Changes in mammary histology and transcriptome profiles by low-dose exposure to environmental phenols at critical windows of development

Gopalakrishnan, Kalpana; Teitelbaum, Susan L.; Lambertini, Luca; Wetmur, James G.; Manservisi, Fabiana; Falcioni, Laura; Panzacchi, Simona; Belpoggi, Fiorella; Chen, Jia

doi:10.1016/j.envres.2016.10.021

Cited by 29 publications

(25 citation statements)

References 65 publications

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“…These chemicals have been used as preservatives in personal care products, pharmaceuticals, and food additives, and have been found to promote cell growth through multiple mechanisms, including estrogenicity (Gonzalez et al 2018, 2019; Okubo et al 2001) and epidermal growth factor receptor signaling (Pan et al 2016). Particularly relevant to our findings of the greatest methyl and ethyl paraben disparities in the youngest non-Hispanic Black women was the finding that early life paraben exposures can alter developing mammary gland morphology and induce gene expression that resembles an early cancer-like state (Gopalakrishnan et al 2017). Use of hair products has been identified as a potential risk factor for breast cancer in non-Hispanic Black women (Stiel et al 2016).…”

Section: Discussionmentioning

confidence: 73%

A comprehensive analysis of racial disparities in chemical biomarker concentrations in United States women, 1999-2014

Nguyen

Kahana

Heidt

et al. 2019

Preprint

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27Background: Stark racial disparities in disease incidence among American women remains a persistent 28 public health challenge. These disparities likely result from complex interactions between genetic, social, 29 lifestyle, and environmental risk factors. The influence of environmental risk factors, such as chemical 30 exposure, however, may be substantial and is poorly understood. 31Objectives: We quantitatively evaluated chemical-exposure disparities by race/ethnicity and age in United 32 States (US) women by using biomarker data for 143 chemicals from the National Health and Nutrition 33 Examination Survey (NHANES) 1999(NHANES) -2014 Methods: We applied a series of survey-weighted, generalized linear models using data from the entire 35 NHANES women population and age-group stratified subpopulations. The outcome was chemical 36 biomarker concentration and the main predictor was race/ethnicity with adjustment for age, socioeconomic 37 status, smoking habits, and NHANES cycle. 38Results: The highest disparities across non-Hispanic Black, Mexican American, Other Hispanic, and other 39 race/multiracial women were observed for pesticides and their metabolites, including 2,5-dichlorophenol, 40 o,p'-DDE, beta-hexachlorocyclohexane, and 2,4-dichlorophenol, along with personal care and consumer 41 product compounds. The latter included parabens, monoethyl phthalate, and several metals, such as mercury 42 and arsenic. Moreover, for Mexican American, Other Hispanic, and non-Hispanic black women, there were 43 several exposure disparities that persisted across age groups, such as higher 2,4-and 2,5-dichlorophenol 44 concentrations. Exposure differences for methyl and propyl parabens, however, were the starkest between 45 non-Hispanic black and non-Hispanic white children with average differences exceeding 4 folds. 46 Discussions: We systematically evaluated differences in chemical exposures across women of various 47 race/ethnic groups and across age groups. Our findings could help inform chemical prioritization in 48 designing epidemiological and toxicological studies. In addition, they could help guide public health 49 interventions to reduce environmental and health disparities across populations.50 51 52The stark racial disparities in disease incidence and health outcomes among American women 53 remains a persistent public health challenge. For example, preterm birth incidence was found to be 54 approximately 60% higher in non-Hispanic Black women relative to non-Hispanic white women (Culhane 55 and Goldenberg 2011). Non-Hispanic Black and Hispanic women are at increased risk of being diagnosed 56 with developing dysglycemia (Marcinkevage et al. 2013) and diabetes (Cowie et al. 2009), relative to non-57 Hispanic white women. Non-Hispanic Black women are also 2-3 times more likely to develop the most 58 aggressive subtype of breast cancer, triple negative, compared to non-Hispanic white women (Carey et al. 59 2006; Stark et al. 2010). Furthermore, relative to non-Hispanic white women, non-Hispanic Black women...

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Section: Discussionmentioning

confidence: 73%

A comprehensive analysis of racial disparities in chemical biomarker concentrations in United States women, 1999-2014

Nguyen

Kahana

Heidt

et al. 2019

Preprint

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“…Hence our rst objective was to adapt the TNBS chronic colitis model to young rats, with low mortality and signi cant brosis before reaching adult age. The window of opportunity was narrow, since in Sprague-Dawley rats the peri-natal period lasts until Postnatal Day 21 (PND 21), the pre-pubertal period until PND 42 (6 weeks) and the pubertal period until PND 63 (9 weeks) (13). We chose to induce colitis starting at 5 weeks of age and all rats were analyzed at 8 weeks of age, before the end of the pubertal period.…”

Section: Discussionmentioning

confidence: 99%

A Polymeric Diet Rich in Transforming Growth Factor Beta 2 Does Not Reduce Inflammation in Chronic 2,4,6-trinitrobenzene Sulfonic Acid Colitis in Pre-pubertal Rats

