» Articles » PMID: 25784850

Bisphenol A and Phthalate Endocrine Disruption of Parental and Social Behaviors

Overview
Journal Front Neurosci
Date 2015 Mar 19
PMID 25784850
Citations 43
Authors
Affiliations
Soon will be listed here.
Abstract

Perinatal exposure to endocrine disrupting chemicals (EDCs) can induce promiscuous neurobehavioral disturbances. Bisphenol A and phthalates are two widely prevalent and persistent EDCs reported to lead to such effects. Parental and social behaviors are especially vulnerable to endocrine disruption, as these traits are programmed by the organizational-activational effects of testosterone and estrogen. Exposure to BPA and other EDCs disrupts normal maternal care provided by rodents and non-human primates, such as nursing, time she spends hunched over and in the nest, and grooming her pups. Paternal care may also be affected by BPA. No long-term study has linked perinatal exposure to BPA or other EDC and later parental behavioral deficits in humans. The fact that the same brain regions and neural hormone substrates govern parental behaviors in animal models and humans suggests that this suite of behaviors may also be vulnerable in the latter. Social behaviors, such as communication, mate choice, pair bonding, social inquisitiveness and recognition, play behavior, social grooming, copulation, and aggression, are compromised in animal models exposed to BPA, phthalates, and other EDCs. Early contact to these chemicals is also correlated with maladaptive social behaviors in children. These behavioral disturbances may originate by altering the fetal or adult gonadal production of testosterone or estrogen, expression of ESR1, ESR2, and AR in the brain regions governing these behaviors, neuropeptide/protein hormone (oxytocin, vasopressin, and prolactin) and their cognate neural receptors, and/or through epimutations. Robust evidence exists for all of these EDC-induced changes. Concern also exists for transgenerational persistence of such neurobehavioral disruptions. In sum, evidence for social and parental deficits induced by BPA, phthalates, and related chemicals is strongly mounting, and such effects may ultimately compromise the overall social fitness of populations to come.

Citing Articles

Should Pregnant Women Consume Probiotics to Combat Endocrine-Disrupting Chemical-Induced Health Risks to Their Unborn Offspring?.

Rosenfeld C Biomedicines. 2024; 12(8).

PMID: 39200093 PMC: 11351870. DOI: 10.3390/biomedicines12081628.


Postnatal maternal care moderates the effects of prenatal bisphenol exposure on offspring neurodevelopmental, behavioral, and transcriptomic outcomes.

Lauby S, Lapp H, Salazar M, Semyrenko S, Chauhan D, Margolis A PLoS One. 2024; 19(6):e0305256.

PMID: 38861567 PMC: 11166292. DOI: 10.1371/journal.pone.0305256.


Exposure of preterm neonates receiving total parenteral nutrition to phthalates and its impact on neurodevelopment at the age of 2 months.

Al-Saleh I, Elkhatib R, Alnuwaysir H, Aldhalaan H, Alismail E, Binmanee A Sci Rep. 2023; 13(1):6969.

PMID: 37117441 PMC: 10141929. DOI: 10.1038/s41598-023-33715-w.


Brief postnatal exposure to bisphenol A affects apoptosis and gene expression in the medial prefrontal cortex and social behavior in rats with sex specificity.

Drzewiecki C, Brinks A, Sellinger E, Doshi A, Koh J, Juraska J Neurotoxicology. 2022; 94:126-134.

PMID: 36442689 PMC: 9839503. DOI: 10.1016/j.neuro.2022.11.011.


Exposure to glyphosate-based herbicide during early stages of development increases insulin sensitivity and causes liver inflammation in adult mice offspring.

Zawoski Gomes E, Teleken J, Vargas R, Alegre-Maller A, Amorim J, Bonfleur M Einstein (Sao Paulo). 2022; 20:eAO6778.

PMID: 35674629 PMC: 9165568. DOI: 10.31744/einstein_journal/2022AO6778.


References
1.
Botelho G, Golin M, Bufalo A, Morais R, Dalsenter P, Martino-Andrade A . Reproductive effects of di(2-ethylhexyl)phthalate in immature male rats and its relation to cholesterol, testosterone, and thyroxin levels. Arch Environ Contam Toxicol. 2009; 57(4):777-84. DOI: 10.1007/s00244-009-9317-8. View

2.
Arnold A, Breedlove S . Organizational and activational effects of sex steroids on brain and behavior: a reanalysis. Horm Behav. 1985; 19(4):469-98. DOI: 10.1016/0018-506x(85)90042-x. View

3.
Wolstenholme J, Rissman E, Connelly J . The role of Bisphenol A in shaping the brain, epigenome and behavior. Horm Behav. 2010; 59(3):296-305. PMC: 3725332. DOI: 10.1016/j.yhbeh.2010.10.001. View

4.
Tang W, Morey L, Cheung Y, Birch L, Prins G, Ho S . Neonatal exposure to estradiol/bisphenol A alters promoter methylation and expression of Nsbp1 and Hpcal1 genes and transcriptional programs of Dnmt3a/b and Mbd2/4 in the rat prostate gland throughout life. Endocrinology. 2011; 153(1):42-55. PMC: 3249669. DOI: 10.1210/en.2011-1308. View

5.
Zhou R, Chen F, Chang F, Bai Y, Chen L . Persistent overexpression of DNA methyltransferase 1 attenuating GABAergic inhibition in basolateral amygdala accounts for anxiety in rat offspring exposed perinatally to low-dose bisphenol A. J Psychiatr Res. 2013; 47(10):1535-44. DOI: 10.1016/j.jpsychires.2013.05.013. View