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Background: While long-term air pollution and noise exposure has been linked to increasing cardiometabolic disease risk, potential effects on body composition remains unclear. This study aimed to investigate the associations of long-term air pollution, noise and body composition., Methods: We used repeated data from the LEAD (Lung, hEart, sociAl, boDy) study conducted in Vienna, Austria. Body mass index (BMI; kg/m 2 ), fat mass index (FMI; z-score), and lean mass index (LMI; z-score) were measured using dual-energy x-ray absorptiometry at the first (t 0 ; 2011-ongoing) and second (t 1 ; 2017-ongoing) examinations. Annual particulate matter (PM 10 ) and nitrogen dioxide (NO 2 ) concentrations were estimated with the GRAMM/GRAL model (2015-2021). Day-evening-night (L den ) and night-time (L night ) noise levels from transportation were modeled for 2017 following the European Union Directive 2002/49/EC. Exposures were assigned to residential addresses. We performed analyses separately in children/adolescents and adults, using linear mixed-effects models with random participant intercepts and linear regression models for cross-sectional and longitudinal associations, respectively. Models were adjusted for co-exposure, lifestyle and sociodemographics., Results: A total of 19,202 observations (nt 0  = 12,717, nt 1  = 6,485) from participants aged 6-86 years (mean age at t 0  = 41.0 years; 52.9 % female; mean PM 10  = 21 µg/m 3 ; mean follow-up time = 4.1 years) were analyzed. Among children and adolescents (age ≤ 18 years at first visit), higher PM 10 exposure was cross-sectionally associated with higher FMI z-scores (0.09 [95 % Confidence Interval (CI): 0.03, 0.16]) and lower LMI z-scores (-0.05 [95 % CI: -0.10, -0.002]) per 1.8 µg/m 3 . Adults showed similar trends in cross-sectional associations as children, though not reaching statistical significance. We observed no associations for noise exposures. Longitudinal analyses on body composition changes over time yielded positive associations for PM 10 , but not for other exposures., Conclusion: Air pollution exposure, mainly PM 10 , was cross-sectionally and longitudinally associated with body composition in children/adolescents and adults. Railway/road-traffic noise exposures showed no associations in both cross-sectional and longitudinal analyses., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Objectives: This paper presents the study design of the Berlin-Brandenburg Air study (BEAR-study). We measure air quality in Berlin and Brandenburg before and after the relocation of aircraft (AC) traffic from Tegel (TXL) airport to the new Berlin-Brandenburg airport (BER) and investigate the association of AC-related ultrafine particles (UFP) with health outcomes in schoolchildren. Methods: The BEAR-study is a natural experiment examining schoolchildren attending schools near TXL and BER airports, and in control areas (CA) away from both airports and associated air corridors. Each child undergoes repeated school-based health-examinations. Total particle number concentration (PNC) and meteorological parameters are continuously monitored. Submicrometer particle number size distribution, equivalent black carbon, and gas-phase pollutants are collected from long-term air quality monitoring stations. Daily source-specific UFP concentrations are modeled. We will analyze short-term effects of UFP on respiratory, cardiovascular, and neurocognitive outcomes, as well as medium and long-term effects on lung growth and cognitive development. Results: We examined 1,070 children (as of 30 November 2022) from 16 schools in Berlin and Brandenburg. Conclusion: The BEAR study increases the understanding of how AC-related UFP affect children's health., Competing Interests: Author SaL was employed by the company Cardinal Health Real-World Evidence and Insights. The remaining authors declare that they do not have any conflicts of interest., (Copyright © 2023 Soppa, Lucht, Ogurtsova, Buschka, López-Vicente, Guxens, Weinhold, Winkler, Wiedensohler, Held, Lüchtrath, Cyrys, Kecorius, Gastmeier, Wiese-Posselt and Hoffmann.)

