Association of long-term exposure to local industry- and traffic-specific particulate matter with arterial blood pressure and incident hypertension.

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≥140mmHg, or diastolic BP≥90mmHg, 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 1km(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 1µg/m(3) of exposure concentration. RESULTS: PM2.5ALL was highly correlated with PM2.5IND (Spearman's ρ=0.92) and moderately with PM2.5TRA (ρ=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, 0.80]) and diastolic (0.25 [0.04, 0.46]) BP. Higher, but less precise estimates were found for PM2.5IND (systolic: 0.55 [-0.05, 1.14]; diastolic: 0.35 [0.03, 0.67]) and PM2.5TRA (systolic: 0.88 [-1.55, 3.31]; diastolic: 0.41 [-0.91, 1.73]). 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 hypertension. CONCLUSIONS: Long-term exposures to all-source and industry-specific PM2.5 were positively related to BP. We could not separate the effects of industry-specific PM2.5 from all-source PM2.5. Estimates with traffic-specific PM2.5 were generally higher but inconclusive.

Comparing land use regression and dispersion modelling to assess residential exposure to ambient air pollution for epidemiological studies.

BACKGROUND: Land-use regression (LUR) and dispersion models (DM) are commonly used for estimating individual air pollution exposure in population studies. Few comparisons have however been made of the performance of these methods. OBJECTIVES: Within the European Study of Cohorts for Air Pollution Effects (ESCAPE) we explored the differences between LUR and DM estimates for NO2, PM10 and PM2.5. METHODS: The ESCAPE study developed LUR models for outdoor air pollution levels based on a harmonised monitoring campaign. In thirteen ESCAPE study areas we further applied dispersion models. We compared LUR and DM estimates at the residential addresses of participants in 13 cohorts for NO2; 7 for PM10 and 4 for PM2.5. Additionally, we compared the DM estimates with measured concentrations at the 20-40 ESCAPE monitoring sites in each area. RESULTS: The median Pearson R (range) correlation coefficients between LUR and DM estimates for the annual average concentrations of NO2, PM10 and PM2.5 were 0.75 (0.19-0.89), 0.39 (0.23-0.66) and 0.29 (0.22-0.81) for 112,971 (13 study areas), 69,591 (7) and 28,519 (4) addresses respectively. The median Pearson R correlation coefficients (range) between DM estimates and ESCAPE measurements were of 0.74 (0.09-0.86) for NO2; 0.58 (0.36-0.88) for PM10 and 0.58 (0.39-0.66) for PM2.5. CONCLUSIONS: LUR and dispersion model estimates correlated on average well for NO2 but only moderately for PM10 and PM2.5, with large variability across areas. DM predicted a moderate to large proportion of the measured variation for NO2 but less for PM10 and PM2.5.

Association between source-specific particulate matter air pollution and hs-CRP: local traffic and industrial emissions.

BACKGROUND: Long-term exposures to particulate matter air pollution (PM2.5 and PM10) and high traffic load have been associated with markers of systemic inflammation. Epidemiological investigations have focused primarily on total PM, which represents a mixture of pollutants originating from different sources. OBJECTIVE: We investigated associations between source-specific PM and high-sensitive C-reactive protein (hs-CRP), an independent predictor of cardiovascular disease. METHODS: We used data from the first (2000-2003) and second examination (2006-2008) of the Heinz Nixdorf Recall study, a prospective population-based German cohort of initially 4,814 participants (45-75 years of age). We estimated residential long-term exposure to local traffic- and industry-specific fine particulate matter (PM2.5) at participants' residences using a chemistry transport model. We used a linear mixed model with a random participant intercept to estimate associations of source-specific PM and natural log-transformed hs-CRP, controlling for age, sex, education, body mass index, low- and high-density lipoprotein cholesterol, smoking variables, physical activity, season, humidity, and city (8,204 total observations). RESULTS: A 1-µg/m3 increase in total PM2.5 was associated with a 4.53% increase in hs-CRP concentration (95% CI: 2.76, 6.33%). hs-CRP was 17.89% (95% CI: 7.66, 29.09%) and 7.96% (95% CI: 3.45, 12.67%) higher in association with 1-µg/m3 increases in traffic- and industry-specific PM2.5, respectively. RESULTS for PM10 were similar. CONCLUSIONS: Long-term exposure to local traffic-specific PM (PM2.5, PM10) was more strongly associated with systemic inflammation than total PM. Associations of local industry-specific PM were slightly stronger but not significantly different from associations with 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.

