Aop: 152

Title

A descriptive phrase which references both the Molecular Initiating Event and Adverse Outcome.It should take the form “MIE leading to AO”. For example, “Aromatase inhibition leading to reproductive dysfunction” where Aromatase inhibition is the MIE and reproductive dysfunction the AO. In cases where the MIE is unknown or undefined, the earliest known KE in the chain (i.e., furthest upstream) should be used in lieu of the MIE and it should be made clear that the stated event is a KE and not the MIE. More help

Interference with thyroid serum binding protein transthyretin and subsequent adverse human neurodevelopmental toxicity

Short name
A name that succinctly summarises the information from the title. This name should not exceed 90 characters. More help
Transthyretin interference

Graphical Representation

A graphical representation of the AOP.This graphic should list all KEs in sequence, including the MIE (if known) and AO, and the pair-wise relationships (links or KERs) between those KEs. More help
Click to download graphical representation template Explore AOP in a Third Party Tool

Authors

The names and affiliations of the individual(s)/organisation(s) that created/developed the AOP. More help

Erik R. Janus; M3 Technical & Regulatory Services; Shepherdstown, WV; <erik@mcubedservices.com>

Kristie Sullivan; Physicians Committee for Responsible Medicine; Washington, DC; <ksullivan@pcrm.org>

Katie Paul-Friedman; US Environmental Protection Agency; Research Triangle Park, NC

Mary Gilbert; National Health and Environmental Effects Research Laboratory; US Environmental Protection Agency; Research Triangle Park, NC; <gilbert.mary@epa.gov>

Kevin M. Crofton; National Center for Computational Toxicology; US Environmental Protection Agency; Research Triangle Park, NC; <crofton.kevin@epa.gov>

Anna van der Zalm; PETA Science Consortium International e.V, Germany; <AnnaZ@thepsci.eu>

Point of Contact

The user responsible for managing the AOP entry in the AOP-KB and controlling write access to the page by defining the contributors as described in the next section.   More help
Allie Always   (email point of contact)

Contributors

Users with write access to the AOP page.  Entries in this field are controlled by the Point of Contact. More help
  • Erik Janus
  • Timo Hamers
  • Kevin Crofton
  • Kristie Sullivan
  • Allie Always

Status

Provides users with information concerning how actively the AOP page is being developed, what type of use or input the authors feel comfortable with given the current level of development, and whether it is part of the OECD AOP Development Workplan and has been reviewed and/or endorsed. OECD Status - Tracks the level of review/endorsement the AOP has been subjected to. OECD Project Number - Project number is designated and updated by the OECD. SAAOP Status - Status managed and updated by SAAOP curators. More help
Author status OECD status OECD project SAAOP status
Under Development: Contributions and Comments Welcome Under Development 1.41 Included in OECD Work Plan
This AOP was last modified on July 16, 2022 18:37

Revision dates for related pages

Page Revision Date/Time
Binding, Transthyretin in serum September 16, 2017 10:16
Displacement, Serum thyroxine (T4) from transthyretin December 17, 2016 17:03
Increased, Free serum thyroxine (T4) September 16, 2017 10:16
Increased, Uptake of thyroxine into tissue December 17, 2016 17:04
Increased, Clearance of thyroxine from serum January 26, 2021 10:41
Thyroxine (T4) in serum, Decreased July 08, 2022 06:52
Thyroxine (T4) in neuronal tissue, Decreased April 04, 2019 09:13
Hippocampal gene expression, Altered August 11, 2018 09:26
Hippocampal anatomy, Altered May 20, 2022 05:45
Hippocampal Physiology, Altered August 11, 2018 09:41
Cognitive Function, Decreased August 09, 2018 11:55
Binding, Transthyretin in serum leads to Displacement, Serum thyroxine (T4) from transthyretin December 09, 2020 14:51
Displacement, Serum thyroxine (T4) from transthyretin leads to Increased, Free serum thyroxine (T4) December 09, 2020 14:51
Increased, Free serum thyroxine (T4) leads to Increased, Clearance of thyroxine from serum January 26, 2021 10:51
Increased, Clearance of thyroxine from serum leads to T4 in serum, Decreased January 26, 2021 10:42
Halogenated phenols March 09, 2017 23:55
Polychlorinated biphenyl November 29, 2016 18:42
Polychlorinated dibenzodioxins March 09, 2017 20:38
Polybrominated diphenyl ethers March 09, 2017 20:40
Isoflavones March 09, 2017 21:14
Perflourinated chemicals March 09, 2017 22:36
Phthalates March 09, 2017 22:37
Tetrabromobisphenol A July 20, 2018 05:36
Clonixin March 10, 2017 00:50
Meclofenamic acid March 10, 2017 00:51
2,6-dinitro-p-cresol March 10, 2017 00:53
Triclopyr March 10, 2017 00:59
2,2',4,4'-Tetrahydroxybenzophenone November 29, 2016 18:42

