Traffic-related air pollution: exposure assesment and respiratory health effects

La contaminació atmosfèrica és un problema de salut pública, causa més de 380 000 morts a la Unió Europea. La present tesis té per objectius avaluar l'exposició i efectes sobre el tracte respiratori de la contaminació provinent del tràfic. Les concentracions exteriors y personals de sulfurs i de carbó són bons indicadors de exposició personal en una ciutat mediterrània; per a PM2.5 hi ha altres fonts a considerar. La molèstia deguda a la contaminació no és un bon indicador d'exposició, però reflecteix la percepció del subjecte. La contaminació que prové del tràfic augmenta els símptomes d'asma y probablement també causa asma en adults. El PM2.5 provinent de la combustió augmenta la permeabilitat de la barrera epitelial pulmonar. El tràfic és una font important de contaminació. Es requereixen eines adequades per a mesurar la seva exposició. La contaminació del tràfic es un factor de risc important per a la salut respiratòria.La contaminación atmosférica es un problema de salud pública, causa 380 000 muertes anuales en la Unión Europea. Esta tesis tiene como objetivo evaluar la exposición a la contaminación debida al tráfico y sus efectos en la salud respiratoria. Los niveles diarios de carbón y sulfuro medidos centralmente son buenos indicadores de exposición personal en una ciudad mediterránea, para PM2.5 fuentes de emisión alternas se tienen que considerar. La molestia debida a la contaminación no es un marcador de exposición, pero es importante porque refleja las percepciones individuales. La contaminación proveniente del tráfico aumento los síntomas del asma, y probablemente también causa asma en adultos. El PM2.5 proveniente de la combustión aumenta la permeabilidad de la barrera epitelial pulmonar. El tráfico es una fuente importante de la contaminación. Herramientas adecuadas para medir su exposición son requeridas. La contaminación del tráfico es un factor de riesgo importante para la salud respiratoria.Air pollution is a major public health concern causing annually 380 000 deaths in the European Union. This thesis aims to study traffic-related air pollution exposure assessment and its association with respiratory effects. Daily levels of carbon and sulphur of outdoor central measurements are good surrogates for personal exposure in a Mediterranean setting; for PM2.5 other sources have to be taken into account. Annoyance due to air pollution is not a valid maker of air pollution exposure but is valuable in its own right as it integrates individual perceptions. Traffic-related air pollution increases asthma symptoms in adults and an association with new asthma onset is suggested. Furthermore, PM2.5 from combustion might lead to an increase in the lung's epithelial barrier permeability. Traffic-related air pollution is a major source of pollution. Adequate tools to assess its exposure are still needed. Traffic-related air pollution is an important risk factor for respiratory morbidity

Traffic-related air pollution: exposure assesment and respiratory health effects

La contaminació atmosfèrica és un problema de salut pública, causa més de 380 000 morts a la Unió Europea. La present tesis té per objectius avaluar l'exposició i efectes sobre el tracte respiratori de la contaminació provinent del tràfic. Les concentracions exteriors y personals de sulfurs i de carbó són bons indicadors de exposició personal en una ciutat mediterrània; per a PM2.5 hi ha altres fonts a considerar. La molèstia deguda a la contaminació no és un bon indicador d'exposició, però reflecteix la percepció del subjecte. La contaminació que prové del tràfic augmenta els símptomes d'asma y probablement també causa asma en adults. El PM2.5 provinent de la combustió augmenta la permeabilitat de la barrera epitelial pulmonar. El tràfic és una font important de contaminació. Es requereixen eines adequades per a mesurar la seva exposició. La contaminació del tràfic es un factor de risc important per a la salut respiratòria.La contaminación atmosférica es un problema de salud pública, causa 380 000 muertes anuales en la Unión Europea. Esta tesis tiene como objetivo evaluar la exposición a la contaminación debida al tráfico y sus efectos en la salud respiratoria. Los niveles diarios de carbón y sulfuro medidos centralmente son buenos indicadores de exposición personal en una ciudad mediterránea, para PM2.5 fuentes de emisión alternas se tienen que considerar. La molestia debida a la contaminación no es un marcador de exposición, pero es importante porque refleja las percepciones individuales. La contaminación proveniente del tráfico aumento los síntomas del asma, y probablemente también causa asma en adultos. El PM2.5 proveniente de la combustión aumenta la permeabilidad de la barrera epitelial pulmonar. El tráfico es una fuente importante de la contaminación. Herramientas adecuadas para medir su exposición son requeridas. La contaminación del tráfico es un factor de riesgo importante para la salud respiratoria.Air pollution is a major public health concern causing annually 380 000 deaths in the European Union. This thesis aims to study traffic-related air pollution exposure assessment and its association with respiratory effects. Daily levels of carbon and sulphur of outdoor central measurements are good surrogates for personal exposure in a Mediterranean setting; for PM2.5 other sources have to be taken into account. Annoyance due to air pollution is not a valid maker of air pollution exposure but is valuable in its own right as it integrates individual perceptions. Traffic-related air pollution increases asthma symptoms in adults and an association with new asthma onset is suggested. Furthermore, PM2.5 from combustion might lead to an increase in the lung's epithelial barrier permeability. Traffic-related air pollution is a major source of pollution. Adequate tools to assess its exposure are still needed. Traffic-related air pollution is an important risk factor for respiratory morbidity

