Association between traffic-related air pollution in schools and cognitive development in primary school children: a prospective cohort study.

Research round-up

BackgroundRoad traffic noise is a prevalent and known health hazard. However, little is known yet about its effect on children’s cognition. We aimed to study the association between exposure to road traffic noise and the development of working memory and attention in primary school children, considering school-outdoor and school-indoor annual average noise levels and noise fluctuation characteristics, as well as home-outdoor noise exposure.Methods and findingsWe followed up a population-based sample of 2,680 children aged 7 to 10 years from 38 schools in Barcelona (Catalonia, Spain) between January 2012 to March 2013. Children underwent computerised cognitive tests 4 times (n = 10,112), for working memory (2-back task, detectability), complex working memory (3-back task, detectability), and inattentiveness (Attention Network Task, hit reaction time standard error, in milliseconds). Road traffic noise was measured indoors and outdoors at schools, at the start of the school year, using standard protocols to obtain A-weighted equivalent sound pressure levels, i.e., annual average levels scaled to human hearing, for the daytime (daytime LAeq, in dB). We also derived fluctuation indicators out of the measurements (noise intermittency ratio, %; and number of noise events) and obtained individual estimated indoor noise levels (LAeq) correcting for classroom orientation and classroom change between years. Home-outdoor noise exposure at home (Lden, i.e., EU indicator for the 24-hour annual average levels) was estimated using Barcelona’s noise map for year 2012, according to the European Noise Directive (2002). We used linear mixed models to evaluate the association between exposure to noise and cognitive development adjusting for age, sex, maternal education, socioeconomical vulnerability index at home, indoor or outdoor traffic-related air pollution (TRAP) for corresponding school models or outdoor nitrogen dioxide (NO2) for home models. Child and school were included as nested random effects.The median age (percentile 25, percentile 75) of children in visit 1 was 8.5 (7.8; 9.3) years, 49.9% were girls, and 50% of the schools were public. School-outdoor exposure to road traffic noise was associated with a slower development in working memory (2-back and 3-back) and greater inattentiveness over 1 year in children, both for the average noise level (e.g., ‒4.83 points [95% CI: ‒7.21, ‒2.45], p-value < 0.001, in 2-back detectability per 5 dB in street levels) and noise fluctuation (e.g., ‒4.38 [‒7.08, ‒1.67], p-value = 0.002, per 50 noise events at street level). Individual exposure to the road traffic average noise level in classrooms was only associated with inattentiveness (2.49 ms [0, 4.81], p-value = 0.050, per 5 dB), whereas indoor noise fluctuation was consistently associated with all outcomes. Home-outdoor noise exposure was not associated with the outcomes. Study limitations include a potential lack of generalizability (58% of mothers with university degree in our study versus 50% in the region) and the lack of past noise exposure assessment.ConclusionsWe observed that exposure to road traffic noise at school, but not at home, was associated with slower development of working memory, complex working memory, and attention in schoolchildren over 1 year. Associations with noise fluctuation indicators were more evident than with average noise levels in classrooms.

Longitudinal association between air pollution exposure at school and cognitive development in school children over a period of 3.5 years

Roles of pollution in the prevalence and exacerbations of allergic diseases in Asia

Background:A few studies have reported associations between traffic-related air pollution exposure at schools and cognitive development. The role of PM components or sources other than traffic on cognitive development has been little explored.Objectives:We aimed to explore the role of PM sources in school air on cognitive development.Methods:A cohort of 2,618 schoolchildren (average age, 8.5 years) belonging to 39 schools in Barcelona (Spain) was followed up for a year. Children completed computerized tests assessing working memory, superior working memory, and inattentiveness during four visits. Particulate matter ≤ 2.5 μm (PM2.5) was measured during two 1-week campaigns in each school, both outdoors and in the classroom. Source apportionment resulted in nine sources: mineral, organic/textile/chalk, traffic, secondary sulfate and organics, secondary nitrate, road dust, metallurgy, sea spray, and heavy oil combustion. Differences in cognitive growth trajectories were assessed with mixed models with age-by-source interaction terms.Results:An interquartile range increase in indoor traffic-related PM2.5 was associated with reductions in cognitive growth equivalent to 22% (95% CI: 2%, 42%) of the annual change in working memory, 30% (95% CI: 6%, 54%) of the annual change in superior working memory, and 11% (95% CI: 0%, 22%) of the annual change in the inattentiveness scale. None of the other PM2.5 sources was associated with adverse effects on cognitive development.Conclusions:Traffic was the only source of fine particles associated with a reduction in cognitive development. Reducing air pollution from traffic at primary schools may result in beneficial effects on cognition.Citation:Basagaña X, Esnaola M, Rivas I, Amato F, Alvarez-Pedrerol M, Forns J, López-Vicente M, Pujol J, Nieuwenhuijsen M, Querol X, Sunyer J. 2016. Neurodevelopmental deceleration by urban fine particles from different emission sources: a longitudinal observational study. Environ Health Perspect 124:1630–1636; http://dx.doi.org/10.1289/EHP209