Abstract

A concise and informative summation of the AOP under development that can stand-alone from the AOP page. The aim is to capture the highlights of the AOP and its potential scientific and regulatory relevance. More help

This AOP describes adverse neurodevelopemental effects that may result from xenobiotic interference with thyroid serum binding protein transthyretin (TTR). Binding of TTR by a xenobiotic (the MIE) during certain developmental windows may disrupt the normal neurodevelopment of mammals through a transient increase in free thyroxine (T4) levels, permitting increased tissue uptake of thyroid hormone (TH), followed by a decrease in both serum and neuronal tissue concentrations. Due to the highly conserved nature of the TTR protein, birds, reptiles, fish and amphibians can also express TTR and be impacted by interference by xeniobiotics. The adverse consequences of TH insufficiency depend both on the severity and developmental timing, indicating that exposure to thyroid toxicants may produce different effects at different developmental windows of exposure. This AOP discusses the potential for developmental TTR interference to adversely impact hippocampal anatomy, function, gene expression and, ultimately, cognitive function.

AOP Development Strategy

Context

Used to provide background information for AOP reviewers and users that is considered helpful in understanding the biology underlying the AOP and the motivation for its development.The background should NOT provide an overview of the AOP, its KEs or KERs, which are captured in more detail below. More help

Transthyretin is one of three ancient, highly conserved serum binding proteins that collectively act to transport thyroid hormone (TH) and thus help maintain normal homeostasis via modulation of the hypothalamic/pituitary/thyroid axis. In addition to TTR, albumin (ALB) and thyroxine-binding globulin (TBG) also serve to transport TH in serum and the relative contribution of each binding protein differs across species. In man, TBG has the greatest affinity for thyroxine (T4), followed by TTR and ALB shows the lowest affinity for T4 while prevalence in serum is the opposite, while in rat, TTR is the major serum transport protein (as rats lack TBG). Interference with TH serum binding proteins is one of several mechanisms through which xenobiotics and environmental contaminants can disrupt normal thyroid endocrine function ("thyroid disruptors") and development of this AOP is expected to contribute towards a fuller understanding of the mechanism of TTR interference and how it may be measured in vitro as part of a larger screening battery for thyroid toxicants.

Strategy

Provides a description of the approaches to the identification, screening and quality assessment of the data relevant to identification of the key events and key event relationships included in the AOP or AOP network.This information is important as a basis to support the objective/envisaged application of the AOP by the regulatory community and to facilitate the reuse of its components.  Suggested content includes a rationale for and description of the scope and focus of the data search and identification strategy/ies including the nature of preliminary scoping and/or expert input, the overall literature screening strategy and more focused literature surveys to identify additional information (including e.g., key search terms, databases and time period searched, any tools used). More help

Summary of the AOP

This section is for information that describes the overall AOP. The information described in section 1 is entered on the upper portion of an AOP page within the AOP-Wiki. This is where some background information may be provided, the structure of the AOP is described, and the KEs and KERs are listed. More help

Events:

Molecular Initiating Events (MIE)
An MIE is a specialised KE that represents the beginning (point of interaction between a prototypical stressor and the biological system) of an AOP. More help
Key Events (KE)
A measurable event within a specific biological level of organisation. More help
Adverse Outcomes (AO)
An AO is a specialized KE that represents the end (an adverse outcome of regulatory significance) of an AOP. More help
Type Event ID Title Short name
MIE 957 Binding, Transthyretin in serum Binding, Transthyretin in serum
KE 958 Displacement, Serum thyroxine (T4) from transthyretin Displacement, Serum thyroxine (T4) from transthyretin
KE 959 Increased, Free serum thyroxine (T4) Increased, Free serum thyroxine (T4)
KE 960 Increased, Uptake of thyroxine into tissue Increased, Uptake of thyroxine into tissue
KE 961 Increased, Clearance of thyroxine from serum Increased, Clearance of thyroxine from serum
KE 281 Thyroxine (T4) in serum, Decreased T4 in serum, Decreased
KE 280 Thyroxine (T4) in neuronal tissue, Decreased T4 in neuronal tissue, Decreased
KE 756 Hippocampal gene expression, Altered Hippocampal gene expression, Altered
KE 757 Hippocampal anatomy, Altered Hippocampal anatomy, Altered
KE 758 Hippocampal Physiology, Altered Hippocampal Physiology, Altered
AO 402 Cognitive Function, Decreased Cognitive Function, Decreased

