Inter-annual trends of ultrafine particles in urban Europe.

Ultrafine particles (UFP, those with diameters ≤ 100 nm), have been reported to potentially penetrate deeply into the respiratory system, translocate through the alveoli, and affect various organs, potentially correlating with increased mortality. The aim of this study is to assess long-term trends (5-11 years) in mostly urban UFP concentrations based on measurements of particle number size distributions (PNSD). Additionally, concentrations of other pollutants and meteorological variables were evaluated to support the interpretations. PNSD datasets from 12 urban background (UB), 5 traffic (TR), 3 suburban background (SUB) and 1 regional background (RB) sites in 15 European cities and 1 in the USA were evaluated. The non-parametric Theil-Sen's method was used to detect monotonic trends. Meta-analyses were carried out to assess the overall trends and those for different environments. The results showed significant decreases in NO, NO2, BC, CO, and particle concentrations in the Aitken (25-100 nm) and the Accumulation (100-800 nm) modes, suggesting a positive impact of the implementation of EURO 5/V and 6/VI vehicle standards on European air quality. The growing use of Diesel Particle Filters (DPFs) might also have clearly reduced exhaust emissions of BC, PM, and the Aitken and Accumulation mode particles. However, as reported by prior studies, there remains an issue of poor control of Nucleation mode particles (smaller than 25 nm), which are not fully reduced with current DPFs, without emission controls for semi-volatile organic compounds, and might have different origins than road traffic. Thus, contrasting trends for Nucleation mode particles were obtained across the cities studied. This mode also affected the UFP and total PNC trends because of the high proportion of Nucleation mode particles in both concentration ranges. It was also found that the urban temperature increasing trends might have also influenced those of PNC, Nucleation and Aitken modes.

Gene-environment interaction in the association of residential greenness and 25(OH) vitamin D.

There is increasing awareness for beneficial health effects of green space surrounding the home, but the underlying mechanisms are not yet fully understood and challenging to study given the correlation with other exposures. Here, the association of residential greenness and vitamin D including a gene-environment interaction is investigated. 25-hydroxyvitamin D (25(OH)D) was measured by electrochemiluminescence at ages 10 and 15 years in participants of two German birth cohorts GINIplus and LISA. Greenness was measured using the Landsat-derived Normalized Difference Vegetation Index (NDVI) in a 500 m buffer surrounding the home. Linear and logistic regression models were applied at both time points adjusted for several covariates (N10Y = 2,504, N15Y = 2,613). In additional analyses vitamin D-related genes, physical activity, time spent outdoors, supplements, and measurement season were investigated as potential confounders or effect modifiers. A 1.5-SD increase in NDVI was significantly associated with increased 25(OH)D values at ages 10 and 15 years (ß10y = 2.41 nmol/l, p=<0.01; ß15y = 2.03 nmol/l, p = 0.02). In stratified analyses, the associations were not seen in participants spending more than 5 h/day outside in summer, having a high physical activity level, taking supplements, or being examined during the winter season. In a subset (n = 1,732) with genetic data, a significant gene-environment interaction of NDVI with CYP2R1, an upstream gene in 25(OH)D synthesis, was observed at age 10 years. When investigating 25(OH)D sufficiency, defined as values above 50 nmol/l, a 1.5-SD increase in NDVI was associated with significantly higher odds of having sufficient 25 (OH)D levels at age 10 years (OR = 1.48, 1.19-1.83). In conclusion, robust associations between residential greenness and 25 (OH)D levels were observed in children and adolescents independent of other confounders and additionally supported by the presence of a gene-environment interaction. Effects of NDVI were stronger in those having lower vitamin D levels at age 10 years due to their covariate profile or genetically lower 25(OH)D synthesis.

Phenomenology of ultrafine particle concentrations and size distribution across urban Europe.

