Austrian Journal of Technical and

et 
al. 2010 on pregnant women, living in a low-
income, predominantly Mexican-immigrant 
community in California showed a significant 
decrease in fecundity associated with PBDE 
exposure in women.
 
Another study conducted by Chevrier et 
al. 2010 measured the concentration of 10 
higher than other U.S. children and 2 to 10 
times higher than U.S. adults. They also found 

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15 
PBDE congeners, free thyroxine (T4), total T4, 
and thyroid-stimulating hormone (TSH) in 270 
pregnant women around the 27th week of 
gestation. Associations between PBDEs and 
free and total T4 were found to be statistically 
insignificant. However, authors did find a 
significant association amongst exposure to 
PBDEs and lower TSH during pregnancy, 
which may have implications for maternal 
health and fetal development. 
A prospective, longitudinal cohort study 
initiated after 11 September 2001, including 
329 mothers who delivered in one of three 
hospitals in lower Manhattan, New York, was 
conducted by Herbstman et al. 2010. Authors 
of this study analyzed 210 cord blood 
specimens for selected PBDE congeners and 
assessed neurodevelopmental effects in the 
children at 12–48 and 72 months of age. 
Results showed that children who had higher 
cord blood concentrations of polybrominated 
diphenyl ethers (PBDEs) scored lower on tests 
of mental and motor development at 1–4 and 6 
years of age. This was the first study to report 
any such associations in humans. 
A similar study was conducted by Roze et 
al. 2009 in The Netherlands on 62 mothers and 
children to estimate associations between 12 
Organohalogen compounds (OHCs), including 
polychlorinated 
biphenyls 
(PCBs) 
and 
brominated diphenyl ether (PBDE) flame 
retardants, measured in maternal serum during 
the 35th week of pregnancy and motor 
performance (coordination, fine motor skills), 
cognition 
(intelligence, 
visual 
perception, visuomotor integration, inhibitory 
control, verbal memory, and attention), and 
behavior scores at 5–6 years of age. Authors 
demonstrated 
for 
the 
first 
time 
that 
transplacental transfer of polybrominated 
flame retardants was associated with the 
development of children at school age. 
Another study was conducted by Rose et al. in 
2010 to measure circulating PBDE levels in 
100 children between 2 and 5 years of age from 
California. The PBDE levels according to this 
study, in 2- to 5-year-old California children 
was 10 to 1,000 fold higher than European 
children, 5 times. 
that diet, indoor environment, and social 
factors influenced children's body burden 
levels. Eating poultry and pork contributed to 
elevated body burdens for nearly all types of 
flame retardants. Study also found that lower 
maternal education was independently and 
significantly associated with higher levels of 
most flame retardant congeners in the children. 
San Antonio Statement on Brominated and 
Chlorinated Flame Retardants 2010: A group 
of 145 prominent scientists from 22 countries 
signed the first-ever consensus statement 
documenting health hazards from flame 
retardant chemicals found at high levels 
in home furniture, electronics, insulation, and 
other products. This statement documents that, 
with limited fire safety benefit, these flame 
retardants can cause serious health issues, and, 
as types of flame retardants are banned, the 
alternatives should be proven safe before being 
used. The group also wants to change 
widespread policies that require use of flame 
retardants. 
A number of recent studies suggest that 
dietary intake is one of the main routes to 
human exposure to PBDEs. In recent years, 
PBDEs 
have 
become 
widespread 
environmental pollutants, while body burden 
in the general population has been increasing. 
The results do show notable coincidences 
between the China, Europe, Japan, and United 
States such as dairy products, fish, and seafood 
being a cause of human exposure to PBDEs 
due to the environmental pollutant. 
A February 2012 study genetically 
engineered female mice to have mutations in 
the x-chromosome MECP2 gene, linked 
to Rett syndrome, a disorder in humans similar 
to autism. After exposure to BDE-47 (a PDBE) 
their offspring, who were also exposed, had 
lower birth weights and survivability and 
showed sociability and learning deficits. A 
January 2013 study of mice showed brain 
damage from BDP-49, via inhibiting of 
the mitochondrial ATP production process 
necessary for brain cells to get energy. 
Toxicity was at very low levels. The study 
offers a possible pathway by which PDBEs 
lead to autism.  
Many halogenated flame retardants with 
aromatic rings, including most brominated 
flame retardants, are likely thyroid hormone 
calcium activity in mitochondria. Exposure to 
PBDEs can also alter neural cell differentiation 
and migration during development Many 

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16 
disruptors. 
The 
thyroid 
hormones 
triiodothyronine 
(T3) 
and thyroxine (T4) carry iodine atoms, another 
halogen, and are structurally similar to many 
aromatic 
halogenated 
flame 
retardants, 
including PCBs, TBBPA, and PBDEs. Such 
flame retardants therefore appear to compete 
for binding sites in the thyroid system, 
interfering 
with 
normal 
function 
of 
thyroid 
transport 
proteins 
(such 
as transthyretin) in vitro and thyroid hormone 
receptors. A 2009 in vivo animal study 
conducted 
by 
the 
US 
Environmental 
Protection Agency (EPA) demonstrated that 
deiodination, active transport, sulfation, 
and glucuronidation may be involved in 
disruption of thyroid homeostasis after 
perinatal exposure to PBDEs during critical 
developmental time points in utero and shortly 
after birth. Disruption of deiodinase as 
reported in the Szabo et al., 2009 in vivo study 
was 
supported 
in 
a 
follow-up