Triclosan in Plasma and Milk from Swedish Nursing Mothers and Their Exposure via Personal Care Products

Stockholm University, Tukholma, Stockholm, Sweden
Science of The Total Environment (Impact Factor: 4.1). 01/2007; 372(1):87-93. DOI: 10.1016/j.scitotenv.2006.08.007
Source: PubMed

ABSTRACT The bactericide triclosan is commonly used in e.g. plastics, textiles and health care products. In vitro studies on rat and human biological systems indicate that triclosan might exert adverse effects in humans. Triclosan has previously been found in human plasma and milk, but neither the primary source of human exposure nor the efficiency of triclosan transfer to human milk is known. In this study, plasma and milk were sampled from 36 mothers and analyzed for triclosan. Scrutinization of the women's personal care products revealed that nine of the mothers used toothpaste, deodorant or soap containing triclosan. Triclosan and/or its metabolites were omnipresent in the analyzed plasma and milk. The concentrations were higher in both plasma and milk from the mothers who used personal care products containing triclosan than in the mothers who did not. This demonstrated that personal care products containing triclosan were the dominant, but not the only, source of systemic exposure to triclosan. The concentrations were significantly higher in plasma than in milk, indicating that infant exposure to triclosan via breast milk is much less than the dose in the mother.

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    • "A study showed a 70 mM TCS cream underwent 10% absorption into human skin, showing absorption into the skin in the millimolar range (Queckenberg, et al. 2010). TCS is detectable in both blood and milk of lactating mothers (Allmyr, et al. 2006). "
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    ABSTRACT: Triclosan (TCS) is an antimicrobial used widely in hospitals and personal care products, at ~10 mm. Human skin efficiently absorbs TCS. Mast cells are ubiquitous key players both in physiological processes and in disease, including asthma, cancer and autism. We previously showed that non-cytotoxic levels of TCS inhibit degranulation, the release of histamine and other mediators, from rat basophilic leukemia mast cells (RBL-2H3), and in this study, we replicate this finding in human mast cells (HMC-1.2). Our investigation into the molecular mechanisms underlying this effect led to the discovery that TCS disrupts adenosine triphosphate (ATP) production in RBL-2H3 cells in glucose-free, galactose-containing media (95% confidence interval EC50 = 7.5-9.7 µm), without causing cytotoxicity. Using these same glucose-free conditions, 15 µm TCS dampens RBL-2H3 degranulation by 40%. The same ATP disruption was found with human HMC-1.2 cells (EC50 4.2-13.7 µm), NIH-3 T3 mouse fibroblasts (EC50 4.8-7.4 µm) and primary human keratinocytes (EC50 3.0-4.1 µm) all with no cytotoxicity. TCS increases oxygen consumption rate in RBL-2H3 cells. Known mitochondrial uncouplers (e.g., carbonyl cyanide 3-chlorophenylhydrazone) previously were found to inhibit mast cell function. TCS-methyl, which has a methyl group in place of the TCS ionizable proton, affects neither degranulation nor ATP production at non-cytotoxic doses. Thus, the effects of TCS on mast cell function are due to its proton ionophore structure. In addition, 5 µm TCS inhibits thapsigargin-stimulated degranulation of RBL-2H3 cells: further evidence that TCS disrupts mast cell signaling. Our data indicate that TCS is a mitochondrial uncoupler, and TCS may affect numerous cell types and functions via this mechanism. Copyright © 2015 John Wiley & Sons, Ltd. Copyright © 2015 John Wiley & Sons, Ltd.
    Journal of Applied Toxicology 07/2015; DOI:10.1002/jat.3209 · 2.98 Impact Factor
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    • "While the reason for this decline with age is unknown, Allmyr et al. (2008) previously reported that in the Australian population, serum triclosan concentrations from all sources varied from 6–10 ng/g in adults 46–60 years and from 6.2–8.7 ng/g for those over 60 years and that on average males from the northeast of Australia had the highest triclosan levels. They further showed that the Australian population had concentrations twice that of a Swedish population, which was thought to reflect differences between the two countries in the use of personal care products containing triclosan (Allmyr et al., 2006a, 2008). While it is possible that the higher triclosan concentrations reported for the Australian population were present in the current study population, no differences in terms of SAEs between the groups were observed, suggesting that the use of the toothpaste did not lead to an increased likelihood of a serious adverse event. "
