Occupational exposure to diesel engine exhaust and serum cytokine levels.
Occupational exposure to diesel engine exhaust and serum cytokine levels.
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DOI：
10.1002/em.22142
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发表时间：
2018-03
影响因子：
2.8
通讯作者：
Zheng Y
中科院分区：
文献类型：
--
作者：
Dai Y;Ren D;Bassig BA;Vermeulen R;Hu W;Niu Y;Duan H;Ye M;Meng T;Xu J;Bin P;Shen M;Yang J;Fu W;Meliefste K;Silverman D;Rothman N;Lan Q;Zheng Y
国际癌症研究机构已将柴油发动机废气（DEE）列为人类肺癌致癌物。鉴于炎症被怀疑是肺癌发生的重要潜在机制，我们使用来自 41 名柴油发动机测试工人和 46 名未暴露对照者的横断面分子流行病学研究数据评估了 DEE 暴露与炎症反应之间的关系。在采血前，对柴油机测试人员进行了重复的 PM2.5 和其他 DEE 成分的个人暴露测量。分析所有受试者的白细胞介素（IL）-1、IL-6、IL-8、肿瘤坏死因子（TNF）-α、巨噬细胞炎症蛋白（MIP）-1β和单核细胞趋化蛋白（MCP）-1等六种炎症生物标志物的血清水平。与未暴露的对照相比，DEE 暴露工人的 MIP-1β 浓度显着降低了约 37% (P < 0.001)，并且在所有受试者 (Ptrend < 0.001) 以及仅暴露受试者 (Ptrend = 0.001) 中，随着 PM2.5 浓度的增加，MIP-1β 浓度呈现出强烈的下降趋势。与未接触 PM2.5 的对照组相比，处于 PM2.5 最高暴露三分位数（>397μg/m3）的工人的 IL-8 和 MIP-1β 水平显着降低。此外，还发现 IL-8 和 MCP-1 的显着负暴露-反应关系与 DEE 暴露工人中 PM2.5 水平的增加有关。鉴于 IL-8、MIP-1β 和 MCP-1 是趋化因子，在招募免疫活性细胞以进行免疫防御和肿瘤细胞清除方面发挥着重要作用，随着 PM2.5 暴露的增加，观察到这些标记物水平较低，这可能有助于深入了解 DEE 促进肺癌的机制。
The International Agency for Research on Cancer has classified diesel engine exhaust (DEE) as a human lung carcinogen. Given that inflammation is suspected to be an important underlying mechanism of lung carcinogenesis, we evaluated the relationship between DEE exposure and the inflammatory response using data from a cross-sectional molecular epidemiology study of 41 diesel engine testing workers and 46 unexposed controls. Repeated personal exposure measurements of PM2.5 and other DEE constituents were taken for the diesel engine testing workers before blood collection. Serum levels of six inflammatory biomarkers including interleukin (IL)-1, IL-6, IL-8, tumor necrosis factor (TNF)-α, macrophage inflammatory protein (MIP)-1β, and monocyte chemotactic protein (MCP)-1 were analyzed in all subjects. Compared to unexposed controls, concentrations of MIP-1β were significantly reduced by ~37% in DEE exposed workers (P < 0.001) and showed a strong decreasing trend with increasing PM2.5 concentrations in all subjects (Ptrend < 0.001) as well as in exposed subjects only (Ptrend = 0.001). Levels of IL-8 and MIP-1β were significantly lower in workers in the highest exposure tertile of PM2.5 (>397μg/m3) compared to unexposed controls. Further, significant inverse exposure-response relationships for IL-8 and MCP-1 were also found in relation to increasing PM2.5 levels among the DEE exposed workers. Given that IL-8, MIP-1β, and MCP-1 are chemokines that play important roles in recruitment of immunocompetent cells for immune defense and tumor cell clearance, the observed lower levels of these markers with increasing PM2.5 exposure may provide insight into the mechanism by which DEE promotes lung cancer.
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DOI：
10.1093/jnci/djs034
发表时间：
2012-06-06
期刊：
Journal of the National Cancer Institute
影响因子：
--
作者：
Silverman DT;Samanic CM;Lubin JH;Blair AE;Stewart PA;Vermeulen R;Coble JB;Rothman N;Schleiff PL;Travis WD;Ziegler RG;Wacholder S;Attfield MD
通讯作者：
Attfield MD
影响因子：
10.3
作者：
Pine, Sharon R.;Mechanic, Leah E.;Harris, Curtis C.
通讯作者：
Harris, Curtis C.
影响因子：
1.7
作者：
Amakawa, K;Terashima, T;Yamaguchi, K
通讯作者：
Yamaguchi, K
影响因子：
1.7
作者：
Saito, Y;Azuma, A;Sugawara, I
通讯作者：
Sugawara, I
影响因子：
10.4
作者：
Vermeulen R;Silverman DT;Garshick E;Vlaanderen J;Portengen L;Steenland K
通讯作者：
Steenland K