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Background: The association between air pollution exposure and emotional and behavioural problems in children is unclear. We aimed to assess prenatal and postnatal exposure to several air pollutants and child's depressive and anxiety symptoms, and aggressive symptoms in children of 7-11 years. Methods: We analysed data of 13182 children from 8 European population-based birth cohorts. Concentrations of nitrogen dioxide (NO2), nitrogen oxides (NOx), particulate matter (PM) with diameters of

Evidence for the effects of air pollution exposure on lung function growth into adolescence is scarce. We investigated associations of air pollution exposure with lung function and lung function growth until age 16.We conducted both longitudinal (n=915) and cross-sectional (n=721) analyses of associations of air pollution exposure with forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) growth from ages eight to 16 and FEV1 and FVC at age 16. We estimated residential concentrations of nitrogen dioxide (NO2), “soot” and particulate matter (PMx, where x is the 50% cut-off aerodynamic diameter in µm) with diameters of 2.5), 10) and 2.5–10 µm (PMcoarse) during the preschool, primary school and secondary school time windows by land use regression models. Associations with (growth in) FEV1 and FVC were analysed by linear (mixed effects) regression.Higher air pollution exposure was associated with reduced FEV1 growth (e.g. adjusted difference −0.26% (95% CI −0.49 to −0.03%) per interquartile range increase in secondary school PM2.5) and lower FEV1 (adjusted difference −2.36% (95% CI −3.76 to −0.94%)), but was not adversely associated with FVC. Associations with FEV1 were stronger in boys than girls and were not modified by asthma status.Higher air pollution exposure may lead to increased airway obstruction, but not reduced lung volume in adolescence.

Background Air pollution has been found to adversely affect children’s lung function. Forced expiratory volume in 1 s and forced vital capacity from spirometry have been studied most frequently, but measurements of airway resistance may provide additional information. We assessed associations of long-term air pollution exposure with airway resistance. Methods We measured airway resistance at age 8 with the interrupter resistance technique (Rint) in participants of the Dutch PIAMA birth cohort study. We linked Rint with estimated annual average air pollution concentrations [nitrogen oxides (NO2, NOx), PM2.5 absorbance (“soot”), and particulate matter

BACKGROUND: Land use regression (LUR) models are commonly used in environmental epidemiology to assign spatially resolved estimates of air pollution to study participants. In this setting, estimated LUR model parameters are assumed to be transportable to a main study (the ''transportability assumption''). We provide an empirical illustration of how violation of this assumption can affect exposure predictions and bias health-effect estimates. METHODS: We based our simulation on two existing LUR models, one for nitrogen dioxide, the other for particulate matter with aerodynamic diameter

Aims: Elevation of a child's blood pressure may cause possible health risks in later life. There is evidence for adverse effects of exposure to air pollution and noise on blood pressure in adults. Little is known about these associations in children. We investigated the associations of air pollution and noise exposure with blood pressure in 12-year-olds. Methods: Blood pressure was measured at age 12 years in 1432 participants of the PIAMA birth cohort study. Annual average exposure to traffic-related air pollution [NO2, mass concentrations of particulate matter with diameters of less than 2.5 μm (PM2.5) and less than 10 μm (PM10), and PM2.5 absorbance] at the participants' home and school addresses at the time of blood pressure measurements was estimated by land-use regression models. Air pollution exposure on the days preceding blood pressure measurements was estimated from routine air monitoring data. Long-term noise exposure was assessed by linking addresses to modelled equivalent road traffic noise levels. Associations of exposures with blood pressure were analysed by linear regression. Effects are presented for an interquartile range increase in exposure. Results: Long-term exposure to NO2 and PM2.5 absorbance were associated with increased diastolic blood pressure, in children who lived at the same address since birth [adjusted mean difference (95% confidence interval) [mmHg] 0.83 (0.06 to 1.61) and 0.75 (-0.08 to 1.58), respectively], but not with systolic blood pressure. We found no association of blood pressure with short-term air pollution or noise exposure. Conclusions: Long-term exposure to traffic-related air pollution may increase diastolic blood pressure in children.

BACKGROUND: Epidemiological evidence on the association between ambient air pollution and breast cancer risk is inconsistent. OBJECTIVE: We examined the association between long-term exposure to ambient air pollution and incidence of postmenopausal breast cancer in European women. METHODS: In 15 cohorts from nine European countries, individual estimates of air pollution levels at the residence were estimated by standardized land-use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE) and Transport related Air Pollution and Health impacts - Integrated Methodologies for Assessing Particulate Matter (TRANSPHORM) projects: particulate matter (PM) ≤2:5 μm, ≤10 μm, and 2:5–10 μm in diameter (PM2:5, PM10, and PMcoarse, respectively); PM2:5 absorbance; nitrogen oxides (NO2 and NOx); traffic intensity; and elemental composition of PM. We estimated cohort-specific associations between breast cancer and air pollutants using Cox regression models, adjusting for major lifestyle risk factors, and pooled cohort-specific estimates using random-effects meta-analyses. RESULTS: Of 74,750 postmenopausal women included in the study, 3,612 developed breast cancer during 991,353 person-years of follow-up. We found positive and statistically insignificant associations between breast cancer and PM2:5 {hazard ratio (HR) =1:08 [95% confidence interval (CI): 0.77, 1.51] per 5 μg/m3 }, PM10 [1.07 (95% CI: 0.89, 1.30) per 10 μg/m3 ], PMcoarse [1.20 (95% CI: 0.96, 1.49 per 5 μg/m3 ], and NO2 [1.02 (95% CI: 0.98, 1.07 per 10 μg/m3 ], and a statistically significant association with NOx [1.04 (95% CI: 1.00, 1.08) per 20 μg/m3, p =0:04]. CONCLUSIONS: We found suggestive evidence of an association between ambient air pollution and incidence of postmenopausal breast cancer in European women. © 2017, Public Health Services, US Dept of Health and Human Services. All rights reserved. Chemicals/CAS: copper, 15158-11-9, 7440-50-8; iron, 14093-02-8, 53858-86-9, 7439-89-6; nickel, 7440-02-0; nitrogen oxide, 11104-93-1; potassium, 7440-09-7; silicon, 7440-21-3; sulfur, 13981-57-2, 7704-34-9; vanadium, 7440-62-2; zinc, 7440-66-6, 14378-32-6

