exchange, Polychlorinated Biphenyls, Polycyclic Aromatic Hydrocarbons, Pregnancy, Prenatal Exposure Delayed Effects, Maternal Exposure
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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