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2627888 
Journal Article 
Abstract 
Changes in pulmonary markers of inflammation and oxidative stress during drastic changes in air pollution during the Beijing Olympic Games 
Kipen, HM; Gong, J; Rich, D; Tong, J; Lu, S; Ohman-Strickland, P; Diehl, S; Huang, W; Wang, Y; Shuo, X; Wang, G; Zhu, T; Zhang, J 
2010 
Yes 
American Journal of Respiratory and Critical Care Medicine
ISSN: 1073-449X
EISSN: 1535-4970 
181 
A1160 
English 
is part of a larger document 3452678 Proceedings of the American Thoracic Society 2010 International Conference, May 14-19, 2010, New Orleans
Rationale: Epidemiologic and experimental studies document that short-term changes in air pollution levels, particularly fine particulate matter (PM2.5), are associated with cardiopulmonary morbidity and mortality. However, the precise mechanisms that underlie these associations are not well-understood, and further exploration of effects of pollution on hypothesized pathogenic pathways is needed. We designed a panel study to examine changes in multiple biomarkers in response to the drastic reductions in Beijing air pollution during the 2008 Olympic period.

Methods: This abstract reports on changes in exhaled breath condensate (EBC) markers of inflammation and oxidative stress among a panel of 128 healthy Chinese medical residents, sampled serially before the Olympics during high pollution, during the lower pollution Olympic period (40%-50% reductions in PM2.5 and NO2 below pre-Olympic levels), and following the Olympics when pollution controls were relaxed. Measurements of ambient PM2.5, NO2, O3, SO2, and CO as well as temperature and relative humidity were assessed hourly and expressed as 24 hour means. EBC samples were collected offline and analyzed for eNO using HPLC-UV. Exhaled Breath condensate (EBC) samples were collected with an EcoScreen II EBC Collector, helium degassed, analyzed for pH, and then stored until analysis for nitrite and nitrate using an HPLC-UV technique. Dose-response analysis of the association between each biomarker and various pollutant species was assessed with random effects regression models and expressed as a percentage change per interquartile range (IQR) change of each pollutant controlling for temperature, relative humidity, gender and day of week.

Results: We observed a significant 7.9% decrease in pH for each IQR increase in PM2.5 (62.6 ug/m^3) 24-47 hours before sampling, and a significant 28% increase in eNO associated with the same IQR increase in the 24 hours before sampling. We also observed significant 8-18% increases in EBC nitrite associated with the 72-95 hours before and 96-119 hours before sampling, while nitrate showed similar significant 9-27% increases for several 24 hour periods 72-168 hours before sampling.

Conclusions: Our data show substantial changes in exhaled breath levels of various molecules thought to reflect the level of inflammation and oxidative/nitrosative stress in the airway as well as systemically. This supports the mechanistic hypothesis that induction of oxidative/nitrosative stress by various constituents of ambient air pollution is responsible for initiation of the adverse health effects documented to result from ambient air pollution. The study was sponsored by HEI 4760-RPFA05-3; NIEHS/NIH 1 R01 ES015864 and P30 ES05022. 
American Thoracic Society 2010 International Conference 
New Orleans, LA 
May 14-19, 2010