Long-term ultrafine particle (UFP) exposure estimates at a fine spatial scale are needed for epidemiological studies. Land use regression (LUR) models were developed and evaluated for six European areas based on repeated 30 min monitoring following standardized protocols. In each area; Basel (Switzerland), Heraklion (Greece), Amsterdam, Maastricht, and Utrecht ("The Netherlands"), Norwich (United Kingdom), Sabadell (Spain), and Turin (Italy), 160-240 sites were monitored to develop LUR models by supervised stepwise selection of GIS predictors. For each area and all areas combined, 10 models were developed in stratified random selections of 90% of sites. UFP prediction robustness was evaluated with the intraclass correlation coefficient (ICC) at 31-50 external sites per area. Models from Basel and The Netherlands were validated against repeated 24 h outdoor measurements. Structure and model R2 of local models were similar within, but varied between areas (e.g., 38-43% Turin; 25-31% Sabadell). Robustness of predictions within areas was high (ICC 0.73-0.98). External validation R2 was 53% in Basel and 50% in The Netherlands. Combined area models were robust (ICC 0.93-1.00) and explained UFP variation almost equally well as local models. In conclusion, robust UFP LUR models could be developed on short-term monitoring, explaining around 50% of spatial variance in longer-term measurements.

Several studies have indicated weakly increased risk for kidney cancer among occupational groups exposed to gasoline vapors, engine exhaust, polycyclic aromatic hydrocarbons and other air pollutants, although not consistently. It was the aim to investigate possible associations between outdoor air pollution at the residence and the incidence of kidney parenchyma cancer in the general population. We used data from 14 European cohorts from the ESCAPE study. We geocoded and assessed air pollution concentrations at baseline addresses by land-use regression models for particulate matter (PM10 , PM2.5 , PMcoarse , PM2.5 absorbance (soot)) and nitrogen oxides (NO2 , NOx ), and collected data on traffic. We used Cox regression models with adjustment for potential confounders for cohort-specific analyses and random effects models for meta-analyses to calculate summary hazard ratios (HRs). The 289,002 cohort members contributed 4,111,908 person-years at risk. During follow-up (mean 14.2 years) 697 incident cancers of the kidney parenchyma were diagnosed. The meta-analyses showed higher HRs in association with higher PM concentration, e.g. HR=1.57 (95%CI: 0.81-3.01) per 5μg/m(3) PM2.5 and HR=1.36 (95%CI: 0.84-2.19) per 10(-5) m(-1) PM2.5 absorbance, albeit never statistically significant. The HRs in association with nitrogen oxides and traffic density on the nearest street were slightly above one. Sensitivity analyses among participants who did not change residence during follow-up showed stronger associations, but none were statistically significant. This study provides suggestive evidence that exposure to outdoor PM at the residence may be associated with higher risk for kidney parenchyma cancer; the results should be interpreted cautiously as associations may be due to chance. This article is protected by copyright. All rights reserved.

BACKGROUND: Few studies on long-term exposure to air pollution and mortality have been reported from Europe. Within the multicentre European Study of Cohorts for Air Pollution Effects (ESCAPE), we aimed to investigate the association between natural-cause mortality and long-term exposure to several air pollutants. METHODS: We used data from 22 European cohort studies, which created a total study population of 367,251 participants. All cohorts were general population samples, although some were restricted to one sex only. With a strictly standardised protocol, we assessed residential exposure to air pollutants as annual average concentrations of particulate matter (PM) with diameters of less than 2.5 μm (PM2.5), less than 10 μm (PM10), and between 10 μm and 2.5 μm (PMcoarse), PM2.5 absorbance, and annual average concentrations of nitrogen oxides (NO2 and NOx), with land use regression models. We also investigated two traffic intensity variables-traffic intensity on the nearest road (vehicles per day) and total traffic load on all major roads within a 100 m buffer. We did cohort-specific statistical analyses using confounder models with increasing adjustment for confounder variables, and Cox proportional hazards models with a common protocol. We obtained pooled effect estimates through a random-effects meta-analysis. FINDINGS: The total study population consisted of 367,251 participants who contributed 5,118,039 person-years at risk (average follow-up 13.9 years), of whom 29,076 died from a natural cause during follow-up. A significantly increased hazard ratio (HR) for PM2.5 of 1.07 (95% CI 1.02-1.13) per 5 μg/m(3) was recorded. No heterogeneity was noted between individual cohort effect estimates (I(2) p value=0.95). HRs for PM2.5 remained significantly raised even when we included only participants exposed to pollutant concentrations lower than the European annual mean limit value of 25 μg/m(3) (HR 1.06, 95% CI 1.00-1.12) or below 20 μg/m(3) (1.07, 1.01-1.13). INTERPRETATION: Long-term exposure to fine particulate air pollution was associated with natural-cause mortality, even within concentration ranges well below the present European annual mean limit value. FUNDING: European Community's Seventh Framework Program (FP7/2007-2011).