The 2017-2019 hourly particle number size distributions (PNSD) from 26 sites in Europe and 1 in the US were evaluated focusing on 16 urban background (UB) and 6 traffic (TR) sites in the framework of Research Infrastructures services reinforcing air quality monitoring capacities in European URBAN & industrial areaS (RI-URBANS) project. The main objective was to describe the phenomenology of urban ultrafine particles (UFP) in Europe with a significant air quality focus. The varying lower size detection limits made it difficult to compare PN concentrations (PNC), particularly PN10-25, from different cities. PNCs follow a TR > UB > Suburban (SUB) order. PNC and Black Carbon (BC) progressively increase from Northern Europe to Southern Europe and from Western to Eastern Europe. At the UB sites, typical traffic rush hour PNC peaks are evident, many also showing midday-morning PNC peaks anti-correlated with BC. These peaks result from increased PN10-25, suggesting significant PNC contributions from nucleation, fumigation and shipping. Site types to be identified by daily and seasonal PNC and BC patterns are: (i) PNC mainly driven by traffic emissions, with marked correlations with BC on different time scales; (ii) marked midday/morning PNC peaks and a seasonal anti-correlation with PNC/BC; (iii) both traffic peaks and midday peaks without marked seasonal patterns. Groups (ii) and (iii) included cities with high insolation. PNC, especially PN25-800, was positively correlated with BC, NO2, CO and PM for several sites. The variable correlation of PNSD with different urban pollutants demonstrates that these do not reflect the variability of UFP in urban environments. Specific monitoring of PNSD is needed if nanoparticles and their associated health impacts are to be assessed. Implementation of the CEN-ACTRIS recommendations for PNSD measurements would provide comparable measurements, and measurements of <10 nm PNC are needed for full evaluation of the health effects of this size fraction.

Residential green space and age at menarche in German and Australian adolescent girls: A longitudinal study.

BACKGROUND: A large multicentre European study reported later onset of menopause among women residing in greener areas. This influence on the timing of a reproductive event like menopause, raises the question whether similar associations can be observed with timing of menarche. We investigated whether exposure to residential green space was related to the age at menarche in German and Australian adolescent girls. METHODS: The analytic samples comprised of 1706 German and 1474 Australian adolescent girls. Percentage of green space was calculated in 1000 m buffers around a residential address or its surrogate at the previous follow-up. Mixed effects Cox proportional hazard models were used to explore the associations. The survival object was the occurrence of menarche at the time of follow-up (15-year follow-up of the German cohorts and the study wave at 14-15 years in the Australian cohort) and number of years since baseline (10-year follow-up in the German cohort and the study wave at 10-11 years in the Australian cohort). Participants who did not reach menarche were included as censored observations. RESULTS: A greener residence was not associated with the age at menarche. Null findings were consistent in the general population and in analyses stratified by socioeconomic status or urbanicity in both countries. Urban residents were more likely to have earlier menarche, and this association was consistent across Germany and Australia. CONCLUSION: The results of our analysis do not support the hypothesis that residing in places with more green space can influence timing of menarche. However, given the limitations of our study, researchers should not be discouraged to further explore environmental risk factors of early menarche.

Longitudinal relationship of particulate matter and metabolic control and severe hypoglycaemia in children and adolescents with type 1 diabetes.

