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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.
2023
Cancer Prev Res
A large prospective study of 76,951 postmenopausal women followed for nearly 17 years found that women reporting the highest levels of stressful life events had a 30% increased risk of developing ER-negative breast cancer compared to those with the lowest stress levels, with no association found for ER-positive breast cancer. The risk was particularly pronounced among widowed women, who showed a 139% increased risk when experiencing high levels of stressful life events. These findings suggest that chronic psychosocial stress may specifically increase risk for ER-negative breast cancer—a more aggressive subtype—and that the impact of stress may be amplified by loss of a spouse, highlighting the potential importance of stress management and social support in breast cancer prevention.
2023
Asian Pac J Cancer Prev
A study of 360 participants found that agricultural workers exposed to pesticides who carry genetic variations that impair their body’s ability to detoxify chemicals (null mutations in GSTT1 and GSTM1 genes) had substantially increased cancer risk, with 4-7 times higher odds of developing lymphoma or breast cancer compared to those with normal detoxification genes. The study also found elevated markers of oxidative stress (cellular damage) in farm workers with these genetic variants who developed leukemia, suggesting that pesticide exposure combined with impaired detoxification capacity triggers cancer development. These findings indicate that certain genetic profiles make agricultural workers particularly vulnerable to pesticide-related cancers, highlighting the importance of protective measures for farm workers and potential genetic screening to identify high-risk individuals.
2023
Breast Cancer Res
This large study of over 181,000 women from the UK Biobank examined whether allostatic load (AL)—a measure of cumulative physiological stress on the body over time—is associated with breast cancer risk. Women with higher AL scores had a significantly increased risk of developing breast cancer, with each one-unit increase in AL associated with a 5% higher risk, and women in the high AL group showing a 17% increased risk compared to those in the low AL group, even after accounting for known risk factors like family history, lifestyle, and genetic factors. The association was found across multiple subgroups and appeared independent of traditional breast cancer risk factors, suggesting that chronic physiological stress may contribute to breast cancer development. These findings indicate that AL could serve as a valuable biomarker for predicting and stratifying breast cancer risk in women.
2021
Cancer Epidemiol Biomarkers Prev
A Spanish case-control study of 1,738 breast cancer cases and 1,910 controls found that occupational heat exposure was associated with a 22% increased risk of breast cancer among women who had ever been exposed. The study found significant dose-response relationships, with risk increasing with both cumulative heat exposure and duration of exposure, and particularly strong associations for hormone receptor-positive breast cancer (38% increased risk). The associations were strongest when not adjusted for detergent exposure, suggesting potential confounding or interaction between these workplace exposures. These findings suggest that chronic workplace heat stress may be a previously underrecognized occupational risk factor for breast cancer, though further research is needed to confirm these results and understand potential interactions with other workplace exposures.
2018
Int J Psychiatry Med
A hospital-based study of 250 breast cancer patients and 250 controls in Turkey found that recent major stressors—particularly those occurring within the last five years—were associated with a 372% increased risk of breast cancer (the strongest factor identified). Other significant risk factors included inadequate social support (83% increased risk), loss of a father during childhood (168% increased risk), family history of cancer (55% increased risk), and history of psychiatric disorders (95% increased risk), suggesting that psychological trauma and social factors may play substantial roles in breast cancer development alongside genetic predisposition.
2018
Breast Cancer Res
A nationwide study of 22,466 Danish female nurses found that long-term exposure to road traffic Noise was associated with increased breast cancer risk, particularly for hormone receptor-positive tumors. For every 10-decibel increase in 24-year average Noise levels at their residence, women showed a 23% increased risk of estrogen receptor-positive (ER+) breast cancer and a 21% increased risk of progesterone receptor-positive (PR+) breast cancer, with no significant association for hormone receptor-negative tumors. The association was especially strong among nurses who worked night shifts, showing a 236% increased risk of ER+ breast cancer compared to a 21% increase in those not working nights. These findings suggest that chronic traffic Noise exposure may contribute to breast cancer development, potentially through stress-related hormonal pathways, with night shift work potentially amplifying this risk.
