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Faire une suggestionMaternal immune response and air pollution exposure during pregnancy: insights from the Early Markers for Autism (EMA) study / Heather E. VOLK in Journal of Neurodevelopmental Disorders, 12 (2020)
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Titre : Maternal immune response and air pollution exposure during pregnancy: insights from the Early Markers for Autism (EMA) study Type de document : texte imprimé Auteurs : Heather E. VOLK, Auteur ; Bo PARK, Auteur ; Calliope HOLLINGUE, Auteur ; Karen L. JONES, Auteur ; Paul ASHWOOD, Auteur ; Gayle C. WINDHAM, Auteur ; Fred LURMAN, Auteur ; Stacey E. ALEXEEFF, Auteur ; Martin KHARRAZI, Auteur ; Michelle PEARL, Auteur ; Judy VAN DE WATER, Auteur ; Lisa A. CROEN, Auteur Langues : Anglais (eng) Mots-clés : Air Pollution/adverse effects Autistic Disorder Biomarkers Case-Control Studies Child Female Humans Immunity Male Pregnancy/immunology Prenatal Exposure Delayed Effects United States Air pollution Autism spectrum disorder Immune response Intellectual disability Prenatal exposure declare. Index. décimale : PER Périodiques Résumé : BACKGROUND: Perinatal exposure to air pollution and immune system dysregulation are two factors consistently associated with autism spectrum disorders (ASD) and other neurodevelopmental outcomes. However, little is known about how air pollution may influence maternal immune function during pregnancy. OBJECTIVES: To assess the relationship between mid-gestational circulating levels of maternal cytokines/chemokines and previous month air pollution exposure across neurodevelopmental groups, and to assess whether cytokines/chemokines mediate the relationship between air pollution exposures and risk of ASD and/or intellectual disability (ID) in the Early Markers for Autism (EMA) study. METHODS: EMA is a population-based, nested case-control study which linked archived maternal serum samples collected during weeks 15-19 of gestation for routine prenatal screening, birth records, and Department of Developmental Services (DDS) records. Children receiving DDS services for ASD without intellectual disability (ASD without ID; n = 199), ASD with ID (ASD with ID; n = 180), ID without ASD (ID; n = 164), and children from the general population (GP; n = 414) with no DDS services were included in this analysis. Serum samples were quantified for 22 cytokines/chemokines using Luminex multiplex analysis technology. Air pollution exposure for the month prior to maternal serum collection was assigned based on the Environmental Protection Agency's Air Quality System data using the maternal residential address reported during the prenatal screening visit. RESULTS: Previous month air pollution exposure and mid-gestational maternal cytokine and chemokine levels were significantly correlated, though weak in magnitude (ranging from - 0.16 to 0.13). Ten pairs of mid-pregnancy immune markers and previous month air pollutants were significantly associated within one of the child neurodevelopmental groups, adjusted for covariates (p < 0.001). Mid-pregnancy air pollution was not associated with any neurodevelopmental outcome. IL-6 remained associated with ASD with ID even after adjusting for air pollution exposure. CONCLUSION: This study suggests that maternal immune activation is associated with risk for neurodevelopmental disorders. Furthermore, that prenatal air pollution exposure is associated with small, but perhaps biologically relevant, effects on maternal immune system function during pregnancy. Additional studies are needed to better evaluate how prenatal exposure to air pollution affects the trajectory of maternal immune activation during pregnancy, if windows of heightened susceptibility can be identified, and how these factors influence neurodevelopment of the offspring. En ligne : https://dx.doi.org/10.1186/s11689-020-09343-0 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] Maternal immune response and air pollution exposure during pregnancy: insights from the Early Markers for Autism (EMA) study [texte imprimé] / Heather E. VOLK, Auteur ; Bo PARK, Auteur ; Calliope HOLLINGUE, Auteur ; Karen L. JONES, Auteur ; Paul ASHWOOD, Auteur ; Gayle C. WINDHAM, Auteur ; Fred LURMAN, Auteur ; Stacey E. ALEXEEFF, Auteur ; Martin KHARRAZI, Auteur ; Michelle PEARL, Auteur ; Judy VAN DE WATER, Auteur ; Lisa A. CROEN, Auteur.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 12 (2020)
