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2025
Front Toxicol
The study examined the estrogenic and anti-estrogenic effects of three endocrine disruptors: Bisphenol A (BPA), which mimics estrogen, 17 -Estradiol (E2), the endogenous nuclear estrogen receptor ligand, and Fulvestrant (FUL), a drug that interferes with proper estrogen function. The experiment measured the influence of the endocrine disruptors in vitro using 2D and 3D T47D and MCF7 cells, which are estrogen receptor-positive human breast cancer cells. The study results concluded that E2 and BPA increased the expression of the estrogen-regulated marker pS2 and decreased TGF 3. Meanwhile, FUL inhibited E2 and BPA’s expression of the estrogen-regulated markers, meaning FUL reversed the effects of the other two endocrine disruptors.
2025
Int J Environ Sci
This study investigated how DEHP (a common plastic additive) affects triple-negative breast cancer (TNBC), the most aggressive form of breast cancer. The researchers found that prolonged DEHP exposure enhanced cancer cell migration and invasion both in laboratory cultures and in animal models by activating a specific protein pathway involving MSI2, which promotes cancer spread and stem cell-like properties. DEHP exposure also reduced levels of a protective microRNA (miR-155-5p), while increasing MSI2 expression, suggesting these molecules work in opposition to each other. The findings identify MSI2 as a potential therapeutic target and prognostic marker for TNBC patients, providing new insights into how plastic additives may contribute to cancer metastasis.
2025
Food Chem Toxicol
An in vitro study examining the effects of Roundup® (a Glyphosate-based herbicide) on non-tumorigenic (MCF10A) and tumorigenic (MCF7 and MDA-MB-231) breast cell lines found that the herbicide affects cells through a non-estrogenic mechanism, impacting both hormone-dependent and -independent cells with dose- and time-dependent toxic and proliferative effects, and altered expression of key breast cancer genes (BRCA1 and BRCA2) even at low doses. Treatment with epigenetic modulators (epidrugs) was able to reverse some Roundup®-induced changes, suggesting the herbicide causes epigenetic modifications that may contribute to breast cancer development. These findings highlight that Glyphosate-based herbicides—widely used in agriculture and recognized as potential carcinogens and endocrine disruptors—may induce epigenetic changes linked to breast cancer risk through mechanisms distinct from estrogenic pathways, underscoring the importance of understanding these mechanisms to develop personalized prevention strategies for populations exposed to agricultural herbicides.
2025
J Hazard Mater
This study investigated whether DEHCH, a newly developed alternative plasticizer, has safer endocrine-disrupting effects compared to conventional phthalates and other alternative plasticizers using computer modeling, cell studies, and zebrafish testing. The researchers found that DEHCH showed lower binding affinity to hormone receptors and did not affect hormone-related gene expression or neurosteroid levels in zebrafish, unlike the other tested plasticizers. In contrast, conventional phthalates (DEHP, DINP) and previously proposed alternatives (DINCH, DEHTP) caused hyperactivity in zebrafish and altered hormone-related gene expression and neurosteroid concentrations. The results suggest that DEHCH may be a safer alternative to both conventional phthalates and previously proposed substitutes in terms of endocrine disruption and neurological effects.
2025
Clin Transl Oncol
A review of 29 studies found that breast cancer patients have distinct imbalances in their gut and breast tissue bacteria that vary based on cancer type, stage, menopause status, body weight, and physical activity, though no single bacterial profile has yet emerged as a reliable biomarker. The research suggests that gut microbiome composition may influence how well breast cancer treatments work, with some beneficial bacteria and their metabolites potentially improving therapy effectiveness or slowing tumor growth. These findings highlight the microbiome as a promising new area for developing personalized breast cancer treatments and improving outcomes, though more research is needed to identify specific bacterial targets and understand the underlying mechanisms.