BACKGROUND: Evidence for the metabolic impact of long-term exposure to air pollution on diabetes is lacking. We investigated the association of particulate matter <10 µm (PM10) and <2.5 µm (PM2.5) with yearly averages of HbA1c, daily insulin dose (IU/kg) and rates of severe hypoglycaemia in type 1 diabetes (T1D). METHODS: We studied data of 44,383 individuals with T1D < 21 years which were documented in 377 German centres within the diabetes prospective follow-up registry (DPV) between 2009 and 2018. Outcomes were aggregated by year and by patient. PM10-and PM2.5-yearly averages prior to the respective treatment year were linked to individuals via the five-digit postcode areas of residency. Repeated measures linear and negative binomial regression were used to study the association between PM-quartiles (Q1 lowest, Q4 highest concentration) and yearly averages of HbA1c, daily insulin dose and rates of severe hypoglycaemia (confounders: sex, time-dependent age, age at diabetes onset, time-dependent type of treatment, migratory background, degree of urbanisation and socioeconomic index of deprivation). RESULTS: Adjusted mean HbA1c increased with PM10 (Q1: 7.96% [95%-CI: 7.95-7.98], Q4: 8.03% [8.02-8.05], p-value<0.001) and with PM2.5 (Q1: 7.97% [7.95-7.99], Q4: 8.02% [8.01-8.04], p < 0.001). Changes in daily insulin dose were inversely related to PM (PM10 and PM2.5: Q1 0.85 IU/kg [0.84-0.85], Q4: 0.83 IU/kg [0.82-0.83], p < 0.001). Adjusted rates of severe hypoglycaemia increased with PM-quartile groups (PM10 Q1:11.2 events/100 PY [10.9-11.5], PM10 Q4: 15.3 [14.9-15.7], p < 0.001; PM2.5 Q1: 9.9 events/100 PY [9.6-10.2], PM2.5 Q4: 14.2 [13.9-14.6], p < 0.001). DISCUSSION: Air pollution was associated with higher HbA1c levels and increased risk of severe hypoglycaemia in people with T1D, consequently indicating a higher risk of diabetes complications. Further studies are needed to explore causal pathways of the observed associations.

Effect of non-optimum ambient temperature on cognitive function of elderly women in Germany.

Non-optimum ambient temperature has been associated with a variety of health outcomes in the elderly population. However, few studies have examined its adverse effects on neurocognitive function. In this study, we explored the temperature-cognition association in elderly women. We investigated 777 elderly women from the German SALIA cohort during the 2007-2010 follow-up. Cognitive function was evaluated using the CERAD-Plus test battery. Modelled data on daily weather conditions were assigned to the residential addresses. The temperature-cognition association over lag 0-10 days was estimated using multivariable regression with distributed lag non-linear model. The daily mean temperature ranged between -6.7 and 26.0 °C during the study period for the 777 participants. We observed an inverse U-shaped association in elderly women, with the optimum temperature (15.3 °C) located at the 68th percentile of the temperature range. The average z-score of global cognitive function declined by -0.31 (95%CI: 0.73, 0.11) for extreme cold (the 2.5th percentile of temperature range) and -0.92 (95%CI: 1.50, -0.33) for extreme heat (the 97.5th percentile of temperature range), in comparison to the optimum temperature. Episodic memory was more sensitive to heat exposure, while semantic memory and executive function were the two cognitive domains sensitive to cold exposure. Individuals living in an urban area and those with a low educational level were particularly sensitive to extreme heat. In summary, non-optimum temperature was inversely associated with cognitive function in elderly women, with the effect size for heat exposure particularly substantial. The strength of association varied by cognitive domains and individual characteristics.

Outdoor air pollution and hormone-assessed pubertal development in children: Results from the GINIplus and LISA birth cohorts.

BACKGROUND: Air pollution is hypothesized to affect pubertal development. However, the few studies on this topic yielded overall mixed results. These studies did not consider important pollutants like ozone, and none of them involved pubertal development assessed by estradiol and testosterone measurements. We aimed to analyze associations between long-term exposure to four pollutants and pubertal development based on sex hormone concentrations among 10-year-old children. METHODS: These cross-sectional analyses were based on the 10-year follow-up medical examinations of 1945 children from the Munich and Wesel centers of the GINIplus and LISA German birth cohorts. Female and male pubertal development was assessed by dichotomizing the concentration of hormones in serum at 18.4 pmol/L and 0.087 nmol/L using the lower limits of quantification for estradiol and testosterone, respectively. Land-use regression models derived annual average concentrations of particulate matter with an aerodynamic diameter < 2.5 and 10 µm (PM2.5 and PM10), as well as spatial models assessed yearly average concentrations of nitrogen dioxide (NO2) and ozone, were calculated at the 10-year residential addresses. To evaluate associations, we utilized logistic regressions adjusted for potential covariates. The analyses were stratified by area and sex. RESULTS: Around 73% of the 943 females and 25% of the 1002 males had a high level of hormones and had already started puberty at the age of 10. Overall, we found no statistically significant associations between exposure to particles (PM2.5 or PM10) and pubertal development. Results on NO2 and ozone were not significant as well; for instance, per 10 µg/m3 increase in ozone concentration, odds ratios and 95% confidence intervals were 0.900 (0.605, 1.339) and 0.830 (0.573, 1.203) for females and males, respectively. Stratified by area, the aforementioned results did not reveal any associations either. CONCLUSIONS: Our study did not observe the associations between ambient air pollutants and pubertal development determined by estradiol and testosterone levels in children. However, due to the current limited number of studies on this topic, our results should be cautiously interpreted. Future longitudinal studies are needed to assess the association.

