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Environ Int. 2019 Nov;132:105064. doi: 10.1016/j.envint.2019.105064. Epub 2019 Aug 13.

Inflammation and acute traffic-related air pollution exposures among a cohort of youth with type 1 diabetes.

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Maryland Institute for Applied Environmental Health, University of Maryland School of Public Health, College Park, MD, USA. Electronic address:
Division of Epidemiology, Department of Public Health Sciences, Pennsylvania State University College of Medicine, Hershey, PA, USA.
Department of Epidemiology, TH Chan Harvard School of Public Health, Boston, MA, USA.
Maryland Institute for Applied Environmental Health, University of Maryland School of Public Health, College Park, MD, USA.
Department of Public Health, Brody School of Medicine, East Carolina University, Greenville, NC 27834, USA.
Department of Epidemiology, Colorado School of Public Health, University of Colorado-Denver Anschutz Medical Center, Denver, CO, USA.
Division of Pediatric Endocrinology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Department of Biostatistical Sciences, Wake Forest University School of Medicine, Winston-Salem, NC, United States.
Division of Metabolism, Endocrinology and Nutrition, Northwest Lipid Metabolism and Diabetes Research Laboratories, Seattle, WA, USA.
Department of Pediatrics, University of Washington, Seattle, USA.
Department of Research & Evaluation, Kaiser Permanente Southern California, Pasadena, CA, USA.
Heart Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC, USA.



Evidence remains equivocal regarding the association of inflammation, a precursor to cardiovascular disease, and acute exposures to ambient air pollution from traffic-related particulate matter. Though youth with type 1 diabetes are at higher risk for cardiovascular disease, the relationship of inflammation and ambient air pollution exposures in this population has received little attention.


Using five geographically diverse US sites from the racially- and ethnically-diverse SEARCH for Diabetes in Youth Cohort, we examined the relationship of acute exposures to PM2.5 mass, Atmospheric Dispersion Modeling System (ADMS)-Roads traffic-related PM concentrations near roadways, and elemental carbon (EC) with biomarkers of inflammation including interleukin-6 (IL-6), c-reactive protein (hs-CRP) and fibrinogen.


Baseline questionnaires and blood were obtained at a study visit. Using a spatio-temporal modeling approach, pollutant exposures for 7 days prior to blood draw were assigned to residential addresses. Linear mixed models for each outcome and exposure were adjusted for demographic and lifestyle factors identified a priori.


Among the 2566 participants with complete data, fully-adjusted models showed positive associations of EC average week exposures with IL-6 and hs-CRP, and PM2.5 mass exposures on lag day 3 with IL-6 levels. Comparing the 25th and 75th percentiles of average week EC exposures resulted in 8.3% higher IL-6 (95%CI: 2.7%,14.3%) and 9.8% higher hs-CRP (95%CI: 2.4%,17.7%). We observed some evidence of effect modification for the relationships of PM2.5 mass exposures with hs-CRP by gender and with IL-6 by race/ethnicity.


Indicators of inflammation were associated with estimated traffic-related air pollutant exposures in this study population of youth with type 1 diabetes. Thus youth with type 1 diabetes may be at increased risk of air pollution-related inflammation. These findings and the racial/ethnic and gender differences observed deserve further exploration.


Diabetes; Inflammation; Traffic-related air pollution

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