Air pollution and subclinical airway inflammation in the SALIA cohort study

Immunity & Ageing

Ursula Krämer²  Thomas Brüning⁵  Swaantje Casjens⁵  Monika Raulf-Heimsoth⁵  Christian Luckhaus³  Thomas Schulte³  Christian Herder⁷  Tom Teichert⁴  Barbara Hoffmann¹  Dorothea Sugiri²  Andrea Vierkötter²  Tamara Schikowski⁶  Mohammad Vossoughi² 

[1] Heinrich Heine University of Düsseldorf, Medical Faculty, Moorenstrasse 5, Düsseldorf 40225, Germany;IUF – Leibniz Research Institute for Environmental Medicine, Auf’m Hennekamp 50, Düsseldorf 40225, Germany;Department of Psychiatry and Psychotherapy, Medical Faculty, Heinrich-Heine-University, Bergische Landstr. 2, Düsseldorf 40629, Germany;Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich Heine University Düsseldorf, Auf’m Hennekamp 65, Düsseldorf 40225, Germany;Institute for Prevention and Occupational Medicine of the German Social Accident Insurance, Institute of the Ruhr-Universität Bochum (IPA), Bürkle-de-la-Camp-Platz 1, Bochum 44789, Germany;University of Basel, Petersplatz 1, Basel 4003, Switzerland;German Center for Diabetes Research (DZD), partner site Düsseldorf, Auf’m Hennekamp 65, Düsseldorf 40225, Germany

关键词: Exhaled breath condensate;    Induced sputum;    Inflammatory markers;    Epidemiology;    Particle exposure;   

Others  :  814033
DOI  :  10.1186/1742-4933-11-5

 received in 2013-09-27, accepted in 2014-03-14,  发布年份 2014

【 摘 要 】

Background

The association between long-term exposure to air pollution and local inflammation in the lung has rarely been investigated in the general population of elderly subjects before. We investigated this association in a population-based cohort of elderly women from Germany.

Methods

In a follow-up examination of the SALIA cohort study in 2008/2009, 402 women aged 68 to 79 years from the Ruhr Area and Borken (Germany) were clinically examined. Inflammatory markers were determined in exhaled breath condensate (EBC) and in induced sputum (IS). We used traffic indicators and measured air pollutants at single monitoring stations in the study area to assess individual traffic exposure and long-term air pollution background exposure. Additionally long-term residential exposure to air pollution was estimated using land-use regression (LUR) models. We applied multiple logistic and linear regression analyses adjusted for age, indoor mould, smoking, passive smoking and socio-economic status and additionally conducted sensitivity analyses.

Results

Inflammatory markers showed a high variability between the individuals and were higher with higher exposure to air pollution. NO derivatives, leukotriene (LT) B₄ and tumour necrosis factor-α (TNF-α) showed the strongest associations. An increase of 9.42 μg/m³ (interquartile range) in LUR modelled NO₂ was associated with measureable LTB₄ level (level with values above the detection limit) in EBC (odds ratio: 1.38, 95% CI: 1.02 -1.86) as well as with LTB₄ in IS (%-change: 19%, 95% CI: 7% - 32%). The results remained consistent after exclusion of subpopulations with risk factors for inflammation (smoking, respiratory diseases, mould infestation) and after extension of models with additional adjustment for season of examination, mass of IS and urban/rural living as sensitivity analyses.

Conclusions

In this analysis of the SALIA study we found that long-term exposure to air pollutants from traffic and industrial sources was associated with an increase of several inflammatory markers in EBC and in IS. We conclude that long-term exposure to air pollution might lead to changes in the inflammatory marker profile in the lower airways in an elderly female population.

【 授权许可】

   
2014 Vossoughi et al.; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

Figure 2.

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