Susceptibility factors relevant for the association between long-term air pollution exposure and incident asthma

In this review, we identified 15 studies in children and 10 studies in adults that assessed the association between long-term exposure to air pollution and incident asthma and that conducted stratified analyses to explore potential susceptibility factors. Overall, adult never-/former smokers seem to be at higher risk of incident asthma due to air pollution. Children without atopy and children from low socioeconomic status families also seem to be at higher risk of incident asthma due to air pollution. While interaction between air pollution and genes involved in the response to oxidative stress pathways have been explored, results are somewhat inconsistent and in need of replication. To evaluate interactions, large sample sizes are necessary, and much more research, including data pooling from existing studies, is needed to further explore susceptibility factors for asthma incidence due to long-term air pollution exposure.SESAP: ANSES EST-2012-16

Susceptibility factors relevant for the association between long-term air pollution exposure and incident asthma

In this review, we identified 15 studies in children and 10 studies in adults that assessed the association between long-term exposure to air pollution and incident asthma and that conducted stratified analyses to explore potential susceptibility factors. Overall, adult never-/former smokers seem to be at higher risk of incident asthma due to air pollution. Children without atopy and children from low socioeconomic status families also seem to be at higher risk of incident asthma due to air pollution. While interaction between air pollution and genes involved in the response to oxidative stress pathways have been explored, results are somewhat inconsistent and in need of replication. To evaluate interactions, large sample sizes are necessary, and much more research, including data pooling from existing studies, is needed to further explore susceptibility factors for asthma incidence due to long-term air pollution exposure.SESAP: ANSES EST-2012-16

Association between air pollution and rhinitis incidence in two European cohorts

Background: The association between air pollution and rhinitis is not well established. Aim: The aim of this longitudinal analysis was to study the association between modeled air pollution at the subjects' home addresses and self-reported incidence of rhinitis. Methods: We used data from 1533 adults from two multicentre cohorts' studies (EGEA and ECRHS). Rhinitis incidence was defined as reporting rhinitis at the second follow-up (2011 to 2013) but not at the first follow-up (2000 to 2007). Annual exposure to NO2, PM10 and PM2.5 at the participants' home addresses was estimated using land-use regression models developed by the ESCAPE project for the 2009–2010 period. Incidence rate ratios (IRR) were computed using Poisson regression. Pooled analysis, analyses by city and meta-regression testing for heterogeneity were carried out. Results: No association between long-term air pollution exposure and incidence of rhinitis was found (adjusted IRR (aIRR) for an increase of 10 μg·m−3 of NO2: 1.00 [0.91–1.09], for an increase of 5 μg·m−3 of PM2.5: 0.88 [0.73–1.04]). Similar results were found in the two-pollutant model (aIRR for an increase of 10 μg·m−3 of NO2: 1.01 [0.87–1.17], for an increase of 5 μg·m−3 of PM2.5: 0.87 [0.68–1.08]). Results differed depending on the city, but no regional pattern emerged for any of the pollutants. Conclusions: This study did not find any consistent evidence of an association between long-term air pollution and incident rhinitis

Long-term exposure to atmospheric metals assessed by mosses and mortality in France

Background: Long-term exposure to air pollution affects health, but little is known about exposure to atmospheric metals. Estimating exposure to atmospheric metals across large spatial areas remains challenging. Metal concentrations in mosses could constitute a useful proxy. Here, we linked moss biomonitoring and epidemiological data to investigate the associations between long-term exposure to metals and mortality. Methods: We modelled and mapped 13 atmospheric metals from a 20-year national moss biomonitoring program to derive exposure estimates across France. In the population-based Gazel cohort, we included 11,382 participants from low to intermediate population density areas and assigned modelled metals to their residential addresses. We distinguished between airborne metals that are primarily of natural origin and those primarily of anthropogenic origin. Associations were estimated between exposure to metals and mortality (natural-cause, cardiovascular and respiratory), using Cox models, with confounder adjustment at individual level. Findings: Between 1996 and 2017, there were 1313 deaths in the cohort (including 181 cardiovascular and 33 respiratory). Exposure to the anthropogenic metals was associated with an increased risk of natural-cause mortality (hazard ratio of 1.16 [1.08-1.24] per interquartile range of exposure), while metals from natural sources were not. Interpretation: Some atmospheric anthropogenic metals may be associated with excess mortality - even in areas with relatively low levels of exposure to air pollution. Consistent with the previous literature, our findings support the use of moss biomonitoring as a tool to assess health effects of air pollution exposure at individual level

