Dataset Information

Air pollution exposure and lung function in children: the ESCAPE project.

ABSTRACT:

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 ?m (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-?g/m3 increase in NOx to -1.77% (95% CI: -3.34, -0.18%) for a 5-?g/m3 increase in PM2.5.

Conclusions

Exposure to air pollution may result in reduced lung function in schoolchildren.

SUBMITTER: Gehring U

PROVIDER: S-EPMC3855518 | biostudies-literature | 2013 Nov-Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Air pollution exposure and lung function in children: the ESCAPE project.

Gehring Ulrike U Gruzieva Olena O Agius Raymond M RM Beelen Rob R Custovic Adnan A Cyrys Josef J Eeftens Marloes M Flexeder Claudia C Fuertes Elaine E Heinrich Joachim J Hoffmann Barbara B de Jongste Johan C JC Kerkhof Marjan M Klümper Claudia C Korek Michal M Mölter Anna A Schultz Erica S ES Simpson Angela A Sugiri Dorothea D Svartengren Magnus M von Berg Andrea A Wijga Alet H AH Pershagen Göran G Brunekreef Bert B

Environmental health perspectives 20130927 11-12

<h4>Background</h4>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.<h4>Objectives</h4>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.<h4>Methods</h4>As part of the European ...[more]

PMID: 24076757

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Project description:ImportanceBreastfeeding and exposure to ambient air pollutants have been found to be independently associated with respiratory health in children; however, previous studies have not examined the association of breastfeeding as a potential moderator of the association.ObjectiveTo assess associations of breastfeeding and air pollution with lung function in children.Design, setting, and participantsUsing a cross-sectional study design, children were recruited from 62 elementary and middle schools located in 7 Chinese cities from April 1, 2012, to October 31, 2013. Data analyses were conducted from November 1, 2018, to March 31, 2019.ExposuresLong-term concentrations of airborne particulate matter with a diameter of 1 μm or less (PM1), airborne particulate matter with a diameter of 2.5 μm or less (PM2.5), airborne particulate matter with a diameter of 10 μm or less (PM10), and nitrogen dioxide were estimated using a spatial statistical model matched to children's geocoded home addresses, and concentrations of PM10, sulfur dioxide, nitrogen dioxide, and ozone were measured by local air monitoring stations.Main outcomes and measuresBreastfeeding was defined as maternal report of having mainly breastfed for longer than 3 months. Lung function was measured using portable electronic spirometers. Using previously published predicted spirometric values for children in Northeast China as the reference, lung impairment was defined as forced vital capacity (FVC) less than 85%, forced expiratory volume in the first second of expiration less than 85%, peak expiratory flow less than 75%, or maximum midexpiratory flow less than 75%.ResultsParticipants included 6740 children (mean [SD] age, 11.6 [2.1] years; 3382 boys [50.2%]). There were 4751 children (70.5%) who were breastfed. Mean (SD) particulate matter concentrations ranged from 46.8 (6.5) μg/m3 for PM1 to 95.6 (9.8) μg/m3 for PM10. The prevalence of lung function impairment ranged from 6.8% for peak expiratory flow to 11.3% for FVC. After controlling for age, sex, and other covariates, 1-interquartile range greater concentration of pollutants was associated with higher adjusted odds ratios (AORs) for lung function impairment by FVC among children who were not breastfed compared with those who were (PM1: AOR, 2.71 [95% CI, 2.02-3.63] vs 1.20 [95% CI, 0.97-1.48]; PM2.5: AOR, 2.27 [95% CI, 1.79-2.88] vs 1.26 [95% CI, 1.04-1.51]; and PM10: AOR, 1.93 [95% CI, 1.58-2.37] vs 1.46 [95% CI, 1.23-1.73]). Younger age (<12 years) was associated with lower lung function impairment among the children who had been breastfed. In children from elementary schools, 1-interquartile range greater concentration of pollutants was associated with higher AORs for lung function impairment by FVC among children who had not been breastfed compared with those who had (PM1: AOR, 6.43 [95% CI, 3.97-10.44] vs 1.89 [95% CI, 1.28-2.80]; PM2.5: AOR, 3.83 [95% CI, 2.63-5.58] vs 1.50 [95% CI, 1.12-2.01]; and PM10: AOR, 2.61 [95% CI, 1.90-3.57] vs 1.52 [95% CI, 1.19-1.95]). Results from linear regression models also showed associations of air pollution with worse lung function among children who were not breastfed compared with their counterparts who were breastfed, especially for FVC (PM1: β, -240.46 [95% CI, -288.71 to -192.21] vs -38.21 [95% CI, -69.27 to -7.16] mL) and forced expiratory volume in the first second of expiration (PM1: β, -201.37 [95% CI, -242.08 to -160.65] vs -30.30 [95% CI, -57.66 to -2.94] mL).Conclusions and relevanceIn this study, breastfeeding was associated with lower risk of lung function impairment among children in China exposed to air pollution, particularly among younger children.

