TY - JOUR
T1 - Inflammation and acute traffic-related air pollution exposures among a cohort of youth with type 1 diabetes
AU - Puett, Robin C.
AU - Yanosky, Jeff D.
AU - Mittleman, Murray A.
AU - Montresor-Lopez, Jessica
AU - Bell, Ronny A.
AU - Crume, Tessa L.
AU - Dabelea, Dana
AU - Dolan, Lawrence M.
AU - D'Agostino, Ralph B.
AU - Marcovina, Santica M.
AU - Pihoker, Catherine
AU - Reynolds, Kristi
AU - Urbina, Elaine
AU - Liese, Angela D.
N1 - Funding Information:
The authors wish to acknowledge the involvement of the South Carolina Clinical & Translational Research Institute, at the Medical University of South Carolina, NIH/National Center for Advancing Translational Sciences (NCATS) grant number UL1 TR000062; Seattle Children's Hospital and the University of Washington, NIH/NCATS grant number UL1 TR00423; University of Colorado Pediatric Clinical and Translational Research Center, NIH/NCATS grant Number UL1 TR000154; the Barbara Davis Center at the University of Colorado at Denver (DERC NIH grant number P30 DK57516); the University of Cincinnati, NIH/NCATS grant number UL1 TR000077; and the Children with Medical Handicaps program managed by the Ohio Department of Health. This study includes data provided by the Ohio Department of Health, which should not be considered an endorsement of this study or its conclusions.
Funding Information:
The SEARCH for Diabetes in Youth Study is indebted to the many youth and their families, and their health care providers, whose participation made this study possible. The authors also thank Linda Li, Jun Chu and James Hibbert for their contributions to the SEARCH Air Study. The SEARCH Air Pollution and Inflammation Ancillary Study is funded by the National Institutes of Health, National Institute of Environmental Health Sciences grant R01 ES019168. SEARCH for Diabetes in Youth is funded by the Centers for Disease Control and Prevention (PA numbers 00097, DP-05-069, and DP-10-001) and supported by the National Institute of Diabetes and Digestive and Kidney Diseases. Kaiser Permanente Southern California (U18DP006133, U48/CCU919219, U01 DP000246, and U18DP002714), University of Colorado Denver (U18DP006139, U48/CCU819241-3, U01 DP000247, and U18DP000247-06A1), Children's Hospital Medical Center (Cincinnati) (U18DP006134, U48/CCU519239, U01 DP000248, and 1U18DP002709), University of North Carolina at Chapel Hill (U18DP006138, U48/CCU419249, U01 DP000254, and U18DP002708), Seattle Children's Hospital (U18DP006136, U58/CCU019235-4, U01 DP000244, and U18DP002710-01), Wake Forest University School of Medicine (U18DP006131, U48/CCU919219, U01 DP000250, and 200-2010-35171). The authors wish to acknowledge the involvement of the South Carolina Clinical & Translational Research Institute, at the Medical University of South Carolina, NIH/National Center for Advancing Translational Sciences (NCATS) grant number UL1 TR000062; Seattle Children's Hospital and the University of Washington, NIH/NCATS grant number UL1 TR00423; University of Colorado Pediatric Clinical and Translational Research Center, NIH/NCATS grant Number UL1 TR000154; the Barbara Davis Center at the University of Colorado at Denver (DERC NIH grant number P30 DK57516); the University of Cincinnati, NIH/NCATS grant number UL1 TR000077; and the Children with Medical Handicaps program managed by the Ohio Department of Health. This study includes data provided by the Ohio Department of Health, which should not be considered an endorsement of this study or its conclusions. The findings and conclusions in this report are those of the authors and do not necessarily represent the official position of the Centers for Disease Control and Prevention or the National Institutes of Health, National Institute of Environmental Health Sciences or National Institute of Diabetes and Digestive and Kidney Diseases.☆ Competing financial interests: none.
Funding Information:
The SEARCH Air Pollution and Inflammation Ancillary Study is funded by the National Institutes of Health , National Institute of Environmental Health Sciences grant R01 ES019168 . SEARCH for Diabetes in Youth is funded by the Centers for Disease Control and Prevention (PA numbers 00097 , DP-05-069 , and DP-10-001 ) and supported by the National Institute of Diabetes and Digestive and Kidney Diseases .
Publisher Copyright:
© 2019 The Authors
PY - 2019/11
Y1 - 2019/11
N2 - Background: 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. Objectives: 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. Methods: 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. Results: 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. Conclusions: 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.
AB - Background: 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. Objectives: 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. Methods: 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. Results: 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. Conclusions: 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.
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U2 - 10.1016/j.envint.2019.105064
DO - 10.1016/j.envint.2019.105064
M3 - Article
C2 - 31419765
AN - SCOPUS:85070519636
SN - 0160-4120
VL - 132
JO - Environment international
JF - Environment international
M1 - 105064
ER -