Exposure and Toxicity Assessment of Ultrafine Particles from Nearby Traffic in Urban Air in Seoul, Korea

OBJECTIVES: We investigated the particle mass size distribution and chemical properties of air pollution particulate matter (PM) in the urban area and its capacity to induce cytotoxicity in human bronchial epithelial (BEAS-2B) cells. METHODS: To characterize the mass size distributions and chemical concentrations associated with urban PM, PM samples were collected by a 10-stage Micro-Orifice Uniform Deposit Impactor close to nearby traffic in an urban area from December 2007 to December 2009. PM samples for in vitro cytotoxicity testing were collected by a mini-volume air sampler with PM(10) and PM(2.5) inlets. RESULTS: The PM size distributions were bi-modal, peaking at 0.18 to 0.32 and 1.8 to 3.2 µm. The mass concentrations of the metals in fine particles (0.1 to 1.8 µm) accounted for 45.6 to 80.4% of the mass concentrations of metals in PM10. The mass proportions of fine particles of the pollutants related to traffic emission, lead (80.4%), cadmium (69.0%), and chromium (63.8%) were higher than those of other metals. Iron was the dominant transition metal in the particles, accounting for 64.3% of the PM(10) mass in all the samples. We observed PM concentration-dependent cytotoxic effects on BEAS-2B cells. CONCLUSIONS: We found that exposure to PM(2.5) and PM(10) from a nearby traffic area induced significant increases in protein expression of inflammatory cytokines (IL-6 and IL-8). The cell death rate and release of cytokines in response to the PM(2.5) treatment were higher than those with PM(10). The combined results support the hypothesis that ultrafine particles from vehicular sources can induce inflammatory responses related to environmental respiratory injury.