Ambient air pollution increases the risk of respiratory mortality, but evidence for impacts on lung function and chronic obstructive pulmonary disease (COPD) is less well established. The aim was to evaluate whether ambient air pollution is associated with lung function and COPD, and explore potential vulnerability factors.We used UK Biobank data on 303 887 individuals aged 40–69 years, with complete covariate data and valid lung function measures. Cross-sectional analyses examined associations of land use regression-based estimates of particulate matter (particles with a 50% cut-off aerodynamic diameter of 2.5 and 10 µm: PM_2.5and PM₁₀, respectively; and coarse particles with diameter between 2.5 μm and 10 μm: PM_coarse) and nitrogen dioxide (NO₂) concentrations with forced expiratory volume in 1 s (FEV₁), forced vital capacity (FVC), the FEV₁/FVC ratio and COPD (FEV₁/FVC <lower limit of normal). Effect modification was investigated for sex, age, obesity, smoking status, household income, asthma status and occupations previously linked to COPD.Higher exposures to each pollutant were significantly associated with lower lung function. A 5 µg·m⁻³increase in PM_2.5concentration was associated with lower FEV₁(−83.13 mL, 95% CI −92.50– −73.75 mL) and FVC (−62.62 mL, 95% CI −73.91– −51.32 mL). COPD prevalence was associated with higher concentrations of PM_2.5(OR 1.52, 95% CI 1.42–1.62, per 5 µg·m⁻³), PM₁₀(OR 1.08, 95% CI 1.00–1.16, per 5 µg·m⁻³) and NO₂(OR 1.12, 95% CI 1.10–1.14, per 10 µg·m⁻³), but not with PM_coarse. Stronger lung function associations were seen for males, individuals from lower income households, and “at-risk” occupations, and higher COPD associations were seen for obese, lower income, and non-asthmatic participants.Ambient air pollution was associated with lower lung function and increased COPD prevalence in this large study.

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, NO_x) 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⁻³increase in NO₂exposure 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⁻³in PM₁₀, but not other PM metrics (PM_2.5, 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: 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. Citation: Jacquemin B, Siroux V, Sanchez M, Carsin AE, Schikowski T, Adam M, Bellisario V, Buschka A, Bono R, Brunekreef B, Cai Y, Cirach M, Clavel-Chapelon F, Declercq C, de Marco R, de Nazelle A, Ducret-Stich RE, Ferretti VV, Gerbase MW, Hardy R, Heinrich J, Janson C, Jarvis D, Al Kanaani Z, Keidel D, Kuh D, Le Moual N, Nieuwenhuijsen MJ, Marcon A, Modig L, Pin I, Rochat T, Schindler C, Sugiri D, Stempfelet M, Temam S, Tsai MY, Varraso R, Vienneau D, Vierkötter A, Hansell AL, Krämer U, Probst-Hensch NM, Sunyer J, Künzli N, Kauffmann F. 2015. Ambient air pollution and adult asthma incidence in six European cohorts (ESCAPE). Environ Health Perspect 123:613–621; http://dx.doi.org/10.1289/ehp.1408206

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 (NO_x) 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 NO_xand 3692 with PM measures. COPD was not associated with NO₂or PM₁₀in any individual cohort. In meta-analyses only NO₂, NO_x, PM₁₀and 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.

Blood biochemistry may provide information on associations between road traffic noise, air pollution, and cardiovascular disease risk. We evaluated this in two large European cohorts (HUNT3, Lifelines). Road traffic noise exposure was modelled for 2009 using a simplified version of the Common Noise Assessment Methods in Europe (CNOSSOS-EU). Annual ambient air pollution (PM₁₀, NO₂) at residence was estimated for 2007 using a Land Use Regression model. The statistical platform DataSHIELD was used to pool data from 144 082 participants aged ≥20 years to enable individual-level analysis. Generalized linear models were fitted to assess cross-sectional associations between pollutants and high-sensitivity C-reactive protein (hsCRP), blood lipids and for (Lifelines only) fasting blood glucose, for samples taken during recruitment in 2006–2013. Pooling both cohorts, an inter-quartile range (IQR) higher day-time noise (5.1 dB(A)) was associated with 1.1% [95% confidence interval (95% CI: 0.02–2.2%)] higher hsCRP, 0.7% (95% CI: 0.3–1.1%) higher triglycerides, and 0.5% (95% CI: 0.3–0.7%) higher high-density lipoprotein (HDL); only the association with HDL was robust to adjustment for air pollution. An IQR higher PM₁₀ (2.0 µg/m³) or NO₂ (7.4 µg/m³) was associated with higher triglycerides (1.9%, 95% CI: 1.5–2.4% and 2.2%, 95% CI: 1.6–2.7%), independent of adjustment for noise. Additionally for NO₂, a significant association with hsCRP (1.9%, 95% CI: 0.5–3.3%) was seen. In Lifelines, an IQR higher noise (4.2 dB(A)) and PM₁₀ (2.4 µg/m³) was associated with 0.2% (95% CI: 0.1–0.3%) and 0.6% (95% CI: 0.4–0.7%) higher fasting glucose respectively, with both remaining robust to adjustment for air/noise pollution. Long-term exposures to road traffic noise and ambient air pollution were associated with blood biochemistry, providing a possible link between road traffic noise/air pollution and cardio-metabolic disease risk.