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Updated: Jun 28, 2026
Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
Neonatal exposure to deca-brominated diphenyl ether (PBDE 209) causes dose-response changes in spontaneous behaviour
N Johansson1, H Viberg, A Fredriksson
1Department of Environmental Toxicology, Uppsala University, Norbyvägen 18 A, S-752 36 Uppsala, Sweden.
Insights
Polybrominated diphenyl ethers (PBDE 209) exposure in neonatal mice caused lasting neurotoxic effects, including hyperactivity and impaired learning. These developmental neurotoxic defects worsened with age and were dose-dependent.
Area of Science:
- Environmental Science
- Toxicology
- Neuroscience
Background:
- Polybrominated diphenyl ethers (PBDEs) are flame retardants found globally in the environment and human tissues.
- Previous studies linked certain PBDEs to developmental neurotoxicity in mice, affecting behavior and the cholinergic system.
Purpose of the Study:
- To investigate the dose-response effects of PBDE 209 on neurodevelopment and behavior in mice.
- To assess the impact of PBDE 209 on the murine cholinergic system and habituation.
Main Methods:
- Neonatal male NMRI mice received a single oral dose of PBDE 209 (1.4–21 micromol/kg).
- Spontaneous behavior, habituation, anxiety-like behavior, and response to nicotine were assessed in adult mice (2 and 4 months old).
Main Results:
- Adult mice exhibited dose-response hyperactivity and reduced habituation, with effects worsening over time.
- Cholinergic system susceptibility, indicated by reduced response to nicotine, was also dose-dependently affected at 4 months of age.
Conclusions:
- PBDE 209 causes developmental neurotoxic defects, including behavioral and cholinergic system impairments.
- PBDE 209 demonstrates potency comparable to lower-brominated PBDEs in inducing neurodevelopmental toxicity.
Abstract:
Polybrominated diphenyl ethers (PBDEs), used as additive flame-retardants, are increasing in the environment and are present in human mother's milk, newborns and toddlers. We reported earlier that several PBDEs, highly brominated PBDEs, caused developmental neurotoxic effects in mice, manifested as persistent aberrations in spontaneous behaviour, habituation capability, learning and memory, and changes in the cholinergic system. The present study was undertaken to explore the dose-response effects of PBDE 209 on spontaneous behaviour, habituation and its effects on the murine cholinergic system. Neonatal male NMRI mice were given 1.4, 2.3, 14 or 21micromol PBDE 209/kg body weight, when 3 days old. The agent was administered as a single oral dose via a metal gastric tube. Spontaneous behaviour and response to the cholinergic agonist nicotine were observed in adult mice at 2 and 4 months of age. Mice were also observed for anxiety-like behaviour in an elevated plus-maze. Adult mice, 2 and 4 months old, showed a dose-response related change in spontaneous behaviour, viz. were hyperactive and showed reduced or lack of habituation, effects that worsen with age. At the adult age of 4 months the susceptibility of the cholinergic system was also affected in a dose-response related manner, viz. reduced and/or hypoactive response to nicotine. This shows that PBDE 209 can be as potent as the lower brominated PBDEs in causing developmental neurotoxic defects.