Background: There is evidence for adverse effects of outdoor air pollution on lung function of children. Quantitative summaries of the effects of air pollution on lung function, however, are lacking due to large differences among studies. Objectives: We aimed to study the association between residential exposure to air pollution and lung function in five European birth cohorts with a standardized exposure assessment following a common protocol. Methods: As part of the European Study of Cohorts for Air Pollution Effects (ESCAPE) we analyzed data from birth cohort studies situated in Germany, Sweden, the Netherlands, and the United Kingdom that measured lung function at 6–8 years of age (n = 5,921). Annual average exposure to air pollution [nitrogen oxides (NO2, NOx), mass concentrations of particulate matter with diameters < 2.5, < 10, and 2.5–10 μm (PM2.5, PM10, and PMcoarse), and PM2.5 absorbance] at the birth address and current address was estimated by land-use regression models. Associations of lung function with estimated air pollution levels and traffic indicators were estimated for each cohort using linear regression analysis, and then combined by random effects meta-analysis. Results: Estimated levels of NO2, NOx, PM2.5 absorbance, and PM2.5 at the current address, but not at the birth address, were associated with small decreases in lung function. For example, changes in forced expiratory volume in 1 sec (FEV1) ranged from –0.86% (95% CI: –1.48, –0.24%) for a 20-μg/m3 increase in NOx to –1.77% (95% CI: –3.34, –0.18%) for a 5-μg/m3 increase in PM2.5. Conclusions: Exposure to air pollution may result in reduced lung function in schoolchildren. Citation: Gehring U, Gruzieva O, Agius RM, Beelen R, Custovic A, Cyrys J, Eeftens M, Flexeder C, Fuertes E, Heinrich J, Hoffmann B, de Jongste JC, Kerkhof M, Klümper C, Korek M, Mölter A, Schultz ES, Simpson A, Sugiri D, Svartengren M, von Berg A, Wijga AH, Pershagen G, Brunekreef B. 2013. Air pollution exposure and lung function in children: the ESCAPE project. Environ Health Perspect 121:1357–1364; http://dx.doi.org/10.1289/ehp.1306770

Background: Few studies have examined the link between air pollution exposure and behavioural problems and learning disorders during late childhood and adolescence. Objectives: To determine whether traffic-related air pollution exposure is associated with hyperactivity/inattention, dyslexia and dyscalculia up to age 15 years using the German GINIplus and LISAplus birth cohorts (recruitment 1995–1999). Methods: Hyperactivity/inattention was assessed using the German parent-completed (10 years) and self-completed (15 years) Strengths and Difficulties Questionnaire. Responses were categorized into normal versus borderline/abnormal. Parent-reported dyslexia and dyscalculia (yes/no) at age 10 and 15 years were defined using parent-completed questionnaires. Individual-level annual average estimates of nitrogen dioxide (NO2), particulate matter (PM)10 mass, PM2.5 mass and PM2.5 absorbance concentrations were assigned to each participant's birth, 10 year and 15 year home address. Longitudinal associations between the air pollutants and the neurodevelopmental outcomes were assessed using generalized estimation equations, separately for both study areas, and combined in a random-effects meta-analysis. Odds ratios and 95% confidence intervals are given per interquartile range increase in pollutant concentration. Results: The prevalence of abnormal/borderline hyperactivity/inattention scores and parental-reported dyslexia and dyscalculia at 15 years of age was 12.9%, 10.5% and 3.4%, respectively, in the combined population (N = 4745). In the meta- analysis, hyperactivity/inattention was associated with PM2.5 mass estimated to the 10 and 15 year addresses (1.12 [1.01, 1.23] and 1.11 [1.01, 1.22]) and PM2.5 absorbance estimated to the 10 and 15 year addresses (1.14 [1.05, 1.25] and 1.13 [1.04, 1.23], respectively). Conclusions: We report associations suggesting a potential link between air pollution exposure and hyperactivity/inattention scores, although these findings require replication. Keywords: Adolescents, Air pollution, Hyperactivity, Inattention, Neurodevelopment

Background Land Use Regression (LUR) is a popular method to explain and predict spatial contrasts in air pollution concentrations, but LUR models for ultrafine particles, such as particle number concentration (PNC) are especially scarce. Moreover, no models have been previously presented for the lung deposited surface area (LDSA) of ultrafine particles. The additional value of ultrafine particle metrics has not been well investigated due to lack of exposure measurements and models. Methods Air pollution measurements were performed in 2011 and 2012 in the eight areas of the Swiss SAPALDIA study at up to 40 sites per area for NO2 and at 20 sites in four areas for markers of particulate air pollution. We developed multi-area LUR models for biannual average concentrations of PM2.5, PM2.5 absorbance, PM10, PMcoarse, PNC and LDSA, as well as alpine, non-alpine and study area specific models for NO2, using predictor variables which were available at a national level. Models were validated using leave-one-out cross-validation, as well as independent external validation with routine monitoring data. Results Model explained variance (R2) was moderate for the various PM mass fractions PM2.5 (0.57), PM10 (0.63) and PMcoarse (0.45), and was high for PM2.5 absorbance (0.81), PNC (0.87) and LDSA (0.91). Study-area specific LUR models for NO2 (R2 range 0.52–0.89) outperformed combined-area alpine (R2 = 0.53) and non-alpine (R2 = 0.65) models in terms of both cross-validation and independent external validation, and were better able to account for between-area variability. Predictor variables related to traffic and national dispersion model estimates were important predictors. Conclusions LUR models for all pollutants captured spatial variability of long-term average concentrations, performed adequately in validation, and could be successfully applied to the SAPALDIA cohort. Dispersion model predictions or area indicators served well to capture the between area variance. For NO2, applying study-area specific models was preferable over applying combined-area alpine/non-alpine models. Correlations between pollutants were higher in the model predictions than in the measurements, so it will remain challenging to disentangle their health effects. Electronic supplementary material The online version of this article (doi:10.1186/s12940-016-0137-9) contains supplementary material, which is available to authorized users.

