Maternal lifestyle and environmental risk factors for autism spectrum disorders
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BACKGROUND: Over the past 10 years, research into environmental risk factors for autism has grown dramatically, bringing evidence that an array of non-genetic factors acting during the prenatal period may influence neurodevelopment. METHODS: This paper reviews the evidence on modifiable preconception and/or prenatal factors that have been associated, in some studies, with autism spectrum disorder (ASD), including nutrition, substance use and exposure to environmental agents. This review is restricted to human studies with at least 50 cases of ASD, having a valid comparison group, conducted within the past decade and focusing on maternal lifestyle or environmental chemicals. RESULTS: Higher maternal intake of certain nutrients and supplements has been associated with reduction in ASD risk, with the strongest evidence for periconceptional folic acid supplements. Although many investigations have suggested no impact of maternal smoking and alcohol use on ASD, more rigorous exposure assessment is needed. A number of studies have demonstrated significant increases in ASD risk with estimated exposure to air pollution during the prenatal period, particularly for heavy metals and particulate matter. Little research has assessed other persistent and non-persistent organic pollutants in association with ASD specifically. CONCLUSIONS: More work is needed to examine fats, vitamins and other maternal nutrients, as well as endocrine-disrupting chemicals and pesticides, in association with ASD, given sound biological plausibility and evidence regarding other neurodevelopmental deficits. The field can be advanced by large-scale epidemiological studies, attention to critical aetiological windows and how these vary by exposure, and use of biomarkers and other means to understand underlying mechanisms.
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Exposures during prenatal and early postnatal developmental windows can exert causal influences on developmental disorders.
“it is believed to be exposures during these times that can exert causal influences on developmental disorders.14,27,28”
From Environmental Chemical Exposures and Autism Spectrum Disorders: A Review of the Epidemiological Evidence (2014) · cites this paper as [14]
Evidence supports prenatal origins for autism.
“Evidence supports the hypothesis of prenatal origins for autism (5)”
From Maternal Intake of Supplemental Iron and Risk of Autism Spectrum Disorder (2014) · cites this paper as [5]
Our systematic review results were generally in concert with previous expert-based narrative reviews that addressed the association of ASD and environmental chemical exposures more broadly.
“Our systematic review results were generally in concert with previous expert-based narrative reviews that addressed the association of ASD and environmental chemical exposures more broadly [18, 65–67].”
From A Systematic Review and Meta-Analysis of Multiple Airborne Pollutants and Autism Spectrum Disorder (2016) · cites this paper as [18]
Environmental factors including pesticides, infection, nutritional factors and maternal biochemistry vary by season, have been hypothesised to be implicated in the aetiology of ASD, and need to be taken into consideration when interpreting the literature on season of conception/birth and risk of ASD.
“These environmental factors include application of pesticides [95], infection [96], nutritional factors [97] and maternal biochemistry [98], all of which have been hypothesised to be implicated in the aetiology of ASD, and need to be taken into consideration when interpreting the literature on season of conception/birth and risk of ASD.”
From Vitamin D and Autism Spectrum Disorder: A Literature Review (2016) · cites this paper as [97]
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- Authors
- Lyall, K., Schmidt, R. J., & Hertz-Picciotto, I.
- Affiliations
- University of California, Davis (US)
- Venue
- International Journal of Epidemiology
- Publisher
- Oxford University Press (OUP)
- Published
- 2014-02-11
- Volume
- 43
- Issue
- 2
- Pages
- 443-464
- ISSN
- 0300-5771 (ISSN-L)
- 1464-3685
- PMC
- PMC3997376
- OpenAlex
- W2106490877
- Cited by
- 427
- References
- 160
- Citations by year
- 2026: 14 · 2025: 28 · 2024: 39 · 2023: 32 · 2022: 39 · 2021: 32 · 2020: 44 · 2019: 45 · 2018: 34 · 2017: 33 · 2016: 39 · 2015: 25 · 2014: 23
- FWCI
- 3.77
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- International Journal of Epidemiology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- U.S. Environmental Protection Agency (R-829388, R-833292)
- National Institutes of Health (ES11269)
- National Institute of Environmental Health Sciences (R01ES020392, R01ES015359, P01ES011269)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (K12HD051958)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Health, Environment, Cognitive Aging
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Keywords
- autism spectrum disorder, maternal lifestyle, prenatal environmental exposure, preconception factors, maternal nutrition, folic acid supplementation, maternal smoking, maternal alcohol use, air pollution exposure, heavy metals, particulate matter, persistent organic pollutants, endocrine disruptors, pesticides, brain development, modifiable risk factors
- MeSH terms
- Alcohol Drinking, Child Development Disorders, Pervasive, Environmental Pollutants, Fatty Acids, Female, Fish Oils, Fish Products, Folic Acid, Humans, Life Style, Pregnancy, Prenatal Exposure Delayed Effects, Risk Factors, Smoking, Vitamins, Preconception Care, Maternal Exposure, Prenatal Nutritional Physiological Phenomena, Fetal Development
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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