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Background: Long-term exposure to ambient air pollution has been linked to childhood-onset asthma, although evidence is still insufficient. Within the multicentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we examined the associations of long-term exposures to particulate matter with a diameter <2.5 µm (PM 2.5 ), nitrogen dioxide (NO 2 ) and black carbon (BC) with asthma incidence in adults., Methods: We pooled data from three cohorts in Denmark and Sweden with information on asthma hospital diagnoses. The average concentrations of air pollutants in 2010 were modelled by hybrid land-use regression models at participants' baseline residential addresses. Associations of air pollution exposures with asthma incidence were explored with Cox proportional hazard models, adjusting for potential confounders., Results: Of 98 326 participants, 1965 developed asthma during a mean follow-up of 16.6 years. We observed associations in fully adjusted models with hazard ratios of 1.22 (95% CI 1.04-1.43) per 5 μg·m -3 for PM 2.5 , 1.17 (95% CI 1.10-1.25) per 10 µg·m -3 for NO 2 and 1.15 (95% CI 1.08-1.23) per 0.5×10 -5  m -1 for BC. Hazard ratios were larger in cohort subsets with exposure levels below the European Union and US limit values and possibly World Health Organization guidelines for PM 2.5 and NO 2 . NO 2 and BC estimates remained unchanged in two-pollutant models with PM 2.5 , whereas PM 2.5 estimates were attenuated to unity. The concentration-response curves showed no evidence of a threshold., Conclusions: Long-term exposure to air pollution, especially from fossil fuel combustion sources such as motorised traffic, was associated with adult-onset asthma, even at levels below the current limit values., Competing Interests: Conflict of interest: S. Liu has nothing to disclose. Conflict of interest: J.T. Jørgensen has nothing to disclose. Conflict of interest: P. Ljungman has nothing to disclose. Conflict of interest: G. Pershagen has nothing to disclose. Conflict of interest: T. Bellander has nothing to disclose. Conflict of interest: K. Leander has nothing to disclose. Conflict of interest: P.K.E. Magnusson has nothing to disclose. Conflict of interest: D. Rizzuto has nothing to disclose. Conflict of interest: U.A. Hvidtfeldt has nothing to disclose. Conflict of interest: O. Raaschou-Nielsen has nothing to disclose. Conflict of interest: K. Wolf has nothing to disclose. Conflict of interest: B. Hoffmann has nothing to disclose. Conflict of interest: B. Brunekreef has nothing to disclose. Conflict of interest: M. Strak has nothing to disclose. Conflict of interest: J. Chen has nothing to disclose. Conflict of interest: A. Mehta has nothing to disclose. Conflict of interest: R.W. Atkinson has nothing to disclose. Conflict of interest: M. Bauwelinck has nothing to disclose. Conflict of interest: R. Varraso has nothing to disclose. Conflict of interest: M-C. Boutron-Ruault has nothing to disclose. Conflict of interest: J. Brandt has nothing to disclose. Conflict of interest: G. Cesaroni has nothing to disclose. Conflict of interest: F. Forastiere has nothing to disclose. Conflict of interest: D. Fecht has nothing to disclose. Conflict of interest: J. Gulliver has nothing to disclose. Conflict of interest: O. Hertel has nothing to disclose. Conflict of interest: K. de Hoogh has nothing to disclose. Conflict of interest: N.A.H. Janssen has nothing to disclose. Conflict of interest: K. Katsouyanni has nothing to disclose. Conflict of interest: M. Ketzel has nothing to disclose. Conflict of interest: J.O. Klompmaker has nothing to disclose. Conflict of interest: G. Nagel has nothing to disclose. Conflict of interest: B. Oftedal has nothing to disclose. Conflict of interest: A. Peters has nothing to disclose. Conflict of interest: A. Tjønneland has nothing to disclose. Conflict of interest: S.P. Rodopoulou has nothing to disclose. Conflict of interest: E Samoli has nothing to disclose. Conflict of interest: D.T. Kristoffersen has nothing to disclose. Conflict of interest: T. Sigsgaard has nothing to disclose. Conflict of interest: M. Stafoggia has nothing to disclose. Conflict of interest: D. Vienneau has nothing to disclose. Conflict of interest: G. Weinmayr has nothing to disclose. Conflict of interest: G. Hoek has nothing to disclose. Conflict of interest: Z.J. Andersen has nothing to disclose., (Copyright ©ERS 2021.)

