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OBM Neurobiology

(ISSN 2573-4407)

OBM Neurobiology is an international peer-reviewed Open Access journal published quarterly online by LIDSEN Publishing Inc. By design, the scope of OBM Neurobiology is broad, so as to reflect the multidisciplinary nature of the field of Neurobiology that interfaces biology with the fundamental and clinical neurosciences. As such, OBM Neurobiology embraces rigorous multidisciplinary investigations into the form and function of neurons and glia that make up the nervous system, either individually or in ensemble, in health or disease. OBM Neurobiology welcomes original contributions that employ a combination of molecular, cellular, systems and behavioral approaches to report novel neuroanatomical, neuropharmacological, neurophysiological and neurobehavioral findings related to the following aspects of the nervous system: Signal Transduction and Neurotransmission; Neural Circuits and Systems Neurobiology; Nervous System Development and Aging; Neurobiology of Nervous System Diseases (e.g., Developmental Brain Disorders; Neurodegenerative Disorders).

OBM Neurobiology publishes a variety of article types (Original Research, Review, Communication, Opinion, Comment, Conference Report, Technical Note, Book Review, etc.). Although the OBM Neurobiology Editorial Board encourages authors to be succinct, there is no restriction on the length of the papers. Authors should present their results in as much detail as possible, as reviewers are encouraged to emphasize scientific rigor and reproducibility.

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Open Access Review

Mental Health Disorders Following Exposure to Endocrine Disruptor Chemicals

Mojtaba Ehsanifar 1,*, Akram Gholami 2, Alireza Esmaeili 3

  1. Department of Environmental Health Engineering, Torbat Jam Faculty of Medical Sciences, Torbat Jam, Iran

  2. Department of Nursing, Torbat Jam Faculty of Medical Sciences, Torbat Jam, Iran

  3. Department of Emergency Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran

* Correspondence: Mojtaba Ehsanifar

Academic Editor: Bart Ellenbroek

Received: October 27, 2024 | Accepted: April 15, 2025 | Published: April 18, 2025

OBM Neurobiology 2025, Volume 9, Issue 2, doi:10.21926/obm.neurobiol.2502285

Recommended citation: Ehsanifar M, Gholami A, Esmaeili A. Mental Health Disorders Following Exposure to Endocrine Disruptor Chemicals. OBM Neurobiology 2025; 9(2): 285; doi:10.21926/obm.neurobiol.2502285.

© 2025 by the authors. This is an open access article distributed under the conditions of the Creative Commons by Attribution License, which permits unrestricted use, distribution, and reproduction in any medium or format, provided the original work is correctly cited.

Abstract

There is growing scientific concern regarding how endocrine-disrupting chemicals (EDCs) impact central nervous system (CNS) disorders. Both anecdotal and preclinical studies suggest a link between EDC exposure and major depressive disorder (MDD), potentially leading to neurodegenerative outcomes. EDCs primarily exhibit their biological effects by interacting with hormone receptors. Nonetheless, there is scientific evidence pointing to dysfunction in the hypothalamic-pituitary-gonadal-adrenal axis, which is linked to neuropsychiatric conditions. Additionally, the global incidence of MDD has risen. Various factors like gender, genetic components, age, hormonal balance, and cultural influences may explain differences in MDD prevalence. Recently, environmental pollutants such as industrial chemicals, emollients, plastics, fungicides, and pesticides have emerged as critical factors influencing this disorder. This review delves into the influence of key phthalate and bisphenol compounds on chronic inflammation and MDD.

Graphical abstract

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Keywords

Major depression; neuroinflammation; environmental exposure; endocrine-disrupting chemicals; indoor pollution; phthalates; bisphenols

1. Introduction

Major Depressive Disorder (MDD), a complex mood disorder, is recognized as a significant global health issue due to the burden it places on public health systems and its prevalence worldwide [1,2,3]. Characterized by enduring low mood, loss of interest in activities, fatigue, and low energy, MDD is one of the most common mental health conditions [4]. It is linked to a lower quality of life, reduced productivity at work, and a heightened risk of mortality from any cause [5]. The inhalation of environmental pollutants contributes to oxidative stress and neuroinflammation, which may trigger MDD [6]. The incidence of MDD is rising, and access to effective treatments is often insufficient [7], making the identification of risk factors and the development of preventive strategies crucial for public health. Research has shown that breathing in pollutants from the air can provoke oxidative stress and inflammation in the brain, potentially causing neurotoxicity that affects dopamine [8]. Evidence links exposure to air pollution with reduced satisfaction with one’s living conditions and self-assessed health, both associated with mental health [9]. This suggests a plausible theory that air pollution could play a role in the development of MDD. Research has explored various aspects, including hormonal changes, genetic predisposition, neurochemicals, and inflammation in the nervous system [10]. Despite significant investment in developing pharmaceuticals for MDD, no truly effective treatments exist, and adherence to treatments is poor, leading to higher rates of treatment failure. Studies, although limited, suggest environmental contaminants such as DEP, DBP, BBP, DEHP, and BPA may be involved in the onset and worsening of MDD symptoms. These findings have led to an examination of such environmental exposures in properly diagnosed patients to understand the underlying mechanisms and factors that contribute to the large patient population [11,12,13]. As bisphenols, phthalates, and other endocrine-disrupting chemicals (EDCs) imitate hormonal actions, this review will delve into how exposure to the principal components of phthalates and bisphenols, commonly found in everyday products, affects men and women diagnosed with depression.