Background: Short-term exposure particulate matter with a diameter of 10 µm or less (PM 10 ) and fine particulate matter (PM 2.5 ) has been associated with heart rate variability (HRV), but exposure to ultrafine particles (UFP) has been less well examined. We investigated the associations between the HRV outcomes and short-term exposure to UFP, PM 10 and PM 2.5 among school-aged children and seniors., Methods: CorPuScula (Coronary, Pulmonary and Sanguis) is a longitudinal, repeated-measure panel study conducted in 2000-2002 in Munich, Germany including 52 seniors (58-94 years old) with 899 observations and 50 children (6-10 years old) with 925 observations. A 10-min resting electrocardiogram was performed to assess resting HRV outcomes [Standard Deviation of Normal to Normal Intervals (SDNN), Root Mean Square of Successive Differences between Normal Heartbeats (RMSSD), Low Frequency power (LF), High Frequency power (HF), ration between low and high frequency (LF/HF)]. UFP and PM exposures were measured near the care home and school yard for seniors and children, respectively. Mean exposures during the day of examination (9-21 h) as well as 3-h, 12-h, 24-h, one-day, and two-day lags were assessed. Linear mixed-effect models were used to investigate the associations between short-term air pollution and HRV outcomes separately in children and seniors. The models were adjusted for sex, age, weather conditions (temperature, precipitation, and water vapor pressure), BMI, lifestyle and medical information. Two and multipollutant models adjusted for NO 2 and O 3 were performed., Results: Among seniors, we observed increases in SDNN, LF, HF and LF/HF ratio after short-term exposure to UFP (hourly and daily lags) in contrast to decreases in SDNN and RMSSD after exposure to PM 10 . Associations were generally robust to two- and multipollutant adjustment. Among children, we observed increases of the LF/HF ratio after short-term exposures to UFP at lags 12 and 24 h. In contrast, we observed decreases of the ratio after exposure to PM 2.5 and PM 10 . Results were largely unchanged for multipollutant modelling, however we found a more pronounced increase in SDNN and LF/HF (UFP lag 12 and 24 h) after adjusting for NO 2 ., Conclusions: Overall, among seniors, we observed associations of UFP and PM 10 exposure with sympathetic responses of the ANS, which play an important role in sudden heart attacks or arrhythmia. Among children we found more inconsistent associations between UFP and a delayed increase in HRV. Adjusting for co-pollutants including NO 2 and O 3 yielded robust results., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The authors DN, KO declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision., (© 2023 Haddad, Ogurtsova, Lucht, Glaubitz, Höppe, Nowak, Angerer and Hoffmann.)

Background: Nonalcoholic fatty liver disease (NAFLD) is a disease characterized by lipid accumulation within hepatocytes, ranging from simple steatosis to steatohepatitis, in the absence of secondary causes of hepatic fat accumulation. Although air pollution (AP) has been associated with several conditions related to NAFLD (e.g., metabolic syndrome, type 2 diabetes mellitus), few studies have explored an association between AP and NAFLD. The aim of the study was to investigate whether exposure to AP is associated with NAFLD prevalence., Methods: We used baseline cross-sectional data (2000-2003) of the Heinz-Nixdorf-Recall cohort study in Germany (baseline n = 4,814), a prospective population-based cohort study in the urbanized Ruhr Area. Mean annual exposure to size-fractioned particulate matter (PM 10 , PM 2.5 , PM coarse , and PM 2.5 abs), nitrogen dioxide, and particle number was assessed using two different exposure models: a chemistry transport dispersion model, which captures urban background AP exposure on a 1 km 2 grid at participant's residential addresses, and a land use regression model, which captures point-specific AP exposure at participant's residential addresses. NAFLD was assessed with the fatty liver index (n = 4,065), with NAFLD defined as fatty liver index ≥60. We estimated ORs of NAFLD per interquartile range of exposure using logistic regression, adjusted for socio-demographic and lifestyle variables., Results: We observed a NAFLD prevalence of 31.7% (n = 1,288). All air pollutants were positively associated with NAFLD prevalence, with an OR per interquartile range for PM 2.5 of 1.11 (95% confidence interval [CI] = 1.00, 1.24) using chemistry transport model, and 1.06 (95% CI = 0.94, 1.19) using the land use regression model, respectively., Conclusion: There was a positive association between long-term AP exposure and NAFLD., Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report. Supported by the German Ministry of Education and Science (BMBF) and the German Aerospace Center (Deutsches Zentrum für Luft- und Raumfahrt, DLR), Bonn, Germany. We acknowledge the support of the Sarstedt AG & Co. (Nümbrecht, Germany) concerning laboratory equipment. This work was supported by the German Research Council (DFG; projects [SI236/8-1, SI236/9-1, HO3314/4-3, HO3314/2-3, HO3314/2-1]). The data is due to data protection issues not available. The code used for this publication is available upon request to the authors., (Copyright © 2023 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.)