Background: Particulate matter (PM) air pollution is a human lung carcinogen; however, the components responsible have not been identified. We assessed the associations between PM components and lung cancer incidence. Methods: We used data from 14 cohort studies in eight European countries. We geocoded baseline addresses and assessed air pollution with land-use regression models for eight elements (Cu, Fe, K, Ni, S, Si, V and Zn) in size fractions of PM2.5 and PM10. We used Cox regression models with adjustment for potential confounders for cohort-specific analyses and random effect models for meta-analysis. Results: The 245,782 cohort members contributed 3,229,220 person–years at risk. During follow-up (mean, 13.1 years), 1878 incident cases of lung cancer were diagnosed. In the meta-analyses, elevated hazard ratios (HRs) for lung cancer were associated with all elements except V; none was statistically significant. In analyses restricted to participants who did not change residence during follow-up, statistically significant associations were found for PM2.5 Cu (HR, 1.25; 95% CI, 1.01–1.53 per 5 ng/m3), PM10 Zn (1.28; 1.02–1.59 per 20 ng/m3), PM10 S (1.58; 1.03–2.44 per 200 ng/m3), PM10 Ni (1.59; 1.12–2.26 per 2 ng/m3) and PM10 K (1.17; 1.02–1.33 per 100 ng/m3). In two-pollutant models, associations between PM10 and PM2.5 and lung cancer were largely explained by PM2.5 S. Conclusions: This study indicates that the association between PM in air pollution and lung cancer can be attributed to various PM components and sources. PM containing S and Ni might be particularly important. Keywords: Air pollution, Particulate matter, Sulfur, Nickel, Cohort study, Lung cancer

Summary Background Previous published analyses have focused on the effect of air pollution on asthma and rhinoconjunctivitis throughout early and middle childhood. However, the role of exposure to air pollution in the development of childhood and adolescent asthma and rhinoconjunctivitis remains unclear. We aimed to assess the longitudinal associations between exposure to air pollution and development of asthma and rhinoconjunctivitis throughout childhood and adolescence. Methods We did a population-based birth cohort study of 14 126 participants from four prospective birth cohort studies from Germany, Sweden, and the Netherlands with 14–16 years of follow-up. We linked repeated questionnaire reports of asthma and rhinoconjunctivitis with annual average air pollution concentrations (nitrogen dioxide [NO 2 ], particulate matter [PM] with a diameter of less than 2·5 μm [PM 2·5 ], less than 10 μm [PM 10 ], and between 2·5 μm and 10 μm [PM coarse ], and PM 2·5 absorbance [indicator of soot]) at the participants' home addresses. We analysed longitudinal associations of air pollution exposure at participants' birth addresses and addresses at the time of follow-up with asthma and rhinoconjunctivitis incidence and prevalence in cohort-specific analyses, with subsequent meta-analysis and pooled analyses. Findings Overall, the risk of incident asthma up to age 14–16 years increased with increasing exposure to NO 2 (adjusted meta-analysis odds ratio [OR] 1·13 per 10 μg/m 3 [95% CI 1·02–1·25]) and PM 2·5 absorbance (1·29 per 1 unit [1·00–1·66]) at the birth address. A similar, albeit non-significant, trend was shown for PM 2·5 and incident asthma (meta-analysis OR 1·25 per 5 μg/m 3 [95% CI 0·94–1·66]). These associations with asthma were more consistent after age 4 years than before that age. There was no indication of an adverse effect of air pollution on rhinoconjunctivitis. Interpretation Exposure to air pollution early in life might contribute to the development of asthma throughout childhood and adolescence, particularly after age 4 years, when asthma can be more reliably diagnosed. Reductions in levels of air pollution could help to prevent the development of asthma in children. Funding The European Union.

Background: Childhood blood pressure is an important predictor of hypertension and cardiovascular disease in adulthood. Evidence for an association between ambient particulate matter (PM) exposure and blood pressure is increasing, but little is known about the relevance of different PM constituents. Objectives: We investigated the association between particulate matter composition and blood pressure at age 12 years. Methods: Annual average concentrations of copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc in particles with diameters of less than 2.5 μm (PM2.5) and 10 μm (PM10) were estimated by land-use regression modeling for the home addresses of the participants of the prospective PIAMA birth cohort study. Associations between element concentrations and blood pressure measurements performed at age 12 years were investigated by linear regression with and without adjustment for confounders. Results: After adjustment for potential confounders we found statistically significant positive associations of diastolic blood pressure with iron, silicon, and potassium in PM10 in children who lived at the same address since birth [mean difference (95% confidence interval) 0.67 (0.02;1.31) mm Hg, 0.85 (0.18;1.52) mm Hg, and 0.75 (0.09;1.41) mm Hg, respectively, per interquartile range increase in exposure]. Also, we found marginally significant (p

The chronic impact of ambient air pollutants on lung function in adults is not fully understood. The objective of this study was to investigate the association of long-term exposure to ambient air pollution with lung function in adult participants from five cohorts in the European Study of Cohorts for Air Pollution Effects (ESCAPE).Residential exposure to nitrogen oxides (NO2, NOx) and particulate matter (PM) was modelled and traffic indicators were assessed in a standardised manner. The spirometric parameters forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) from 7613 subjects were considered as outcomes. Cohort-specific results were combined using meta-analysis.We did not observe an association of air pollution with longitudinal change in lung function, but we observed that a 10 μg·m−3 increase in NO2 exposure was associated with lower levels of FEV1 (−14.0 mL, 95% CI −25.8 to −2.1) and FVC (−14.9 mL, 95% CI −28.7 to −1.1). An increase of 10 μg·m−3 in PM10, but not other PM metrics (PM2.5, coarse fraction of PM, PM absorbance), was associated with a lower level of FEV1 (−44.6 mL, 95% CI −85.4 to −3.8) and FVC (−59.0 mL, 95% CI −112.3 to −5.6). The associations were particularly strong in obese persons.This study adds to the evidence for an adverse association of ambient air pollution with lung function in adults at very low levels in Europe.