The mediating role of lung function on air pollution-induced cardiopulmonary mortality in elderly women: The SALIA cohort study with 22-year mortality follow-up.

BACKGROUND: Air pollution exposure is associated with reduced lung function and increased cardio-pulmonary mortality (CPM). OBJECTIVES: We analyzed the potential mediating effect of reduced lung function on the association between air pollution exposure and CPM. METHODS: We used data from the German SALIA cohort including 2527 elderly women (aged 51-56 years at baseline 1985-1994) with 22-year follow-up to CPM. Exposures to PM10, PM2.5, PM2.5 absorbance, NO2 and NOx were assessed by land-use regression modelling and back-extrapolated to estimate exposures at baseline. Lung function (FVC, FEV1) was measured by spirometry and transformed to GLI z-scores. Adjusted Cox proportional hazards and causal proportional hazards mediation analysis models were fitted. RESULTS: The survival analysis showed that reduced lung function (z-scores of FVC or FEV1 below 5% predicted) reflected significantly lower survival probability from CPM (p < 0.0001). Longterm exposures to NOx and NO2 were associated with increased risks of CPM (eg. HR = 1.215; 95%CI: 1.017-1.452 for IQR increase in NOx and HR = 1.209; 95%CI: 1.011-1.445 for IQR increase in NO2) after adjusting for reduced lung function and additional covariates. The associations of PM2.5 absorbance and CPM remained significant in models adjusted for FEV1/FVC, but the associations with PM10 and PM2.5 were not significant. The mediation analysis showed significant indirect effects of NO2 and NOx on CPM mediated through reduced FEV1 and FVC. The largest indirect effects were found for exposures to NO2 (HR = 1.037; 95%CI: 1.005-1.070) and NOx (HR = 1.028; 95%CI: 1.004-1.052) mediated through reduced FVC. The mediated proportion effect ranged from 13.9% to 19.6% in fully adjusted models. DISCUSSION: This study provides insights into the mechanism of reduced lung function in association between long-term air pollution exposure and CPM. The mediated effect was substantial for exposure to nitrogen oxides (NOx and NO2), but less pronounced for PM10 and PM2.5.

Air pollution and IgE sensitization in 4 European birth cohorts-the MeDALL project.

