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      Risks of dioxins resulting from high exposure via breast-feeding?

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      Archives of Toxicology
      Springer Berlin Heidelberg

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          Abstract

          Commentary to, Martin van den Berg, Karin Kypke, Alexander Kotz, Angelika Tritscher, Seoung Yong Lee, Katarina Magulova, Heidelore Fiedler & Rainer Malisch. WHO/UNEP global surveys of PCDDs, PCDFs, PCBs and DDTs in human milk and benefit-risk evaluation of breastfeeding. Archives of Toxicology, January 2017, Volume 91, Issue 1, pp 83–96. As part of the article by Martin van den Berg and others, the authors compare possible risks and benefits of breast-feeding in relation to the levels of PCDDs and PCDFs (“dioxins”) and other persistent compounds. For dioxins, a “safe level” of 0.2 pg WHO-TEQ per g fat of mother’s milk was calculated, using the lower WHO-TDI of 1 pg/kg b.w., a fat content of 3.5% and a daily consumption of 125 g/kg b.w. This is a simple and correct calculation—if it makes sense to apply the TDI to breastfed infants in this way. For dioxins, the TDI also considers the extremely long biological half-life of the compounds in order to prevent a critical body burden in the child-bearing age (females) or in aged people possibly associated with health effects. Therefore, a slight and temporary exceedance of the TDI is acceptable, but what about breast-feeding? What about dioxin body burden of infants who are exclusively breastfed for up to 6 months, taking up, for example, 44 pg/kg b.w. per day during this period in case of a maternal body burden of 10 pg/g fat (using the same numbers for the calculation as above)? At first glance, such a calculation gives rise to a concern regarding a critical body burden, primarily for females in the child-bearing age. Kinetic models predict the expected big difference in dioxin body burden between formula-fed and breast-fed infants at the end of the breast-feeding period (Kreuzer et al. 1997; Kerger et al. 2007). However, concentrations in the former breast-fed child decline rapidly thereafter, due to the fast growth of body mass and body fat, and an age-dependent elimination half-life (Kerger et al. 2006) may also contribute to this process. Within a few years, this leads to an assimilation of the child’s dioxin concentrations to the slowly increasing concentrations of a child who has never been breastfed. These model predictions were validated by measured data. Therefore, former breast- and formula-fed girls living under otherwise identical conditions are not expected to differ with respect to their body burden in the child-bearing age, as long as the contamination of mother’s milk does not greatly exceed the current background range (WHO-TEQ <20 pg/g fat). In conclusion, no increased risk results from breast-feeding of girls for their future offspring during the in-utero period. Another question is, whether the temporarily (up to a few years) higher dioxin body burden in breast-fed children during a period of possibly higher susceptibility is associated with health risks. Indeed, infants exclusively breastfed for 6 months according to current recommendations, reached dioxin levels comparable to or even slightly higher than those of their mothers (Abraham et al. 1996, 1998). Numerous studies have focused on the question of possible health risks or changes in laboratory parameters in children breastfed for a longer period. Currently, there is no serious evidence for any of that. Even after the Seveso accident in 1976, no health effects have been reported for children primarily exposed via breast-feeding. Dioxin levels in human milk are strongly decreasing in industrialized countries—in Germany from mean values of about 35 pg WHO-TEQ pg per g milk fat at the end of the 1980s to 6.3 WHO-TEQ pg per g milk fat in 2009 (BfR 2011; more recent data not available). These numbers are 175 and 32 times higher than the proposed “safe level” of 0.2 pg WHO-TEQ per g milk fat, respectively. Scientifically, establishing such a “safe level” with these dramatic exceedances without serious evidence for negative health effects appears questionable. Of course, dioxins are unwanted contaminants and should be further reduced with special emphasis on possible in-utero effects. However, from the pediatrician’s view on the current dioxin levels in human milk from industrialized countries (<20 pg WHO-TEQ per g fat), it makes no sense to point out putative dioxin risks of breast-feeding over and over again, even if the final conclusion is that the benefits are higher than the risks. This may contribute to unnecessary confusion of parents and health professionals, and thereby bears the risk of negatively influencing breast-feeding rates.

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          2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and congeners in infants. A toxicokinetic model of human lifetime body burden by TCDD with special emphasis on its uptake by nutrition.