Background: ambient particulate matter (PM) exposure is associated with children's respiratory health. little is known about the importance of different PM constituents. We investigated the effects of PM constituents on asthma, allergy, and lung function until the age of 11-12 years. Methods: For 3,702 participants of a prospective birth cohort study, questionnaire-reported asthma and hay fever and measurements of allergic sensitization and lung function were linked with annual average concentrations of copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc in particles with diameters of less than 2.5 and 10 μm (PM2.5 and PM10) at birth addresses and current addresses from land-use regression models. exposure-health relations were analyzed by multiple (repeated measures) logistic and linear regressions. Results: asthma incidence and prevalence of asthma symptoms and rhinitis were positively associated with zinc in PM10 at the birth address (odds ratio [95% confidence interval] per interquartile range increase in exposure 1.13 [1.02, 1.25], 1.08 [1.00, 1.17], and 1.16 [1.04, 1.30], respectively). Moreover, asthma symptoms were positively associated with copper in PM10 at the current address (1.06 [1.00, 1.12]). allergic sensitization was positively associated with copper and iron in PM10 at the birth address (relative risk [95% con-fidence interval] 1.07 [1.01, 1.14] and 1.10 [1.03, 1.18]) and current address. Forced expiratory volume in 1 second was negatively associated with copper and iron in PM2.5 (change [95% confidence interval]-2.1% [-1.1,-0.1%] and-1.0% [-2.0,-0.0%]) and FeF75-50 with copper in PM10 at the current address (-2.3% [-4.3,-0.3%]). Conclusion: PM constituents, in particular iron, copper, and zinc, reflecting poorly regulated non-tailpipe road traffic emissions, may increase the risk of asthma and allergy in schoolchildren.

Emerging evidence indicates that near-roadway pollution (NRP) in ambient air has adverse health effects. However, specific components of the NRP mixture responsible for these effects have not been established. A major limitation for health studies is the lack of exposure models that estimate NRP components observed in epidemiological studies over fine spatial scale of tens to hundreds of meters. In this study, exposure models were developed for fine-scale variation in biologically relevant elemental carbon (EC). Measurements of particulate matter (PM) and EC less than 2.5 mu m in aerodynamic diameter (EC2.5) and of PM and EC of nanoscale size less than 0.2 mu m were made at up to 29 locations in each of eight Southern California Children's Health Study communities. Regression-based prediction models were developed using a guided forward selection process to identify traffic variables and other pollutant sources, community physical characteristics and land use as predictors of PM and EC variation in each community. A combined eight-community model including only CALINE4 near-roadway dispersion-estimated vehicular emissions accounting for distance, distance-weighted traffic volume, and meteorology, explained 51% of the EC0.2 variability. Community-specific models identified additional predictors in some communities; however, in most communities the correlation between predicted concentrations from the eight-community model and observed concentrations stratified by community was similar to those for the community-specific models. EC2.5 could be predicted as well as EC0.2. EC2.5 estimated from CALINE4 and population density explained 53% of the within-community variation. Exposure prediction was further improved after accounting for between-community heterogeneity of CALINE4 effects associated with average distance to Pacific Ocean shoreline (to 61% for EC0.2) and for regional NOx pollution (to 57% for EC2.5). PM fine spatial scale variation was poorly predicted in both size fractions. In conclusion, models of exposure that include traffic measures such as C.ALINE4 can provide useful estimates for EC0.2 and EC2.5 on a spatial scale appropriate for health studies of NRP in selected Southern California communities. (C) 2013 Elsevier Ltd. All rights reserved.

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.

Background: Evidence on the long-term effects of air pollution exposure on childhood allergy is limited.Objective: We investigated the association between air pollution exposure and allergic sensitization to common allergens in children followed prospectively during the first 10 years of life.Methods: Five European birth cohorts participating in the European Study of Cohorts for Air Pollution Effects project were included: BAMSE (Sweden), LISAplus and GINIplus (Germany), MAAS (Great Britain), and PIAMA (The Netherlands). Land-use regression models were applied to assess the individual residential outdoor levels of particulate matter with an aerodynamic diameter of less than 2.5 mm (PM2.5), the mass concentration of particles between 2.5 and 10 mm in size, and levels of particulate matter with an aerodynamic diameter of less than 10 mm (PM10), as well as measurement of the blackness of PM2.5 filters and nitrogendioxide and nitrogen oxide levels. Blood samples drawn at 4 to 6 years of age, 8 to 10 years of age, or both from more than 6500 children were analyzed for allergen-specific serum IgE against common allergens. Associations were assessed by using multiple logistic regression and subsequent meta-analysis.Results: The prevalence of sensitization to any common allergen within the 5 cohorts ranged between 24.1% and 40.4% at the age of 4 to 6 years and between 34.8% and 47.9% at the age of 8 to 10 years. Overall, air pollution exposure was not associated with sensitization to any common allergen, with odds ratios ranging from 0.94 (95% CI, 0.63-1.40) for a 1 x 10(-5) . m(-1) increase in measurement of the blackness of PM2.5 filters to 1.26 (95% CI, 0.90-1.77) for a 5 mu g/m(3) increase in PM2.5 exposure at birth address. Further analyses did not provide consistent evidence for a modification of the air pollution effects by sex, family history of atopy, or moving status.Conclusion: No clear associations between air pollution exposure and development of allergic sensitization in children up to 10 years of age were revealed.