2024
Environ Health Perspect
Researchers analyzed 279 chemicals known to cause mammary tumors in rodents and identified 642 additional chemicals that activate estrogen or progesterone signaling, finding that tumor-causing chemicals were significantly more likely to stimulate hormone production, activate estrogen receptors, or damage DNA—characteristics that likely increase breast cancer risk in humans. The study found that more mammary carcinogens worked by increasing hormone production than by directly activating estrogen receptors, with chemicals showing stronger hormone-disrupting effects being most likely to cause tumors, demonstrating a clear dose-response relationship. These findings suggest that hundreds of chemicals currently in use may pose unrecognized breast cancer risks and should not be assumed safe without specific testing for breast effects, with the strongest evidence chemicals prioritized for exposure reduction and improved testing methods needed to identify additional hazardous substances. The research provides a framework for identifying and regulating chemicals that may contribute to breast cancer through hormone disruption and genetic damage—mechanisms supported by both animal and human studies.
2023
Chemosphere
A community-based intervention study (REDUXE) examined the effects of discontinuing paraben and phthalate-containing personal care products over 28 days by collecting paired fine needle aspirates of breast tissue from healthy volunteers before and after intervention, finding striking reversal of cancer-associated phenotypes including PI3K-AKT/mTOR pathway alterations, autophagy, and apoptotic signaling networks, along with significant reductions in urinary paraben and phthalate metabolites. Post-intervention breast tissue showed “normalizing” changes in estrogen-modulated gene expression pathways, estrogen receptor alpha:beta ratios, and cell cycle S-phase fraction when treated with 17β-estradiol in vitro, demonstrating functional improvement in cellular responses. This paradigm-shifting study reveals that persistent exposure to xenoestrogens from daily-use personal care products produces unfavorable pro-carcinogenic cellular changes in human breast tissue that can be reversed through short-term avoidance, suggesting that reducing xenoestrogen exposure from consumer products may suppress cancer-promoting phenotypes and represents a viable approach for breast cancer prevention.
2023
Toxicol Sci
A high-throughput transcriptomic study using MCF-7 breast cancer cells exposed to BPA and 15 alternative chemicals (0.0005-100 µM for 48 hours) found that 8 alternative chemicals activated estrogen receptor alpha (ERα), with bisphenol AF identified as the most potent, followed by BPA and bisphenol C, and benchmark concentration analysis revealing that BPA and transcriptionally active alternatives enriched similar gene sets associated with increased cell division and cancer-related processes at comparable concentrations. Global transcriptomic and ERα-specific points of departure produced highly consistent potency rankings, and pathway analysis showed that active alternatives induced hazards similar to BPA through shared molecular mechanisms. These findings reveal that many BPA replacement chemicals used since initial 2010 Canadian regulatory action are not safer alternatives and may pose similar or greater hazards at comparable exposure levels despite being data-poor compounds with limited toxicological assessment, supporting the use of transcriptomic profiling for read-across risk assessment of structurally related chemicals and raising concerns about regrettable substitution in which one harmful chemical is simply replaced with equally harmful alternatives.
2023
Endocrinology
Methylparaben (MP) and propylparaben (PP) are preservatives commonly found in food, and cosmetics which activate estrogen receptors (ER) in the body. Research shows that these parabens can promote mammary tumor growth and metastasis. This study tested female mice with exposure to MP and PP within levels deemed safe by the FDA. Even within FDA approved levels, there was significant increase in mammary tumor volume. Cellular analysis revealed that these parabens affected the expression of genes, some linked to breast cancer. This research highlights potential risks of parabens in promoting breast cancer.
2022
Biomedicines
This study investigates the effects of di-(2-ethylhexyl) phthalate (DEHP), a common plasticizer, on female rats. It found that exposure to DEHP, even at realistic environmental doses, led to significant disruptions in the rats’ reproductive and thyroid systems. More specifically it found that even low exposure to DEHP over a period of 21 days resulted in a significant decrease in the levels of estrogen and progesterone, which correlated with damage to ovarian follicles. Additionally, the thyroid showed signs of damage, including alterations in hormone regulation. The data in this study suggests that DEHP can potentially lead reproductive issues and impaired ovarian and thyroid gland function.
2022
Endocrinology
A review examining PFAS (found in nonstick cookware, food packaging, and stain-resistant fabrics) and parabens (used in personal care products) found that exposure to these endocrine-disrupting chemicals is linked to breast cancer development, with marginalized and socially disadvantaged communities facing disproportionately higher exposures due to structural racism and inequitable environmental conditions. These disparities in chemical exposure may contribute to poorer breast cancer outcomes in these populations, yet breast cancer research continues to underrepresent these communities, limiting our ability to address treatment disparities and improve survival rates. The authors emphasize the urgent need to both reduce EDC exposures in vulnerable communities and increase research inclusion of diverse populations to understand how environmental injustices intersect with breast cancer risk and develop interventions that address these health inequities.