BACKGROUND: Whether long-term exposure air to pollution has effects on allergic sensitization is controversial. OBJECTIVE: Our aim was to investigate associations of air pollution exposure at birth and at the time of later biosampling with IgE sensitization against common food and inhalant allergens, or specific allergen molecules, in children aged up to 16 years. METHODS: A total of 6163 children from 4 European birth cohorts participating in the Mechanisms of the Development of ALLergy [MeDALL] consortium were included in this meta-analysis of the following studies: Children, Allergy, Milieu, Stockholm, Epidemiology (BAMSE) (Sweden), Influences of Lifestyle-Related Factors on the Human Immune System and Development of Allergies in Childhood (LISA)/German Infant Study on the Influence of Nutrition Intervention PLUS Environmental and Genetic Influences on Allergy Development (GINIplus) (Germany), and Prevention and Incidence of Asthma and Mite Allergy (PIAMA) (The Netherlands). The following indicators were modeled by land use regression: individual residential outdoor levels of particulate matter with aerodynamic diameters less than 2.5 µm, less than 10 µm, and between 2.5 and 10 µm; PM2.5 absorbance (a measurement of the blackness of PM2.5 filters); and nitrogen oxides levels. Blood samples drawn at ages 4 to 6 (n = 5989), 8 to 10 (n = 6603), and 15 to 16 (n = 5825) years were analyzed for IgE sensitization to allergen extracts by ImmunoCAP. Additionally, IgE against 132 allergen molecules was measured by using the MedALL microarray chip (n = 1021). RESULTS: Air pollution was not consistently associated with IgE sensitization to any common allergen extract up to age 16 years. However, allergen-specific analyses suggested increased risks of sensitization to birch (odds ratio [OR] = 1.12 [95% CI = 1.01-1.25] per 10-µg/m3 increase in NO2 exposure). In a subpopulation with microarray data, IgE to the major timothy grass allergen Phleum pratense 1 (Phl p 1) and the cat allergen Felis domesticus 1 (Fel d 1) greater than 3.5 Immuno Solid-phase Allergen Chip standardized units for detection of IgE antibodies were related to PM2.5 exposure at birth (OR = 3.33 [95% CI = 1.40-7.94] and OR = 4.98 [95% CI = 1.59-15.60], respectively, per 5-µg/m3 increase in exposure). CONCLUSION: Air pollution exposure does not seem to increase the overall risk of allergic sensitization; however, sensitization to birch as well as grass pollen Phl p 1 and cat Fel d 1 allergen molecules may be related to specific pollutants.

Ambient air pollution is associated with airway inflammation in older women: a nested cross-sectional analysis.

BACKGROUND: Air pollution is a risk factor for chronic obstructive pulmonary disease (COPD). Fraction of exhaled nitric oxide (FeNO) could be a useful biomarker for health effects of air pollutants. However, there were limited data from older populations with higher prevalence of COPD and other inflammatory conditions. METHODS: We obtained data from the German Study on the influence of Air pollution on Lung function, Inflammation and Ageing. Spirometry and FeNO were measured by standard techniques. Air pollutant exposures were estimated following the European Study of Cohorts for Air Pollution Effects protocols, and ozone (O3) measured at the closest ground level monitoring station. Multiple linear regression models were fitted to FeNO with each pollutant separately and adjusted for potential confounders. RESULTS: In 236 women (mean age 74.6 years), geometric mean FeNO was 15.2ppb. Almost a third (n=71, 30.1%) of the women had some chronic inflammatory respiratory condition. A higher FeNO concentration was associated with exposures to fine particles (PM2.5), PM2.5absorbance and respirable particles (PM10). There were no significant associations with PMcoarse, NO2, NOx, O3 or length of major roads within a 1 km buffer. Restricting the analysis to participants with a chronic inflammatory respiratory condition, with or without impaired lung function produced similar findings. Adjusting for diabetes did not materially alter the findings. There were no significant interactions between individual pollutants and asthma or current smoking. CONCLUSIONS: This study adds to the evidence to reduce ambient PM2.5 concentrations as low as possible to protect the health of the general population.

The role of air pollution in cognitive impairment and decline.

The biological pathways and the extent to which air pollution can affect the cognitive decline in the elderly is not fully understood. In recent years, the impact of air pollution on cognitive impairment has become an active area of epidemiological research and several studies provided supporting evidence. This short review focuses on epidemiological studies in older adults investigating the associations between long-term air pollution exposure and cognitive impairment and decline. Most studies were observational studies and reported assessment of cognitive function using different cognitive scores and air pollution exposure in adults older than 50 years. The results from these studies indicate that exposure to ambient air pollution can have adverse effects on cognitive decline and impairment, but the overall results are heterogeneous and not fully conclusive. The number of epidemiological studies are still limited and additional longer-term studies are needed to confirm the findings. Understanding the relationship between air pollution and cognitive impairment is important to develop preventive measures and to address the needs of people living with cognitive impairment.

Air pollution is associated with depressive symptoms in elderly women with cognitive impairment.