Rationale: Prospective cohort studies have shown that chronic exposure to particulate matter and traffic-related air pollution is associated with reduced survival. However, the effects on nonmalignant respiratory mortality are less studied, and the data reported are less consistent. Objectives: We have investigated the relationship of long-term exposure to air pollution and nonmalignant respiratory mortality in 16 cohorts with individual level data within the multicenter European Study of Cohorts for Air Pollution Effects (ESCAPE). Methods: Data from 16 ongoing cohort studies from Europe were used. The total number of subjects was 307,553. There were 1,559 respiratory deaths during follow-up. Measurements and Main Results: Air pollution exposure was estimated by land use regression models at the baseline residential addresses of study participants and traffic-proximity variables were derived from geographical databases following a standardized procedure within, the ESCAPE study. Cohort-specific hazard ratios obtained by Cox proportional hazard models from standardized individual cohort analyses were combined using metaanalyses. We found no significant associations between air pollution exposure and nonmalignant respiratory mortality. Most hazard ratios were slightly below unity, with the exception of the traffic-proximity indicators. Conclusions: In this study of 16 cohorts, there was no-association between air pollution exposure and nonmalignant respiratory mortality.

BACKGROUND: A recent meta-analysis suggested evidence for an effect of exposure to ambient air pollutants on risk of certain congenital heart defects. However, few studies have investigated the effects of traffic-related air pollutants with sufficient spatial accuracy. OBJECTIVES: We estimated associations between congenital anomalies and exposure to traffic-related air pollution in Barcelona, Spain. METHOD: Cases with nonchromosomal anomalies (n = 2,247) and controls (n = 2,991) were selected from the Barcelona congenital anomaly register during 1994-2006. Land use regression models from the European Study of Cohorts for Air Pollution Effects (ESCAPE), were applied to residential addresses at birth to estimate spatial exposure to nitrogen oxides and dioxide (NOx, NO2), particulate matter with diameter ≤ 10 μm (PM10), 10-2.5 μm (PMcoarse), ≤ 2.5 μm (PM2.5), and PM2.5 absorbance. Spatial estimates were adjusted for temporal trends using data from routine monitoring stations for weeks 3-8 of each pregnancy. Logistic regression models were used to calculate odds ratios (ORs) for 18 congenital anomaly groups associated with an interquartile-range (IQR) increase in exposure estimates. RESULTS: In spatial and spatiotemporal exposure models, we estimated statistically significant associations between an IQR increase in NO2 (12.2 μg/m3) and coarctation of the aorta (ORspatiotemporal = 1.15; 95% CI: 1.01, 1.31) and digestive system defects (ORspatiotemporal = 1.11; 95% CI: 1.00, 1.23), and between an IQR increase in PMcoarse (3.6 μg/m3) and abdominal wall defects (ORspatiotemporal = 1.93; 95% CI: 1.37, 2.73). Other statistically significant increased and decreased ORs were estimated based on the spatial model only or the spatiotemporal model only, but not both. CONCLUSIONS: Our results overall do not indicate an association between traffic-related air pollution and most groups of congenital anomalies. Findings for coarctation of the aorta are consistent with those of the previous meta-analysis. This work was jointly supported by the EUROCAT (European Surveillance of Congenital Anomalies) Joint Action, funded by the Public Health Programme 2008–2013 of the European Commission (grant agreement 20102204); the ARIBA (Air Pollution and Pregnancy in Barcelona) project, funded by a Fondo de Investigación Sanitaria (FIS) (grant agreement PI081109); and by the ESCAPE (European Study of Cohorts for Air Pollution Effects) project, funded under the European Union’s Seventh Framework Programme (grant agreement 211250). A.S. is funded by an Instituto de Salud Carlos III-FEDER fellowship (PFIS grant FI 10/00476). P.D. is funded by a Ramón y Cajal fellowship (RYC-2012-10995) awarded by the Spanish Ministry of Economy and Finance.

