•All-source AP exposure associated with DM incidence.•Traffic-specific AP exposure shows strongest association with DM.•Possible mediation through decreased adiponectin levels.
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.
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.
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.
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 from traffic poses higher risk of stroke than from industrial sources.•No association found between exposure to air pollution and risk of CHD.•Among PM components NH4 and SO4 have ...higher effect on cardiovascular health.
Few studies have examined the risk of long-term exposure to source-specific airborne pollutants on incidence of cerebrovascular and cardiovascular events.
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).
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.
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.
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.
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.
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).
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.
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.
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.
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.
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.
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.
•Air pollution associated with diabetes-related biomarkers in non-diabetic adults•Differing temporal patterns of association for each biomarker•Negative association with adiponectin seen primarily in lean individuals
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).
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
(
), (
), and nitrogen dioxide (
) 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.
While no clear associations were observed in the full study sample (mean age 59.1 (
) 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
higher exposure to
(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%).
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.
Lung function depends nonlinearly on age and height, so that the use of age and height specific reference values is required. The widely used age and height specific GLI (Global Lung Initiative) ...z-scores derived from cross-sectional data, however, have not been proven for validity in an elderly population or for longitudinal data. Therefore, we aimed to test their validity in a population of elderly women followed prospectively for more than 20 years.
We used spirometric data (forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) and FEV1/FVC) from the SALIA cohort of German women (baseline: 1985-1994 (aged 55 years), follow-up: 2008/2009 and 2012/2013). We calculated GLI-z-scores for baseline and follow-up examination separately (cross-sectional evaluation) and individual differences in z-scores between baseline and follow-up (longitudinal evaluation) for healthy never-smoking women.
GLI reference values for FEV1, FVC and FEV1/FVC were cross-sectionally and longitudinally equivalent with our SALIA data. The mean change in z-scores between baseline and follow-up was 0.33 for FEV1, 0.38 for FVC and -0.10 for FEV1/FVC.
In conclusion, GLI z-scores fit cross-sectionally and longitudinally with FEV1, FVC and FEV1/FVC measured in women from Germany which indicates that they can be used in longitudinal association analyses.
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 PM
2.5
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.
Particulate air pollution is linked to impaired respiratory health. We analyzed particle emissions from common indoor sources (candles burning (CB), toasting bread (TB), frying sausages (FS)) and ...lung function in 55 healthy volunteers (mean age 33.0 years) in a randomized cross-over controlled exposure study. Lung-deposited particle surface area concentration (PSC), size-specific particle number concentration (PNC) up to 10 µm, and particle mass concentration (PMC) of PM1, PM2.5 and PM10 were determined during exposure (2 h). FEV1, FVC and MEF25%-75% was measured before, 4 h and 24 h after exposure. Wilcoxon-rank sum tests (comparing exposure scenarios) and mixed linear regression using particle concentrations and adjusting for personal characteristics, travel time and transportation means before exposure sessions were performed. While no effect was seen comparing the exposure scenarios and in the unadjusted model, inverse associations were found for PMC from CB and FS in relation to FEV1 and MEF25%-75%. with a change in 10 µg/m3 in PM2.5 from CB being associated with a change in FEV1 of -19 mL (95%-confidence interval:-43; 5) after 4 h. PMC from TB and PNC of UFP were not associated with lung function changes, but PSC from CB was. Elevated indoor fine particles from certain sources may be associated with small decreases in lung function in healthy adults.
Two commonly used models to assess air pollution concentration for investigating health effects of air pollution in epidemiological studies are Land Use Regression (LUR) models and Dispersion and ...Chemistry Transport Models (DCTM). Both modeling approaches have been applied in the Ruhr area, Germany, a location where multiple cohort studies are being conducted. Application of these different modelling approaches leads to differences in exposure estimation and interpretation due to the specific characteristics of each model. We aimed to compare both model approaches by means of their respective aims, modeling characteristics, validation, temporal and spatial resolution, and agreement of residential exposure estimation, referring to the air pollutants PM2.5, PM10, and NO2. Residential exposure referred to air pollution exposure at residences of participants of the Heinz Nixdorf Recall Study, located in the Ruhr area. The point-specific ESCAPE (European Study of Cohorts on Air Pollution Effects)-LUR aims to temporally estimate stable long-term exposure to local, mostly traffic-related air pollution with respect to very small-scale spatial variations (≤100 m). In contrast, the EURAD (European Air Pollution Dispersion)-CTM aims to estimate a time-varying average air pollutant concentration in a small area (i.e., 1 km2), taking into account a range of major sources, e.g., traffic, industry, meteorological conditions, and transport. Overall agreement between EURAD-CTM and ESCAPE-LUR was weak to moderate on a residential basis. Restricting EURAD-CTM to sources of local traffic only, respective agreement was good. The possibility of combining the strengths of both applications will be the next step to enhance exposure assessment.
Background:
Recent epidemiological studies investigating the modifying effect of air temperature in ozone–mortality associations lack consensus as how to adjust for nonlinear and lagged temperature ...effect in addition to including an interaction term.
Methods:
We evaluated the influence of temperature confounding control on temperature-stratified ozone–mortality risks in a time series setting in eight European cities and 86 US cities, respectively. To investigate potential residual confounding, we additionally incorporated next day’s ozone in models with differing temperature control.
Results:
Using only a categorical variable for temperature or only controlling nonlinear effect of low temperatures yielded highly significant ozone effects at high temperatures but also significant residual confounding in both regions. Adjustment for nonlinear effect of temperature, especially high temperatures, substantially reduced ozone effects at high temperatures and residual confounding.
Conclusions:
Inadequate control for confounding by air temperature leads to residual confounding and an overestimation of the temperature-modifying effect in studies of ozone-related mortality.
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