Endocrine disrupting chemicals and breast cancer: a systematic review of epidemiological studies

Wan, Murphy Lam Yim; Co, Vanessa Anna; El‐Nezami, Hani

doi:10.1080/10408398.2021.1903382

Cited by 92 publications

(49 citation statements)

References 275 publications

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“…This capability enables these substances to mimic and/ or antagonize the hormone function. Although current evidence is not fully conclusive of their mechanism of action, exposure to these compounds has been associated with an increased risk of breast cancer (47). We found that exposed patients present an increased frequency of hormone (ER/PR) negative tumors.…”

Section: Discussionmentioning

confidence: 61%

Somatic DNA Damage Response and Homologous Repair Gene Alterations and Its Association With Tumor Variant Burden in Breast Cancer Patients With Occupational Exposure to Pesticides

et al. 2022

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Homologous recombination is a crucial pathway that is specialized in repairing double-strand breaks; thus, alterations in genes of this pathway may lead to loss of genomic stability and cell growth suppression. Pesticide exposure potentially increases cancer risk through several mechanisms, such as the genotoxicity caused by chronic exposure, leading to gene alteration. To analyze this hypothesis, we investigated if breast cancer patients exposed to pesticides present a different mutational pattern in genes related to homologous recombination (BRCA1, BRCA2, PALB2, and RAD51D) and damage-response (TP53) concerning unexposed patients. We performed multiplex PCR-based assays and next-generation sequencing (NGS) of all coding regions and flanking splicing sites of BRCA1, BRCA2, PALB2, TP53, and RAD51D in 158 unpaired tumor samples from breast cancer patients on MiSeq (Illumina) platform. We found that exposed patients had tumors with more pathogenic and likely pathogenic variants than unexposed patients (p = 0.017). In general, tumors that harbored a pathogenic or likely pathogenic variant had a higher mutational burden (p < 0.001). We also observed that breast cancer patients exposed to pesticides had a higher mutational burden when diagnosed before 50 years old (p = 0.00978) and/or when carrying BRCA1 (p = 0.0138), BRCA2 (p = 0.0366), and/or PALB2 (p = 0.00058) variants, a result not found in the unexposed group. Our results show that pesticide exposure impacts the tumor mutational landscape and could be associated with the carcinogenesis process, therapy response, and disease progression. Further studies should increase the observation period in exposed patients to better evaluate the impact of these findings.

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Section: Discussionmentioning

confidence: 61%

Somatic DNA Damage Response and Homologous Repair Gene Alterations and Its Association With Tumor Variant Burden in Breast Cancer Patients With Occupational Exposure to Pesticides

et al. 2022

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“…2,4-dichlorophenol [196], o-nitrotoluene [197] Cancer Human DDT/DDE [15,213], DES [138] a Air pollution/PAHs [219] , PFOS [216], PFHxS [216], PFDA [216]), b DDT/DDE [17], organophosphate pesticides [17], phthalates (MCPP [213], MCNP [213], MCOP [213], MEHP [213], DEHP [17,213], DBP [17], DEP [17], MEP [17], MECPP [17]), a Air pollution [15,17,215], PAHs [17], zearalenone [213], organic dyes [17,226], metals ( a Hg [17], As [17])…”

Section: Experimental Studiesmentioning

confidence: 99%

“…However, chemicals that alter normal MG development and function in rodent studies have also been detected in blood and urine of women, and those biomarkers of exposure have been associated with breast cancer risk. Recent systematic reviews highlight strong epidemiological evidence showing that DDT and its metabolites, TCDD, air pollution (e.g., PAHs, NO 2 , PM 2.5 , and heavy metals), organic solvents, and pharmaceutical estrogens (e.g., DES) are associated with increased risk of breast cancer, with some increasing the risk of premenopausal breast cancer, which is less likely to be confounded by age-related risk or demographic factors [15,17,[213][214][215]. In addition, estrogen + progestin HRT after menopause has also been shown to increase breast cancer risk [138].…”

