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Annu Rev Public Health. 2017 Mar 20;38:81-102. doi: 10.1146/annurev-publhealth-031816-044318. Epub 2016 Dec 21.

The Changing Epidemiology of Autism Spectrum Disorders.

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A.J. Drexel Autism Institute, Philadelphia, Pennsylvania 19104; email:
Kaiser Permanente Division of Research, Oakland, California 94612.
Department of Epidemiology, University of North Carolina Gillings School of Public Health, Chapel Hill, North Carolina 27599.
Wendy Klag Center for Autism and Developmental Disabilities, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21205.
Department of Mental Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21205.
Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21205.
Department of Epidemiology and Biostatistics, Drexel University School of Public Health, Philadelphia, Pennsylvania 19104.
Department of Medical Epidemiology and Biostatistics and Department of Public Health Sciences, Karolinska Institute, SE 171-77 Stockholm, Sweden.
Department of Economics and Business, National Centre for Register-Based Research, Aarhus University, DK-8210 Aarhus, Denmark.
Department of Public Health, Section for Epidemiology, Aarhus University, DK-8000 Aarhus, Denmark.
Lundbeck Foundation Initiative for Integrative Psychiatric Research, Aarhus, Denmark.
California Department of Public Health, Division of Environmental and Occupational Disease Control, Richmond, California 94805.


Autism spectrum disorder (ASD) is a complex neurodevelopmental condition with lifelong impacts. Genetic and environmental factors contribute to ASD etiology, which remains incompletely understood. Research on ASD epidemiology has made significant advances in the past decade. Current prevalence is estimated to be at least 1.5% in developed countries, with recent increases primarily among those without comorbid intellectual disability. Genetic studies have identified a number of rare de novo mutations and gained footing in the areas of polygenic risk, epigenetics, and gene-by-environment interaction. Epidemiologic investigations focused on nongenetic factors have established advanced parental age and preterm birth as ASD risk factors, indicated that prenatal exposure to air pollution and short interpregnancy interval are potential risk factors, and suggested the need for further exploration of certain prenatal nutrients, metabolic conditions, and exposure to endocrine-disrupting chemicals. We discuss future challenges and goals for ASD epidemiology as well as public health implications.


air pollution; autism; environmental exposures; epidemiology; gene-environment interaction; genetics

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