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Introduction: The beneficial effect of improving air quality on lung function in the elderly remains unclear. We examined associations between decline in air pollutants and lung function, and effect modifications by genetics and body mass index (BMI), in elderly German women., Methods: Data were analysed from the prospective SALIA (Study on the influence of Air pollution on Lung function, Inflammation and Aging) study (n=601). Spirometry was conducted at baseline (1985-1994; age 55 years), in 2007-2010 and in 2012-2013. Air pollution concentrations at home addresses were determined for each time-point using land-use regression models. Global Lung Initiative 2012 z-scores were calculated. Weighted genetic risk scores (GRSs) were determined from lung function-related risk alleles and used to investigate interactions with improved air quality. Multiple linear mixed models were fitted., Results: Air pollution levels decreased substantially during the study period. Reduction of air pollution was associated with an increase in z-scores for forced expiratory volume in 1 s (FEV 1 ) and the FEV 1 /forced vital capacity ratio. For a decrease of 10 µg·m -3 in nitrogen dioxide (NO 2 ), the z-score for FEV 1 increased by 0.14 (95% CI 0.01-0.26). However, with an increasing number of lung function-related risk alleles, the benefit from improved air quality decreased (GRS×NO 2 interaction: p=0.029). Interactions with BMI were not significant., Conclusions: Reduction of air pollution is associated with a relative improvement of lung function in elderly women, but also depends on their genetic make-up., Competing Interests: Conflict of interest: D. Hüls has nothing to disclose. Conflict of interest: D. Sugiri has nothing to disclose. Conflict of interest: M.J. Abramson reports grants from Pfizer, grants from Boehringer Ingelheim, assistance with conference attendance and honoraria for consultancy from Sanofi, outside the submitted work. Conflict of interest: B. Hoffmann has nothing to disclose. Conflict of interest: H. Schwender has nothing to disclose. Conflict of interest: K. Ickstadt has nothing to disclose. Conflict of interest: U. Krämer has nothing to disclose. Conflict of interest: T. Schikowski has nothing to disclose., (Copyright ©ERS 2019.)

Background: Among the many risk factors for the development of atopic eczema (AE), the influence of air pollution has recently been discussed more often. A systematic review about this topic however is lacking., Aims: Which effects of outdoor air pollution (particles, nitric oxides, sulfur dioxide, ozone or general traffic exhaust emissions) on AE can be demonstrated in a systematic analysis of available environmental epidemiologic studies?, Methods: All environmental epidemiologic studies on AE and air pollution found in the literature database PubMed were identified. The most important key figures of these studies were tabulated, the quality of evidence was graded and the studies described., Results: A total of 57 studies were identified. Only one of the 15 cross-sectional studies with a large-scale exposure assessment found a significant association between AE and air pollution. In contrast 23 of 30 studies with small-scale exposure assessment found a significant association between AE and traffic related emissions-especially from trucks. Of the 30 studies, 14 were cohort studies (1 adult, 13 birth cohorts). The sole adult cohort found an association with intrinsic AE. In the East Asian cohorts (all published since 2015), an association between maternal exposure to traffic-related pollution and incidence of AE in the offspring was found. This was less clear in cohorts from Europe/US or simply not investigated. In 5/5 panel studies (all from South Korea), symptom severity of AE was found to be significantly and positively related to outdoor air pollution., Conclusions: In a systematic analysis of environmental epidemiologic studies about air pollution and AE rather good evidence was found that, based on small-scale exposure measurements, especially truck traffic emissions increased AE prevalence, while large-scale exposure to larger particles (PM10) or SO 2 was without effect. Considering pathophysiologic aspects traffic exhaust emissions seem to affect both skin barrier function and activation of immune responses.

Air pollution has been associated with impaired lung and cognitive function, especially impairment in visuo-construction performance (VCP). In this article, we evaluate whether the effect of air pollution on VCP is mediated by lung function.We used data from the SALIA cohort (baseline 1985-1994 and follow-up 2007-2010) including 587 women aged 55 years at baseline. Particulate matter (PM) and nitrogen dioxide (NO 2 ) exposures at baseline were estimated via land-use regression models. Lung function was characterised by averages between baseline and follow-up. We used age- and height-controlled Global Lung Initiative (GLI) z-scores of forced expiratory volume in 1 s (FEV 1 ), forced vital capacity (FVC) and FEV 1 /FVC. VCP was assessed at follow-up with the CERAD-Plus neuropsychological test battery and causal mediation analysis was conducted.An increase of one interquartile range in FEV 1 and FVC was positively associated with VCP (β=0.18 (95% CI 0.02-0.34) and β=0.23 (95% CI 0.07-0.39), respectively). The proportion of the association between NO 2 on VCP mediated by FEV 1 was 6.2% and this was higher in never smokers (7.2%) and non-carriers of the APOE-ε4 allele (11.2%). However, none of the mediations were statistically significant.In conclusion, air pollution associated VCP was partially mediated by lung function. Further studies on the mechanisms underlying this pathway are required to develop new strategies to prevent air pollution induced cognitive impairment., Competing Interests: Conflict of interest: M.J. Abramson has received investigator initiated grants for unrelated research from Pfizer and Boehringer-Ingelheim, and reimbursement for congress attendance from Sanofi., (Copyright ©ERS 2018.)

