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Occupational exposure to carbon black nanoparticles increases inflammatory vascular disease risk: an implication of an ex vivo biosensor assay
Particle and Fibre Toxicology ( IF 10 ) Pub Date : 2020-09-29 , DOI: 10.1186/s12989-020-00378-8
Jinglong Tang 1 , Wenting Cheng 1 , Jinling Gao 1 , Yanting Li 1 , Ruyong Yao 2 , Nathaniel Rothman 3 , Qing Lan 3 , Matthew J Campen 4 , Yuxin Zheng 1 , Shuguang Leng 1, 5, 6
Affiliation  

Among manufactured or engineered nanoparticles, carbon black (CB) has largest production worldwide and is also an occupational respiratory hazard commonly seen in rubber industry. Few studies have assessed the risk for cardiovascular disease in carbon black exposed populations. An endothelial biosensor assay was used to quantify the capacity of sera from 82 carbon black packers (CBP) and 106 non-CBPs to induce endothelial cell activation ex vivo. The mediation effect of circulatory proinflammatory factors on the association between carbon black exposure and endothelial cell activation was assessed and further validated using in vitro intervention experiments. The average elemental carbon level inside carbon black bagging facilities was 657.0 μg/m3, which was 164-fold higher than that seen in reference areas (4.0 μg/m3). A global index was extracted from mRNA expression of seven candidate biosensor genes using principal component analysis and used to quantify the magnitude of endothelial cell activation. This global index was found to be significantly altered in CBPs compared to non-CBPs (P < 0.0001), however this difference did not vary by smoking status (P = 0.74). Individual gene analyses identified that de novo expression of key adhesion molecules (e.g., ICAM and VCAM) and chemotactic factors (e.g., CCL2, CCL5, and CXCL8) responsible for the recruitment of leukocytes was dramatically induced in CBPs with CXCL8 showing the highest fold of induction (relative quantification = 9.1, P < 0.0001). The combination of mediation analyses and in vitro functional validation confirmed TNF-α, IL-1β, and IL-6 as important circulatory factors mediating the effects of carbon black exposure on endothelial cell activation responses. Inflammatory mediators in sera from CBPs may bridge carbon black exposure and endothelial cell activation response assessed ex vivo. CBPs may have elevated risk for cardiovascular diseases when comorbidity exists. Our study may serve as a benchmark for understanding health effects of engineered carbon based nanoparticles with environmental and occupational health relevance.

中文翻译:

职业暴露于炭黑纳米颗粒会增加炎症性血管疾病的风险:离体生物传感器测定的含义

在制造或设计的纳米颗粒中,炭黑(CB)在世界范围内产量最大,并且也是橡胶工业中常见的职业性呼吸道危害。很少有研究评估暴露于炭黑人群中心血管疾病的风险。内皮生物传感器测定法用于量化来自82个炭黑封隔器(CBP)和106个非CBP的血清离体诱导内皮细胞活化的能力。使用体外干预实验评估并进一步验证了循环促炎因子对炭黑暴露与内皮细胞活化之间关系的介导作用。炭黑装袋设施内的平均元素碳水平为657.0μg/ m3,比参考区域(4.0μg/ m3)高164倍。使用主成分分析从七个候选生物传感器基因的mRNA表达中提取全局指数,并用于量化内皮细胞激活的程度。与非CBP相比,发现该CBP中的总体指数发生了显着变化(P <0.0001),但是这种差异并未因吸烟状况而变化(P = 0.74)。个别基因分析发现,在负责CBP的CBP中,诱导了主要粘附分子(例如ICAM和VCAM)和趋化因子(例如CCL2,CCL5和CXCL8)的从头表达,其中CXCL8的折叠倍数最高。诱导(相对定量= 9.1,P <0.0001)。中介分析与体外功能验证相结合,证实了TNF-α,IL-1β,IL-6和IL-6是重要的循环因子,介导炭黑暴露对内皮细胞激活反应的影响。CBP血清中的炎性介质可能桥接炭黑暴露和离体评估的内皮细胞活化反应。存在合并症时,CBP可能会增加心血管疾病的风险。我们的研究可作为了解工程碳基纳米颗粒对环境和职业健康的健康影响的基准。
更新日期:2020-09-29
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