Nonatopic eczema in elderly women: Effect of air pollution and genes.

BACKGROUND: Although many risk factors have been described for atopic eczema in children, little is known about the eczema phenotype in middle-aged or elderly adults. OBJECTIVE: We sought to examine the association between air pollution, atopy, and eczema in adulthood. METHODS: This analysis was based on 834 women from the Study on the influence of Air pollution on Lung Function, Inflammation and Ageing cohort in Germany. Incident symptoms of eczema after age 55 years and prevalent symptoms of eczema 12 months or less before investigation were assessed by means of questionnaire at the second follow-up (2007-2010). Total serum IgE levels were measured at baseline (1985-1994) and in 2007-2010. Exposure to air pollution was assessed by using land-use regression. Adjusted logistic regression models were applied to estimate the association between air pollution and incident and prevalent symptoms of eczema. Weighted genetic risk scores were used to investigate the effect of atopic eczema-related risk alleles on this association. RESULTS: Exposures to oxides of nitrogen (nitrogen dioxide and nitrogen oxides) and particulate matter (fine particulate matter with an aerodynamic diameter of ≤2.5 µm [PM2.5] and particulate matter with an aerodynamic diameter of <10 µm) were significantly associated with increased odds of incident eczema (eg, with PM2.5 per 4.7 µg/m3; odds ratio, 1.45; 95% CI, 1.06-1.99). These associations were slightly more pronounced with nonatopic eczema (eg, with PM2.5; odds ratio of 1.65 and 95% CI of 1.15-2.34 for participants without hay fever or increased IgE levels). Associations with air pollution were stronger in carriers of fewer risk alleles for atopic eczema. CONCLUSION: Nonatopic eczema in the elderly is associated with traffic-related air pollutants, and this phenotype differs from genetically driven atopic eczema.

Impact of long-term air pollution exposure on metabolic control in children and adolescents with type 1 diabetes: results from the DPV registry.

AIMS/HYPOTHESIS: Studies on the association between air pollution and metabolic control in children and adolescents with type 1 diabetes are rare and findings are inconsistent. We examined the relationship between air pollution variables (particulate matter with an aerodynamic diameter <10 µm [PM10], NO2 and accumulated ozone exposure [O3-AOT]) and metabolic variables (HbA1c and daily insulin dose [U/kg body weight]) in children and adolescents with type 1 diabetes. METHODS: We investigated 37,372 individuals with type 1 diabetes aged <21 years, documented between 2009 and 2014 in 344 German centres of the prospective diabetes follow-up registry (Diabetes-Patienten-Verlaufsdokumentation [DPV]). Long-term air pollution exposure (annual and quinquennial means) data were linked to participants via the five-digit postcode areas of residency. Cross-sectional multivariable regression analysis was used to examine the association between air pollution and metabolic control. RESULTS: After comprehensive adjustment, an interquartile range increase in O3-AOT was associated with a lower HbA1c (-3.7% [95% CI -4.4, -3.0]). The inverse association between O3-AOT and HbA1c persisted after additional adjustment for degree of urbanisation or additional adjustment for PM10. Moreover, the inverse association remained stable in further sensitivity analyses. No significant associations between HbA1c and PM10 or NO2 were found. No association was observed between any of the three air pollutants and insulin dose. CONCLUSIONS/INTERPRETATION: The inverse association between O3-AOT and HbA1c could not be explained by regional differences in diabetes treatment or by other differences between urban and rural areas. Furthermore, our results remained stable in sensitivity analyses. Further studies on the association between air pollution and HbA1c in children and adolescents with type 1 diabetes are needed to confirm our observed association and to elucidate underlying mechanisms.

The role of air pollution and lung function in cognitive impairment.

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 (NO2) 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 (FEV1), forced vital capacity (FVC) and FEV1/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 FEV1 and FVC was positively associated with VCP (ß=0.18 (95% CI 0.02-0.34) and ß=0.23 (95% CI 0.07-0.39), respectively). The proportion of the association between NO2 on VCP mediated by FEV1 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.

Urban upbringing and childhood respiratory and allergic conditions: A multi-country holistic study.

