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A platform for research: civil engineering, architecture and urbanism
All-source and source-specific air pollution and 10-year diabetes Incidence: Total effect and mediation analyses in the Heinz Nixdorf recall study
Highlights All-source AP exposure associated with DM incidence. Traffic-specific AP exposure shows strongest association with DM. Possible mediation through decreased adiponectin levels.
Abstract Background An increasing number of studies have been published recently on the association between ambient air pollution (AP) and incident diabetes mellitus (DM), but studies investigating source-specific AP toxicity and potential mediating pathways are rare. We investigated the associations of all-source, traffic-specific, and industry-specific outdoor AP exposure with 10-year incidence of DM and potential mediation via inflammation-associated biomarkers. Methods Data from participants of the prospective Heinz Nixdorf Recall cohort study who attended the baseline (t0; 2000–2003), 5-year follow-up (t1; 2006–2008), and 10-year follow-up (t2; 2011–2015) examinations was used. For participants without DM at baseline (determined using information on physician diagnosis and glucose-lowering medication), residential long-term exposure (total, traffic-specific, and industry-specific) to particulate matter (PM2.5, PM10), nitrogen dioxide (NO2), and accumulation mode particle number concentration (PNAM) were estimated using a chemistry transport model. Covariate-adjusted modified Poisson regression models with robust standard errors were applied to estimate relative risks (RR) for the associations between baseline AP and incident DM at t2. Mediation analyses for adiponectin, high-sensitivity C-reactive protein (hsCRP), and interleukin-1 receptor antagonist (IL-1RA) were conducted to estimate natural direct and indirect effects. Results Of the 4,814 participants at t0, 2,451 participants (mean baseline age: 58.2 years) were included in the main analysis. Interquartile range (IQR) increases in total PM10 and PNAM were associated with increased risk of DM (e.g., RR: 1.25 [95% Confidence Interval (CI): 1.02, 1.53] per 3.8 µg/m3 PM10). Whereas traffic-specific exposures were associated with DM risk for all air pollutants (e.g., RR: 1.24 [95% CI: 1.06, 1.46] per 0.3 µg/m3 PM10), significant associations for industry exposures were limited to NO2 and PNAM (e.g., RR: 1.24 [95% CI: 1.03, 1.49] per 230 particles/mL PNAM). Potential mediation of the association between AP and DM was observed for adiponectin but not for hsCRP and IL-1RA. Conclusion Our study shows that long-term exposure to total and source-specific ambient AP may increase DM risk, with consistent results observed across traffic-specific exposures. Decreases in adiponectin may play a potential role along the causal pathway.
All-source and source-specific air pollution and 10-year diabetes Incidence: Total effect and mediation analyses in the Heinz Nixdorf recall study
Highlights All-source AP exposure associated with DM incidence. Traffic-specific AP exposure shows strongest association with DM. Possible mediation through decreased adiponectin levels.
Abstract Background An increasing number of studies have been published recently on the association between ambient air pollution (AP) and incident diabetes mellitus (DM), but studies investigating source-specific AP toxicity and potential mediating pathways are rare. We investigated the associations of all-source, traffic-specific, and industry-specific outdoor AP exposure with 10-year incidence of DM and potential mediation via inflammation-associated biomarkers. Methods Data from participants of the prospective Heinz Nixdorf Recall cohort study who attended the baseline (t0; 2000–2003), 5-year follow-up (t1; 2006–2008), and 10-year follow-up (t2; 2011–2015) examinations was used. For participants without DM at baseline (determined using information on physician diagnosis and glucose-lowering medication), residential long-term exposure (total, traffic-specific, and industry-specific) to particulate matter (PM2.5, PM10), nitrogen dioxide (NO2), and accumulation mode particle number concentration (PNAM) were estimated using a chemistry transport model. Covariate-adjusted modified Poisson regression models with robust standard errors were applied to estimate relative risks (RR) for the associations between baseline AP and incident DM at t2. Mediation analyses for adiponectin, high-sensitivity C-reactive protein (hsCRP), and interleukin-1 receptor antagonist (IL-1RA) were conducted to estimate natural direct and indirect effects. Results Of the 4,814 participants at t0, 2,451 participants (mean baseline age: 58.2 years) were included in the main analysis. Interquartile range (IQR) increases in total PM10 and PNAM were associated with increased risk of DM (e.g., RR: 1.25 [95% Confidence Interval (CI): 1.02, 1.53] per 3.8 µg/m3 PM10). Whereas traffic-specific exposures were associated with DM risk for all air pollutants (e.g., RR: 1.24 [95% CI: 1.06, 1.46] per 0.3 µg/m3 PM10), significant associations for industry exposures were limited to NO2 and PNAM (e.g., RR: 1.24 [95% CI: 1.03, 1.49] per 230 particles/mL PNAM). Potential mediation of the association between AP and DM was observed for adiponectin but not for hsCRP and IL-1RA. Conclusion Our study shows that long-term exposure to total and source-specific ambient AP may increase DM risk, with consistent results observed across traffic-specific exposures. Decreases in adiponectin may play a potential role along the causal pathway.
All-source and source-specific air pollution and 10-year diabetes Incidence: Total effect and mediation analyses in the Heinz Nixdorf recall study
Lucht, Sarah (author) / Hennig, Frauke (author) / Moebus, Susanne (author) / Ohlwein, Simone (author) / Herder, Christian (author) / Kowall, Bernd (author) / Jöckel, Karl-Heinz (author) / Hoffmann, Barbara (author)
2020-01-13
Article (Journal)
Electronic Resource
English
Ambient air pollution , Incident diabetes , Mediation , Particulate matter , Inflammation , AP , air pollution , ATC , anatomical therapeutic chemical classification system , BMI , body mass index , CI , confidence interval , CV , coefficient of variation , DAG , directed acyclic graph , dB(A) , A-weighted decibels , DZD , german center for diabetes research , ETS , environmental tobacco smoke , EURAD , EURopean air pollution dispersion , HbA1c , glycated hemoglobin A1c , HNR , heinz nixdorf recall , hsCRP , high sensitivity C-reactive protein , IKK , IκB Kinase , IL-1RA , interleukin-1 receptor antagonist , IQR , Interquartile range , IUTA , institute of energy and environmental technology , JNK , c-Jun N-terminal kinase , L<inf>den</inf> , 24-hour weighted noise , NDE , natural direct effect , NIE , natural indirect effect , NO<inf>2</inf> , nitrogen dioxide , PM<inf>2.5</inf> , particulate matter with aerodynamic diameter ≤2.5 µm mass concentration , PM<inf>10</inf> , particulate matter with aerodynamic diameter ≤10 µm mass concentration , PN<inf>AM</inf> , accumulation mode particle number concentration , PY , pack-years , r , correlation coefficient , RIU , rhenish institute for environmental research , RR , relative risk , SES , socioeconomic status , t<inf>0</inf> , baseline examination , t<inf>1</inf> , 5-year follow-up examination , t<inf>2</inf> , 10-year follow-up examination , TNF-α , tumor necrosis factor alpha , UFP , ultrafine particles , WHO , world health organization