title: Association between traffic-related air pollution, subclinical inflammation and impaired glucose metabolism: results from the SALIA study.
abstract: 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.
authors: Institute of Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
authors: Tom
authors: T
authors: Teichert
authors: Mohammad
authors: M
authors: Vossoughi
authors: Andrea
authors: A
authors: Vierkötter
authors: Dorothea
authors: D
authors: Sugiri
authors: Tamara
authors: T
authors: Schikowski
authors: Thomas
authors: T
authors: Schulte
authors: Michael
authors: M
authors: Roden
authors: Christian
authors: C
authors: Luckhaus
authors: Christian
authors: C
authors: Herder
authors: Ursula
authors: U
authors: Krämer
mesh_terms: D000368:Aged; D000393:Air Pollutants / Q000009:adverse effects; D000397:Air Pollution / Q000009:adverse effects*; D015415:Biomarkers; D001786:Blood Glucose / Q000737:chemistry; D003924:Diabetes Mellitus, Type 2 / Q000097:blood; D004781:Environmental Exposure / Q000009:adverse effects; D004784:Environmental Monitoring / Q000379:methods; D005260:Female; D005858:Germany; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000473:pathology*; D008875:Middle Aged; D009589:Nitrogen Oxides / Q000032:analysis; D012044:Regression Analysis; D012111:Residence Characteristics; D001335:Vehicle Emissions
chemical_list: D000393:Air Pollutants; D015415:Biomarkers; D001786:Blood Glucose; D009589:Nitrogen Oxides; D001335:Vehicle Emissions; D005947:Glucose