Borm P J, Schins R P, Derhaag T J, Kant I, Jorna T H
Department of Health Risk Analysis, University of Limburg, Maastricht, the Netherlands.
Chest. 1996 Apr;109(4):1078-85. doi: 10.1378/chest.109.4.1078.
Grain dust is well known to cause both acute and chronic respiratory disorders, and endotoxins are considered key components in this. Since endotoxins are known to elicit proinflammatory mediators, we investigated cytokine (tumor necrosis factor [TNF], interleukin-6, interleukin-8) release and a number of proinflammatory and anti-inflammatory proteins (soluble TNF receptors, lipopolysaccharide (LPS) binding protein, bactericidal permeability increasing protein (BPI), C-reactive protein) in plasma of workers exposed to grain dust. In two surveys during 1 week, lung function was measured daily before and after the shift, using flow-volume curves and/or forced oscillation measurements. On Monday and Friday, blood samples (30 mL) were drawn and cytokine release was determined by enzyme-linked immunosorbent assay in supernatant of isolated monocytes or whole blood culture, either unstimulated or on the ex vivo stimulation with 3 ng/mL or 1,000 ng/mL endotoxin. Individual exposures were determined from stationary dust measurements at every workplace combined with personal task analysis during all shifts. In both surveys, no cross-week change in lung function parameters was observed. In the first survey (average exposure: 20.2 mg/m3), monocyte spontaneous TNF release was increased sevenfold cross week (p<0.001) and was significantly related both to individual dust exposure (r=0.62) of that week and the increase in soluble TNF receptor 75 kD (r=0.85). In the second survey, where average exposure was much lower (3.67 mg/m3), impedance parameters indicated a significant improvement of airway function, and cross-week changes in inflammatory markers were minimal. Therefore, we conclude that inflammatory events can be used to monitor adverse respiratory effects of moderate grain dust exposure.
众所周知，谷物粉尘会引发急性和慢性呼吸道疾病，内毒素被认为是其中的关键成分。由于已知内毒素会引发促炎介质，我们研究了接触谷物粉尘的工人血浆中细胞因子（肿瘤坏死因子 [TNF]、白细胞介素-6、白细胞介素-8）的释放以及一些促炎和抗炎蛋白（可溶性TNF受体、脂多糖 (LPS) 结合蛋白、杀菌通透性增加蛋白 (BPI)、C反应蛋白）。在为期1周的两次调查中，每天在轮班前和轮班后使用流量-容积曲线和/或强迫振荡测量来测量肺功能。在周一和周五采集血样（30 mL），通过酶联免疫吸附测定法测定分离的单核细胞或全血培养上清液中细胞因子的释放，培养上清液未受刺激或用3 ng/mL或1000 ng/mL内毒素进行体外刺激。根据每个工作场所的固定粉尘测量结果以及所有轮班期间的个人任务分析来确定个体接触情况。在两次调查中，均未观察到肺功能参数的跨周变化。在第一次调查中（平均接触量：20.2 mg/m³），单核细胞自发TNF释放跨周增加了7倍（p<0.001），并且与该周的个体粉尘接触量（r=0.62）和可溶性TNF受体75 kD的增加（r=0.85）均显著相关。在第二次调查中，平均接触量要低得多（3.67 mg/m³），阻抗参数表明气道功能有显著改善，炎症标志物的跨周变化最小。因此，我们得出结论，炎症事件可用于监测中度谷物粉尘接触对呼吸道的不良影响。
