The Berlin-Brandenburg Air Study-A Methodological Study Paper of a Natural Experiment Investigating Health Effects Related to Changes in Airport-Related Exposures.

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.

Long-term exposure to air pollution and prevalent nonalcoholic fatty liver disease.

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 (PM10, PM2.5, PMcoarse, and PM2.5abs), 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 km2 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 PM2.5 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.

Short-term exposure to ultrafine and fine particulate matter with multipollutant modelling on heart rate variability among seniors and children from the CorPuScula (coronary, pulmonary, sanguis) longitudinal study in Germany.

Background: Short-term exposure particulate matter with a diameter of 10 µm or less (PM10) and fine particulate matter (PM2.5) 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, PM10 and PM2.5 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 NO2 and O3 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 PM10. 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 PM2.5 and PM10. 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 NO2. Conclusions: Overall, among seniors, we observed associations of UFP and PM10 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 NO2 and O3 yielded robust results.

Association between Long-Term Air Pollution, Chronic Traffic Noise, and Resting-State Functional Connectivity in the 1000BRAINS Study.

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 (PM10, PM2.5, and PM2.5 absorbance), accumulation mode particle number (PNAM), and nitrogen dioxide (NO2) was estimated applying land-use regression and chemistry transport models. Noise exposures were assessed as weighted 24-h (Lden) and nighttime (Lnight) 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 PM2.5 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.

Long-term air pollution, noise, and structural measures of the Default Mode Network in the brain: Results from the 1000BRAINS cohort.

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 [PM10]; diameter ≤2.5 µm [PM2.5]), PM2.5 absorbance (PM2.5abs), nitrogen dioxide (NO2), and accumulation mode particulate number concentration (PNAM) 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., PM10 mean: 27.5 µg/m3). 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 PM2.5abs) 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.

Air Pollution and Polyclonal Elevation of Serum Free Light Chains: An Assessment of Adaptive Immune Responses in the Prospective Heinz Nixdorf Recall Study.

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 (t0: 2000-2003; t1: 2006-2008; and t2: 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 2.5µm (PM10 and PM2.5 respectively), nitrogen dioxide (NO2), and particle number concentrations (accumulation mode; PNAM) 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 NO2 (14.1µg/m³). Across the different pollutants, NO2 showed strongest associations with FLC, followed by PM10 and PNAM. Effect estimates for traffic-related exposures were mostly higher compared with total exposures. Although NO2 and PNAM estimates remained stable upon adjustment for PM, PM estimates decreased considerably upon adjustment for NO2 and PNAM. DISCUSSION: Our results suggest that middle-term AP exposures in particular might be positively associated with activation of the adaptive IS. Traffic-related PM, PNAM, and NO2 showed strongest associations. https://doi.org/10.1289/EHP7164.

Air Pollution and Progression of Atherosclerosis in Different Vessel Beds-Results from a Prospective Cohort Study in the Ruhr Area, Germany.

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 ≤2.5µm (PM2.5), (PM10), and nitrogen dioxide (NO2) 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 µg/m3 higher exposure to PM2.5 (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.

Long-term exposure to ambient source-specific particulate matter and its components and incidence of cardiovascular events - The Heinz Nixdorf Recall study.

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 NO2 and total and source-specific PM10, PM2.5, accumulation mode particle number concentration (PNAM), 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/m3 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 PM2.5 were 1.16 (1.02-1.34), 2.53 (1.07-5.97), and 1.27 (1.03-1.56) per 1 µg/m3 increase, respectively. PM components showed no substantially different effects from those of total PM per IQR, but higher associations were observed for NH4 and SO4 per 1 µg/m3. 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, NH4 and SO4 showed higher effects. No effect was observed for PM and CHD.

Associations of Air Pollution and Noise with Local Brain Structure in a Cohort of Older Adults.

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 (PM10, PM2.5, PM2.5abs), accumulation mode particle number (PNAM), and nitrogen oxides (NOx, NO2), 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-µg/m3 PM10, 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.