Relationships Between Two Key Events (Including MIEs and AOs)

This table summarizes all of the KERs of the AOP and is populated in the AOP-Wiki as KERs are added to the AOP.Each table entry acts as a link to the individual KER description page. More help

Network View

This network graphic is automatically generated based on the information provided in the MIE(s), KEs, AO(s), KERs and Weight of Evidence (WoE) summary tables. The width of the edges representing the KERs is determined by its WoE confidence level, with thicker lines representing higher degrees of confidence. This network view also shows which KEs are shared with other AOPs. More help

Prototypical Stressors

A structured data field that can be used to identify one or more “prototypical” stressors that act through this AOP. Prototypical stressors are stressors for which responses at multiple key events have been well documented. More help

Life Stage Applicability

The life stage for which the AOP is known to be applicable. More help
Life stage Evidence
Development Moderate

Taxonomic Applicability

Latin or common names of a species or broader taxonomic grouping (e.g., class, order, family) can be selected.In many cases, individual species identified in these structured fields will be those for which the strongest evidence used in constructing the AOP was available. More help
Term Scientific Term Evidence Link
rat Rattus norvegicus High NCBI

Sex Applicability

The sex for which the AOP is known to be applicable. More help
Sex Evidence
Mixed Moderate

Overall Assessment of the AOP

Addressess the relevant biological domain of applicability (i.e., in terms of taxa, sex, life stage, etc.) and Weight of Evidence (WoE) for the overall AOP as a basis to consider appropriate regulatory application (e.g., priority setting, testing strategies or risk assessment). More help

Domain of Applicability

Addressess the relevant biological domain(s) of applicability in terms of sex, life-stage, taxa, and other aspects of biological context. More help

Essentiality of the Key Events

The essentiality of KEs can only be assessed relative to the impact of manipulation of a given KE (e.g., experimentally blocking or exacerbating the event) on the downstream sequence of KEs defined for the AOP. Consequently, evidence supporting essentiality is assembled on the AOP page, rather than on the independent KE pages that are meant to stand-alone as modular units without reference to other KEs in the sequence. The nature of experimental evidence that is relevant to assessing essentiality relates to the impact on downstream KEs and the AO if upstream KEs are prevented or modified. This includes: Direct evidence: directly measured experimental support that blocking or preventing a KE prevents or impacts downstream KEs in the pathway in the expected fashion. Indirect evidence: evidence that modulation or attenuation in the magnitude of impact on a specific KE (increased effect or decreased effect) is associated with corresponding changes (increases or decreases) in the magnitude or frequency of one or more downstream KEs. More help

Molecular Initiating Event Summary, Key Event Summary Provide an overall assessment of the essentiality for the key events in the AOP. Support calls for individual key events can be included in the molecular initiating event, key event, and adverse outcome tables above.

In vivo evidence for MIE

Kohrle et al (1989) added 10 μmol/L 3-methyl-4’,6-dihydroxy-3’,5-dibromo-flavone (EMD 21388) to pooled rat serum and measured displacement of [125I]-T4 from TTR. EMD21388 was synthesized using “molecular drug design” (and resembles T4) to help confirm previous findings that certain flavonoid deiodinase inhibitors also displaced thyroxine (T4) for TTR (or T3-binding prealbumin). Displacement of [125I] from TTR in rat serum was analyzed by gel electrophoresis (PAGE) and individual serum samples were assayed for T3 and T4 content by RIA and % free TH by equilibrium dialysis (lower limit of detectability 0.3 ug/dL for T4). There was a significant increase in % free T4 (0.031 to 0.124), which was dose-dependent and resulted in complete inhibition of [125I]-T4/TTR at 8-10 umol (radiolabeled TH were displaced primarily to albumin).