Background: Older adults show a high variability in cognitive performance that cannot be explained by aging alone. Although research has linked air pollution and noise to cognitive impairment and structural brain alterations, the potential impact of air pollution and noise on functional brain organization is unknown., Objective: This study examined the associations between long-term air pollution and traffic noise with measures of functional brain organization in older adults. We hypothesize that exposures to high air pollution and noise levels are associated with age-like changes in functional brain organization, shown by less segregated brain networks., Methods: Data from 574 participants (44.1% female, 56-85 years of age) in the German 1000BRAINS study (2011-2015) were analyzed. Exposure to particulate matter ( PM 10 , PM 2.5 , and PM 2.5 absorbance), accumulation mode particle number ( PN AM ), and nitrogen dioxide ( NO 2 ) was estimated applying land-use regression and chemistry transport models. Noise exposures were assessed as weighted 24-h ( L den ) and nighttime ( L night ) means. Functional brain organization of seven established brain networks (visual, sensorimotor, dorsal and ventral attention, limbic, frontoparietal and default network) was assessed using resting-state functional brain imaging data. To assess functional brain organization, we determined the degree of segregation between networks by comparing the strength of functional connections within and between networks. We estimated associations between air pollution and noise exposure with network segregation, applying multiple linear regression models adjusted for age, sex, socioeconomic status, and lifestyle variables., Results: Overall, small associations of high exposures with lesser segregated networks were visible. For the sensorimotor networks, we observed small associations between high air pollution and noise and lower network segregation, which had a similar effect size as a 1-y increase in age [e.g., in sensorimotor network, - 0.006 (95% CI: - 0.021 , 0.009) per 0.3 × 10 - 5 / m increase in PM 2.5 absorbance and - 0.004 (95% CI: - 0.006 , - 0.002 ) per 1-y age increase]., Conclusion: High exposure to air pollution and noise was associated with less segregated functional brain networks. https://doi.org/10.1289/EHP9737.

Background: While evidence suggests that long-term air pollution (AP) and noise may adversely affect cognitive function, little is known about whether environmental exposures also promote structural changes in underlying brain networks. We therefore investigated the associations between AP, traffic noise, and structural measures of the Default Mode Network (DMN), a functional brain network known to undergo specific changes with age., Methods: We analyzed data from 579 participants (mean age at imaging: 66.5 years) of the German 1000BRAINS study. Long-term residential exposure to particulate matter (diameter ≤10 μm [PM 10 ]; diameter ≤2.5 μm [PM 2.5 ]), PM 2.5 absorbance (PM 2.5abs ), nitrogen dioxide (NO 2 ), and accumulation mode particulate number concentration (PN AM ) was estimated using validated land use regression and chemistry transport models. Long-term outdoor traffic noise was modeled at participants' homes based on a European Union's Environmental Noise Directive. As measures of brain structure, cortical thickness and local gyrification index (lGI) values were calculated for DMN regions from T1-weighted structural brain images collected between 2011 and 2015. Associations between environmental exposures and brain structure measures were estimated using linear regression models, adjusting for demographic and lifestyle characteristics., Results: AP exposures were below European Union standards but above World Health Organization guidelines (e.g., PM 10 mean: 27.5 μg/m 3 ). A third of participants experienced outdoor 24-h noise above European recommendations. Exposures were not consistently associated with lGI values in the DMN. We observed weak inverse associations between AP and cortical thickness in the right anterior DMN (e.g., -0.010 mm [-0.022, 0.002] per 0.3 unit increase in PM 2.5abs ) and lateral part of the posterior DMN., Conclusion: Long-term AP and noise were not consistently associated with structural parameters of the DMN in the brain. While weak associations were present between AP exposure and cortical thinning of right hemispheric DMN regions, it remains unclear whether AP might influence DMN brain structure in a similar way as aging., (Copyright © 2021 Elsevier GmbH. All rights reserved.)