Background: Few studies have investigated effects of air pollution on the incidence of cerebrovascular events. Objectives: We assessed the association between long-term exposure to multiple air pollutants and the incidence of stroke in European cohorts. Methods: Data from 11 cohorts were collected, and occurrence of a first stroke was evaluated. Individual air pollution exposures were predicted from land-use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE). The exposures were: PM2.5 [particulate matter (PM) ≤ 2.5 μm in diameter], coarse PM (PM between 2.5 and 10 μm), PM10 (PM ≤ 10 μm), PM2.5 absorbance, nitrogen oxides, and two traffic indicators. Cohort-specific analyses were conducted using Cox proportional hazards models. Random-effects meta-analysis was used for pooled effect estimation. Results: A total of 99,446 study participants were included, 3,086 of whom developed stroke. A 5-μg/m3 increase in annual PM2.5 exposure was associated with 19% increased risk of incident stroke [hazard ratio (HR) = 1.19, 95% CI: 0.88, 1.62]. Similar findings were obtained for PM10. The results were robust to adjustment for an extensive list of cardiovascular risk factors and noise coexposure. The association with PM2.5 was apparent among those ≥ 60 years of age (HR = 1.40, 95% CI: 1.05, 1.87), among never-smokers (HR = 1.74, 95% CI: 1.06, 2.88), and among participants with PM2.5 exposure < 25 μg/m3 (HR = 1.33, 95% CI: 1.01, 1.77). Conclusions: We found suggestive evidence of an association between fine particles and incidence of cerebrovascular events in Europe, even at lower concentrations than set by the current air quality limit value. Citation: Stafoggia M, Cesaroni G, Peters A, Andersen ZJ, Badaloni C, Beelen R, Caracciolo B, Cyrys J, de Faire U, de Hoogh K, Eriksen KT, Fratiglioni L, Galassi C, Gigante B, Havulinna AS, Hennig F, Hilding A, Hoek G, Hoffmann B, Houthuijs D, Korek M, Lanki T, Leander K, Magnusson PK, Meisinger C, Migliore E, Overvad K, Östenson CG, Pedersen NL, Pekkanen J, Penell J, Pershagen G, Pundt N, Pyko A, Raaschou-Nielsen O, Ranzi A, Ricceri F, Sacerdote C, Swart WJ, Turunen AW, Vineis P, Weimar C, Weinmayr G, Wolf K, Brunekreef B, Forastiere F. 2014. Long-term exposure to ambient air pollution and incidence of cerebrovascular events: results from 11 European cohorts within the ESCAPE project. Environ Health Perspect 122:919–925; http://dx.doi.org/10.1289/ehp.1307301

Evidence for a role of long-term particulate matter exposure on acute respiratory infections is growing. However, which components of particulate matter may be causative remains largely unknown. We assessed associations between eight particulate matter elements and early-life pneumonia in seven birth cohort studies (Ntotal = 15,980): BAMSE (Sweden), GASPII (Italy), GINIplus and LISAplus (Germany), INMA (Spain), MAAS (United Kingdom) and PIAMA (The Netherlands). Annual average exposure to copper, iron, potassium, nickel, sulfur, silicon, vanadium and zinc, each respectively derived from particles with aerodynamic diameters ≤ 10 μm (PM10) and 2.5 μm (PM2.5), were estimated using standardized land use regression models and assigned to birth addresses. Cohort-specific associations between these exposures and parental reports of physician-diagnosed pneumonia between birth and two years were assessed using logistic regression models adjusted for host and environmental covariates and total PM10 or PM2.5 mass. Combined estimates were calculated using random-effects meta-analysis. There was substantial within and between-cohort variability in element concentrations. In the adjusted meta-analysis, pneumonia was weakly associated with zinc derived from PM10 (OR: 1.47 (95% CI: 0.99, 2.18) per 20 ng/m3 increase). No other associations with the other elements were consistently observed. The independent effect of particulate matter mass remained after adjustment for element concentrations. In conclusion, associations between particulate matter mass exposure and pneumonia were not explained by the elements we investigated. Zinc from PM10 was the only element which appeared independently associated with a higher risk of early-life pneumonia. As zinc is primarily attributable to non-tailpipe traffic emissions, these results may suggest a potential adverse effect of non-tailpipe emissions on health. This research received funding from the European Community's Seventh Framework Program (FP7/2007-2011): ESCAPE (grant agreement number: 211250) and TRANSPHORM (ENV.2009.1.2.2.1). The Swedish Research Council FORMAS, the Stockholm County Council, the Swedish Foundation for Health Care Sciences and Allergy Research, and the Swedish Environmental Protection Agency supported BAMSE. The Italian Ministry of Health (ex art.12 D.Lgs 502/92, 2001) supported GASPII. The GINIplus study was supported for the first three years by grants of the Federal Ministry for Education, Science, Research and Technology (grant no. 01 EE 9401-4). The LISAplus study was supported by grants 01 EG 9732 and 01 EG 9705/2 from the Federal Ministry for Education, Science, Research and Technology, by the Federal Ministry for Environment (IUF, FKZ 20462296) and by the Helmholtz Zentrum München, Munich Center of Health. The Netherlands Organization for Health Research and Development, The Netherlands Organization for Scientific Research, The Netherlands Asthma Fund, The Netherlands Ministry of Spatial Planning, Housing, and the Environment and The Netherlands Ministry of Health, Welfare and Sport supported PIAMA. An Asthma UK Grant 04/014, the Moulton Charitable Trust, the James Trust and Microsoft Research supported MAAS. Grants from the Spanish Ministry of Health-Instituto de Salud Carlos III (Red INMA G03/176, CB06/02/0041, FISPI041436, FIS-PI081151, FIS-PI042018, FIS-PI09/02311, FIS-PI06/0867, FIS-PS09/00090, FIS-FEDER 03/1615, 04/1509, 04/1112, 04/1931, 05/1079, 05/1052, 06/1213, 07/0314, and 09/02647), Generalitat de Catalunya-CIRIT 1999SGR 00241, Conselleria de Sanitat Generalitat Valenciana, Universidad de Oviedo, Obra social Cajastur, Department of Health of the Basque Government (2005111093 and 2009111069), Provincial Government of Gipuzkoa (DFG06/004 and DFG08/001) and Fundación Roger Torné supported INMA.