2021
Oncol Rep
A review of organophosphorus pesticides (OPs)—among the most commonly used insecticides—and their association with hormone-mediated cancer found that OPs combined with estrogen induce transformation events in human breast epithelial cells, with in vitro studies showing these substances cause genomic instability through inactivation of tumor-suppressor genes and activation of oncogenes. Studies using immortalized non-tumorigenic human breast epithelial cell lines (MCF-10F) demonstrated that OPs like malathion and parathion, particularly in the presence of estrogen, affect cell cycle regulation, epidermal growth factor signaling pathways, drug metabolism, and genomic stability, leading to cellular transformation and signs of carcinogenesis. The findings suggest hormone-mediated carcinogenic effects of these widely used insecticides on breast cancer risk in women, with experimental models revealing the multistep process by which normal breast cells transform into malignant ones through combined exposure to environmental pesticides and estrogen, providing mechanistic insights into how occupational and environmental OP exposure may contribute to breast cancer development.
2021
Adv Pharmacol
A comprehensive review examining endocrine-disrupting chemicals (EDCs) in breast tissue concludes that hundreds of these environmental chemicals are entering human breast tissue and contributing to the global rise in breast cancer incidence through multiple biological mechanisms. Laboratory studies demonstrate that EDCs can activate all the established “hallmarks of cancer” in human breast cancer cells—even at concentrations measured in actual human breast tissue—with effects amplified when chemicals are present as mixtures rather than individually. The authors argue that EDCs must now be formally recognized as a breast cancer risk factor to enable prevention strategies that include reducing environmental chemical exposures, particularly given that the varied mixtures of EDCs found in individual breast tissues act through overlapping mechanisms to promote cancer development.
2020
Mol Cell Endocrinol
A review of EPA pesticide registration documents found that 28 pesticides cause mammary tumors in animals and five alter mammary gland development, yet the agency’s risk assessments often dismiss these findings or don’t evaluate their implications for breast cancer risk. Many of these pesticides work through hormone-disrupting pathways that could affect breast tissue, including common chemicals like malathion, atrazine, and triclopyr. The authors argue that current testing guidelines don’t adequately assess effects on the mammary gland and call for re-evaluation of several widely-used pesticides based on stronger standards informed by breast cancer biology.
2019
Environ Res
This study investigated how DEHP (a common plastic additive) and its metabolite MEHP affect breast cancer-related markers in T-47D breast cancer cells exposed to various concentrations for 4 days. The researchers found that high-dose DEHP (10,000 nM) and low-dose MEHP (0.1 nM) significantly increased cell proliferation without causing cell death, and DEHP also increased progesterone receptor (PR) protein levels and nuclear accumulation. When cells were treated with a progesterone receptor blocker (Mifepristone), the increased cell growth was completely prevented and PR nuclear levels were partially reduced, indicating that DEHP promotes breast cancer cell proliferation through progesterone receptor activation. The findings suggest that DEHP exposure may increase breast cancer risk by activating progesterone signaling pathways, though the exact mechanisms and long-term consequences require further investigation.
2019
PLOS One
Bisphenol AF (BPAF)—a chemical increasingly used to replace BPA in consumer products—shows even stronger estrogen-like effects than BPA and promotes the growth of estrogen receptor-positive (ER+) breast cancer cells through multiple hormone signaling pathways. Laboratory studies revealed that BPAF stimulates cancer cell proliferation by activating estrogen receptors and upregulating AREG, a growth-promoting gene, with blocking either estrogen receptors or AREG preventing BPAF’s cancer-promoting effects. These findings challenge the assumption that BPA alternatives are safer, demonstrating that BPAF may pose equal or greater breast cancer risks than the chemical it’s replacing, and highlight the urgent need for human studies to assess BPAF’s impact on breast cancer risk before its continued widespread use in products marketed as “BPA-free.”
