Air Pollution Reduction during the Beijing Olympics: Impact on Respiratory and Cardiovascular Diseases

Abstract:

Numerous epidemiologic studies document that daily or hourly 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 pollution effects on hypothesized pathogenic pathways is indicated. We present a panel study that examines changes in multiple biomarkers of cardiovascular and respiratory health in response to the drastic reductions in air pollution during the 2008 Olympics. The study is being carried out in 131 healthy medical students living on a University campus in Beijing. Each of the study participants is repeatedly measured two times before, during, and after the Beijing Olympics for a large suite of biomarkers reflecting lung and systemic inflammation, vascular endothelial dysfunction, blood coagulation, autonomic dysfunction, and oxidative stress. Air pollution measurements of daily concentrations made on the campus showed a 41% reduction in PM2.5 from pre-Olympic level of 97 µg/m3, a 49% reduction in NO2 from pre-Olympic level of 28 ppb, 53% reduction in CO from pre-Olympic level of 1.32 ppb, and a 18% reduction in SO2 from pre-Olympic level of 9.7 ppb. At the time this abstract is written, we only have preliminary data available on two biomarkers measured before and during the Olympics. One biomarker is nitrite ion in exhaled breath condensate, a novel biomarker of pulmonary oxidative stress. The other biomarker is nitric oxide in exhaled breath (FENO), a biomarker of pulmonary inflammation. In the pre-Olympic period, breath condensate nitrite averaged 8.52 ± 5.39 µM and decreased to 5.41 ± 3.05 µM after approximately 2 weeks of the Olympic pollution reductions. FENO decreased from 13.1 ± 6.4 ppb to 5.0 ± 5.2 ppb during the same period. These preliminary data support the hypothesis that induction of pulmonary inflammation via oxidative stress is a prominent mechanism to explain the effects of air pollution. Pending data will examine other prominent hypothesized mechanisms of PM cardiopulmonary health effects. These findings also have important public health implications. Cleaner air during the Beijing Olympics is directly translated into reduced body burden of oxidative stress and inflammation even in young healthy adults. Pending data are expected to show similar improvements in other respiratory and cardiovascular endpoints during the Olympic period, providing objective and molecular biology evidence for the improvement of public health resulting from air pollution interventions.