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Faire une suggestionMaternal Exposure to Pesticides and Risk of Autism Spectrum Disorders in Offspring: A Meta-analysis / Li WANG in Journal of Autism and Developmental Disorders, 52-4 (April 2022)
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Titre : Maternal Exposure to Pesticides and Risk of Autism Spectrum Disorders in Offspring: A Meta-analysis Type de document : texte imprimé Auteurs : Li WANG, Auteur ; Shiming TANG, Auteur ; Songjie WU, Auteur ; Lihua YAO, Auteur ; Dezhen SU, Auteur ; Ying WANG, Auteur Article en page(s) : p.1640-1651 Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder/chemically induced/epidemiology Female Humans Maternal Exposure/statistics & numerical data Pesticides/toxicity Self Report Autism Meta-analysis Pesticides Risk factor Index. décimale : PER Périodiques Résumé : This meta-analysis was conducted to estimate the overall association between maternal exposure to pesticides and risk of ASD in offspring. PubMed, EMBASE, Web of Science, and the PsycINFO were searched until December 30, 2020 to include eligible studies. Eight studies with 50,426 participants, 5810 of whom had ASD, were involved in the study. Overall, the summary OR (95% confidence interval) of ASDs in offspring for maternal exposure to pesticide estimated by residential proximity measures and self-report was 1.88 (1.10-3.20). However, maternal exposure to pesticide measured by biomarkers was not associated with an increased risk of ASDs (pooled OR 1.13; 95% CI 0.83-1.54). Further well-designed studies are needed to confirm our findings. En ligne : http://dx.doi.org/10.1007/s10803-021-05063-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=475
in Journal of Autism and Developmental Disorders > 52-4 (April 2022) . - p.1640-1651[article] Maternal Exposure to Pesticides and Risk of Autism Spectrum Disorders in Offspring: A Meta-analysis [texte imprimé] / Li WANG, Auteur ; Shiming TANG, Auteur ; Songjie WU, Auteur ; Lihua YAO, Auteur ; Dezhen SU, Auteur ; Ying WANG, Auteur . - p.1640-1651.
Langues : Anglais (eng)
in Journal of Autism and Developmental Disorders > 52-4 (April 2022) . - p.1640-1651
Mots-clés : Autism Spectrum Disorder/chemically induced/epidemiology Female Humans Maternal Exposure/statistics & numerical data Pesticides/toxicity Self Report Autism Meta-analysis Pesticides Risk factor Index. décimale : PER Périodiques Résumé : This meta-analysis was conducted to estimate the overall association between maternal exposure to pesticides and risk of ASD in offspring. PubMed, EMBASE, Web of Science, and the PsycINFO were searched until December 30, 2020 to include eligible studies. Eight studies with 50,426 participants, 5810 of whom had ASD, were involved in the study. Overall, the summary OR (95% confidence interval) of ASDs in offspring for maternal exposure to pesticide estimated by residential proximity measures and self-report was 1.88 (1.10-3.20). However, maternal exposure to pesticide measured by biomarkers was not associated with an increased risk of ASDs (pooled OR 1.13; 95% CI 0.83-1.54). Further well-designed studies are needed to confirm our findings. En ligne : http://dx.doi.org/10.1007/s10803-021-05063-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=475 Maternal Exposures Associated with Autism Spectrum Disorder in Jamaican Children / MacKinsey A. CHRISTIAN in Journal of Autism and Developmental Disorders, 48-8 (August 2018)
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Titre : Maternal Exposures Associated with Autism Spectrum Disorder in Jamaican Children Type de document : texte imprimé Auteurs : MacKinsey A. CHRISTIAN, Auteur ; Maureen SAMMS-VAUGHAN, Auteur ; Michelle LEE, Auteur ; Jan BRESSLER, Auteur ; Manouchehr HESSABI, Auteur ; Megan L. GROVE, Auteur ; Sydonnie SHAKESPEARE-PELLINGTON, Auteur ; Charlene COORE-DESAI, Auteur ; Jody-Ann REECE, Auteur ; Katherine A. LOVELAND, Auteur ; Eric BOERWINKLE, Auteur ; Mohammad H. RAHBAR, Auteur Article en page(s) : p.2766-2778 Langues : Anglais (eng) Mots-clés : Autism spectrum disorder Fever Jamaica Pesticides Physical trauma Volatile organic compounds Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder with poorly understood etiology. Many maternal exposures during pregnancy and breastfeeding potentially interfere with neurodevelopment. Using data from two age- and sex-matched case-control studies in Jamaica (n = 298 pairs), results of conditional logistic regression analyses suggest that maternal exposures to fever or infection (matched odds ratio (MOR) = 3.12, 95% CI 1.74-5.60), physical trauma (MOR 2.02, 95% CI 1.01-4.05), and oil-based paints (MOR 1.99, 95% CI 1.14-3.46) may be associated with ASD. Additionally, maternal exposure to oil-based paints may modify the relationship between maternal exposure to pesticides and ASD, which deepens our understanding of the association between pesticides and ASD. En ligne : http://dx.doi.org/10.1007/s10803-018-3537-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367
in Journal of Autism and Developmental Disorders > 48-8 (August 2018) . - p.2766-2778[article] Maternal Exposures Associated with Autism Spectrum Disorder in Jamaican Children [texte imprimé] / MacKinsey A. CHRISTIAN, Auteur ; Maureen SAMMS-VAUGHAN, Auteur ; Michelle LEE, Auteur ; Jan BRESSLER, Auteur ; Manouchehr HESSABI, Auteur ; Megan L. GROVE, Auteur ; Sydonnie SHAKESPEARE-PELLINGTON, Auteur ; Charlene COORE-DESAI, Auteur ; Jody-Ann REECE, Auteur ; Katherine A. LOVELAND, Auteur ; Eric BOERWINKLE, Auteur ; Mohammad H. RAHBAR, Auteur . - p.2766-2778.
