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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 (n(obs)= 7,108) of the population-based Heinz Nixdorf Recall study at baseline (2000-2003) and follow-up examination (2006-2008). Daily fine particulate matter (aerodynamic diameter <= 2.5 mu m, PM2.5; aerodynamic diameter <= 10 mu m, 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 mu g/m(3)]. 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 mu g/m(3)]. 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 findi

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 PM(2.5)abs) 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 mu g/m(3)). 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 mu g/m(3)) and 1.19 (95%-CI 0.98-1.44, IQR = 1.5 mu g/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 NO2 and prevalent MetS.

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) followup examinations of the German Heinz Nixdorf Recall cohort study of 4814 participants (45-75 years). 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 (1.9 mu g/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: 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.

Investigations of adverse effects of air pollution (AP) and ambient noise on cognitive functions are apparently scarce, and findings seem to be inconsistent. The aim of this study was to examine the associations of long-term exposure to AP and traffic noise with cognitive performance. At the second examination of the population-based Heinz Nixdorf Recall study (2006-2008), cognitive performance was evaluated in 4086 participants. Long-term residential exposure to size-specific particulate matter (PM) and nitrogen oxides (NOx) with land use regression, to and traffic noise (weighted 24-h (L-DEN) and nighttime (L-NIGHT) means), was assessed according to the European Union (EU) Directive 2002/49/EC. Multiple regression models were calculated for the relationship of environmental exposures with a global cognitive score (GCS) and in five cognitive subtests, using single- and two-exposure models. In fully adjusted models, several AP metrics were negatively associated with four of five subtests and with GCS. For example, an interquartile range increase in PM2.5 was correlated with verbal fluency, labyrinth test, and immediate and delayed verbal recall. A 10 dB(A) elevation in L-DEN and L-NIGHT was associated with GCS. Similar but not significant associations were found for the cognitive subtests. In two-exposure models including noise and air pollution simultaneously, the associations did not change markedly for air pollution, but attenuated numerically for noise. Long-term exposures to AP and traffic noise are negatively correlated with subtests related to memory and executive functions. There appears to be little evidence for mutual confounding.

Background: Long-term exposure to fine particulate matter (PM2.5) may lead to increased blood pressure (BP). The role of industry- and traffic-specific PM2.5 remains unclear. Objective: We investigated the associations of residential long-term source-specific PM2.5 exposure with arterial BP and incident hypertension in the population-based Heinz Nixdorf Recall cohort study. Methods: We defined hypertension as systolic BP >= 140 mmHg, or diastolic BP >= 90 mmHg, or current use of BP lowering medication. Long-term concentrations of PM2.5 from all local sources (PM2.5ALL), local industry (PM2.5IND) and traffic (PM2.5TRA) were modeled with a dispersion and chemistry transport model (EURAD-CTM) with a 1 km(2) resolution. We performed a cross-sectional analysis with BP and prevalent hypertension at baseline, using linear and logistic regression, respectively, and a longitudinal analysis with incident hypertension at 5-year follow-up, using Poisson regression with robust variance estimation. We adjusted for age, sex, body mass index, lifestyle, education, and major road proximity. Change in BP (mmHg), odds ratio (OR) and relative risk (RR) for hypertension were calculated per 1 mu g/m(3) of exposure concentration. Results: PM2.5ALL was highly correlated with PM25IND. (Spearman's rho = 0.92) and moderately with PM2.5TRA (rho = 0.42). In adjusted cross-sectional analysis with 4539 participants, we found positive associations of PM2.5ALL with systolic (0.42 [95%-CI: 0.03, 0.801) and diastolic (0.25 [0.04, 0.461] BP. Higher, but less precise estimates were found for PM2.5IND (systolic: 0.55 [-0.05, 1.14]; diastolic: 0.35 [0.03, 0.671) and PM2.5TRA (systolic: 0.88 [-1.55, 3.31]; diastolic: 0.41 [-0.91, 1.731). We found crude positive association of PM2.5TRA with prevalence (OR 1.41 [1.10, 1.80]) and incidence of hypertension (RR 1.38 [1.03,1.85]), attenuating after adjustment (OR 1.19 [0.90, 1.58] and RR 1.28 [0.94, 1.72]). We found no association of PM2.5ALL and PM2.5IND with

Background and Purpose-Carotid intima-media thickness is a marker for subclinical atherosclerosis that predicts subsequent clinical cardiovascular events. The aim of this study was to identify chromosomal loci with linkage or association to common carotid intima-media thickness. Methods-Nuclear families were recruited using the single parental proband sib-pair design. Genotype data were available for 546 individuals from 132 nuclear families of the Bonn IMT Family Study using the Affymetrix GeneChip Human Mapping 250K Sty chip. Multipoint logarithm of the odds (LOD) scores were determined with the quantitative trait locus statistic implemented in multipoint engine for rapid likelihood. Linkage analysis and family-based association tests were conducted. Data from 2471 German participants from the HNR (Heinz Nixdorf Recall) Study were used for subsequent replication. Results-Two new genomic regions with suggestive linkage (LOD>2) were identified on chromosome 4 (LOD=2.26) and on chromosome 17 (LOD=2.01). Previously reported linkage findings were replicated on chromosomes 13 and 14. Fifteen single nucleotide polymorhisms, located on chromosomes 4, 6, and 9, revealed P<10(-4) in the family-based association analyses. One of these signals was replicated in HNR (rs2416804, 1-sided P=1.60x10(-3), located in the gene TRAF1). Conclusions-This study presents the first genome-wide linkage and association study of common carotid intima-media thickness in the German population. Alleles of rs2416804 in TRAF1 were identified as being linked and associated with carotid intima-media thickness. Further studies are needed to evaluate the contribution of this locus to the development of atherosclerosis.

Epidemiological evidence on the associations between exposure to ultrafine particles (UFP), with aerodynamic electrical mobility diameters <100 nm, and health is limited. We gathered data on UFP from five European cities within 2001-2011 to investigate associations between short-term changes in concentrations and respiratory hospitalisations.We applied city-specific Poisson regression models and combined city-specific estimates to obtain pooled estimates. We evaluated the sensitivity of our findings to co-pollutant adjustment and investigated effect modification patterns by period of the year, age at admission and specific diagnoses.Our results for the whole time period do not support an association between UFP and respiratory hospitalisations, although we found suggestive associations among those 0-14 years old. We nevertheless report consistent adverse effect estimates during the warm period of the year, statistically significant after lag 2 when an increase by 10 000 particles per cm(3) was associated with a 4.27% (95% CI 1.68-6.92%) increase in hospitalisations. These effect estimates were robust to particles' mass or gaseous pollutants adjustment.Considering that our findings during the warm period may reflect better exposure assessment and that the main source of non-soluble UFP in urban areas is traffic, our results call for improved regulation of traffic emissions.