Urban particulate matter air pollution is associated with subclinical atherosclerosis: results from the HNR (Heinz Nixdorf Recall) study.

OBJECTIVES: The aim of this study was to investigate the association of long-term residential exposure to fine particles with carotid intima-media thickness (CIMT). BACKGROUND: Experimental and epidemiological evidence suggest that long-term exposure to air pollution might have a causal role in atherogenesis, but epidemiological findings are still inconsistent. We investigate whether urban particulate matter (PM) air pollution is associated with CIMT, a marker of subclinical atherosclerosis. METHODS: We used baseline data (2000 to 2003) from the HNR (Heinz Nixdorf Recall) study, a population-based cohort of 4,814 participants, 45 to 75 years of age. We assessed residential long-term exposure to PM with a chemistry transport model and measured distance to high traffic. Multiple linear regression was used to estimate associations of air pollutants and traffic with CIMT, adjusting for each other, city of residence, age, sex, diabetes, and lifestyle variables. RESULTS: Median CIMT of the 3,380 analyzed participants was 0.66 mm (interquartile range 0.16 mm). An interdecile range increase in PM(2.5) (4.2 µg/m(3)), PM(10) (6.7 µg/m(3)), and distance to high traffic (1,939 m) was associated with a 4.3% (95% confidence interval [CI]: 1.9% to 6.7%), 1.7% (95% CI: -0.7% to 4.1%), and 1.2% (95% CI: -0.2% to 2.6%) increase in CIMT, respectively. CONCLUSIONS: Our study shows a clear association of long-term exposure to PM(2.5) with atherosclerosis. This finding strengthens the hypothesized role of PM(2.5) as a risk factor for atherogenesis.

Influence of short-term exposure to ultrafine and fine particles on systemic inflammation.

Daily to monthly variations in fine particulate matter have been linked to systemic inflammatory responses. It has been hypothesized that smaller particles resulting from combustion processes confer higher toxicity. We aim to analyze the association between short-term exposure to ultrafine and fine particles and systemic inflammation. We use baseline data (2000-2003) of the Heinz Nixdorf Recall Study, a population-based cohort study of 4,814 participants in the Ruhr Area in Germany. A chemistry transport model was applied to model daily surface concentrations of particulate air pollutants on a grid of 1 km(2). Exposure included particle number (PN) and particulate matter mass concentration with an aerodynamic diameter < or = 2.5 microm (PM(2.5)) and < or = 10 microm (PM(10)). Generalized additive models were used to explore the relation of air pollutants using single day lags and averaging times of up to 28 days with high-sensitivity C-reactive protein (hs-CRP). We adjusted for meteorology, season, time trend, and personal characteristics. Median hs-CRP level in the 3,999 included participants was 1.5 mg/l. Median daily concentration of PN was 8,414 x 10(4)/ml (IQR 4,580 x 10(4)/ml), of PM(2.5) 14.5 microg/m(3) (IQR 11.5 microg/m(3)) and of PM(10) 18.5 microg/m(3) (IQR 13.9 microg/m(3)). A positive association between PN and hs-CRP could be observed only for single day lags and for averaged PN concentrations with higher estimates for longer averaging times. The highest hs-CRP-increase of 7.1% (95%-CI: 1.9, 12.6%) was found for the 21-day average. These results support the hypothesis that short-term exposure to traffic-related particles might lead to detrimental cardiovascular health effects via an inflammatory mechanism.

Chronic residential exposure to particulate matter air pollution and systemic inflammatory markers.