2025
JAMA Netw Open
A cross-sectional study of 121 Black and White women with breast cancer found that chronic stressors—including perceived stress, inadequate social support, discrimination, and neighborhood deprivation—were associated with harmful immune and tumor changes, with particularly pronounced effects in Black women who also lived in significantly more socioeconomically deprived neighborhoods. Higher stress, discrimination, and neighborhood deprivation were linked to increased systemic inflammation, immune-suppressive tumor environments (including tumor-promoting M2 macrophages), and elevated tumor mutational burden, while greater social support was associated with beneficial immune-stimulatory changes including increased natural killer cells in breast tissue. Black women showed distinct stress-related immunologic signatures including enhanced chemotaxis, immune suppression at the systemic level, and increased tumor-associated myeloid cells, suggesting that chronic psychosocial and environmental stressors may biologically contribute to breast cancer disparities by creating a pro-tumorigenic immune environment—findings that underscore the urgent need for interventions addressing social determinants of health as cancer prevention strategies.
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.
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.
2024
Maturitas
A comprehensive review of breast cancer disparities highlights that Non-Hispanic Black women experience markedly elevated breast cancer mortality due to multifactorial causes, including unique risk profiles such as higher prevalence of early-onset triple-negative breast cancer, specific reproductive risk factors, obesity patterns traced to infant feeding practices, and barriers to genetic risk assessment and high-risk referrals. The authors propose risk- and race-based screening strategies given the prevalence of aggressive early-onset disease in young Black women, emphasize the importance of early hereditary/familial risk identification while addressing challenges in interpreting uncertain genetic results, and stress the need for culturally sensitive approaches to healthy lifestyle promotion and clinical trial participation. Addressing breast cancer disparities requires tackling social determinants of health, educating patients and clinicians about factors driving outcome inequities, building trust to foster adherence and follow-up, and encouraging participation in targeted research to better serve all communities and reduce the disproportionate burden of breast cancer mortality in Black women.
2023
Cancer Causes Control
A review examining how low socioeconomic status (SES) contributes to early chronic disease onset and reduced life expectancy found that neighborhood-level factors—including environmental pollutants, deprivation, social isolation, structural racism, and discrimination—create chronic life stress that affects molecular processes like DNA methylation, inflammation, and immune response, contributing to more aggressive tumor biology, particularly in Black Americans. Despite decades of research showing associations between neighborhood factors and cancer outcomes in marginalized communities, the biological mechanisms linking SES to cancer disparities remain poorly understood, though emerging evidence suggests chronic stress pathways may play a central role. The authors summarize current methods for measuring neighborhood-level deprivation, discrimination, and structural racism in cancer disparities research and recommend adopting a multi-faceted intersectional approach to reduce cancer health inequities and develop effective interventions promoting health equity.
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
Asian Pac J Cancer Prev
A matched case-control study of 187 breast cancer patients and 187 controls in Asia found that irregular sleep patterns and severe stress were the strongest modifiable risk factors, with irregular sleep associated with a staggering 3,311% increased breast cancer risk and severe stress showing a 574% increased risk. Poor sleep quality showed an even more dramatic 1,029% increased risk, while regular multivitamin use was associated with a 238% increased risk—a surprising finding requiring further investigation—and having a first child before age 30 was protective with a 56% risk reduction. Notably, none of the traditional non-modifiable risk factors (such as family history) showed significant associations in this study, suggesting that modifiable lifestyle factors—particularly sleep quality and stress management—may be critically important targets for breast cancer prevention in Asian populations experiencing rapidly rising breast cancer rates.
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.
2020
Int J Cancer
A population-based case-control study of 3,030 breast cancer cases and 3,402 controls in Ontario, Canada found that iron intake’s effects on breast cancer risk varied by menopausal status, hormone receptor subtype, and antioxidant-related genotypes: among premenopausal women, dietary nonheme iron was positively associated with ER-/PR- breast cancer, while among postmenopausal women, supplemental iron reduced overall risk (OR=0.68; 95% CI: 0.51-0.91) but dietary heme iron increased ER-/PR- risk (OR=1.69; 95% CI: 1.16-2.47). GSTT1 and GSTM1/GSTT1 polymorphisms modified these associations, with higher dietary iron most strongly linked to increased risk among women with genetic deletions affecting antioxidant capacity (p<0.05). These findings suggest that iron's impact on breast cancer development through oxidative stress mechanisms depends on iron source (heme vs. nonheme, dietary vs. supplemental), menopausal status, tumor hormone receptor status, and individual genetic variation in oxidative stress defense.
