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2024
Sci Total Environ
A Chinese study of 226 breast cancer cases and 990 controls found that exposure to certain perfluoroalkyl substances (PFAS), particularly perfluorononanoic acid (PFNA) and perfluoroheptanoic acid (PFHpA), was associated with increased mitochondrial DNA copy number (mtDNAcn) in blood, which in turn was linked to breast cancer risk. Women with the highest mtDNAcn levels had a 234% increased risk of breast cancer and a 271% increased risk of postmenopausal breast cancer compared to those with the lowest levels. The study found that mtDNAcn mediated about 15% of the relationship between PFHpA exposure and breast cancer, suggesting that PFAS may increase breast cancer risk partly by affecting mitochondrial function. These findings provide new insights into how PFAS chemicals may contribute to breast cancer development through effects on cellular energy production and mitochondrial health.
2024
Environ Res
A decade-long study of 135 breast cancer cases and 540 controls found that exposure to PFAS (perfluoroalkyl substances) was strongly associated with increased breast cancer risk, with mixed PFAS exposure showing more than double the odds of developing the disease. Several specific PFAS compounds—including PFBA, PFOS, PFHxS, and PFDA—were identified as particularly significant risk factors, with some associations appearing exclusively in premenopausal women. The findings suggest that premenopausal women should be especially cautious about PFAS exposure, as these persistent “forever chemicals” may pose a substantial breast cancer risk.
2022
Environ Health
This large Chinese case-control study of 373 breast cancer patients and 657 controls found that higher plasma levels of PFOA and PFDA were positively associated with breast cancer risk, with PFOA showing particularly strong associations with hormone receptor-positive and HER2-positive breast cancers (47%, 36%, and 62% increased odds, respectively). Interestingly, the study found that PFTrDA (a longer-chain PFAS) was inversely associated with breast cancer risk, though the reasons for this protective effect are unclear. The findings add to growing international evidence linking PFAS exposure to breast cancer, demonstrating that these “forever chemicals” pose breast cancer risks not just in Europe and America but also in Asian populations. These results are concerning because PFOS was found at the highest concentrations in blood samples from both cases and controls, indicating widespread population exposure to these persistent environmental contaminants in Chin
2022
Environ Pollut
This Chinese prospective study of over 1,200 women found that higher baseline plasma concentrations of PFOA and PFHpA (a shorter-chain PFAS) were associated with 35% and 20% increased risk of developing breast cancer, respectively, with similar or stronger associations seen in postmenopausal women. When researchers examined the combined effect of all perfluorinated carboxylic acids together, they found a 19% increased breast cancer risk for each quartile increase in exposure, with PFOA accounting for more than half of this effect. Importantly, this is the first study to identify PFHpA—a shorter-chain PFAS increasingly used as a replacement for longer-chain compounds—as a breast cancer risk factor, raising concerns that newer “replacement” PFAS chemicals may not be safer alternatives. These prospective findings strengthen the evidence that PFAS exposure is a modifiable risk factor for breast cancer and support the need to regulate PFAS as an entire chemical class rather than individual compounds.
2022
Toxics
A meta-analysis of eight studies examining the relationship between PFAS chemicals and breast cancer found that two specific PFAS compounds—PFOA and PFHxS—were associated with significantly increased breast cancer risk, showing 32% and 79% elevated risk respectively. Surprisingly, PFNA showed a protective association with 24% reduced risk, while PFOS showed no association with breast cancer risk, though all findings had substantial statistical heterogeneity between studies. The researchers concluded that certain PFAS compounds may be potential breast cancer risk factors, with concerning evidence that even low-level exposures could have harmful impacts on human health, highlighting the need for further research to clarify the varied effects of different PFAS chemicals on breast cancer development.
2021
Environ Res
This large U.S. study using NHANES data found that multiple PFAS chemicals were associated with increased odds of both breast and ovarian cancer, with dose-response relationships showing dramatically higher risks at the highest exposure levels—women in the highest quartile of exposure had 130% increased odds for breast cancer (up to 607% for PFHxS) and 77-125% increased odds for ovarian cancer compared to those in the lowest quartile. Different PFAS chemicals showed stronger correlations with different cancers: PFOA was most strongly correlated with breast cancer while PFHxS was most strongly correlated with ovarian cancer, suggesting these endocrine-disrupting chemicals may affect different hormone-sensitive tissues through distinct mechanisms. No associations were found with prostate or uterine cancers. These findings are particularly concerning because PFAS are ubiquitous environmental contaminants found in everyday products and the water supply, and the strong dose-response relationships suggest that reducing PFAS exposure could potentially lower the risk of these estrogen-related cancers in women.
