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Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
Prenatal exposure to bisphenol - A is associated with dysregulated perinatal innate cytokine response and elevated
Sui-Ling Liao1, Li-Chen Chen2, Ming-Han Tsai1
1Community Medicine Research Center, Chang Gung Memorial Hospital at Keelung, Keelung, Taiwan; Department of Pediatrics, Chang Gung Memorial Hospital at Keelung, Keelung, Taiwan; Chang Gung University, College of Medicine, Taoyuan, Taiwan.
Insights
Prenatal bisphenol-A (BPA) exposure did not increase childhood allergy risk or impair infant lung function. However, BPA altered early immune biomarkers, suggesting a potential role in allergy development that warrants further investigation.
Area of Science:
- Environmental Health
- Immunology
- Pediatrics
Background:
- Conflicting reports exist on the link between prenatal bisphenol-A (BPA) exposure and childhood allergy development.
- This study investigates BPA's impact on objective allergy markers, including cytokine profiles, atopic sensitization, and infant lung function (ILF).
Purpose of the Study:
- To determine the association between prenatal BPA exposure and objective outcomes related to childhood allergy.
- To assess BPA's impact on immune biomarkers and infant lung function.
- To evaluate the relationship between prenatal BPA exposure and clinical allergic symptoms.
Main Methods:
- A cohort of 274 children with cord BPA data was followed until age 3.
- Assessed IgE levels and Toll-like receptor (TLR) stimulated cytokine production annually.
- Measured ILF and determined allergic outcomes via questionnaires and physician assessments.
Main Results:
- Prenatal BPA exposure showed a significant association with cord blood IgE levels and altered perinatal cytokine production (TNF-α, IL-6).
- These associations were not sustained beyond birth.
- No correlation was found between prenatal BPA concentration and ILF measurements or childhood allergic symptoms.
Conclusions:
- Prenatal BPA exposure was not linked to an increased risk of childhood allergy or impaired ILF.
- Despite the lack of direct clinical association, BPA's impact on perinatal immune biomarkers suggests a potential role in allergy development.
- Further research is needed to fully understand the long-term implications of prenatal BPA exposure on allergic diseases.
Background:
Reports on the relationship between prenatal exposure to bisphenol-A (BPA) and the development of childhood allergy have been conflicting. This study aimed to investigate the impact of prenatal BPA exposure on several objective outcomes such as cytokine profile, atopic sensitization, and infant lung function (ILF) tests in addition to clinical allergic symptoms.
Methods:
A subset of 274 children from the PATCH cohort study with available cord BPA data were followed until 3 years of age. Total and specific IgE level and Toll-like receptor (TLR) stimulated cytokine production were assessed yearly since birth. ILF such as tidal volume, VmaxFRC, airway resistance and compliance were performed at least once before the age of 2 years. Allergic outcome was determined by questionnaires and physician's assessment.
Results:
There was significant association between BPA concentration and IgE level in the cord blood (p < 0.01), but the correlation was no longer significant at ages 1 through 3 years. In addition, cord BPA concentration was associated with dysregulated TLR stimulated TNF-α and IL-6 production, but the correlation was significant only at birth. No relationship was found between cord BPA concentration and ILF measurements or allergic symptoms (wheezing, rhino-conjunctivitis, or eczema) throughout early childhood.
Conclusion:
Results showed that prenatal exposure to BPA was not associated with increased risk of childhood allergy or impaired ILF. However, with its impact on biomarkers for allergy such as alterations in perinatal cytokine profile and elevated cord IgE level, the potential role of prenatal BPA exposure on the development of allergy cannot be disregarded.
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