Genetic and environmental risk factors contribute to the pathogenesis of Alzheimer's dementia. Besides known genetic risk factors like the apolipoprotein (APO) Eε4 allele, single nuclear polymorphisms (SNPs) of the estrogen receptors (ESRs) are candidate genetic risk factors, while air pollution represents an environmental risk factor for dementia. Effects of these risk factors and their interaction were investigated in the SALIA cohort of 834 non-demented elderly women. Cognitive function was assessed by the CERAD-plus test battery. Air pollution was estimated by land use regression (LUR) models. Genotyping was carried out for nine ESR1 and ESR2 SNPs and two ApoE SNPs. Carriers of minor ESR2 alleles showed significantly reduced cognitive performance in the CERAD total score with most pronounced deficits in semantic memory (rs1256062, rs10144225, and rs2274705) and executive function (rs1256062). The minor allele effects of ESR2 were stronger in carriers of APOEε4 for the cognitive domain 'executive function' (p value of interaction 0.023 for rs1256062). The investigated ESR1 SNPs were not associated with cognition. Furthermore, we found a significant gene-environment interaction between the ESR2 SNP rs1256062 and air pollution on cognition. Carriers of two major alleles of rs1256062 were more susceptible for an air pollution-induced decrease in performance of 'figure copying' than carriers of minor alleles (p value of interaction, e.g., 0.031 for PM 2.5 ). In conclusion, ESR2 but not ESR1 minor alleles were associated with lower cognitive performance in elderly women with an indication of a gene-gene interaction with APOEε4. We also found indications for gene-environment interactions of ESR2 with traffic-related air pollution exposure on cognitive performance.

An increasing number of epidemiological studies suggest that adverse health effects of air pollution may be related to particulate matter (PM) composition, particularly trace metals. However, we lack comprehensive data on the spatial distribution of these elements. We measured PM2.5 and PM10 in twenty study areas across Europe in three seasonal two-week periods over a year using Harvard impactors and standardized protocols. In each area, we selected street (ST), urban (UB) and regional background (RB) sites (totaling 20) to characterize local spatial variability. Elemental composition was determined by energy-dispersive X-ray fluorescence analysis of all PM2.5 and PM10 filters. We selected a priori eight (Cu, Fe, K, Ni, S, Si, V, Zn) well-detected elements of health interest, which also roughly represented different sources including traffic, industry, ports, and wood burning. PM elemental composition varied greatly across Europe, indicating different regional influences. Average street to urban background ratios ranged from 0.90 (V) to 1.60 (Cu) for PM2.5 and from 0.93 (V) to 2.28 (Cu) for PM10. Our selected PM elements were variably correlated with the main pollutants (PM2.5, PM10, PM2.5 absorbance, NO2 and NOx) across Europe: in general, Cu and Fe in all size fractions were highly correlated (Pearson correlations above 0.75); Si and Zn in the coarse fractions were modestly correlated (between 0.5 and 0.75); and the remaining elements in the various size fractions had lower correlations (around 0.5 or below). This variability in correlation demonstrated the distinctly different spatial distributions of most of the elements. Variability of PM10_Cu and Fe was mostly due to within-study area differences (67% and 64% of overall variance, respectively) versus between-study area and exceeded that of most other traffic-related pollutants, including NO2 and soot, signaling the importance of non-tailpipe (e.g., brake wear) emissions in PM., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Introduction: The impact of outdoor air pollution exposure on long-term lung development and potential periods of increased lung susceptibility remain unknown. This study assessed associations between early-life and current residential exposure to air pollution and lung function at 15-years of age in two German birth cohorts., Methods: Fifteen year-old participants living in an urban and rural area in Germany underwent spirometry before and after bronchodilation (N=2266). Annual average (long-term) exposure to nitrogen dioxide (NO(2)), particles with aerodynamic diameters less than 2.5 μg/m(3) (PM2.5) mass and less than 10 μg/m(3) (PM(10)) mass, PM(2.5) absorbance and ozone were estimated to each participant's birth-, 10- and 15-year home address using land-use regression and kriging (ozone only) modelling. Associations between lung function variables and long-term pollutant concentrations were assessed using linear regression models adjusted for host and environmental covariates and recent short-term air pollution exposures., Results: Long-term air pollution concentrations assessed to the birth-, 10- and 15-year home addresses were not associated with lung function variables, before and after bronchodilation, in the complete or study area specific populations. However, several lung function variables were negatively associated with long-term NO2 concentrations among asthmatics. For example, NO(2) estimated to the 15-year home address was associated with the ratio of forced expiratory volume in one second to forced vital capacity (FEV(1)/FVC) and the mean flow rate between 25% and 75% of FVC (-3.5%, 95% confidence interval [-6.0, -1.0] and -297.4 ml/s [-592.6, -2.1] per 5.9 μg/m(3) increase in NO(2), respectively). Nearly all effect estimates for the associations between the short-term PM(2.5) mass, PM(10) mass and ozone concentrations and the lung function variables were negative in the complete population., Conclusions: Early-life and current long-term air pollution exposures and lung function at the age of 15 years were not associated in the complete study population. Asthmatics may represent a vulnerable group., (Copyright © 2015 Elsevier GmbH. All rights reserved.)

Background: Studies have shown associations between mortality and long-term exposure to particulate matter air pollution. Few cohort studies have estimated the effects of the elemental composition of particulate matter on mortality., Objectives: Our aim was to study the association between natural-cause mortality and long-term exposure to elemental components of particulate matter., Methods: Mortality and confounder data from 19 European cohort studies were used. Residential exposure to eight a priori-selected components of particulate matter (PM) was characterized following a strictly standardized protocol. Annual average concentrations of copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc within PM size fractions ≤ 2.5 μm (PM2.5) and ≤ 10 μm (PM10) were estimated using land-use regression models. Cohort-specific statistical analyses of the associations between mortality and air pollution were conducted using Cox proportional hazards models using a common protocol followed by meta-analysis., Results: The total study population consisted of 291,816 participants, of whom 25,466 died from a natural cause during follow-up (average time of follow-up, 14.3 years). Hazard ratios were positive for almost all elements and statistically significant for PM2.5 sulfur (1.14; 95% CI: 1.06, 1.23 per 200 ng/m3). In a two-pollutant model, the association with PM2.5 sulfur was robust to adjustment for PM2.5 mass, whereas the association with PM2.5 mass was reduced., Conclusions: Long-term exposure to PM2.5 sulfur was associated with natural-cause mortality. This association was robust to adjustment for other pollutants and PM2.5.

