Maria Foraster

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

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.

Transportation noise and blood pressure in a population-based sample of adults

Background: There is some evidence for an association between traffic noise and ischemic heart disease; however, associations with blood pressure have been inconsistent, and little is known about health effects of railway noise. Objectives: We aimed to investigate the effects of railway and traffic noise exposure on blood pressure; a secondary aim was to address potentially susceptible subpopulations. Methods: We performed adjusted linear regression analyses using data from 6,450 participants of the second survey of the Swiss Study on Air Pollution and Lung Disease in Adults (SAPALDIA 2) to estimate the associations of daytime and nighttime railway and traffic noise (A-weighted decibels) with systolic blood pressure (SBP) and diastolic blood pressure (DBP; millimeters of mercury). Noise data were provided by the Federal Office for the Environment. Stratified analyses by self-reported hypertension, cardiovascular disease (CVD), and diabetes were performed. Results: Mean noise exposure during the day and night was 51 dB(A) and 39 dB(A) for traffic noise, respectively, and 19 dB(A) and 17 dB(A) for railway noise. Adjusted regression models yielded significant effect estimates for a 10 dB(A) increase in railway noise during the night [SBP β = 0.84; 95% confidence interval (CI): 0.22, 1.46; DBP β = 0.44; 95% CI: 0.06, 0.81] and day (SBP β = 0.60; 95% CI: 0.07, 1.13). Additional adjustment for nitrogen dioxide left effect estimates almost unchanged. Stronger associations were estimated for participants with chronic disease. Significant associations with traffic noise were seen only among participants with diabetes. Conclusion: We found evidence of an adverse effect of railway noise on blood pressure in this cohort population. Traffic noise was associated with higher blood pressure only in diabetics, possibly due to low exposure levels. The study results imply more severe health effects by transportation noise in vulnerable populations, such as adults with hypertension, diabetes, or CVD.

Local determinants of road traffic noise levels versus determinants of air pollution levels in a Mediterranean city.

BACKGROUND Both traffic-related noise and air pollution have been associated with cardiovascular disease (CVD). Spatial correlations between these environmental stressors may entail mutual confounding in epidemiological studies investigating their long-term effects. Few studies have investigated their correlation - none in Spain - and results differ among cities. OBJECTIVES We assessed the contribution of urban land-use and traffic variables to the noise-air pollution correlation in Girona town, where an investigation of the chronic effects of air pollution and noise on CVD takes place (REGICOR-AIR). METHODOLOGY Outdoor annual mean concentrations of nitrogen dioxide (NO(2)) derived from monthly passive sampler measurements were obtained at 83 residential locations. Long-term average traffic-related noise levels from a validated model were assigned to each residence. Linear regression models were fitted both for NO(2) and noise. RESULTS The correlation between NO(2) and noise (L(24h)) was 0.62. However, the correlation differed across the urban space, with lower correlations at sites with higher traffic density and in the modern downtown. Traffic density, distance from the location to the sidewalk and building density nearby explained 35.6% and 73.2% of the variability of NO(2) and noise levels, respectively. The correlation between the residuals of the two models suggested the presence of other unmeasured common variables. CONCLUSIONS The substantial correlation between traffic-related noise and NO(2), endorsed by common determinants, and the dependence of this correlation on complex local characteristics call for careful evaluations of both factors to ultimately assess their cardiovascular effects.

Arterial Blood Pressure and Long-Term Exposure to Traffic-Related Air Pollution: An Analysis in the European Study of Cohorts for Air Pollution Effects (ESCAPE)