2021
Sci Total Environ
This Japanese case-control study of 405 matched pairs of women found that higher serum concentrations of PFAS chemicals were generally associated with reduced breast cancer risk rather than increased risk, with women in the highest exposure quartile showing 79-85% lower odds of breast cancer for linear isomers of PFOS and PFOA. However, the study revealed important differences between chemical structures: among postmenopausal women, while the linear form of one PFAS (PFTrDA) was protective, the branched form showed a marginally increased risk (74% higher odds approaching significance at medium exposure levels). These unexpected inverse associations contrast with several other studies showing increased breast cancer risk from PFAS exposure, highlighting the complexity of PFAS research and the importance of distinguishing between different chemical structures (branched vs. linear isomers) that may have opposite health effects, though the reasons for these protective associations remain unclear and warrant further investigation.
2025
Environ Pollut
This study examined the combined toxic effects of nanoplastic particles (NPs) and DEHP plasticizer on mouse mammary epithelial cells, finding that co-exposure caused severe cell death (pyroptosis), inflammation, and oxidative stress. The researchers discovered that the combination damaged mitochondria and increased endoplasmic reticulum stress, leading to disrupted cellular energy production and membrane integrity. Notably, co-exposure enhanced communication between cellular organelles (ER-mitochondria crosstalk), involving increased calcium levels and expanded contact areas between these structures. The findings reveal new molecular mechanisms by which plastic particles and plasticizers can work together to damage mammary gland tissue, providing insights into potential breast health risks from environmental plastic pollution.
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.
2024
Environ Int
A study in mice found that exposure to DEHP—a common chemical used to make plastics flexible—disrupts the gut-mammary connection, causing changes in gut bacteria, intestinal inflammation, and direct damage to mammary (breast) tissue that could impair milk production. DEHP altered gut microbiome composition (increasing some bacteria while decreasing others), changed blood metabolite levels, and its breakdown product (MEHP) triggered cell death in mammary tissue through multiple pathways. These findings raise concerns about DEHP exposure from plastics affecting both human breast health and dairy production in livestock, while identifying potential therapeutic targets to counteract the chemical’s harmful effects on the gut-breast axis.
2024
Heliyon
A mouse study found that ginger volatile oil (GVO) reduced triple-negative breast cancer tumor growth in animals exposed to bisphenol A (BPA), a common plastic chemical known to promote cancer, with the effect linked to restoration of healthy gut bacteria. BPA exposure disrupted the gut microbiome by reducing bacterial diversity and beneficial bacteria like Lactobacillus, but treatment with ginger oil reversed these changes and increased the ratio of beneficial bacteria while decreasing harmful bacteria. The findings suggest that ginger compounds may counteract BPA’s cancer-promoting effects through their impact on the gut microbiome, offering a potential dietary strategy to mitigate harm from plastic chemical exposure, though human studies are needed to confirm these results.
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
Gut Microbes
A mouse study revealed that Vitamin D receptor (VDR) deficiency in the gut lining leads to bacterial imbalance (dysbiosis), increased intestinal permeability (“leaky gut”), and bacterial migration to breast tissue, significantly increasing breast tumor formation. Mice lacking intestinal VDR developed larger and more numerous breast tumors, with harmful bacteria like Streptococcus found in the tumor tissue, while beneficial bacteria that normally protect against cancer were depleted. However, treatment with butyrate (a beneficial bacterial byproduct) or the probiotic Lactobacillus plantarum reduced breast tumors by restoring gut barrier function and reducing inflammation, demonstrating a direct gut-breast axis. These findings suggest that maintaining gut health through adequate Vitamin D, beneficial bacteria, and a healthy microbiome may be a promising strategy for breast cancer prevention, though human studies are needed to confirm these results.
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
Sci Total Environ
In a transgenic mouse model (MMTV-Erbb2) that naturally develops mammary tumors, mice given oral cadmium (3.6 mg/L in drinking water for 23 weeks) developed palpable tumors significantly earlier and showed accelerated tumor growth compared with unexposed controls. Cadmium exposure increased the proliferation marker Ki-67, enhanced focal necrosis and new blood vessel formation in mammary tumors, and triggered greater intratumoral glutamine metabolism. Notably, disrupting gut microbiota with antibiotics delayed tumor onset and reduced tumor weight, implicating gut-microbiome–mediated metabolic reprogramming in cadmium-driven mammary tumorigenesis.
