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Comperative Experiment on the Toxicity of Particulate Matter from Different Cities

Author: ZhaoXueBin
Tutor: YangLei
School: Huazhong University of Science and Technology
Course: Occupational and Environmental Health
Keywords: Haze PM2.5 Vascular endothelial cell Oxidative stress Comparative study Animal study Inflammation
CLC: R114
Type: Master's thesis
Year: 2011
Downloads: 17
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Abstract

In recent years, along with the rapid economic development the air in region of Pearl River Delta has been more and more polluted, which led to a disastrous climate phenomenon known as atmospheric haze. Currently, more attention to the reasons for the formation of such weather, but rarley to health effects. The haze weather manifests mainly in the reduction of air quality and the visibility. However, it is well known that visibility is related to the particulate matter concentration. The particulate matter （PM） is one kind of complex mixture, and its chemical composition is decided by sources with different geographical environment and industries especially. Its toxicity, especially in a comparative point of view, was sometimes reported internationally but rarely in China. Therefore, toxicity of particulate matter gathered from 4 cities Guangzhou, Dongguan, Shenzhen and Zhaoqing in the region is to be compared through experiments in vivo and in vitro, and also with the purpose to explore its possible mechanisms.PartⅠIn vitro study on toxic effects to human vascular endothelial cells by particulate matters from different Chinese citiesObjective:To observe toxic effects of particulate matter on human umbilical vein endothelial cells and to explore its mechanism.Methods:Airborne particulate matter PM_2.5 was collected in 4 cities of south China, i.e., Guangzhou, Dongguan, Shenzhen and Zhaoqing in 2009. The cells were exposed to the PM_2.5 in different dose of 10, 50, 100, 200, 300μg/ml for 24h, and then NO production, LDH release, SOD activity and viability of the cells （MTT） were measured. During analysis the toxicity was compared using the city Zhaoqing as reference, and regression slope as a unified parameter.Results:The NO production and LDH release increased, and SOD MTT decreased significantly with increase in dose （p <0.05）, which was observed in every city samples. If compared between cities, the PM of Guangzhou and Shenzhen produced more NO at higher dose than that of Zhaoqing （p <0.05）. The PM of Guangzhou, Dongguan and Shenzhen inhibited SOD more serious than the reference （p <0.05）. The Shenzhen PM resulted in more LDH release significantly than that of Zhaoqing （p <0.05）, which was found in the Guangzhou and Dongguan PM only at higher dose. The cell survival rate in the PM group Guangzhou and Shenzhen was significantly lower the reference of Zhaoqing （p <0.05）. The regression analysis showed that the Guangzhou PM had the highest toxicity in the aspect of LDH leakage and cell death, the Shenzhen particle was toxic at the highest level in producing NO and inhibiting SOD activity, and in contrast the toxicity of Zhaoqing PM was at the lowest in NO, SOD and LDH. In addition the NO and LDH were correlated with MTT negatively, and SOD with MTT positively, at a significant level （P <0.01）.Conclusion:The PM_2.5 from the city of Guangzhou, Dongguan and Shenzhen showed more severe toxicity than the reference, which seams to be related to the haze whether. The toxicity of PM from different areas was not homogeneous. The indicator of NO, SOD and LDH was correlated closely to cell death, suggesting that oxidative stress might be a mechanism of cardiovascular toxicity caused by airborne particles. Objective:With an animal experiment to compare the toxicity of particulate matter from different cities, and to explore the mechanism from point view of oxidative stress and inflammation.Methods:Airborne particulate matter PM_2.5 was collected in 4 cities of south China in 2009. Experimental animals were SD rats, dividing into 3 dosage groups, one control group, each one including 7 aninals. Particulate matters were administered to rats for one time by intratracheal instillation at the dose of 10mg/kg, 3mg/kg, and 1mg/kg respectively, and with the same volume of saline for control group. In each group there were 7 animals. The rats were sacrificed 48 hours or 28 days after the treatment. Heart, lungs, liver, kidney and spleen were taken for organ coefficient. Bronchoalveolar lavage fluid （BALF） and serum were collected as biological samples at that time periods. Parameters of TP, LDH, SOD, IL-6 and TNF-a in BALF, and TP, LDH, SOD, IL-6 and CRP in serum were determined. During analysis the PM of city Zhaoqing as reference and regression slope as a unified parameter were used to compare the toxicity.Results:The particles from Dongguan led to the grouth of rats slowing down significantly as compared to the control group and that of other regions （p<0.05）. The organ coefficient increased with increase in dose, and the lung coefficient increased significantly （p<0.05）. The particles from Guangzhou induced spleen coefficient increased significantly at high dose （p<0.05）. The level of TP, LDH, IL-6, and TNF-a increased, and SOD decreased in BALF with increase in dose. The LDH, IL-6 and CRP in serum increased with doses and significantly as compared to the control group （p<0.05）. Talking about the time effect the parameters after particle exposure for 48 hours changed more significantly than that of exposure for 28 days （p<0.05）, either observed in BALF and serium. When comparing between regions, the Guangzhou PM had the highest toxicity in producing IL-6, CRP in the serum and inhibiting SOD activity. The Dongguan PM had the highest toxicity in producing IL-6 in BALF. Shenzhen PM had the highest toxicity in producing TNF-a in BALF. And in contrast the toxicity of Zhaoqing PM was at the lowest in all aspects.Conclusion:The particle matters from the city of Guangzhou, Dongguan and Shenzhen showed more severe toxicity than the reference, which seems to be related to the haze whether. All the perameters changed significantly in the time period of 48h after exposure than that of the 28d group. In addition, oxidative stress and inflammation might be a mechanism.

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