Endocrine Disrupters: A Review of Some Sources, Effects, and Mechanisms of Actions on Behaviour and Neuroendocrine Systems
Open accessAbstract
Some environmental contaminants interact with hormones and may exert adverse consequences as a result of their actions as endocrine disrupting chemicals (EDCs). Exposure in people is typically a result of contamination of the food chain, inhalation of contaminated house dust or occupational exposure. EDCs include pesticides and herbicides (such as dichlorodiphenyl trichloroethane or its metabolites), methoxychlor, biocides, heat stabilisers and chemical catalysts (such as tributyltin), plastic contaminants (e.g. bisphenol A), pharmaceuticals (i.e. diethylstilbestrol; 17α‐ethinylestradiol) or dietary components (such as phytoestrogens). The goal of this review is to address the sources, effects and actions of EDCs, with an emphasis on topics discussed at the International Congress on Steroids and the Nervous System. EDCs may alter reproductively‐relevant or nonreproductive, sexually‐dimorphic behaviours. In addition, EDCs may have significant effects on neurodevelopmental processes, influencing the morphology of sexually‐dimorphic cerebral circuits. Exposure to EDCs is more dangerous if it occurs during specific ‘critical periods’ of life, such as intrauterine, perinatal, juvenile or puberty periods, when organisms are more sensitive to hormonal disruption, compared to other periods. However, exposure to EDCs in adulthood can also alter physiology. Several EDCs are xenoestrogens, which can alter serum lipid concentrations or metabolism enzymes that are necessary for converting cholesterol to steroid hormones. This can ultimately alter the production of oestradiol and/or other steroids. Finally, many EDCs may have actions via (or independent of) classic actions at cognate steroid receptors. EDCs may have effects through numerous other substrates, such as the aryl hydrocarbon receptor, the peroxisome proliferator‐activated receptor and the retinoid X receptor, signal transduction pathways, calcium influx and/or neurotransmitter receptors. Thus, EDCs, from varied sources, may have organisational effects during development and/or activational effects in adulthood that influence sexually‐dimorphic, reproductively‐relevant processes or other functions, by mimicking, antagonising or altering steroidal actions.
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NO endocrine disruption by GEN, BPA, and other EDCs has been found in parvocellular aspects of AVP signaling.
“Concomitant work focused on the parvocellular aspects of AVP signaling has also found evidence of NO endocrine disruption by GEN, BPA, and other EDCs (39, 74, 151).”
From Endocrine Disruption of Vasopressin Systems and Related Behaviors (2017) · cites this paper as [39]
In “EDCs Influence Brain Morphology” (page unavailable), the review reports that embryonic exposure to genistein, DES, or DDE significantly demasculinized the sexually dimorphic parvocellular AVT system in Japanese quail. That is contrary to the claim of no endocrine disruption in this system. The passage concerns avian AVT, the counterpart the review discusses alongside mammalian AVP; it does not establish a BPA effect on parvocellular AVP signaling. (LLM, conf=0.85)
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Experimental — accuracy not yet measuredDisruption of steroid hormone action was found to be causal in reproductive outcomes of EDC exposure, particularly during critical developmental windows.
“Invariably, disruption of steroid hormone action was found to be causal, particularly during critical developmental windows (39–41).”
From Endocrine Disruption of Vasopressin Systems and Related Behaviors (2017) · cites this paper as [39]
The Introduction says EDCs can act by mimicking, antagonizing, or altering endogenous steroids, and the Summary/Conclusions says exposure during critical developmental phases may have more salient reproductive effects. But the review does not establish that disrupted steroid action was invariably causal: the Summary/Conclusions also identifies effects through other pathways and uses qualified language. (LLM, conf=0.88)
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“Concomitant work focused on the parvocellular aspects of AVP signaling has also found evidence of NO endocrine disruption by GEN, BPA, and other EDCs (39, 74, 151).”
BackgroundSelf-citation
- Authors
- Frye, C., Bo, E., Calamandrei, G., Calzà, L., Dessì‐Fulgheri, F., Fernández, M., Fusani, L., Kah, O., Kajta, M., Le Page, Y., Patisaul, H. B., Venerosi, A., Wojtowicz, A. K., & Panzica, G. C.
- Affiliations
- University at Albany, State University of New York (US)
- Neuroscience Institute Cavalieri Ottolenghi (IT)
- Istituto Superiore di Sanità (IT)
- University of Bologna (IT)
- University of Florence (IT)
- University of Ferrara (IT)
- Centre National de la Recherche Scientifique (FR)
- Maj Institute of Pharmacology (PL)
- North Carolina State University (US)
- Politecnico di Torino (IT)
- Corresponding author
- Frye, C.
- ORCID
- Venue
- Journal of Neuroendocrinology
- Publisher
- Wiley
- Published
- 2011-12-20
- Volume
- 24
- Issue
- 1
- Pages
- 144-159
- ISSN
- 0953-8194 (ISSN-L)
- 1365-2826
- PMC
- PMC3245362
- OpenAlex
- W2158159969
- Cited by
- 431
- References
- 19
- Citations by year
- 2026: 8 · 2025: 19 · 2024: 22 · 2023: 20 · 2022: 13 · 2021: 44 · 2020: 24 · 2019: 31 · 2018: 37 · 2017: 43 · 2016: 41 · 2015: 41 · 2014: 39 · 2013: 31 · 2012: 16
- FWCI
- 2.82
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Journal of Neuroendocrinology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion)
- Florence Research (University of Florence) (submittedVersion)
- Institutional Research Information System University of Turin (University of Turin) (submittedVersion, other-oa)
- Institutional Research Information System University of Ferrara (University of Ferrara) (submittedVersion, other-oa)
- Funders
- U.S. Public Health Service (067698)
- National Institute of Mental Health (MH-067698, R01MH067698)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sexual Differentiation and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Keywords
- endocrine disruptors, neuroendocrine system, behavioral effects, brain development, sexual dimorphism, xenoestrogens, steroid hormone receptors, aryl hydrocarbon receptor, peroxisome proliferator-activated receptors, retinoid X receptor, pesticide exposure, bisphenol A, phytoestrogens, estradiol, reproductive behavior, plastic contaminants, pharmaceuticals
- MeSH terms
- Bisphenol A Compounds, Animals, Behavior, Animal, Benzhydryl Compounds, Brain, Environmental Pollutants, Humans, Phenols, Puberty, Reproduction, Phytoestrogens, Endocrine Disruptors
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