Sofie De Prins1, Evi Dons2, Martine Van Poppel3, Luc Int Panis4, Els Van de Mieroop5, Vera Nelen6, Bianca Cox7, Tim S Nawrot8, Caroline Teughels9, Greet Schoeters10, Gudrun Koppen11. 1. Environmental Risk and Health Unit, VITO (Flemish Institute for Technological Research), Boeretang 200, B-2400 Mol, Belgium; Faculty of Pharmaceutical, Biomedical and Veterinary Sciences, University of Antwerp, Universiteitsplein 1, B-2610 Antwerp, Belgium. Electronic address: sofie.deprins@vito.be. 2. Environmental Risk and Health Unit, VITO (Flemish Institute for Technological Research), Boeretang 200, B-2400 Mol, Belgium. Electronic address: evi.dons@vito.be. 3. Environmental Risk and Health Unit, VITO (Flemish Institute for Technological Research), Boeretang 200, B-2400 Mol, Belgium. Electronic address: martine.vanpoppel@vito.be. 4. Environmental Risk and Health Unit, VITO (Flemish Institute for Technological Research), Boeretang 200, B-2400 Mol, Belgium; Transportation Research Institute (IMOB), Hasselt University, Wetenschapspark 5 Bus 6, B-3590 Diepenbeek, Belgium. Electronic address: luc.intpanis@vito.be. 5. Environment and Health Unit, Provincial Institute of Hygiene, Kronenburgstraat 45, B-2000 Antwerp, Belgium. Electronic address: els.vandemieroop@pih.provant.be. 6. Environment and Health Unit, Provincial Institute of Hygiene, Kronenburgstraat 45, B-2000 Antwerp, Belgium. Electronic address: vera.nelen@pih.provant.be. 7. Centre for Environmental Sciences, Hasselt University, Agoralaan Gebouw D, B-3590 Diepenbeek, Belgium. Electronic address: bianca.cox@uhasselt.be. 8. Centre for Environmental Sciences, Hasselt University, Agoralaan Gebouw D, B-3590 Diepenbeek, Belgium. Electronic address: tim.nawrot@uhasselt.be. 9. Environment & Health, Flemish Government, Department of Environment, Nature and Energy, Koning Albert II-laan 20 Bus 8, B-1000 Brussels, Belgium. Electronic address: caroline.teughels@lne.vlaanderen.be. 10. Environmental Risk and Health Unit, VITO (Flemish Institute for Technological Research), Boeretang 200, B-2400 Mol, Belgium; Faculty of Pharmaceutical, Biomedical and Veterinary Sciences, University of Antwerp, Universiteitsplein 1, B-2610 Antwerp, Belgium. Electronic address: greet.schoeters@vito.be. 11. Environmental Risk and Health Unit, VITO (Flemish Institute for Technological Research), Boeretang 200, B-2400 Mol, Belgium. Electronic address: gudrun.koppen@vito.be.
Abstract
BACKGROUND: The current study aimed at assessing the associations between black carbon (BC) exposure and markers for airway inflammation and oxidative stress in primary school children in a Western European urban area. METHODS: In 130 children aged 6-12 years old, the fraction of exhaled nitric oxide (FeNO), exhaled breath condensate (EBC) pH, 8-isoprostane and interleukin (IL)-1β were measured in two seasons. BC concentrations on the sampling day (2-h average, 8:00-10:00 AM) and on the day before (24-h average) were assessed using measurements at a central monitoring site. Land use regression (LUR) models were applied to estimate weekly average BC exposure integrated for the time spent at home and at school, and seasonal average BC exposure at the home address. Associations between exposure and biomarkers were tested using linear mixed effect regression models. Next to single exposure models, models combining different BC exposure metrics were used. RESULTS: In single exposure models, an interquartile range (IQR) increase in 2-h BC (3.10 μg/m(3)) was linked with a 5.9% (95% CI: 0.1 to 12.0%) increase in 8-isoprostane. FeNO increased by 16.7% (95% CI: 2.2 to 33.2%) per IQR increase in 24-h average BC (4.50 μg/m(3)) and by 12.1% (95% CI: 2.5 to 22.8%) per IQR increase in weekly BC (1.73 μg/m(3)). IL-1β was associated with weekly and seasonal (IQR=1.70 μg/m(3)) BC with respective changes of 38.4% (95% CI: 9.0 to 75.4%) and 61.8% (95% CI: 3.5 to 153.9%) per IQR increase in BC. An IQR increase in weekly BC was linked with a lowering in EBC pH of 0.05 (95% CI: -0.10 to -0.01). All associations were observed independent of sex, age, allergy status, parental education level and meteorological conditions on the sampling day. Most of the associations remained when different BC exposure metrics were combined in multiple exposure models, after additional correction for sampling period or after exclusion of children with airway allergies. In additional analyses, FeNO was linked with 24-h PM10 levels, but the effect size was smaller than for BC. 8-Isoprostane was not linked with either 2-h or 24-h concentrations of PM2.5 or PM10. CONCLUSION: BC exposure on the morning of sampling was associated with airway oxidative stress while 24-h and weekly exposures were linked with airway inflammation.
BACKGROUND: The current study aimed at assessing the associations between black carbon (BC) exposure and markers for airway inflammation and oxidative stress in primary school children in a Western European urban area. METHODS: In 130 children aged 6-12 years old, the fraction of exhaled nitric oxide (FeNO), exhaled breath condensate (EBC) pH, 8-isoprostane and interleukin (IL)-1β were measured in two seasons. BC concentrations on the sampling day (2-h average, 8:00-10:00 AM) and on the day before (24-h average) were assessed using measurements at a central monitoring site. Land use regression (LUR) models were applied to estimate weekly average BC exposure integrated for the time spent at home and at school, and seasonal average BC exposure at the home address. Associations between exposure and biomarkers were tested using linear mixed effect regression models. Next to single exposure models, models combining different BC exposure metrics were used. RESULTS: In single exposure models, an interquartile range (IQR) increase in 2-h BC (3.10 μg/m(3)) was linked with a 5.9% (95% CI: 0.1 to 12.0%) increase in 8-isoprostane. FeNO increased by 16.7% (95% CI: 2.2 to 33.2%) per IQR increase in 24-h average BC (4.50 μg/m(3)) and by 12.1% (95% CI: 2.5 to 22.8%) per IQR increase in weekly BC (1.73 μg/m(3)). IL-1β was associated with weekly and seasonal (IQR=1.70 μg/m(3)) BC with respective changes of 38.4% (95% CI: 9.0 to 75.4%) and 61.8% (95% CI: 3.5 to 153.9%) per IQR increase in BC. An IQR increase in weekly BC was linked with a lowering in EBC pH of 0.05 (95% CI: -0.10 to -0.01). All associations were observed independent of sex, age, allergy status, parental education level and meteorological conditions on the sampling day. Most of the associations remained when different BC exposure metrics were combined in multiple exposure models, after additional correction for sampling period or after exclusion of children with airway allergies. In additional analyses, FeNO was linked with 24-h PM10 levels, but the effect size was smaller than for BC. 8-Isoprostane was not linked with either 2-h or 24-h concentrations of PM2.5 or PM10. CONCLUSION: BC exposure on the morning of sampling was associated with airway oxidative stress while 24-h and weekly exposures were linked with airway inflammation.
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