Impact of commuting exposure to traffic-related air pollution on cognitive development in children walking to school

Traffic-Related Air Pollution in Relation to Incidence and Prognosis of Coronary Heart Disease

Introduction Traffic pollution comprises toxic air pollutants and noise. Air pollution has been associated with infant mortality, and there is also evidence for small effects on birth weight. Research on noise and birth outcomes is limited, but an association with low birthweight is suggested. This study investigates traffic-related air and noise pollution exposures in relation to birth outcomes and infant mortality. Methods The study population comprises 882713 live births and 5452 stillbirths in the Greater London area from 2003-2010. Monthly concentrations of primary traffic air pollutants (NO2, NOx, exhaust and non-exhaust PM2.5 and PM10) and regional/urban background air pollutants (Ozone, and total PM2.5 and PM10) have been estimated using a dispersion model at 20m x 20m resolution. Time-weighted average air pollution estimates at address-level have been calculated for pregnancy and post-natal time windows. Annual road traffic noise levels have been modeled at address-level using the TRAffic Noise EXposure (TRANEX) model. We are analysing the relationship between air pollutant/noise exposures and birth weight, small-for-gestational-age (SGA), stillbirth and infant mortality, adjusting for potential confounders (e.g. maternal age, smoking and deprivation). Results Mean time-weighted average pregnancy exposures were 75μg/m3 for NOx, 15μg/m3 for PM2.5 and 24μg/m3 for PM10, and mean noise exposures were 58dB (day-time) and 53dB (night-time). Preliminary results suggest that traffic-related air pollution and noise exposures during pregnancy are independently associated with reduced mean birth weight and elevated risk of SGA. Conclusions The study is in progress and will be the largest to date examining environmental noise exposures and birth outcomes. This study combines highly spatially refined address-level exposure assessment for both noise and air pollutants, and will improve understanding of the relative influences of these co-exposures upon fetal/infant health.

Background and Aim: Environmental justice issues surround population exposure to ambient air pollution; however, few studies have specifically examined traffic air pollution (a pollutant with localized concentration patterns) and pregnancy exposures (maternal-infant dyads may be particularly susceptible to air pollution effects). How socioeconomic and demographic disparities may change over time is also unclear but could have important policy implications. Methods: We identified ~ 6.9 million pregnant mothers in Texas from 1996 to 2016 using individual-level vital statistics records. We estimated traffic air pollution exposures using full residential addresses and calculated the total vehicle miles travelled (VMT) within 300 m, assigned nitrogen dioxide (NO2) concentrations from a spatial-temporal land use regression model (an indicator of vehicle tailpipe emissions), and linked the National Air Toxic Agency cancer risk index from vehicles emissions to maternal addresses. From census tract data, we examined median household income. We quantified annual absolute and relative mean percent differences in traffic air pollution across socio-demographic indicators of maternal race and ethnicity, educational attainment, and maternal birthplace. Results: We observed marked differences in traffic air pollution exposures by all socio-demographic variables examined. Overall, the strongest disparities were seen among non-White and foreign-born pregnancies. While the absolute level of disparity shrank from 1996 to 2016 (e.g., in 1996 Black individuals were exposed to NO2 levels 1.8 ppb higher than white individuals, while in 2016 NO2 levels were 1.5 ppb higher among Black compared to white individuals), the relative level of disparity continued to increase. Within census tracts (i.e., neighborhoods), we also observed sizeable disparities among socioeconomic and demographic groups. Conclusion: Despite considerable reductions in traffic-related air pollution, the magnitude of disparity has increased when we compared groups with lower socioeconomic positioning to their higher socioeconomic positioned counterparts. Keywords: traffic-related air pollution, pregnancy, environmental justice