Background: Air pollution has been suggested as a risk factor for chronic obstructive pulmonary disease (COPD), but evidence is sparse and inconsistent., Objectives: We examined the association between long-term exposure to low-level air pollution and COPD incidence., Methods: Within the 'Effects of Low-Level Air Pollution: A Study in Europe' (ELAPSE) study, we pooled data from three cohorts, from Denmark and Sweden, with information on COPD hospital discharge diagnoses. Hybrid land use regression models were used to estimate annual mean concentrations of particulate matter with a diameter < 2.5 µm (PM 2.5 ), nitrogen dioxide (NO 2 ), and black carbon (BC) in 2010 at participants' baseline residential addresses, which were analysed in relation to COPD incidence using Cox proportional hazards models., Results: Of 98,058 participants, 4,928 developed COPD during 16.6 years mean follow-up. The adjusted hazard ratios (HRs) and 95% confidence intervals for associations with COPD incidence were 1.17 (1.06, 1.29) per 5 µg/m 3 for PM 2.5 , 1.11 (1.06, 1.16) per 10 µg/m 3 for NO 2 , and 1.11 (1.06, 1.15) per 0.5 10 -5 m -1 for BC. Associations persisted in subset participants with PM 2.5 or NO 2 levels below current EU and US limit values and WHO guidelines, with no evidence for a threshold. HRs for NO 2 and BC remained unchanged in two-pollutant models with PM 2.5 , whereas the HR for PM 2.5 was attenuated to unity with NO 2 or BC., Conclusions: Long-term exposure to low-level air pollution is associated with the development of COPD, even below current EU and US limit values and possibly WHO guidelines. Traffic-related pollutants NO 2 and BC may be the most relevant., (Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.)

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 NO 2 . 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. NO 2 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. NO 2 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 NO 2 exposure with lung function.

Background: Research based on cluster analyses led to the identification of particular phenotypes confirming phenotypic heterogeneity of asthma. The long-term clinical course of asthma phenotypes defined by clustering analysis remains unknown, although it is a key aspect to underpin their clinical relevance. We aimed to estimate risk of poor asthma events between asthma clusters identified 20 years earlier., Methods: The study relied on two cohorts of adults with asthma with 20-year follow-up, ECRHS (European Community Respiratory Health Survey) and EGEA (Epidemiological study on Genetics and Environment of Asthma). Regression models were used to compare asthma characteristics (current asthma, asthma exacerbations, asthma control, quality of life, and FEV 1 ) at follow-up and the course of FEV 1  between seven cluster-based asthma phenotypes identified 20 years earlier., Results: The analysis included 1325 adults with ever asthma. For each asthma characteristic assessed at follow-up, the risk for adverse outcomes differed significantly between the seven asthma clusters identified at baseline. As compared with the mildest asthma phenotype, ORs (95% CI) for asthma exacerbations varied from 0.9 (0.4 to 2.0) to 4.0 (2.0 to 7.8) and the regression estimates (95% CI) for FEV 1 % predicted varied from 0.6 (-3.5 to 4.6) to -9.9 (-14.2 to -5.5) between clusters. Change in FEV 1 over time did not differ significantly across clusters., Conclusion: Our findings show that the long-term risk for poor asthma outcomes differed between comprehensive adult asthma phenotypes identified 20 years earlier, and suggest a strong tracking of asthma activity and impaired lung function over time., (© 2018 EAACI and John Wiley and Sons A/S. Published by John Wiley and Sons Ltd.)

Asthma, rhinitis, and eczema are complex diseases with multiple genetic and environmental factors interlinked through IgE-associated and non-IgE-associated mechanisms. Mechanisms of the Development of ALLergy (MeDALL; EU FP7-CP-IP; project no: 261357; 2010-2015) studied the complex links of allergic diseases at the clinical and mechanistic levels by linking epidemiologic, clinical, and mechanistic research, including in vivo and in vitro models. MeDALL integrated 14 European birth cohorts, including 44,010 participants and 160 cohort follow-ups between pregnancy and age 20 years. Thirteen thousand children were prospectively followed after puberty by using a newly standardized MeDALL Core Questionnaire. A microarray developed for allergen molecules with increased IgE sensitivity was obtained for 3,292 children. Estimates of air pollution exposure from previous studies were available for 10,000 children. Omics data included those from historical genome-wide association studies (23,000 children) and DNA methylation (2,173), targeted multiplex biomarker (1,427), and transcriptomic (723) studies. Using classical epidemiology and machine-learning methods in 16,147 children aged 4 years and 11,080 children aged 8 years, MeDALL showed the multimorbidity of eczema, rhinitis, and asthma and estimated that only 38% of multimorbidity was attributable to IgE sensitization. MeDALL has proposed a new vision of multimorbidity independent of IgE sensitization, and has shown that monosensitization and polysensitization represent 2 distinct phenotypes. The translational component of MeDALL is shown by the identification of a novel allergic phenotype characterized by polysensitization and multimorbidity, which is associated with the frequency, persistence, and severity of allergic symptoms. The results of MeDALL will help integrate personalized, predictive, preventative, and participatory approaches in allergic diseases., (Copyright © 2016 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)

