Flame retardants cause brain damage in young mice

Reduced adaptability, hyperactivity, and disturbances in memory and learning functions. These are deficiencies mice and rats evince when exposed to bromide flame retardants, such as those found in computers, textiles, and other materials in our surroundings, during the period when the brain develops most rapidly.

Our environment contains a multitude of pollutants, including bromide flame retardants (polybromide diphenylethers, PBDEs) used in plastics, electronic circuit boards, computers, construction materials, and synthetic textiles. Both in Sweden and around the globe PBDEs are wide-spread, and ever greater concentrations have been found in the environment, as well as in human breast milk, over the last few decades. An individual can be exposed to PBDEs throughout his/her lifetime, including the breast-feeding period, when substances are transmitted to the infant via breast milk.

In many mammals, the so-called neo-natal period is characterized by rapid development and growth of the undeveloped brain. It has previously been shown that various toxic substances can induce permanent injuries to the brain function in mice exposed during this period of development. In mice and rats this phase lasts through the first 3-4 weeks after birth. In humans, on the other hand, it starts during the third trimester of pregnancy and continues throughout the first two years of life.

In his dissertation, Henrik Viberg has identified a definable critical phase during the period of rapid development and growth of the brain, when the brain is extremely sensitive to low doses of PBDEs. He demonstrates that the presence of PBDEs, and/or their metabolites, in the brain during this critical phase led to permanently altered spontaneous behavior, reduced adaptability to new environments, and hyperactivity in the adult individual­-deficiencies that grew worse with age. Moreover, there were disturbances in memory and learning functions in adult individuals as well as changes in the so-called cholinergic system, which is tied to behavior, memory, and learning. The capacity of PBDEs to cause these neurotoxic effects does not seem to be dependent on sex, lineage, or species.

The fact that PBDEs themselves can induce neurotoxic developmental effects and that these effects are similar to those previously observed regarding polychloride biphenyls (PBCs) means that greater attention should be paid to the neurotoxic impact of PBDEs-­and possible cumulative effects between PBDEs and other pollutants in our environment.