Background: Residential exposure to air pollution (AP) has been shown to activate the immune system (IS). Although innate immune responses to AP have been studied extensively, investigations on the adaptive IS are scarce., Objectives: The aim of this study was to investigate the association between short- to long-term AP exposure and polyclonal free light chains (FLC) produced by plasma cells., Methods: We used repeated data from three examinations ( t 0 : 2000-2003; t 1 : 2006-2008; and t 2 : 2011-2015) of the population-based German Heinz Nixdorf Recall cohort of initially 4,814 participants (45-75 y old). Residential exposure to total and source-specific particulate matter (PM) with an aerodynamic diameter of 10 or 2.5 μ m ( PM 10 and PM 2.5 respectively), nitrogen dioxide ( NO 2 ), and particle number concentrations (accumulation mode; PN AM ) was estimated using a chemistry transport model with different time windows (1- to 365-d mean ± standard deviation) before blood draw. We applied linear mixed models with a random participant intercept to estimate associations between total, traffic- and industry-related AP exposures and log-transformed FLC, controlling for examination time, sociodemographic and lifestyle variables, estimated glomerular filtration rate and season., Results: Analyzing 9,933 observations from 4,455 participants, we observed generally positive associations between AP exposures and FLC. We observed strongest associations with middle-term exposures, e.g., 3.0% increase in FLC (95% confidence interval: 1.8%, 4.3%) per interquartile range increase in 91-d mean of NO 2 ( 14.1 μ g / m ³ ). Across the different pollutants, NO 2 showed strongest associations with FLC, followed by PM 10 and PN AM . Effect estimates for traffic-related exposures were mostly higher compared with total exposures. Although NO 2 and PN AM estimates remained stable upon adjustment for PM, PM estimates decreased considerably upon adjustment for NO 2 and PN AM ., Discussion: Our results suggest that middle-term AP exposures in particular might be positively associated with activation of the adaptive IS. Traffic-related PM, PN AM , and NO 2 showed strongest associations. https://doi.org/10.1289/EHP7164.

Objectives: Due to inconsistent epidemiological evidence on health effects of air pollution on progression of atherosclerosis, we investigated several air pollutants and their effects on progression of atherosclerosis, using carotid intima media thickness (cIMT), coronary calcification (CAC), and thoracic aortic calcification (TAC)., Methods: We used baseline (2000-2003) and 5-y follow-up (2006-2008) data from the German Heinz Nixdorf Recall cohort study, including 4,814 middle-aged adults. Residence-based long-term air pollution exposure, including particulate matter (PM) with aerodynamic diameter ≤ 2.5 μ m ( PM 2.5 ), ( PM 10 ), and nitrogen dioxide ( NO 2 ) was assessed using chemistry transport and land use regression (LUR) models. cIMT was quantified as side-specific median IMT assessed from standardized ultrasound images. CAC and TAC were quantified by computed tomography using the Agatston score. Development (yes/no) and progression of atherosclerosis (change in cIMT and annual growth rate for CAC/TAC) were analyzed with logistic and linear regression models, adjusting for age, sex, lifestyle variables, socioeconomic status, and traffic noise., Results: While no clear associations were observed in the full study sample (mean age 59.1 ( ± 7.6 ) y; 53% female), most air pollutants were marginally associated with progression of atherosclerosis in participants with no or low baseline atherosclerotic burden. Most consistently for CAC, e.g., a 1.5   μ g / m 3 higher exposure to PM 2.5 (LUR) yielded an estimated odds ratio of 1.19 [95% confidence interval (CI): 1.03, 1.39] for progression of CAC and an increased annual growth rate of 2% (95% CI: 1%, 4%)., Conclusion: Our study suggests that development and progression of subclinical atherosclerosis is associated with long-term air pollution in middle-aged participants with no or minor atherosclerotic burden at baseline, while overall no consistent associations are observed. https://doi.org/10.1289/EHP7077.