BACKGROUND: Long-term exposure to urban air pollution may accelerate atherogenesis, but mechanisms are still unclear. The induction of a low-grade systemic inflammatory state is a plausible mechanistic pathway. OBJECTIVES: We analyzed the association of residential long-term exposure to particulate matter (PM) and high traffic with systemic inflammatory markers. METHODS: We used baseline data from the German Heinz Nixdorf Recall Study, a population-based, prospective cohort study of 4,814 participants that started in 2000. Fine PM [aerodynamic diameter

Residential traffic exposure and coronary heart disease: results from the Heinz Nixdorf Recall Study.

Traffic is one of the major sources of environmental pollution in metropolitan areas, emitting pollutants such as particulate matter and noise. Epidemiological evidence links both particulate matter (PM) and noise to cardiovascular disease and increased cardiovascular mortality. Short-term exposure to traffic may trigger acute cardiovascular events. Long-term residential traffic exposure is associated with the degree of subclinical atherosclerosis, prevalence of coronary heart disease and incidence of myocardial infarction. This review will present recent epidemiological findings regarding long-term exposure to traffic and its association with coronary heart disease, using results from the Heinz Nixdorf Recall Study, an ongoing prospective cohort study of 4814 unselected participants living in three large adjacent cities of the highly industrialized Ruhr Area in western Germany. Special focus is placed on the association of long-term traffic exposure with subclinical atherosclerosis, the major underlying pathology for cardiovascular disease.

Residential exposure to urban air pollution, ankle-brachial index, and peripheral arterial disease.

BACKGROUND: Long-term exposure to particulate air pollution has been associated with increased cardiovascular disease. Biologic pathways for this association are not fully understood. METHODS: We examined the association of urban air pollution with atherosclerosis of the peripheral vascular bed, using baseline data (2000-2003) from 4348 participants in a population-based cohort study in the German Ruhr Area. Levels of annual fine particulate matter (PM2.5) exposure, derived from a dispersion and chemistry transport model, were assigned to the participants' home addresses. Residential traffic exposure was assessed by the distance between residence and major roads (federal and state highways). Using multiple regression analyses and controlling for individual level risk factors, we examined the association of PM2.5 and traffic with the ankle-brachial index and prevalence of peripheral arterial disease, defined as an index of less than 0.9 or a history of treatment for peripheral artery disease. RESULTS: Living within 101-200, 51-100, and 50 m of a major road was associated with an adjusted absolute decrease in ankle-brachial index of -0.015 (95% confidence interval [CI] = -0.030 to 0.0), -0.002 (-0.021 to 0.016) and -0.024 (-0.047 to -0.001), respectively. Stronger associations were seen in women, whereas no clear association was found in men. Individuals living within 50 m of a major road had an OR of 1.77 (1.01-2.1) for peripheral arterial disease compared with those living more than 200 m away. Associations with PM2.5 were inconsistent. CONCLUSIONS: This study adds to the evidence that long-term residential exposure to traffic is associated with atherosclerosis.

Residence close to high traffic and prevalence of coronary heart disease.

AIMS: Long-term exposure to urban air pollution may accelerate atherogenesis and increase cardiopulmonary mortality. We aim to examine the relationship between the long-term residential exposure to traffic and prevalence of coronary heart disease (CHD). METHODS AND RESULTS: We used baseline data from the German Heinz Nixdorf RECALL study, a population-based, prospective cohort study. For 3399 participants from two cities, we assessed the long-term personal traffic exposure and background air pollution, comparing residents living within 150 m of major roads with those living further away. The principal outcome variable was clinically manifest CHD. We evaluated the association with multivariable logistic regression, controlling for background air pollution and individual level risk factors. Of 3399 participants, 242 (7.1%) had CHD. The crude odds ratio (OR) for prevalence of CHD at high traffic exposure was significantly elevated (1.62, 95%CI 1.12-2.34) and rose to 1.85 (95%CI 1.21-2.84) after adjusting for cardiovascular risk factors and background air pollution. Subgroup analysis showed stronger effects for men (OR 2.33, 95%CI 1.44-3.78), participants younger than 60 years (OR 2.67, 95%CI 1.24-5.74) and never-smokers (OR 2.72, 95%CI 1.40-5.29). CONCLUSION: This study provides epidemiological evidence that the long-term exposure to traffic-related emissions may be an important risk factor for CHD.