Mots-clés : Air Pollution/adverse effects Autistic Disorder Biomarkers Case-Control Studies Child Female Humans Immunity Male Pregnancy/immunology Prenatal Exposure Delayed Effects United States Air pollution Autism spectrum disorder Immune response Intellectual disability Prenatal exposure declare. Index. décimale : PER Périodiques Résumé : BACKGROUND: Perinatal exposure to air pollution and immune system dysregulation are two factors consistently associated with autism spectrum disorders (ASD) and other neurodevelopmental outcomes. However, little is known about how air pollution may influence maternal immune function during pregnancy. OBJECTIVES: To assess the relationship between mid-gestational circulating levels of maternal cytokines/chemokines and previous month air pollution exposure across neurodevelopmental groups, and to assess whether cytokines/chemokines mediate the relationship between air pollution exposures and risk of ASD and/or intellectual disability (ID) in the Early Markers for Autism (EMA) study. METHODS: EMA is a population-based, nested case-control study which linked archived maternal serum samples collected during weeks 15-19 of gestation for routine prenatal screening, birth records, and Department of Developmental Services (DDS) records. Children receiving DDS services for ASD without intellectual disability (ASD without ID; n = 199), ASD with ID (ASD with ID; n = 180), ID without ASD (ID; n = 164), and children from the general population (GP; n = 414) with no DDS services were included in this analysis. Serum samples were quantified for 22 cytokines/chemokines using Luminex multiplex analysis technology. Air pollution exposure for the month prior to maternal serum collection was assigned based on the Environmental Protection Agency's Air Quality System data using the maternal residential address reported during the prenatal screening visit. RESULTS: Previous month air pollution exposure and mid-gestational maternal cytokine and chemokine levels were significantly correlated, though weak in magnitude (ranging from - 0.16 to 0.13). Ten pairs of mid-pregnancy immune markers and previous month air pollutants were significantly associated within one of the child neurodevelopmental groups, adjusted for covariates (p < 0.001). Mid-pregnancy air pollution was not associated with any neurodevelopmental outcome. IL-6 remained associated with ASD with ID even after adjusting for air pollution exposure. CONCLUSION: This study suggests that maternal immune activation is associated with risk for neurodevelopmental disorders. Furthermore, that prenatal air pollution exposure is associated with small, but perhaps biologically relevant, effects on maternal immune system function during pregnancy. Additional studies are needed to better evaluate how prenatal exposure to air pollution affects the trajectory of maternal immune activation during pregnancy, if windows of heightened susceptibility can be identified, and how these factors influence neurodevelopment of the offspring. En ligne : https://dx.doi.org/10.1186/s11689-020-09343-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=573 Prenatal exposure to air pollution and maternal stress predict infant individual differences in reactivity and regulation and socioemotional development / Ran LIU in Journal of Child Psychology and Psychiatry, 63-11 (November 2022)
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Titre : Prenatal exposure to air pollution and maternal stress predict infant individual differences in reactivity and regulation and socioemotional development Type de document : texte imprimé Auteurs : Ran LIU, Auteur ; Mariah DESERISY, Auteur ; Nathan A. FOX, Auteur ; Julie B. HERBSTMAN, Auteur ; Virginia A. RAUH, Auteur ; Beatrice BEEBE, Auteur ; Amy E. MARGOLIS, Auteur Article en page(s) : p.1359-1367 Langues : Anglais (eng) Mots-clés : Infant Pregnancy Male Adolescent Female Humans Prenatal Exposure Delayed Effects/psychology Individuality Air Pollution/adverse effects Air Pollutants/adverse effects Polycyclic Aromatic Hydrocarbons Polycyclic aromatic