Early life exposure to air pollution poses a significant risk to brain development from direct exposure to toxicants or via indirect mechanisms involving the circulatory, pulmonary or gastrointestinal systems. In children, exposure to traffic related air pollution has been associated with adverse effects on cognitive, behavioral and psychomotor development. We aimed to determine whether childhood exposure to traffic related air pollution is associated with regional differences in brain volume and cortical thickness among children enrolled in a longitudinal cohort study of traffic related air pollution and child health. We used magnetic resonance imaging to obtain anatomical brain images from a nested subset of 12 year old participants characterized with either high or low levels of traffic related air pollution exposure during their first year of life. We employed voxel-based morphometry to examine group differences in regional brain volume, and with separate analyses, changes in cortical thickness. Smaller regional gray matter volumes were determined in the left pre- and post-central gyri, the cerebellum, and inferior parietal lobe of participants in the high traffic related air pollution exposure group relative to participants with low exposure. Reduced cortical thickness was observed in participants with high exposure relative to those with low exposure, primarily in sensorimotor regions of the brain including the pre- and post-central gyri and the paracentral lobule, but also within the frontal and limbic regions. These results suggest that significant childhood exposure to traffic related air pollution is associated with structural alterations in brain.

The molecular mechanisms that promote pathologic alterations in human physiology mediated by short-term exposure to traffic pollutants remains not well understood. This work was to develop mechanistic networks to determine which specific pathways are activated by real-world exposures of traffic-related air pollution (TRAP) during rest and moderate physical activity (PA). A controlled crossover study to compare whole blood gene expression pre and post short-term exposure to high and low of TRAP was performed together with systems biology analysis. Twenty-eight healthy volunteers aged between 21 and 53years were recruited. These subjects were exposed during 2h to different pollution levels (high and low TRAP levels), while either cycling or resting. Global transcriptome profile of each condition was performed from human whole blood samples. Microarrays analysis was performed to obtain differential expressed genes (DEG) to be used as initial input for GeneMANIA software to obtain protein-protein (PPI) networks. Two networks were found reflecting high or low TRAP levels, which shared only 5.6 and 15.5% of its nodes, suggesting specific cell signaling pathways being activated in each environmental condition. However, gene ontology analysis of each PPI network suggests that each level of TRAP regulate common members of NF-κB signaling pathway. Our work provides the first approach describing mechanistic networks to understand TRAP effects on a system level.

BackgroundThere is evidence that ambient air pollution is associated with increased risk of infant mortality. Road traffic is a major contributor to ambient air pollution, but it also generates noise. This study investigates long-term exposure to both traffic-related air and noise pollution and risk of infant mortality. MethodsWe conducted a matched case-control study of infant deaths (deaths occurring in 1st year of life) from singleton births across Greater London from 2003-2010. Controls were singleton births in the study area between 2003-2010 surviving to age 1. Cases were matched to controls (n&amp;#61;29) on birthdate and sex. Monthly concentrations of NO2, NOX, source-specific traffic-related PM2.5, PM2.5, PM10 and ozone were estimated at 20x20m resolution using a dispersion model, and time-weighted averages calculated for pregnancy/trimesters and birth to case death at address-level. Road traffic noise was modelled at address-level. We analysed the relationship between air pollutants/noise and infant mortality using conditional logistic regression, with adjustment for confounding. ResultsThe study population comprises 3390 infant deaths (69% neonatal, 31% postneonatal). Average air pollutant exposures for cases from birth to death were 42&amp;#956;g/m3 NO2, 77&amp;#956;g/m3 NOx, 15&amp;#956;g/m3 PM2.5, 24&amp;#956;g/m3 PM10 and 31&amp;#956;g/m3 O3. Average day- and night-time noise levels were 58 and 53 dB respectively. Higher road traffic air pollution and noise exposures were particularly associated with non-White ethnicity and lower socio-economic status. Preliminary results from adjusted single-pollutant models suggest increased risk of infant mortality associated with higher ozone exposure, but not with other air pollutants or noise. Analyses of joint air pollution&amp;#8211;noise exposures are currently underway. ConclusionsTo our knowledge, this is the first epidemiological study to investigate risk of infant mortality in relation to both road traffic air pollution and noise co-exposures.