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.

Epidemiological studies indicate that asthmatic children are more susceptible to traffic-related air pollution exposure than non-asthmatic children. Local and systemic inflammation in combination with oxidative stress have been suggested as a possible susceptibility factor. We investigated effect modification by asthma status for the association between air pollution exposure and systemic effects using whole blood cytokine responsiveness as an inflammatory marker. The study was nested within the two German birth cohort studies GINIplus and LISAplus and initially designed as a random sub-sample enriched with asthmatic children. Using data from 27 asthmatic and 59 non-asthmatic six-year-old children we measured the production of Interleukin-6 (IL)-6, IL-8, IL-10, monocyte chemotactic protein-1 (MCP-1), tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in whole blood after ex-vivo stimulation with urban particulate matter (EHC-93). Air pollution exposure (nitrogen dioxide (NO2), nitrogen oxides (NOx), particulate matter with an aerodynamic diameter <10μm (PM10), particulate matter with an aerodynamic diameter <2.5μm (PM2.5mass), coarse particulate matter (PMcoarse) and PM2.5absorbance (PM2.5abs)) was modelled for children´s home addresses applying land-use regression. To assess effect modification by asthma status linear regression models with multiplicative interaction terms were used. In asthmatics exposure to NO2 was associated with higher production of pro-inflammatory cytokines: adjusted means ratio (MR) 2.22 (95% confidence interval 1.22-4.04) for IL-6 per 2.68µg/m³ NO2. The interaction term between asthma status and NO2 exposure was significant. Results for NOx, PM10, PM2.5mass and PM2.5abs were in the same direction. No association between air pollution and cytokine responsiveness was found in the group of non-asthmatic children and in the overall group. Traffic-related air pollution exposure is associated with higher pro-inflammatory cytokine responsiveness in whole blood of asthmatic children., (Copyright © 2015 Elsevier Inc. All rights reserved.)

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.)

Evidence for a role of long-term particulate matter exposure on acute respiratory infections is growing. However, which components of particulate matter may be causative remains largely unknown. We assessed associations between eight particulate matter elements and early-life pneumonia in seven birth cohort studies (N total=15,980): BAMSE (Sweden), GASPII (Italy), GINIplus and LISAplus (Germany), INMA (Spain), MAAS (United Kingdom) and PIAMA (The Netherlands). Annual average exposure to copper, iron, potassium, nickel, sulfur, silicon, vanadium and zinc, each respectively derived from particles with aerodynamic diameters ≤ 10 μm (PM10) and 2.5 μm (PM2.5), were estimated using standardized land use regression models and assigned to birth addresses. Cohort-specific associations between these exposures and parental reports of physician-diagnosed pneumonia between birth and two years were assessed using logistic regression models adjusted for host and environmental covariates and total PM10 or PM2.5 mass. Combined estimates were calculated using random-effects meta-analysis. There was substantial within and between-cohort variability in element concentrations. In the adjusted meta-analysis, pneumonia was weakly associated with zinc derived from PM10 (OR: 1.47 (95% CI: 0.99, 2.18) per 20 ng/m(3) increase). No other associations with the other elements were consistently observed. The independent effect of particulate matter mass remained after adjustment for element concentrations. In conclusion, associations between particulate matter mass exposure and pneumonia were not explained by the elements we investigated. Zinc from PM10 was the only element which appeared independently associated with a higher risk of early-life pneumonia. As zinc is primarily attributable to non-tailpipe traffic emissions, these results may suggest a potential adverse effect of non-tailpipe emissions on health., (Copyright © 2014 The Authors. Published by Elsevier GmbH.. All rights reserved.)

Background: Long-term exposure to air pollution has been hypothesized to elevate arterial blood pressure (BP). The existing evidence is scarce and country specific., Objectives: We investigated the cross-sectional association of long-term traffic-related air pollution with BP and prevalent hypertension in European populations., Methods: We analyzed 15 population-based cohorts, participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE). We modeled residential exposure to particulate matter and nitrogen oxides with land use regression using a uniform protocol. We assessed traffic exposure with traffic indicator variables. We analyzed systolic and diastolic BP in participants medicated and nonmedicated with BP-lowering medication (BPLM) separately, adjusting for personal and area-level risk factors and environmental noise. Prevalent hypertension was defined as ≥ 140 mmHg systolic BP, or ≥ 90 mmHg diastolic BP, or intake of BPLM. We combined cohort-specific results using random-effects meta-analysis., Results: In the main meta-analysis of 113,926 participants, traffic load on major roads within 100 m of the residence was associated with increased systolic and diastolic BP in nonmedicated participants [0.35 mmHg (95% CI: 0.02, 0.68) and 0.22 mmHg (95% CI: 0.04, 0.40) per 4,000,000 vehicles × m/day, respectively]. The estimated odds ratio (OR) for prevalent hypertension was 1.05 (95% CI: 0.99, 1.11) per 4,000,000 vehicles × m/day. Modeled air pollutants and BP were not clearly associated., Conclusions: In this first comprehensive meta-analysis of European population-based cohorts, we observed a weak positive association of high residential traffic exposure with BP in nonmedicated participants, and an elevated OR for prevalent hypertension. The relationship of modeled air pollutants with BP was inconsistent.