insert Fig 2 from Kohrle et al 1989

One to 4 hours following ip delivery of 2 μmol/100 g BW to euthyroid Sprague-Dawley rats (a dose that is 1000x higher than daily T4 production in rat), inhibition of [125I]-T4/TTR binding was observed. T4 decreased from 5.6 to 2.3 ug/dl after 1 hour and remained low while % free T4 increased from 0.035 to 0.091 and remained high; however, free T4 did not change. TSH decreased to very low values after 2 hours and increased slightly, despite no change in the free TH concentration (hypothyroid rats did not show changes in serum TSH following EMD 21388 administration). Lueprasitsakul et al (1990) performed a series of experiments with Sprague-Dawley rats using smaller doses of EMD 21388 (up to 2 μmol /100 g BW) and the same measurement methods (RIA, equilibrium dialysis). Administration of 2 μmol of EMD 21388 inhibited [125I]-T4/TTR binding within a few minutes, displacing [125I] to albumin to a greater degree of magnitude, due to slight differences in preparing the EMD 21388 solutions. Dose-dependent decreases in displacement were found with decreasing dose.

insert Figure 1 & Figure 2

Following a single dose of 2 μmol, a significant decrease was seen in total serum T4 after 10 minutes that persisted, % free T4 also increased immediately (peaked after 10 minutes) and stayed elevated and a significant increase in free T4 was observed within three minutes that stayed elevated for 60 minutes. Following a single dose of 0.3 μmol, decreased [125I]-T4/TTR binding was observed reaching a nadir after 10 minutes and slowly recovering over the 180-minute experiment. The % free T4 and serum free T4 both increased and returned to normal after 180 minutes as well while total serum T4 hit a nadir after 10 minutes and mostly recovered. Serum TSH decreased after 20 minutes, significantly at the nadir hit after 60 minutes.

Evidence Assessment

Addressess the biological plausibility, empirical support, and quantitative understanding from each KER in an AOP. More help

Known Modulating Factors

Modulating factors (MFs) may alter the shape of the response-response function that describes the quantitative relationship between two KES, thus having an impact on the progression of the pathway or the severity of the AO.The evidence supporting the influence of various modulating factors is assembled within the individual KERs. More help

Quantitative Understanding

Optional field to provide quantitative weight of evidence descriptors.  More help

Considerations for Potential Applications of the AOP (optional)

Addressess potential applications of an AOP to support regulatory decision-making.This may include, for example, possible utility for test guideline development or refinement, development of integrated testing and assessment approaches, development of (Q)SARs / or chemical profilers to facilitate the grouping of chemicals for subsequent read-across, screening level hazard assessments or even risk assessment. More help

References

List of the literature that was cited for this AOP. More help

Abdalla, S.M. and A.C. Bianco. (2014) Defending plasma T3 is a biological priority.  Clin. Endocrinol. (Oxf)  81(5): 633-641.

Alshehri, B., D’Souza, D. G., Lee, J. Y., Petratos, S., & Richardson, S. J. (2015). The Diversity of Mechanisms Influenced by Transthyretin in Neurobiology: Development, Disease and Endocrine Disruption. Journal of Neuroendocrinology, 27(5), 303–323. http://doi.org/10.1111/jne.12271

Andrea, T.A., R.R. Cavalieri, I.D. Goldfine and E.C. Jorgensen (1980) Binding of thyroid hormones and analogues to the human plasma protein prealbumin. Biochemistry  19(1): 55-63.

Aqai, P., C. Fryganas, M. Mizuguchi, W. Haasnoot and M.W. Nielen. (2012) Triple bioaffinity mass spectrometry concept for thyroid transporter ligands.  Anal. Chem.  84(15): 6488-6493.

Athanasiadou, M., S.N. Cuadra, G. Marsh, A> Bergman, and K. Jakobsson. (2008) Polybrominated diphenyl ethers (PBDEs) and bioaccumulative hydroxylated PBDE metabolites in young humans from Managua, Nicaragua.  Environ. Health Perspect. 116(3): 400-408.

Barter, R.A. and C.D. Klaassen. (1994) Reduction of thyroid hormone levels and alteration of thyroid function by four representative UDP-glucuronosyltransferase inducers in rats.  Toxicol. Appl. Pharmacol.  128(1): 9-17.

Blake, C.C., J.M. Burridge and S.J. Oatley. (1978) X-ray analysis of thyroid hormone binding to prealbumin. Biochem Soc. Trans. 6(6): 1114-1118.

Bloom, M.S., J.E. Vena, J.R. Olson and P.J. Kostyniak.  (2009)  Assessment of polychlorinated biphenyl congeners, thyroid stimulating hormone, and free thyroxine among New York state anglers.  Int. J. Hyg. Environ. Health  212(6): 599-611.