Does the oxidative stress play a role in the associations between outdoor air pollution and persistent asthma in adults? Findings from the EGEA study

Background: Evidences that oxidative stress plays a role in the associations between outdoor air pollution and asthma are growing. We aimed to study the role of plasma fluorescent oxidation products levels (FlOPs; an oxidative stress-related biomarker), as potential mediators, in the associations between outdoor air pollution and persistent asthma. Methods: Analyses were conducted in 204 adult asthmatics followed up in the French case-control and family study on asthma (EGEA; the Epidemiological study of the Genetic and Environmental factors of Asthma). Persistent asthma was defined as having current asthma at EGEA2 (baseline, 2003-2007) and EGEA3 (follow-up, 2011-2013). Exposures to nitrogen dioxide, nitrogen oxides, road traffic, particulate matter with a diameter ≤ 10 μm (PM10) and ≤ 2.5 μm were estimated by ESCAPE models (2009-2010), and ozone (O3) by IFEN models (2004). We used a mediation analysis to assess the mediated effect by FlOPs levels and the interaction between FlOPs levels and air pollution. Results: FlOPs levels increased with PM10 and O3 (adjusted β = 0.04 (95%CI 0.001-0.08), aβ = 0.04 (95%CI 0.009-0.07) per 10 μg/m3, respectively), and the risk of persistent asthma increased with FlOPs levels (aOR = 1.81 (95%CI 1.08-3.02)). The risk of persistent asthma decreased with exposures to NO2, NOx and PM2.5 (aOR ranging from 0.62 to 0.94), and increased with exposures to PM10, O3, O3-summer and road traffic, the greater effect being observed for O3 (aOR = 1.78, 95% CI 0.73-4.37, per 10 μg/m3). Using mediation analysis, we observed a positive total effect (aOR = 2.16, 95%CI 0.70-11.9), a positive direct effect of O3 on persistent asthma (OR = 1.68, 95%CI 0.57-7.25), and a positive indirect effect mediated by FIOPs levels (aOR = 1.28 (95%CI 1.01-2.29)) accounting for 41% of the total effect. Conclusions: Our results add insights on the role of oxidative stress in the association between air pollution and persistent asthma.This work was supported by the National Hospital program of clinical research [PHRC-national 2012, EvAdA]; ANR-CES-2009; Region Nord Pas-de-Calais; Merck Sharp & Dohme (MSD); the GA2LEN (Global Allergy and Asthma European Network) project; the Fonds AGIR pour les maladies chroniques and ESCAPE [FP7/2007–2011, Grant Nr.211250]

Systematic review protocol to define classical IgE-associated diseases from birth to adolescence: the MeDALL study

BACKGROUND: Classical disease phenotypes are mainly based on descriptions of symptoms and the hypothesis that a given pattern of symptoms provides a diagnosis. With refined technologies there is growing evidence that disease expression in patients is much more diverse and subtypes need to be defined to allow a better targeted treatment. One of the aims of the Mechanisms of the Development of Allergy Project (MeDALL,FP7) is to re-define the classical phenotypes of IgE-associated allergic diseases from birth to adolescence, by consensus among experts using a systematic review of the literature and identify possible gaps in research for new disease markers. This paper describes the methods to be used for the systematic review of the classical IgE-associated phenotypes applicable in general to other systematic reviews also addressing phenotype definitions based on evidence. METHODS/DESIGN: Eligible papers were identified by PubMed search (complete database through April 2011). This search yielded 12,043 citations. The review includes intervention studies (randomized and clinical controlled trials) and observational studies (cohort studies including birth cohorts, case-control studies) as well as case series. Systematic and non-systematic reviews, guidelines, position papers and editorials are not excluded but dealt with separately. Two independent reviewers in parallel conducted consecutive title and abstract filtering scans. For publications where title and abstract fulfilled the inclusion criteria the full text was assessed. In the final step, two independent reviewers abstracted data using a pre-designed data extraction form with disagreements resolved by discussion among investigators. DISCUSSION: The systematic review protocol described here allows to generate broad,multi-phenotype reviews and consensus phenotype definitions. The in-depth analysis of the existing literature on the classification of IgE-associated allergic diseases through such a systematic review will 1) provide relevant information on the current epidemiologic definitions of allergic diseases, 2) address heterogeneity and interrelationships and 3) identify gaps in knowledge.This work was supported by the European Commission’s Seventh Framework Programme under grant/nagreement No. 261357 (Mechanisms of the Development of ALLergy, Framework Programme 7 N° 264357/n(MeDALL paper N°7

