Research Results

Beta Version

Use the search bar below to find studies, or apply one or more filters to narrow your results. See our list of keywords to guide your search.

Search by keyword

Try these: air pollutionalcoholbisphenolshormonespersonal care productspesticidesplastic

Filter by Risk Factors
Filter by Protective Factors
Filter by Exposure Sources
Filter by Chemical Classes

Sort By

  • Relevance
  • Title (A to Z)
  • Title (Z to A)
  • Publication Year (Ascending)
  • Publication Year (Descending)
  • Authors (A to Z)
  • Authors (Z to A)

Specific microbiome patterns and their association with breast cancer: the intestinal microbiota as a potential biomarker and therapeutic strategy.

Amaro-da-Cruz et al,

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.

Diethyl-hexyl-cyclohexane (Eco-DEHCH) is a safer phthalate alternative that does not elicit neuroendocrine disrupting effects.

Kang et al,

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.

Prolonged DEHP exposure enhances the stemness and metastatic potential of TNBC cells in an MSI2-dependent manner.

Jadhao et al,

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.

The endoplasmic reticulum-mitochondrial crosstalk involved in nanoplastics and di(2-ethylhexyl) phthalate co-exposure induced the damage to mouse mammary epithelial cells.

Wang et al,

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.

Plastic additives affect estrogenic pathways and lipid metabolism in precision – cut – liver slices in Atlantic cod (Gadus morhua).

Andersen et al,

2025

Sci Totl Environ

This study investigated the effects of three common plastic additives (DEHP, BPA, and benzotriazoles) on Atlantic cod liver tissue using precision-cut liver slices exposed to various concentrations of these chemicals individually and in mixtures. The researchers found that BPA and chemical mixtures caused estrogenic effects, significantly increasing vitellogenin (a female egg protein) production and related gene expression in male juvenile cod. The study also observed changes in liver metabolism genes, with mixture exposures showing potentially different effects than individual chemical exposures. The results suggest these plastic additives can disrupt hormone systems in fish, with BPA being the primary driver of estrogenic effects, though the interaction effects between chemicals require further investigation.

Edodes Cultured Extract Regulates Immune Stress During Puberty and Modulates MicroRNAs Involved in Mammary Gland Development and Breast Cancer Suppression.

Yasavoli-Sharahi et al,

2024

Cancer Med

A mouse study found that exposure to bacterial toxins (lipopolysaccharides or LPS) during puberty—a critical period for breast development—caused lasting inflammation and changes in gene expression that increased breast cancer risk later in life. Researchers discovered that a prebiotic supplement derived from shiitake mushrooms (AHCC) could counteract these harmful effects by reducing inflammation, regulating immune signaling molecules, and blocking cancer-promoting gene activity in mammary tissue. The findings suggest that gut health and inflammation during puberty may influence long-term breast cancer risk, and that dietary interventions like prebiotics might offer a preventive strategy, though human studies are needed to confirm these results.

Application of the Key Characteristics Framework to Identify Potential Breast Carcinogens Using Publicly Available in Vivo, in Vitro, and in Silico Data.

Kay et al,

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.

Ginger volatile oil inhibits the growth of MDA-MB-231 in the bisphenol A environment by altering gut microbial diversity.

Luo et al,

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.

Environmental endocrine disrupting chemical-DEHP exposure-provoked biotoxicity about microbiota-gut-mammary axis in lactating mice via multi-omics technologies.

Xu et al,

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.

Intestinal Vitamin D receptor protects against extraintestinal breast cancer tumorigenesis.

Zhang et al,

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.

Food Thermal Labels are a Source of Dietary Exposure to Bisphenol S and Other Color Developers.