Section: Epidemiological Studiesmentioning

confidence: 99%

“…In addition, estrogen + progestin HRT after menopause has also been shown to increase breast cancer risk [138]. More limited evidence suggests associations between breast cancer and exposure to certain PFAS, PCBs, PBDEs, oral contraceptives, phthalates, hair dyes, and organophosphate pesticides [15,17,213,216]. Increasing breast cancer rates in women who are too young to be recommended for yearly mammograms (< 40 years old) lend further support to the hypothesis that early life exposures can be carcinogenic [11,17,[217][218][219][220][221][222].…”

Section: Epidemiological Studiesmentioning

confidence: 99%

See 1 more Smart Citation

Chemical Effects on Breast Development, Function, and Cancer Risk: Existing Knowledge and New Opportunities

Kay

Cardona²,

Rudel³

et al. 2022

Curr Envir Health Rpt

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Population studies show worrisome trends towards earlier breast development, difficulty in breastfeeding, and increasing rates of breast cancer in young women. Multiple epidemiological studies have linked these outcomes with chemical exposures, and experimental studies have shown that many of these chemicals generate similar effects in rodents, often by disrupting hormonal regulation. These endocrine-disrupting chemicals (EDCs) can alter the progression of mammary gland (MG) development, impair the ability to nourish offspring via lactation, increase mammary tissue density, and increase the propensity to develop cancer. However, current toxicological approaches to measuring the effects of chemical exposures on the MG are often inadequate to detect these effects, impairing our ability to identify exposures harmful to the breast and limiting opportunities for prevention. This paper describes key adverse outcomes for the MG, including impaired lactation, altered pubertal development, altered morphology (such as increased mammographic density), and cancer. It also summarizes evidence from humans and rodent models for exposures associated with these effects. We also review current toxicological practices for evaluating MG effects, highlight limitations of current methods, summarize debates related to how effects are interpreted in risk assessment, and make recommendations to strengthen assessment approaches. Increasing the rigor of MG assessment would improve our ability to identify chemicals of concern, regulate those chemicals based on their effects, and prevent exposures and associated adverse health effects.

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“…A growing body of evidence from animal and human studies links exposure to environmental chemicals with increased risks of developing breast cancer. Among them are endocrine-disrupting chemicals (EDCs) [4][5][6]. EDCs are exogenous chemicals that can interfere with endogenous hormone action with key characteristics, including activating or antagonizing hormone receptors or altering receptor expression and downstream signaling events in the sensitive cells [7].…”

Section: Introductionmentioning

confidence: 99%

Minireview: Parabens Exposure and Breast Cancer

Hager

Chen

Zhao

2022

IJERPH

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There is increasing recognition that environmental exposure to chemicals, such as endocrine-disruptive chemicals (EDCs), contributes to the development of breast cancer. Parabens are a group of EDCs commonly found in personal care products, foods, and pharmaceuticals. Systemic exposure to parabens has been confirmed by the ubiquitous detection of parabens in human blood and urine samples. Although evidence from in vivo and epidemiological studies linking parabens exposure to breast cancer is limited, the current evidence suggests that parabens may negatively interfere with some endocrine and intracrine targets relevant to breast carcinogenesis. So far, most studies have focused on a single paraben’s effects and the direct modulating effects on estrogen receptors or the androgen receptor in vitro. Recent studies have revealed that parabens can modulate local estrogen-converting enzymes, 17β-hydroxysteroid dehydrogenase 1 and 2 and increase local estrogen levels. Also, parabens can crosstalk with the human epidermal growth factor receptor 2 (HER2) pathway and work with ER signaling to increase pro-oncogenic c-Myc expression in ER+/HER2+ breast cancer cells. Future studies investigating paraben mixtures and their crosstalk with other EDCs or signaling pathways both in vitro and in vivo in the context of breast cancer development are warranted.

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Endocrine disrupting chemicals and breast cancer: a systematic review of epidemiological studies

Cited by 92 publications

References 275 publications

Somatic DNA Damage Response and Homologous Repair Gene Alterations and Its Association With Tumor Variant Burden in Breast Cancer Patients With Occupational Exposure to Pesticides

Somatic DNA Damage Response and Homologous Repair Gene Alterations and Its Association With Tumor Variant Burden in Breast Cancer Patients With Occupational Exposure to Pesticides

Chemical Effects on Breast Development, Function, and Cancer Risk: Existing Knowledge and New Opportunities

Minireview: Parabens Exposure and Breast Cancer

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