Breast cancer risk and chemical exposure: New evidence points to triclosan as a key culprit

By Vijay Kumar MalesuReviewed by Susha Cheriyedath, M.Sc.Feb 4 2025

New research reveals that a common antibacterial chemical, triclosan, may significantly increase breast cancer risk in younger and overweight women. With endocrine disruptors everywhere in daily life, are we unknowingly increasing our cancer risk?

Study: Associations between phenol and paraben exposure and the risk of developing breast cancer in adult women: a cross-sectional study. Image Credit: Mouse family / Shutterstock

In a recent study published in the journal Scientific Reports, researchers assessed the association between exposure to endocrine-disrupting chemicals, specifically phenols and parabens, and the risk of developing breast cancer in adult women.

Background

Did you know that nearly every person has traces of endocrine-disrupting chemicals in their body? These chemicals, found in skincare products, plastics, and even food packaging, mimic hormones and may contribute to serious health risks. Breast cancer is the most commonly diagnosed malignancy in women, with global incidence rates rising steadily. While genetic and hormonal factors contribute significantly to its onset, environmental exposures are increasingly recognized as potential risk factors. Despite growing evidence linking these chemicals to endocrine disorders, their role in breast cancer remains inconclusive. Further research is essential to clarify these associations and guide public health policies.

About the Study

This cross-sectional study utilized data from the National Health and Nutrition Examination Survey (NHANES) from 2005 to 2014. A total of 4,455 adult women were included, with urinary concentrations of bisphenol A, triclosan, benzophenone-3, methyl paraben, ethyl paraben, propyl paraben, and butyl paraben measured using high-performance liquid chromatography-tandem mass spectrometry. Breast cancer diagnosis was determined through self-reported medical history.

Multivariable logistic regression models, adjusted for potential confounders including age, race, body mass index, and lifestyle factors, were employed to evaluate associations between chemical exposures and breast cancer risk. Data were analyzed using weighted quantile sum regression and Bayesian Kernel Machine Regression models to assess combined exposure effects. Urinary concentrations were log-transformed for normalization, and restricted cubic spline modeling (p=0.007) confirmed a statistically significant nonlinear relationship between triclosan exposure and breast cancer risk. Stratified analyses were performed based on age, body mass index, and race.

Statistical significance was set at p<0.05, and all analyses accounted for NHANES survey design weights. Ethics approval and participant consent were obtained through the Centers for Disease Control and Prevention institutional review board. Data were publicly available and analyzed using R software.

Study Results

Among the 4,455 women included in the study, 134 had a breast cancer diagnosis. The mean age was 47.52 years, with a higher prevalence of breast cancer among older and overweight participants. Non-Hispanic White women exhibited the highest incidence.

Urinary triclosan concentrations were significantly associated with breast cancer risk, with adjusted odds ratios indicating a 2.33-fold increased risk in the second quartile (p<0.001) and a 1.94-fold increased risk in the third quartile (p=0.006). A nonlinear relationship was observed, with breast cancer risk peaking at moderate triclosan levels before declining at higher concentrations. This inverted U-shaped association was statistically significant (p=0.007).

No significant overall association was identified for other phenols or parabens. However, stratified analyses revealed that ethyl and butyl paraben exposure was linked to increased breast cancer risk specifically among women with BMI < 25 kg/m² (p<0.05). White women and those under 60 years exhibited stronger associations between triclosan exposure and breast cancer risk.

Weighted quantile sum (WQS) regression found that triclosan contributed over 50% to the overall exposure index influencing breast cancer risk. However, Bayesian Kernel Machine Regression (BKMR) did not confirm a significant overall mixture effect, highlighting complex interactions.

The detection rates of methyl paraben and propyl paraben exceeded 95%, reflecting widespread exposure in the population. Benzophenone-3 was detected in nearly all samples, emphasizing its ubiquitous presence. Spearman correlation analysis showed moderate positive associations among the urinary chemicals, with the strongest correlation observed between methyl paraben and propyl paraben. Triclosan concentrations were weakly correlated with other metabolites, suggesting distinct exposure sources or metabolic pathways.

The findings suggest that moderate triclosan exposure may contribute to breast cancer risk, particularly in overweight and younger women. No definitive association was observed for bisphenol A, contradicting some prior studies linking it to breast cancer. However, the researchers note that previous studies have reported mixed results, particularly in animal models and smaller cohorts. These discrepancies may stem from differences in study design, exposure measurement, and participant characteristics.

Conclusions

To summarize, this study highlights a significant association between urinary triclosan levels and breast cancer risk, particularly among younger and overweight women. While no overall link was found for other phenols and parabens, stratified analysis showed that ethyl and butyl paraben exposure was significantly associated with increased risk in leaner women (BMI < 25 kg/m², p<0.05). The nonlinear relationship observed for triclosan underscores the complexity of endocrine-disrupting chemical effects.

While triclosan appeared to play a significant role, Bayesian Kernel Machine Regression did not confirm a significant overall effect of the chemical mixture, suggesting complex interactions. Given the widespread use of these chemicals, further research is necessary to elucidate causal mechanisms and inform regulatory policies.

Limitations of this study include its cross-sectional design, which prevents causal inference, reliance on self-reported breast cancer diagnoses (which may introduce recall bias), and single urinary measurements, which do not account for long-term exposure variations. Public health interventions should prioritize reducing exposure to potentially harmful environmental chemicals, particularly among high-risk populations, to reduce breast cancer risk.