Background: Few studies have examined the risk of long-term exposure to source-specific airborne pollutants on incidence of cerebrovascular and cardiovascular events., Objectives: We aimed to estimate the effect of long-term exposure to source-specific air pollution and particulate matter (PM) components on incidence of stroke, coronary heart disease (CHD), and total cardiovascular events (CVE) in the population-based Heinz Nixdorf Recall study (HNR)., Methods: We used baseline (2000-2003) and 14-year follow-up data of the HNR Study, an ongoing population-based prospective cohort study in Western Germany. Participants' residential mean exposures to NO 2 and total and source-specific PM 10 , PM 2.5 , accumulation mode particle number concentration (PN AM ), and PM components were modelled using a dispersion and chemical transport model. We used Cox regression to evaluate the effect of pollutants (per 1 μg/m 3 increase and per interquartile range - IQR) on risk of stroke and CHD, adjusting for socio-demographic characteristics, lifestyle risk factors and nighttime traffic noise exposure., Results: In 4,105 included participants (aged 45-76 at baseline, 52.5% women), we observed 118 cases of first stroke and 373 cases of first CHD during 46,748 person-years under risk. The median survival time within the cohort was 13.3 years. No effect of exposure to ambient air pollution on risk of CHD was observed, but distinct effects were observed for stroke. Ambient traffic-specific PM showed a stronger effect on stroke than industry-specific PM: hazard ratios (95% confidence interval) for total, traffic-specific, and industry-specific PM 2.5 were 1.16 (1.02-1.34), 2.53 (1.07-5.97), and 1.27 (1.03-1.56) per 1 μg/m 3 increase, respectively. PM components showed no substantially different effects from those of total PM per IQR, but higher associations were observed for NH 4 and SO 4 per 1 μg/m 3 . However, the exposure contrast of ammonium and sulfate components was very low., Conclusion: Traffic-specific PM exhibited stronger effects than total and industry-specific PM on risk of stroke. Among components, NH 4 and SO 4 showed higher effects. No effect was observed for PM and CHD., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Background: Despite the importance of understanding associations of air pollution and noise exposure with loss of neurocognitive performance, studies investigating these exposures and local brain structure are limited., Objective: We estimated associations of residential air pollution and noise exposures with neurocognitive test performance and the local gyrification index (lGI), a marker for local brain atrophy, among older adults., Methods: For n = 615 participants from the population-based 1000BRAINS study, based on the German Heinz Nixdorf Recall study, we assessed residential exposures to particulate matter ( PM 10 , PM 2.5 , PM 2.5 abs ), accumulation mode particle number ( PN AM ), and nitrogen oxides ( NO x , NO 2 ), using land-use regression and chemistry transport models. Weighted 24-h and nighttime noise were modeled according to the European noise directive. We evaluated associations of air pollution and noise exposure at the participants' 2006-2008 residential addresses with neurocognitive test performance and region-specific lGI values ( n = 590 ) from magnetic resonance imaging, both assessed in 2011-2015, using linear regression and adjusting for demographic and personal characteristics., Results: Air pollution and noise were associated with language and short-term/working memory and with local atrophy of the fronto-parietal network (FPN), a functional resting-state network associated with these cognitive processes. For example, per 2 - μ g / m 3 PM 10 , local brain atrophy was more pronounced in the posterior brain regions of the FPN, with a - 0.02 [95% confidence interval (CI): - 0.04 , 0.00] lower lGI. In contrast, in the anterior regions of the FPN, weighted 24-h and nighttime noise were associated with less local brain atrophy [e.g., 0.02 (95% CI: 0.00, 0.04) for 10  dB (A) 24-h noise]., Conclusions: Air pollution and noise exposures were associated in opposite directions with markers of local atrophy of the FPN in the right brain hemisphere in older adults, suggesting that both chronic air pollution and noise exposure may influence the physiological aging process of the brain. https://doi.org/10.1289/EHP5859.