          Contents of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and of 16 further congeners--polychlorinated dibenzodioxins and dibenzofuranes (PCDD/PCDF)--were determined in lipids of adipose tissue and of livers of 3 stillborns and of 17 infants (0.43-44 weeks old) who died from sudden infant death syndrome. International toxic equivalents (I-TEq) calculated for the sum of TCDD together with all of the 16 congeners (1.55-29.63 ng/kg lipids of adipose tissue, n = 20; 2.05-57.73 ng/kg liver lipids, n = 19) were within the range of or lower than the values published for adults. TCDD concentrations in lipids of breast-fed infants were higher (0.38-4.1 ng/kg lipids of adipose tissue, n = 9; 0.49-3.9 ng/kg liver lipids, n = 8) compared to non breast-fed subjects (0.16-0.76 ng/kg lipids of adipose tissue, n = 8; 0.29-0.71 ng/kg liver lipids, n = 7). Neither I-TEq values nor TCDD concentrations exceeded values published for adults. Since even in stillborns PCDD/PCPF were found (I-TEq, 9.70-10.83 ng/kg lipids of adipose tissue, 6.17-8.83 ng/kg liver lipids; TCDD, 1.3-2.1 ng/kg lipids of adipose tissue, 0.76-1.5 ng/kg liver lipids; n = 3), transplacental exposure has to be deduced. All of the findings concerning TCDD concentrations in the organism become intelligible on the basis of a physiological toxicokinetic model which was developed to describe the body burden of TCDD for the entire human lifetime in dependence of TCDD uptake from contaminated nutrition. The model reflects sex and age dependent changes in the following parameters: body weight, volumes of liver, adipose and muscle tissue, food consumption, and excretion of faeces. TCDD is supposed to be taken up orally, to be distributed freely in lipids of the organism and to be eliminated unchanged by excretion in lipids of faeces as well as by metabolism in the liver. The model was used to predict the half-life of elimination of TCDD (4 months in newborns increasing to approximately 5 years in adults) and concentrations of this compound in lipids of adipose tissue, blood, liver and faeces at different ages. Furthermore, the influence of breast-feeding on the TCDD burden of a mother, her milk and her child was simulated. The model was validated by means of own data gained in adipose tissue and livers of infants and also using a series of values measured by other authors in mother's milk and in tissues and faeces of infants and adults. Predictions as well as experimental findings demonstrate a distinct increase in the TCDD body burden of breast-fed infants. Generally, it can be concluded for the excretion of unchanged, non-volatile, non protein bound highly lipophilic compounds that their half-life is short in infants (approximately 5 months) and increases to approximately 10 years reached between 40 and 60 years of age.
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            Intake, fecal excretion, and body burden of polychlorinated dibenzo-p-dioxins and dibenzofurans in breast-fed and formula-fed infants.

            To assess toxicokinetics of polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs), oral intake and fecal excretion were measured in two breast-fed infants and one formula-fed infant during the 1st y of life. The intake of these compounds was up to 50 times higher in the breast-fed infants. In these children, fecal excretion of the main tetra- to hexachlorinated congeners was less than 9% of the intake at age of 1 and 5 mo, indicating almost complete intestinal absorption during breast-feeding. In contrast, distinctly higher fecal excretion rates were observed for the hepta- and octachlorinated compounds. Despite much lower PCDD/PCDF intake after weaning, concentrations in stool fat did not decrease substantially. We conclude that concentrations in fecal fat more or less reflect those in body fat. Additionally, PCDD/PCDF concentrations were measured in blood fat of all infants (and in a second formula-fed baby) at the age of 11 mo. International toxicity equivalent (I-TEq) concentrations in the formula-fed infants were less than 25% of maternal values and about 10 times lower than in the infants breast-fed for 6-7 mo. In the latter, a distinct accumulation was found for the tetra- to hexachlorinated congeners compared with maternal concentrations. We conclude that accumulation of PCDDs and PCDFs in infants is as high as expected on the basis of intake data and assuming complete absorption and negligible elimination during the 1st y of life.
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              Age- and Concentration-Dependent Elimination Half-Life of 2,3,7,8-Tetrachlorodibenzo-p-dioxin in Seveso Children

              Objective Pharmacokinetic and statistical analyses are reported to elucidate key variables affecting 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) elimination in children and adolescents. Design We used blood concentrations to calculate TCDD elimination half-life. Variables examined by statistical analysis include age, latency from exposure, sex, TCDD concentration and quantity in the body, severity of chloracne response, body mass index, and body fat mass. Participants Blood was collected from 1976 to 1993 from residents of Seveso, Italy, who were 400 ppt for children 400–700 ppt.
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                Author and article information

                Contributors
                klaus.abraham@bfr.bund.de
                Journal
                Arch Toxicol
                Arch. Toxicol
                Archives of Toxicology
                Springer Berlin Heidelberg (Berlin/Heidelberg )
                0340-5761
                1432-0738
                18 March 2017
                18 March 2017
                2017
                : 91
                : 7
                : 2703-2704
                Affiliations
                ISNI 0000 0000 8852 3623, GRID grid.417830.9, Department of Food Safety, , German Federal Institute for Risk Assessment (BfR), ; Max-Dohrn-Str. 8-10, 10589 Berlin, Germany
                Article
                1952
                10.1007/s00204-017-1952-7
                5489633
                28315924
                465b5209-1ba6-4620-93ae-39577bff70a8
                © The Author(s) 2017

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                : 1 February 2017
                : 1 March 2017
                Categories
                Letter to the Editor, News and Views
                Custom metadata
                © Springer-Verlag GmbH Germany 2017

                Toxicology
                Toxicology

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