All-source and source-specific air pollution and 10-year diabetes Incidence: Total effect and mediation analyses in the Heinz Nixdorf recall study.

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 (t0; 2000-2003), 5-year follow-up (t1; 2006-2008), and 10-year follow-up (t2; 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 (PM2.5, PM10), nitrogen dioxide (NO2), and accumulation mode particle number concentration (PNAM) 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 t2. 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 t0, 2,451 participants (mean baseline age: 58.2 years) were included in the main analysis. Interquartile range (IQR) increases in total PM10 and PNAM were associated with increased risk of DM (e.g., RR: 1.25 [95% Confidence Interval (CI): 1.02, 1.53] per 3.8 µg/m3 PM10). 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/m3 PM10), significant associations for industry exposures were limited to NO2 and PNAM (e.g., RR: 1.24 [95% CI: 1.03, 1.49] per 230 particles/mL PNAM). 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.

Circulating lipids, mammographic density, and risk of breast cancer in the Nurses' Health Study and Nurses' Health Study II.

PURPOSE: Epidemiologic evidence supports an association between high mammographic density and increased breast cancer risk yet etiologic mechanisms remain largely unknown. Mixed evidence exists as to whether circulating lipid levels influence mammographic density and breast cancer risk. Therefore, we examined these associations in the Nurses' Health Study (NHS) and Nurses' Health Study II (NHSII), two large prospective cohorts with information on PMD and circulating lipid measures, long follow-up, and breast cancer risk factor and outcome data. METHODS: We conducted a nested case-control study among women in the NHS and NHSII. Percent mammographic density (PMD) was measured using Cumulus software, a computer-assisted method, on digitized film mammograms. Cross-sectional associations between circulating lipids [total cholesterol (n = 1,502), high-density lipoprotein (HDL-C; n = 579), and triglycerides (n = 655)] and PMD were evaluated among controls. All analyses were stratified by menopausal status at time of mammogram. Relative risks for breast cancer by lipid and PMD measures were estimated among postmenopausal women in the full nested case-control study (cases/controls for cholesterol, HDL-C, and triglycerides were 937/975, 416/449, and 506/537, respectively). RESULTS: There were no significant associations between circulating lipid levels and PMD among healthy women, irrespective of menopausal status. The association between PMD and breast cancer risk among postmenopausal women was not modified by circulating lipid levels (p interaction = 0.83, 0.80, and 0.34 for total cholesterol, HDL-C, and triglycerides, respectively). CONCLUSION: Overall, no association was observed between lipid levels and PMD, and there was no evidence that lipid levels modified the association between PMD and breast cancer risk.

Air pollution and diabetes-related biomarkers in non-diabetic adults: A pathway to impaired glucose metabolism?

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 (t0; 2000-2003) and first follow-up (t1; 2006-2008) examinations of the prospective Heinz Nixdorf Recall (HNR) cohort study in Germany. Participants' residential mean exposures to PM10, PM2.5, NO2, and accumulation mode particle number concentration (PNAM) 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 (nt0 = 3626, nt1 = 3101) from 4052 participants of the HNR study (52% women; ages 45-76 years at t0). For all air pollutants, medium-term exposures (60- to 120-day) were negatively associated with adiponectin (e.g., 91-day PNAM: -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 PM10: 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.

Indoor and outdoor road traffic noise and incident diabetes mellitus: Results from a longitudinal German cohort study.

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 (Lden) and night-time (Lnight) 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 (NO2 or PM2.5). RESULTS: A 10-dB(A) increase in outdoor road traffic noise (Lden) was associated with an RR of 1.09 (95% confidence interval, 0.96-1.24) for T2DM in the fully adjusted model. Models including PM2.5 or NO2 yielded RRs of 1.09 (0.96-1.24) and 1.11 (0.97-1.27), respectively. In analyses with road traffic noise (Lden) 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.