BACKGROUND: Studies on air pollution and depression in the elderly are limited and the results are heterogeneous. OBJECTIVES: We examined the association of ambient air pollution exposure and diagnosis and symptoms of depression in the elderly; and whether any associations were confounded or modified by cognitive decline. METHODS: We enrolled 821 elderly women from the German SALIA cohort (follow-up examination, 2007-2010). Self-reported depressive symptoms and level of cognition were evaluated using the CESD-R Scale and the CERAD-Plus test, respectively. We used two depression endpoints for analyses: self-reported doctor diagnosis of depression and frequency of depressive symptoms (CESD-R score). Long-term concentrations of particulate matter (PM) size fractions and nitrogen oxides (NOx) modeled by land-use regression were assigned to home addresses. Cross-sectional associations were assessed using adjusted logistic and linear regression models. RESULTS: Concentrations of coarse particles (PMcoarse), fine particles (PM2.5 and PM2.5 abs) and NO2 were significantly associated with diagnosis of depression (e.g. for PM2.5 OR = 1.62, 95%CI: 1.06, 2.46 and for NO2 OR = 1.54, 95% CI: 1.08, 2.19). Similarly, an increase of one interquartile range in PM10, PM2.5, NO2 and NOx was associated with depressive symptoms assessed with the CESD-R score (e.g. for PM2.5 16.2% difference in the mean; 95% CI: 5.8%, 26.5% and for NO2 14.5%; 95% CI: 4.8%, 24.2%). These associations were stronger in women with cognitive decline (e.g. Pint for PM2.5:0.022 and NO2:0.017) compared to women with normal cognition. In addition, living less than 100 m distance to major roads was significantly associated with diagnosis (OR = 1.99, 95% CI: 1.14, 3.47) and symptoms (19.7%; 95% CI: 4.3%, 35.1%) of depression. We did not observe any interaction effect of cognition on prior diagnosis of depression. CONCLUSIONS: Exposure to air pollution was associated with diagnosis of depression and depressive symptoms in elderly women. Women with impaired cognition may be at greater risk of depressive symptoms when exposed to air pollution.

Prenatal and postnatal exposure to air pollution and emotional and aggressive symptoms in children from 8 European birth cohorts.

BACKGROUND: The association between air pollution exposure and emotional and behavioural problems in children is unclear. We aimed to assess prenatal and postnatal exposure to several air pollutants and child's depressive and anxiety symptoms, and aggressive symptoms in children of 7-11 years. METHODS: We analysed data of 13182 children from 8 European population-based birth cohorts. Concentrations of nitrogen dioxide (NO2), nitrogen oxides (NOx), particulate matter (PM) with diameters of ≤10 µm (PM10), ≤ 2.5 µm (PM2.5), and between 10 and 2.5 µm (PMcoarse), the absorbance of PM2.5 filters (PM2.5abs), and polycyclic aromatic hydrocarbons (PAHs) were estimated at residential addresses of each participant. Depressive and anxiety symptoms and aggressive symptoms were assessed at 7-11 years of age using parent reported tests. Children were classified in borderline/clinical range or clinical range using validated cut offs. Region specific models were adjusted for various socio-economic and lifestyle characteristics and then combined using random effect meta-analysis. Multiple imputation and inverse probability weighting methods were applied to correct for potential attrition bias. RESULTS: A total of 1896 (14.4%) children were classified as having depressive and anxiety symptoms in the borderline/clinical range, and 1778 (13.4%) as having aggressive symptoms in the borderline/clinical range. Overall, 1108 (8.4%) and 870 (6.6%) children were classified as having depressive and anxiety symptoms, and aggressive symptoms in the clinical range, respectively. Prenatal exposure to air pollution was not associated with depressive and anxiety symptoms in the borderline/clinical range (e.g. OR 1.02 [95%CI 0.95 to 1.10] per 10 µg/m3 higher NO2) nor with aggressive symptoms in the borderline/clinical range (e.g. OR 1.04 [95%CI 0.96 to 1.12] per 10 µg/m3 higher NO2). Similar results were observed for the symptoms in the clinical range, and for postnatal exposures to air pollution. CONCLUSIONS: Overall, our results suggest that prenatal and postnatal exposure to air pollution is not associated with depressive and anxiety symptoms or aggressive symptoms in children of 7 to 11 years old.

