Eriksson,
P, E Jakobsson and A Fredriksson. 2001. Brominated Flame
Retardants: A Novel Class of Developmental Neurotoxicants in Our
Environment? Environmental
Health Perspectives 109:903-908.
Eriksson
et al. present data on the developmental neurotoxicology
of brominated
flame retardants, showing that two different types of
these ubiquitous contaminants cause permanent changes in behavior
of mice if they have been exposed shortly after birth.
Both induce changes in spontaneous behavior that worsen as the mouse
ages. One also impaired learning and memory in adult mice after
neonatal exposure. These results, in combination with data indicating
that these compounds are persistent, bioaccumulative and increasing
exponentially in different animals, including humans, raise significant
public health concerns about these compounds.
What
did they do? Eriksson et al. exposed neonatal
male mice to three different types of brominated flame retardants,
2 polybrominated diphenyl ethers (BDE-47 and BDE-99) and a brominated
bisphenol (TBBPA). Doses used were moderately low, ranging from
just beneath 1 ppm to just over 20 ppm. Each experimental animal
received a single oral dose on day 10 after birth.
At
two months and four months after birth, spontaneous behavior was
measured in the mice by quantifying their movements in a specially-designed
cage. Then at five months of age, the mice were placed in a maze
to determine how quickly they learned it and in a final test, how
well they remembered what they had learned.
What
did they find? Two months after receiving a single low-dose
exposure to both BDE-47 and BDE-99, mice demonstrated significant
changes in patterns of spontaneous behavior that increased with
dose, while those exposed to TBBPA did not. The changes involved
differences in the amount of locomotion and the frequency with which
they raised themselves upward, a normal behavior of unconstrained
mice. The differences did not follow a simple pattern, but instead
involved a suppression of spontaneous behaviors compared to controls
during the early phase of the experiment, but then late in the experiment
they became more active than controls.
When
the mice were tested two months later, i.e., 4 months after birth,
Eriksson et al. found that these same patterns persisted
but had strengthened statistically.
Eriksson
et al. also asked whether the ability of the animals to
habituate
to a new environment as they aged was affected by the treatments.
They found that the ability to habituate declined significantly
for animals treated with BDE-47 and BDE-99 but not for TBBPA. This
effect was seen at both 1.4 and 21 ppm BDE-99 but only at 21 ppm
BDE-47.
In
the maze experiment, no differences were seen in the rate of learning
the maze. When the maze was reconfigured, however, the control animals
adapted more rapidly. The animals treated with BDE-99 also appeared
less capable of responding to the changed conditions.
What
does it mean? The most important conclusion from this research
is that relatively low levels of two types of polybrominated diphenyl
ethers affected the behavior of mice that had been exposed only
a single time during neonatal development. Ericksson et al.
conclude that BDE-47 and BDE-49 cause "cause permanent aberrations
in spontaneous behavior" and also eroded habituation capability,
and learning and memory.
This
finding supports the proposal that PBDEs are developmental neurotoxicants
and is consistent with earlier
findings that they interfere with thyroid hormone function.
Ericksson et al.'s results also indicate that the neurotoxicity
of different BDE congeners will vary.
With
PBDEs continuing to increase in human and wildlife tissues, these
findings reinforce the urgency of developing better understanding
of their developmental impacts. Because of their high persistence
and bioaccumulative nature, moreover, strong measures to constrain
PBDE releases into the environment should be implemented immediately.
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