2. Methodology

A systematic search was conducted across multiple databases, including PubMed, Scopus, and Web of Science, using keywords such as Mental Health Disorders, Environmental exposure, Endocrine Disruptor Compounds (EDCs), and neuroinflammation. The review includes studies published between 2010 and 2023, ensuring that the most current findings are represented. The inclusion criteria were focused on peer-reviewed articles that involved both animal and human models and specifically examined EDCs’ effects on MDD and endocrine functions. Studies not related to EDCs, those involving other pollutants, or those that lacked MDD insights were excluded. The selected studies were synthesized to assess consistent findings on EDCs’ ability to induce oxidative stress, including the production of reactive oxygen species (ROS) and inflammation, as well as their endocrine-disrupting effects and MDD.

3. Neuroinflammation and MDD

Inflammation and neuropsychiatric disorders, including MDD, are closely connected. MDD can trigger inflammatory responses, while inflammation can exacerbate MDD and other similar disorders. Patients with MDD show diagnostic markers of inflammation, such as activated sensors and elevated circulating inflammatory signals targeting multiple tissues [4,14]. Inflammation can drive the clinical advancement and pathology of these conditions. Proinflammatory cytokines can alter mood, behavior, and cognition by reducing the availability of brain monoamines, initiating neuroendocrine reactions, impairing brain plasticity, and promoting excitotoxicity (increasing glutamate levels). Studies indicate that the source of ongoing inflammation often involves environmental EDC exposures that promote inflammation. Additionally, changes in neuroendocrine regulation, metabolism, diet/microbiota, and unhealthy behaviors contribute to inflammation [15,16]. The four elements central to an inflammatory reaction include: (1) Inflammatory inducers or pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs); (2) Sensory receptors in immune cells that detect these inducers; (3) Inflammatory mediators prompted by these sensors (like reactive oxygen species, cytokines, chemokines, and prostaglandins); (4) Target tissues affected by these mediators. Individuals with mood disorders and MDD present numerous indicators of immune dysfunction across cellular, molecular, and tissue levels. Environmental stressors are tied to higher circulating inflammatory triggers, notably DAMPs, which are endogenous molecules that amplify following cellular oxidative stress and damage. These molecules, when present outside of cells due to stress or necrosis, act as DAMPs [17]. DAMPs include circulating uric acid, extracellular ATP, heat shock proteins (HSPs), and oxidized molecules. Research demonstrates that environmental and psychological stresses can elevate these DAMPs, catalyzing nervous and peripheral system inflammatory responses [18]. Beyond tissue harm, stress-induced DAMPs can incite systemic inflammation. There is documented evidence of heightened circulating DAMPs in neurological and psychiatric conditions, with particularly elevated serum uric acid and HSP70 levels in MDD and Bipolar Disorder (BD) [19,20]. MDD patients have immune cells with heightened activation in response to DAMPs or PAMPs. Individuals with BD often show increased TLR receptor presence in peripheral monocytes and lymphocytes, as well as heightened TLR-mediated intracellular signaling [21]. Furthermore, elevated serum interleukin (IL)-1 and IL-18 levels have been detected in MDD patients [22]. Studies have found a positive correlation between oxidative stress and inflammatory markers and MDD symptoms [23]. Patients with MDD also exhibit higher levels of inflammatory mediators. Research has found that proinflammatory cytokines and their receptors, along with acute phase reactants like CRP, chemokines, and soluble adhesive molecules, are highly present in plasma and peripheral blood of those with BD, MDD, and schizophrenia [24,25,26]. The increase of innate immune cells, such as activated T cells, monocytes, and neutrophils, correlates with cell activation and growth [27,28]. Greater inflammation levels are linked to the progression or intensity of MDD symptoms. Indeed, heightened CRP and IL-6 levels can provoke depressive episodes in MDD patients [29], while remission is linked to reduced inflammatory markers [30]. It is notable that both the number and intensity of inflammatory disorders influence depression severity [31].

