Academic journal article Environmental Health Perspectives

Behavioral Changes in Aging but Not Young Mice after Neonatal Exposure to the Polybrominated Flame Retardant decaBDE

Academic journal article Environmental Health Perspectives

Behavioral Changes in Aging but Not Young Mice after Neonatal Exposure to the Polybrominated Flame Retardant decaBDE

Article excerpt

BACKGROUND: After several decades of commercial use, the flame-retardant chemicals polybrominated diphenyl ethers (PBDEs) and their metabolites are pervasive environmental contaminants and are detected in the human body. Decabrominated diphenyl ether (decaBDE) is currently the only PBDE in production in the United States.

OBJECTIVES: Little is known about the health effects of decaBDE. In the present study we examined the effects of neonatal decaBDE exposure on behavior in mice at two ages.

METHODS: Neonatal male and female C57BL6/J mice were exposed to a daily oral dose of 0, 6, or 20 mg/kg decaBDE from postnatal days 2 through 15. Two age groups were examined: a cohort that began training during young adulthood and an aging cohort of littermates that began training at 16 months of age. Both cohorts were tested on a series of operant procedures that included a fixed-ratio 1 schedule of reinforcement, a fixed-interval (FI) 2-min schedule, and a light-dark visual discrimination.

RESULTS: We observed minimal effects on the light-dark discrimination in the young cohort, with no effects on the other tasks. The performance of the aging cohort was significantly affected by decaBDE. On the FI schedule, decaBDE exposure increased the overall response rate. On the light--dark discrimination, older treated mice learned the task more slowly, made fewer errors on the first-response choice of a trial but more perseverative errors after an initial error, and had lower latencies to respond compared with controls. Effects were observed in both dose groups and sexes on various measures.

CONCLUSIONS: These findings suggest that neonatal decaBDE exposure produces effects on behavioral tasks in older but not younger animals. The behavioral mechanisms responsible for the pattern of observed effects may include increased impulsivity, although further research is required.

KEY WORDS: behavior, behavioral effects, C57BL6 mouse, decabrominated diphenyl ether, fixed interval, fixed ratio, impulsivity, neonatal exposure, PBDE, perseveration, visual discrimination. Environ Health Perspect 117:1903-1911 (2009). doi:10.1289/ehp.l 1814 available via http:lldx.doi. org/ [Online 17 June 2009]


Polybrominated diphenyl ethers (PBDEs) are a class of flame-retardant chemicals used in a variety of products, including textiles, plastics, and foam. PBDE levels have increased exponentially in the environment, wildlife, and human tissue since their introduction in the 1970s, with current doubling times of 2-3 years (Environmental Working Group 2003; Meironyte and Noren 1999; Rayne et al. 2003). Tissue levels of PBDEs in humans in the United States are 10-70 times higher than in Europe (Johnson-Restrepo et al. 2005; Schecter et al. 2003; Sjodin et al. 2008).

Two commercial mixtures, pentaBDE and octaBDE, are no longer produced in the United States or Europe. However, the fully substituted 2, 2', 3, 3', 4, 4', 5, 5', 6, 6-brominated diphenyl ether (decaBDE) continues to be widely used in the worldwide market. DecaBDE, like other PBDE congeners, is accumulated and bioconcentraced up the food chain (Burreau et al. 2004; Elliott et al. 2005; Jaspers et al. 2005, 2006; Vorkamp et al. 2005). It is readily absorbed after oral exposure (Morck et al. 2003), crosses the placenta (Guvenius et al. 2003; Mazdai et al. 2003), and is excreted into breast milk (Guvenius et al. 2003; She 2005). DecaBDE is a dominant congener in house dust in the United States (Allen et al. 2007; Staplccon et al. 2005).

PBDEs may have effects on the nervous system similar to those of polychlorinated biphenyls (PCBs), a well-known class of developmental neurotoxicants in humans and animals. PBDEs and PCBs are structurally similar and produced similar effects on calcium homeostasis and second-messenger systems (Kodavanti and Derr-Yellin 2002; Kodavanti and Ward 2005; Kodavanti et al. 2005). Developmental exposure to either Aroclor 1254 or decaBDE disrupted a number of cell-signaling pathways in the hippocampus that are associated with cell proliferation, migration, axonal and dendritic extension, and synaptogenesis (Pruitt et al. …

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