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Environ Int. 2014 Sep;70:32-49. doi: 10.1016/j.envint.2014.05.013. Epub 2014 Jun 3.

Associations between ambient air pollution and blood markers of inflammation and coagulation/fibrinolysis in susceptible populations.

Author information

1
ESC-Environmental Science Center, University of Augsburg, Universitätsstr. 2, 86135 Augsburg, Germany; Institute of Epidemiology II, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany. Electronic address: regina.pickford@helmholtz-muenchen.de.
2
Institute of Epidemiology II, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany. Electronic address: regina.hampel@helmholtz-muenchen.de.
3
Institute of Epidemiology II, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany. Electronic address: susanne.breitner@helmholtz-muenchen.de.
4
ESC-Environmental Science Center, University of Augsburg, Universitätsstr. 2, 86135 Augsburg, Germany; Institute of Epidemiology II, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany. Electronic address: cyrys@helmholtz-muenchen.de.
5
Institute of Epidemiology II, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany. Electronic address: ute.kraus@helmholtz-muenchen.de.
6
Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, Environmental Protection Agency, Research Triangle Park, Durham, NC 27709, USA. Electronic address: carter.jackie@epamail.epa.gov.
7
Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, Environmental Protection Agency, Research Triangle Park, Durham, NC 27709, USA. Electronic address: dailey.lisa@epamail.epa.gov.
8
Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, Environmental Protection Agency, Research Triangle Park, Durham, NC 27709, USA. Electronic address: devlin.robert@epamail.epa.gov.
9
Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, Environmental Protection Agency, Research Triangle Park, Durham, NC 27709, USA. Electronic address: diaz-sanchez.david@epamail.epa.gov.
10
Department of Internal Medicine II-Cardiology, University of Ulm Medical Centre, Albert-Einstein-Allee 23, 89081 Ulm, Germany. Electronic address: wolfgang.koenig@uniklinik-ulm.de.
11
Department of Environmental Medicine, Lung Biology and Disease Program, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA. Electronic address: Richard_Phipps@URMC.Rochester.edu.
12
Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, Environmental Protection Agency, Research Triangle Park, Durham, NC 27709, USA. Electronic address: silbajoris.robert@epamail.epa.gov.
13
ESC-Environmental Science Center, University of Augsburg, Universitätsstr. 2, 86135 Augsburg, Germany. Electronic address: soentgen@wzu.uni-augsburg.de.
14
Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, Environmental Protection Agency, Research Triangle Park, Durham, NC 27709, USA. Electronic address: soukup.joleen@epamail.epa.gov.
15
Institute of Epidemiology II, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany; German Center for Diabetes Research (DZD e.V.), Neuherberg, Germany. Electronic address: peters@helmholtz-muenchen.de.
16
Institute of Epidemiology II, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany. Electronic address: alexandra.schneider@helmholtz-muenchen.de.

Abstract

The pathophysiological pathways linking particulate air pollution to cardiovascular disease are still not fully understood. We examined the association between ambient air pollutants and blood markers of inflammation and coagulation/fibrinolysis in three potentially susceptible populations. Three panels of non-smoking individuals were examined between 3/2007 and 12/2008: 1) with type 2 diabetes mellitus (T2D, n=83), 2) with impaired glucose tolerance (IGT, n=104), and 3) with a potential genetic predisposition which could affect detoxifying and inflammatory pathways (n=87) defined by the null polymorphism for glutathione S-transferase M1 (GSTM1) in combination with a certain single nucleotide polymorphism on the C-reactive protein (CRP) or the fibrinogen gene. Study participants had blood drawn up to seven times every four to six weeks. In total, 1765 blood samples were analysed for CRP, interleukin (IL)-6, soluble CD40 ligand (sCD40L), fibrinogen, myeloperoxidase (MPO), and plasminogen activator inhibitor-1 (PAI-1). Hourly mean values of particulate air pollutants, particle number concentrations in different size ranges and gaseous pollutants were collected at fixed monitoring sites and individual 24hour averages calculated. Associations between air pollutants and blood markers were analysed for each panel separately and taking the T2D panel and the IGT panel together, using additive mixed models adjusted for long-term time trend and meteorology. For the panel with potential genetic susceptibility, CRP and MPO increased for most lags, especially with the 5-day average exposure (% change of geometric mean and 95% confidence interval: 22.9% [12.0;34.7] for CRP and 5.0% [0.3;9.9] for MPO per interquartile range of PM2.5). Small positive associations were seen for fibrinogen while sCD40L, PAI-1 and IL-6 mostly decreased in association with air pollution concentrations. Except for positive associations for fibrinogen we did not see significant results with the two other panels. Participants with potential genetic susceptibility showed a clear association between inflammatory blood biomarkers and ambient air pollutants. Our results support the hypothesis that air pollution increases systemic inflammation especially in susceptible populations which may aggravate atherosclerotic diseases and induce multi-organ damage.

KEYWORDS:

Air pollution; CRP; Coagulation; Diabetes; GSTM1; Inflammation

PMID:
24907704
DOI:
10.1016/j.envint.2014.05.013
[Indexed for MEDLINE]

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