hydrocarbons infancy maternal stress reactivity and regulation socioemotional development Index. décimale : PER Périodiques Résumé : BACKGROUND: Humans are ubiquitously exposed to air pollutants including polycyclic aromatic hydrocarbons (PAH). Although most studies of prenatal exposures have focused on psychopathology in childhood or adolescence, the effects of air pollutants on early emerging individual differences in reactivity and regulation are of growing concern. Our study is the first to report effects of prenatal exposure to PAH and maternal stress on infant reactivity and regulation. METHODS: Participants included 153 infants (74 girls and 79 boys). Prenatal exposure to PAH was measured via personal air monitoring during the third trimester of pregnancy. Maternal perceived stress was measured via self-report. We assessed infant orienting/regulation (OR), surgency (SE), and negative affectivity (NA) at 4 months using the Infant Behavior Questionnaire. We measured infant socioemotional outcomes at 12 months using the Brief Infant-Toddler Social & Emotional Assessment Questionnaire. RESULTS: Infants with higher prenatal PAH exposure and of mothers with higher stress had lower OR at 4 months, which predicted lower competence at 12 months. Infants with higher prenatal PAH exposure had lower SE at 4 months, which predicted more behavioral problems at 12 months. Prenatal exposure to PAH had no effects on infant NA at 4 months, although NA was associated with greater behavioral problems at 12 months. CONCLUSIONS: Infant reactivity and regulation, as early makers of child psychopathology, can facilitate timely and targeted screening and possibly prevention of disorders caused, in part, by environmental pollution. A multifaceted approach to improve environmental quality and reduce psychosocial stress is necessary to improve the developmental outcomes of children and most specially children from disadvantaged communities that disproportionately experience these environmental exposures. En ligne : http://dx.doi.org/10.1111/jcpp.13581 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=490
in Journal of Child Psychology and Psychiatry > 63-11 (November 2022) . - p.1359-1367[article] Prenatal exposure to air pollution and maternal stress predict infant individual differences in reactivity and regulation and socioemotional development [texte imprimé] / Ran LIU, Auteur ; Mariah DESERISY, Auteur ; Nathan A. FOX, Auteur ; Julie B. HERBSTMAN, Auteur ; Virginia A. RAUH, Auteur ; Beatrice BEEBE, Auteur ; Amy E. MARGOLIS, Auteur . - p.1359-1367.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 63-11 (November 2022) . - p.1359-1367
Mots-clés : Infant Pregnancy Male Adolescent Female Humans Prenatal Exposure Delayed Effects/psychology Individuality Air Pollution/adverse effects Air Pollutants/adverse effects Polycyclic Aromatic Hydrocarbons Polycyclic aromatic hydrocarbons infancy maternal stress reactivity and regulation socioemotional development Index. décimale : PER Périodiques Résumé : BACKGROUND: Humans are ubiquitously exposed to air pollutants including polycyclic aromatic hydrocarbons (PAH). Although most studies of prenatal exposures have focused on psychopathology in childhood or adolescence, the effects of air pollutants on early emerging individual differences in reactivity and regulation are of growing concern. Our study is the first to report effects of prenatal exposure to PAH and maternal stress on infant reactivity and regulation. METHODS: Participants included 153 infants (74 girls and 79 boys). Prenatal exposure to PAH was measured via personal air monitoring during the third trimester of pregnancy. Maternal perceived stress was measured via self-report. We assessed infant orienting/regulation (OR), surgency (SE), and negative affectivity (NA) at 4 months using the Infant Behavior Questionnaire. We measured infant socioemotional outcomes at 12 months using the Brief Infant-Toddler Social & Emotional Assessment Questionnaire. RESULTS: Infants with higher prenatal PAH exposure and of mothers with higher stress had lower OR at 4 months, which predicted lower competence at 12 months. Infants with higher prenatal PAH exposure had lower SE at 4 months, which predicted more behavioral problems at 12 months. Prenatal