Posted: November 30th, 2024

Prenatal Exposure to Bisphenol-A as a Causative Agent for Improper Fetal Development in Mammals

Prenatal Exposure to Bisphenol-A as a Causative Agent for Improper Fetal Development
I. Abstract
II. Introduction
A. Background Information:
in Mammals.
1. Bisphenol-A is a chemical heavily employed in the confection of
polycarbonate plastic-based packaging goods (Jalal et al., 2018).
2. Fetuses and young children are more sensitive to the effects of BPA exposure
(Lee et al., 2018).
3. BPA predominantly targets crucial steps in the premature life of mammals
(Lee et al., 2008).
B. Problem: Bisphenol-A content in the maternal body has been found to negatively
interfere with normal fetal development (Lee et al., 2008).
C. Main statement: The purpose of this review is to provide an overview of the
mechanisms via which BPA affects mammals during early life stages.
III. Body of the Review
A. Developmental anomalies attributed to BPA.
1. Primordial follicle formation is noticeably compromised in the presence of
Bisphenol-A.
a. Inhibition of meiotic activity in oocyte disturbs primordial follicle
creation (Zhang et al., 2012).
b. Anticipated and excessive transition of primordial to primary follicles
unleashed by BPA depletes primordial pool (Hu et al., 2018).

2. BPA exposure hinders neurological development.
a. Structure of the forming brain allows BPA to easily bypass barriers
and interfere with developmental phases (Negri-Cesi, 2015).
b. BPA is able to alter genetic expression in brain tissue during perinatal
stages (Casas et al., 2015).
3. Maternal exposure to BPA negatively affects the offspring’s gonadal
development and future reproductive success.
a. Male descendants from mothers with noticeable placental BPA
accumulation were found to experience diminished sperm count
(Gaskins, Hauser and Minguez-Alarcon, 2017).
b. Human fetal testes xenograft showed poor differentiation and reduced
cell count in pregnant mice exposed to BPA (Eladak et al., 2018).
c. BPA negatively impacts the development of the female reproductive
system (Galloway et al., 2016).
B. The impact of maternal Bisphenol-A exposure on prenatal endocrine function.
1. BPA toxicity has been found to negatively impact thyroid function.
a. Thyroid hormone-dependent mechanisms were found to be affected by
BPA (Viguié et al., 2013).
b. Disruption of enzymes that play a vital role in the maintenance of
thyroidal homeostasis in fetuses (Guignard et al., 2017).
C. Immunological impairments associated with BPA.
1. Maternal exposure to BPA can impact the strength of immune responses in
newborn babies.

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a. Moderate levels of BPA led to suppressed antigen sensitization and
decreased immunogenicity to enteric infections (Ménard et al., 2014).
b. BPA treatments on mice models caused increased immunoglobin and
interferon-γ expression and low lymphocyte count (Elhami and
Sadeghi, 2016).
2. Exposure to BPA during embryonic development leads to airway
inflammation.
IV. Conclusions
a. Attenuated doses of intratracheal BPA enhanced Th2 responses and
induced swelling (Koike et al., 2018).
b. Late gestational exposure accelerates maturation of proximal airways
secretory cells (Van Winkle et al., 2013).
A. Various studies provide evidence of negative outcomes induced by BPA during
the gestational period. Developmental, endocrinal and immunological
irregularities have been reported.
1. Experimental studies offered sufficient evidence to conclude that BPA
negatively affects mammalian development.
B. Limitations of the studies: The group of studies consulted showed very concise
findings overall. However, there were some limitations that may have skewed the
results.
1. Animal models employed have ontogenetic timings that differed from those of
humans.

2. Exposure routes explored in experimental designs were not representative of
the most common routs of exposure in humans (Hu et al., 2018)
3. Dosages employed to test BPA interactions with brain functions are not
designed for replications in human samples (Negri-Cesi, 2015).
4. Inaccurate exposure information led to inconclusive findings in investigations
for child neurophysiological development (Casas et al., 2015).
C. Future work needed in the field, knowledge gaps: Despite obtaining clear results

in most trials, there is room for improvements towards more informative
experimentations.
1. Humanized models for appropriate extrapolation to human development
2. Testing of physiologically-relevant doses.
3. Exposure routes that more closely resemble human exposure routes

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Fetal exposure to bisphenol a affects the primordial follicle formation by inhibiting the
meiotic progression of oocytes. Molecular Biology Reports, 39(5), 5651–5657.

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