Langues : Anglais (eng)
in Journal of Autism and Developmental Disorders > 48-8 (August 2018) . - p.2766-2778
Mots-clés : Autism spectrum disorder Fever Jamaica Pesticides Physical trauma Volatile organic compounds Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder with poorly understood etiology. Many maternal exposures during pregnancy and breastfeeding potentially interfere with neurodevelopment. Using data from two age- and sex-matched case-control studies in Jamaica (n = 298 pairs), results of conditional logistic regression analyses suggest that maternal exposures to fever or infection (matched odds ratio (MOR) = 3.12, 95% CI 1.74-5.60), physical trauma (MOR 2.02, 95% CI 1.01-4.05), and oil-based paints (MOR 1.99, 95% CI 1.14-3.46) may be associated with ASD. Additionally, maternal exposure to oil-based paints may modify the relationship between maternal exposure to pesticides and ASD, which deepens our understanding of the association between pesticides and ASD. En ligne : http://dx.doi.org/10.1007/s10803-018-3537-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367 Translational outcomes relevant to neurodevelopmental disorders following early life exposure of rats to chlorpyrifos / Elizabeth L. BERG in Journal of Neurodevelopmental Disorders, 12 (2020)
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Titre : Translational outcomes relevant to neurodevelopmental disorders following early life exposure of rats to chlorpyrifos Type de document : texte imprimé Auteurs : Elizabeth L. BERG, Auteur ; Tianna M. CHING, Auteur ; Donald A. BRUUN, Auteur ; Josef K. RIVERA, Auteur ; Milo CAREAGA, Auteur ; Jacob ELLEGOOD, Auteur ; Jason P. LERCH, Auteur ; Markus WÖHR, Auteur ; Pamela J. LEIN, Auteur ; Jill L. SILVERMAN, Auteur Langues : Anglais (eng) Mots-clés : Animals Autism Spectrum Disorder Brain Chlorpyrifos/toxicity Female Male Pregnancy Prenatal Exposure Delayed Effects Rats Rats, Sprague-Dawley United States Animal models Autism Behavior Chlorpyrifos Imaging Neurodevelopment Pesticides Rat Social Toxicology Usv Vocalization Index. décimale : PER Périodiques Résumé : BACKGROUND: Neurodevelopmental disorders (NDDs), including intellectual disability, attention deficit hyperactivity disorder (ADHD), and autism spectrum disorder (ASD), are pervasive, lifelong disorders for which pharmacological interventions are not readily available. Substantial increases in the prevalence of NDDs over a relatively short period may not be attributed solely to genetic factors and/or improved diagnostic criteria. There is now a consensus that multiple genetic loci combined with environmental risk factors during critical periods of neurodevelopment influence NDD susceptibility and symptom severity. Organophosphorus (OP) pesticides have been identified as potential environmental risk factors. Epidemiological studies suggest that children exposed prenatally to the OP pesticide chlorpyrifos (CPF) have significant mental and motor delays and strong positive associations for the development of a clinical diagnosis of intellectual delay or disability, ADHD, or ASD. METHODS: We tested the hypothesis that developmental CPF exposure impairs behavior relevant to NDD phenotypes (i.e., deficits in social communication and repetitive, restricted behavior). Male and female rat pups were exposed to CPF at 0.1, 0.3, or 1.0 mg/kg (s.c.) from postnatal days 1-4. RESULTS: These CPF doses did not significantly inhibit acetylcholinesterase activity in the blood or brain but significantly impaired pup ultrasonic vocalizations (USV) in both sexes. Social communication in juveniles via positive affiliative 50-kHz USV playback was absent in females exposed to CPF at 0.3 mg/kg and 1.0 mg/kg. In contrast, this CPF exposure paradigm had no significant effect on gross locomotor abilities or contextual and cued fear memory. Ex vivo magnetic resonance imaging largely found no differences between the CPF-exposed rats and the corresponding vehicle controls using strict false discovery correction; however, there were interesting trends in females in the 0.3 mg/kg dose group. CONCLUSIONS: This work generated and characterized a rat model of developmental CPF exposure that exhibits adverse behavioral phenotypes resulting from perinatal exposures at levels that did not significantly inhibit acetylcholinesterase activity in the brain or blood. These data suggest that current regulations regarding safe levels of CPF need to be reconsidered. En ligne : https://dx.doi.org/10.1186/s11689-020-09342-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=573