OBJECTIVE: We integratively assessed the effect of different indoor and outdoor environmental exposures early in life on respiratory and allergic health conditions among children from (sub-) urban areas. METHODS: This study included children participating in four ongoing European birth cohorts located in three different geographical regions: INMA (Spain), LISAplus (Germany), GINIplus (Germany) and BAMSE (Sweden). Wheezing, bronchitis, asthma and allergic rhinitis throughout childhood were assessed using parental-completed questionnaires. We designed "environmental scores" corresponding to different indoor, green- and grey-related exposures (main analysis, a-priori-approach). Cohort-specific associations between these environmental scores and the respiratory health outcomes were assessed using random-effects meta-analyses. In addition, a factor analysis was performed based on the same exposure information used to develop the environmental scores (confirmatory analysis, data-driven-approach). RESULTS: A higher early exposure to the indoor environmental score increased the risk for wheezing and bronchitis within the first year of life (combined adjusted odds ratio: 1.20 [95% confidence interval: 1.13-1.27] and 1.28 [1.18-1.39], respectively). In contrast, there was an inverse association with allergic rhinitis between 6 and 8 years (0.85 [0.79-0.92]). There were no statistically significant associations for the outdoor related environmental scores in relation to any of the health outcomes tested. The factor analysis conducted confirmed these trends. CONCLUSION: Although a higher exposure to indoor related exposure through occupants was associated with an increased risk for wheezing and bronchitis within the 1st year, it might serve as a preventive mechanism against later childhood allergic respiratory outcomes in urbanized environments through enhanced shared contact with microbial agents.

Estrogen receptor beta polymorphisms and cognitive performance in women: associations and modifications by genetic and environmental influences.

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 PM2.5). 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.

Residential greenness and blood lipids in children: A longitudinal analysis in GINIplus and LISAplus.

INTRODUCTION: There is some evidence of decreased cardiovascular disease (CVD) mortality and morbidity among adults residing in greener places. Among others, blood lipids are well established risk factors for CVD. In our previous study, we observed the inverse association between greenness and blood pressure in 10-year-old children. In the current study, we investigated whether there is also a link between residential greenness and blood lipids in 10- and 15-year-old children. METHODS: Complete data on blood lipids (total cholesterol, HDL, LDL and triglyceride), residential greenness (NDVI in 100-m, 300- and 500-m buffers around residences) and confounders were available for 1,552 participants at 10 and 15 years of age, residing in two study areas of two German birth cohorts - GINIplus and LISAplus. Longitudinal associations between NDVI and blood lipids were assessed by generalized estimation equations. RESULTS: No associations were observed between residential greenness in any of the chosen buffers and blood lipids in children (e.g., change in blood lipids per interquartile increase in NDVI in 100-m buffer for total cholesterol and LDL: means ratio=1.00 (95% confidence interval: 0.99-1.01), for triglyceride: 0.98 (0.96-1.00)). No area- or sex-varying effects were evident. Change of the residence between 10 and 15 years also did not yield any consistent associations. CONCLUSIONS: There is no evidence of an association between greenness and blood lipids in 10- and 15-years old children.

Effects of long-term exposure to air pollution on natural-cause mortality: an analysis of 22 European cohorts within the multicentre ESCAPE project.

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).

Long-term Exposure to Particulate Matter Constituents and the Incidence of Coronary Events in 11 European Cohorts.

BACKGROUND: Long-term exposure to particulate matter (PM) has been associated with increased cardiovascular morbidity and mortality but little is known about the role of the chemical composition of PM. This study examined the association of residential long-term exposure to PM components with incident coronary events. METHODS: Eleven cohorts from Finland, Sweden, Denmark, Germany, and Italy participated in this analysis. 5,157 incident coronary events were identified within 100,166 persons followed on average for 11.5 years. Long-term residential concentrations of PM < 10 µm (PM10), PM < 2.5 µm (PM2.5), and a priori selected constituents (copper, iron, nickel, potassium, silicon, sulfur, vanadium, and zinc) were estimated with land-use regression models. We used Cox proportional hazard models adjusted for a common set of confounders to estimate cohort-specific component effects with and without including PM mass, and random effects meta-analyses to pool cohort-specific results. RESULTS: A 100 ng/m³ increase in PM10 K and a 50 ng/m³ increase in PM2.5 K were associated with a 6% (hazard ratio and 95% confidence interval: 1.06 [1.01, 1.12]) and 18% (1.18 [1.06, 1.32]) increase in coronary events. Estimates for PM10 Si and PM2.5 Fe were also elevated. All other PM constituents indicated a positive association with coronary events. When additionally adjusting for PM mass, the estimates decreased except for K. CONCLUSIONS: This multicenter study of 11 European cohorts pointed to an association between long-term exposure to PM constituents and coronary events, especially for indicators of road dust.