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.)

Background: Negative effects of long-term exposure to particulate matter (PM) on lung function have been shown repeatedly. Spatial differences in the composition and toxicity of PM may explain differences in observed effect sizes between studies., Methods: We conducted a multicenter study in 5 European birth cohorts-BAMSE (Sweden), GINIplus and LISAplus (Germany), MAAS (United Kingdom), and PIAMA (The Netherlands)-for which lung function measurements were available for study subjects at the age of 6 or 8 years. Individual annual average residential exposure to copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc within PM smaller than 2.5 μm (PM2.5) and smaller than 10 μm (PM10) was estimated using land-use regression models. Associations between air pollution and lung function were analyzed by linear regression within cohorts, adjusting for potential confounders, and then combined by random effects meta-analysis., Results: We observed small reductions in forced expiratory volume in the first second, forced vital capacity, and peak expiratory flow related to exposure to most elemental pollutants, with the most substantial negative associations found for nickel and sulfur. PM10 nickel and PM10 sulfur were associated with decreases in forced expiratory volume in the first second of 1.6% (95% confidence interval = 0.4% to 2.7%) and 2.3% (-0.1% to 4.6%) per increase in exposure of 2 and 200 ng/m, respectively. Associations remained after adjusting for PM mass. However, associations with these elements were not evident in all cohorts, and heterogeneity of associations with exposure to various components was larger than for exposure to PM mass., Conclusions: Although we detected small adverse effects on lung function associated with annual average levels of some of the evaluated elements (particularly nickel and sulfur), lower lung function was more consistently associated with increased PM mass.

Background: Accumulating evidence from laboratory animal and human studies suggests that air pollution exposure during pregnancy affects cognitive and psychomotor development in childhood., Methods: We analyzed data from 6 European population-based birth cohorts-GENERATION R (The Netherlands), DUISBURG (Germany), EDEN (France), GASPII (Italy), RHEA (Greece), and INMA (Spain)-that recruited mother-infant pairs from 1997 to 2008. Air pollution levels-nitrogen oxides (NO2, NOx) in all regions and particulate matter (PM) with diameters of <2.5, <10, and 2.5-10 μm (PM2.5, PM10, and PMcoarse, respectively) and PM2.5 absorbance in a subgroup-at birth addresses were estimated by land-use regression models, based on monitoring campaigns performed primarily between 2008 and 2011. Levels were back-extrapolated to exact pregnancy periods using background monitoring sites. Cognitive and psychomotor development was assessed between 1 and 6 years of age. Adjusted region-specific effect estimates were combined using random-effects meta-analysis., Results: A total of 9482 children were included. Air pollution exposure during pregnancy, particularly NO2, was associated with reduced psychomotor development (global psychomotor development score decreased by 0.68 points [95% confidence interval = -1.25 to -0.11] per increase of 10 μg/m in NO2). Similar trends were observed in most regions. No associations were found between any air pollutant and cognitive development., Conclusions: Air pollution exposure during pregnancy, particularly NO2 (for which motorized traffic is a major source), was associated with delayed psychomotor development during childhood. Due to the widespread nature of air pollution exposure, the public health impact of the small changes observed at an individual level could be considerable.

Background: Geographical variation in the prevalence of sensitization to aeroallergens may reflect differences in exposure to risk factors such as having older siblings, being raised on a farm or other unidentified exposures., Objective: We wanted to measure geographical variation in skin prick test positivity and assess whether it was explained by differences in family size and/or farm exposure. We also compared prevalence in younger and older subjects., Methods: Within the Global Allergy and Asthma European Network (GA(2) LEN) survey, we measured the prevalence of skin prick positivity to a panel of allergens, and geometric mean serum total immunoglobulin E (IgE), in 3451 participants aged 18-75 years in 13 areas of Europe. Estimated prevalence was standardized to account for study design. We compared prevalence estimates in younger and older subjects and further adjusted for age, gender, smoking history, farm exposure, number of older siblings and body mass index (BMI)., Results: Skin prick test positivity to any one of the measured allergens varied within Europe from 31.4% to 52.9%. Prevalence of sensitization to single allergens also varied. Variation in serum total IgE was less marked. Younger participants had higher skin prick sensitivity prevalence, but not total IgE, than older participants. Geographical variation remained even after adjustment for confounders., Conclusion: Geographical variation in the prevalence of skin prick test positivity in Europe is unlikely to be explained by geographical variation in gender, age, smoking history, farm exposure, family size and BMI. Higher prevalence in younger, compared to older, adults may reflect cohort-associated increases in sensitization or the influence of ageing on immune or tissue responses., (© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background: Air pollution has been associated with cardiovascular mortality, but it remains unclear as to whether specific pollutants are related to specific cardiovascular causes of death. Within the multicenter European Study of Cohorts for Air Pollution Effects (ESCAPE), we investigated the associations of long-term exposure to several air pollutants with all cardiovascular disease (CVD) mortality, as well as with specific cardiovascular causes of death., Methods: Data from 22 European cohort studies were used. Using a standardized protocol, study area-specific air pollution exposure at the residential address was characterized as annual average concentrations of the following: nitrogen oxides (NO2 and NOx); particles with diameters of less than 2.5 μm (PM2.5), less than 10 μm (PM10), and 10 μm to 2.5 μm (PMcoarse); PM2.5 absorbance estimated by land-use regression models; and traffic indicators. We applied cohort-specific Cox proportional hazards models using a standardized protocol. Random-effects meta-analysis was used to obtain pooled effect estimates., Results: The total study population consisted of 367,383 participants, with 9994 deaths from CVD (including 4,992 from ischemic heart disease, 2264 from myocardial infarction, and 2484 from cerebrovascular disease). All hazard ratios were approximately 1.0, except for particle mass and cerebrovascular disease mortality; for PM2.5, the hazard ratio was 1.21 (95% confidence interval = 0.87-1.69) per 5 μg/m and for PM10, 1.22 (0.91-1.63) per 10 μg/m., Conclusion: In a joint analysis of data from 22 European cohorts, most hazard ratios for the association of air pollutants with mortality from overall CVD and with specific CVDs were approximately 1.0, with the exception of particulate mass and cerebrovascular disease mortality for which there was suggestive evidence for an association.

