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Background: Emerging evidence suggests that air pollution may contribute to childhood asthma development. We estimated the burden of incident childhood asthma that may be attributable to outdoor nitrogen dioxide (NO 2 ), particulate matter ≤2.5 µm in diameter (PM 2.5 ) and black carbon (BC) in Europe., Methods: We combined country-level childhood incidence rates and pooled exposure-response functions with childhood (age 1-14 years) population counts, and exposure estimates at 1 540 386 1 km×1 km cells, across 18 European countries and 63 442 419 children. Annual average pollutant concentrations were obtained from a validated and harmonised European land-use regression model. We investigated two exposure reduction scenarios. For the first, we used recommended annual World Health Organization (WHO) air quality guideline values. For the second, we used the minimum air pollution levels recorded across 41 studies in the underlying meta-analysis., Results: NO 2 ranged from 1.4 to 70.0 µg·m -3 , with a mean of 11.8 µg·m -3 . PM 2.5 ranged from 2.0 to 41.1 µg·m -3 , with a mean of 11.6 µg·m -3 . BC ranged from 0.003 to 3.7×10 -5  m -1 , with a mean of 1.0×10 -5  m -1 . Compliance with the NO 2 and PM 2.5 WHO guidelines was estimated to prevent 2434 (0.4%) and 66 567 (11%) incident cases, respectively. Meeting the minimum air pollution levels for NO 2 (1.5 µg·m -3 ), PM 2.5 (0.4 µg·m -3 ) and BC (0.4×10 -5  m -1 ) was estimated to prevent 135 257 (23%), 191 883 (33%) and 89 191 (15%) incident cases, respectively., Conclusions: A significant proportion of childhood asthma cases may be attributable to outdoor air pollution and these cases could be prevented. Our estimates underline an urgent need to reduce children's exposure to air pollution., Competing Interests: Conflict of interest: H. Khreis has nothing to disclose. Conflict of interest: M. Cirach has nothing to disclose. Conflict of interest: N. Mueller has nothing to disclose. Conflict of interest: K. de Hoogh has nothing to disclose. Conflict of interest: G. Hoek has nothing to disclose. Conflict of interest: M.J. Nieuwenhuijsen has nothing to disclose. Conflict of interest: D. Rojas-Rueda has nothing to disclose., (Copyright ©ERS 2019.)

We assessed the effect of three different indices of urban built environment on allergic and respiratory conditions.This study involved 2472 children participating in the ongoing INMA birth cohort located in two bio-geographic regions (Euro-Siberian and Mediterranean) in Spain. Residential surrounding built environment was characterised as 1) residential surrounding greenness based on satellite-derived normalised difference vegetation index (NDVI), 2) residential proximity to green spaces and 3) residential surrounding greyness based on urban land use patterns. Information on wheezing, bronchitis, asthma and allergic rhinitis up to age 4 years was obtained from parent-completed questionnaires. Logistic regression and generalised estimating equation modelling were performed.Among children from the Euro-Siberian region, higher residential surrounding greenness and higher proximity to green spaces were negatively associated with wheezing. In the Mediterranean region, higher residential proximity to green spaces was associated with a reduced risk for bronchitis. A higher amount of residential surrounding greyness was found to increase the risk for bronchitis in this region.Associations between indices of urban residential greenness and greyness with respiratory diseases differ by region. The pathways underlying these associations require further exploration., Competing Interests: Conflict of interest: None declared., (Copyright ©ERS 2017.)

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., (Copyright ©ERS 2015.)

The role of air pollution in chronic obstructive pulmonary disease (COPD) remains uncertain. The aim was to assess the impact of chronic exposure to air pollution on COPD in four cohorts using the standardised ESCAPE exposure estimates. Annual average particulate matter (PM), nitrogen oxides (NOx) and road traffic exposure were assigned to home addresses using land-use regression models. COPD was defined by NHANES reference equation (forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) less than the lower limit of normal) and the Global Initiative for Chronic Obstructive Lung Disease criterion (FEV1/FVC <0.70) and categorised by severity in non-asthmatics. We included 6550 subjects with assigned NOx and 3692 with PM measures. COPD was not associated with NO2 or PM10 in any individual cohort. In meta-analyses only NO2, NOx, PM10 and the traffic indicators were positively, although not significantly, associated with COPD. The only statistically significant associations were seen in females (COPD prevalence using GOLD: OR 1.57, 95% CI 1.11-2.23; and incidence: OR 1.79, 95% CI 1.21-2.68). None of the principal results were statistically significant, the weak positive associations of exposure with COPD and the significant subgroup findings need to be evaluated in further well standardised cohorts followed up for longer time, and with time-matched exposure assignments., (©ERS 2014.)

The origin(s) of systemic inflammation in patients with chronic obstructive pulmonary disease (COPD) is unclear. We investigated the impact of exposure to ambient air pollution on systemic biomarkers of inflammation (C-reactive protein (CRP), tumour necrosis factor-α, interleukin (IL)-6, IL-8 and fibrinogen) and tissue repair (hepatocyte growth factor (HGF)) in 242 clinically stable COPD patients (mean age 67.8 years and forced expiratory volume in 1 s 71.3% predicted) in Barcelona, Spain, in 2004-2006. A spatiotemporal exposure assessment framework was applied to predict ambient nitrogen dioxide (NO2) and levels of particles with a 50% cut-off aerodynamic diameter of 2.5 μm (PM2.5) at each participant's home address during 10 periods of 24 h (lags 1-10) and 1 year prior to the blood sampling date. We used linear regression models to estimate associations between biomarkers and exposure levels. An interquartile range (IQR) increase in NO2 exposure in lag 5 was associated with 51%, 10% and 9% increases in CRP, fibrinogen and HGF levels respectively. We also observed 12% and 8% increases in IL-8 associated with an IQR increase in NO2 exposure in lag 3 and over the year before sampling, respectively. These increases were larger in former smokers. The results for PM2.5 were not conclusive. These results show that exposure to ambient NO2 increases systemic inflammation in COPD patients, especially in former smokers., (©ERS 2014.)