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Description of key information

Key value for chemical safety assessment

Effect on neurotoxicity: via oral route

Endpoint conclusion
Endpoint conclusion:
no adverse effect observed

Additional information

Several studies were published in respect to Neurotoxicity of TBBA:


Saegusa et al. (2012) studied the effect of TBBA on neurodevelopment in relation to thyroid homeostatis. Neuronal development of neonatal rats was studied after their dams were exposed to 10,000 ppm TBBA in their diet.

Results: There was an increase in reelin-expressing interneurons in the dentate hilus and a slight increase in apoptotic bodies in offspring of pregnant rats, but these effects were not reversible by PND 77. Further TBBA did not cause any developmental  hypothyroidism in these animals, by means of no dose related changes in thyroid serum lvels (Saegusa et al. (2009) There was an access of mature neurons in the hilus at later stages, but these effects were also reversible and there were no effects on organ weight cjangesin the brain or thyroid. Overall, it was concluded that there was no obvious developmental hypothyroidism caused by TBBPA in these studies (Saegusa et al. 2009, 2012)  

In a study by Viberg and Eriksson (2011) Neonate mice were exposed via oral administration to a single low dose (11.5 mg/kg/bw) of TBBPA. Results: TBBPA did not appear to affect the levels of proteins involved in maturation of the brain, neural growth or synaptogenesis in the the neonate mice. However, there was a decrease in binding sites of the nicotinic ligand cytisine in frontal cortex, but not in the parietal cortex or hippocampus of 17 day old mice.

Earlier developmental neurotoxicity studies did not observe any adverse effects upon neurodevelopment or effects upon behavior, auditory startle habitutation, learning or memory in perinatal or adult rats (Eriksson et al. 1998, 2001; Schroeder 2002; Hass et al. 2003). Furthermore, an acute neurobehavioral study by Nakajima et al. (2009) observed behavioral changes, but these effects were not considered to be treatment related.

Kiciński et al. (2012) examined neurobehavioural function in adolescents and low level exposure to TBBPA, did not find any consistent associations with performance in neurobehavioural tests and levels of TBBPA measured in blood.

Motor activity was measured in Sprague Dawley rat pups. No effects on motor activity were observed on PNDs 1, 21, or 60 after oral gavage administration of TBBPA up to 1000 mg/kg to dams from 10 weeks Premating through gestation, lactation, and waening of F2 litters (Williams and DeSesso, 2010). Overall, although it was found that TBBPA is cytoxotic to neuronal cells in vitro, the available in vivo studies in rodents were negative and there were no permanent adverse effects in brain development.



Saegusa Y, Fujimoto H, Woo G, Ohishi T, Wang L, Mitsumori K, Nishikawa A, Shibutani M. 2012. Transient aberration of neuronal development in the hippocampal dentate gyrus after developmental exposure to brominated flame retardants in rats. Arch Toxicol 86(9):1431-1442 


Viberg H and Eriksson P. 2011. Differences in neonatal neurotoxicity of brominated flame retardants, PBDE 99 and TBBPA, in mice. Toxicology 289(1):59-65.


Eriksson P, Jakobsson E, and Fredriksson A. 1998. Developmental neurorotoxicity of brominated flameretardants, polybrominated diphenyl ethers and tetrabromo-bisphenol A. Organohal Compd, Polymer Additives and Monomers 35:375-377. [cited in EU RAR 2008].


Eriksson P, Jakobsson E, Fredriksson A. 2001. Brominated flame retardants: a novel class of developmental neurorotoxins in our environment. Environ Health Perspect 109(9):903-908. [cited in EU RAR 2008].


Schroeder, R. 2002. An oral two generation reproductive, fertility, and developmental neurobehavioral study in tetrabromobisphenol A in rats. Study ID Number: 474-004. MPI Research, Inc., Mattawan, MI. Study abstract available inHPV data summary and test plan for phenol, 4,4’-isopropylidenbis[ 2,6- dibromo- (Tetrabromobisphenol A, TBBPA). Prepared by American Chemistry Council Brominated Flame Retardant Industry Panel (BFRIP)


Hass H, Wamberg C, Ladefoged O, Dalgaard M, Rye L, Vinggard A. 2003. Developmental neurotoxicity of tertabromobisphenol A in rats. (Unpublished). [cited in EU RAR 2008]


 Nakajima A, Saigusa D, Tetsu N, Yamakuni T, Tomiokka Y, Hishinuma T. 2009. Neurobehavioral effects of tetrabromobisphenol A, a brominated flame retardant in mice. Toxicol Letters 189 (1):78-83.


Kiciński M, Viaene MK, Den Hond E, Schoeters G, Covaci A, Dirtu AC, Nelen V, Bruckers L, Croes K,Sioen I, Baeyens W, Van Larebeke N, and Nawrot TS. 2012. Neurobehavioral function and low-level exposure to brominated flame retardants in adolescents: A cross-sectional study. Environ Health 11:86.


Williams A.L., and DeSesso, J.M. 2010. The potential of selected brominated flame retardants to affect neurological development. J. Toxicol. Environ. Healt B, 13, 411-448.


Saegusa Y, Fujimoto H, Woo G, Inoue K, sumori K, Hirose M, Nishikawa A, Shibutani M. 2009Takahashi M, MitOhishi T, Wang L, Mitsumori K, Nishikawa A, Shibutani M. 2012.

Developmental toxicity of brominated flame retardants, TBBPA and 1,2,5,6,9,10-hexabromocyclododecane, in rat offspring after maternal exposure from mid-gestation through lactation. Reproductive Toxicol 28: 456- 467.

Justification for selection of effect on neurotoxicity via oral route endpoint:
see below summary in discussion section

Justification for classification or non-classification

The available data do not indicate adverse neurotoxic effects. No classification is justified for the endpoint.