Back to table of contents Previous article Next article Clinical & Research NewsFull AccessAutism Linked to Air Pollution In Preschool ChildrenJoan Arehart-TreichelJoan Arehart-TreichelSearch for more papers by this authorPublished Online:18 Jan 2013https://doi.org/10.1176/appi.pn.2013.1a3AbstractA pollution-based case-control study suggests that being exposed to high levels of traffic-induced air pollution, such as that emitted on freeways, might be a risk factor for autism.Could exposure to traffic-related air pollution contribute to autism? A study published online November 26, 2012, in Archives of General Psychiatry and funded by the National Institute of Environmental Health Sciences suggests so.Traffic-related air pollution has been shown to induce inflammation. Inflammation may be involved in some forms of autism, according to emerging evidence.Tyler Olson/ShutterstockTwo years ago, Heather Volk, Ph.D., an assistant professor of research at the University of Southern California, and her colleagues found a provocative association between living near a freeway and autism. This association implied that traffic air pollution might be a culprit in autism.They decided to conduct another study to test the hypothesis. The cohort included 279 preschool children with autism and 145 preschool children with typical development (controls). In addition to vehicle-emission rates, the researchers used local meteorological data, traffic volume, and road geometry to construct mathematical models of traffic-related air pollution in the areas where the subjects lived. The researchers then used the models as well as the addresses of the subjects to see whether they could find any links between traffic air pollution and autism.They could. The children residing in areas with the highest levels of traffic air pollution were three times more likely to have autism than were the children residing in areas with the lowest levels. Moreover, the children with autism were twice as likely as controls to have been exposed to high levels of traffic air pollution during their mothers’ pregnancy and three times as likely as controls to have been exposed to high levels of traffic air pollution during the first year of life. Some specific traffic air pollutants—nitrogen dioxide and particulate matter—were likewise associated with autism during pregnancy and the first year of life. Finally, the findings remained solid even when demographic and socioeconomic factors as well as maternal smoking during pregnancy were considered.“This study is a major contribution to the literature regarding factors potentially involved in the cause of autism,” Christopher McDougle, M.D., a professor of autism at Harvard Medical School, said during an interview. “While we know that genetic contributions exist, it is also clear that environmental factors are also important. To date, few environmental factors related to the cause of autism have been identified by rigorous scientific investigation.”There are also some possible routes whereby traffic air pollution could lead to autism, McDougle pointed out. “Previous research has shown that concentrations of particulate air pollutants, such as polycyclic aromatic hydrocarbons, can reduce the expression of genes, including the MET receptor tyrosine kinase gene, which is important in early life neurodevelopment and is markedly reduced in the brains of people with autism. Traffic-related air pollution has also been shown to induce inflammation after both short- and long-term exposure. Emerging evidence demonstrates that inflammation may also be involved in some forms of autism.”“We are currently studying whether genes involved in brain development and genes that help the body metabolize toxins interact with air pollution exposure to alter autism risk,” Volk told Psychiatric News. “We are also working to study whether there are particular time points when exposure may be important.” ■An abstract of “Traffic-Related Air Pollution, Particulate Matter, and Autism” is posted at http://archpsyc.jamanetwork.com/article.aspx?articleid=1393589#qundefined. ISSUES NewArchived

Road traffic air and noise pollution exposure assessment – A review of tools and techniques

Recent studies suggest that exposure to both traffic-related air pollution (TrAP) and to road traffic noise (RTN) are independent risk factors for cardiovascular disease (CVD). While the exact pathophysiologic mechanisms are not known, plausible biological models exist for both associations. This paper describes interventions and mitigating measures aimed at reducing both air and noise pollution emitted from traffic. Nine types of interventions are examined within the four strategic themes of (i) land-use planning and transportation management, (ii) reduction of vehicle emissions, (iii) modification of existing structures, and (iv) behavioral change. Not all interventions result in concomitant reductions of air and noise pollutant exposures. Most interventions that rely on a scientific basis to reduce CVD are directed at reducing TrAP. Interventions identified with the greatest potential benefits focus on the pollutant source, such as reductions in traffic volume and air pollutant emissions, and are more easily realized, and likely cheaper, if they are considered in the land-use planning stages with less reliance on behavioral changes.