Maria Jose Rosa1, Beizhan Yan2, Steven N Chillrud3, Luis M Acosta4, Adnan Divjan5, Judith S Jacobson6, Rachel L Miller7, Inge F Goldstein8, Matthew S Perzanowski9. 1. Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, 722 W 168th Street, 11th floor, New York, NY 10032, United States. Electronic address: maria.rosa@mssm.edu. 2. Lamont-Doherty Earth Observatory, Columbia University, Comer Building, Rm 203, Palisades, NY 10964, United States. Electronic address: yanbz@ldeo.columbia.edu. 3. Lamont-Doherty Earth Observatory, Columbia University, Comer Building, Rm 203, Palisades, NY 10964, United States. Electronic address: chilli@ldeo.columbia.edu. 4. Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, 722 W 168th Street, 11th floor, New York, NY 10032, United States. Electronic address: la181@columbia.edu. 5. Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, 722 W 168th Street, 11th floor, New York, NY 10032, United States. Electronic address: ad708@columbia.edu. 6. Department of Epidemiology, Mailman School of Public Health, Columbia University, 722 W 168th Street, R732, New York, NY 10032, United States. Electronic address: jsj4@columbia.edu. 7. Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, 722 W 168th Street, 11th floor, New York, NY 10032, United States; Division of Pulmonary, Allergy, Critical Care Medicine, Department of Medicine, Columbia, University College of Physicians and Surgeons, 630 W 168th Street, PHE-101, New York, NY 10032, United States. Electronic address: rlm14@columbia.edu. 8. Department of Epidemiology, Mailman School of Public Health, Columbia University, 722 W 168th Street, R732, New York, NY 10032, United States. Electronic address: ifg2@columbia.edu. 9. Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, 722 W 168th Street, 11th floor, New York, NY 10032, United States. Electronic address: mp2217@columbia.edu.
Abstract
BACKGROUND: Exposure to airborne black carbon (BC) has been associated with asthma development, respiratory symptoms and decrements in lung function. However, the mechanism through which BC may lead to respiratory symptoms has not been completely elucidated. Oxidative stress has been suggested as a potential mechanism through which BC might lead to adverse health outcomes. Exhaled breath condensate (EBC) allows for the non-invasive collection of airway lining fluid containing biomarkers of oxidative stress like 8-isoprostane, a stable by-product of lipid peroxidation. Therefore, we sought to characterize the association between domestic airborne BC concentrations and 8-isoprostane in EBC. MATERIALS AND METHODS: Seven- and eight-year-old children participated in an asthma case-control study in New York City. During home visits, air samples and EBC were collected. Seven day averages of domestic levels of particulate matter <2.5μm (PM2.5), BC and environmental tobacco smoke (ETS) were measured. Urea and 8-isoprostane were measured by liquid chromatography tandem mass spectrometry (LC/MS/MS) in EBC. RESULTS: In univariate models, PM2.5 and BC, but not ETS, were significantly associated with increases in 8-isoprostane in the EBC (β=0.006 and β=0.106 respectively, p<0.05 for both). These associations remained statistically significant for both PM2.5 and BC after adjustment for covariates. In a co-pollutant model including PM2.5, BC and ETS, only BC remained a statistically significant predictor of 8-isoprostane (p<0.05). CONCLUSIONS: Our findings suggest the BC fraction of PM might contain exposure relevant to increased oxidative stress in the airways.
BACKGROUND: Exposure to airborne black carbon (BC) has been associated with asthma development, respiratory symptoms and decrements in lung function. However, the mechanism through which BC may lead to respiratory symptoms has not been completely elucidated. Oxidative stress has been suggested as a potential mechanism through which BC might lead to adverse health outcomes. Exhaled breath condensate (EBC) allows for the non-invasive collection of airway lining fluid containing biomarkers of oxidative stress like 8-isoprostane, a stable by-product of lipid peroxidation. Therefore, we sought to characterize the association between domestic airborne BC concentrations and 8-isoprostane in EBC. MATERIALS AND METHODS: Seven- and eight-year-old children participated in an asthma case-control study in New York City. During home visits, air samples and EBC were collected. Seven day averages of domestic levels of particulate matter <2.5μm (PM2.5), BC and environmental tobacco smoke (ETS) were measured. Urea and 8-isoprostane were measured by liquid chromatography tandem mass spectrometry (LC/MS/MS) in EBC. RESULTS: In univariate models, PM2.5 and BC, but not ETS, were significantly associated with increases in 8-isoprostane in the EBC (β=0.006 and β=0.106 respectively, p<0.05 for both). These associations remained statistically significant for both PM2.5 and BC after adjustment for covariates. In a co-pollutant model including PM2.5, BC and ETS, only BC remained a statistically significant predictor of 8-isoprostane (p<0.05). CONCLUSIONS: Our findings suggest the BC fraction of PM might contain exposure relevant to increased oxidative stress in the airways.
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