Background: Long-term exposure to air pollution has been hypothesized to elevate arterial blood pressure (BP). The existing evidence is scarce and country specific. Objectives: We investigated the cross-sectional association of long-term traffic-related air pollution with BP and prevalent hypertension in European populations. Methods: We analyzed 15 population-based cohorts, participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE). We modeled residential exposure to particulate matter and nitrogen oxides with land use regression using a uniform protocol. We assessed traffic exposure with traffic indicator variables. We analyzed systolic and diastolic BP in participants medicated and nonmedicated with BP-lowering medication (BPLM) separately, adjusting for personal and area-level risk factors and environmental noise. Prevalent hypertension was defined as ≥ 140 mmHg systolic BP, or ≥ 90 mmHg diastolic BP, or intake of BPLM. We combined cohort-specific results using random-effects meta-analysis. Results: In the main meta-analysis of 113,926 participants, traffic load on major roads within 100 m of the residence was associated with increased systolic and diastolic BP in nonmedicated participants [0.35 mmHg (95% CI: 0.02, 0.68) and 0.22 mmHg (95% CI: 0.04, 0.40) per 4,000,000 vehicles × m/day, respectively]. The estimated odds ratio (OR) for prevalent hypertension was 1.05 (95% CI: 0.99, 1.11) per 4,000,000 vehicles × m/day. Modeled air pollutants and BP were not clearly associated. Conclusions: In this first comprehensive meta-analysis of European population-based cohorts, we observed a weak positive association of high residential traffic exposure with BP in nonmedicated participants, and an elevated OR for prevalent hypertension. The relationship of modeled air pollutants with BP was inconsistent. Citation: Fuks KB, Weinmayr G, Foraster M, Dratva J, Hampel R, Houthuijs D, Oftedal B, Oudin A, Panasevich S, Penell J, Sommar JN, Sørensen M, Tittanen P, Wolf K, Xun WW, Aguilera I, Basagaña X, Beelen R, Bots ML, Brunekreef B, Bueno-de-Mesquita HB, Caracciolo B, Cirach M, de Faire U, de Nazelle A, Eeftens M, Elosua R, Erbel R, Forsberg B, Fratiglioni L, Gaspoz JM, Hilding A, Jula A, Korek M, Krämer U, Künzli N, Lanki T, Leander K, Magnusson PK, Marrugat J, Nieuwenhuijsen MJ, Östenson CG, Pedersen NL, Pershagen G, Phuleria HC, Probst-Hensch NM, Raaschou-Nielsen O, Schaffner E, Schikowski T, Schindler C, Schwarze PE, Søgaard AJ, Sugiri D, Swart WJ, Tsai MY, Turunen AW, Vineis P, Peters A, Hoffmann B. 2014. Arterial blood pressure and long-term exposure to traffic-related air pollution: an analysis in the European Study of Cohorts for Air Pollution Effects (ESCAPE). Environ Health Perspect 122:896–905; http://dx.doi.org/10.1289/ehp.1307725

Residential proximity to major roads and term low birth weight: the roles of air pollution, heat, noise, and road-adjacent trees.

Background: Maternal residential proximity to roads has been associated with adverse pregnancy outcomes. However, there is no study investigating mediators or buffering effects of road-adjacent trees on this association. We investigated the association between mothers’ residential proximity to major roads and term low birth weight (LBW), while exploring possible mediating roles of air pollution (PM2.5, PM2.5–10, PM10, PM2.5 absorbance, nitrogen dioxide, and nitrogen oxides), heat, and noise and buffering effect of road-adjacent trees on this association. Methods: This cohort study was based on 6438 singleton term births in Barcelona, Spain (2001–2005). Road proximity was measured as both continuous distance to and living within 200 m from a major road. We assessed individual exposures to air pollution, noise, and heat using, respectively, temporally adjusted land-use regression models, annual averages of 24-hour noise levels across 50 m and 250 m, and average of satellite-derived land-surface temperature in a 50-m buffer around each residential address. We used vegetation continuous fields to abstract tree coverage in a 200-m buffer around major roads. Results: Living within 200 m of major roads was associated with a 46% increase in term LBW risk; an interquartile range increase in heat exposure with an 18% increase; and third-trimester exposure to PM2.5, PM2.5–10, and PM10 with 24%, 25%, and 26% increases, respectively. Air pollution and heat exposures together explained about one-third of the association between residential proximity to major roads and term LBW. Our observations on the buffering of this association by road-adjacent trees were not consistent between our 2 measures of proximity to major roads. Conclusion: An increased risk of term LBW associated with proximity to major roads was partly mediated by air pollution and heat exposures.

