Academic journal article Environmental Health Perspectives

Influence of Tetrabromobisphenol A, with or without Concurrent Triclosan, upon Bisphenol A and Estradiol Concentrations in Mice

Academic journal article Environmental Health Perspectives

Influence of Tetrabromobisphenol A, with or without Concurrent Triclosan, upon Bisphenol A and Estradiol Concentrations in Mice

Article excerpt

Introduction

Tetrabromobisphenol A (TBBPA; CAS 79-94-7) is the most-produced flame retardant, with global use over 170,000 metric tons/y (Environment Canada and Health Canada 2013). Approximately 80% of TBBPA is used in reactive applications, where it is covalently bound to the polymer of epoxy resins for printed circuit boards in electronics equipment (Colnot et al. 2014; Shaw et al. 2014). The remaining 20% of TBBPA is used in additive applications, where it is physically blended with rather than chemically bound to the polymer, as in plastic housing for electronics equipment (Colnot et al. 2014; Shaw et al. 2014). Both reactive- and additive-treated products release TBBPA into the environment (Malkoske et al. 2016; Shaw et al. 2014). TBBPA has been detected in soil and sediment (Lee et al. 2015; Wang J et al. 2015; Zhu et al. 2014), surface and waste water (Kim et al. 2016; Xiong et al. 2015), and air and indoor dust (La Guardia and Hale 2015; Ni and Zeng 2013; Wang W et al. 2015; Wu et al. 2016b). Nonoccupational TBBPA exposure in humans occurs via inhalation and ingestion of dust, as well as through dermal contact with dust and free (unreacted) TBBPA in consumer products (Abdallah 2016; Knudsen et al. 2015). TBBPA is bioavailable in humans, as shown by its detection in human serum (Cariou et al. 2008; Fujii et al. 2014), plasma (Ho et al. 2017), breast milk (Abdallah and Harrad 2011; Fujii et al. 2014; Nakao et al. 2015), and adipose tissue (Cariou et al. 2008; Johnson-Restrepo et al. 2008).

The potential for TBBPA to act as an endocrine-disrupting chemical is not well understood. Mechanisms of endocrine disruption by TBBPA could include actions on estrogen, androgen, glucocorticoid, or thyroid hormone receptors, or combinations of any or all of these receptors (Beck et al. 2016; Hamers et al. 2006; Huang et al. 2013). Considering evidence of estrogenic actions, some studies found that TBBPA binds to estrogen receptor (ER) a in in vitro assays (Li et al. 2010; Olsen et al. 2003; Suzuki et al. 2013), whereas other studies found that TBBPA failed to bind ER[alpha] in in vitro assays (Dorosh et al. 2011; Hamers et al. 2006; Lee et al. 2012; Meerts et al. 2001; Miller et al. 2001; Molina-Molina et al. 2013; Riu et al. 2011a, 2011b) and in molecular modeling studies (Zhuang et al. 2014). More recent work has examined indirect mechanisms of estrogenicity whereby TBBPA disrupts estrogen homeostasis (Honkisz and Wojtowicz 2015; Lai et al. 2015; Sanders et al. 2016; Wikoff et al. 2016). One proposed mechanism is that TBBPA inhibits the metabolism of 17[beta]-estradiol (E2), thus increasing its bioavailability, via interactions with conjugating enzymes (Lai et al. 2015; Sanders et al. 2016; Wikoff et al. 2016). These enzymes include estrogen sulfotransferase (SULT), UDP-glucuronosyltransferase (UGT), cytochrome p450 (CYP), and 17[beta]-hydroxysteroid dehydrogenase (17[beta]-HSD) (Dumas and Diorio 2011; Wikoff et al. 2016). Another proposed mechanism is that TBBPA enhances E2 secretion via actions on aromatase (CYP19) expression (Honkisz and Wojtowicz 2015).

We previously demonstrated in vivo interactions among bisphenol A (BPA), E2, and triclosan (CAS 3,380-34-5), an antimicrobial agent found in soaps and cosmetics. Compared with vehicle-treated animals, male and female mice given a single dose of 0.6-18 mg triclosan showed greater concentrations of [sup.14]C-BPA in blood serum and in reproductive and other tissues (Pollock et al. 2014). Similarly, female mice given a single dose of 1-2 mg triclosan showed greater concentrations of exogenous 3H-E2 in the uterus and natural E2 in urine than did vehicle-treated animals (Pollock et al. 2016). Blastocyst implantation in inseminated female mice can be disrupted by high doses of BPA (Berger et al. 2007, 2008, 2010; Borman et al. 2015) and triclosan (Crawford and deCatanzaro 2012); lower doses of each substance that were insufficient on their own disrupted implantation when combined (Crawford and deCatanzaro 2012). …

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