Search

BACKGROUND: Traffic-related air pollution is emerging as a risk factor for Alzheimer's disease (AD) and impaired brain development. Individual differences in vulnerability to air pollution may involve the ∊4 allele of Apolipoprotein E (APOE) gene, the primary genetic risk factor for AD. OBJECTIVE: We analyzed whether the association between traffic air pollution and neurodevelopmental outcomes is modified by APOE ∊4 status in children. METHODS: Data on parent-reported behavior problems (total difficulties scores, Strengths and Difficulties Questionnaire), teacher-reported attentiondeficit hyperactivity disorder (ADHD) symptom scores, cognitive performance trajectories (computerized tests of inattentiveness and working memory repeated 2-4 times during January 2012-March 2013), and APOE genotypes were obtained for 1,667 children age 7-11 y attending 39 schools in or near Barcelona. Basal ganglia volume (putamen, caudate, and globus pallidum) was measured in 163 of the children by MRI (October 2012-April 2014.) Average annual outdoor polycyclic aromatic hydrocarbons (PAHs), elemental carbon (EC), and nitrogen dioxide (NO2 concentrations were estimated based on measurements at each school (two 1-wk campaigns conducted 6 months apart in 2012). RESULTS: APOE ∊4 allele carriers had significantly higher behavior problem scores than noncarriers, and adverse associations with PAHs and NO2 were stronger or limited to ∊4 carriers for behavior problem scores (P-interaction 0.03 and 0.04), caudate volume (P-interaction 0.04 and 0.03), and inattentiveness trajectories (P-interaction 0.15 and 0.08, respectively). Patterns of associations with the same outcomes were similar for EC. CONCLUSION: PAHs, EC, and NO2 were associated with higher behavior problem scores, smaller reductions in inattentiveness over time, and smaller caudate volume in APOE ∊4 allele carriers in our study population, and corresponding associations were weak or absent among ∊4 noncarriers. These findings support a potential role of APOE in biological mechanisms that may contribute to associations between air pollution and neurobehavioral outcomes in children. [ABSTRACT FROM AUTHOR]

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 (PM[sub 2.5]) 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 PM[sub 2.5] 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: Basagafia X, Esnaola M, Rivas I, Amato F, Alvarez-Pedrerol M, Forns J, Lôpez-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 [ABSTRACT FROM AUTHOR]

BACKGROUND: The available evidence of the effects of air pollution and noise on behavioral development is limited, and it overlooks exposure at schools, where children spend a considerable amount of time. OBJECTIVE: We aimed to investigate the associations of exposure to traffic-related air pollutants (TRAPs) and noise at school on behavioral development of schoolchildren. METHODS: We evaluated children 7-11 years of age in Barcelona (Catalonia, Spain) during 2012-2013 within the BREATHE project. Indoor and outdoor concentrations of elemental carbon (EC), black carbon (BC), and nitrogen dioxide (NO[sub 2]) were measured at schools in two separate 1-week campaigns. In one campaign we also measured noise levels inside classrooms. Parents filled out the strengths and difficulties questionnaire (SDQ) to assess child behavioral development, while teachers completed the attention deficit/hyperactivity disorder criteria of the DSM-IV (ADHD-DSM-IV) list to assess specific ADHD symptomatology. Negative binomial mixed-effects models were used to estimate associations between the exposures and behavioral development scores. RESULTS: Interquartile range (IQR) increases in indoor and outdoor EC, BC, and NO2 concentrations were positively associated with SDQ total difficulties scores (suggesting more frequent behavioral problems) in adjusted multivariate models, whereas noise was significantly associated with ADHD-DSM-IV scores. CONCLUSION: In our study population of 7- to 11-year-old children residing in Barcelona, exposure to TRAPs at school was associated with increased behavioral problems in schoolchildren. Noise exposure at school was associated with more ADHD symptoms. [ABSTRACT FROM AUTHOR]

BACKGROUND: Dozens of studies link acute exposure to particulate matter (PM) air pollution with premature mortality and morbidity, but questions remain about which species and sources in the vast PM mixture are responsible for the observed health effects. Although a few studies exist on the effects of species and sources in U.S. cities, European cities.which have a higher proportion of diesel engines and denser urban populations.have not been well characterized. Information on the effects of specific sources could aid in targeting pollution control and in articulating the biological mechanisms of PM. OBJECTIVES: Our study examined the effects of various PM sources on daily mortality for 2003 through 2007 in Barcelona, a densely populated city in the northeast corner of Spain. METHODS: Source apportionment for PM ≤2.5 μm and ≤10 m in aerodynamic diameter (PM2.5 and PM10) using positive matrix factorization identified eight different factors. Case-crossover regression analysis was used to estimate the effects of each factor. RESULTS: Several sources of PM2.5, including vehicle exhaust, fuel oil combustion, secondary nitrate/organics, minerals, secondary sulfate/organics, and road dust, had statistically significant associations (p <.0.05) with all-cause and cardiovascular mortality. Also, in some cases relative risks for a respective interquartile range increase in concentration were higher for specific sources than for total PM2.5 mass. CONCLUSIONS: These results along with those from our multisource models suggest that traffic, sulfate from shipping and long-range transport, and construction dust are important contributors to the adverse health effects linked to PM. [ABSTRACT FROM AUTHOR]

Background: Traffic-related air pollution is emerging as a risk factor for Alzheimer's disease (AD) and impaired brain development. Individual differences in vulnerability to air pollution may involve the ε4 allele of Apolipoprotein E ( APOE ) gene, the primary genetic risk factor for AD., Objective: We analyzed whether the association between traffic air pollution and neurodevelopmental outcomes is modified by APOE ε4 status in children., Methods: Data on parent-reported behavior problems (total difficulties scores, Strengths and Difficulties Questionnaire), teacher-reported attention-deficit hyperactivity disorder (ADHD) symptom scores, cognitive performance trajectories (computerized tests of inattentiveness and working memory repeated 2-4 times during January 2012-March 2013), and APOE genotypes were obtained for 1,667 children age 7-11 y attending 39 schools in or near Barcelona. Basal ganglia volume (putamen, caudate, and globus pallidum) was measured in 163 of the children by MRI (October 2012-April 2014.) Average annual outdoor polycyclic aromatic hydrocarbons (PAHs), elemental carbon (EC), and nitrogen dioxide (NO 2 ) concentrations were estimated based on measurements at each school (two 1-wk campaigns conducted 6 months apart in 2012)., Results: APOE ε4 allele carriers had significantly higher behavior problem scores than noncarriers, and adverse associations with PAHs and NO 2 were stronger or limited to ε4 carriers for behavior problem scores ( P -interaction 0.03 and 0.04), caudate volume ( P -interaction 0.04 and 0.03), and inattentiveness trajectories ( P -interaction 0.15 and 0.08, respectively). Patterns of associations with the same outcomes were similar for EC., Conclusion: PAHs, EC, and NO 2 were associated with higher behavior problem scores, smaller reductions in inattentiveness over time, and smaller caudate volume in APOE ε4 allele carriers in our study population, and corresponding associations were weak or absent among ε4 noncarriers. These findings support a potential role of APOE in biological mechanisms that may contribute to associations between air pollution and neurobehavioral outcomes in children. https://doi.org/10.1289/EHP2246.