Air Pollution and Glucose Metabolism: An Analysis in Non-Diabetic Participants of the Heinz Nixdorf Recall Study.

BACKGROUND: Despite the importance of understanding the connection between air pollution exposure and diabetes, studies investigating links between air pollution and glucose metabolism in nondiabetic adults are limited. OBJECTIVE: We aimed to estimate the association of medium-term air pollution exposures with blood glucose and glycated hemoglobin A1c (HbA1c) among nondiabetics. METHODS: This study included observations from nondiabetic participants (nobs=7,108) of the population-based Heinz Nixdorf Recall study at baseline (2000­2003) and follow-up examination (2006­2008). Daily fine particulate matter (aerodynamic diameter≤2.5 µm, PM2.5; aerodynamic diameter≤10 µm, PM10), accumulation mode particle number (PNAM), and nitrogen dioxide (NO2) exposures were estimated at participants' residences using the spatiotemporal European Air Pollution Dispersion (EURAD) chemistry transport model. We evaluated the associations between medium-term air pollution exposures (28- and 91-d means) and glucose metabolism measures using mixed linear regression and adjusting for season, meteorology, and personal characteristics. A range of other exposure windows (1-, 2-, 3-, 7-, 14-, 45-, 60-, 75-, 105-, 120-, and 182-d means) were also evaluated to identify potentially relevant biological windows. RESULTS: We observed positive associations between PM2.5 and PNAM exposures and blood glucose levels [e.g., 28-d PM2.5: 0.91 mg/dL (95% CI: 0.38, 1.44) per 5.7 µg/m3]. PM2.5, PM10, and PNAM exposures were positively associated with HbA1c [e.g., 91-d PM2.5: 0.07 p.p. (95% CI: 0.04, 0.10) per 4.0 µg/m3]. Mean exposures during longer exposure windows (75- to 105-d) were most strongly associated with HbA1c, whereas 7- to 45-d exposures were most strongly associated with blood glucose. NO2 exposure was not associated with blood glucose or with HbA1c. CONCLUSIONS: Medium-term PM and PNAM exposures were positively associated with glucose measures in nondiabetic adults. These findings indicate that reducing ambient air pollution levels may decrease the risk of diabetes. https://doi.org/10.1289/EHP2561.

Long-term exposure to airborne particulate matter and NO2 and prevalent and incident metabolic syndrome - Results from the Heinz Nixdorf Recall Study.

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 NO2 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 (PM10, PM2.5, PMcoarse, and PM2.5abs) and nitrogen dioxide (NO2) 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). NO2 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/m3). PM10 and PM2.5 were both borderline positively associated with MetS incidence, with ORs of 1.14 (95%-CI 0.99-1.32, IQR = 2.1 µg/m3) and 1.19 (95%-CI 0.98-1.44, IQR = 1.5 µg/m3) 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 NO2 and prevalent MetS.

Is long-term particulate matter and nitrogen dioxide air pollution associated with incident monoclonal gammopathy of undetermined significance (MGUS)? An analysis of the Heinz Nixdorf Recall study.

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 NO2 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 NO2 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 PMcoarse was associated with incident MGUS (OR per IQR (1.9µg/m3): 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: PM2.5 2.03 (1.08-3.80); PM10 1.97 (1.05-3.67); PMcoarse 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.

Vitamin Variation in Capsicum Spp. Provides Opportunities to Improve Nutritional Value of Human Diets.

Chile peppers, native to the Americas, have spread around the world and have been integrated into the diets of many cultures. Much like their heat content, nutritional content can vary dramatically between different pepper types. In this study, a diverse set of chile pepper types were examined for nutrient content. Some pepper types were found to have high levels of vitamin A, vitamin C, or folate. Correlations between nutrient content, species, cultivation status, or geographic region were limited. Varietal selection or plant breeding offer tools to augment nutrient content in peppers. Integration of nutrient rich pepper types into diets that already include peppers could help combat nutrient deficiencies by providing a significant portion of recommended daily nutrients.