Systematic review of prenatal exposure to endocrine disrupting chemicals and autism spectrum disorder in offspring

Autism ◽  
2021 ◽  
pp. 136236132110399
Author(s):  
Salvador Marí-Bauset ◽  
Isabel Peraita-Costa ◽  
Carolina Donat-Vargas ◽  
Agustín Llopis-González ◽  
Amelia Marí-Sanchis ◽  
...  

Epidemiological studies, which can have inherent methodological limitations, are used to study the relation between endocrine disrupting chemicals and autism spectrum disorder. The objective is to systematically review the treatment of methodological limitations and assess the quality and strength of the findings in the available literature. The quality and strength of the evidence were evaluated using the Navigation Guide Systematic Review Methodology. The overall quality and strength of the available studies were “moderate” and “limited,” respectively. Risk of bias due to the methodological limitations regarding the exclusion of potential confounding factors and the lack of accuracy of exposure assessment methods were the most prevalent and were also considered to arrive at these results. The omnipresence of endocrine disrupting chemicals, their persistence and bioaccumulation, and the biological plausibility of the association between prenatal exposure to these and later development of autism spectrum disorder highlight the need to carry out well-designed epidemiological studies that overcome the methodological limitations observed in the currently available literature in order to be able to inform public policy to prevent exposure to these potentially harmful chemicals. Lay abstract Autism spectrum disorders comprise a complex group with many subtypes of behaviorally defined neurodevelopmental abnormalities in two core areas: deficits in social communication and fixated, restricted, repetitive, or stereotyped behaviors and interests each with potential unique risk factors and characteristics. The underlying mechanisms and the possible causes of autism spectrum disorder remain elusive and while increased prevalence is undoubtable, it is unclear if it is a reflection of diagnostic improvement or emerging risk factors such as endocrine disrupting chemicals. Epidemiological studies, which are used to study the relation between endocrine disrupting chemicals and autism spectrum disorder, can have inherent methodological challenges that limit the quality and strength of their findings. The objective of this work is to systematically review the treatment of these challenges and assess the quality and strength of the findings in the currently available literature. The overall quality and strength were “moderate” and “limited,” respectively. Risk of bias due to the exclusion of potential confounding factors and the lack of accuracy of exposure assessment methods were the most prevalent. The omnipresence of endocrine disrupting chemicals and the biological plausibility of the association between prenatal exposure and later development of autism spectrum disorder highlight the need to carry out well-designed epidemiological studies that overcome the methodological challenges observed in the currently available literature in order to be able to inform public policy to prevent exposure to these potentially harmful chemicals and aid in the establishment of predictor variables to facilitate early diagnosis of autism spectrum disorder and improve long-term outcomes.

Epidemiology ◽  
2019 ◽  
Vol 30 (3) ◽  
pp. 418-426 ◽  
Author(s):  
Ghassan B. Hamra ◽  
Kristen Lyall ◽  
Gayle C. Windham ◽  
Antonia M. Calafat ◽  
Andreas Sjödin ◽  
...  

2021 ◽  
Vol 2021 (1) ◽  
Author(s):  
Jennifer L. Ames ◽  
Ghassan B. Hamra ◽  
Kimberly P. Berger ◽  
Martin Kharrazi ◽  
Kristen Lyall ◽  
...  

Toxics ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 97
Author(s):  
Tristan Furnary ◽  
Rolando Garcia-Milian ◽  
Zeyan Liew ◽  
Shannon Whirledge ◽  
Vasilis Vasiliou

Recent epidemiological studies suggest that prenatal exposure to acetaminophen (APAP) is associated with increased risk of Autism Spectrum Disorder (ASD), a neurodevelopmental disorder affecting 1 in 59 children in the US. Maternal and prenatal exposure to pesticides from food and environmental sources have also been implicated to affect fetal neurodevelopment. However, the underlying mechanisms for ASD are so far unknown, likely with complex and multifactorial etiology. The aim of this study was to explore the potential effects of APAP and pesticide exposure on development with regards to the etiology of ASD by highlighting common genes and biological pathways. Genes associated with APAP, pesticides, and ASD through human research were retrieved from molecular and biomedical literature databases. The interaction network of overlapping genetic associations was subjected to network topology analysis and functional annotation of the resulting clusters. These genes were over-represented in pathways and biological processes (FDR p < 0.05) related to apoptosis, metabolism of reactive oxygen species (ROS), and carbohydrate metabolism. Since these three biological processes are frequently implicated in ASD, our findings support the hypothesis that cell death processes and specific metabolic pathways, both of which appear to be targeted by APAP and pesticide exposure, may be involved in the etiology of ASD. This novel exposures-gene-disease database mining might inspire future work on understanding the biological underpinnings of various ASD risk factors.


Author(s):  
Judit Biosca-Brull ◽  
Cristian Pérez-Fernández ◽  
Santiago Mora ◽  
Beatriz Carrillo ◽  
Helena Pinos ◽  
...  

Autism spectrum disorder (ASD) is a complex set of neurodevelopmental pathologies characterized by impoverished social and communicative abilities and stereotyped behaviors. Although its genetic basis is unquestionable, the involvement of environmental factors such as exposure to pesticides has also been proposed. Despite the systematic analyses of this relationship in humans, there are no specific reviews including both human and preclinical models. The present systematic review summarizes, analyzes, and discusses recent advances in preclinical and epidemiological studies. We included 45 human and 16 preclinical studies. These studies focused on Organophosphates (OP), Organochlorine (OC), Pyrethroid (PT), Neonicotinoid (NN), Carbamate (CM), and mixed exposures. Preclinical studies, where the OP Chlorpyrifos (CPF) compound is the one most studied, pointed to an association between gestational exposure and increased ASD-like behaviors, although the data are inconclusive with regard to other ages or pesticides. Studies in humans focused on prenatal exposure to OP and OC agents, and report cognitive and behavioral alterations related to ASD symptomatology. The results of both suggest that gestational exposure to certain OP agents could be linked to the clinical signs of ASD. Future experimental studies should focus on extending the analysis of ASD-like behaviors in preclinical models and include exposure patterns similar to those observed in human studies.


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