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2627889 
Journal Article 
Abstract 
Changes in biomarkers of systemic inflammation following drastic changes in air pollution during the Beijing Olympics 
Kipen, HM; Rich, D; Tong, J; Lu, S; Ohman-Strickland, P; Diehl, S; Huang, W; Gong, J; Wang, Y; Wang, G; Zhu, T; Zhang, J 
2010 
Yes 
American Journal of Respiratory and Critical Care Medicine
ISSN: 1073-449X
EISSN: 1535-4970 
181 
A1161 
English 
WOS:000208771000162 
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, further exploration of hypothesized mechanistic pathways underlying these associations is needed. We have designed a panel study to examine changes in multiple biomarkers in response to the drastic reductions in air pollution during the 2008 Beijing Olympics.

Methods: We assessed changes in biomarkers of systemic inflammation among 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), and following the Olympics when pollution controls were relaxed. Measurements of ambient PM2.5, NO2, O3, SO3, and CO as well as temperature and relative humidity were assessed hourly and expressed as 24 hour averages. Plasma fibrinogen, von Willebrand Factor (vWF), and CRP, as well as blood WBC and RBC were assessed at each time point. Analyses of the dose-response relationship between each biomarker and pollutant species were conducted using random effects regression models, controlling for temperature and relative humidity, with changes presented per interquartile range (IQR) increase in pollutant.

Results: WBC showed no significant changes associated with any pollutant. RBC decreased by 0.6% at lag 0 with an IQR increase in PM2.5 (65.9 ug/m^3), decreased by 0.7 and 1.1% at lags 1 and 2 with increased ozone (27.5 ppb), decreased by 0.5% at lag 0 with increased NO2, and increased by 0.4% at lag 1 with increased CO (0.54 ppm). Increases of 1.5% and 1.7% in fibrinogen were associated with IQR increases in CO and NO2 at lag 0, although there was a paradoxical decrease at lags 0-3 with ozone and at lag 5 with PM2.5. vWF increased by up to 4.6% and 7.3% at lags 1 though 6, with increased PM2.5 and sulfate and by up to 5.9% for lags 0 through 6 with CO. The odds of a detectable CRP increased by 31% and 27% with increased CO at lags 0 and 1.

Conclusions: Our data show substantial changes in blood levels of various biomarkers thought to reflect the level of systemic inflammation. This supports the mechanistic hypothesis that induction of systemic inflammation by various constituents of ambient air pollution is in pathways responsible for initiation of the adverse cardiopulmonary health effects from ambient air pollution. 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