Comparison of coronary artery calcification, carotid intima-media thickness and ankle-brachial index for predicting 10-year incident cardiovascular events in the general population.

AIMS: To compare the predictive value of coronary artery calcification (CAC), carotid intima-media thickness (CIMT) and ankle-brachial index (ABI) in a primary prevention cohort depending on risk factor profile to determine which of the three markers improves cardiovascular (CV) risk discrimination best in which risk group. METHODS AND RESULTS: We quantified CAC, CIMT, and ABI in 3108 subjects (mean age 59.2 ± 7.7, 47.1% male) without prevalent CV diseases from the population-based Heinz Nixdorf Recall study. Associations with incident major CV events (coronary event, stroke, CV death; n = 223) were assessed during a follow-up period of 10.3 ± 2.8 years with Cox proportional regressions in the total cohort and stratified by Framingham risk score (FRS) groups. Discrimination ability was evaluated with Harrell's C. All three markers were associated with CV events (hazard ratio [95% confidence interval (CI)]: CAC: 1.31 (1.23-1.39) per 1-unit increase in log(CAC + 1) vs. CIMT: 1.27 (1.13-1.43) per 1 SD vs. ABI: 1.30 (1.14-1.49) per 1 SD, in FRS adjusted models). Considering reclassification, CAC lead to highest reclassification in the total cohort, while also for CIMT and ABI significant improvement in net-reclassification was observed [NRI (95% CI): CAC: 0.55 (0.42-0.69); CIMT: 0.32 (0.19-0.45); ABI: 0.19 (0.10-0.28)]. CONCLUSION: Coronary artery calcification provides the best discrimination of risk compared with CIMT and ABI, particularly in the intermediate risk group, whereas CIMT may be an alternative measure for reassurance in the low risk group.

Arterial blood pressure responses to short-term exposure to fine and ultrafine particles from indoor sources - A randomized sham-controlled exposure study of healthy volunteers.

OBJECTIVES: Particulate air pollution is linked to adverse cardiovascular effects. The aim of the study was to investigate the effect of short-term exposure to indoor particles on blood pressure (BP). METHODS: We analyzed the association of particle emissions from indoor sources (candle burning, toasting bread, frying sausages) with BP changes in 54 healthy volunteers in a randomized cross-over controlled exposure study. Particle mass concentration (PMC), size-specific particle number concentration (PNC) and lung-deposited particle surface area concentration (PSC) were measured during the 2h exposure. Systolic and diastolic blood pressure were measured before, during, directly, 2, 4 and 24h after exposure. We performed multiple mixed linear regression analyses of different particle metrics and BP. RESULTS: BP significantly increased with increasing PMC, PSC and PNC resulting from toasting bread. For example, an increase per 10µg/m3 PM10 and PM2.5, systolic BP increased at all time points with largest changes 1h after exposure initiation of 1.5mmHg (95%-CI: 1.1; 1.9) and of 2.2mmHg (95%-CI: 1.3; 3.1), respectively. CONCLUSIONS: Our study suggests an association of short-term exposure to fine and ultrafine particles emitted from toasting bread with increases in BP. Particles emitted from frying sausages and candle burning did not consistently affect BP.

Linkage and Association Analysis Identifies TRAF1 Influencing Common Carotid Intima-Media Thickness.

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=1.60×10-3, 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.

Exposure to ultrafine particles and respiratory hospitalisations in five European cities.

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.

Long-term air pollution and traffic noise exposures and cognitive function:A cross-sectional analysis of the Heinz Nixdorf Recall study.

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 (LDEN) and nighttime (LNIGHT) 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 LDEN and LNIGHT 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.

Association of short-term ozone and temperature with sleep disordered breathing.

Scarce evidence suggests that ambient air pollution and temperature might play a role in incidence and severity of sleep disordered breathing (SDB). We investigated the association of short-term exposure to fine particulate matter (particles with a 50% cut-off aerodynamic diameter of 10 µm (PM10)), ozone and temperature with SDB in the general population. Between 2006 and 2008, 1773 participants (aged 50-80 years) of the Heinz Nixdorf Recall study underwent screening for SDB, as defined by the apnoea-hypopnoea index (AHI). We assessed daily exposure to PM10, ozone, temperature and humidity. We used multiple linear regression to estimate associations of daily PM10, ozone levels and temperature on the day of screening, adjusting for relative humidity, season, age, sex, body mass index, education, smoking habits, alcohol consumption and physical activity. In the study population, the mean±sd AHI was 11.2±11.4 events·h(-1). Over all seasons, an interquartile range increase in temperature (8.6°C) and ozone (39.5 µg·m(-3)) was associated with a 10.2% (95% CI 1.2-20.0%) and 10.1% (95% CI 2.0-18.9%) increase in AHI, respectively. Associations for temperature were stronger in summer, yielding a 32.4% (95% CI 0.0-75.3%) increase in AHI per 8.6°C (p-value for season-temperature interaction 0.08). We observed that AHI was not associated with PM10. This study suggests that short-term variations in ozone concentration and temperature are associated with SDB.

