Abstract
Autism spectrum disorder (ASD) is a neurodevelopmental condition of heterogeneous etiology. While it is widely recognized that genetic and environmental factors and their interactions contribute to autism phenotypes, their precise causal mechanisms remain poorly understood. This article reviews our current understanding of environmental risk factors of ASD and their presumed adverse physiological mechanisms. It comprehensively maps the significance of parental age, teratogenic compounds, perinatal risks, medication, smoking and alcohol use, nutrition, vaccination, toxic exposures, as well as the role of extreme psychosocial factors. Further, we consider the role of potential protective factors such as folate and fatty acid intake. Evidence indicates an increased offspring vulnerability to ASD through advanced maternal and paternal age, valproate intake, toxic chemical exposure, maternal diabetes, enhanced steroidogenic activity, immune activation, and possibly altered zinc–copper cycles and treatment with selective serotonin reuptake inhibitors. Epidemiological studies demonstrate no evidence for vaccination posing an autism risk. It is concluded that future research needs to consider categorical autism, broader autism phenotypes, as well as autistic traits, and examine more homogenous autism variants by subgroup stratification. Our understanding of autism etiology could be advanced by research aimed at disentangling the causal and non-causal environmental effects, both founding and moderating, and gene–environment interplay using twin studies, longitudinal and experimental designs. The specificity of many environmental risks for ASD remains unknown and control of multiple confounders has been limited. Further understanding of the critical windows of neurodevelopmental vulnerability and investigating the fit of multiple hit and cumulative risk models are likely promising approaches in enhancing the understanding of role of environmental factors in the etiology of ASD.
Highlights
Autism spectrum disorder (ASD) is an early onset neurodevelopmental condition defined in the DSM-5 by alterations in social communication and interaction in conjunction with repetitive, inflexible behaviors and circumscribed interests causing significant impairment in major life areas [1, 2] and reduced quality of life [3]
The DSM-5 criteria for ASD includes a specifier recommending that the potential role of medical and genetic conditions, and environmental factors associated with atypical neurodevelopment leading to ASD be considered
Research examining the etiology of autism across the last 25 years has been dominated by a focus on genetic factors; there is increasing awareness of the potential significance of environmental influences in the etiology of ASD
Summary
Autism spectrum disorder (ASD) is an early onset neurodevelopmental condition defined in the DSM-5 by alterations in social communication and interaction in conjunction with repetitive, inflexible behaviors and circumscribed interests causing significant impairment in major life areas [1, 2] and reduced quality of life [3]. Adverse reactions linked to air pollution include neuroinflammation and oxidative stress [187,188,189,190], with a recent systematic review and meta-analysis identifying 23 studies examining its association with autism reporting ORs of 1.07 (95% CI 1.06–1.08) per 10-μg/m3 increase in PM10 exposure (k = 6 studies) and 2.32 (95% CI 2.15–2.51) per 10-μg/m3 increase in PM2.5 exposure (k = 3 studies) [191], concluding that modest evidence exists for the toxicity of air pollution during early development These findings provide support for public health policies aiming to limit exposure to harmful airborne contaminants. There is evidence that some probiotic bacteria migrate from the mother to the child [245], with probiotic supplementation during pregnancy a promising, but as yet unexplored field of future investigation in autism protective factors [246]
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