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.