Thyroid hormone metabolism and environmental chemical exposure

<p>Abstract</p> <p>Background</p> <p>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 polybrom...

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Main Authors: Leijs Marike M, ten Tusscher Gavin W, Olie Kees, van Teunenbroek Tom, van Aalderen Wim MC, de Voogt Pim, Vulsma Tom, Bartonova Alena, Krayer von Krauss Martin, Mosoiu Claudia, Riojas-Rodriguez Horacio, Calamandrei Gemma, Koppe Janna G
Format: Article
Language:English
Published: BMC 2012-06-01
Series:Environmental Health
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spelling doaj-c1f1d8558385489c8033852823294abc2020-11-24T21:50:29ZengBMCEnvironmental Health1476-069X2012-06-0111Suppl 1S1010.1186/1476-069X-11-S1-S10Thyroid hormone metabolism and environmental chemical exposureLeijs Marike Mten Tusscher Gavin WOlie Keesvan Teunenbroek Tomvan Aalderen Wim MCde Voogt PimVulsma TomBartonova AlenaKrayer von Krauss MartinMosoiu ClaudiaRiojas-Rodriguez HoracioCalamandrei GemmaKoppe Janna G<p>Abstract</p> <p>Background</p> <p>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.</p> <p>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.</p> <p>Methods</p> <p>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.</p> <p>Results</p> <p>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.</p> <p>Conclusion</p> <p>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.</p>
collection DOAJ
language English
format Article
sources DOAJ
author Leijs Marike M
ten Tusscher Gavin W
Olie Kees
van Teunenbroek Tom
van Aalderen Wim MC
de Voogt Pim
Vulsma Tom
Bartonova Alena
Krayer von Krauss Martin
Mosoiu Claudia
Riojas-Rodriguez Horacio
Calamandrei Gemma
Koppe Janna G
spellingShingle Leijs Marike M
ten Tusscher Gavin W
Olie Kees
van Teunenbroek Tom
van Aalderen Wim MC
de Voogt Pim
Vulsma Tom
Bartonova Alena
Krayer von Krauss Martin
Mosoiu Claudia
Riojas-Rodriguez Horacio
Calamandrei Gemma
Koppe Janna G
Thyroid hormone metabolism and environmental chemical exposure
Environmental Health
author_facet Leijs Marike M
ten Tusscher Gavin W
Olie Kees
van Teunenbroek Tom
van Aalderen Wim MC
de Voogt Pim
Vulsma Tom
Bartonova Alena
Krayer von Krauss Martin
Mosoiu Claudia
Riojas-Rodriguez Horacio
Calamandrei Gemma
Koppe Janna G
author_sort Leijs Marike M
title Thyroid hormone metabolism and environmental chemical exposure
title_short Thyroid hormone metabolism and environmental chemical exposure
title_full Thyroid hormone metabolism and environmental chemical exposure
title_fullStr Thyroid hormone metabolism and environmental chemical exposure
title_full_unstemmed Thyroid hormone metabolism and environmental chemical exposure
title_sort thyroid hormone metabolism and environmental chemical exposure
publisher BMC
series Environmental Health
issn 1476-069X
publishDate 2012-06-01
description <p>Abstract</p> <p>Background</p> <p>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.</p> <p>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.</p> <p>Methods</p> <p>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.</p> <p>Results</p> <p>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.</p> <p>Conclusion</p> <p>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.</p>
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