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

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

Long-term exposure to fine particulate matter and incidence of type 2 diabetes mellitus in a cohort study: effects of total and traffic-specific air pollution.

BACKGROUND: Studies investigating the link between long-term exposure to air pollution and incidence of diabetes are still scarce and results are inconsistent, possibly due to different compositions of the particle mixture. We investigate the long-term effect of traffic-specific and total particulate matter (PM) and road proximity on cumulative incidence of diabetes mellitus (mainly type 2) in a large German cohort. METHODS: We followed prospectively 3607 individuals without diabetes at baseline (2000-2003) from the Heinz Nixdorf Recall Study in Germany (mean follow-up time 5.1 years). Mean annual exposures to total as well as traffic-specific PM10 and PM2.5 at residence were estimated using a chemistry transport model (EURAD, 1 km(2) resolution). Effect estimates for an increase of 1 µg/m(3) in PM were obtained with Poisson regression adjusting for sex, age, body mass index, lifestyle factors, area-level and individual-level socio-economic status, and city. RESULTS: 331 incident cases developed. Adjusted RRs for total PM10 and PM2.5 were 1.05 (95%-CI: 1.00;1.10) and 1.03 (95%-CI: 0.95;1.12), respectively. Markedly higher point estimates were found for local traffic-specific PM with RRs of 1.36 (95%-CI: 0.98;1.89) for PM10 and 1.36 (95%-CI: 0.97;1.89) for PM2.5. Individuals living closer than 100 m to a busy road had a more than 30% higher risk (1.37;95%-CI: 1.04;1.81) than those living further than 200 m away. CONCLUSIONS: Long-term exposure to total PM increases type two diabetes risk in the general population, as does living close to a major road. Local traffic-specific PM was related to higher risks for type two diabetes than total PM.

Are air pollution and traffic noise independently associated with atherosclerosis: the Heinz Nixdorf Recall Study.

AIMS: Living close to high traffic has been linked to subclinical atherosclerosis, however it is not clear, whether fine particulate matter (PM) air pollution or noise, two important traffic-related exposures, are responsible for the association. We investigate the independent associations of long-term exposure to fine PM and road traffic noise with thoracic aortic calcification (TAC), a reliable measure of subclinical atherosclerosis. METHODS AND RESULTS: We used baseline data (2000-2003) from the German Heinz Nixdorf Recall Study, a population-based cohort of 4814 randomly selected participants. We assessed residential long-term exposure to PM with a chemistry transport model, and to road traffic noise using façade levels from noise models as weighted 24 h mean noise (Lden) and night-time noise (Lnight). Thoracic aortic calcification was quantified from non-contrast enhanced electron beam computed tomography. We used multiple linear regression to estimate associations of environmental exposures with ln(TAC+1), adjusting for each other, individual, and neighbourhood characteristics. In 4238 participants (mean age 60 years, 49.9% male), PM2.5 (aerodynamic diameter ≤2.5 µm) and Lnight are both associated with an increasing TAC-burden of 18.1% (95% CI: 6.6; 30.9%) per 2.4 µg/m(3) PM2.5 and 3.9% (95% CI 0.0; 8.0%) per 5dB(A) Lnight, respectively, in the full model and after mutual adjustment. We did not observe effect measure modification of the PM2.5 association by Lnight or vice versa. CONCLUSION: Long-term exposure to fine PM and night-time traffic noise are both independently associated with subclinical atherosclerosis and may both contribute to the association of traffic proximity with atherosclerosis.

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.

Investigation of air pollution and noise on progression of thoracic aortic calcification: results of the Heinz Nixdorf Recall Study.

AIMS: Air pollution and noise are potential risk factors for subclinical atherosclerosis. Longitudinal analyses, especially on the interplay of these environmental factors, are scarce and inconsistent. Hence we investigated long-term traffic-related exposure to air pollution and noise with the development and progression of thoracic aortic calcification, a marker of subclinical atherosclerosis. METHODS: We used baseline (2000-2003) and follow-up (2006-2008) data from the German Heinz Nixdorf Recall cohort study, including 4814 middle-aged adults. Residence-based air pollution (PM2.5 (aerodynamic diameter ≤ 2.5 µm), PM10, nitrogen dioxide and particle number), and noise was assessed with dispersion models. Thoracic aortic calcification was quantified from non-contrast enhanced electron beam computed tomography. The presence and extent of thoracic aortic calcification progression were analysed with multiple logistic and linear regression models, respectively, adjusting for age, sex, lifestyle variables, socioeconomic status and respective co-exposure. RESULTS: We observed no association in the full study sample (n = 3155, mean age 59.1 (±7.6) years, 52.8% women). While an interquartile range in particle number and night-time noise yielded odds ratios of 1.20 (1.03, 1.40) and 1.21 (1.00, 1.46) for binary thoracic aortic calcification progression, and 0.02 (-0.01, 0.05) and 0.04 (0.00, 0.07) higher growth rates of thoracic aortic calcification in participants with baseline thoracic aortic calcification less than 10, negative findings were observed in those with baseline thoracic aortic calcification of 10 or greater. Results were similar for other pollutants and daytime noise. CONCLUSION: Our study shows no overall associations. Subgroup analyses suggest independent associations of traffic-related air pollution and noise with the development and progression of subclinical atherosclerosis in participants with no or minor thoracic aortic calcification at baseline, in contrast to negative findings in those with advanced calcification.

