ArticleEnvironmental research2024
Gestational exposure to organophosphate esters and autism spectrum disorder and other non-typical development in a cohort with elevated familial likelihood.
Article in Environmental research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Pollutant Burden in Autism Spectrum Disorder: Mechanistic Convergence, Genetic Susceptibility, and Clinical Translation.Current issues in molecular biology · 2026Review
- Prenatal exposure to organophosphate ester flame retardants and child cognition: Findings from the environmental influences on child Health Outcomes cohort.Environmental pollution (Barking, Essex : 1987) · 2026Article
- Gestational exposures to mixtures of multiple chemical classes and autism spectrum disorder in the MARBLES study.Environmental research · 2025Article
- Prenatal exposure to organophosphate ester flame retardants and behavioral outcomes in early childhood in the Environmental influences on Child Health Outcomes (ECHO) cohort.Environment international · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors.
Funding
Abstract
backgroundGestational exposure to organophosphate esters (OPEs) is known to affect offspring neurodevelopment in animal studies. However, epidemiological evidence is inconsistent.
methodsParticipants were 277 mother-child pairs from MARBLES (Markers of Autism Risk in Babies - Learning Early Signs), a cohort with elevated familial likelihood of autism spectrum disorder (ASD). Nine OPE biomarker concentrations were quantified in maternal urine collected during the 2nd or 3rd trimesters of pregnancy. At age 3 years, children underwent clinical assessment for ASD and were classified into ASD, other non-typical development (non-TD), or typical development (TD). Multinomial logistic regression was used to estimate associations between each OPE biomarker and relative risk ratios for ASD and non-TD compared to TD. We examined effect modification by child sex and socioeconomic status. We also conducted a secondary analysis by using a continuous measure of ASD symptom severity as an outcome. Quantile-based g-computation was performed to examine the associations for an OPE mixture.
resultsOverall, no significant association was observed between the concentrations of each OPE biomarker or their mixture and relative risk for either ASD or non-TD. Effect modifications by child sex and maternal education were not observed. When the analysis was stratified by homeownership, among non-homeowners, ASD likelihood was increased with increased levels of bis(1-chloro-2-propyl) phosphate, bis(butoxyethyl) phosphate, and sum of di-n-butyl phosphate and di-iso-butyl phosphate (DBUP/DIBP) (p
conclusionThere was no clear evidence of gestational OPE exposure in association with relative risk for ASD; however, potential effect modification by homeownership was observed. Although our cohort includes children with elevated familial likelihood of ASD, this is the first study investigating the association between gestational OPE exposure and clinically-diagnosed ASD. Further research is needed to confirm our findings in the general population.
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