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    ABSTRACT: Adverse effects of long-term usage of triclosan-containing toothpaste in humans are currently unknown. We assessed the effect of long-term use of 0.3% triclosan-toothpaste on serious adverse events (SAEs) in patients with cardiovascular disease (CVD). 438 patients with a history of stable CVD were entered into the 5-year longitudinal Cardiovascular and Periodontal Study at Prince Charles Hospital, Brisbane, Australia and randomised into test (triclosan) or placebo groups. There were no significant differences in demographics or clinical features between the groups. Patients were examined at baseline, and annually for 5-years. SAEs were classified according to the System Organ Classes defined by MedDRA (Medical Dictionary for Regulatory Activities). Results were analysed using chi square and Kaplan Meier analysis. Overall, 232 patients (123 in the triclosan group; 109 in the placebo group) experienced 569 SAEs (288 in the triclosan group and 281 in the placebo group). There was no significant difference between the groups in numbers of patients experiencing SAEs (p=0.35) or specific cardiovascular SAEs (p=0.82), nor in time to the first SAE or first cardiovascular SAE, irrespective of gender, age or BMI after adjusting for multiple comparisons (p>0.05). The adjusted odds of experiencing an SAE were estimated to increase by 2.7% for each year of age (p=0.02) and the adjusted odds of experiencing a cardiovascular SAE were estimated to increase by 5.1% for each unit increase in BMI (p=0.02). Most cardiovascular events were related to unstable angina or myocardial infarcts, 21 were associated with arrhythmia and 41 were vascular events such as aortic aneurysm and cerebrovascular accident. Within the limitations of the present study the data suggest that the use of triclosan-toothpaste may not be associated with any increase in SAEs in this CVD population. The long-term impact of triclosan on hormone-related disease, such as cancer, in humans remains to be determined.
    Science of The Total Environment 11/2014; 508. DOI:10.1016/j.scitotenv.2014.11.052 · 4.10 Impact Factor
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    • "Over the last 30 years the widespread use of antimicrobials has led to contamination of the aquatic environment (Halden and Paull, 2004; Houtman et al., 2004; Kolpin et al., 2002; Ying and Kookana, 2007). Human exposure to these compounds has also been described (Allmyr et al., 2006a,b; Calafat et al., 2008). UV filters are widely used in personal care products due to growing concerns about skin cancer. "
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    ABSTRACT: Industrial chemicals, antimicrobials, drugs and personal care products have been reported as global pollutants which enter the food chain. Some of them have also been classified as endocrine disruptors based on results of various studies employing a number of in vitro/vivo tests. The present study employed a mammalian reporter gene assay to assess the effects of known and emerging contaminants on estrogen nuclear receptor transactivation.Out of fifty-nine compounds assessed, estrogen receptor agonistic activity was observed for parabens (n = 3), UV filters (n = 6), phthalates (n = 4) and a metabolite, pyrethroids (n = 9) and their metabolites (n = 3). Two compounds were estrogen receptor antagonists while some of the agonists enhanced 17β-estradiol mediated response.This study reports five new compounds (pyrethroids and their metabolites) possessing estrogen agonist activity and highlights for the first time that pyrethroid metabolites are of particular concern showing much greater estrogenic activity than their parent compounds.
    Toxicology in Vitro 10/2014; 29(1). DOI:10.1016/j.tiv.2014.10.014 · 2.90 Impact Factor
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