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2025
JAMA Netw Open
In a cross-sectional study involving Black and White women participating in the NCI Maryland Breast Cancer Study, the investigators examined associations between neighborhood-level deprivation, air pollution (PM₂.₅) and presence of breast tissue crown-like structures (CLS-B) plus DNA methylation patterns. Higher PM₂.₅ exposure and greater neighborhood deprivation were associated with increased odds of having CLS-B (OR for PM₂.₅ 2.32, 95% CI: 1.12–4.78). The findings point to how socio-environmental disadvantage and pollution may influence breast adipose inflammation and epigenetic changes linked to cancer risk.
2025
Sci Total Environ
This review examines the relationship between DEHP (a common plastic additive) and cancer development, noting that while epidemiological studies suggest a link between DEHP exposure and increased cancer risk, the specific mechanisms need further clarification. The research shows that DEHP influences multiple aspects of cancer biology, including cell growth, spread, and drug resistance, through various molecular pathways involving hormone receptors, inflammation, and genetic modifications. DEHP’s carcinogenic effects operate through complex mechanisms including PI3K/AKT signaling, estrogen receptor activation, and oxidative stress. Understanding these molecular pathways could help develop targeted strategies to prevent and treat cancers associated with DEHP exposure.
2022
Cancer Epiemiol
The first Indian case-control study examining phthalates (chemicals widely used in plastics, cosmetics, and food packaging) and breast cancer found that women with higher urinary levels of di-butyl phthalate (DBP) had 1.5 times increased breast cancer risk, while those with higher DEHP levels had nearly 3 times increased risk. Analysis of breast tumor tissue revealed mutations in several genes known to respond to phthalate exposure, affecting pathways involved in hormones, metabolism, and cancer development. These findings suggest that exposure to certain phthalates may increase breast cancer risk through genetic changes, though larger studies are needed to confirm these results and understand how early-life exposures might contribute to cancer development later in life.
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
Ecotoxicol Env Saf
A Mendelian randomization study using genetic data from European populations found that specific endocrine-disrupting chemicals (EDCs) were causally associated with different breast cancer subtypes: n-butyl paraben (n-BuP) increased Luminal A risk, mono-methyl phthalate decreased Luminal B risk, and mono-iso-butyl phthalate (MiBP) increased triple-negative breast cancer risk. Mediation analysis revealed that blood metabolites—including caffeic acid sulfate and caffeine metabolism ratios—partially explained the n-BuP effect on Luminal A, while methylsuccinate mediated the MiBP effect on triple-negative cancer, and epigenetic analysis identified specific DNA methylation sites associated with EDC exposure and breast cancer risk. These findings provide the first genetic evidence suggesting causal relationships between specific EDC exposures and breast cancer subtypes through distinct metabolic and epigenetic pathways, identifying potential biomarkers for early detection and highlighting the heterogeneous effects of different EDCs on breast cancer biology—underscoring the need for chemical-specific and subtype-specific prevention strategies rather than treating all EDCs or breast cancers as uniform entities.
2024
Environ Health Perspect
A mouse study examining DNA methylation changes from lead and DEHP (phthalate) exposure during pregnancy and early development found that the brain (cerebral cortex) showed the most epigenetic changes (66% for lead, 57% for DEHP), with alterations concentrated in gene regulatory regions that control gene expression. The research identified imprinted genes—particularly Gnas and Grb10—as targets of both chemical exposures across multiple tissues, with some DNA methylation signatures in blood matching those in target organs like liver and brain, suggesting blood tests could potentially detect toxic exposures affecting other organs. Notably, lead exposure caused consistent hypermethylation of the Grb10 gene’s control region in both blood and liver of male offspring, providing preliminary evidence that epigenetic changes in easily accessible blood samples might serve as biomarkers for chemical exposures affecting critical organs like the brain. These findings are significant for breast cancer prevention because early-life exposures to lead and phthalates can alter epigenetic programming in ways that may increase disease risk decades later, and identifying blood-based biomarkers could enable early detection of harmful exposures during vulnerable developmental windows.