Background: An increasing number of studies have been published recently on the association between ambient air pollution (AP) and incident diabetes mellitus (DM), but studies investigating source-specific AP toxicity and potential mediating pathways are rare. We investigated the associations of all-source, traffic-specific, and industry-specific outdoor AP exposure with 10-year incidence of DM and potential mediation via inflammation-associated biomarkers., Methods: Data from participants of the prospective Heinz Nixdorf Recall cohort study who attended the baseline (t 0 ; 2000-2003), 5-year follow-up (t 1 ; 2006-2008), and 10-year follow-up (t 2 ; 2011-2015) examinations was used. For participants without DM at baseline (determined using information on physician diagnosis and glucose-lowering medication), residential long-term exposure (total, traffic-specific, and industry-specific) to particulate matter (PM 2.5 , PM 10 ), nitrogen dioxide (NO 2 ), and accumulation mode particle number concentration (PN AM ) were estimated using a chemistry transport model. Covariate-adjusted modified Poisson regression models with robust standard errors were applied to estimate relative risks (RR) for the associations between baseline AP and incident DM at t 2 . Mediation analyses for adiponectin, high-sensitivity C-reactive protein (hsCRP), and interleukin-1 receptor antagonist (IL-1RA) were conducted to estimate natural direct and indirect effects., Results: Of the 4,814 participants at t 0 , 2,451 participants (mean baseline age: 58.2 years) were included in the main analysis. Interquartile range (IQR) increases in total PM 10 and PN AM were associated with increased risk of DM (e.g., RR: 1.25 [95% Confidence Interval (CI): 1.02, 1.53] per 3.8 µg/m 3 PM 10 ). Whereas traffic-specific exposures were associated with DM risk for all air pollutants (e.g., RR: 1.24 [95% CI: 1.06, 1.46] per 0.3 µg/m 3 PM 10 ), significant associations for industry exposures were limited to NO 2 and PN AM (e.g., RR: 1.24 [95% CI: 1.03, 1.49] per 230 particles/mL PN AM ). Potential mediation of the association between AP and DM was observed for adiponectin but not for hsCRP and IL-1RA., Conclusion: Our study shows that long-term exposure to total and source-specific ambient AP may increase DM risk, with consistent results observed across traffic-specific exposures. Decreases in adiponectin may play a potential role along the causal pathway., (Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: While prior studies have linked air pollution (AP) to diabetes prevalence and incidence, few have investigated whether AP exposure is also associated with alterations in diabetes-related biomarkers in metabolically healthy adults., Objective: To evaluate the associations between short-, medium-, and long-term AP and diabetes-related biomarkers (adiponectin, interleukin-1 receptor antagonist [IL-1RA], high sensitivity C-reactive protein [hsCRP], fibrinogen) in persons without diabetes., Methods: Adiponectin, IL-1RA, hsCRP, and fibrinogen were measured in blood samples collected at the baseline (t 0 ; 2000-2003) and first follow-up (t 1 ; 2006-2008) examinations of the prospective Heinz Nixdorf Recall (HNR) cohort study in Germany. Participants' residential mean exposures to PM 10 , PM 2.5 , NO 2 , and accumulation mode particle number concentration (PN AM ) were estimated for several time windows (1- to 365-day) prior to examination using a dispersion and chemistry transport model. We fitted covariate-adjusted linear mixed effects models using a random participant intercept and investigated effect modification by obesity status., Results: We analyzed 6727 observations (n t0  = 3626, n t1  = 3101) from 4052 participants of the HNR study (52% women; ages 45-76 years at t 0 ). For all air pollutants, medium-term exposures (60- to 120-day) were negatively associated with adiponectin (e.g., 91-day PN AM : -2.51% change [-3.40%, -1.53%] per interquartile [IQR] increase). Several short-, medium-, and long-term AP exposures were positively associated with IL-1RA (e.g., 365-day PM 10 : 2.64% change [1.25%, 4.22%] per IQR increase). Long-term exposures were positively associated with hsCRP level while no consistent patterns were observed for fibrinogen. Stronger associations