Effects of diesel exhaust particles compositions on cytotoxicity of human coronary artery endothelial cells
Date Issued
2007
Date
2007
Author(s)
Fan, Ching-Wen
DOI
en-US
Abstract
Ambient particulate matter has been considered associated with increased cardiovascular diseases. These associations are strongest for fine particles (PM2.5), of which combustion-derived diesel exhaust particles are important components. Particle sizes, chemical compositions are generally considered responsible for their toxic responses. However, the mechanisms of these effects are not well-certified.
The purpose of this study is to investigate organic extracts of DEP (OE-DEP), supernatant OE-DEP, and pellet OE-DEP induced cytotoxicity on human coronary artery endothelial cell (HCAEC) at different particle sizes. A ten-stage micro-orifice uniform deposit impactor (MOUDITM) was used to collect DEP within a size range of 10, 5.6, 3.2, 1.8, 1.0, 0.56, 0.32, 0.18, 0.1, 0.056 µm and <0.056 µm from the platform of an intercity bus station, in Taipei, Taiwan. DEP was collected between 08:00 a.m. and 06:00 p.m. A total of 23 samples were taken between September 2006 and April 2007. Metal contents of submicron/ultrafine fraction OE-DEP were analyzed by inductively coupled plasma-mass spectrometry (ICP-MS). OE-DEP-induced endothelial dysfunctions and inflammatory effects were evaluated by nitrite oxide (NO), endothelin-1 (ET-1), and interleukin-6 (IL-6). All statistical analyses are undertaken by SAS software.
The mass concentrations of DEP exhibited a trimodal size distribution peaking at 3.2, 0.56, and <0.056 µm, respectively, in our samples. The mean concentrations with standard deviations (percentage of PM10) of coarse fraction (PM10-1), submicrometer fraction (PM1-0.1), and ultrafine fraction (PM0.1) were 29.3±9.6 (49.5%), 23.6±14.6 (39.9%), and 6.2±2.5 (10.5%) μg/m3, respectively. Zn was both the most abundant element in submicrometer and ultrafine OE-DEP. HCAEC exposed to 30μg/mL OE-DEP for 4h affected endothelial function by decreasing NO concentration in culture and suppressing ET-1 production. OE-DEP stimulated IL-6 production in submicrometer fraction but suppressed IL-6 production in ultrafine fraction. After the removal of supernatant OE-DEP, pellet OE-DEP was showed to be less cytotoxic on HCAEC. Cr, Cu, and Zn were found to induce IL-6 production. Co, Cr, and Cu were found to be associated with ET-1 secretion. Those results suggest that the chemical composition is more potent than particle size on determining endothelial dysfunctions and inflammatory effects.
Subjects
柴油排放微粒
金屬
人類冠狀動脈內皮細胞
NO
ET-1
IL-6
diesel exhaust particle
metal
human coronary artery endothelial cell
SDGs
Type
thesis
File(s)![Thumbnail Image]()
Loading...
Name
ntu-96-R94841004-1.pdf
Size
23.31 KB
Format
Adobe PDF
Checksum
(MD5):727586903c43cbb7e806f9c4881d9613