4. Influence of Environmental Pollutants on MDD Patients

EDCs do not directly cause neuronal tissue damage or cell death. However, they can indirectly disrupt the structure and function of the nervous system through neuroendocrine-related mechanisms [32]. EDCs may affect the brain through two main pathways: disrupting neuroendocrine processes originating in the hypothalamus and affecting steroid hormone receptors and signaling pathways throughout the brain [33]. Studies have highlighted that various factors, including genetics, age, hormonal conditions, and socio-cultural elements, contribute to the differing prevalence of MDD [34]. According to the World Health Organization (WHO), MDD is a mood disorder involving neurochemical, hormonal, and inflammatory alterations [35,36]. It is also noted that the incidence of MDD is twice as high in women compared to men [37]. Environmental pollutants, such as plastics, industrial chemicals, emollients, fungicides, and pesticides, have emerged as significant contributors to this disorder [34]. The exposure to these pollutants, particularly EDCs, has been linked with various neurological conditions like autism spectrum disorder and attention-deficit/hyperactivity disorder [38,39]. Some EDCs, including the additive DEHP, regulate the hypothalamic-pituitary-adrenal axis, which plays a crucial role in neurological and reproductive functions [40]. Bisphenols and phthalates, common ambient pollutants, disrupt homeostasis across different bodily systems. Predominantly found in dairy products, these compounds have permeated diverse sources such as air, food, and water globally, posing significant health risks [41,42]. Being lipophilic, they are readily absorbed through the skin and can leach from plastics with changes in temperature or pH, entering the body through ingestion. Once inside, bisphenols and phthalates antagonize steroid receptors, altering signaling pathways typically activated by natural ligands [43,44]. Notably, exposure to emollients, phthalates, and bisphenols during crucial life stages can detrimentally impact health [45]. This indicates that pathways involving maternal-infant interactions, perinatal exposure, and adulthood could be linked to heightened susceptibility to MDD.

5. Gender-Specific Effects of Pollutant Exposure in MDD

MDD is linked with changes in neurotransmitter systems, including serotonergic, noradrenergic, dopaminergic, and cholinergic pathways. Estrogens such as estradiol (E2) enhance serotonergic system efficiency through transcriptional regulation of TPH-2, 5-HT (SERT or 5-HTT), and monoamine oxidase A and B (MAO). Hence, E2 is attributed to significant antidepressant functions [46,47]. The combination of serotonin reuptake inhibitors, sertraline and fluoxetine, with E2, has shown promising outcomes in treating depression among older women [48]. It is crucial to note that malfunctions in MAOs are significant in sustaining and developing MDD [49]. Additionally, MDD occurrence often corresponds with hormonal disturbances in women [50,51]. EDCs interrupt regular hormonal functions and can impair hormone-sensitive organ systems such as the brain. In animal studies, EDC exposure resulted in inadequate methylation of genes in the brain, hampering neuronal development and function across generations [52,53]; possibly influencing depression development. Estrogen receptors, which are present in immune cells, may exhibit either pro- or anti-inflammatory effects based on the tissue type of the cell. Estradiol contributes to Th1 and Th2 response modulation [54], where an imbalance in Th2 response is clinically associated with MDD [55]. The influence of varying EDCs in modulating Th1 and Th2 responses remains underexplored. Exposure to BPA in early life stages corresponded with a shift towards Th2 response in female mice [56]. BBP, an asymmetric high molecular weight phthalate used to plasticize PVC products, has been found in higher serum concentrations in women than men, existing in dual forms [11]. As the most active estrogenic phthalate, BBP can adjust several genes dependent on hormonal cues [57]. Its linkage to endometriosis is significant due to direct associations with high blood concentrations of this contaminant [12]. Various phthalates also reduce E2 levels by repressing gene expression of aromatase, the enzyme responsible for E2 production, thereby extending the estrous cycle and hindering mouse ovulation [58]. Given E2's pivotal role in managing multiple systems and its essential antidepressant capability, it's crucial to concurrently evaluate EDC and E2 levels in MDD patients to recalibrate hormonal balance. Moreover, numerous unknown pleiotropic impacts of phthalates on neural functions are recognized [59]. Research measuring BBP metabolite concentrations demonstrated larger quantities in women's serum in contrast to men's [60]. The higher BBP serum levels observed in women are likely linked to more frequent use of cosmetics and medications, as phthalates are present in pharmaceutical capsules and packaging materials [61].

