Association Between Traffic-Related Air Pollution, Subclinical Inflammation and Impaired Glucose Metabolism: Results From the SALIA Study

PLoS One. 2013 Dec 10;8(12):e83042. doi: 10.1371/journal.pone.0083042. eCollection 2013.


Background: Environmental and lifestyle factors regulate the expression and release of immune mediators. It has been hypothesised that ambient air pollution may be such an external factor and that the association between air pollution and impaired glucose metabolism may be attributable to inflammatory processes. Therefore, we assessed the associations between air pollution, circulating immune mediators and impaired glucose metabolism.

Methods: We analysed concentrations of 14 pro- and anti-inflammatory immune mediators as well as fasting glucose and insulin levels in plasma of 363 women from the Study on the influence of Air pollution on Lung function, Inflammation and Aging (SALIA, Germany). Exposure data for a group of pollutants such as nitrogen oxides (NO2, NOx) and different fractions of particulate matter were available for the participants' residences. We calculated the association between the pollutants and impaired glucose metabolism by multiple regression models.

Results: The study participants had a mean age of 74.1 (SD 2.6) years and 48% showed impaired glucose metabolism based on impaired fasting glucose or previously diagnosed type 2 diabetes. Only long-term exposure NO2 and NOx concentrations showed positive associations (NO2: OR 1.465, 95% CI 1.049-2.046, NOx: OR 1.409, 95% CI 1.010-1.967) per increased interquartile range of NO2 (14.65 µg/m(3)) or NOx (43.16 µg/m(3)), respectively, but statistical significance was lost after correction for multiple comparisons. Additional adjustment for circulating immune mediators or the use of anti-inflammatory medication had hardly any impact on the observed ORs.

Conclusions: Our results suggest that exposure to nitrogen oxides may contribute to impaired glucose metabolism, but the associations did not reach statistical significance so that further studies with larger sample sizes are required to substantiate our findings. Our data do not preclude a role of inflammatory mechanisms in adipose or other tissues which may not be reflected by immune mediators in plasma.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Air Pollutants / adverse effects
  • Air Pollution / adverse effects*
  • Biomarkers
  • Blood Glucose / chemistry
  • Diabetes Mellitus, Type 2 / blood
  • Environmental Exposure / adverse effects
  • Environmental Monitoring / methods
  • Female
  • Germany
  • Glucose / metabolism*
  • Humans
  • Inflammation / pathology*
  • Middle Aged
  • Nitrogen Oxides / analysis
  • Regression Analysis
  • Residence Characteristics
  • Vehicle Emissions


  • Air Pollutants
  • Biomarkers
  • Blood Glucose
  • Nitrogen Oxides
  • Vehicle Emissions
  • Glucose

Grant support

This study was supported by research grants from the Deutsche Forschungsgemeinschaft (DFG; HE-4510/2-1, KR 1938/3-1, LU 691/4-1). SALIA received funds from the Ministry of the Environment of the state North Rhine-Westphalia (Düsseldorf, Germany) and the Federal Ministry of the Environment (Berlin, Germany). The follow-up investigation was funded by the DGUV (German statutory accident assurance) VT 266.1. Exposure assessment (ESCAPE-data) was funded by the European Community’s Seventh Framework Program (FP7/2007-2011) under grant agreement number 211250. The German Diabetes Center is funded by the German Federal Ministry of Health (Berlin, Germany) and the Ministry of Innovation, Science and Research of the State of North Rhine-Westphalia (Düsseldorf, Germany). This study was supported in part by a grant from the German Federal Ministry of Education and Research (BMBF) to the German Center for Diabetes Research (DZD e.V.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.