2024
Int J Environ Res Public Health
A systematic review of 25 epidemiological studies (2013-2022) found that seven out of eight investigated outdoor air pollutants showed significant associations with increased breast cancer risk, with benzo[a]pyrene showing the strongest relationship. The review found that 100% of studies examining nitrogen oxides (NOₓ), 83% of PM₂.₅ studies, 69% of nitrogen dioxide (NO₂) studies, and 43% of PM₁₀ studies demonstrated positive associations with breast cancer risk, with hazard ratios ranging from 1.05-1.56 and odds ratios from 1.03-1.86, while ozone and cadmium showed negative or no associations. These findings strengthen the evidence that outdoor air pollution—particularly traffic-related pollutants and fine particulate matter—contributes to breast cancer development, though the authors note that further research is needed to establish causal mechanisms, particularly through epigenetic pathways, and acknowledge that the review’s focus on English-language articles from developed countries may limit generalizability.
2024
Int J Mol Sci
This comprehensive review covers breast cancer biology from classification and risk factors through diagnosis and treatment, highlighting how the disease varies by subtype and between racial groups. The review examines both traditional factors like staging systems and molecular subtypes (Luminal A/B, Triple Negative, HER2-enriched) as well as emerging research on genetic mutations, epigenetic changes, and microbiome imbalances that may contribute to breast cancer development and progression. Recent evidence suggests that disruptions in the body’s microbial communities may play a role in breast cancer, with patterns potentially differing across populations, adding a new dimension to understanding racial disparities in breast cancer outcomes.
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.
2023
Front Oncol
A study of 80 Black and White women with breast cancer at Emory University Hospitals (2008-2017) examined associations between contemporary neighborhood redlining—a structural racism measure derived from Home Mortgage Disclosure Act data—and DNA methylation patterns in breast tumor tissue. Contemporary redlining was significantly associated with aberrant methylation at 5 CpG sites (FDR<0.10) in genes implicated in breast carcinogenesis, inflammation, immune function, and stress response (ANGPT1, PRG4), with additional top sites showing interaction by ER status and association with mortality; redlining was also associated with epigenetic age acceleration (β=5.35; 95% CI: 0.30-10.4 by Hannum metric). These novel findings suggest that structural racism—manifested through discriminatory housing policies leading to inequitable social and environmental exposures—may biologically embed in the breast tumor epigenome through altered DNA methylation patterns, potentially contributing to documented racial disparities in breast cancer outcomes and highlighting the need for further research on epigenetic mechanisms linking neighborhood-level structural racism to cancer prognosis.
2022
Eur J Epidemiol
A comprehensive study combining meta-analysis of observational data with genetic (Mendelian randomization) analysis found that each 10 grams per day increase in alcohol consumption was associated with a 4% increased breast cancer risk, and importantly, genetic predisposition to problematic alcohol use showed a 76% increased risk even after accounting for alcohol quantity consumed. The study identified four specific DNA methylation sites (epigenetic modifications) affected by alcohol—near the CDC7, ZNF318, RIN3, and RP11-867G23.13 genes—where alcohol-induced changes were causally linked to increased breast cancer risk, providing mechanistic insight into how alcohol drives carcinogenesis. These findings confirm that even low-dose alcohol consumption increases breast cancer risk and suggest that the harm stems not just from the amount consumed but from pathological drinking patterns and specific epigenetic changes that could serve as targets for prevention strategies.
2022
Biomed Pharmacother
A review of endocrine-disrupting chemicals (EDCs)—ubiquitous substances found in cosmetics, plastic food packaging, and medicines that enter the body through skin, digestive, or respiratory routes—examined their toxic effects even at microgram doses on the female reproductive system and genetic mechanisms. EDCs disrupt endocrine functions by binding to steroid hormone receptors, interfering with hormone synthesis and secretion, and modulating epigenetic processes that can lead to gene expression disturbances, contributing to neoplastic diseases, neurological disorders, circulatory problems, and reproductive dysfunction. Prenatal exposure can affect offspring development, with particular impacts on ovarian function leading to reduced fertility through disturbances in steroid receptor function, steroidogenesis, and gametogenesis. The review emphasizes that despite widespread exposure to these chemicals in everyday products, continued research is needed to fully understand their effects on the female reproductive system and potential transgenerational impacts mediated through epigenetic mechanisms.
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.
