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      Association between Traffic-Related Air Pollution in Schools and Cognitive Development in Primary School Children: A Prospective Cohort Study

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          Abstract

          Background

          Air pollution is a suspected developmental neurotoxicant. Many schools are located in close proximity to busy roads, and traffic air pollution peaks when children are at school. We aimed to assess whether exposure of children in primary school to traffic-related air pollutants is associated with impaired cognitive development.

          Methods and Findings

          We conducted a prospective study of children ( n = 2,715, aged 7 to 10 y) from 39 schools in Barcelona (Catalonia, Spain) exposed to high and low traffic-related air pollution, paired by school socioeconomic index; children were tested four times (i.e., to assess the 12-mo developmental trajectories) via computerized tests ( n = 10,112). Chronic traffic air pollution (elemental carbon [EC], nitrogen dioxide [NO2], and ultrafine particle number [UFP; 10–700 nm]) was measured twice during 1-wk campaigns both in the courtyard (outdoor) and inside the classroom (indoor) simultaneously in each school pair. Cognitive development was assessed with the n-back and the attentional network tests, in particular, working memory (two-back detectability), superior working memory (three-back detectability), and inattentiveness (hit reaction time standard error). Linear mixed effects models were adjusted for age, sex, maternal education, socioeconomic status, and air pollution exposure at home.

          Children from highly polluted schools had a smaller growth in cognitive development than children from the paired lowly polluted schools, both in crude and adjusted models (e.g., 7.4% [95% CI 5.6%–8.8%] versus 11.5% [95% CI 8.9%–12.5%] improvement in working memory, p = 0.0024). Cogently, children attending schools with higher levels of EC, NO2, and UFP both indoors and outdoors experienced substantially smaller growth in all the cognitive measurements; for example, a change from the first to the fourth quartile in indoor EC reduced the gain in working memory by 13.0% (95% CI 4.2%–23.1%). Residual confounding for social class could not be discarded completely; however, the associations remained in stratified analyses (e.g., for type of school or high-/low-polluted area) and after additional adjustments (e.g., for commuting, educational quality, or smoking at home), contradicting a potential residual confounding explanation.

          Conclusions

          Children attending schools with higher traffic-related air pollution had a smaller improvement in cognitive development.

          Abstract

          In a prospective cohort study, Jordi Sunyer and colleagues examine the association between traffic-related air pollution and 12 month cognitive development trajectories in primary school children in Barcelona.

          Editors' Summary

          Background

          Human brain development is a complex and lengthy process. During pregnancy, the basic structures of the brain are formed, and the neural circuits that will eventually control movement, speech, memory, and other cognitive (thinking) functions, as well as the function of many organs, begin to be established. By the time of birth, the brain is about a quarter of its adult size, and the neural circuits that control vital bodily functions such as breathing are well developed. By contrast, the cerebral cortex—the brain region that is involved in thought and action—is poorly developed. Much of the development of the cerebral cortex happens during the first two years of life. For example, babies usually learn to crawl at about nine months. Other aspects of brain function take longer to develop. Thus, the cognitive functions that are essential for learning undergo considerable development between the ages of 6 and 10 years, and further brain changes occur during adolescence.

          Why Was This Study Done?

          Exposure to the air pollutants produced by the combustion of fossil fuels by vehicles during pregnancy or infancy has been associated with delays in cognitive development. Moreover, experiments in animals suggest that traffic-related air pollution is a developmental neurotoxicant—a factor that disrupts brain development. However, although many schools are located next to busy roads and although traffic-related air pollution levels peak during school hours, it is not known whether exposure of school-age children to traffic-related air pollutants impairs their cognitive development and thus their ability to learn. Here, in a prospective cohort study (the BREATHE study), the researchers assess whether exposure of children aged 7–10 years to traffic-related air pollutants in schools in Barcelona, Spain, is associated with impaired cognitive development. A prospective cohort study is an observational investigation that studies groups (cohorts) of individuals who differ with respect to a specific factor to determine how exposure to this factor affects specific outcomes.

          What Did the Researchers Do and Find?

          The researchers used computerized tests to measure the development of working memory (the system that holds multiple pieces of transitory information in the mind where they can be manipulated), superior working memory (working memory that involves continuous updating of the working memory buffer), and attentiveness every three months over a 12-month period in 2,715 primary school children attending 39 schools exposed to high or low levels of traffic-related air pollution and paired by socioeconomic index. That is, the researchers compared three cognitive development outcomes in the children attending each school where exposure to air pollution was high with the same outcomes in children attending a school with a similar socioeconomic index where exposure to pollution was low; school pairing was undertaken to avoid “confounding” by social class, a factor that is known to affect cognitive development. Statistical analyses of these data indicated that the increase in cognitive development over time among children attending highly polluted schools was less than that among children attending paired lowly polluted schools, even after adjusting for additional factors that affect cognitive development. Thus, for example, there was an 11.5% 12-month increase in working memory at the lowly polluted schools but only a 7.4% 12-month increase in working memory at the highly polluted schools. Other analyses indicated that children attending schools with higher levels of traffic-related air pollutants in either the courtyard or in the classroom experienced a substantially smaller increase over the 12-month study in all three cognitive measurements than those attending schools with lower levels of pollutants.

