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Prenatal and early-life diesel exhaust exposure causes autism-like behavioral changes in mice

BACKGROUND: Escalating prevalence of autism spectrum disorders (ASD) in recent decades has triggered increasing efforts in understanding roles played by environmental risk factors as a way to address this widespread public health concern. Several epidemiological studies show associations between dev...

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Autores principales: Chang, Yu-Chi, Cole, Toby B., Costa, Lucio G.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5910592/
https://www.ncbi.nlm.nih.gov/pubmed/29678176
http://dx.doi.org/10.1186/s12989-018-0254-4
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author Chang, Yu-Chi
Cole, Toby B.
Costa, Lucio G.
author_facet Chang, Yu-Chi
Cole, Toby B.
Costa, Lucio G.
author_sort Chang, Yu-Chi
collection PubMed
description BACKGROUND: Escalating prevalence of autism spectrum disorders (ASD) in recent decades has triggered increasing efforts in understanding roles played by environmental risk factors as a way to address this widespread public health concern. Several epidemiological studies show associations between developmental exposure to traffic-related air pollution and increased ASD risk. In rodent models, a limited number of studies have shown that developmental exposure to ambient ultrafine particulates or diesel exhaust (DE) can result in behavioral phenotypes consistent with mild ASD. We performed a series of experiments to determine whether developmental DE exposure induces ASD-related behaviors in mice. RESULTS: C57Bl/6J mice were exposed from embryonic day 0 to postnatal day 21 to 250–300 μg/m(3) DE or filtered air (FA) as control. Mice exposed developmentally to DE exhibited deficits in all three of the hallmark categories of ASD behavior: reduced social interaction in the reciprocal interaction and social preference tests, increased repetitive behavior in the T-maze and marble-burying test, and reduced or altered communication as assessed by measuring isolation-induced ultrasonic vocalizations and responses to social odors. CONCLUSIONS: These findings demonstrate that exposure to traffic-related air pollution, in particular that associated with diesel-fuel combustion, can cause ASD-related behavioral changes in mice, and raise concern about air pollution as a contributor to the onset of ASD in humans. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12989-018-0254-4) contains supplementary material, which is available to authorized users.
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spelling pubmed-59105922018-05-02 Prenatal and early-life diesel exhaust exposure causes autism-like behavioral changes in mice Chang, Yu-Chi Cole, Toby B. Costa, Lucio G. Part Fibre Toxicol Research BACKGROUND: Escalating prevalence of autism spectrum disorders (ASD) in recent decades has triggered increasing efforts in understanding roles played by environmental risk factors as a way to address this widespread public health concern. Several epidemiological studies show associations between developmental exposure to traffic-related air pollution and increased ASD risk. In rodent models, a limited number of studies have shown that developmental exposure to ambient ultrafine particulates or diesel exhaust (DE) can result in behavioral phenotypes consistent with mild ASD. We performed a series of experiments to determine whether developmental DE exposure induces ASD-related behaviors in mice. RESULTS: C57Bl/6J mice were exposed from embryonic day 0 to postnatal day 21 to 250–300 μg/m(3) DE or filtered air (FA) as control. Mice exposed developmentally to DE exhibited deficits in all three of the hallmark categories of ASD behavior: reduced social interaction in the reciprocal interaction and social preference tests, increased repetitive behavior in the T-maze and marble-burying test, and reduced or altered communication as assessed by measuring isolation-induced ultrasonic vocalizations and responses to social odors. CONCLUSIONS: These findings demonstrate that exposure to traffic-related air pollution, in particular that associated with diesel-fuel combustion, can cause ASD-related behavioral changes in mice, and raise concern about air pollution as a contributor to the onset of ASD in humans. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12989-018-0254-4) contains supplementary material, which is available to authorized users. BioMed Central 2018-04-20 /pmc/articles/PMC5910592/ /pubmed/29678176 http://dx.doi.org/10.1186/s12989-018-0254-4 Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Chang, Yu-Chi
Cole, Toby B.
Costa, Lucio G.
Prenatal and early-life diesel exhaust exposure causes autism-like behavioral changes in mice
title Prenatal and early-life diesel exhaust exposure causes autism-like behavioral changes in mice
title_full Prenatal and early-life diesel exhaust exposure causes autism-like behavioral changes in mice
title_fullStr Prenatal and early-life diesel exhaust exposure causes autism-like behavioral changes in mice
title_full_unstemmed Prenatal and early-life diesel exhaust exposure causes autism-like behavioral changes in mice
title_short Prenatal and early-life diesel exhaust exposure causes autism-like behavioral changes in mice
title_sort prenatal and early-life diesel exhaust exposure causes autism-like behavioral changes in mice
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5910592/
https://www.ncbi.nlm.nih.gov/pubmed/29678176
http://dx.doi.org/10.1186/s12989-018-0254-4
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