Abstract
Background: The prevalence of neurodevelopmental disorders, such as ASD and ADHD, is increasing. This might at least partly be explained by an increased awareness of symptoms and a shift in diagnosis. However, further studies of the incidence of ASD and ADHD are warranted. Evidence has been accumulating that fetal exposure to endocrine disrupting chemicals (EDCs) can cause neurodevelopmental damage. Objective: To determine a link between fetal EDCs exposure and ASD and/or ADHD. Methods: A systemic review of the literature (PubMed) was performed. The primary search terms were: ‘prenatal exposure delayed effects’ and ‘EDCs’, and ‘autistic disorder’ or ‘attention deficit disorder with hyperactivity’. Secondary search terms were combinations of ‘maternal exposure’ with ‘developmental disabilities/chemically induced’ and ‘neurotoxins’, all with the limiters ‘child’, ‘English’, and ‘human’. Results: Fetal exposure to EDCs appears to affect the HPA-axis, leading to disturbed fetal thyroid metabolism and androgen and estrogen homeostasis and therefore possibly disturbed neurodevelopment. Furthermore, fetal exposure to EDCs, organochlorine pesticides in particular, is associated with an elevated risk of ASD and ADHD. Different gene expression in those children due to fetal EDCs exposure is reported. Conclusion: Evidence is emerging that fetal exposure to EDCs contributes to the increasing prevalence of ASD and ADHD. However, prospective long term cohort studies are necessary to confirm these observations.
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