in Journal of Neurodevelopmental Disorders > 12 (2020)[article] Translational outcomes relevant to neurodevelopmental disorders following early life exposure of rats to chlorpyrifos [texte imprimé] / Elizabeth L. BERG, Auteur ; Tianna M. CHING, Auteur ; Donald A. BRUUN, Auteur ; Josef K. RIVERA, Auteur ; Milo CAREAGA, Auteur ; Jacob ELLEGOOD, Auteur ; Jason P. LERCH, Auteur ; Markus WÖHR, Auteur ; Pamela J. LEIN, Auteur ; Jill L. SILVERMAN, Auteur.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 12 (2020)
Mots-clés : Animals Autism Spectrum Disorder Brain Chlorpyrifos/toxicity Female Male Pregnancy Prenatal Exposure Delayed Effects Rats Rats, Sprague-Dawley United States Animal models Autism Behavior Chlorpyrifos Imaging Neurodevelopment Pesticides Rat Social Toxicology Usv Vocalization Index. décimale : PER Périodiques Résumé : BACKGROUND: Neurodevelopmental disorders (NDDs), including intellectual disability, attention deficit hyperactivity disorder (ADHD), and autism spectrum disorder (ASD), are pervasive, lifelong disorders for which pharmacological interventions are not readily available. Substantial increases in the prevalence of NDDs over a relatively short period may not be attributed solely to genetic factors and/or improved diagnostic criteria. There is now a consensus that multiple genetic loci combined with environmental risk factors during critical periods of neurodevelopment influence NDD susceptibility and symptom severity. Organophosphorus (OP) pesticides have been identified as potential environmental risk factors. Epidemiological studies suggest that children exposed prenatally to the OP pesticide chlorpyrifos (CPF) have significant mental and motor delays and strong positive associations for the development of a clinical diagnosis of intellectual delay or disability, ADHD, or ASD. METHODS: We tested the hypothesis that developmental CPF exposure impairs behavior relevant to NDD phenotypes (i.e., deficits in social communication and repetitive, restricted behavior). Male and female rat pups were exposed to CPF at 0.1, 0.3, or 1.0 mg/kg (s.c.) from postnatal days 1-4. RESULTS: These CPF doses did not significantly inhibit acetylcholinesterase activity in the blood or brain but significantly impaired pup ultrasonic vocalizations (USV) in both sexes. Social communication in juveniles via positive affiliative 50-kHz USV playback was absent in females exposed to CPF at 0.3 mg/kg and 1.0 mg/kg. In contrast, this CPF exposure paradigm had no significant effect on gross locomotor abilities or contextual and cued fear memory. Ex vivo magnetic resonance imaging largely found no differences between the CPF-exposed rats and the corresponding vehicle controls using strict false discovery correction; however, there were interesting trends in females in the 0.3 mg/kg dose group. CONCLUSIONS: This work generated and characterized a rat model of developmental CPF exposure that exhibits adverse behavioral phenotypes resulting from perinatal exposures at levels that did not significantly inhibit acetylcholinesterase activity in the brain or blood. These data suggest that current regulations regarding safe levels of CPF need to be reconsidered. En ligne : https://dx.doi.org/10.1186/s11689-020-09342-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=573 Understanding environmental contributions to autism: Causal concepts and the state of science / Irva HERTZ-PICCIOTTO in Autism Research, 11-4 (April 2018)
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Titre : Understanding environmental contributions to autism: Causal concepts and the state of science Type de document : texte imprimé Auteurs : Irva HERTZ-PICCIOTTO, Auteur ; Rebecca J. SCHMIDT, Auteur ; Paula KRAKOWIAK, Auteur Article en page(s) : p.554-586 Langues : Anglais (eng) Mots-clés : autism spectrum disorder causal inference diabetes environmental risk factors epigenetics gene-environment interaction nutrition pesticides pre- and peri-natal risk factors Index. décimale : PER Périodiques Résumé : The complexity of neurodevelopment, the rapidity of early neurogenesis, and over 100 years of research identifying environmental influences on neurodevelopment serve as backdrop to understanding factors that influence risk and severity of autism spectrum disorder (ASD). This Keynote Lecture, delivered at the May 2016 annual meeting of the International Society for Autism Research, describes concepts of causation, outlines the trajectory of research on nongenetic factors beginning in the 1960s, and briefly reviews the current state of this science. Causal concepts are introduced, including root causes; pitfalls in interpreting time trends as clues to etiologic factors; susceptible time windows for exposure; and implications of a multi-factorial model of ASD. An historical background presents early research into the origins of ASD. The epidemiologic literature from the last fifteen years is briefly but critically reviewed for potential roles of, for example, air pollution, pesticides, plastics, prenatal vitamins, lifestyle and family factors, and