for adiponectin were observed among non-obese participants., Conclusion: In persons without diabetes, we observed differing patterns of association between AP and diabetes-related biomarkers across a range of exposure windows, supporting the hypothesis that AP may play a role in the development of diabetes., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Road traffic noise affects a large number of people in urbanized areas. Recent epidemiological evidence indicates that environmental noise exposure may not only be associated with cardiovascular but also with cardio-metabolic outcomes. This prospective cohort study investigated the effect of outdoor and indoor residential road traffic noise on incident type 2 diabetes mellitus (T2DM)., Methods: We used data from 3,396 participants of age 45-75 years of the Heinz Nixdorf Recall study being non-diabetic at baseline (2000-2003). T2DM was defined via blood glucose level, incident intake of an anti-diabetic drug during follow-up or self-reported physician diagnosis at follow-up examination (2005-2008). Weighted 24-h (L den ) and night-time (L night ) mean road traffic noise was assessed according to the European Union directive 2002/49/EC. Road traffic noise exposure indoors was modeled taking into account the participants' room orientation, ventilation behavior and window insulation (n = 2,697). We applied Poisson regression analyses to estimate relative risks (RRs) of incident T2DM, adjusting for demographic characteristics, lifestyle factors, and air pollution exposure (NO 2 or PM 2.5 )., Results: A 10-dB(A) increase in outdoor road traffic noise (L den ) was associated with an RR of 1.09 (95% confidence interval, 0.96-1.24) for T2DM in the fully adjusted model. Models including PM 2.5 or NO 2 yielded RRs of 1.09 (0.96-1.24) and 1.11 (0.97-1.27), respectively. In analyses with road traffic noise (L den ) exposure indoors, we observed similar RRs with smaller confidence intervals (1.11 [1.01-1.21])., Conclusions: Our analyses suggest that long-term exposure to indoor and outdoor road traffic noise may increase the risk of developing T2DM, independent of air pollution exposure., Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report., (Copyright © 2018 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of Environmental Epidemiology. All rights reserved.)

Introduction: Recently, epidemiological studies have found a link between air pollution (AP) and individual components of the metabolic syndrome (MetS), a condition predisposing to cardiometabolic diseases. However, very few studies have explored a possible association between air pollution and MetS., Objective: We analyzed the effects of long-term exposure to airborne particulate matter and NO 2 on prevalence and incidence of MetS., Methods: We used data of the population-based prospective Heinz Nixdorf Recall study (baseline 2000-2003) to investigate the association(s) between AP exposure and MetS prevalence at baseline (n = 4457) and MetS incidence at first follow-up visit (n = 3074; average follow-up: 5.1 years). Mean annual exposure to size-fractioned particulate matter (PM 10 , PM 2.5 , PM coarse , and PM 2.5 abs) and nitrogen dioxide (NO 2 ) was assessed using a land use regression model. MetS was defined as central obesity plus two out of four additional risk factors (i.e., elevated triglycerides, reduced high-density lipoprotein cholesterol, elevated blood pressure or elevated plasma glucose). We estimated odds ratios (ORs) of MetS prevalence and incidence per interquartile range (IQR) of exposure, adjusting for demographic and lifestyle variables., Results: We observed a MetS prevalence of 20.7% (n = 922) and an incidence of 9.7% (n = 299). NO 2 was positively associated with MetS prevalence, with an OR increase per IQR of 1.12 (95%-CI 1.02-1.24, IQR = 6.1 μg/m 3 ). PM 10 and PM 2.5 were both borderline positively associated with MetS incidence, with ORs of 1.14 (95%-CI 0.99-1.32, IQR = 2.1 μg/m 3 ) and 1.19 (95%-CI 0.98-1.44, IQR = 1.5 μg/m 3 ) per IQR, respectively., Conclusion: In summary, we found a weak positive association between air pollution and MetS. The strongest and most consistent effects were observed between NO 2 and prevalent MetS., (Copyright © 2018. Published by Elsevier Ltd.)