Dupont-Lucas

Marion‐Letellier

Pala

et al. 2020

Preprint

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Background: Pediatric Crohn’s disease is characterized by a higher incidence of complicated phenotypes. Murine models help to better understand the dynamic process of intestinal fibrosis and test therapeutic interventions. Pre-pubertal models are lacking. We aimed to adapt a model of chronic colitis to pre-pubertal rats and test if a polymeric diet rich in TGF-β2 could reduce TNBS-induced intestinal inflammation and fibrosis. Methods: Colitis was induced in 20 five-week-old Sprague-Dawley male rats by weekly rectal injections of increasing doses of TNBS (90 mg/kg, 140 mg/kg and 180 mg/kg) for 3 weeks, while 10 controls received phosphate-buffered saline (PBS). Rats were anesthetized using ketamine and chlorpromazine. After first administration of TNBS, 10 rats were fed exclusively MODULEN IBD® powder, while remaining rats were fed breeding chow. Colitis was assessed one week after last dose of TNBS by histopathology and magnetic resonance colonography (MRC). Results: Histological inflammation and fibrosis scores were higher in TNBS group than controls (p<0.05 for both). MRC showed increased colon wall thickness in TNBS group compared to controls (p<0.01), and increased prevalence of strictures and target sign (p<0.05). Colon expression of COL1A1, CTGF, α-SMA and COX-2 did not differ between TNBS rats and controls. TNBS colitis was not associated with growth failure. Treatment with MODULEN IBD® was associated with growth failure, increased colon weight/length ratio (p<0.01), but did not affect histological scores or MRI characteristics. Colon expression of α-SMA was significantly lower in the MODULEN group vs. controls (p=0.005).Conclusion: Features of chronic colitis were confirmed in this model, based on MRC and histopathology. Treatment with MODULEN did not reverse inflammation or fibrosis.

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“…However, recent work on rats exposed to an environmental dose of triclosan (0.05 mg/kg/day) during a long period, from birth PND1 to reproductive stage and lactation (PND146), showed different results. Triclosan induced morphological changes of the mammary gland by increasing adipose tissue and decreasing the proportion of lobular tissue, but further transcriptomic and gene set enrichment analysis showed that genes upregulated by triclosan treatment during that exposure were homologous to genes downregulated in breast cancer in humans; conversely, genes downregulated by triclosan are homologous to certain genes upregulated in breast cancer [ 68 ]. These results suggest that the model species, timing of exposure, and/or dose can have significantly different effects; further studies should be undertaken to better understand how triclosan can affect the development of breast cancer.…”

Section: Edcs and Breast Cancermentioning

confidence: 99%

Emerging Estrogenic Pollutants in the Aquatic Environment and Breast Cancer

Lecomte

Habauzit

Charlier

et al. 2017

Genes

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The number and amount of man-made chemicals present in the aquatic environment has increased considerably over the past 50 years. Among these contaminants, endocrine-disrupting chemicals (EDCs) represent a significant proportion. This family of compounds interferes with normal hormonal processes through multiple molecular pathways. They represent a potential risk for human and wildlife as they are suspected to be involved in the development of diseases including, but not limited to, reprotoxicity, metabolic disorders, and cancers. More precisely, several studies have suggested that the increase of breast cancers in industrialized countries is linked to exposure to EDCs, particularly estrogen-like compounds. Estrogen receptors alpha (ERα) and beta (ERβ) are the two main transducers of estrogen action and therefore important targets for these estrogen-like endocrine disrupters. More than 70% of human breast cancers are ERα-positive and estrogen-dependent, and their development and growth are not only influenced by endogenous estrogens but also likely by environmental estrogen-like endocrine disrupters. It is, therefore, of major importance to characterize the potential estrogenic activity from contaminated surface water and identify the molecules responsible for the hormonal effects. This information will help us understand how environmental contaminants can potentially impact the development of breast cancer and allow us to fix a maximal limit to the concentration of estrogen-like compounds that should be found in the environment. The aim of this review is to provide an overview of emerging estrogen-like compounds in the environment, sum up studies demonstrating their direct or indirect interactions with ERs, and link their presence to the development of breast cancer. Finally, we emphasize the use of in vitro and in vivo methods based on the zebrafish model to identify and characterize environmental estrogens.

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Changes in mammary histology and transcriptome profiles by low-dose exposure to environmental phenols at critical windows of development

Cited by 29 publications

References 65 publications

A comprehensive analysis of racial disparities in chemical biomarker concentrations in United States women, 1999-2014

A comprehensive analysis of racial disparities in chemical biomarker concentrations in United States women, 1999-2014

A Polymeric Diet Rich in Transforming Growth Factor Beta 2 Does Not Reduce Inflammation in Chronic 2,4,6-trinitrobenzene Sulfonic Acid Colitis in Pre-pubertal Rats

Emerging Estrogenic Pollutants in the Aquatic Environment and Breast Cancer

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