Rationale: Prospective cohort studies have shown that chronic exposure to particulate matter and traffic-related air pollution is associated with reduced survival. However, the effects on nonmalignant respiratory mortality are less studied, and the data reported are less consistent., Objectives: We have investigated the relationship of long-term exposure to air pollution and nonmalignant respiratory mortality in 16 cohorts with individual level data within the multicenter European Study of Cohorts for Air Pollution Effects (ESCAPE)., Methods: Data from 16 ongoing cohort studies from Europe were used. The total number of subjects was 307,553. There were 1,559 respiratory deaths during follow-up., Measurements and Main Results: Air pollution exposure was estimated by land use regression models at the baseline residential addresses of study participants and traffic-proximity variables were derived from geographical databases following a standardized procedure within the ESCAPE study. Cohort-specific hazard ratios obtained by Cox proportional hazard models from standardized individual cohort analyses were combined using metaanalyses. We found no significant associations between air pollution exposure and nonmalignant respiratory mortality. Most hazard ratios were slightly below unity, with the exception of the traffic-proximity indicators., Conclusions: In this study of 16 cohorts, there was no association between air pollution exposure and nonmalignant respiratory mortality.

Background: There is growing evidence that air pollutants are associated with the risk of type 2 diabetes. Subclinical inflammation may be a mechanism linking air pollution with diabetes. Information is lacking whether air pollution also contributes to worse metabolic control in newly diagnosed type 2 diabetes. We examined the hypothesis that residential particulate matter (PM10) is associated with HbA1c concentration in newly diagnosed type 2 diabetes., Methods: Nationwide regional levels of particulate matter with a diameter of ≤ 10 µm (PM10) were obtained in 2009 from background monitoring stations in Germany (Federal Environmental Agency) and assigned to place of residency of 9,102 newly diagnosed diabetes patients registered in the DPV database throughout Germany (age 65.5 ± 13.5 yrs; males: 52.1%). Mean HbA1c (%) levels stratified for air pollution quartiles (PM10 in µg/m(3)) were estimated using linear regression models adjusting for age, sex, BMI, diabetes duration, geographic region, year of ascertainment, and social indicators., Findings: In both men and women, adjusted HbA1c was significantly lower in the lowest quartile of PM10 exposure in comparison to quartiles Q2-Q4. Largest differences in adjusted HbA1c (95% CI) were seen comparing lowest quartiles of exposure with highest quartiles (men %: -0.42 (-0.62; -0.23)/mmol/mol: -28.11 (-30.30; -26.04), women, %: -0.28 (-0.47; -0.09)/mmol/mol: -0.28 (-0.47; -0.09))., Interpretation: Air pollution may be associated with higher HbA1c levels in newly diagnosed type 2 diabetes patients. Further studies are warranted to examine this association.

Background: Few studies on long-term exposure to air pollution and mortality have been reported from Europe. Within the multicentre European Study of Cohorts for Air Pollution Effects (ESCAPE), we aimed to investigate the association between natural-cause mortality and long-term exposure to several air pollutants., Methods: We used data from 22 European cohort studies, which created a total study population of 367,251 participants. All cohorts were general population samples, although some were restricted to one sex only. With a strictly standardised protocol, we assessed residential exposure to air pollutants as annual average concentrations of particulate matter (PM) with diameters of less than 2.5 μm (PM2.5), less than 10 μm (PM10), and between 10 μm and 2.5 μm (PMcoarse), PM2.5 absorbance, and annual average concentrations of nitrogen oxides (NO2 and NOx), with land use regression models. We also investigated two traffic intensity variables-traffic intensity on the nearest road (vehicles per day) and total traffic load on all major roads within a 100 m buffer. We did cohort-specific statistical analyses using confounder models with increasing adjustment for confounder variables, and Cox proportional hazards models with a common protocol. We obtained pooled effect estimates through a random-effects meta-analysis., Findings: The total study population consisted of 367,251 participants who contributed 5,118,039 person-years at risk (average follow-up 13.9 years), of whom 29,076 died from a natural cause during follow-up. A significantly increased hazard ratio (HR) for PM2.5 of 1.07 (95% CI 1.02-1.13) per 5 μg/m(3) was recorded. No heterogeneity was noted between individual cohort effect estimates (I(2) p value=0.95). HRs for PM2.5 remained significantly raised even when we included only participants exposed to pollutant concentrations lower than the European annual mean limit value of 25 μg/m(3) (HR 1.06, 95% CI 1.00-1.12) or below 20 μg/m(3) (1.07, 1.01-1.13)., Interpretation: Long-term exposure to fine particulate air pollution was associated with natural-cause mortality, even within concentration ranges well below the present European annual mean limit value., Funding: European Community's Seventh Framework Program (FP7/2007-2011)., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Background: Air pollution and obesity are hypothesized to contribute to accelerated decline in lung function with age through their inflammatory properties., Objective: We investigated whether the previously reported association between improved air quality and lung health in the population-based SAPALDIA cohort is modified by obesity., Methods: We used adjusted mixed-model analyses to estimate the association of average body mass index (BMI) and changes in particulate matter with aerodynamic diameter ≤ 10 µm (PM10; ΔPM10) with lung function decline over a 10-year follow-up period., Results: Lung function data and complete information were available for 4,664 participants. Age-related declines in lung function among participants with high average BMI were more rapid for FVC (forced vital capacity), but slower for FEV1/FVC (forced expiratory volume in 1 sec/FVC) and FEF25-75 (forced expiratory flow at 25-75%) than declines among those with low or normal average BMI. Improved air quality was associated with attenuated reductions in FEV1/FVC, FEF25-75, and FEF25-75/FVC over time among low- and normal-BMI participants, but not overweight or obese participants. The attenuation was most pronounced for ΔFEF25-75/FVC (30% and 22% attenuation in association with a 10-μg/m3 decrease in PM10 among low- and normal-weight participants, respectively.), Conclusion: Our results point to the importance of considering health effects of air pollution exposure and obesity in parallel. Further research must address the mechanisms underlying the observed interaction.