The role of socioeconomic status in the association of lung function and air pollution-A pooled analysis of three adult ESCAPE cohorts

Ambient air pollution is a leading environmental risk factor and its broad spectrum of adverse health effects includes a decrease in lung function. Socioeconomic status (SES) is known to be associated with both air pollution exposure and respiratory function. This study assesses the role of SES either as confounder or effect modifier of the association between ambient air pollution and lung function. Cross-sectional data from three European multicenter adult cohorts were pooled to assess factors associated with lung function, including annual means of home outdoor NO2. Pre-bronchodilator lung function was measured according to the ATS-criteria. Multiple mixed linear models with random intercepts for study areas were used. Three different factors (education, occupation and neighborhood unemployment rate) were considered to represent SES. NO2 exposure was negatively associated with lung function. Occupation and neighborhood unemployment rates were not associated with lung function. However, the inclusion of the SES-variable education improved the models and the air pollution-lung function associations got slightly stronger. NO2 associations with lung function were not substantially modified by SES-variables. In this multicenter European study we could show that SES plays a role as a confounder in the association of ambient NO2 exposure with lung function.SAPALDIA Research support: The Swiss National Science Foundation (grants no 33CS30-177506/1, 33CS30-148470/1&2, 33CSCO-134276/1, 33CSCO-108796, 324730_135673, 3247BO-104283, 3247BO-104288, 3247BO-104284, 3247-065896, 3100-059302, 3200-052720, 3200-042532, 4026-028099, PMPDP3_129021/1, PMPDP3_141671/1), the Federal Office for the Environment, the Federal Office of Public Health, the Federal Office of Roads and Transport, the canton’s government of Aargau, Basel-Stadt, Basel-Land, Geneva, Luzern, Ticino, Valais, and Zürich, the Swiss Lung League, the canton’s Lung League of Basel Stadt/ Basel Landschaft, Geneva, Ticino, Valais, Graubünden and Zurich, Stiftung ehemals Bündner Heilstätten, SUVA, Freiwillige Akademische Gesellschaft, UBS Wealth Foundation, Talecris Biotherapeutics GmbH, Abbott Diagnostics, Klinik Barmelweid, Hirslanden Klinik Aarau, European Commission 018996 (GABRIEL), Wellcome Trust WT 084703MA, Exposomics EC FP7 grant(Grant agreement No: 308610)

Systematic review protocol to define classical IgE-associated diseases from birth to adolescence: the MeDALL study

BACKGROUND: Classical disease phenotypes are mainly based on descriptions of symptoms and the hypothesis that a given pattern of symptoms provides a diagnosis. With refined technologies there is growing evidence that disease expression in patients is much more diverse and subtypes need to be defined to allow a better targeted treatment. One of the aims of the Mechanisms of the Development of Allergy Project (MeDALL,FP7) is to re-define the classical phenotypes of IgE-associated allergic diseases from birth to adolescence, by consensus among experts using a systematic review of the literature and identify possible gaps in research for new disease markers. This paper describes the methods to be used for the systematic review of the classical IgE-associated phenotypes applicable in general to other systematic reviews also addressing phenotype definitions based on evidence. METHODS/DESIGN: Eligible papers were identified by PubMed search (complete database through April 2011). This search yielded 12,043 citations. The review includes intervention studies (randomized and clinical controlled trials) and observational studies (cohort studies including birth cohorts, case-control studies) as well as case series. Systematic and non-systematic reviews, guidelines, position papers and editorials are not excluded but dealt with separately. Two independent reviewers in parallel conducted consecutive title and abstract filtering scans. For publications where title and abstract fulfilled the inclusion criteria the full text was assessed. In the final step, two independent reviewers abstracted data using a pre-designed data extraction form with disagreements resolved by discussion among investigators. DISCUSSION: The systematic review protocol described here allows to generate broad,multi-phenotype reviews and consensus phenotype definitions. The in-depth analysis of the existing literature on the classification of IgE-associated allergic diseases through such a systematic review will 1) provide relevant information on the current epidemiologic definitions of allergic diseases, 2) address heterogeneity and interrelationships and 3) identify gaps in knowledge.This work was supported by the European Commission’s Seventh Framework Programme under grant/nagreement No. 261357 (Mechanisms of the Development of ALLergy, Framework Programme 7 N° 264357/n(MeDALL paper N°7