Road Traffic Noise at the Residence, Annoyance, and Cognitive Function in Elderly Women.

The detrimental effects of traffic noise on cognition in children are well documented. Not much is known about the health effects in adults. We investigated the association of residential exposure to road traffic noise and annoyance due to road traffic noise with cognitive function in a cohort of 288 elderly women from the longitudinal Study on the influence of Air pollution on Lung function, Inflammation and Aging (SALIA) in Germany. Residential noise levels-weighted 24-h mean (LDEN) and nighttime noise (LNIGHT)-were modeled for the most exposed facade of dwellings and dichotomized at ≥50 dB(A). Traffic noise annoyance (day and night) was estimated by questionnaire. Cognitive function was assessed using the Consortium to Establish a Registry on Alzheimer's Disease (CERAD-Plus) Neuropsychological Assessment Battery. The modeled noise levels were associated with impaired total cognition and the constructional praxis domain, independently of air pollution. Self-reported noise annoyance was associated with better performance in semantic memory and constructional praxis domains. This finding should be interpreted with caution since we could not control for potential confounding by hearing loss. Noise levels and annoyance were associated, but their health effects seemed mutually independent.

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.

Modeling of air pollutant concentrations in an industrial region of Turkey.

The hourly SO2 and PM10 concentrations in ambient air of the Kutahya city located at the western part of Turkey have exceeded the air quality limits in winter months since several years. The region has major industrial plants including lignite-fired power plants and open-cast mining activities, residential areas, and traffic sources. To obtain and quantify the sector-wise anthropogenic emissions and spatial distribution of the major pollutants including SO2, NO x , PM10, and CO, a comprehensive emission inventory with 1-km spatial resolution was prepared for the year of 2014, and the AERMOD dispersion model was used to predict ambient air concentrations in a domain of 140 km by 110 km. Validation of the model results was also done referring to in situ routine measurements at two monitoring stations located in the study area. Total emissions of SO2, PM10, NO x , and CO in the study area were calculated as 64,399, 9770, 24,627, and 29,198 tons/year, respectively. The results showed that industrial plants were the largest sources of SO2, NO x , and PM10 emissions, while residential heating and road traffic were the most contributing sectors for CO emissions. Three major power plants in the region with total annual lignite consumption of 10 million tons per year were main sources of high SO2 concentrations, while high PM10 concentrations mainly originated from two major open-cast lignite mines. Major contributors of high NO x and CO concentrations were traffic including highways and urban streets, and residential heating with high lignite consumption in urban areas. Results of the dispersion model run with the emission inventory resulted in partially high index of agreement (0.75) with SO2 measured in the urban station within the modeled area.

Effects of ambient air pollution on respiratory tract complaints and airway inflammation in primary school children.

Respiratory health effects of ambient air pollution were studied in 605 school children 9 to 13 years in Eskisehir, Turkey. Each child performed a fractional exhaled nitric oxide (FENO) measurement and a lung function test (LFT). Self-reported respiratory tract complaints (having cold, complaints of throat, runny nose and shortness of breath/wheezing) in the last 7 days and on the day of testing were also recorded. As acute health outcomes were investigated, weekly average ambient concentrations of ozone (O3), nitrogen dioxide (NO2) and sulfur dioxide (SO2) were determined by passive sampling in the school playgrounds simultaneously with the health survey. Effects of air pollution on respiratory tract complaints and exhaled NO/lung function were estimated by multivariate logistic regression and multivariate linear mixed effects models, respectively. Upper respiratory tract complaints were significantly (p<0.05) associated with weekly average O3 concentrations during the health survey (adjusted odds ratios (OR) of 1.21 and 1.28 for a 10 µgm(-3) increment for having cold and a runny nose on day of testing, respectively). FENO levels were significantly (p<0.05) increased in children with various upper respiratory tract complaints (ratio in FENO varied between 1.16 and 1.40). No significant change in FENO levels was detected in association with any of the measured pollutants (p ≥ 0.05). Lung function was not associated with upper respiratory tract complaints and FENO levels. Peak Expiratory Flow (PEF) levels were negatively associated with weekly average O3 levels for children without upper respiratory tract complaints. In summary, elevated levels of air pollutants increased respiratory tract complaints in children.

