Exposure and Toxicity Assessment of Ultrafine Particles from Nearby Traffic in Urban Air in Seoul, Korea.
- Author:
Ji Yeon YANG
1
;
Jin Yong KIM
;
Ji Young JANG
;
Gun Woo LEE
;
Soo Hwan KIM
;
Dong Chun SHIN
;
Young Wook LIM
Author Information
1. Institute for Environmental Research, Yonsei University College of Medicine, Seoul, Korea. envlim@yuhs.ac
- Publication Type:In Vitro ; Original Article
- Keywords:
Cell toxicity;
Transition metals;
Ultrafine particles;
Vehicle source
- MeSH:
Air Pollution;
Bays;
Cadmium;
Cell Death;
Chromium;
Cytokines;
Humans;
Iron;
Korea*;
Metals;
Particulate Matter;
Seoul*
- From:Environmental Health and Toxicology
2013;28(1):e2013007-
- CountryRepublic of Korea
- Language:English
-
Abstract:
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 PM10 and PM2.5 inlets. RESULTS: The PM size distributions were bi-modal, peaking at 0.18 to 0.32 and 1.8 to 3.2 microm. The mass concentrations of the metals in fine particles (0.1 to 1.8 microm) 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 PM10 mass in all the samples. We observed PM concentration-dependent cytotoxic effects on BEAS-2B cells. CONCLUSIONS: We found that exposure to PM2.5 and PM10 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 PM2.5 treatment were higher than those with PM10. The combined results support the hypothesis that ultrafine particles from vehicular sources can induce inflammatory responses related to environmental respiratory injury.