2020
Medicina
A systematic review of 12 studies examining nurses and shift work found that most studies showed an association between breast cancer and consecutive rotating night shifts prolonged over time, with risk increasing particularly during early adulthood and after 5 or more years of working 6 or more consecutive night shifts. The review identified disruption of circadian rhythm and alterations in peripheral clock genes and reproductive hormones as key mechanisms linking night shift work to breast cancer development, with potential roles for melatonin suppression and epigenetic changes including telomere alterations. These findings are particularly concerning given that nursing is a predominantly female profession requiring 24-hour staffing, suggesting the need for workplace policies that limit consecutive night shifts and total years of night work exposure, along with further research to establish definitive causal mechanisms and identify protective strategies for the millions of women working night shifts globally.
2018
Environ Res
A study of women from the Western New York Exposures and Breast Cancer Study examined associations between early life air pollution exposure (total suspended particulates and traffic emissions as proxies for polycyclic aromatic hydrocarbons) and DNA methylation of nine genes in breast tumor tissue, finding nominally significant associations including higher TSP at first birth associated with altered SCGB3A1 (OR=0.48) and SYK (OR=1.86) methylation, and traffic emissions at menarche associated with increased SYK methylation (OR=2.37), though none remained significant after multiple comparison adjustment. These preliminary findings provide suggestive evidence that ambient air pollution exposure during critical developmental windows (birth, menarche, first birth) may influence epigenetic methylation patterns of tumor suppressor genes in breast tissue, potentially representing a mechanism linking early life environmental exposures to later breast cancer risk. Larger studies assessing more methylation sites are warranted to confirm whether air pollution exposure during vulnerable life stages causes lasting epigenetic changes that contribute to breast cancer development.
2018
Oncol Rep
This study investigated whether exposure to bisphenol A (BPA) and phthalate metabolites affects breast cancer risk through epigenetic changes in the ADAM33 gene, which plays a role in cancer progression. The researchers conducted a case-control study with 44 breast cancer patients and 22 controls, analyzing ADAM33 gene methylation patterns in blood samples and measuring urinary concentrations of endocrine-disrupting chemicals. They found that certain phthalate metabolites (MEHHP, MECPP, MEOHP) were positively associated with increased methylation of the ADAM33 gene, which was linked to higher gene expression levels. Surprisingly, the study suggests these phthalate metabolites may have a protective effect against breast cancer by increasing ADAM33 methylation and expression, contrary to the typical expectation that endocrine disruptors increase cancer risk.
2018
Cancer Epidemiol Biomark Prev
A systematic review and meta-analysis of 24 studies found suggestive evidence that physical activity may reduce breast cancer risk through increased global DNA methylation, with higher activity levels showing a trend toward higher methylation (19% standardized mean difference) and higher methylation associated with a 30% reduced breast cancer risk, though neither association reached statistical significance overall. Subgroup analyses revealed that the protective pathway became clearer when examining long-term physical activity patterns and prospective cohort studies specifically, where both associations were statistically significant. This is the first systematic review to examine the complete biological pathway linking physical activity to breast cancer prevention through epigenetic mechanisms, suggesting that exercise may alter DNA methylation patterns in ways that protect against cancer development—a finding that could help explain how physical activity exerts its well-established cancer-preventive effects at the molecular level.
2017
Molec Cell Endocrinol
This study examines the role of environmental estrogen-like endocrine-disrupting chemicals (EEDs) in breast cancer development. EEDs are synthetic compounds that mimic estrogen, and the ones being studied in this paper include polychlorinated biphenyls (PCBs), bisphenol A (BPA), and phthalates. The results of the study show that of the EEDs tested, only one type of PCB, PCB138, had a strong association with the formation of breast cancer, where as phthalates (and it metabolites) but and BPA showed no strong correlation. Additionaly, the researchers identify that these EEDs promote the proliferation of breast cancer cells, induce epigenetic changes that may increase susceptibility to cancer, as well as alter developmental pathways during critical windows of breast development.
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.
2014
Aging Dis
The following review article described how exposure to EDCs during early development can lead to adverse health outcomes later in life through epigenetic mechanisms based on existing studies. The article emphasizes that exposure to EDCs during critical developmental periods such as in utero and early childhood, can have lasting effects on health since, during these periods, the body’s systems are particularly vulnerable to exposures. Additionally, the article finds a link between early-life exposure to EDCs and increased risk of various health issues later on in life, including metabolic disorders and cancers. The suspected mechanism by which these chemicals do this is thought to be mediated by epigenetic changes, which are changes to gene expression without altering the DNA. Therefore, the article emphasizes understanding how exposure during such sensitive periods in development can pose such drastic problems later on in life.