We assessed whether long-term exposure to air pollution is associated with all-cause and cause-specific mortality during a period of declining particulate matter concentrations. Approximately 4800 women aged 55 years from North Rhine-Westphalia, Germany, were followed for up to 18 years. Exposure to air pollution was assessed in two ways: (1) using the distance between the residential address and the nearest major road, as calculated from Geographic Information System data and (2) calculating 1-year average particulate matter concentrations below 10 µm (PM(10)) and nitrogen dioxide (NO(2)) levels using data from the nearest air-monitoring station data to the subjects' residences. Ninety-two per cent of all subjects lived in the same community during the entire follow-up period. Associations between mortality and exposure were assessed using Cox's proportional hazards models, including confounder adjustment. Sixteen per cent of women passed away during the follow-up period. An increase of 7 μg/m(3) PM(10) (IQR) was associated with an increased HR for all-cause (HR 1.15, 95% CI (1.04 to 1.27)), cardiopulmonary (HR 1.39, 95% CI (1.17 to 1.64)), and lung cancer mortality (HR 1.84, 95% CI (1.23 to 2.74)). An increase of 16 μg/m(3) (IQR) NO(2) exposure was associated with all-cause (HR 1.18, 95% CI (1.07 to 1.30)) and cardiopulmonary mortality (HR 1.55, 95% CI (1.30 to 1.84)). The association between cardiopulmonary mortality and PM(10) was reduced for the extended follow-up period, during which PM(10) concentrations (but not NO(2) concentrations) were lower. Living close to a major road was associated with an increased relative risk for all-cause, cardiopulmonary and respiratory mortality. These associations were temporally stable. Long-term exposure to ambient PM(10) and NO(2) was associated with increased mortality rates.

The causes of adult-onset asthma are poorly established, and the asthmogenic role of air pollution has been investigated primarily in children. This review assesses the current evidence of the association between air pollution and asthma incidence among subjects free of asthma at least until late childhood. Seven publications from five study populations fulfilled the inclusion criteria (one case-control and six cohort studies). All but one used markers of local traffic-related air pollution to characterize long-term exposure. Those studies reported similar associations with traffic-related air pollution. However, protocols, definitions of asthma, and exposure assignment were rather heterogeneous, and three publications relied on the same study; thus we abstain from meta-analytic summaries. Reported patterns of effect modification (e.g., by sex, atopy, or smoking) were inconsistent. Overall, the role of traffic-related air pollution in adult-onset asthma is less conclusive than in childhood asthma. Larger studies with more consistent definitions of phenotypes and exposure assessment for local traffic-related pollutants (e.g., ultrafine particles) are needed. Pooling existing cohorts such as in the ongoing European ESCAPE and TRANSPHORM consortia are promising steps. There is, however, a need for large-scale megacohorts to investigate these effects in standardized ways and to identify the most susceptible populations., (Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.)

Background: Extensive epidemiological studies have provided evidence of an association between elevated outdoor particulate air pollution and adverse health effects. However, while people typically spend majority of time indoors, there is limited knowledge on airborne indoor particles and on the correlation between the concentrations of indoor particles and health effects. Even insights into the influence of differently sized indoor particles on human health are still rare., Objective: The association between differentially sized indoor air particles and the development of respiratory diseases was studied for three year aged children., Methods: Short-term measurements of particle mass and number concentrations were carried out in children's rooms. Information on possible particle sources (smoking habits, type of heating, and traffic) and respiratory outcomes were obtained from questionnaires. Measured indoor particle concentrations were correlated with possible sources of indoor particles and with respiratory health impacts., Results: Daily smoking, smoking more than 5 cigarettes per day at home and traffic density in front of the window of children's room were found to be related to indoor exposure by particles of different diameters. High indoor particle exposures were associated with an increased risk for the development of obstructive bronchitis and in some extent of non-obstructive bronchitis. The strongest impact was observed for the mass concentration of particles <1 μm and the number concentration of particles >0.5 μm. The risk increases still remain significant if tested for stability changing the number of adjustment variables or omitting randomly selected cases, respectively., Conclusion: Our results show significant associations between indoor particle concentrations and the risks for respiratory diseases in young children. The applied short-term measurements can help to assess the health risks of indoor particles with different sizes within epidemiological studies., (Copyright © 2010 Elsevier B.V. All rights reserved.)

