지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2013.12
- 수록면
- 32 - 40 (9page)
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초록· 키워드
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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 ㎛. The mass concentrations of the metals in fine particles (0.1 to 1.8 ㎛) 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.
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 ㎛. The mass concentrations of the metals in fine particles (0.1 to 1.8 ㎛) 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.
목차
Introduction
Materials and Methods
Results
Discussion
References
참고문헌 (19)
참고문헌 신청
Harrison RM / 1995 / The chemical composition of airborne particles in the UK atmosphere / Sci Total Environ 168(3):195~214
Schwartz J / 1999 / Episodes of high coarse particle concentrations are not associated with increased mortality / Environ Health Perspect 107(5):339~342
Wilson WE / 1997 / Fine particles and coarse particles: concentration relationships relevant to epidemiologic studies / J Air Waste Manag Assoc 47(12):1238~1249
Oberdorster G / 1995 / Association of particulate air pollution and acute mortality: involvement of ultrafine particles / Inhal Toxicol 7(1):111~124
Seaton A / 1995 / Particulate air pollution and acute health effects / Lancet 345(8943):176~178
Schwartz J / 1999 / Episodes of high coarse particle concentrations are not associated with increased mortality / Environ Health Perspect 107(5):339~342
Wilson WE / 1997 / Fine particles and coarse particles: concentration relationships relevant to epidemiologic studies / J Air Waste Manag Assoc 47(12):1238~1249
Oberdorster G / 1995 / Association of particulate air pollution and acute mortality: involvement of ultrafine particles / Inhal Toxicol 7(1):111~124
Seaton A / 1995 / Particulate air pollution and acute health effects / Lancet 345(8943):176~178
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UCI(KEPA) : I410-ECN-0101-2015-530-001447589