Xu et al,

2023

Environ Sci Technol

This review investigates the migration of bisphenols and alternative color developers from thermal labels on cling-wrapped fresh food, identifying them as significant dietary sources of these compounds. While no BPA was found in packaging, high concentrations of bisphenol S (BPS) and other alternatives were detected, particularly in thermal labels. Migration studies revealed that BPS and related compounds leach into food, especially fish, raising potential health concerns. These findings highlight the need for further risk assessments regarding these alternative chemicals in food packaging due to past findings about BPA being an endocrine disruptor. This will help mitigate exposure risks and ensure consumer safety.

Chronic Exposure to Low Levels of Parabens Increases Mammary Cancer Growth and Metastasis in Mice.

Tong et al,

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.

Environmental cadmium exposure facilitates mammary tumorigenesis via reprogramming gut microbiota-mediated glutamine metabolism in MMTV-Erbb2 mice.

Yue et al,

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.

Endocrine-Disrupting Chemicals and Breast Cancer: Disparities in Exposure and Importance of Research Inclusivity.

Santaliz Casiano et al,

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.

Endoglin Modulates TGFβR2 Induced VEGF and Proinflammatory Cytokine Axis Mediated Angiogenesis in Prolonged DEHP-Exposed Breast Cancer Cells.

Jadhao et al,

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.

Update on the Health Effects of Bisphenol A: Overwhelming Evidence of Harm.

Vom Saal et al,

2021

Endocrinology

A comprehensive review of bisphenol A (BPA) research spanning over 20 years—from the landmark 1997 study showing reproductive effects in male mouse offspring at 2 µg/kg/day through the CLARITY-BPA study designed to bridge regulatory and scientific disagreements—found that thousands of animal studies and over 100 epidemiological studies report adverse effects at low doses, with CLARITY-BPA showing effects at 2.5 µg/kg/day, leading independent experts to recommend dropping the lowest observed adverse effect level 20,000-fold from 50,000 to 2.5 µg/kg/day. Despite this overwhelming evidence, the FDA continues to assert BPA is safe by rejecting low-dose data as “not biologically plausible” based on four incorrect assumptions criticized by the Endocrine Society as violating basic principles of endocrinology: that dose responses must be monotonic, thresholds exist below which there are no effects, both sexes must respond similarly, and only traditional toxicological guideline studies are valid. The review highlights a fundamental divide between regulatory approaches and endocrine science, demonstrating that traditional toxicology methods are insufficient for evaluating endocrine-disrupting chemicals like BPA, which can cause non-monotonic dose responses, sex-specific effects, and low-dose effects that challenge conventional assumptions about chemical safety, yet regulatory agencies continue to ignore modern endocrinology principles in favor of outdated toxicological paradigms.

Signs of carcinogenicity induced by parathion, malathion, and estrogen in human breast epithelial cells (Review).

Calaf et al,

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.

Oral administration of tartrazine (E102) accelerates the incidence and the development of 7,12-dimethylbenz(a) anthracene (DMBA)-induced breast cancer in rats.

Zingue et al,

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.

Biodegradable polymers and their nano-composites for the removal of endocrine-disrupting chemicals (EDCs) from wastewater: A review

Sharabati et al,

2021

Environ Res

Biodegradable polymers are emerging as a promising solution for removing endocrine-disrupting chemicals (EDCs) from wastewater. EDC’s, found in pharmaceuticals, pesticides, and personal care products pose serious health risks, impacting the endocrine system and disrupting reproductive health. Traditional water treatments often fail to fully remove EDCs. Biodegradable polymers, with strong adsorptive properties, offer a sustainable and effective method, helping to minimize EDC exposure and protect human and environmental health.

US EPA’s regulatory pesticide evaluations need clearer guidelines for considering mammary gland tumors and other mammary gland effects.

Cardona et al,

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.

Environmental chemicals and breast cancer: An updated review of epidemiological literature informed by biological mechanisms.

