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Association between Urinary Phenols and Parabens as Well as Breast Cancer.

Wu et al,

2025

Iran J of Pub Health

This study of nearly 5,000 U.S. women found that exposure to triclosan—an antibacterial chemical once commonly found in soaps, toothpaste, and other personal care products—was associated with more than double the breast cancer risk at moderate exposure levels, while propylparaben (a preservative in cosmetics and foods) showed a protective association. However, when researchers examined the combined effect of multiple phenols and parabens together, they found no significant association with breast cancer, suggesting these chemicals may have complex and sometimes opposing effects. These mixed findings highlight the need for more research to understand how individual chemicals versus chemical mixtures affect breast cancer risk, especially since people are typically exposed to multiple chemicals simultaneously in everyday products.

Multi-pollutant exposure profiles associated with breast cancer risk: A Bayesian profile regression analysis in the French E3N cohort.

Giampiccolo et al,

2024

Environ Int

A comprehensive French study of over 10,000 women examined exposure to eight different air pollutants simultaneously and identified that women exposed to high levels of nitrogen dioxide (NO₂), particulate matter, and PCB153 had a 38-61% increased risk of breast cancer compared to women with low pollution exposure. Using advanced statistical modeling that groups women by their combined pollution exposure patterns rather than examining pollutants individually, researchers found that specific combinations of high pollutant exposures were strongly associated with elevated breast cancer risk. This study provides important evidence that the combined “cocktail effect” of multiple air pollutants, particularly traffic-related pollution (NO₂) and industrial chemicals (PCB153), may significantly increase breast cancer risk beyond what individual pollutants cause alone.

Multiple xenoestrogen air pollutants and breast cancer risk: Statistical approaches to investigate combined exposures effect.

Amadou et al,

2024

Environ Pollut

A French study of over 10,000 women found that combined exposure to a mixture of four hormone-disrupting air pollutants (benzo[a]pyrene, cadmium, dioxin, and PCB153) was associated with an approximately 10-11% increased risk of breast cancer. Using advanced statistical methods that account for simultaneous exposure to multiple pollutants rather than examining each separately, researchers found that benzo[a]pyrene, cadmium, and PCB153 showed the strongest individual contributions to increased breast cancer risk within the mixture. This research provides important evidence that the cumulative effect of multiple air pollutants acting together on hormone pathways may be a significant risk factor for breast cancer development.

Breast Cancer Incidence and Exposure to Metalworking Fluid in a Cohort of Female Autoworkers.

Garcia et al,

2018

Am J Epidemiol

A cohort study of 4,503 female autoworkers in Michigan exposed to metalworking fluids (MWFs)—oil and chemical mixtures used in metal manufacturing—found that increased exposure to straight mineral oil MWFs was associated with a 13% increased breast cancer risk per interquartile range increase in cumulative exposure. Among younger women who developed premenopausal breast cancer, exposure to synthetic MWFs (chemical lubricants without oil) showed elevated risk, suggesting potentially different carcinogenic mechanisms in younger versus older women. This occupational study addresses a critical gap in breast cancer research by providing quantitative exposure-response data for a specific chemical mixture affecting a large workforce, offering one of the few leads on modifiable environmental risk factors for breast cancer.

Urban Neighborhood and Residential Factors Associated with Breast Cancer in African American Women: a Systematic Review.

Smith et al,

2018

Discov Oncol

This systematic review examined the relation of 4 neighborhood factors on breast cancer incidence and prognosis among African-American women: neighborhood socioeconomic status (nSES), residential segregation, spatial access to mammography, and residential pollution. The authors found that nSES, residential segregation and access to mammography were all related to stage at diagnosis, and nSES and living in more segregated areas were both associated with mortality. Residential pollution was not associated with increased risk of breast cancer in the studies reviewed.

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.

Associations between phenol and paraben exposure and the risk of developing breast cancer in adult women: a cross-sectional study.