In a cross-sectional study performed in 2000, an unexpected positive association between nickel (Ni) in ambient air, urinary Ni content and the prevalence of Ni sensitization in a subgroup of 6-yr-old children living near a steel mill was observed. Between 2005 and 2006, in a different and larger study population, we examined if Ni from ambient air or urinary Ni concentration was related to Ni sensitization in children living next to Ni-emitting steel mills. We studied 749 school beginners living in four Ni-polluted industrial areas of North Rhine-Westphalia, Germany. We assessed Ni in ambient air, Ni in urine from children and mothers, and Ni in tap water, conducted patch tests in children (including the NiSO(4)-dilution test) and collected questionnaire data. Statistics were done by linear and logistic regression analyses, adjusted for covariates. At increased Ni concentration in ambient air (unit of increase: 10 ng/m(3)), urinary Ni concentrations rose in both mothers (9.1%; 95% CI: 6.8-11.4%) and children (2.4%; 95% CI: 0.4-4.4%). The prevalence of Ni sensitization in children was associated with increased Ni from ambient air (unit of increase: 18 ng/m(3); odds ratio 1.28; 95% CI: 1.25-1.32) and urinary Ni concentration (unit of increase: 7.1 μg/L; odds ratio 2.4; 95% CI: 1.20-4.48). Ni in ambient air of areas with Ni-emitting factories contributes to internal Ni exposure in residents via inhalation and, furthermore, is a risk factor for the development of Ni sensitization in children., (Copyright © 2010 Elsevier Inc. All rights reserved.)

For decades, extrinsic skin aging has been known to result from chronic exposure to solar radiation and, more recently, to tobacco smoke. In this study, we have assessed the influence of air pollution on skin aging in 400 Caucasian women aged 70-80 years. Skin aging was clinically assessed by means of SCINEXA (score of intrinsic and extrinsic skin aging), a validated skin aging score. Traffic-related exposure at the place of residence was determined by traffic particle emissions and by estimation of soot in fine dust. Exposure to background particle concentration was determined by measurements of ambient particles at fixed monitoring sites. The impact of air pollution on skin aging was analyzed by linear and logistic regression and adjusted for potential confounding variables. Air pollution exposure was significantly correlated to extrinsic skin aging signs, in particular to pigment spots and less pronounced to wrinkles. An increase in soot (per 0.5 × 10(-5) per m) and particles from traffic (per 475  kg per year and square km) was associated with 20% more pigment spots on forehead and cheeks. Background particle pollution, which was measured in low residential areas of the cities without busy traffic and therefore is not directly attributable to traffic but rather to other sources of particles, was also positively correlated to pigment spots on face. These results indicate that particle pollution might influence skin aging as well.

Background and Objective: Nickel is one of the most prevalent causes of contact allergy in the general population. This study focuses on human exposure to airborne nickel and its potential to induce allergic sensitization., Materials and Methods: The study group consisted of 309 children at school-starter age living in the West of Germany in the vicinity of two industrial sources and in a rural town without nearby point sources of nickel. An exposure assessment of nickel in ambient air was available for children in the Ruhr district using routinely monitored ambient air quality data and dispersion modelling. Internal nickel exposure was assessed by nickel concentrations in morning urine samples of the children., Results: The observed nickel sensitization prevalence rates varied between 12.6% and 30.7%. Statistically significant associations were showed between exposure to nickel in ambient air and urinary nickel concentration as well as between urinary nickel concentration and nickel sensitization. Furthermore, an elevated prevalence of nickel sensitization was associated with exposure to increased nickel concentrations in ambient air., Conclusion: The observed associations support the assumption that inhaled nickel in ambient air might be a risk factor for nickel sensitization; further studies in larger collectives are necessary.

Objective: Risk-assessment for environmental odors and the development of an appropriate guideline for protection against undue odor annoyance have long been hampered by the difficulties of assessing odor exposure and community annoyance responses. In recent years, however, dose-response associations between frequency of odor events and odor annoyance level in the affected population were established. However, the influence of hedonic tone (pleasantness-unpleasantness) and perceived odor strength (intensity) on the degree of odor annoyance have long been neglected in such studies and accompanying guidelines. In order to close this gap a pertinent field study was conducted in the vicinity of six odor emitting plants, two with pleasant (sweets production, rusk bakery), with neutral (textile production, seed oil production), and with presumably unpleasant odor emissions (fat refinery, cast iron production)., Methods: A standardized sensory method was developed (described in Part I in the accompanying paper) to quantify intensity and hedonic tone within the assessment of odor exposure by systematic field inspection with trained observers. Additionally, exposure-information, the degree of annoyance, and the frequency of general health complaints and irritation symptoms were collected from the exposed residents through direct interviews. Multiple logistic regression analysis was used to establish dose-response associations between odor frequency, intensity and hedonic tone as independent variables and annoyance or symptom reporting as the dependent variable., Results: It is shown that exposure-annoyance as well as exposure-symptom associations are strongly influenced by odor hedonic. Whereas pleasant odors induced little to no annoyance, both neutral and unpleasant ones did. Additional inclusion of odor intensity did not improve the prediction of odor annoyance. Frequency of reported symptoms was found to be exclusively mediated by annoyance. The results are discussed in terms of environmental stress emphasizing the WHO-definition of health., Conclusions: Based on these findings the existing German guideline against undue odor annoyance was modified.