Branchi, I., E. Alleva and L.G. Costa.  (2002)  Effects of perinatal exposure to a polybrominated diphenyl ether (PBDE 99) on mouse neurobehavioural development.  Neurotoxicology  23(3): 375-384.

Brouwer, a, & van den Berg, K. J. (1986). Binding of a metabolite of 3,4,3’,4'-tetrachlorobiphenyl to transthyretin reduces serum vitamin A transport by inhibiting the formation of the protein complex carrying both retinol and thyroxin. Toxicology and Applied Pharmacology, 85(3), 301–312.

Calvo, R.M., E. Jauniaux, B. Gulbis, M. Asuncion, C. Gervy, B. Contempre and G. Morreale de Escobar.  (2002)  Fetal tissues are exposed to biologically relevant free thyroxine concentrations during early phases of development.  J. Clin. Endocrinol. Metab.  87(4); 1768-1777.

Cao, J., L.H. Guo, B. Wan and Y. Wei. (2011) In vitro fluorescence displacement investigation of thyroxine transport disruption by bisphenol A.  J. Environ Sci, (China)  23(2): 315-321.

Cao, J., Y. Lin, L.H. Guo, A.Q. Zhang, Y. Wei and Y. Yang. (2010) Structure-based investigation on the binding interaction of hydroxylated polybrominated diphenyl ethers with thyroxine transport proteins.  Toxicology  277(1-3): 20-28.

Chan, S.Y., J.A. Franklyn, H.N. Pemberton, J.N. Bulmer, T.J. Visser, C.J. McCabe and M.D. Kilby.  (2006)  Monocarboxylate transporter 8 expression in the human placenta: the effects of severe intrauterine growth restriction.  J. Endocrinol.  189(3): 465-471.

Chan, S., S. Kachilele, C.J. McCabe, L.A. Tannahill, K. Boelaert, N.J. Gittoes, T.J. Visser, J.A. Franklyn and M.D. Kilby.  (2002)  Early expression of thyroid hormone deiodinases and receptors in human fetal cerebral cortex.  Brain Res. Dev. Brain Res.  138(2): 109-116.

Chang, S.C., J.R. Thibodeaux, M.L. Eastvold, D.J. Ehresman, J.A. Bjork, J.W. Froehlich, C. Lau, R.J. Singh, K.B. Wallace and J.L. Butenhoff. (2008) Thyroid hormone status and pituitary function in adult rats given oral doses of perfluorooctanesulfonate (PFOS).  Toxicology  243(3): 330-339.

Chanoine, J.-P., Alex, S., Fang, S. L., Stone, S., Leonard, J. L., Kohrle, J., & Braverman, L. E. (1992). Role of transthyretin in the transport of thyroxine from the blood to the choroid plexus, the cerebrospinal fluid and the brain. Endocrinology, 130(2), 933–938.

Chauhan, K. R., Kodavanti, P. R. S., & McKinney, J. D. (2000). Assessing the Role of ortho-Substitution on Polychlorinated Biphenyl Binding to Transthyretin, a Thyroxine Transport Protein. Toxicology and Applied Pharmacology, 162(1), 10–21. http://doi.org/10.1006/taap.1999.8826

Cheek, A.O., K. Kow, J. Chen and J.A. McLachlan. (1999) Potential mechanisms of thyroid disruption in humans: interaction of organochlorine compounds with thyroid receptor, transthyretin, and thyroid-binding globulin.  Environ. Health Perspect.  107(4): 273-278.

Chevrier, J., K.G. Harley, A. Bradman, M. Gharbi, A. Sjodin and B. Eskenazi.  (2010)  Polybrominated diphenyl ether (PBDE) flame retardants and thyroid hormone during pregnancy.  Environ. Health Perspect.  118(10) : 1444-1449.

Chopra, I.J., P. Taing and L. Mikus. (1996) Direct determination of free triiodothyronine (T3) in undiluted serum by equilibrium dialysis/radioimmunoassay (RIA).  Thyroid  6(4): 255-259.

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Dallaire, R., G. Muckle, E. Dewailly, S.W. Jacobson, J.L. Jacobson, T.M. Sandanger, C.D. Sandau and P. Ayotte. (2009a)  Thyroid hormone levels of pregnant inuit women and their infants exposed to environmental contaminants.  Environ. Health Perspect.  117(6): 1014-1020.

