Background: Autism spectrum disorders (ASD) are a growing concern with
more than 1 in every 68 children affected in the United States by age 8. Limited scientific
advances have been made regarding the etiology of autism, with general agreement
that both genetic and environmental factors contribute to this disorder.
Objective: To explore the link between exposure to PBDE, mitochondrial dysfunction and autism risk.
Results: Perinatal exposures to PBDEs may contribute to the etiology or morbidity of ASD including mitochondrial dysfunction
based on (i) their increased environmental abundance and human exposures, (ii) their activity towards implicated
in neuronal development and synaptic plasticity including mitochondria, and (iii) their bioaccumulation in mitochondria.
Conclusion: In this review, we propose that PBDE, and possibly other environmental exposures, during child development
can induce or compound mitochondrial dysfunction, which in conjunction with a dysregulated antioxidant response,
increase a child’s susceptibility of autism.