Marcin Szwed , Alethea V. de Jesus , Bartosz Kossowski , Hedyeh Ahmadi , Emilia Rutkowska , Yarema Mysak , Clemens Baumbach , Katarzyna Kaczmarek-Majer , Anna Degórska , Krzysztof Skotak , Katarzyna Sitnik-Warchulska , Małgorzata Lipowska , James Grellier , Iana Markevych , Megan M. Herting
{"title":"来自ABCD和NeuroSmog研究的空气污染和学龄儿童皮质髓磷脂T1w/T2w比值估计。","authors":"Marcin Szwed , Alethea V. de Jesus , Bartosz Kossowski , Hedyeh Ahmadi , Emilia Rutkowska , Yarema Mysak , Clemens Baumbach , Katarzyna Kaczmarek-Majer , Anna Degórska , Krzysztof Skotak , Katarzyna Sitnik-Warchulska , Małgorzata Lipowska , James Grellier , Iana Markevych , Megan M. Herting","doi":"10.1016/j.dcn.2025.101538","DOIUrl":null,"url":null,"abstract":"<div><div>Air pollution affects human health and may disrupt brain maturation, including axon myelination, critical for efficient neural signaling. Here, we assess the impact of prenatal and current long-term particulate matter (PM) and nitrogen dioxide (NO<sub>2</sub>) exposure on cortical T1w/T2w ratios – a proxy for myelin content – in school-age children from the Adolescent Brain Cognitive Development (ABCD) Study (United States; N = 2021) and NeuroSmog study (Poland; N = 577), using Siemens scanners. Across both samples, we found that NO<sub>2</sub> and PM were not significantly associated with cortical T1w/T2w except for one association of PM<sub>10</sub> with lower T1w/T2w in the precuneus in NeuroSmog. Superficially, ABCD Study analyses including data from all scanner types (Siemens, GE, Philips; N = 3089) revealed a negative association between NO₂ exposure and T1w/T2w ratios. However, this finding could be an artifact of between-site sociodemographic differences and large scanner-type-related measurement differences. While significant associations between air pollution and cortical myelin were largely absent, these findings do not rule out the possibility that air pollution affects cortical myelin during other exposure periods/stages of neurodevelopment. Future research should examine these relationships across diverse populations and developmental periods using unified analysis methods to better understand the potential neurotoxic effects of air pollution.</div></div>","PeriodicalId":49083,"journal":{"name":"Developmental Cognitive Neuroscience","volume":"73 ","pages":"Article 101538"},"PeriodicalIF":4.6000,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Air pollution and cortical myelin T1w/T2w ratio estimates in school-age children from the ABCD and NeuroSmog studies.\",\"authors\":\"Marcin Szwed , Alethea V. de Jesus , Bartosz Kossowski , Hedyeh Ahmadi , Emilia Rutkowska , Yarema Mysak , Clemens Baumbach , Katarzyna Kaczmarek-Majer , Anna Degórska , Krzysztof Skotak , Katarzyna Sitnik-Warchulska , Małgorzata Lipowska , James Grellier , Iana Markevych , Megan M. Herting\",\"doi\":\"10.1016/j.dcn.2025.101538\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Air pollution affects human health and may disrupt brain maturation, including axon myelination, critical for efficient neural signaling. Here, we assess the impact of prenatal and current long-term particulate matter (PM) and nitrogen dioxide (NO<sub>2</sub>) exposure on cortical T1w/T2w ratios – a proxy for myelin content – in school-age children from the Adolescent Brain Cognitive Development (ABCD) Study (United States; N = 2021) and NeuroSmog study (Poland; N = 577), using Siemens scanners. Across both samples, we found that NO<sub>2</sub> and PM were not significantly associated with cortical T1w/T2w except for one association of PM<sub>10</sub> with lower T1w/T2w in the precuneus in NeuroSmog. Superficially, ABCD Study analyses including data from all scanner types (Siemens, GE, Philips; N = 3089) revealed a negative association between NO₂ exposure and T1w/T2w ratios. However, this finding could be an artifact of between-site sociodemographic differences and large scanner-type-related measurement differences. While significant associations between air pollution and cortical myelin were largely absent, these findings do not rule out the possibility that air pollution affects cortical myelin during other exposure periods/stages of neurodevelopment. 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Air pollution and cortical myelin T1w/T2w ratio estimates in school-age children from the ABCD and NeuroSmog studies.
Air pollution affects human health and may disrupt brain maturation, including axon myelination, critical for efficient neural signaling. Here, we assess the impact of prenatal and current long-term particulate matter (PM) and nitrogen dioxide (NO2) exposure on cortical T1w/T2w ratios – a proxy for myelin content – in school-age children from the Adolescent Brain Cognitive Development (ABCD) Study (United States; N = 2021) and NeuroSmog study (Poland; N = 577), using Siemens scanners. Across both samples, we found that NO2 and PM were not significantly associated with cortical T1w/T2w except for one association of PM10 with lower T1w/T2w in the precuneus in NeuroSmog. Superficially, ABCD Study analyses including data from all scanner types (Siemens, GE, Philips; N = 3089) revealed a negative association between NO₂ exposure and T1w/T2w ratios. However, this finding could be an artifact of between-site sociodemographic differences and large scanner-type-related measurement differences. While significant associations between air pollution and cortical myelin were largely absent, these findings do not rule out the possibility that air pollution affects cortical myelin during other exposure periods/stages of neurodevelopment. Future research should examine these relationships across diverse populations and developmental periods using unified analysis methods to better understand the potential neurotoxic effects of air pollution.
期刊介绍:
The journal publishes theoretical and research papers on cognitive brain development, from infancy through childhood and adolescence and into adulthood. It covers neurocognitive development and neurocognitive processing in both typical and atypical development, including social and affective aspects. Appropriate methodologies for the journal include, but are not limited to, functional neuroimaging (fMRI and MEG), electrophysiology (EEG and ERP), NIRS and transcranial magnetic stimulation, as well as other basic neuroscience approaches using cellular and animal models that directly address cognitive brain development, patient studies, case studies, post-mortem studies and pharmacological studies.