Impact of long-term air pollution exposure on metabolic control in children and adolescents with type 1 diabetes: results from the DPV registry
Studies on the association between air pollution and metabolic control in children and adolescents with type 1 diabetes are rare and findings are inconsistent. We examined the relationship between air pollution variables (particulate matter with an aerodynamic diameter <10 μm [PM10], NO2 and accumulated ozone exposure [O3-AOT]) and metabolic variables (HbA1c and daily insulin dose [U/kg body weight]) in children and adolescents with type 1 diabetes.
We investigated 37,372 individuals with type 1 diabetes aged <21 years, documented between 2009 and 2014 in 344 German centres of the prospective diabetes follow-up registry (Diabetes-Patienten-Verlaufsdokumentation [DPV]). Long-term air pollution exposure (annual and quinquennial means) data were linked to participants via the five-digit postcode areas of residency. Cross-sectional multivariable regression analysis was used to examine the association between air pollution and metabolic control.
After comprehensive adjustment, an interquartile range increase in O3-AOT was associated with a lower HbA1c (−3.7% [95% CI −4.4, −3.0]). The inverse association between O3-AOT and HbA1c persisted after additional adjustment for degree of urbanisation or additional adjustment for PM10. Moreover, the inverse association remained stable in further sensitivity analyses. No significant associations between HbA1c and PM10 or NO2 were found. No association was observed between any of the three air pollutants and insulin dose.
The inverse association between O3-AOT and HbA1c could not be explained by regional differences in diabetes treatment or by other differences between urban and rural areas. Furthermore, our results remained stable in sensitivity analyses. Further studies on the association between air pollution and HbA1c in children and adolescents with type 1 diabetes are needed to confirm our observed association and to elucidate underlying mechanisms.
KeywordsAir pollution HbA1c Insulin Metabolic control Ozone Particulate matter Type 1 diabetes
German Health Interview and Examination Survey for Children and Adolescents
Cooperative Health Research in the Region of Augsburg, Germany
Accumulated ozone exposure
Particulate matter with an aerodynamic diameter <10 μm
Standard deviation score
The authors thank all participating centres of the DPV Initiative, especially those collaborating in this investigation (listed in the ESM). We thank the German Federal Environmental Agency (Umweltbundesamt [UBA], Department II 4.2) for providing the air pollution data.
SL contributed to data management, data analysis and manuscript writing and editing. JR contributed to data analysis and manuscript writing and editing. DS and TS contributed to data analysis and manuscript editing. BT, DK and WR reviewed the manuscript and contributed to interpretation of data and manuscript editing. RWH is the principal investigator of the study and contributed to data analysis and manuscript writing and editing. All co-authors approved the final version to be published. RWH is the guarantor of this work and, as such, had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
The study was financially supported by the Federal Ministry of Education and Research within the German Competence Network Diabetes Mellitus (grant 01GI1106), which was integrated into the German Centre for Diabetes Research (DZD) as of January 2015. This project has received funding from the Innovative Medicines Initiative 2 Joint Undertaking under grant agreement no. 115797 (INNODIA). This joint undertaking receives support from the Union’s Horizon 2020 research and innovation programme and ‘EFPIA’, ‘JDRF’ and ‘The Leona M. and Harry B. Helmsley Charitable Trust’. Additional support was provided by the German Diabetes Association (DDG). Sponsors were not involved in data acquisition or analysis.
Duality of interest
The authors declare that there is no duality of interest associated with this manuscript.
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