Cytogenetic biomonitoring of primary school children exposed to air pollutants: micronuclei analysis of buccal epithelial cells.

There is an increasing attempt in the world to determine the exposures of children to environmental chemicals. To analyze the genotoxic effect of air pollution, micronucleus (MN) assay was carried out in buccal epithelial cells (BECs) of children living in an urban city of Turkey. Children from two schools at urban-traffic and suburban sites were investigated in summer and winter seasons for the determination of BEC-MN frequency (per mille) and frequency of BEC with MN (per mille). The same children were also recruited for lung function measurements within a MATRA project ("Together Towards Clean Air in Eskisehir and Iskenderun") Measured NO2 and SO2 concentrations did not exceed the European Union (EU) limit levels either in urban-traffic or suburban regions. Higher O3 concentrations were measured in the suburban site especially in the summer period. Particulate matter (PM2.5 and PM10) levels which did not differ statistically between two regions were above the EU limits in general. Although BEC-MN frequencies of children living in the suburban sites were higher in general, the difference between two regions was not significant either in the summer or winter periods. BEC-MN frequencies of the urban-traffic children were found to be significantly higher in summer period (mean ± SD, 2.68 ± 1.99) when compared to winter period (1.64 ± 1.59; p = 0.004). On the other hand, no seasonality was observed for the suburban children. Similar results have been obtained in the BEC frequency with MN in our study. In summer, BEC-MN frequencies were significantly increased with the decrease in pulmonary function levels based on forced expiratory flow between 25 and 75% of vital capacity (FEF25-75%) levels (p < 0.05). As a conclusion, children living in urban-traffic and suburban areas in the city of Eskisehir exhibited similar genotoxicity. Seasonal variation in genotoxicity may be interpreted as relatively high ozone levels and increasing time spent at outdoors in the summer.

Effects of air pollution on lung function and symptoms of asthma, rhinitis and eczema in primary school children.

Health effects of ambient air pollution were studied in three groups of schoolchildren living in areas (suburban, urban and urban-traffic) with different air pollution levels in Eskisehir, Turkey. This study involved 1,880 students aged between 9 and 13 years from 16 public primary schools. This two-season study was conducted from January 2008 through March 2009. Symptoms of asthma, rhinitis and eczema were determined by the International Study of Asthma and Allergies in Childhood questionnaire in 2008. Two lung function tests were performed by each child for summer and winter seasons with simultaneous ambient air measurements of ozone (O3), nitrogen dioxide (NO2) and sulfur dioxide (SO2) by passive sampling. Effects of air pollution on impaired lung function and symptoms in schoolchildren were estimated by multivariate logistic regression analyses. Girls with impaired lung function (only for the summer season evaluation) were more observed in suburban and urban areas when compared to urban-traffic area ([odds ratio (OR) = 1.49; 95 % confidence interval (CI) 1.04-2.14] and [OR = 1.69 (95 % CI 1.06-2.71)] for suburban vs. urban-traffic and urban vs. urban-traffic, respectively). Significant association between ambient ozone concentrations and impaired lung function (for an increase of 10 µg m(-3)) was found only for girls for the summer season evaluation [OR = 1.11 (95 % CI 1.03-1.19)]. No association was found for boys and for the winter season evaluation. No association was found between any of the measured air pollutants and symptoms of current wheeze, current rhinoconjunctivitis and current itchy rash. The results of this study showed that increasing ozone concentrations may cause a sub-acute impairment in lung function of school aged children.