BACKGROUND: Few studies have investigated traffic-related air pollution as a risk factor for respiratory infections during early childhood. OBJECTIVES: We aimed to investigate the association between air pollution and pneumonia, croup, and otitis media in 10 European birth cohorts--BAMSE (Sweden), GASPII (Italy), GINIplus and LISAplus (Germany), MAAS (United Kingdom), PIAMA (the Netherlands), and four INMA cohorts (Spain)--and to derive combined effect estimates using meta-analysis. METHODS: Parent report of physician-diagnosed pneumonia, otitis media, and croup during early childhood were assessed in relation to annual average pollutant levels [nitrogen dioxide (NO2), nitrogen oxide (NOx), particulate matter≤2.5 μm (PM2.5), PM2.5 absorbance, PM10, PM2.5-10 (coarse PM)], which were estimated using land use regression models and assigned to children based on their residential address at birth. Identical protocols were used to develop regression models for each study area as part of the ESCAPE project. Logistic regression was used to calculate adjusted effect estimates for each study, and random-effects meta-analysis was used to calculate combined estimates. RESULTS: For pneumonia, combined adjusted odds ratios (ORs) were elevated and statistically significant for all pollutants except PM2.5 (e.g., OR=1.30; 95% CI: 1.02, 1.65 per 10-μg/m3 increase in NO2 and OR=1.76; 95% CI: 1.00, 3.09 per 10-μg/m3 PM10). For otitis media and croup, results were generally null across all analyses except for NO2 and otitis media (OR=1.09; 95% CI: 1.02, 1.16 per 10-μg/m3). CONCLUSION: Our meta-analysis of 10 European birth cohorts within the ESCAPE project found consistent evidence for an association between air pollution and pneumonia in early childhood, and some evidence for an association with otitis media., qwqwqw, The research leading to these results was funded by the European Community’s Seventh Framework Program (FP7/2007–2011) under grant 211250. The BAMSE study was supported by the Swedish Research Council FORMAS (for Environment, Agricultural Sciences and Spatial Planning), the Stockholm County Council, the Swedish Foundation for Health Care Sciences and Allergy Research, and the Swedish Environmental Protection Agency. The GINIplus study was supported for the first 3 years by the Federal Ministry for Education, Science, Research and Technology, Germany (interventional arm) and Helmholtz Zentrum München, Germany (former GSF; National Research Center for Environment and Health) (observational arm). The LISAplus study was supported by grants from the Federal Ministry for Education, Science, Research and Technology, Germany; Helmholtz Zentrum München, Germany (former GSF); Helmholtz Centre for Environmental Research–UFZ, Germany; Marien-Hospital Wesel, Germany; and Pediatric Practice, Bad Honnef, Germany. The PIAMA study is supported by The Netherlands Organization for Health search and Development; The Netherlands Organization for Scientific Research; The Netherlands Asthma Fund; The Netherlands Ministry of Spatial Planning, Housing, and the Environment; and The Netherlands Ministry of Health, Welfare, and Sport. MAAS was supported by an Asthma UK Grant (04/014); the JP Moulton Charitable Foundation, UK; and the James Trust and Medical Research Council, UK (G0601361). INMA was funded by grants from the Spanish Ministry of Health-Instituto de Salud Carlos III (Red INMA G03/176,CB06/02/0041, FISPI041436, FIS-PI081151, FIS-PI042018, FIS-PI09/02311, FIS-PI06/0867, FIS-PS09/00090, FIS-FEDER 03/1615, 04/1509, 04/1112, 04/1931, 05/1079, 05/1052, 06/1213,07/0314, and 09/02647); Generalitat de Catalunya-CIRIT, Spain (1999SGR 00241); Conselleria de Sanitat Generalitat Valenciana, Spain; Universidad de Oviedo, Obra social Cajastur, Spain; Department of Health of the Basque Government, Spain (2005111093 and 2009111069); Provincial Government of Gipuzkoa (DFG06/004 and DFG08/001), Spain; and Fundación Roger Torné, Spain. GASPII was funded by The Italian Ministry of Health (ex art.12 D.Lgs 502/92, 2001), MacIntyre, E.A., Gehring, U., Mölter, A., Fuertes, E., Klümper, C., Krämer, U., Quass, U., Hoffmann, B., Gascon, M., Brunekreef, B., Koppelman, G.H., Beelen, R., Hoek, G., Birk, M., de Jongste, J.C., Smit, H.A., Cyrys, J., Gruzieva, O., Korek, M., Bergström, A., Agius, R.M., de Vocht, F., Simpson, A., Porta, D., Forastiere, F., Badaloni, C., Cesaroni, G., Esplugues, A., Fernández-Somoano, A., Lerxundi, A., Sunyer, J., Cirach, M., Nieuwenhuijsen, M.J., Pershagen, G., Heinrich, J.

The aim of this study was to determine the effect of six traffic-related air pollution metrics (nitrogen dioxide, nitrogen oxides, particulate matter with an aerodynamic diameter 10), PM2.5, coarse particulate matter and PM2.5 absorbance) on childhood asthma and wheeze prevalence in five European birth cohorts: MAAS (England, UK), BAMSE (Sweden), PIAMA (the Netherlands), GINI and LISA (both Germany, divided into north and south areas).Land-use regression models were developed for each study area and used to estimate outdoor air pollution exposure at the home address of each child. Information on asthma and current wheeze prevalence at the ages of 4–5 and 8–10 years was collected using validated questionnaires. Multiple logistic regression was used to analyse the association between pollutant exposure and asthma within each cohort. Random-effects meta-analyses were used to combine effect estimates from individual cohorts.The meta-analyses showed no significant association between asthma prevalence and air pollution exposure (e.g. adjusted OR (95%CI) for asthma at age 8–10 years and exposure at the birth address (n=10377): 1.10 (0.81–1.49) per 10 μg·m-3 nitrogen dioxide; 0.88 (0.63–1.24) per 10 μg·m-3 PM10; 1.23 (0.78–1.95) per 5 μg·m-3 PM2.5). This result was consistently found in initial crude models, adjusted models and further sensitivity analyses.This study found no significant association between air pollution exposure and childhood asthma prevalence in five European birth cohorts.