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Review
. 2015 Mar 3:9:57.
doi: 10.3389/fnins.2015.00057. eCollection 2015.

Bisphenol A and phthalate endocrine disruption of parental and social behaviors

Affiliations
Review

Bisphenol A and phthalate endocrine disruption of parental and social behaviors

Cheryl S Rosenfeld. Front Neurosci. .

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.

Keywords: EDC; bisphenol A; brain development; epigenetics; neuropeptides; phthalate; rodent models; xenoestrogen.

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Figures

Figure 1
Figure 1
Steroidogenesis of androgens and estrogens. Evidence exists that all of the shaded enzymes required in the synthesis of these hormones are altered by BPA and/or phthalate exposure.

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References

    1. Adewale H. B., Todd K. L., Mickens J. A., Patisaul H. B. (2011). The impact of neonatal bisphenol–a exposure on sexually dimorphic hypothalamic nuclei in the female rat. Neurotoxicology 32, 38–49 10.1016/j.neuro.2010.07.008 - DOI - PMC - PubMed
    1. Akingbemi B. T., Ge R., Klinefelter G. R., Zirkin B. R., Hardy M. P. (2004a). Phthalate-induced Leydig cell hyperplasia is associated with multiple endocrine disturbances. Proc. Natl. Acad. Sci. U.S.A. 101, 775–780. 10.1073/pnas.0305977101 - DOI - PMC - PubMed
    1. Akingbemi B. T., Sottas C. M., Koulova A. I., Klinefelter G. R., Hardy M. P. (2004b). Inhibition of testicular steroidogenesis by the xenoestrogen bisphenol A is associated with reduced pituitary luteinizing hormone secretion and decreased steroidogenic enzyme gene expression in rat Leydig cells. Endocrinology 145, 592–603. 10.1210/en.2003-1174 - DOI - PubMed
    1. Akingbemi B. T., Youker R. T., Sottas C. M., Ge R., Katz E., Klinefelter G. R., et al. . (2001). Modulation of rat Leydig cell steroidogenic function by di(2-ethylhexyl)phthalate. Biol. Reprod. 65, 1252–1259. 10.1095/biolreprod65.4.1252 - DOI - PubMed
    1. Arnold A. P., Breedlove S. M. (1985). Organizational and activational effects of sex steroids on brain and behavior: a reanalysis. Horm. Behav. 19, 469–498. 10.1016/0018-506X(85)90042-X - DOI - PubMed