2019
Molecules
A study examined the effects of four common herbicides (MCPA, mesotrione, bifenox, and dichlobenil) on breast cancer cells and found that these pesticides, which can remain as residues in plant-based foods, showed harmful effects on cancer cells at physiological concentrations. The researchers also tested whether traumatic acid (TA), a beneficial natural compound found in food, could counteract the effects of these herbicides when cells were exposed to both together. Results showed that TA, in a concentration-dependent manner, was able to influence and potentially reduce some of the effects of the tested herbicides on certain breast cancer cell lines. This research highlights concerns about herbicide residues in food as potential contributors to cancer risk while also suggesting that naturally occurring food compounds like traumatic acid might help mitigate some pesticide effects, though more research is needed to understand real-world implications.
2019
Environ Pollut
This study investigated how three endocrine-disrupting chemicals (BPA, BBP, and DEHP) affect estrogen receptor alpha (ERα) activity under normal and low-oxygen (hypoxic) conditions in breast and endometrial cancer cells. The researchers found that BPA and BBP activated ERα at specific concentrations, while DEHP did not, but all three chemicals enhanced ERα-mediated gene activity and decreased ERα protein levels under hypoxic conditions. BPA and BBP also affected hypoxia-related factors, decreasing hypoxia-inducible factor-1 activity while increasing VEGF (a blood vessel growth factor) secretion in breast cancer cells, whereas DEHP had different effects. The findings suggest that these endocrine disruptors can alter ERα regulation under low-oxygen conditions, which may influence disease processes since hypoxia is common in tumors and other pathological states.
2018
Tox Lett
This study investigated how butyl benzyl phthalate (BBP), a common environmental contaminant linked to breast cancer, promotes cancer cell growth and identified the molecular mechanisms involved. The researchers found that BBP increased proliferation in both estrogen receptor-positive (MCF-7) and negative (MDA-MB-231) breast cancer cells by promoting cell cycle progression and upregulating growth-promoting proteins while downregulating tumor suppressor proteins. For the first time, the study revealed that BBP works through modulating microRNA-19a/b, which targets the tumor suppressor gene PTEN, leading to activation of the AKT signaling pathway that promotes cell growth. These findings provide new insights into how BBP contributes to breast cancer development at the molecular level and suggest potential targets for intervention.
2018
PLOS One
This study investigated how phthalates affect the growth of normal breast cells (MCF-10A) when grown alongside breast fibroblasts derived from tissue near estrogen receptor (ER) positive and negative breast cancers. The researchers found that only fibroblasts from ER-positive breast cancer tissue significantly stimulated breast cell proliferation, and when these co-cultures were exposed to estrogen or three phthalates (BBP, DBP, DEHP), cell growth increased significantly along with markers of cell division and estrogen receptor expression. The effects of phthalates on normal breast cells were similar to those of estrogen and depended on estrogen receptor activity, suggesting that phthalates act through hormone-mediated pathways. The study concludes that phthalates should be considered potential endocrine disruptors with breast cancer risk implications, even at low concentrations, particularly in the presence of estrogen-responsive tissue.
2018
Food Chem Tox
A systematic review of 25 studies examining phthalates (plastic chemicals) and breast cancer found that while laboratory studies show certain phthalates can activate estrogen receptors and promote cancer cell growth, epidemiological studies in humans have produced mixed and inconclusive results. The main source of phthalate exposure is through diet—particularly from food and beverages in plastic packaging—but current human studies have significant limitations in how they measure exposure and account for other risk factors. The review calls for better-designed future studies that use hair samples instead of urine for more accurate long-term exposure assessment, include dietary factors and genetic markers as confounders, and investigate phthalates’ effects beyond just estrogen-driven cancers to include all breast cancer subtypes.
2015
Carcinogenesis
This study explores the linkage between environmental chemical exposures and cellular resistance to cell death, a carcinogenic trait. The researchers in this study specifically investigate BPA, chlorothalonil, dibutyl phthalate, and more because of their disruptive effects that may be involved in these carcinogenic pathways. The researchers found that arsenic interferes with cellular signaling pathways and induces oxidative stress, leading to impaired apoptosis; dioxins bind to aryl hydrocarbon receptors (AHRs), which alters gene expression and disrupts normal cell death processes; BPA mimics the estrogen hormone, affecting hormonal balance and promoting cell survival pathways that inhibit cell death. By allowing cells to evade cell death, these environmental chemicals can promote the survival of cells with genetic mutations and therefore increase the risk of cancer development.
