Seasonal variation in chemical composition of size-segregated urban air particles and the inflammatory activity in the mouse lung
Seasonal variation in chemical composition of size-segregated urban air particles and the inflammatory activity in the mouse lung
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DOI：
10.3109/08958370902862426
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发表时间：
2010-01-01
影响因子：
2.1
通讯作者：
Salonen, R. O.
中科院分区：
文献类型：
--
作者：
Happo, M. S.;Hirvonen, M. -R.;Salonen, R. O.
我们研究了四种尺寸范围（PM10-2.5、PM2.5-1、PM1-0.2和PM0.2）的城市空气颗粒样本的化学成分和体内炎症活性的季节变化。样本是在赫尔辛基使用大容量级联冲击器（HVCI）收集的。健康C57BL/6J小鼠气管内灌注单剂量（10 mg/kg）颗粒样品。肺灌洗，测定支气管肺泡灌洗液（BALF）炎症和组织损伤指标：细胞因子（肿瘤坏死因子[TNF]- α、白细胞介素[IL]-6和角化细胞衍生趋化因子[KC]）在4小时，总细胞数和总蛋白浓度在12小时。PM10-2.5和PM2.5-1样品的炎症效力远高于PM1-0.2和PM0.2样品。在等质量基础上，秋季样品的相对炎症活性最高，但当估计每立方米空气的颗粒质量时，春季样品具有最高的炎症潜力。来自交通的重悬浮土壤物质和其他非废气颗粒物质与PM10-2.5和PM2.5-1样品的高炎症活性有关。PM1-0.2和PM0.2样品中的次级无机离子与炎症活性呈不一致的负相关或正相关。PM1-0.2和PM0.2样品中不完全燃烧示踪剂和大气氧化有机物没有系统的季节变化，这可能解释了它们与炎症活性的低相关性。综上所述，在一个相对清洁的北欧城市，来自交通的道路粉尘和其他非排气颗粒物质的再悬浮是城市空气可吸入颗粒炎症活性的主要来源。
We investigated the seasonal variations in the chemical composition and in vivo inflammatory activity of urban air particulate samples in four size ranges (PM10-2.5, PM2.5-1, PM1-0.2, and PM0.2). The samples were collected in Helsinki using a high-volume cascade impactor (HVCI). Healthy C57BL/6J mice were intratracheally instilled with a single dose (10 mg/kg) of the particulate samples. The lungs were lavaged and the bronchoalveolar lavage fluid (BALF) was assayed for indicators of inflammation and tissue damage: cytokines (tumor necrosis factor [TNF]-alpha, interleukin [IL]-6, and keratinocyte-derived chemokine [KC]) at 4 h, and total cell number and total protein concentration at 12 h. The PM10-2.5 and PM2.5-1 samples had much higher inflammatory potency than the PM1-0.2 and PM0.2 samples. The relative inflammatory activities of the autumn samples were the highest on an equal mass basis, but when estimated for the particulate mass per cubic meter of air, the springtime samples had the highest inflammatory potential. Resuspended soil material and other non-exhaust particulate material from traffic were associated with a high inflammatory activity of the PM10-2.5 and PM2.5-1 samples. Secondary inorganic ions in the PM1-0.2 and PM0.2 samples had inconsistent negative or positive correlations with the inflammatory activity. There were no systematic seasonal variations in the tracers of incomplete combustion and atmospherically oxidized organics in the PM1-0.2 and PM0.2 samples, which probably explains their low correlations with the inflammatory activity. In conclusion, in a relatively clean Nordic city, the resuspension of road dust and other non-exhaust particulate material from traffic were the major sources of inflammatory activity of urban air inhalable particles.