中文摘要：

目的 评价瓷厂和钨矿生产性粉尘对血管内皮细胞的直接损伤作用,探讨粉尘引发心血管疾病的机制.方法 以人脐静脉内皮细胞（HUVEC）株HUV-EC-C为作用细胞,以瓷厂、钨矿作业点收集的生产性粉尘为实验粉尘,以中国标准石英为对照,将粉尘配制成25、50、100、200、400μg/ml浓度与HUVEC共培养24 h,测定细胞乳酸脱氢酶（LDH）活力、细胞的活力噻唑蓝（MTT）、一氧化氮（NO）和肿瘤坏死因子-α（TNF-α）的释放量.结果 瓷厂和钨矿作业点的生产性粉尘均能使HUVEC细胞培养液中LDH活力升高,释放NO及TNF-α水平升高,并随粉尘浓度升高呈现明确的剂量-反应关系.瓷厂和钨矿作业点生产性粉尘均能导致HUVEC细胞活力下降,呈剂量-反应关系.石英粉尘诱导HUVEC培养液中LDH活力升高的能力明显高于瓷厂和钨矿的生产性粉尘,差异有统计学意义（P＜0.05）.瓷厂和钨矿生产性粉尘诱导HUVEC细胞活力下降及释放NO的能力相近且与标准石英相当.在较低剂量组（25、50、100μg/ml）时,瓷厂和钨矿生产性粉尘诱导TNF-α的释放量与标准石英相当,差异无统计学意义（P＞0.05）,而在较高剂量组（200、400 μg/ml）时,标准石英诱导TNF-α的释放量明显高于瓷厂和钨矿生产性粉尘,差异有统计学意义（P＜0.05）.结论 不同来源的生产性粉尘及标准石英均能损伤血管内皮细胞,诱导TNF-α释放,引起不同程度的生物学效应.

英文摘要：

Objective To assess direct adverse effects of occupational dusts from pottery factories and tungsten mines on vascular endothelial cells in vitro test. Methods Human umbilical vein endothelial cell （HUVEC） line HUV-EC-C were used as target cells. HUVEC were then treated with respirable dust particles from workplaces in pottery factories and tungsten mines in concentrations of 25,50,100,200 and 400μg/ml for 24 h. Standard quartz was used as control. LDH activity, cell viability, the release of NO and TNF-α levels were determined to assess the biological responses of the dust particles. Results Dose-response relationships between the dust concentrations and the enhancement of the LDH activity, the release of NO and TNF-α were found in both dust particles from pottery factories and tungsten mines. The cell viability decreased with the increase of dust concentration from 25 to 400 μg/ml. Compared with the dust particles from workplaces, the quartz dust induced significantly higher LDH activity （P〈0.05） after cultured with HUVEC. No significant difference of releases of NO were observed among the dust particles from workplaces and standard quartz. However, significantly higher levels of TNF-α were induced by standard quartz compared with dust samples from workplaces at concentrations of 200, 400μg/ml. Conclusion Occupational dust particles from workplaces and quartz could induce the injury and the releases of TNF-α from HUVEC.