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Environ Health. 2012 Jun 28;11:S10. doi: 10.1186/1476-069X-11-S1-S10.

Thyroid hormone metabolism and environmental chemical exposure.

Environmental health : a global access science source

Marike M Leijs, Gavin W ten Tusscher, Kees Olie, Tom van Teunenbroek, Wim M C van Aalderen, Pim de Voogt, Tom Vulsma, Alena Bartonova, Martin Krayer von Krauss, Claudia Mosoiu, Horacio Riojas-Rodriguez, Gemma Calamandrei, Janna G Koppe

Affiliations

  1. Department of Paediatrics and Neonatology, Emma Children's Hospital Academic Medical Centre, Amsterdam, The Netherlands.

PMID: 22759492 PMCID: PMC3388438 DOI: 10.1186/1476-069X-11-S1-S10

Abstract

BACKGROUND: Polychlorinated dioxins and -furans (PCDD/Fs) and polychlorinated-biphenyls (PCBs) are environmental toxicants that have been proven to influence thyroid metabolism both in animal studies and in human beings. In recent years polybrominated diphenyl ethers (PBDEs) also have been found to have a negative influence on thyroid hormone metabolism. The lower brominated flame retardants are now banned in the EU, however higher brominated decabromo-diphenyl ether (DBDE) and the brominated flame retardant hexabromocyclododecane (HBCD) are not yet banned. They too can negatively influence thyroid hormone metabolism. An additional brominated flame retardant that is still in use is tetrabromobisphenol-A (TBBPA), which has also been shown to influence thyroid hormone metabolism.Influences of brominated flame retardants, PCDD/F's and dioxin like-PCBs (dl-PCB's) on thyroid hormone metabolism in adolescence in the Netherlands will be presented in this study and determined if there are reasons for concern to human health for these toxins. In the period 1987-1991, a cohort of mother-baby pairs was formed in order to detect abnormalities in relation to dioxin levels in the perinatal period. The study demonstrated that PCDD/Fs were found around the time of birth, suggesting a modulation of the setpoint of thyroid hormone metabolism with a higher 3,3', 5,5'tetrathyroxine (T4) levels and an increased thyroid stimulating hormone (TSH). While the same serum thyroid hormone tests (- TSH and T4) were again normal by 2 years of age and were still normal at 8-12 years, adolescence is a period with extra stress on thyroid hormone metabolism. Therefore we measured serum levels of TSH, T4, 3,3',5- triiodothyronine (T3), free T4 (FT4), antibodies and thyroxine-binding globulin (TBG) in our adolescent cohort.

METHODS: Vena puncture was performed to obtain samples for the measurement of thyroid hormone metabolism related parameters and the current serum dioxin (PCDD/Fs), PCB and PBDE levels.

RESULTS: The current levels of T3 were positively correlated to BDE-99. A positive trend with FT4 and BDE-99 was also seen, while a positive correlation with T3 and dl-PCB was also seen. No correlation with TBG was seen for any of the contaminants. Neither the prenatal nor the current PCDD/F levels showed a relationship with the thyroid parameters in this relatively small group.

CONCLUSION: Once again the thyroid hormone metabolism (an increase in T3) seems to have been influenced by current background levels of common environmental contaminants: dl-PCBs and BDE-99. T3 is a product of target organs and abnormalities might indicate effects on hormone transporters and could cause pathology. While the influence on T3 levels may have been compensated, because the adolescents functioned normal at the time of the study period, it is questionable if this compensation is enough for all organs depending on thyroid hormones.

References

  1. Acta Paediatr. 2001 Nov;90(11):1292-8 - PubMed
  2. Toxicol Lett. 2004 Jun 15;151(1):51-61 - PubMed
  3. Environ Health Perspect. 2007 Oct;115(10):1519-26 - PubMed
  4. Lancet. 1992 May 23;339(8804):1303 - PubMed
  5. Early Hum Dev. 1998 Feb 27;50(3):283-92 - PubMed
  6. Toxicol Sci. 2009 Jul;110(1):107-16 - PubMed
  7. Environ Health Perspect. 2009 Apr;117(4):605-10 - PubMed
  8. Toxicology. 2008 Mar 12;245(1-2):76-89 - PubMed
  9. Environ Health Perspect. 2003 Sep;111(12):1519-23 - PubMed
  10. Int Arch Occup Environ Health. 2005 Aug;78(7):584-92 - PubMed
  11. Environ Sci Technol. 2008 Mar 15;42(6):2195-200 - PubMed
  12. Int Arch Occup Environ Health. 2001 Apr;74(3):184-8 - PubMed
  13. Environ Health Perspect. 1998 Jun;106 Suppl 3:875-80 - PubMed
  14. Science. 1988 Jul 15;241(4863):334-6 - PubMed
  15. Environ Health Perspect. 2009 Feb;117(2):197-202 - PubMed
  16. Acta Paediatr Suppl. 1999 May;88(429):49-54 - PubMed
  17. Environ Sci Technol. 2007 Oct 15;41(20):6961-8 - PubMed
  18. J Toxicol Environ Health. 1989;27(2):165-71 - PubMed
  19. Neurotoxicol Teratol. 1990 Jul-Aug;12(4):319-26 - PubMed
  20. Pediatr Res. 1995 Sep;38(3):404-10 - PubMed
  21. N Engl J Med. 1999 Aug 19;341(8):549-55 - PubMed
  22. Toxicol Sci. 2001 May;61(1):76-82 - PubMed
  23. J Pediatr. 1988 Dec;113(6):991-5 - PubMed
  24. Chemosphere. 1996 Oct;33(7):1317-26 - PubMed
  25. Environ Sci Technol. 1984 Mar 1;18(3):78A-90A - PubMed
  26. Acta Paediatr Suppl. 2006 Oct;95(453):55-64 - PubMed
  27. Toxicol Ind Health. 1998 Jan-Apr;14(1-2):59-84 - PubMed
  28. Neonatology. 2009;96(2):120-4 - PubMed
  29. Lancet. 2004 Oct 16-22;364(9443):1435-7 - PubMed
  30. Chemosphere. 2008 Oct;73(7):1036-41 - PubMed
  31. Toxicol Lett. 2003 Sep 30;144(2):173-82 - PubMed
  32. Environ Health Perspect. 2004 Jan;112(1):9-17 - PubMed
  33. Arch Environ Health. 2001 Mar-Apr;56(2):138-43 - PubMed
  34. Acta Paediatr. 1994 Jun;83(6):583-7 - PubMed
  35. Chemosphere. 2008 Sep;73(2):176-81 - PubMed

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