Abstract
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.