Xiong et al,

2025

Sci Rep

A large U.S. study of 4,455 people found that exposure to triclosan (TRS)—an antibacterial chemical commonly found in soaps, toothpaste, and personal care products—was associated with more than double the risk of breast cancer at moderate exposure levels, with the relationship following an inverted U-shape pattern. The association was strongest among overweight individuals, people under 60 years old, and white participants, while other tested chemicals (including bisphenol A, benzophenone-3, and parabens) showed no significant link to breast cancer risk. These findings suggest that triclosan exposure may be an important modifiable risk factor for breast cancer, particularly for certain population groups, though more research is needed to understand the underlying mechanisms and confirm causality.

Personal Care Products, Socioeconomic Status, and Endocrine-Disrupting Chemical Mixtures in Black Women.

Schildroth et al,

2024

Environ Sci Technol

A study of 751 reproductive-aged Black women found that the relationship between personal care product (PCP) use and exposure to endocrine-disrupting chemicals (EDCs) varied significantly by socioeconomic status (SES), with different patterns of chemical exposure from the same products depending on women’s education, income, and employment. For example, vaginal powder use was associated with higher phenol exposure (a class of EDCs) among lower SES women but showed no such association in higher SES women, suggesting that product formulations, brands, or usage patterns may differ across SES groups. These findings highlight that Black women face inequitable EDC exposures that are influenced by both race and socioeconomic factors, underscoring the need for targeted public health interventions that address these intersecting disparities in chemical exposures from everyday products

Exposure to air pollutants and breast cancer risk: mediating effects of metabolic health biomarkers in a nested case-control study within the E3N-Generations cohort.

Mercoeur et al,

2024

Breast Cancer Res

A nested case-control study within the French E3N-Generations cohort examined 523 breast cancer cases and 523 matched controls to investigate whether thirteen metabolic health biomarkers mediate the relationship between exposure to three air pollutants (nitrogen dioxide, PCB153, and benzo[a]pyrene) and breast cancer risk. The study found that benzo[a]pyrene exposure was associated with a significant 2.32-fold increased breast cancer risk (highest vs. lowest quartile), PCB153 showed inconsistent positive associations, and nitrogen dioxide showed no association; among biomarkers, estradiol was associated with increased breast cancer risk (OR = 1.22 per SD). Four-way decomposition mediation analysis revealed suggestive evidence that albumin, HDL and LDL cholesterol, parathormone, and estradiol may partially mediate the associations between all three pollutants and breast cancer risk, though findings were limited by statistical power. These results provide preliminary mechanistic insights suggesting that air pollutants may influence breast cancer risk through alterations in metabolic biomarkers—particularly lipid metabolism and hormone regulation—though larger studies are needed to confirm these pathways and establish the clinical significance of these mediating effects in the relationship between environmental exposures and breast cancer development.

Reduction of daily-use parabens and phthalates reverses accumulation of cancer-associated phenotypes within disease-free breast tissue of study subjects.

Dairkee et al,

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.

Environmental mixtures and breast cancer: identifying co-exposure patterns between understudied vs breast cancer-associated chemicals using chemical inventory informatics.

Koval et al,

2022

J Expo Sci Environ Epidemiol

A comprehensive analysis of 6,793 chemicals in commercial use identified 50 high-priority understudied chemicals that frequently co-occur with known breast cancer-associated chemicals in everyday exposure sources like food, consumer products, and personal care items. Using chemical databases and structural similarity analyses, researchers found these understudied chemicals share physicochemical properties with established mammary carcinogens and potential endocrine disruptors, yet have not been adequately evaluated for breast cancer risk. The findings highlight that real-world chemical exposures occur as mixtures rather than isolated compounds, and that focusing solely on individual well-known chemicals may miss important combination effects—underscoring the urgent need for mixtures-based research in clinical, epidemiological, and toxicological studies to better understand and prevent environmentally-driven breast cancer.

