The DOI matches its Crossref record; 86 of the 88 references it cites were found in a registry or an index.
Prenatal Exposures to Persistent and Non‐Persistent Organic Compounds and Effects on Immune System Development
Open accessAbstract
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, 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]
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“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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- 10.1038/sj.mp.4000923 · DOI
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Cited by
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The health effects of ambient PM2.5 and potential mechanisms
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The Changing Epidemiology of Autism Spectrum Disorders
Lyall, K., Croen, L., Daniels, J., Fallin, M. D., Ladd-Acosta, C., Lee, B. K., Park, B. Y., Snyder, N. W., Schendel, D., Volk, H., et al. (2017) · Annual Review of Public Health · doi:10.1146/annurev-publhealth-031816-044318 · Cited by 1,011
Human Health and Ocean Pollution
Landrigan, P. J., Stegeman, J. J., Fleming, L. E., Allemand, D., Anderson, D. M., Backer, L. C., Brücker-Davis, F., Chevalier, N., Corra, L., Czerucka, D., et al. (2020) · Annals of Global Health · doi:10.5334/aogh.2831 · Cited by 885
Health and environmental effects of persistent organic pollutants
Alharbi, O. M. L., Basheer, A. A., Khattab, R. A., & Ali, I. (2018) · Journal of Molecular Liquids · doi:10.1016/j.molliq.2018.05.029 · Cited by 756
The contribution of environmental exposure to the etiology of autism spectrum disorder
Bölte, S., Girdler, S., & Marschik, P. B. (2019) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-018-2988-4 · Cited by 509
Metadata
- 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
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