Background: Short-term exposure to air pollution has adverse effects among patients with asthma, but whether long-term exposure to air pollution is a cause of adult-onset asthma is unclear., Objective: We aimed to investigate the association between air pollution and adult onset asthma., Methods: Asthma incidence was prospectively assessed in six European cohorts. Exposures studied were annual average concentrations at home addresses for nitrogen oxides assessed for 23,704 participants (including 1,257 incident cases) and particulate matter (PM) assessed for 17,909 participants through ESCAPE land-use regression models and traffic exposure indicators. Meta-analyses of cohort-specific logistic regression on asthma incidence were performed. Models were adjusted for age, sex, overweight, education, and smoking and included city/area within each cohort as a random effect., Results: In this longitudinal analysis, asthma incidence was positively, but not significantly, associated with all exposure metrics, except for PMcoarse. Positive associations of borderline significance were observed for nitrogen dioxide [adjusted odds ratio (OR) = 1.10; 95% CI: 0.99, 1.21 per 10 μg/m3; p = 0.10] and nitrogen oxides (adjusted OR = 1.04; 95% CI: 0.99, 1.08 per 20 μg/m3; p = 0.08). Nonsignificant positive associations were estimated for PM10 (adjusted OR = 1.04; 95% CI: 0.88, 1.23 per 10 μg/m3), PM2.5 (adjusted OR = 1.04; 95% CI: 0.88, 1.23 per 5 μg/m3), PM2.5absorbance (adjusted OR = 1.06; 95% CI: 0.95, 1.19 per 10-5/m), traffic load (adjusted OR = 1.10; 95% CI: 0.93, 1.30 per 4 million vehicles × meters/day on major roads in a 100-m buffer), and traffic intensity (adjusted OR = 1.10; 95% CI: 0.93, 1.30 per 5,000 vehicles/day on the nearest road). A nonsignificant negative association was estimated for PMcoarse (adjusted OR = 0.98; 95% CI: 0.87, 1.14 per 5 μg/m3)., Conclusions: Results suggest a deleterious effect of ambient air pollution on asthma incidence in adults. Further research with improved personal-level exposure assessment (vs. residential exposure assessment only) and phenotypic characterization is needed.

Rationale: The temporal stability of adult asthma phenotypes identified using clustering methods has never been addressed. Longitudinal cluster-based methods may provide novel insights in the study of the natural history of asthma., Objectives: To compare the stability of cluster-based asthma phenotype structures a decade apart in adults and to address the individuals' phenotypic transition across these asthma phenotypes., Methods: The latent transition analysis was applied on longitudinal data (twice, 10 yr apart) from 3,320 adults with asthma who took part in the European Community Respiratory Health Survey, the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults, or the Epidemiological Study on Genetics and Environment of Asthma. Nine variables covering personal and phenotypic characteristics measured twice, 10 years apart, were simultaneously considered., Measurements and Main Results: Latent transition analysis identifies seven asthma phenotypes (prevalence range, 8.4-20.8%), mainly characterized by the level of asthma symptoms (low, moderate, high), the allergic status, and pulmonary function. Phenotypes observed 10 years apart showed strong similarities. The probability of membership in the same asthma phenotype at both times varied across phenotypes from 54 to 88%. Different transition patterns were observed across phenotypes. Transitions toward increased asthma symptoms were more frequently observed among nonallergic phenotypes as compared with allergic phenotypes. Results showed a strong stability of the allergic status over time., Conclusions: Adult asthma phenotypes identified by a clustering approach, 10 years apart, were highly consistent. This study is the first to model the probabilities of transitioning over time between comprehensive asthma phenotypes.

Cough is a common symptom that affects a large proportion of the general population, but has been somewhat neglected in the epidemiological literature in the recent years. Various types of coughs are described based on life-long epidemiological surveys. Using published and unpublished data from three epidemiological studies (the European Community Respiratory Health survey, the French Epidemiological study on the Genetics and environment of asthma (EGEA) and the French E3N study), some specific aspects are discussed in detail. Phenotypic heterogeneity according to chronicity, or its productive nature, or its daytime or nocturnal characteristics are discussed. The association of cough with asthma and gender is described, together with its evolution over a 12-year period. The potential for genetic studies of cough is discussed., (Copyright © 2010 Elsevier Ltd. All rights reserved.)