Breast cancer and urinary metal mixtures in Mexican women.

Mérida-Ortega et al,

2022

Environ Res

A case-control study of 499 breast cancer patients and 499 controls in Northern Mexico found that women with breast cancer had distinct patterns of urinary metal exposure, with higher concentrations of tin and lower concentrations of vanadium, cobalt, and molybdenum compared to controls. Using principal component analysis to identify metal mixtures, researchers discovered two distinct exposure patterns with opposite breast cancer associations: a mixture containing chromium, nickel, antimony, aluminum, lead, and tin showed a 15% increased risk, while a mixture of molybdenum and cobalt showed a 44% reduced risk. This is the first study to identify specific urinary metal mixture profiles associated with breast cancer, highlighting that metals may interact synergistically or antagonistically rather than acting independently, and underscoring the critical need for mixture-based approaches in environmental health research—since real-world exposures involve multiple simultaneous contaminants whose combined effects may differ substantially from predictions based on individual metals alone—along with mechanistic studies to understand how metal interactions influence breast carcinogenesis.

Endocrine disrupting chemicals and breast cancer cells.

Darbre et al,

2021

Adv Pharmacol

A comprehensive review examining endocrine-disrupting chemicals (EDCs) in breast tissue concludes that hundreds of these environmental chemicals are entering human breast tissue and contributing to the global rise in breast cancer incidence through multiple biological mechanisms. Laboratory studies demonstrate that EDCs can activate all the established “hallmarks of cancer” in human breast cancer cells—even at concentrations measured in actual human breast tissue—with effects amplified when chemicals are present as mixtures rather than individually. The authors argue that EDCs must now be formally recognized as a breast cancer risk factor to enable prevention strategies that include reducing environmental chemical exposures, particularly given that the varied mixtures of EDCs found in individual breast tissues act through overlapping mechanisms to promote cancer development.

In utero exposure to poly- and perfluoroalkyl substances (PFASs) and subsequent breast cancer.

Cohn et al,

2020

Repro Toxicol

A 54-year follow-up study of 102 breast cancer cases and 310 matched controls among 9,300 daughters born 1959-1967 in the Child Health and Development Studies cohort found that high maternal perinatal levels of N-ethyl-perfluorooctane sulfonamido acetic acid (EtFOSAA, a precursor to PFOS) combined with high maternal cholesterol predicted a 3.6-fold increased breast cancer risk in daughters by age 52 (95% CI: 1.1-11.6), while maternal PFOS alone was paradoxically associated with decreased risk. These robust findings—consistent across alternative modeling approaches and independent of other maternal factors—demonstrate that prenatal exposure to specific PFAS compounds during critical developmental windows can influence breast cancer risk decades later, revealing multigenerational health consequences of persistent environmental chemicals. The results emphasize the critical importance of studying internal PFAS doses and chemical mixture exposures during vulnerable early-life periods for breast cancer prevention, particularly as current and future generations face continued ubiquitous exposure to these persistent compounds, though experimental validation and replication in additional epidemiological cohorts are needed to confirm causality and inform prevention strategies.

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.

Disruptive environmental chemicals and cellular mechanisms that confer resistance to cell death.

Narayanan et al,

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.

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.

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.

Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: focus on the cancer hallmark of tumor angiogenesis.

Hu et al,

2015

Carcinogenesis

This paper examined how low doses of environmental chemical mixtures may contribute to cancer development by promoting tumor angiogenesis, and the formation of new blood vessels that supply nutrients to tumors. The authors identified chemicals that may interfere with these angiogenic pathways, such as those involving vascular endothelial growth factor (VEGF) and hypoxia-inducible factors (HIFs). Chemicals disrupting these pathways can lead to uncontrolled blood vessel formation in tumors. However, there is a need for further research to understand the combined effects of low-dose chemical exposures on angiogenesis and cancer risk.

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