Pozzi Roberta, De Berardis Barbara, Paoletti Luigi, Guastadisegni Cecilia
Laboratory of Environmental Hygiene, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy.
Toxicology. 2003 Feb 1;183(1-3):243-54. doi: 10.1016/s0300-483x(02)00545-0.
Increased incidence of mortality and morbidity due to cardiopulmonary complications has been found to associate with elevated levels of urban air particles with an aerodynamic diameter <10 micron, PM10 and <2.5 micron, PM2.5. Respirable particles reach the lower respiratory tract where they are phagocytized by alveolar macrophages. Depending on particle composition, exposed macrophages may produce inflammatory mediators. A cascade impactor sampler was used to collect size-fractionated urban air particles. Particulate matter from the city of Rome (Italy) were collected onto stainless steel plates, and recovered using alcohol. The murine monocytic/macrophagic RAW 264.7 cell line was used to compare the ability of PM2.5-10, PM2.5 and carbon black to cause cell injury, such as arachidonic acid (AA) release, tumour necrosis factor alpha (TNF alpha) and interleukin (IL)-6 production. All test particles have been used at the same concentrations 30 and 120 microg/ml. Treatment with PM2.5-10 and PM2.5 induced significant AA release after 5 h of exposure at both concentrations, while carbon black was effective only at the higher concentration. After 5 h of incubation, PM2.5-10 and PM2.5 at 120 microg/ml induced 10 times the amount of TNF alpha than carbon black particles. The urban air particles-stimulated TNF alpha production decreased after 24 h of incubation while carbon black-stimulated TNF alpha was not. IL-6 production was induced by PM2.5 and by PM2.5-10 but not by carbon black. Carbon black was consistently less effective than the urban particles, suggesting that, the contaminants adsorbed on the particles are responsible for the release of inflammatory mediators.
人们发现，由于心肺并发症导致的死亡率和发病率增加与空气动力学直径小于10微米的城市空气颗粒物（PM10）以及小于2.5微米的城市空气颗粒物（PM2.5）水平升高有关。可吸入颗粒物会到达下呼吸道，在那里被肺泡巨噬细胞吞噬。根据颗粒物的成分，暴露的巨噬细胞可能会产生炎症介质。使用串联冲击式采样器收集按粒径分级的城市空气颗粒物。将来自意大利罗马市的颗粒物收集到不锈钢板上，并用酒精回收。使用鼠单核细胞/巨噬细胞RAW 264.7细胞系比较PM2.5 - 10、PM2.5和炭黑导致细胞损伤的能力，如花生四烯酸（AA）释放、肿瘤坏死因子α（TNFα）和白细胞介素（IL）-6的产生。所有测试颗粒物均以30和120微克/毫升的相同浓度使用。在两种浓度下暴露5小时后，用PM2.5 - 10和PM2.5处理均诱导出显著的AA释放，而炭黑仅在较高浓度下有效。孵育5小时后，120微克/毫升的PM2.5 - 10和PM2.5诱导产生的TNFα量是炭黑颗粒的10倍。孵育24小时后，城市空气颗粒物刺激产生的TNFα量减少，而炭黑刺激产生的TNFα量则没有减少。IL - 6的产生由PM2.5和PM2.5 - 10诱导，但不由炭黑诱导。炭黑的效果始终低于城市颗粒物，这表明吸附在颗粒物上的污染物是炎症介质释放的原因。