maternal obstetric and metabolic conditions during her pregnancy. Three examples from the case-control CHildhood Autism Risks from Genes and the Environment Study are probed to illustrate methodological approaches to central challenges in observational studies: capturing environmental exposure; causal inference when a randomized controlled clinical trial is either unethical or infeasible; and the integration of genetic, epigenetic, and environmental influences on development. We conclude with reflections on future directions, including exposomics, new technologies, the microbiome, gene-by-environment interaction in the era of -omics, and epigenetics as the interface of those two. As the environment is malleable, this research advances the goal of a productive and fulfilling life for all children, teen-agers and adults. Autism Res 2018, 11: 554-586. (c) 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: This Keynote Lecture, delivered at the 2016 meeting of the International Society for Autism Research, discusses evidence from human epidemiologic studies of prenatal factors contributing to autism, such as pesticides, maternal nutrition and her health. There is no single cause for autism. Examples highlight the features of a high-quality epidemiology study, and what comprises a compelling case for causation. Emergent research directions hold promise for identifying potential interventions to reduce disabilities, enhance giftedness, and improve lives of those with ASD. En ligne : http://dx.doi.org/10.1002/aur.1938 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=358
in Autism Research > 11-4 (April 2018) . - p.554-586[article] Understanding environmental contributions to autism: Causal concepts and the state of science [texte imprimé] / Irva HERTZ-PICCIOTTO, Auteur ; Rebecca J. SCHMIDT, Auteur ; Paula KRAKOWIAK, Auteur . - p.554-586.
Langues : Anglais (eng)
in Autism Research > 11-4 (April 2018) . - p.554-586
Mots-clés : autism spectrum disorder causal inference diabetes environmental risk factors epigenetics gene-environment interaction nutrition pesticides pre- and peri-natal risk factors Index. décimale : PER Périodiques Résumé : The complexity of neurodevelopment, the rapidity of early neurogenesis, and over 100 years of research identifying environmental influences on neurodevelopment serve as backdrop to understanding factors that influence risk and severity of autism spectrum disorder (ASD). This Keynote Lecture, delivered at the May 2016 annual meeting of the International Society for Autism Research, describes concepts of causation, outlines the trajectory of research on nongenetic factors beginning in the 1960s, and briefly reviews the current state of this science. Causal concepts are introduced, including root causes; pitfalls in interpreting time trends as clues to etiologic factors; susceptible time windows for exposure; and implications of a multi-factorial model of ASD. An historical background presents early research into the origins of ASD. The epidemiologic literature from the last fifteen years is briefly but critically reviewed for potential roles of, for example, air pollution, pesticides, plastics, prenatal vitamins, lifestyle and family factors, and maternal obstetric and metabolic conditions during her pregnancy. Three examples from the case-control CHildhood Autism Risks from Genes and the Environment Study are probed to illustrate methodological approaches to central challenges in observational studies: capturing environmental exposure; causal inference when a randomized controlled clinical trial is either unethical or infeasible; and the integration of genetic, epigenetic, and environmental influences on development. We conclude with reflections on future directions, including exposomics, new technologies, the microbiome, gene-by-environment interaction in the era of -omics, and epigenetics as the interface of those two. As the environment is malleable, this research advances the goal of a productive and fulfilling life for all children, teen-agers and adults. Autism Res 2018, 11: 554-586. (c) 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: This Keynote Lecture, delivered at the 2016 meeting of the International Society for Autism Research, discusses evidence from human epidemiologic studies of prenatal factors contributing to autism, such as pesticides, maternal nutrition and her health. There is no single cause for autism. Examples highlight the features of a high-quality epidemiology study, and what comprises a compelling case for causation. Emergent research directions hold promise for identifying potential interventions to reduce disabilities, enhance giftedness, and improve lives of those with ASD. En ligne : http://dx.doi.org/10.1002/aur.1938 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=358