Cross-sectional associations between air pollution and chronic bronchitis: an ESCAPE meta-analysis across five cohorts.

BACKGROUND: This study aimed to assess associations of outdoor air pollution on prevalence of chronic bronchitis symptoms in adults in five cohort studies (Asthma-E3N, ECRHS, NSHD, SALIA, SAPALDIA) participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE) project. METHODS: Annual average particulate matter (PM(10), PM(2.5), PM(absorbance), PM(coarse)), NO(2), nitrogen oxides (NO(x)) and road traffic measures modelled from ESCAPE measurement campaigns 2008-2011 were assigned to home address at most recent assessments (1998-2011). Symptoms examined were chronic bronchitis (cough and phlegm for ≥3 months of the year for ≥2 years), chronic cough (with/without phlegm) and chronic phlegm (with/without cough). Cohort-specific cross-sectional multivariable logistic regression analyses were conducted using common confounder sets (age, sex, smoking, interview season, education), followed by meta-analysis. RESULTS: 15 279 and 10 537 participants respectively were included in the main NO(2) and PM analyses at assessments in 1998-2011. Overall, there were no statistically significant associations with any air pollutant or traffic exposure. Sensitivity analyses including in asthmatics only, females only or using back-extrapolated NO(2) and PM10 for assessments in 1985-2002 (ECRHS, NSHD, SALIA, SAPALDIA) did not alter conclusions. In never-smokers, all associations were positive, but reached statistical significance only for chronic phlegm with PM(coarse) OR 1.31 (1.05 to 1.64) per 5 µg/m(3) increase and PM(10) with similar effect size. Sensitivity analyses of older cohorts showed increased risk of chronic cough with PM(2.5abs) (black carbon) exposures. CONCLUSIONS: Results do not show consistent associations between chronic bronchitis symptoms and current traffic-related air pollution in adult European populations.

Air pollution during pregnancy and childhood cognitive and psychomotor development: six European birth cohorts.

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.

Long-term exposure to air pollution and cardiovascular mortality: an analysis of 22 European cohorts.

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.

Investigating the spill-over hypothesis: analysis of the association between local inflammatory markers in sputum and systemic inflammatory mediators in plasma.

Exposure to air pollutants represents a risk factor not only for respiratory diseases and lung cancer, but also for cardiometabolic diseases. It has been hypothesised that local inflammation in the lung and systemic subclinical inflammation are linked by impaired lung function and the spill-over of proinflammatory factors from the lung into the circulation which could act as intermediaries between environmental exposures and disease risk. We wanted to investigate whether local and systemic inflammatory markers are associated, which would support the spill-over hypothesis. Sputum and plasma samples were obtained from 257 women of the German SALIA cohort. We performed immunoassays to measure multiple biomarkers of airway inflammation in sputum as well as cytokines, chemokines and soluble adhesion molecules in plasma. Correlations were calculated and adjusted for potentially confounding variables. Even though several significant associations were detected between inflammatory mediators in sputum and plasma, correlation coefficients were rather low ranging from r≥-0.20 to r≤0.20. Comparatively stronger associations were observed between nitrite, eosinophil cationic protein, leukotrienes C/D/E4 and interleukin-8 in sputum. Notably, correlations were positive with all proinflammatory biomarkers and interleukin-1 receptor antagonist in plasma, whereas negative correlations were observed with the anti-inflammatory adipokine adiponectin. In conclusion, local inflammation in the lung and systemic subclinical inflammation appear mainly independently regulated in elderly women from the general population. Although we found multiple significant correlations between inflammatory biomarkers in sputum and plasma, our results do not provide clear support for the spill-over hypothesis.