6. Exposure to Phthalates and Bisphenols Effects in MDD Patients

Studies suggest that phthalates may encourage Th2 differentiation, as observed in vitro, in vivo, and through epidemiological research on asthma [62]. Research has evaluated serum E2 levels in MDD patients, identifying them to be around 175-85 pg/ml in males and 55 pg/ml in females [63,64]. Several investigations have sought to measure bisphenols and phthalates in different biological fluids [65,66], but there is still no data on their serum levels in MDD patients. Among phthalates, two are characterized by high molecular weight, primarily found in plastic products, while another two are low molecular weight compounds, often located in cosmetics and personal care items [65,67]. It is presumed that following BPA exposure and its absorption, it is quickly metabolized into an inactive form (glucuronic acid) and excreted with a half-life of about 5 hours [68]. The half-life of phthalates varies with molecular weight. Low molecular weight phthalates, like DBP and DEP, are quickly hydrolyzed to monoesters and excreted, while high molecular weight phthalates, like BBP and DEHP, undergo hydrolysis followed by multi-step oxidative metabolism [59,65]. Evidence exists that the enzyme β-glucuronidase, found in multiple tissues, can generate and release the active BPA form within the body [69]. Since BPA is lipophilic, it can potentially migrate and accumulate in tissues, fostering bioaccumulation concerns. Some argue against this notion, pointing out that animals and humans frequently encounter BPA and similar substances. Given BPA’s ability to revert to its active form, is it feasible to measure unconjugated parent metabolites? Should we assess various contaminants in the blood and tissues to gauge potential bodily effects? [68]. The lipophilicity of BBP [70] may aid in its central nervous system transport and storage, potentially leading to MDD. BBP exposure also reduces serotonin (5-HT) levels, affecting adenylyl cyclase activation via G protein-coupled receptors (GPCRs). This enzyme, by using ATP, converts it into cAMP through an energy-reliant process, potentially disrupting protein kinase A activation and eventually lowering CREB phosphorylation levels. These sequences might result in behavioral dysfunction, oxidative harm, or pathological brain changes, as noted in mouse studies [71]. Regarding phthalates' cellular impacts, DBP seems to augment reactive oxygen levels [72], which may significantly damage neurons. Reports indicate that different phthalates alter sex enzymes and hormone processes in male and female animal models [73]. In vivo models suggest that these hormonal disruptions might lead to conditions analogous to human MDD, evidenced by cognitive decline and impaired learning and memory. Perinatal phthalate exposure notably affects mouse hippocampal impairment. It downregulates androgen receptor and expression, indicating potential placental and brain barrier crossings [74,75], Previous research on air pollutant transmission across the blood-brain barrier (BBB), brain inflammation including hippocampal cytokine gene expression and behavioral modifications [76,77,78] implies that phthalates might contribute to air pollutant BBB crossing and memory, learning, anxiety, [79] and depression in mice [80] Prenatal phthalate exposure is linked to hippocampal disruption, demonstrated by reduced androgen and estrogen receptor expression in mice [74] and placental barrier crossings [75], hinting at possible BBB penetration. Furthermore, early life phthalate and other EDCs exposure might impair neuronal function through brain methylation profile alteration [81], increasing the risk of neurological disorders such as adult MDD. Postnatal DEHP exposure reportedly impacts male mice's hippocampal growth but spares females [82]. DEHP may alter the female hippocampal lipid profile, raising sphingomyelin and phosphatidylcholine levels, with no such effects found in males, suggesting potential female protective neuro-properties [83]. Bisphenol research revealed no significant BPA and BPS disparities between depressed and healthy individuals [84]. Possibly due to limited depressed patient studies. There’s growing biological evidence of environmental pollutant roles in disorders like MDD, though strong clinical data supporting this link is still missing [85].

7. Conclusions

Research indicates that chronic inflammation plays a mediating role in the link between exposure to EDCs and symptoms of MDD. The variance in MDD prevalence across different studies may stem from using diverse measurement scales for MDD, population composition variations, and sample size discrepancies. Studies consistently demonstrate a robust association between elevated concentrations of phthalates found in urine and MDD symptoms, although the precise mechanism by which phthalate exposure leads to MDD remains unclear. This review highlights the pivotal role of EDCs, particularly benzyl butyl phthalate (BBP), in potentially causing or exacerbating mental disorders such as MDD and other psychiatric issues. Nonetheless, a definitive conclusion requires further investigation involving a broader population, including comprehensive surveys of EDC exposure and assessments of their serum concentrations alongside measurements of metabolites, neurotransmitters, serum levels of E2, other hormone concentrations, lipid and methylation profiles, and varied cytokines. These evaluations will crucially offer a global perspective on the impact of EDCs in a significant subset of MDD patients. Elevated EDC levels correlate with an increased risk of MDD, and chronic inflammation is identified as a risk factor. Findings indicate that general inflammatory factors partly mediate the relationship between EDC exposure and heightened MDD risk. This new analytical framework is a valuable tool to understand the effects of exposure to EDCs, including phthalates, on MDD.

Abbreviations

Acknowledgments

We thank Dr. Ehsanifar Research Lab. Tehran, Iran.

Author Contributions

All the authors contributed to writing, reviewing and editing the manuscript.

Funding

This review received no external funding and was initiated and funded by Dr. Ehsanifar Research Lab, Tehran, Iran.

Competing Interests

The authors declare that they have no competing interests.

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