2023
Cancer Epidemiol Biomark Prev
A systematic review and meta-analysis of 34 observational studies and 3 Mendelian randomization studies found that women with the highest levels of C-reactive protein (CRP)—a marker of systemic inflammation—had a 13% increased breast cancer risk compared to those with the lowest levels, though the quality of evidence was rated as very low to moderate. While adiponectin showed a protective association (24% reduced risk), this finding was not supported by genetic evidence from Mendelian randomization studies, and there was little evidence that other inflammatory markers like TNFα and IL-6 affected breast cancer risk. These findings suggest that while chronic low-grade inflammation measured by CRP may modestly increase breast cancer risk, the overall role of inflammation in breast cancer development remains unclear, with limited support beyond CRP—highlighting the need for higher-quality prospective studies and mechanistic research to clarify whether inflammation is truly causal or merely a marker of other underlying processes that drive breast carcinogenesis.
2022
Molec Carcinogen
A case-control study of 708 breast cancer patients and 598 controls from Long Island found that paraben exposure—particularly methylparaben—was associated with significantly increased breast cancer risk among women with hypomethylated (undermethylated) DNA, showing a 46% increased risk in the highest versus lowest exposure group and a 32% increased risk per one-quantile increase in combined paraben exposure. Importantly, paraben exposure was specifically associated with breast tumors characterized by hypomethylation of the CCND2 gene promoter, with methylparaben showing a 25% increased risk and combined parabens showing a 55% increased risk for this tumor subtype. These findings suggest that parabens—ubiquitous preservatives in personal care products—may contribute to breast cancer development through epigenetic mechanisms, particularly in women with pre-existing DNA methylation abnormalities, identifying a potentially vulnerable subpopulation and a specific molecular pathway through which these chemicals may promote carcinogenesis.
2022
Talanta Open
This study developed a sensitive analytical method to detect steroid hormones (progestins, estrogens, androgens, and glucocorticoids) in fruits and vegetables, using strawberry, carrot, and spinach as test samples. The optimized extraction procedure uses ultrasonic extraction with minimal methanol, followed by clean-up and analysis via HPLC-ESI-MS/MS, achieving good recoveries at concentrations of 10-50 ng/g. The method was successfully applied to additional produce (raspberry, radish, arugula) and used to analyze market-purchased samples, where some steroids were detected at low ng/g levels. These findings are consistent with existing literature on steroid hormone accumulation in edible plants as emerging environmental pollutants.
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
BMC Complement Med Ther
This study focused on the effect that tartrazine (E102), a common yellow food dye, had on the progression of breast cancer in rats that were exposed to 7,12-Dimethylbenz(a)anthracene (DMBA), a polycyclic aromatic hydrocarbons (PAH) that is widely known for its carcinogenicity. The researchers discovered that tartrazine accelerated the development and growth of tumors in the rats with 100% of rats having early incidents of breast cancer when exposed to both DMBA and tartrazin, and only 80% having early incidence when exposed to DMBA alone. The authors also hypothesized that tartrazine could cause oxidative stress, leading to DNA damage by producing Reactive Oxygen Species. These results may apply to humans as well, and raise concerns about the safety of prolonged or high-dose exposure to synthetic food dyes like tartrazine, especially in individuals who may already have other risk factors for cancer.
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.
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
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.
2017
Sci Rep
An experimental study in mice using fluorescent polystyrene microplastics (5 μm and 20 μm diameter) found that microplastics accumulated in liver, kidney, and gut with tissue distribution and kinetics strongly dependent on particle size. Exposure induced disturbances in energy and lipid metabolism, oxidative stress, and altered blood biomarkers of neurotoxicity, as revealed through biochemical analyses and metabolomic profiling. This study provides new evidence for adverse health consequences of microplastic exposure in mammals, demonstrating tissue-specific accumulation patterns and systemic metabolic disruptions, though information about microplastic toxicity in mammals remains limited compared to marine organisms despite the ubiquitous environmental presence of these particles in oceans, rivers, soil, food, and even table salt.
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
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
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.
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.