Air pollution and subclinical airway inflammation in the SALIA cohort study.

BACKGROUND: The association between long-term exposure to air pollution and local inflammation in the lung has rarely been investigated in the general population of elderly subjects before. We investigated this association in a population-based cohort of elderly women from Germany. METHODS: In a follow-up examination of the SALIA cohort study in 2008/2009, 402 women aged 68 to 79 years from the Ruhr Area and Borken (Germany) were clinically examined. Inflammatory markers were determined in exhaled breath condensate (EBC) and in induced sputum (IS). We used traffic indicators and measured air pollutants at single monitoring stations in the study area to assess individual traffic exposure and long-term air pollution background exposure. Additionally long-term residential exposure to air pollution was estimated using land-use regression (LUR) models. We applied multiple logistic and linear regression analyses adjusted for age, indoor mould, smoking, passive smoking and socio-economic status and additionally conducted sensitivity analyses. RESULTS: Inflammatory markers showed a high variability between the individuals and were higher with higher exposure to air pollution. NO derivatives, leukotriene (LT) B4 and tumour necrosis factor-α (TNF-α) showed the strongest associations. An increase of 9.42 µg/m3 (interquartile range) in LUR modelled NO2 was associated with measureable LTB4 level (level with values above the detection limit) in EBC (odds ratio: 1.38, 95% CI: 1.02 -1.86) as well as with LTB4 in IS (%-change: 19%, 95% CI: 7% - 32%). The results remained consistent after exclusion of subpopulations with risk factors for inflammation (smoking, respiratory diseases, mould infestation) and after extension of models with additional adjustment for season of examination, mass of IS and urban/rural living as sensitivity analyses. CONCLUSIONS: In this analysis of the SALIA study we found that long-term exposure to air pollutants from traffic and industrial sources was associated with an increase of several inflammatory markers in EBC and in IS. We conclude that long-term exposure to air pollution might lead to changes in the inflammatory marker profile in the lower airways in an elderly female population.

A cross-sectional analysis of the effects of residential greenness on blood pressure in 10-year old children: results from the GINIplus and LISAplus studies.

BACKGROUND: According to Ulrich's psychoevolutionary theory, contact with green environments mitigates stress by activating the parasympathetic system, (specifically, by decreasing blood pressure (BP)). Experimental studies have confirmed this biological effect. However, greenness effects on BP have not yet been explored using an observational study design. We assessed whether surrounding residential greenness is associated with BP in 10 year-old German children. METHODS: Systolic and diastolic BPs were assessed in 10 year-old children residing in the Munich and Wesel study areas of the German GINIplus and LISAplus birth cohorts. Complete exposure, outcome and covariate data were available for 2,078 children. Residential surrounding greenness was defined as the mean of Normalized Difference Vegetation Index (NDVI) values, derived from Landsat 5 TM satellite images, in circular 500-m buffers around current home addresses of participants. Generalized additive models assessed pooled and area-specific associations between BP and residential greenness categorized into area-specific tertiles. RESULTS: In the pooled adjusted model, the systolic BP of children living at residences with low and moderate greenness was 0.90 ± 0.50 mmHg (p-value = 0.073) and 1.23 ± 0.50 mmHg (p-value = 0.014) higher, respectively, than the systolic BP of children living in areas of high greenness. Similarly, the diastolic BP of children living in areas with low and moderate greenness was 0.80 ± 0.38 mmHg (p-value = 0.033) and 0.96 ± 0.38 mmHg (p-value = 0.011) higher, respectively, than children living in areas with high greenness. These associations were not influenced by environmental stressors (temperature, air pollution, noise annoyance, altitude and urbanisation level). When stratified by study area, associations were significant among children residing in the urbanised Munich area but null for those in the rural Wesel area. CONCLUSIONS: Lower residential greenness was positively associated with higher BP in 10 year-old children living in an urbanised area. Further studies varying in participants' age, geographical area and urbanisation level are required.

Development of land use regression models for particle composition in twenty study areas in Europe.