exposure to PAH had no effects on infant NA at 4 months, although NA was associated with greater behavioral problems at 12 months. CONCLUSIONS: Infant reactivity and regulation, as early makers of child psychopathology, can facilitate timely and targeted screening and possibly prevention of disorders caused, in part, by environmental pollution. A multifaceted approach to improve environmental quality and reduce psychosocial stress is necessary to improve the developmental outcomes of children and most specially children from disadvantaged communities that disproportionately experience these environmental exposures. En ligne : http://dx.doi.org/10.1111/jcpp.13581 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=490 Prenatal exposure to air pollution is associated with altered brain structure, function, and metabolism in childhood / Bradley S. PETERSON in Journal of Child Psychology and Psychiatry, 63-11 (November 2022)
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Titre : Prenatal exposure to air pollution is associated with altered brain structure, function, and metabolism in childhood Type de document : texte imprimé Auteurs : Bradley S. PETERSON, Auteur ; Ravi BANSAL, Auteur ; Siddhant SAWARDEKAR, Auteur ; Carlo NATI, Auteur ; Eman R. ELGABALAWY, Auteur ; Lori A. HOEPNER, Auteur ; Wanda GARCIA, Auteur ; Xuejun HAO, Auteur ; Amy E. MARGOLIS, Auteur ; Frederica PERERA, Auteur ; Virginia A. RAUH, Auteur Article en page(s) : p.1316-1331 Langues : Anglais (eng) Mots-clés : Male Adolescent Pregnancy Female Humans Child Prenatal Exposure Delayed Effects/metabolism Prospective Studies Air Pollution/adverse effects Brain Particulate Matter/adverse effects/analysis/metabolism Polycyclic Aromatic Hydrocarbons Air Pollutants Air pollution arterial spin labeling diffusion tensor imaging magnetic resonance imaging magnetic resonance spectroscopy particulate matter polycyclic aromatic hydrocarbons Index. décimale : PER Périodiques Résumé : BACKGROUND: Prenatal exposure to air pollution disrupts cognitive, emotional, and behavioral development. The brain disturbances associated with prenatal air pollution are largely unknown. METHODS: In this prospective cohort study, we estimated prenatal exposures to fine particulate matter (PM(2.5) ) and polycyclic aromatic hydrocarbons (PAH), and then assessed their associations with measures of brain anatomy, tissue microstructure, neurometabolites, and blood flow in 332 youth, 6-14 years old. We then assessed how those brain disturbances were associated with measures of intelligence, ADHD and anxiety symptoms, and socialization. RESULTS: Both exposures were associated with thinning of dorsal parietal cortices and thickening of postero-inferior and mesial wall cortices. They were associated with smaller white matter volumes, reduced organization in white matter of the internal capsule and frontal lobe, higher metabolite concentrations in frontal cortex, reduced cortical blood flow, and greater microstructural organization in subcortical gray matter nuclei. Associations were stronger for PM(2.5) in boys and PAH in girls. Youth with low exposure accounted for most significant associations of ADHD, anxiety, socialization, and intelligence measures with cortical thickness and white matter volumes, whereas it appears that high exposures generally disrupted these neurotypical brain-behavior associations, likely because strong exposure-related effects increased the variances of these brain measures. CONCLUSIONS: The commonality of effects across exposures suggests PM(2.5) and PAH disrupt brain development through one or more common molecular pathways, such as inflammation or oxidative stress. Progressively higher exposures were associated with greater disruptions in local volumes, tissue organization, metabolite concentrations, and blood flow throughout cortical and subcortical brain regions and the white matter pathways interconnecting them. Together these affected regions comprise cortico-striato-thalamo-cortical circuits, which support the regulation of thought, emotion, and behavior. En ligne : http://dx.doi.org/10.1111/jcpp.13578 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=490
