Abstract
The increasing prevalence of neurodevelopmental disorders, especially autism spectrum disorders (ASD) and attention deficit hyperactivity disorder (ADHD), calls for more research into the identification of etiologic and risk factors. The Developmental Origin of Health and Disease (DOHaD) hypothesizes that the environment during fetal and childhood development affects the risk for many chronic diseases in later stages of life, including neurodevelopmental disorders. Epigenetics, a term describing mechanisms that cause changes in the chromosome state without affecting DNA sequences, is suggested to be the underlying mechanism, according to the DOHaD hypothesis. Moreover, many neurodevelopmental disorders are also related to epigenetic abnormalities. Experimental and epidemiological studies suggest that exposure to prenatal environmental toxicants is associated with neurodevelopmental disorders. In addition, there is also evidence that environmental toxicants can result in epigenetic alterations, notably DNA methylation. In this review, we first focus on the relationship between neurodevelopmental disorders and environmental toxicants, in particular maternal smoking, plastic-derived chemicals (bisphenol A and phthalates), persistent organic pollutants, and heavy metals. We then review studies showing the epigenetic effects of those environmental factors in humans that may affect normal neurodevelopment.
Highlights
Neurodevelopmental disorders are a group of conditions characterized by impairments of social skills or intelligence with onset in the developmental period
A number of research have pointed out the relationship between in utero exposure to environmental toxicants and an increase in the risk of neurodevelopmental disorders; several lines of research describe the changes in epigenetic markers, mainly on DNA methylation
The Developmental Origin of Health and Disease (DOHaD) hypothesis in particular is mainly based on cohort epidemiological studies and proposes epigenetics as its underlying mechanism
Summary
Neurodevelopmental disorders are a group of conditions characterized by impairments of social skills or intelligence with onset in the developmental period. The reasons for the increasing trend in ASD and ADHD are still controversial; explanations include changes in diagnostic criteria, reporting methods, or other factors such as environment, culture, and social-economic status that may affect the prevalence of neurodevelopmental disorders [7,8,9]. A birth cohort study from 1911 by the same group found that the lower the birth weight, the higher the cardiovascular disease mortality rate, hypertension, and impaired glucose tolerance rate [10,11,12,13] From these findings, Barker et al proposed an “adult-onset of fetal origin” hypothesis called “Barker’s hypothesis,” stating that a low nutritional environment in the fetal stage increases the risk of chronic diseases in adulthood, which is the concept underlying the Developmental Origin of Health and Disease (DOHaD) [14]. We focus on reviewing the relationship between maternal exposure to environmental toxicants and neurodevelopmental disorders and propose epigenetics as the linking mechanism
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