Land Use Regression (LUR) models have been used to describe and model spatial variability of annual mean concentrations of traffic related pollutants such as nitrogen dioxide (NO2), nitrogen oxides (NOx) and particulate matter (PM). No models have yet been published of elemental composition. As part of the ESCAPE project, we measured the elemental composition in both the PM10 and PM2.5 fraction sizes at 20 sites in each of 20 study areas across Europe. LUR models for eight a priori selected elements (copper (Cu), iron (Fe), potassium (K), nickel (Ni), sulfur (S), silicon (Si), vanadium (V), and zinc (Zn)) were developed. Good models were developed for Cu, Fe, and Zn in both fractions (PM10 and PM2.5) explaining on average between 67 and 79% of the concentration variance (R(2)) with a large variability between areas. Traffic variables were the dominant predictors, reflecting nontailpipe emissions. Models for V and S in the PM10 and PM2.5 fractions and Si, Ni, and K in the PM10 fraction performed moderately with R(2) ranging from 50 to 61%. Si, NI, and K models for PM2.5 performed poorest with R(2) under 50%. The LUR models are used to estimate exposures to elemental composition in the health studies involved in ESCAPE.

Development of Land Use Regression models for PM(2.5), PM(2.5) absorbance, PM(10) and PM(coarse) in 20 European study areas; results of the ESCAPE project.

Land Use Regression (LUR) models have been used increasingly for modeling small-scale spatial variation in air pollution concentrations and estimating individual exposure for participants of cohort studies. Within the ESCAPE project, concentrations of PM(2.5), PM(2.5) absorbance, PM(10), and PM(coarse) were measured in 20 European study areas at 20 sites per area. GIS-derived predictor variables (e.g., traffic intensity, population, and land-use) were evaluated to model spatial variation of annual average concentrations for each study area. The median model explained variance (R(2)) was 71% for PM(2.5) (range across study areas 35-94%). Model R(2) was higher for PM(2.5) absorbance (median 89%, range 56-97%) and lower for PM(coarse) (median 68%, range 32- 81%). Models included between two and five predictor variables, with various traffic indicators as the most common predictors. Lower R(2) was related to small concentration variability or limited availability of predictor variables, especially traffic intensity. Cross validation R(2) results were on average 8-11% lower than model R(2). Careful selection of monitoring sites, examination of influential observations and skewed variable distributions were essential for developing stable LUR models. The final LUR models are used to estimate air pollution concentrations at the home addresses of participants in the health studies involved in ESCAPE.

The SCINEXA: a novel, validated score to simultaneously assess and differentiate between intrinsic and extrinsic skin ageing.

BACKGROUND: Studies on the pathogenesis of skin ageing as well as efficacy testing of cosmetic and aesthetic measures to prevent or reverse skin ageing require - as an easy to use method - a validated non-invasive clinical score, which allows to simultaneously assess and differentiate between intrinsic (=chronological) and extrinsic (=photo-) skin ageing. Such an ideal score, however, does currently not exist. OBJECTIVES: We developed a novel skin ageing score 'SCINEXA' comprising 5 items indicative of intrinsic and 18 items highly characteristic of extrinsic skin ageing. These items were used to define an index (index(discr)) that allowed differentiating between intrinsic versus extrinsic skin ageing. In order to validate the 'SCINEXA', we asked whether it can be used to discriminate regular sunbed users, which have been chronically exposed to ultraviolet radiation and thus are prone to photoageing, from non-sunbed users, which were considered paradigmatic for intrinsic skin ageing. METHODS: For this purpose, 58 non-sunbed users and 16 regularly sunbed users were assessed. In addition to the clinical examination of the 23 score items potential confounders were considered by questionnaire. RESULTS: By employing the index(discr), we were able to classify 92% of all study subjects correctly as sunbed or non-sunbed users. Specifically, an index above 2 was associated with sunbed use and thus extrinsic skin ageing, whereas an index below 2 indicated intrinsic skin ageing. CONCLUSION: The novel 'SCINEXA' is suitable for the simultaneous assessment of intrinsic and extrinsic skin ageing.

Residential and school greenspace and academic performance: Evidence from the GINIplus and LISA longitudinal studies of German adolescents.

