The prevalence of Autism Spectrum Disorder (ASD) has increased dramatically in recent decades, supporting the claim of an autism epidemic. Systematic monitoring of ASD allows estimating prevalence and identifying potential sources of variation over time and geographical areas. At present, ASD prevalence estimates are available worldwide, coming either from surveillance systems using existing health and educational databases or from population studies specifically performed. In the present article, we present a review of the ASD prevalence estimates published since 2014. Data confirm a high variability in prevalence across the world, likely due to methodological differences in case detection, and the consistent increase of prevalence estimates within each geographical area.

A significant body of evidence supports the multifactorial etiology of neurodevelopmental disorders (NDDs) affecting children. The present review focuses on early exposure to environmental chemicals as a risk factor for neurodevelopment, and presents the major lines of evidence derived from epidemiological studies, underlying key uncertainties and research needs in this field. We introduce the exposome concept that, encompassing the totality of human environmental exposures to multiple risk factors, aims at explaining individual vulnerability and resilience to early chemical exposure. In this framework, we synthetically review the role of variable gene backgrounds, the involvement of epigenetic mechanisms as well as the function played by potential effect modifiers such as socioeconomic status. We describe laboratory rodent studies where the neurodevelopmental effects of environmental chemicals are assessed in the presence of either a “vulnerable” gene background or adverse pregnancy conditions (i.e., maternal stress). Finally, we discuss the need for more descriptive and “lifelike” experimental models of NDDs, to identify candidate biomarkers and pinpoint susceptible groups or life stages to be translated to large prospective studies within the exposome framework.