Background: Exposure to air pollution activates the innate immune system and influences the adaptive immune system in experimental settings. We investigated the association of residential long-term exposure to particulate matter (PM) and NO 2 air pollution with monoclonal gammopathy of undetermined significance (MGUS) as a marker of adaptive immune system activation., Methods: We used data from the baseline (2000-2003), 5-year (2006-2008) and 10-year (2011-2015) follow-up examinations of the German Heinz Nixdorf Recall cohort study of 4814 participants (45-75years). Residential exposure to PM size fractions and NO 2 was estimated by land-use regression (ESCAPE-LUR, annual mean 2008/2009) and dispersion chemistry transport models (EURAD-CTM, 3-year mean at baseline). We used logistic regression to estimate the effects of air pollutants on incident MGUS, adjusting for age, sex, education, smoking status, physical activity, and BMI. As a non-linear approach, we looked at quartiles (2-4) of the air pollutants in comparison to quartile 1., Results: Of the 3949 participants with complete data, 100 developed MGUS during the 10-year follow-up. In the main model, only PM coarse was associated with incident MGUS (OR per IQR (1.9μg/m 3 ): 1.32, 95% CI 1.04-1.67). We further found positive associations between PM size fractions estimated by ESCAPE-LUR and incident MGUS by quartiles of exposure (OR Q4 vs Q1: PM 2.5 2.03 (1.08-3.80); PM 10 1.97 (1.05-3.67); PM coarse 1.98 (1.09-3.60))., Conclusions: Our results indicate that an association between long-term exposure to PM and MGUS may exist. Further epidemiologic studies are needed to corroborate this possible link., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

The Double Chooz experiment presents an indication of reactor electron antineutrino disappearance consistent with neutrino oscillations. An observed-to-predicted ratio of events of 0.944±0.016(stat)±0.040(syst) was obtained in 101 days of running at the Chooz nuclear power plant in France, with two 4.25 GW(th) reactors. The results were obtained from a single 10 m(3) fiducial volume detector located 1050 m from the two reactor cores. The reactor antineutrino flux prediction used the Bugey4 flux measurement after correction for differences in core composition. The deficit can be interpreted as an indication of a nonzero value of the still unmeasured neutrino mixing parameter sin(2)2θ(13). Analyzing both the rate of the prompt positrons and their energy spectrum, we find sin(2)2θ(13)=0.086±0.041(stat)±0.030(syst), or, at 90% C.L., 0.017

The aim of the study was to evaluate an educational video designed to modify the pain concept of chronic pain patients. It is commonly described that chronic pain patients foster an illness model which is dominated by purely medical assumptions about causes of pain and its modulation and treatment. Furthermore the mostly unrealistic hope for total pain relief which is expected from the pain expert guides the patients' seek for help. These concepts are most probable very dysfunctional in a multidisciplinary pain management setting, where psychological interventions are important elements of the treatment. Therefore the video was designed to initiate changes in the patient's attitude towards a multimodal model of pain. The educational pain video was evaluated in an experimental design using a control group to whom a different video on a health related topic (nutrition) was presented. The Ss participating in the study were 47 chronic pain patients of a pain ambulance and 42 patients of a pain clinic (inpatient setting). The results showed that after viewing the pain video the groups differed significantly in their pain concept as predicted. The use of an educational video, like the one evaluated, seems useful to initiate first steps in illness concept modification by expanding and enriching the patients attitude by assumptions about the influence of psychological factors on pain maintenance and management and shaping realistic attitudes towards treatment.