2020
Environ Res
A systematic review of 100 publications across 56 epidemiologic studies found that research enriched with women at higher baseline breast cancer risk—through family history, early-onset disease, or genetic susceptibility—consistently showed stronger and more frequent associations between environmental chemical exposures and breast cancer compared to average-risk populations. Specifically, 80% of studies enriched with family history or early-onset cases showed significant associations with exposures including PAHs, air pollution, DDT, PCBs, PFAS, metals, personal care products, and occupational chemicals, while 74% of studies examining genetic susceptibility found significant gene-environment interactions for various pollutants in women with variants affecting carcinogen metabolism, DNA repair, and oxidative stress. These findings suggest that the inconsistent evidence for environmental chemicals and breast cancer in the literature may partly stem from studying predominantly average-risk populations who may be less susceptible to environmental carcinogens, highlighting the critical need for future research to focus on high-risk populations and measure exposures during key windows of susceptibility (puberty, pregnancy, menopause) to more accurately capture the role of environmental chemicals in breast cancer development.
2019
Breast Cancer Res Treat
A systematic review and meta-analysis of 11 cohort studies found that a history of stressful life events was associated with an 11% increased risk of breast cancer (pooled risk ratio: 1.11, 95% CI: 1.03-1.19). While the increase is modest, the finding suggests that psychological stress may play a role in breast cancer development and that women who experience significant life stressors could benefit from psychological and counseling services as a potential preventive measure. These results add to growing evidence linking chronic stress exposure to cancer risk and underscore the importance of addressing mental health and stress management as part of comprehensive breast cancer prevention strategies.
2019
Environ Int
Advanced glycation end products (AGEs), formed during the processing of foods at high temperatures, act as endocrine disruptors and are linked to various health risks. These compounds accumulate in the body over time, promoting oxidative stress, aging, diabetes, and other degenerative diseases. Processed foods, often convenient and inexpensive, are significant sources of AGEs, contributing to hormonal disruption and potential long-term health effects. Choosing minimally processed, whole foods can help reduce exposure to these harmful compounds and support overall hormonal balance, reinforcing the importance of food quality in maintaining long-term health and well-being.
2018
BMC Pub Health
A mixed ecological and case-control study in Australia found that obesity occurring between ages 31-40 was independently associated with a 250% increased breast cancer risk in middle-aged women, though no direct association was found between alcohol consumption and breast cancer in the case-control analysis despite ecological correlations. The study revealed that stress was ecologically linked to both alcohol consumption and obesity but not directly to breast cancer incidence, suggesting that stress may influence breast cancer risk indirectly through health behaviors rather than representing a “missing link” as hypothesized. These findings highlight a critical window for breast cancer prevention: obesity in the decade before age 40 appears particularly risky, supporting targeted weight management interventions for women in their 30s, while the complex interrelationships between stress, alcohol, obesity, and breast cancer warrant further investigation using longitudinal designs that can capture temporal sequences and cumulative exposures across women’s reproductive years.
2018
Psycho-Oncology
A prospective cohort study of 2,739 women from 990 Australasian families at increased familial breast cancer risk followed participants over multiple 3-year assessment periods, measuring acute and chronic life stressors, social support, and personality characteristics (optimism, anger control, antiemotionality) to determine their association with breast cancer development. During follow-up, 103 women were diagnosed with breast cancer, but Cox proportional hazard regression analysis found no significant associations between any stressor or psychosocial variable and breast cancer risk in either unadjusted or adjusted models (total acute stressors HR = 1.03, p = .19; total chronic stressors HR = 1.0, p = .98). The study concludes that stress, social support, and personality characteristics do not appear to influence breast cancer risk, even in women with increased familial susceptibility. The researchers emphasize that women should focus their prevention efforts on evidence-based risk reduction strategies rather than worrying about stress or personality factors as contributors to breast cancer development, addressing a longstanding concern about the potential role of psychological factors in cancer development.
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 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.
2022
Metabolites
This study investigates the effects of the insecticide chlorpyrifos on rice plants. High concentrations of chlorpyrifos inhibited growth, increased oxidative stress, and led to lipid peroxidation, as indicated by elevated malondialdehyde (MDA) levels. Antioxidant enzyme activities increased, and protein synthesis was negatively impacted. Significant changes in amino acids and organic acids, including increased proline and glutathione, were observed, suggesting a stress response. Just as chlorpyrifos induces oxidative stress in plants, similar mechanisms may occur in humans, leading to cellular damage and increasing the risk of chronic diseases such as cancer.