BACKGROUND: Few studies have reported the association between greenspace and academic performance at school level. We examined associations between both residential and school greenspace and individual school grades in German adolescents. METHODS: German and maths grades from the latest school certificate, residential and school greenspace, and covariates were available for 1351 10 and 15 years old Munich children and 1078 Wesel children from two German birth cohorts - GINIplus and LISA. Residential and school greenspace was assessed by the Normalized Difference Vegetation Index (NDVI), tree cover, and (in Munich only) proportion of agricultural land, forest, and urban green space in 500-m and 1000-m circular buffers. Longitudinal associations between each exposure-outcome pair were assessed by logistic mixed effects models with person and school as random intercepts and adjusted for potential confounders. RESULTS: No associations were observed between any of the greenspace variables and grades in Wesel children. Several statistically significant associations were observed with German and maths grades in Munich children, however associations were inconsistent across sensitivity analyses. CONCLUSIONS: There is no evidence of an association of higher greenspace at residence, school or combined with improved academic performance in German adolescents from the GINIplus and LISA longitudinal studies.

Tropospheric ozone and skin aging: Results from two German cohort studies.

During the last two decades, it has been well established that a short-term exposure to ozone (O3) elicits an oxidative stress response in human and mouse skin, which leads to aberrant transcriptional expression of genes consistent with increased skin aging. Whether a long-term exposure to ambient O3 is associated with any skin aging traits, has remained unclear. We addressed this question in two elderly German cohorts: the SALIA study (806 women aged 66-79 years), and the BASE-II study (1207 men and women aged 60-84 years). Five-year mean residential exposure to O3 was modeled as the number of days with maximum daily 8-h mean O3 concentrations ≥120 µg/m3 per year in the wider neighborhood (5-digit postcode) of a participant's residence. Extrinsic (environmentally induced) skin aging traits - coarse wrinkles and pigment spots (lentigines) on the face - were assessed by means of SCINEXA™, a validated visual score previously shown to be well suited to measure extrinsic facial skin aging in cohort studies. We observed positive associations of O3 exceedances with coarse wrinkles in the face, but not with pigment spots. These associations were present in each cohort as well as in the combined sample of both cohorts. They were independent of chronic ultraviolet radiation exposure as the most obvious confounder, and also of co-pollutants such as particulate matter and nitrogen dioxide. Thus, long-term exposure to elevated concentrations of tropospheric O3 appears to contribute to skin aging.

Does respiratory health contribute to the effects of long-term air pollution exposure on cardiovascular mortality?

BACKGROUND: There is growing epidemiological evidence that short-term and long-term exposure to high levels of air pollution may increase cardiovascular morbidity and mortality. In addition, epidemiological studies have shown an association between air pollution exposure and respiratory health. To what extent the association between cardiovascular mortality and air pollution is driven by the impact of air pollution on respiratory health is unknown. The aim of this study was to investigate whether respiratory health at baseline contributes to the effects of long-term exposure to high levels of air pollution on cardiovascular mortality in a cohort of elderly women. METHOD: We analyzed data from 4750 women, aged 55 at the baseline investigation in the years 1985-1994. 2593 of these women had their lung function tested by spirometry. Respiratory diseases and symptoms were asked by questionnaire. Ambient air pollution exposure was assessed by the concentrations of NO2 and total suspended particles at fixed monitoring sites and by the distance of residency to a major road. A mortality follow-up of these women was conducted between 2001 and 2003. For the statistical analysis, Cox' regression was used. RESULTS: Women with impaired lung function or pre-existing respiratory diseases had a higher risk of dying from cardiovascular causes. The impact of impaired lung function declined over time. The risk ratio (RR) of women with forced expiratory volume in one second (FEV1) of less than 80% predicted to die from cardiovascular causes was RR = 3.79 (95%CI: 1.64-8.74) at 5 years survival time and RR = 1.35 (95%CI: 0.66-2.77) at 12 years. The association between air pollution levels and cardiovascular death rate was strong and statistically significant. However, this association did only change marginally when including indicators of respiratory health into the regression analysis. Furthermore, no interaction between air pollution and respiratory health on cardiovascular mortality indicating a higher risk of those with impaired respiratory health could be detected. CONCLUSION: Respiratory health is a predictor for cardiovascular mortality. In women followed about 15 years after the baseline investigation at age 55 years long-term air pollution exposure and impaired respiratory health were independently associated with increased cardiovascular mortality.