Do EDCs contribute to the rise in ASD ?

Are endocrine disrupting compounds environmental risk factors for autism spectrum disorder?

2018 Study Highlights

  • The increasing prevalence of autism spectrum disorder (ASD) has stimulated research on contributory environmental factors.
  • Human exposures to a broad group of ubiquitously dispersed endocrine disrupting compounds (EDCs) are steadily increasing.
  • Prenatal EDC exposures have been shown to associate with ASD-traits as well as neurobehaviors in both humans and animals.
  • Gene expression profiling of EDC-exposed animals and cultured human cells reveals transcriptomic changes associated with ASD.
  • Transgenerational effects of EDCs on neurobehaviors suggest potential epigenetic contributions to the heritability of ASD.


Recent research on the etiology of autism spectrum disorder (ASD) has shifted in part from a singular focus on genetic causes to the involvement of environmental factors and their gene interactions. This shift in focus is a result of the rapidly increasing prevalence of ASD coupled with the incomplete penetrance of this disorder in monozygotic twins. One such area of environmentally focused research is the association of exposures to endocrine disrupting compounds (EDCs) with elevated risk for ASD. EDCs are exogenous chemicals that can alter endogenous hormone activity and homeostasis, thus potentially disrupting the action of sex and other natural hormones at all stages of human development. Inasmuch as sex hormones play a fundamental role in brain development and sexual differentiation, exposure to EDCs in utero during critical stages of development can have lasting neurological and other physiological influences on the developing fetus and, ultimately, the child as well as adult.

This review will focus on the possible contributions of EDCs to autism risk and pathogenesis by first discussing the influence of endogenous sex hormones on the autistic phenotype, followed by a review of documented human exposures to EDCs and associations with behaviors relevant to ASD. Mechanistic links between EDC exposures and aberrant neurodevelopment and behaviors are then considered, with emphasis on EDC-induced transcriptional profiles derived from animal and cellular studies. Finally, this review will discuss possible mechanisms through which EDC exposure can lead to persistent changes in gene expression and phenotype, which may in turn contribute to transgenerational inheritance of ASD.

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