          What Do These Findings Mean?

          These findings suggest that, compared with attendance at schools exposed to low levels of traffic-related air pollution, attendance at schools exposed to high levels of traffic-related air pollution is associated with a smaller increase in cognitive development over a 12-month period among 7- to 10-year-old children in Barcelona. The accuracy of these findings may be limited by residual confounding. That is, the children attending schools where traffic-related pollution is high might have shared other unknown characteristics that affected their cognitive development. Importantly, these findings do not prove that traffic-related air pollution causes impairment of cognitive development. Rather, they suggest that the developing brain may be vulnerable to traffic-related air pollution well into middle childhood, a conclusion that has implications for the design of air pollution regulations and for the location of new schools.

          Additional Information

          Please access these websites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001792.

          Related collections

          Most cited references29

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          Attention-deficit hyperactivity disorder.

          Attention-deficit hyperactivity disorder (ADHD) is a disorder of inattention, impulsivity, and hyperactivity that affects 8-12% of children worldwide. Although the rate of ADHD falls with age, at least half of children with the disorder will have impairing symptoms in adulthood. Twin, adoption, and molecular genetic studies show ADHD to be highly heritable, and other findings have recorded obstetric complications and psychosocial adversity as predisposing risk factors. Converging evidence from animal and human studies implicates the dysregulation of frontal-subcortical-cerebellar catecholaminergic circuits in the pathophysiology of ADHD, and molecular imaging studies suggest that abnormalities of the dopamine transporter lead to impaired neurotransmission. Studies during the past decade have shown the safety and effectiveness of new non-stimulant drugs and long-acting formulations of methylphenidate and amfetamine. Other investigations have also clarified the appropriate role of targeted psychosocial treatments in the context of ongoing pharmacotherapy.
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            Socioeconomic Status Modifies Heritability of IQ in Young Children

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              The outdoor air pollution and brain health workshop.

              Accumulating evidence suggests that outdoor air pollution may have a significant impact on central nervous system (CNS) health and disease. To address this issue, the National Institute of Environmental Health Sciences/National Institute of Health convened a panel of research scientists that was assigned the task of identifying research gaps and priority goals essential for advancing this growing field and addressing an emerging human health concern. Here, we review recent findings that have established the effects of inhaled air pollutants in the brain, explore the potential mechanisms driving these phenomena, and discuss the recommended research priorities/approaches that were identified by the panel. Copyright © 2012 Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                PLoS Med
                PLoS Med
                plos
                plosmed
                PLoS Medicine
                Public Library of Science (San Francisco, CA USA )
                1549-1277
                1549-1676
                3 March 2015
                March 2015
                : 12
                : 3
                : e1001792
                Affiliations
                [1 ]Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Catalonia, Spain
                [2 ]Pompeu Fabra University, Barcelona, Catalonia, Spain
                [3 ]Consortium for Biomedical Research in Epidemiology and Public Health (CIBERESP), Madrid, Spain
                [4 ]Institut Hospital del Mar d’Investigacions Mèdiques–Parc de Salut Mar, Barcelona, Catalonia, Spain
                [5 ]Institute of Environmental Assessment and Water Research (IDAEA-CSIC), Barcelona, Catalonia, Spain
                [6 ]Learning Disabilities Unit (UTAE), Neuropediatrics Department, Hospital Sant Joan de Déu, Universitat de Barcelona, Barcelona, Spain
                Simon Fraser University, CANADA
                Author notes

                The authors have declared that no competing interests exist.

                Conceived and designed the experiments: JS XQ. Performed the experiments: MAP JF MLV ESG MF IR MV TM AA MN NSG. Analyzed the data: ME RGE XB MC MAP MF. Contributed reagents/materials/analysis tools: MN ME XB. Wrote the paper: JS ME MAP JF IR MLV ESG MF RGE XB MV MC TM AA NSG MN XQ. Agree with manuscript results and conclusions: JS ME MAP JF IR MLV ESG MF RGE XB MV MC TM AA NSG MN XQ. All authors have read, and confirm that they meet, ICMJE criteria for authorship.

                Article
                PMEDICINE-D-14-02920
                10.1371/journal.pmed.1001792
                4348510
                25734425
                62f9df87-d588-4e3f-9ceb-4411f4ea024d
                Copyright @ 2015

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

                History
                : 16 September 2014
                : 9 January 2015
                Page count
                Figures: 6, Tables: 8, Pages: 24
                Funding
                The research leading to these results has received funding from the European Research Council under the ERC Grant Agreement number 268479 – the BREATHE project. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Research Article
                Custom metadata
                Data are from the BREATHE study whose authors may be contacted at CREAL ( http://www.creal.cat/projectebreathe/).

                Medicine
                Medicine

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