Dallaire, R., E. Dewailly, D. Pereg, S. Dery and P. Ayotte.  (2009b)  Thyroid function and plasma concentrations of polyhalogenated compounds in Inuit adults.  Environ. Health Perspect.  117(9): 1380-1386.

Darnerud, P.O., D. Morse, E. Klasson-Wehler and A Brouwer.  (1996)  Binding of a 3,3', 4,4'-tetrachlorobiphenyl (CB-77) metabolite to fetal transthyretin and effects on fetal thyroid hormone levels in mice.  Toxicology  106(1-3): 105-114.

De Escobar, G.M., M.J. Obregon and F.E. del Rey.  (2004)  Maternal thyroid hormones early in pregnancy and fetal brain development.  Best Pract. Res. Clin. Endocrinol. Metab.  18(2): 225-248.

Dirinck, E., A.C. Dirtu, G. Malarvanna, A. Covaci, P.G. Jorens and L.F. Van Gall. (2016) A Preliminary Link between Hydroxylated Metabolites of Polychlorinated Biphenyls and Free Thyroxin in Humans.  Int. J. Environ. Res. Public Health  13(4): 421.

Eguchi, A., K. Nomiyama, N. Minh Tue, P.T. Trang, P. Hung Viet, S. Takahashi and S. Tanabe.  (2015)  Residue profiles of organohalogen compounds in human serum from e-waste recycling sites in North Vietnam: Association with thyroid hormone levels.  Environ. Res.  137: 440-449.

Emerson, C.H., J.H. Cohen III, R.A Yung, S. Alex and S.L. Fang. (1990) Gender-related differences of serum thyroxine-binding proteins in the rat. Acta Endocrinol. (Copenh)  123(1): 72-78.

Erratico, C.A., A. Steitz and S.M. Bandiera. (2013) Biotransformation of 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) by human liver microsomes: identification of cytochrome P450 2B6 as the major enzyme involved.  Chem. Res. Toxicol.  26(5): 721-731.

Erratico, C.A., S.C. Moffatt and S.M. Bandiera. (2011) Comparative oxidative metabolism of BDE-47 and BDE-99 by rat hepatic microsomes.  Toxicol. Sci.  123(1): 37-47.

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Ferguson, R.N., H. Edelhoch, H.A. Saroff, J. Robbins and H.J. Cahnmann (1975) Negative cooperativity in the binding of thyroxine to human serum prealbumin. Preparation of tritium-labeled 8-anilino-1-naphthalenesulfonic acid.  Biochemistry  14(2): 282-289.

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Gutshall, D.M., G.D. Pilcher and A.E. Langley. (1989) Mechanism of the serum thyroid hormone lowering effect of perfluoro-n-decanoic acid (PFDA) in rats. J. Toxicol. Environ. Health   28(1): 53-65.

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Hagmar, L., J. Bjork, A. Sjodin, A. Bergman and E.M. Erfurth. (2001b) Plasma levels of persistent organohalogens and hormone levels in adult male humans.  Arch. Environ. Health  56(2): 138-143.

Hallgren, S., T. Sinjari, H. Hakansson and P.O. Darnerud. (2001) Effects of polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs) on thyroid hormone and vitamin A levels in rats and mice.  75(4): 200-208.

Hallgren, S. and P.O. Darnerud. (2002) Polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs) and chlorinated paraffins (CPs) in rats-testing interactions and mechanisms for thyroid hormone effects.  Toxicology  177(203): 227-243.

Hamers, T., J.H. Kamstra, E. Sonneveld, A.J. Murk, M.H. Kester, P.L. Andersson, J. Legler and A. Brouwer. (2006) In vitro profiling of the endocrine-disrupting potency of brominated flame retardants.  Toxicol. Sci.  92(1): 157-173.

Hamers, T., Kamstra, E. Sonneveld, A.J. Murk, T.J. Visser, M.J. Van Velzen, A. Brouwer and A. Bergman. (2008) Biotransformation of brominated flame retardants into potentially endocrine-disrupting metabolites, with special attention to 2,2',4,4'-tetrabromodiphenyl ether (BDE-47).  Mol. Nutr. Food Res.  52(2): 284-298.

Harley, K.G., A.R. Marks, J. Chevrier, A. Bradman, A. Sjodin and B. Eskenazi.  (2010)  PBDE concentrations in women's serum and fecundability.  Environ. Health Perspect.  118(5): 699-704.

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