Westberg Håkan, Elihn Karine, Andersson Eva, Persson Bodil, Andersson Lennart, Bryngelsson Ing-Liss, Karlsson Cathe, Sjögren Bengt
Department of Occupational and Environmental Medicine, Örebro University Hospital, 701 85, Örebro, Sweden.
Department of Applied Environmental Science, Atmospheric Science Unit, Stockholm University, 106 91, Stockholm, Sweden.
Int Arch Occup Environ Health. 2016 Jul;89(5):813-22. doi: 10.1007/s00420-016-1119-5. Epub 2016 Feb 13.
To study the relationship between exposure to airborne particles in a pulp and paper mill and markers of inflammation and coagulation in blood.
Personal sampling of inhalable dust was performed for 72 subjects working in a Swedish pulp and paper mill. Stationary measurements were used to study concentrations of total dust, respirable dust, PM10 and PM2.5, the particle surface area and the particle number concentrations. Markers of inflammation, interleukins (IL-1b, IL-6, IL-8, and IL-10), C-reactive protein (CRP), serum amyloid A (SAA), and fibrinogen and markers of coagulation factor VIII, von Willebrand, plasminogen activator inhibitor, and D-dimer were measured in plasma or serum. Sampling was performed on the last day of the work free period of 5 days, before and after the shift the first day of work and after the shifts the second and third day. In a mixed model analysis, the relationship between particulate exposures and inflammatory markers was determined. Sex, age, smoking, and BMI were included as covariates.
The average 8-h time-weighted average (TWA) air concentration levels of inhalable dust were 0.30 mg/m(3), range 0.005-3.3 mg/m(3). The proxies for average 8-h TWAs of respirable dust were 0.045 mg/m(3). Significant and consistent positive relations were found between several exposure metrics (PM 10, total and inhalable dust) and CRP, SAA and fibrinogen taken post-shift, suggesting a dose-effect relationship.
This study supports a relationship between occupational particle exposure and established inflammatory markers, which may indicate an increased risk of cardiovascular disease.
研究在一家纸浆造纸厂接触空气中颗粒物与血液中炎症和凝血标志物之间的关系。
对瑞典一家纸浆造纸厂工作的72名受试者进行可吸入粉尘的个人采样。采用定点测量来研究总粉尘、可吸入粉尘、PM10和PM2.5的浓度、颗粒表面积和颗粒数浓度。在血浆或血清中测量炎症标志物白细胞介素(IL-1β、IL-6、IL-8和IL-10)、C反应蛋白(CRP)、血清淀粉样蛋白A(SAA)、纤维蛋白原以及凝血因子VIII、血管性血友病因子、纤溶酶原激活物抑制剂和D-二聚体的标志物。采样在5天工作空闲期的最后一天、工作第一天轮班前和后以及工作第二天和第三天轮班后进行。在混合模型分析中,确定颗粒物暴露与炎症标志物之间的关系。将性别、年龄、吸烟和体重指数作为协变量纳入。
可吸入粉尘的平均8小时时间加权平均(TWA)空气浓度水平为0.30毫克/立方米,范围为0.005 - 3.3毫克/立方米。可吸入粉尘的平均8小时TWA的替代值为0.045毫克/立方米。发现几个暴露指标(PM10、总粉尘和可吸入粉尘)与轮班后采集的CRP、SAA和纤维蛋白原之间存在显著且一致的正相关关系,表明存在剂量 - 效应关系。
本研究支持职业性颗粒物暴露与既定炎症标志物之间的关系,这可能表明心血管疾病风险增加。