2015
Environ Health Perspect
This study investigates how low concentrations of Bisphenol A (BPA) affect DNA integrity and cell proliferation in breast cells, focusing on the involvement of the oncogene c-Myc. They found that exposure to low doses of BPA resulted in significant DNA damage in estrogen receptor-alpha (ERα)-negative mammary cells, meaning that BPA can promote cancer in ways independent of standard estrogen receptor pathways. Additionally, BPA exposure led to the upregulation of c-Myc, which is a gene known to regulate cell proliferation and death., and the study did observe enhanced proliferation of ERα-negative mammary cells upon BPA exposure. This suggests that BPA may promote cancer pathways through c-Myc activation. This was then confirmed when the researchers silenced c-Myc gene expression and found that oncogenic effects in the presence of BPA were decreased. Overall, these findings raise concerns about BPA’s potential role in breast cancer formation, even at low exposure levels.
2015
Carcinogenesis
This study explores the relationship between chemical carcinogens, cellular senescence, and the process of cellular immortalization, which is a sign of cancer development. The article discusses how certain chemicals can disrupt normal cellular processes, leading to cellular senescence, the process where cells stop dividing but remain metabolically active. This thereby enables the progression of cancer. These chemicals interfere with key regulatory pathways, such as those involving the p53 and pRb proteins, which are crucial for maintaining the balance between cell division and arrest. The authors emphasize that exposure to certain chemicals can lead to disruptions to cellular senescence pathways.
2015
Carcinogenesis
A review examining the intersection of environmental toxicants, immune function, and cancer development argues that common chemicals like bisphenol A, atrazine, and phthalates can disrupt the delicate balance between pro- and anti-inflammatory immune responses, potentially contributing to tumor development through immune system dysfunction. The authors highlight that while the role of immunity in cancer is well-established, research on how environmental chemicals affect immune cells as co-factors in cancer causation remains underdeveloped compared to studies on autoimmunity and allergies. The review calls for increased research using systems biology approaches to better understand how chemical exposures disturb inflammatory pathways and immune molecules involved in tumor-associated inflammation, arguing that chemically induced immune perturbations represent an important but understudied mechanism of environmental carcinogenesis.
2012
Environ Health Perspect
This study analyzed 213 everyday products, including cosmetics, cleaners, and personal care items, for endocrine-disrupting chemicals (EDCs) and asthma-related compounds. Testing revealed 55 chemicals, with fragranced products and sunscreens containing the highest levels. Vinyl products were also found to contain significant amounts of bis(2-ethylhexyl) phthalate (DEHP), a known EDC. Many harmful chemicals were not listed on product labels, limiting consumer ability to avoid them. These results highlight the presence of potentially harmful chemicals in commonly used products, raising concerns about their widespread use in household and personal care items.
2024
Chemosphere
When tea is made using a polypropylene teabag, it could be releasing over 1 billion tiny plastic particles into every milliliter of your tea. A typical cup of tea is about 240 mL, so that could be nearly 300 billion particles per cup. An experimental study simulating tea preparation from three commercial teabags found substantial release of micro/nanoplastics (MNPLs), with teabags made of nylon-6, polypropylene, and cellulose releasing 8.18×10⁶ to 1.20×10⁹ nanoparticles per mL (particle sizes 136-244 nm), along with microfibers. In vitro exposure of three human intestinal cell lines (Caco-2, HT29, HT29-MTX) to 100 μg/mL of these nanoparticles for 24 hours revealed significant cell-type-specific uptake patterns: polypropylene nanoparticles were preferentially taken up by mucus-secreting HT29-MTX cells, cellulose nanoparticles by HT29 and HT29-MTX cells, and nylon-6 nanoparticles by Caco-2 cells. These findings highlight that everyday items like teabags represent a significant, previously underappreciated source of human MNPL exposure beyond environmental contamination, with billions of nanoparticles released per serving that are readily internalized by intestinal cells, underscoring the urgent need to investigate potential health effects of dietary plastic exposure from food packaging and preparation materials.