Rodgers et al,

2018

Environ Res

A systematic review of 158 studies examining environmental chemicals and breast cancer found the strongest evidence for increased risk from exposures during critical developmental periods (in utero, adolescence, pregnancy) to DDT, dioxins, PFOSA, air pollution, and occupational solvents, with risk estimates ranging from 1.4 to 5 times higher. A landmark 50-year study that captured DDT exposure during windows of breast development showed particularly elevated risks, while research on genetic variations found that women with certain DNA repair gene variants had higher breast cancer risk from PAH (polycyclic aromatic hydrocarbon) exposure. However, most studies failed to assess exposure timing during biologically relevant windows of susceptibility, and many current-use chemicals in consumer products remain inadequately studied, with major challenges including reconstructing decades-old exposures and measuring rapidly metabolized chemicals in complex real-world mixtures.

Environmental immune disruptors, inflammation and cancer risk.

Thompson et al,

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.

New exposure biomarkers as tools for breast cancer epidemiology, biomonitoring, and prevention: a systematic approach based on animal evidence.

Rudel et al,

2014

Environ Health Perspect

This review of exposure biomarkers for chemicals potentially linked to breast cancer identified methods for 102 chemicals causing mammary tumors in rodents, finding biomarkers for nearly 75% of them, with human exposure biomarkers existing for 62 chemicals (45 measured in non-occupationally exposed populations) and the CDC tracking 23 of them. Among rodent mammary carcinogens with >50% population detection frequency were PAHs (98%), methyleugenol (98%), PFOA (>50%), chlordane (>50%), acrylamide (>50%), and benzene (>50%), indicating near-universal exposure to multiple mammary carcinogens, with several additional chemicals showing >50% detection of urinary metabolites including ethylene oxide, acrylonitrile, fenvalerate, and vinyl chloride (71-75%). The study found consistent carcinogenicity between humans and rodents for many chemicals, though limited data exists for direct effects in humans, and emphasizes the availability of biomonitoring tools and resources to advance breast cancer prevention efforts. The findings underscore that populations are ubiquitously exposed to multiple known mammary carcinogens simultaneously, highlighting the urgent need for biomonitoring programs to assess mixed exposures and inform prevention strategies targeting modifiable environmental risk factors for breast cancer.

Designing Endocrine Disruption Out of the Next Generation of Chemicals.

Schug et al,

2013

Green Chemistry

Scientists have developed TiPED (Tiered Protocol for Endocrine Disruption), a voluntary five-tier testing system designed to help chemists identify hormone-disrupting properties in new chemicals during the design phase—before they enter consumer products—ranging from computer-based predictions to cell and animal studies. The protocol was created by experts in green chemistry and environmental health to broadly test whether new chemicals can mimic or block hormones or interfere with hormone signaling, which is critical for preventing endocrine disruption that can contribute to diseases like breast cancer. Testing of six known endocrine disruptors with different mechanisms of action successfully identified all of them, demonstrating the protocol’s effectiveness, though the system will continue evolving as scientific understanding advances. This tool represents an important shift toward preventing chemical hazards at the design stage rather than discovering them years later after widespread human exposure, which could significantly reduce public health risks including breast cancer.

Endocrine disruptors and asthma-associated chemicals in consumer products.

Dodson et al,

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.

Environmental pollutants and breast cancer: epidemiologic studies.

Brody et al,

2007

Cancer

A comprehensive review found that while laboratory studies have identified numerous environmental chemicals that cause breast tumors in animals or mimic estrogen, human epidemiological evidence is strongest for PAHs (found in air pollution and grilled foods) and PCBs (banned industrial chemicals), particularly in women with certain genetic variations affecting how their bodies process these chemicals and hormones. Evidence linking dioxins and organic solvents to breast cancer is limited but suggestive, while many chemicals identified as mammary carcinogens in animal studies have never been investigated in human populations due to challenges in measuring past exposures and the decades-long delay between exposure and cancer diagnosis. The review argues that given these methodological limitations in human studies, policymakers should rely more heavily on animal and laboratory evidence to develop regulations that reduce chemical exposures, as waiting for definitive human proof may unnecessarily delay prevention strategies that could reduce breast cancer rates.

No results found.

You have Successfully Subscribed!

Share This