Air Pollution, Subclinical Inflammation and the Risk of Type 2 Diabetes



Air pollution represents an important environmental risk factor for a number of health conditions. Particulate matter and gaseous compounds increase the risk of chronic and acute respiratory diseases, cardiovascular disease and lung cancer. Additional studies indicate that long-term exposure to air pollutants also contributes to the development and progression of type 2 diabetes. As the most common metabolic disease, type 2 diabetes and its chronic complications are important determinants of morbidity and mortality worldwide.

This article aims to provide an overview of the currently available data on the relationship between air pollution and type 2 diabetes with specific focus on epidemiological studies. Inflammatory processes have been discussed as mechanisms that mediate this association. Therefore, we first discuss the role of subclinical inflammation in the pathogenesis of type 2 diabetes and subsequently the impact of air pollutants on the immune system. We conclude that despite accumulating evidence linking (i) air pollution and proinflammatory processes, (ii) air pollution and risk of type 2 diabetes and (iii) subclinical inflammation and type 2 diabetes, there is a surprising lack of studies addressing this complex relationship in prospective cohorts. Therefore, it is currently not possible to quantify which proportion of the risk of type 2 diabetes can be attributed to air pollution-related immune activation and to what extent the risk of type 2 diabetes can be reduced by reducing air pollution levels.


Modifiable Risk Factor International Diabetes Federation Impaired Glucose Metabolism Subclinical Inflammation Soluble Adhesion Molecule 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.



This study was supported by research grants from the Deutsche Forschungsgemeinschaft (DFG; HE-4510/2-1, KR 1938/3-1, LU 691/4-1). This work was supported by the Ministry of Innovation, Science and Research of the State of North Rhine-Westphalia (MIWF NRW) and the German Federal Ministry of Health (BMG). 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.). We thank Kirti Kaul (German Diabetes Center) for critically reading the manuscript and for helpful discussions.


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© Springer-Verlag Wien 2016

Authors and Affiliations

  1. 1.Institute for Clinical DiabetologyGerman Diabetes Center, Leibniz Center for Diabetes Research at Heinrich Heine University DüsseldorfDüsseldorfGermany
  2. 2.German Center for Diabetes Research (DZD e.V.)DüsseldorfGermany

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