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Int J Hyg Environ Health. 2016 Aug;219(6):527-35. doi: 10.1016/j.ijheh.2016.05.008. Epub 2016 May 26.

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

Author information

1
Environmental Epidemiology Group, Institute of Occupational, Social and Environmental Medicine, Center for Health and Society, Heinrich-Heine-University of Düsseldorf, University Hospital of Düsseldorf, Umweltepidemiologie, POB 10 10 07, 40001 Düsseldorf, Germany. Electronic address: kateryna.fuks@uni-duesseldorf.de.
2
Institute of Epidemiology of Ulm University, Helmholtzstrasse 16, 89081 Ulm, Germany. Electronic address: gudrun.weinmayr@uni-ulm.de.
3
Environmental Epidemiology Group, Institute of Occupational, Social and Environmental Medicine, Center for Health and Society, Heinrich-Heine-University of Düsseldorf, University Hospital of Düsseldorf, Umweltepidemiologie, POB 10 10 07, 40001 Düsseldorf, Germany. Electronic address: frauke.hennig@uni-duesseldorf.de.
4
Environmental Epidemiology Group, Institute of Occupational, Social and Environmental Medicine, Center for Health and Society, Heinrich-Heine-University of Düsseldorf, University Hospital of Düsseldorf, Umweltepidemiologie, POB 10 10 07, 40001 Düsseldorf, Germany. Electronic address: liliana.tzivian@med.uni-duesseldorf.de.
5
Institute for Medical Informatics, Biometry and Epidemiology, University Hospital Essen, The University of Duisburg-Essen, Hufelandstraße 55, 45122 Essen, Germany. Electronic address: susanne.moebus@uk-essen.de.
6
Rhenish Institute for Environmental Research at the University of Cologne, Aachener Strasse 209, 50931 Cologne, Germany. Electronic address: hermann.jakobs@riu.uni-koeln.de.
7
Rhenish Institute for Environmental Research at the University of Cologne, Aachener Strasse 209, 50931 Cologne, Germany. Electronic address: michael.memmesheimer@riu.uni-koeln.de.
8
West German Heart Centre of Essen, University Hospital Essen, The University of Duisburg-Essen, Hufelandstraße 55, 45122 Essen, Germany. Electronic address: hagen.kaelsch@uk-essen.de.
9
Institute for Medical Informatics, Biometry and Epidemiology, University Hospital Essen, The University of Duisburg-Essen, Hufelandstraße 55, 45122 Essen, Germany. Electronic address: silke.andrich@ddz.uni-duesseldorf.de.
10
Institute for Medical Informatics, Biometry and Epidemiology, University Hospital Essen, The University of Duisburg-Essen, Hufelandstraße 55, 45122 Essen, Germany. Electronic address: michael.nonnemacher@uk-essen.de.
11
Institute for Medical Informatics, Biometry and Epidemiology, University Hospital Essen, The University of Duisburg-Essen, Hufelandstraße 55, 45122 Essen, Germany. Electronic address: raimund.erbel@uk-essen.de.
12
Institute for Medical Informatics, Biometry and Epidemiology, University Hospital Essen, The University of Duisburg-Essen, Hufelandstraße 55, 45122 Essen, Germany. Electronic address: k-h.joeckel@uk-essen.de.
13
Environmental Epidemiology Group, Institute of Occupational, Social and Environmental Medicine, Center for Health and Society, Heinrich-Heine-University of Düsseldorf, University Hospital of Düsseldorf, Umweltepidemiologie, POB 10 10 07, 40001 Düsseldorf, Germany. Electronic address: b.hoffmann@uni-duesseldorf.de.

Abstract

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.

KEYWORDS:

Blood pressure; Hypertension; Industrial emissions; Particulate matter; Source-specific air pollution; Traffic emissions

PMID:
27318724
DOI:
10.1016/j.ijheh.2016.05.008
[Indexed for MEDLINE]

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