Background: Living close to major roads or highways has been suggested to almost double the risk of dying from cardiopulmonary causes. We assessed whether long-term exposure to air pollution originating from motorized traffic and industrial sources is associated with total and cause-specific mortality in a cohort of women living in North Rhine-Westphalia, Germany., Methods: The study was a follow-up of a series of cross-sectional studies carried out during the 1980s and 1990s on the health of women (age 50-59 years). Approximately 4800 women were followed up for vital status and migration. Exposure to air pollution was defined by distance to major roads calculated from Geographic Information System data and by 1- and 5-year average nitrogen dioxide (NO2) and particle (PM10) concentrations calculated from air monitoring station data. We analyzed associations between exposure and mortality using Cox's proportional hazards models adjusting for confounders. Relative risks (RRs) refer to an interquartile range increase in exposure (16 microg/m for NO2; 7 microg/m for PM10)., Results: During the follow-up period, 8% of the women died, 3% from cardiopulmonary causes. Cardiopulmonary mortality was associated with living within a 50-meter radius of a major road (adjusted RR = 1.70; 95% confidence interval = 1.02-2.81), with NO2 (1.57; 1.23-2.00 for 1-year average), and with PM10 (1.34; 1.06-1.71 for 1-year average). Exposure to NO2 was also associated with all-cause mortality (1.17; 1.02-1.34). No association was seen with noncardiopulmonary nonlung cancer mortality., Conclusions: Living close to major roads and chronic exposure to NO2 and PM10 may be associated with an increased mortality due to cardiopulmonary causes.

Between 1991 and 2000, ambient air pollution in East Germany changed to resemble West German pollution levels: The concentration of total suspended particles (TSPs) decreased on a broad scale while traffic increased. During that time, we analyzed total lung capacity (TLC) and airway resistance (R(aw)) of East and West German children. We tested children 5-7 years of age (n = 2,574) with cooperation-independent body plethysmography in repeated cross sections. We used random-effect models to determine the mutually adjusted association between lung function and short-term and chronic particle exposure and its interaction with living near a busy road. Annual averages of TSPs declined from 77 to 44 microg/m2; averages on the day of investigation declined from 133 to 30 microg/m2. Differences in lung function between East and West German children vanished during the investigation time. The association of TSPs with R(aw) and TLC was stronger in children living > 50 m away from busy roads. East German children from this group had an R(aw) 2.5% higher [95% confidence interval (CI), 0.0-5.1%] per 40-microg/m2 increase of daily TSP averages. TLC decreased by 6.2% (95% CI, 0.04-11.6%) per 40-microg/m2 increase in annual mean TSPs, and this effect was equally pronounced in East and West Germany. TSP exposure decreased on a broad scale between 1991 and 2000. Lower concentrations of TSPs were associated with better measures of lung function in 6-year-old children. For children living near busy roads, this effect was diminished.

Particles in the air influence mortality and morbidity even in concentrations which were considered harmless. This report examines their role in allergies. Studies on children from areas with different degrees of pollution show that the "classical" type of air pollution with high amounts of coarse particles apparently does not induce allergies. Nearly all studies, which characterized exposure on a smaller spatial scale, found that symptoms of asthma and allergic rhinitis were more common in children exposed to traffic-related pollution. Time series and panel studies demonstrate that particle pollution contributes to asthma aggravation. Whether this applies to eczema or allergic rhinitis has hardly been investigated. Overall the studies suggest a special role for traffic-related particles.

Background: East-West comparison studies in Europe find higher prevalences of infectious airway diseases and lower prevalences of allergies in eastern areas. Pollution from sulphur dioxide (SO2) or total suspended particles (TSP) are discussed as causes of this difference., Methods: In four differently polluted areas of East Germany where pollution decreased dramatically between 1989 and 1995 cross-sectional studies in about 7-year-old children were repeated every year between 1991 and 1995. In two differently polluted areas of West Germany studies with the same design were done in 1991 and 1994. In all, 19090 children participated in the study. Thirteen different questions about airway diseases and allergies were evaluated. Logistic regression was used to adjust for confounding., Results: With the exception of pneumonia, all infectious airway diseases and irritations of the airways show a steeper temporal decrease in East than in West Germany or are positively associated with either SO2 or TSP in East Germany. For allergies and related symptoms no differences in time trends could be detected or no association with SO2 or TSP could be seen in East Germany., Conclusion: Most airway diseases were more frequent in East than in West Germany in 1991 and were associated with SO2 or TSP. The decrease in these pollutants between 1991 and 1995 has already had a favourable effect. An effect of SO2 or TSP pollution on allergies and related symptoms could not be detected. This pollution does not protect against the development of allergies.

The aim of this study was to investigate the relationship between different levels of air pollution and IgG antibody titers against tetanus toxoid in sera of 6 year old children (n = 354). Additionally, other parameters of the humoral immune response (immunoglobulins G, A, M, total IgE, complement component C3c, C-reactive protein (CRP)) were analysed. The index areas were Leipzig, Magdeburg (Saxony/Saxe-Anhalt), and Duisburg, Dortmund (Ruhr region). The control areas were Osterburg and Borken. IgG antibodies against tetanus toxoid were measured by ELISA in sera of children vaccinated three times DPT in early childhood. The other humoral parameters were measured by nephelometry. In comparison to the control area Borken the sera of children living in the index areas Duisburg and Dortmund showed a lower antibody titer. There were no differences between the index areas (Leipzig, Magdeburg) and the control area Osterburg. It has to be taken into account that the choice of Osterburg as a control area is problematic because of the lack of data on air pollution. Statistically, there was no relationship between antibody titer against tetanus toxoid and the additionally measured parameters of the humoral immune response.