in Journal of Child Psychology and Psychiatry > 63-11 (November 2022) . - p.1316-1331[article] Prenatal exposure to air pollution is associated with altered brain structure, function, and metabolism in childhood [texte imprimé] / Bradley S. PETERSON, Auteur ; Ravi BANSAL, Auteur ; Siddhant SAWARDEKAR, Auteur ; Carlo NATI, Auteur ; Eman R. ELGABALAWY, Auteur ; Lori A. HOEPNER, Auteur ; Wanda GARCIA, Auteur ; Xuejun HAO, Auteur ; Amy E. MARGOLIS, Auteur ; Frederica PERERA, Auteur ; Virginia A. RAUH, Auteur . - p.1316-1331.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 63-11 (November 2022) . - p.1316-1331
Mots-clés : Male Adolescent Pregnancy Female Humans Child Prenatal Exposure Delayed Effects/metabolism Prospective Studies Air Pollution/adverse effects Brain Particulate Matter/adverse effects/analysis/metabolism Polycyclic Aromatic Hydrocarbons Air Pollutants Air pollution arterial spin labeling diffusion tensor imaging magnetic resonance imaging magnetic resonance spectroscopy particulate matter polycyclic aromatic hydrocarbons Index. décimale : PER Périodiques Résumé : BACKGROUND: Prenatal exposure to air pollution disrupts cognitive, emotional, and behavioral development. The brain disturbances associated with prenatal air pollution are largely unknown. METHODS: In this prospective cohort study, we estimated prenatal exposures to fine particulate matter (PM(2.5) ) and polycyclic aromatic hydrocarbons (PAH), and then assessed their associations with measures of brain anatomy, tissue microstructure, neurometabolites, and blood flow in 332 youth, 6-14 years old. We then assessed how those brain disturbances were associated with measures of intelligence, ADHD and anxiety symptoms, and socialization. RESULTS: Both exposures were associated with thinning of dorsal parietal cortices and thickening of postero-inferior and mesial wall cortices. They were associated with smaller white matter volumes, reduced organization in white matter of the internal capsule and frontal lobe, higher metabolite concentrations in frontal cortex, reduced cortical blood flow, and greater microstructural organization in subcortical gray matter nuclei. Associations were stronger for PM(2.5) in boys and PAH in girls. Youth with low exposure accounted for most significant associations of ADHD, anxiety, socialization, and intelligence measures with cortical thickness and white matter volumes, whereas it appears that high exposures generally disrupted these neurotypical brain-behavior associations, likely because strong exposure-related effects increased the variances of these brain measures. CONCLUSIONS: The commonality of effects across exposures suggests PM(2.5) and PAH disrupt brain development through one or more common molecular pathways, such as inflammation or oxidative stress. Progressively higher exposures were associated with greater disruptions in local volumes, tissue organization, metabolite concentrations, and blood flow throughout cortical and subcortical brain regions and the white matter pathways interconnecting them. Together these affected regions comprise cortico-striato-thalamo-cortical circuits, which support the regulation of thought, emotion, and behavior. En ligne : http://dx.doi.org/10.1111/jcpp.13578 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=490 Cerebral cortex and blood transcriptome changes in mouse neonates prenatally exposed to air pollution particulate matter / Amin HAGHANI in Journal of Neurodevelopmental Disorders, 13 (2021)
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Titre : Cerebral cortex and blood transcriptome changes in mouse neonates prenatally exposed to air pollution particulate matter Type de document : texte imprimé Auteurs : Amin HAGHANI, Auteur ; Jason I. FEINBERG, Auteur ; Kristy C. LEWIS, Auteur ; Christine LADD-ACOSTA, Auteur ; Richard G. JOHNSON, Auteur ; Andrew E. JAFFE, Auteur ; Constantinos SIOUTAS, Auteur ; Caleb E. FINCH, Auteur ; Daniel B. CAMPBELL, Auteur ; Todd E. MORGAN, Auteur ; Heather E. VOLK, Auteur Langues : Anglais (eng) Mots-clés : Air Pollutants/toxicity Air Pollution/adverse effects Animals Cerebral Cortex Female Male Mice Particulate Matter/toxicity Pregnancy Transcriptome Blood RNA sequencing nPM Index. décimale : PER Périodiques Résumé : BACKGROUND: Prenatal exposure to air pollutants is associated with increased risk for neurodevelopmental