Comparisons of Ultrafine and Fine Particles in Their Associations with Biomarkers Reflecting Physiological Pathways

[Image: see text] Using a quasi-experimental opportunity offered by greatly restricted air pollution emissions during the Beijing Olympics compared to before and after the Olympics, we conducted the current study to compare ultrafine particles (UFPs) and fine particles (PM(2.5)) in their associations with biomarkers reflecting multiple pathophysiological pathways linking exposure and cardiorespiratory events. Number concentrations of particles (13.0–764.7 nm) and mass concentrations of PM(2.5) were measured at two locations within 9 km from the residence and workplace of 125 participating Beijing residents. Each participant was measured 6 times for biomarkers of autonomic function (heart rate, systolic and diastolic blood pressures), hemostasis (von Willebrand factor, soluble CD40 ligand, and P-selectin), pulmonary inflammation and oxidative stress (exhaled nitric oxide and exhaled breath condensate pH, malondialdehyde, and nitrite), and systemic inflammation and oxidative stress (urinary malondialdehyde and 8-hydroxy-2′-deoxyguanosine, plasma fibrinogen, and white blood cells). Linear mixed models were used to estimate associations of biomarkers with UFPs and PM(2.5) measured 1–7 days prior to biomarker measurements (lags). We found that the correlation coefficient for UFPs at two locations (∼9 km apart) was 0.45, and at the same location, the correlation coefficient for PM(2.5) vs UFPs was −0.18. Changes in biomarker levels associated with increases in UFPs and PM(2.5) were comparable in magnitude. However, associations of certain biomarkers with UFPs had different lag patterns compared to those with PM(2.5), suggesting that the ultrafine size fraction (≤100 nm) and the fine size fraction (∼100 nm to 2.5 μm) of PM(2.5) are likely to affect PM-induced pathophysiological pathways independently.