The role of depressive symptoms within the association of long-term exposure to indoor and outdoor traffic noise and cognitive function - Results from the Heinz Nixdorf Recall study.

OBJECTIVES: Traffic noise is negatively associated with cognitive function, and its perception can differ between depressed and non-depressed people. We studied the role of depressive symptoms in the association between traffic noise and cognitive function. We studied the role of depressive symptoms in the association between traffic noise and cognitive function. METHODS: During the first follow-up examination (2006-2008) of the German Heinz Nixdorf Recall study, cognitive function (five subtests and an additive global summary score, GCS) and depressive symptoms (CES-D score) were assessed in 2745 participants (aged 50-80, 49.8% women). Mild cognitive impairment (MCI) was diagnosed according to the Petersen criteria in 380 participants. Long-term exposure to traffic noise was modeled as weighted 24-h mean (LDEN) and night-time mean (LNIGHT) at the façade of the baseline addresses, and was corrected for indoors (LDEN_IN and LNIGHT_IN). We developed multiple linear and logistic regression models adjusted for individual-level characteristics to investigate cross-sectionally the role of depressive symptoms in the association of traffic noise with cognitive function. RESULTS: Overall, 8.6% participants had depressive symptoms. The median noise values were LDEN 52.1 dB(A) and LDEN_IN 34.7 dB(A). Associations were slightly stronger for cognitive subtests in those with severe depression (CES-D>21), i.e., per 10 dB(A) LDEN and verbal fluency: ß = -0.04 [-0.11; 0.03] for CES-D≤21 and ß = -0.09 [-0.24; -0.06] for CES-D>21. Additional adjustment of the main model for CES-D did not change the association between noise and cognitive outcomes. Estimates using indoor noise exposure were generally stronger and more precise. CONCLUSIONS: Depressed people may be more susceptible to adverse effects of noise than non-depressed. Modeled estimates of indoor noise exposure is possibly a more appropriate measure of exposure.

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.

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.

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.

Effects of short-term exposure to fine and ultrafine particles from indoor sources on arterial stiffness - A randomized sham-controlled exposure study.

OBJECTIVES: Particulate air pollution is linked to adverse cardiovascular effects, including arterial stiffness. The aim of the study was to investigate the effect of short-term exposure to indoor fine and ultrafine particles on augmentation index (AIx), augmentation pressure (AP), and pulse wave velocity (PWV), early signs of vascular damage. METHODS: We analyzed the association of particle emissions from typical indoor sources (candle burning - CB, toasting bread - TB, and frying sausages - FS) with changes in pulse wave analysis indices in 55 healthy adults in a randomized cross-over controlled exposure study. Particle mass concentration (PMC), size-specific particle number concentration (PNC) and lung-deposited particle surface area concentration (PSC) were measured during the 2 h exposure. AIx and AP were measured before, directly, 2, 4 and 24 h after exposure. PWV was measured directly and 24 h after exposure. We performed multiple mixed linear regression analyses of different particle metrics and AIx, AP and PWV. RESULTS: The highest mean PMC was observed during FS reaching a maximum of 210 µg/m3 PM10. The maximal PNC for UFP <100 nm was reached during CB with 2.3 million particles/cm3. PSC was similar across all three exposures (about 3000 µm2/cm³). Strongest associations between different particles metrics and arterial stiffness indices could be observed for UFP from CB and FS and for PMC from TB. The highest mean increase could be observed for the UFP fraction <10 nm, measured during CB, and AIx with an increase of 9.5%-points (95%-CI: 3.1; 15.9). PSC seemed to follow the pattern of PNC. PM10 and PM2.5 from TB led to clear changes in AIx with biggest increases for PM10 of 5.8%-points (95%-CI: 3.2; 8.4) 2 h after exposure and for PM2.5 of 8.1%-points (95%-CI: 2.5; 13.7) directly after exposure. CONCLUSIONS: Our study indicates effects of indoor exposure to fine and ultrafine particles on systemic arterial stiffness indices that depend on the indoor source as well as on particle metric. Differences in size-specific physical characteristics of source-specific particles might account for these differential effects. We did not observe clear and stable associations of indoor particle exposure and PWV.

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.