Association between Long-Term Exposure to Traffic-Related Air Pollution and Subclinical Atherosclerosis: The REGICOR Study

Background: Epidemiological evidence of the effects of long-term exposure to air pollution on the chronic processes of atherogenesis is limited. Objective: We investigated the association of long-term exposure to traffic-related air pollution with subclinical atherosclerosis, measured by carotid intima media thickness (IMT) and ankle–brachial index (ABI). Methods: We performed a cross-sectional analysis using data collected during the reexamination (2007–2010) of 2,780 participants in the REGICOR (Registre Gironí del Cor: the Gerona Heart Register) study, a population-based prospective cohort in Girona, Spain. Long-term exposure across residences was calculated as the last 10 years’ time-weighted average of residential nitrogen dioxide (NO2) estimates (based on a local-scale land-use regression model), traffic intensity in the nearest street, and traffic intensity in a 100 m buffer. Associations with IMT and ABI were estimated using linear regression and multinomial logistic regression, respectively, controlling for sex, age, smoking status, education, marital status, and several other potential confounders or intermediates. Results: Exposure contrasts between the 5th and 95th percentiles for NO2 (25 µg/m3), traffic intensity in the nearest street (15,000 vehicles/day), and traffic load within 100 m (7,200,000 vehicle-m/day) were associated with differences of 0.56% (95% CI: –1.5, 2.6%), 2.32% (95% CI: 0.48, 4.17%), and 1.91% (95% CI: –0.24, 4.06) percent difference in IMT, respectively. Exposures were positively associated with an ABI of > 1.3, but not an ABI of < 0.9. Stronger associations were observed among those with a high level of education and in men ≥ 60 years of age. Conclusions: Long-term traffic-related exposures were associated with subclinical markers of atherosclerosis. Prospective studies are needed to confirm associations and further examine differences among population subgroups.

High blood pressure and long-term exposure to indoor noise and air pollution from road traffic

Background: Traffic noise has been associated with prevalence of hypertension, but reports are inconsistent for blood pressure (BP). To ascertain noise effects and to disentangle them from those suspected to be from traffic-related air pollution, it may be essential to estimate people’s noise exposure indoors in bedrooms. Objectives: We analyzed associations between long-term exposure to indoor traffic noise in bedrooms and prevalent hypertension and systolic (SBP) and diastolic (DBP) BP, considering long-term exposure to outdoor nitrogen dioxide (NO2). Methods: We evaluated 1,926 cohort participants at baseline (years 2003–2006; Girona, Spain). Outdoor annual average levels of nighttime traffic noise (Lnight) and NO2 were estimated at postal addresses with a detailed traffic noise model and a land-use regression model, respectively. Individual indoor traffic Lnight levels were derived from outdoor Lnight with application of insulations provided by reported noise-reducing factors. We assessed associations for hypertension and BP with multi-exposure logistic and linear regression models, respectively. Results: Median levels were 27.1 dB(A) (indoor Lnight), 56.7 dB(A) (outdoor Lnight), and 26.8 μg/m3 (NO2). Spearman correlations between outdoor and indoor Lnight with NO2 were 0.75 and 0.23, respectively. Indoor Lnight was associated both with hypertension (OR = 1.06; 95% CI: 0.99, 1.13) and SBP (β = 0.72; 95% CI: 0.29, 1.15) per 5 dB(A); and NO2 was associated with hypertension (OR = 1.16; 95% CI: 0.99, 1.36), SBP (β = 1.23; 95% CI: 0.21, 2.25), and DBP (β⊇= 0.56; 95% CI: –0.03, 1.14) per 10 μg/m3. In the outdoor noise model, Lnight was associated only with hypertension and NO2 with BP only. The indoor noise–SBP association was stronger and statistically significant with a threshold at 30 dB(A). Conclusion: Long-term exposure to indoor traffic noise was associated with prevalent hypertension and SBP, independently of NO2. Associations were less consistent for outdoor traffic Lnight and likely affected by collinearity. Citation: Foraster M, Künzli N, Aguilera I, Rivera M, Agis D, Vila J, Bouso L, Deltell A, Marrugat J, Ramos R, Sunyer J, Elosua R, Basagaña X. 2014. High blood pressure and long-term exposure to indoor noise and air pollution from road traffic. Environ Health Perspect 122:1193–1200; http://dx.doi.org/10.1289/ehp.1307156

Association of long-term exposure to traffic-related air pollution with blood pressure and hypertension in an adult population-based cohort in Spain (the REGICOR study).