Project description:Although ambient air pollution has been linked to reduced lung function in healthy children, longitudinal analyses of pollution effects in asthmatic patients are lacking.We sought to investigate pollution effects in a longitudinal asthma study and effect modification by controller medications.We examined associations of lung function and methacholine responsiveness (PC20) with ozone, carbon monoxide (CO), nitrogen dioxide, and sulfur dioxide concentrations in 1003 asthmatic children participating in a 4-year clinical trial. We further investigated whether budesonide and nedocromil modified pollution effects. Daily pollutant concentrations were linked to ZIP/postal code of residence. Linear mixed models tested associations of within-subject pollutant concentrations with FEV1 and forced vital capacity (FVC) percent predicted, FEV1/FVC ratio, and PC20, adjusting for seasonality and confounders.Same-day and 1-week average CO concentrations were negatively associated with postbronchodilator percent predicted FEV1 (change per interquartile range, -0.33 [95% CI, -0.49 to -0.16] and -0.41 [95% CI, -0.62 to -0.21], respectively) and FVC (-0.19 [95% CI, -0.25 to -0.07] and -0.25 [95% CI, -0.43 to -0.07], respectively). Longer-term 4-month CO averages were negatively associated with prebronchodilator percent predicted FEV1 and FVC (-0.36 [95% CI, -0.62 to -0.10] and -0.21 [95% CI, -0.42 to -0.01], respectively). Four-month averaged CO and ozone concentrations were negatively associated with FEV1/FVC ratio (P < .05). Increased 4-month average nitrogen dioxide concentrations were associated with reduced postbronchodilator FEV1 and FVC percent predicted. Long-term exposures to sulfur dioxide were associated with reduced PC20 (percent change per interquartile range, -6% [95% CI, -11% to -1.5%]). Treatment augmented the negative short-term CO effect on PC20.Air pollution adversely influences lung function and PC20 in asthmatic children. Treatment with controller medications might not protect but rather worsens the effects of CO on PC20. This clinical trial design evaluates modification of pollution effects by treatment without confounding by indication.

Project description:BackgroundPrenatal exposure to air pollutants has been suggested as a possible etiologic factor for the occurrence of autism spectrum disorder.ObjectivesWe aimed to assess whether prenatal air pollution exposure is associated with childhood autistic traits in the general population.MethodsOurs was a collaborative study of four European population-based birth/child cohorts-CATSS (Sweden), Generation R (the Netherlands), GASPII (Italy), and INMA (Spain). Nitrogen oxides (NO2, NOx) and particulate matter (PM) with diameters of ? 2.5 ?m (PM2.5), ? 10 ?m (PM10), and between 2.5 and 10 ?m (PM(coarse)), and PM2.5 absorbance were estimated for birth addresses by land-use regression models based on monitoring campaigns performed between 2008 and 2011. Levels were extrapolated back in time to exact pregnancy periods. We quantitatively assessed autistic traits when the child was between 4 and 10 years of age. Children were classified with autistic traits within the borderline/clinical range and within the clinical range using validated cut-offs. Adjusted cohort-specific effect estimates were combined using random-effects meta-analysis.ResultsA total of 8,079 children were included. Prenatal air pollution exposure was not associated with autistic traits within the borderline/clinical range (odds ratio = 0.94; 95% CI: 0.81, 1.10 per each 10-?g/m3 increase in NO2 pregnancy levels). Similar results were observed in the different cohorts, for the other pollutants, and in assessments of children with autistic traits within the clinical range or children with autistic traits as a quantitative score.ConclusionsPrenatal exposure to NO2 and PM was not associated with autistic traits in children from 4 to 10 years of age in four European population-based birth/child cohort studies.CitationGuxens M, Ghassabian A, Gong T, Garcia-Esteban R, Porta D, Giorgis-Allemand L, Almqvist C, Aranbarri A, Beelen R, Badaloni C, Cesaroni G, de Nazelle A, Estarlich M, Forastiere F, Forns J, Gehring U, Ibarluzea J, Jaddoe VW, Korek M, Lichtenstein P, Nieuwenhuijsen MJ, Rebagliato M, Slama R, Tiemeier H, Verhulst FC, Volk HE, Pershagen G, Brunekreef B, Sunyer J. 2016. Air pollution exposure during pregnancy and childhood autistic traits in four European population-based cohort studies: the ESCAPE Project. Environ Health Perspect 124:133-140; http://dx.doi.org/10.1289/ehp.1408483.

Project description:BackgroundTelomere length is a molecular marker of biological aging.ObjectiveHere we investigated whether early-life exposure to residential air pollution was associated with leukocyte telomere length (LTL) at 8 y of age.MethodsIn a multicenter European birth cohort study, HELIX (Human Early Life Exposome) ([Formula: see text]), we estimated prenatal and 1-y childhood exposure to nitrogen dioxide ([Formula: see text]), particulate matter with aerodynamic diameter [Formula: see text] ([Formula: see text]), and proximity to major roads. Average relative LTL was measured using quantitative real-time polymerase chain reaction (qPCR). Effect estimates of the association between LTL and prenatal, 1-y childhood air pollution, and proximity to major roads were calculated using multiple linear mixed models with a random cohort effect and adjusted for relevant covariates.ResultsLTL was inversely associated with prenatal and 1-y childhood [Formula: see text] and [Formula: see text] exposures levels. Each standard deviation (SD) increase in prenatal [Formula: see text] was associated with a [Formula: see text] (95% CI: [Formula: see text], [Formula: see text]) change in LTL. Prenatal [Formula: see text] was nonsignificantly associated with LTL ([Formula: see text] per SD increase; 95% CI: [Formula: see text], 0.6). For each SD increment in 1-y childhood [Formula: see text] and [Formula: see text] exposure, LTL shortened by [Formula: see text] (95% CI: [Formula: see text], [Formula: see text]) and [Formula: see text] (95% CI: [Formula: see text], 0.1), respectively. Each doubling in residential distance to nearest major road during childhood was associated with a 1.6% (95% CI: 0.02, 3.1) lengthening in LTL.ConclusionLower exposures to air pollution during pregnancy and childhood were associated with longer telomeres in European children at 8 y of age. These results suggest that reductions in traffic-related air pollution may promote molecular longevity, as exemplified by telomere length, from early life onward. https://doi.org/10.1289/EHP4148.

Dataset Information

Air pollution exposure and lung function in children: the ESCAPE project.

Background

Objectives

Methods

Results

Conclusions

Publications

Air pollution exposure and lung function in children: the ESCAPE project.

Similar Datasets

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