and neurodegenerative disorders. However, few studies have identified transcriptional changes related to air pollutant exposure. METHODS: RNA sequencing was used to examine transcriptomic changes in blood and cerebral cortex of three male and three female mouse neonates prenatally exposed to traffic-related nano-sized particulate matter (nPM) compared to three male and three female mouse neonates prenatally exposed to control filter air. RESULTS: We identified 19 nPM-associated differentially expressed genes (nPM-DEGs) in blood and 124 nPM-DEGs in cerebral cortex. The cerebral cortex transcriptional responses to nPM suggested neuroinflammation involvement, including CREB1, BDNF, and IFNγ genes. Both blood and brain tissues showed nPM transcriptional changes related to DNA damage, oxidative stress, and immune responses. Three blood nPM-DEGs showed a canonical correlation of 0.98 with 14 nPM-DEGS in the cerebral cortex, suggesting a convergence of gene expression changes in blood and cerebral cortex. Exploratory sex-stratified analyses suggested a higher number of nPM-DEGs in female cerebral cortex than male cerebral cortex. The sex-stratified analyses identified 2 nPM-DEGs (Rgl2 and Gm37534) shared between blood and cerebral cortex in a sex-dependent manner. CONCLUSIONS: Our findings suggest that prenatal nPM exposure induces transcriptional changes in the cerebral cortex, some of which are also observed in blood. Further research is needed to replicate nPM-induced transcriptional changes with additional biologically relevant time points for brain development. En ligne : https://dx.doi.org/10.1186/s11689-021-09380-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=574
in Journal of Neurodevelopmental Disorders > 13 (2021)[article] Cerebral cortex and blood transcriptome changes in mouse neonates prenatally exposed to air pollution particulate matter [texte imprimé] / Amin HAGHANI, Auteur ; Jason I. FEINBERG, Auteur ; Kristy C. LEWIS, Auteur ; Christine LADD-ACOSTA, Auteur ; Richard G. JOHNSON, Auteur ; Andrew E. JAFFE, Auteur ; Constantinos SIOUTAS, Auteur ; Caleb E. FINCH, Auteur ; Daniel B. CAMPBELL, Auteur ; Todd E. MORGAN, Auteur ; Heather E. VOLK, Auteur.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 13 (2021)
Mots-clés : Air Pollutants/toxicity Air Pollution/adverse effects Animals Cerebral Cortex Female Male Mice Particulate Matter/toxicity Pregnancy Transcriptome Blood RNA sequencing nPM Index. décimale : PER Périodiques Résumé : BACKGROUND: Prenatal exposure to air pollutants is associated with increased risk for neurodevelopmental and neurodegenerative disorders. However, few studies have identified transcriptional changes related to air pollutant exposure. METHODS: RNA sequencing was used to examine transcriptomic changes in blood and cerebral cortex of three male and three female mouse neonates prenatally exposed to traffic-related nano-sized particulate matter (nPM) compared to three male and three female mouse neonates prenatally exposed to control filter air. RESULTS: We identified 19 nPM-associated differentially expressed genes (nPM-DEGs) in blood and 124 nPM-DEGs in cerebral cortex. The cerebral cortex transcriptional responses to nPM suggested neuroinflammation involvement, including CREB1, BDNF, and IFNγ genes. Both blood and brain tissues showed nPM transcriptional changes related to DNA damage, oxidative stress, and immune responses. Three blood nPM-DEGs showed a canonical correlation of 0.98 with 14 nPM-DEGS in the cerebral cortex, suggesting a convergence of gene expression changes in blood and cerebral cortex. Exploratory sex-stratified analyses suggested a higher number of nPM-DEGs in female cerebral cortex than male cerebral cortex. The sex-stratified analyses identified 2 nPM-DEGs (Rgl2 and Gm37534) shared between blood and cerebral cortex in a sex-dependent manner. CONCLUSIONS: Our findings suggest that prenatal nPM exposure induces transcriptional changes in the cerebral cortex, some of which are also observed in blood. Further research is needed to replicate nPM-induced transcriptional changes with additional biologically relevant time points for brain development. En ligne : https://dx.doi.org/10.1186/s11689-021-09380-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=574

