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Association of exposure to metals and polycyclic aromatic hydrocarbons with expression of Receptor of Advanced Clycation End Products in welding workers

机译:金属和多环芳烃接触结合与焊接工人高级凝肝末端产物受体表达的关联

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Shipyard welders will expose to fine particulate, aerosols, dust, metal fumes, polycyclic aromatic hydrocarbons (PAHs) and other substances during the work process. Modifiable environmental factors including particulate matter and its components drive endogenous formation Advanced glycation end-products (AGEs) overwhelm innate defenses of antioxidant and activate pro-inflammatory and pro-oxidant receptors for advanced glycation end-products (RAGE) associated cardiovascular effects have not been explored. This study was in a cross-sectional design. Study subjects consisted of 53 welders and 29 office workers from a shipyard of northern Taiwan. Participants were asked to wear PM2.5 samplers during their working hours on the first weekday (Monday) and collected urine and fasting blood samples on the next day (Tuesday) morning. Monocytic receptor of advanced glycation end products expression was assessed flow cytometry. AGEs, IL-6, TNF-a were analyzed by ELISA kits. Urinary metal concentration was analyzed by ICP- MS. Statistical analysis was conducted using SPSS 22.0. It showed Log(Ni) (B=0.329, 95% CI 0.031 to 0.172, p=0.006), or Log(Fe) ( β = 0.258, 95% CI 0.044 to 0.556, p = 0.022) was positively associated with Log(AGEs) adjusting for creatinine, age, smoking status, and work group. Log(Cr) (B = 0.236, 95% CI 0.018 to 0.337, p = 0.03), Log(Ni) (B = 0.225, 95% CI 0.006 to 0.133, p=0.032), or Log(Cd) (p=0.309, 95% CI 0.006 to 0.139, p=0.028) was positively associated with the Log(RAGE), respectively. Log(RAGE) was found statistically significant with IL-6 (P = 0.294, 95% CI 0.083 to 0.732, p = 0.014). The possible mechanism is that the metal or PAHs adsorbed on the fine particles from welding fume might cause the increasing AGEs concentration, and then react with the receptor to produce the inflammatory reaction. We conclude that exposure to welding fume particles is associated with increasing AGEs levels and RAGE expression.
机译:造船厂焊工将在工作过程中暴露于细颗粒剂,气雾剂,尘,金属烟雾,多环芳香烃(PAHs)和其它物质。改变的环境因素,包括颗粒物质和它的组件驱动的内源性形成高级糖基化终产物(AGEs)的抗氧化剂的压倒先天防御并激活促炎症和促氧化剂受体晚期糖化终产物(RAGE)相关的心血管效果并没有探讨。这项研究是一个横断面设计。研究对象包括53名焊工和29名办公室工作人员从台湾北部的造船厂。在第一个工作日(周一),收集尿液并在第二天空腹血样(星期二)上午工作时间参加者被要求穿PM2.5采样器。的晚期糖化终产物的表达单核细胞受体进行了评估流式细胞术。的AGEs,IL-6,TNF-α的通过ELISA试剂盒进行分析。尿金属浓度是通过ICP-MS分析。统计分析采用SPSS 22.0进行。这表明日志(Ni)的(B = 0.329,95%CI 0.031至0.172,P = 0.006),或日志(Fe)的(β= 0.258,95%CI 0.044〜0.556,P = 0.022)呈正日志相关联( AGEs)的调整肌酐,年龄,吸烟状况和工作组。日志(Cr)的(B = 0.236,95%CI 0.018〜0.337,P = 0.03),对数(Ni)的(B = 0.225,95%CI为0.006〜0.133,P = 0.032),或日志(CD)(p值= 0.309,95%CI为0.006〜0.139,p = 0.028)呈正的日志(RAGE)相关联。日志(RAGE)被发现统计学显著与IL-6(P = 0.294,95%CI 0.083至0.732,P = 0.014)。可能的机制是,金属或多环芳烃吸附于微粒从焊接烟尘可能会导致增加的AGE浓度,然后与受体以产生炎症反应发生反应。我们的结论是暴露于焊接烟尘颗粒与终产物水平和RAGE表达增加有关。

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