Background: Long-term exposure to traffic-related air pollution may increase blood pressure (BP) and induce hypertension. However, evidence supporting these associations is limited, and they may be confounded by exposure to traffic noise and biased due to inappropriate control for use of BP-lowering medications. Objectives: We evaluated the associations of long-term traffic-related air pollution with BP and prevalent hypertension, adjusting for transportation noise and assessing different methodologies to control for BP-lowering medications. Methods: We measured systolic (SBP) and diastolic BP (DBP) at baseline (years 2003–2005) in 3,700 participants, 35–83 years of age, from a population-based cohort in Spain. We estimated home outdoor annual average concentrations of nitrogen dioxide (NO2) with a land-use regression model. We used multivariate linear and logistic regression. Results: A 10-μg/m3 increase in NO2 levels was associated with 1.34 mmHg (95% CI: 0.14, 2.55) higher SBP in nonmedicated individuals, after adjusting for transportation noise. Results were similar in the entire population after adjusting for medication, as commonly done, but weaker when other methods were used to account for medication use. For example, when 10 mmHg were added to the measured SBP levels of medicated participants, the association was β = 0.78 (95% CI: –0.43, 2.00). NO2 was not associated with hypertension. Associations of NO2 with SBP and DBP were stronger in participants with cardiovascular disease, and the association with SBP was stronger in those exposed to high traffic density and traffic noise levels ≥ 55 dB(A). Conclusions: We observed a positive association between long-term exposure to NO2 and SBP, after adjustment for transportation noise, which was sensitive to the methodology used to account for medication. Citation: Foraster M, Basagaña X, Aguilera I, Rivera M, Agis D, Bouso L, Deltell A, Marrugat J, Ramos R, Sunyer J, Vila J, Elosua R, Künzli N. 2014. Association of long-term exposure to traffic-related air pollution with blood pressure and hypertension in an adult population–based cohort in Spain (the REGICOR study). Environ Health Perspect 122:404–411; http://dx.doi.org/10.1289/ehp.1306497

Measurement Error in Epidemiologic Studies of Air Pollution Based on Land-Use Regression Models

Land-use regression (LUR) models are increasingly used to estimate air pollution exposure in epidemiologic studies. These models use air pollution measurements taken at a small set of locations and modeling based on geographical covariates for which data are available at all study participant locations. The process of LUR model development commonly includes a variable selection procedure. When LUR model predictions are used as explanatory variables in a model for a health outcome, measurement error can lead to bias of the regression coefficients and to inflation of their variance. In previous studies dealing with spatial predictions of air pollution, bias was shown to be small while most of the effect of measurement error was on the variance. In this study, we show that in realistic cases where LUR models are applied to health data, bias in health-effect estimates can be substantial. This bias depends on the number of air pollution measurement sites, the number of available predictors for model selection, and the amount of explainable variability in the true exposure. These results should be taken into account when interpreting health effects from studies that used LUR models.

Urban and transport planning related exposures and mortality : a health impact assessment for cities

Background: By 2050, nearly 70% of the global population is projected to live in urban areas. Because the environments we inhabit affect our health, urban and transport designs that promote healthy living are needed. Objective: We estimated the number of premature deaths preventable under compliance with international exposure recommendations for physical activity (PA), air pollution, noise, heat, and access to green spaces. Methods: We developed and applied the Urban and TranspOrt Planning Health Impact Assessment (UTOPHIA) tool to Barcelona, Spain. Exposure estimates and mortality data were available for 1,357,361 residents. We compared recommended with current exposure levels. We quantified the associations between exposures and mortality and calculated population attributable fractions to estimate the number of premature deaths preventable. We also modeled life-expectancy and economic impacts. Results: We estimated that annually, nearly 20% of mortality could be prevented if international recommendations for performance of PA; exposure to air pollution, noise, and heat; and access to green space were followed. Estimations showed that the greatest portion of preventable deaths was attributable to increases in PA, followed by reductions of exposure to air pollution, traffic noise, and heat. Access to green spaces had smaller effects on mortality. Compliance was estimated to increase the average life expectancy by 360 (95% CI: 219, 493) days and result in economic savings of 9.3 (95% CI: 4.9, 13.2) billion EUR/year. Conclusions: PA factors and environmental exposures can be modified by changes in urban and transport planning. We emphasize the need for a) the reduction of motorized traffic through the promotion of active and public transport and b) the provision of green infrastructure, both of which are suggested to provide opportunities for PA and for mitigation of air pollution, noise, and heat. Citation: Mueller N, Rojas-Rueda D, Basagaña X, Cirach M, Cole-Hunter T, Dadvand P, Donaire-Gonzalez D, Foraster M, Gascon M, Martinez D, Tonne C, Triguero-Mas M, Valentín A, Nieuwenhuijsen M. 2017. Urban and transport planning related exposures and mortality: a health impact assessment for cities. Environ Health Perspect 125:89–96; http://dx.doi.org/10.1289/EHP220