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首页> 外文期刊>Occupational and environmental medicine >Increased alveolar nitric oxide and systemic inflammation markers in silica-exposed workers
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Increased alveolar nitric oxide and systemic inflammation markers in silica-exposed workers

机译：接触二氧化硅的工人的肺泡一氧化氮和全身炎症指标增加

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Background: Exposure to silica dust may cause inflammatory responses, primarily in the lungs, although systemic effects have also been reported. Alveolar inflammation can be demonstrated by increased alveolar concentration of nitric oxide (NO), but information on the effects of silica dust on exhaled NO is sparse. Inflammatory mediators including cytokines are known to take part in silica-induced processes, but the role of adipokines has not been studied previously. Objectives: The aim of the study was to investigate the pulmonary and systemic inflammatory responses to occupational exposure to silica dust. Methods: The authors examined 94 silica-exposed workers and 35 healthy volunteers. The authors also measured alveolar NO concentration, bronchial NO flux and the plasma levels of proinflammatory cytokines, interleukin (IL)-6 and IL-8, and the adipokines, adipsin, leptin, adiponectin and resistin. Results: After adjusting for age, body mass index and pack-years of tobacco smoking, silica exposure was associated with significantly higher levels of alveolar NO (p=0.001), indicating inflammatory effects of silica in the peripheral lung. In addition, increased plasma concentrations of IL-6, adiponectin, adipsin and resistin were significantly associated with silica exposure (p=0.002, p=0.034, p<0.001 and p=0.048, respectively). Conclusions: In conclusion, measurement of alveolar NO concentration and plasma cytokine and adipokine levels seems to offer a modern means to demonstrate the inflammatory effects of exposure to silica. These measures might be useful in finding subjects with a significant immune response to silica particles and thus at higher risk of developing silicosis or other immunological diseases associated with exposure to silica, but further research is needed.
机译：背景：接触二氧化硅尘土可能会引起炎症反应，主要是在肺部，尽管也有全身作用的报道。一氧化氮（NO）的肺泡浓度升高可证明肺泡发炎，但有关二氧化硅粉尘对呼出NO的影响的信息很少。已知包括细胞因子在内的炎性介质参与了二氧化硅诱导的过程，但是脂肪因子的作用尚未得到研究。目的：该研究的目的是研究职业性接触硅尘对肺和全身的炎症反应。方法：作者检查了94名接触二氧化硅的工人和35名健康志愿者。作者还测量了肺泡NO浓度，支气管NO通量以及促炎细胞因子，白介素（IL）-6和IL-8以及脂肪因子，脂肪酶，瘦素，脂联素和抵抗素的血浆水平。结果：在调整了年龄，体重指数和吸烟年限后，暴露于二氧化硅与肺泡NO水平显着升高（p = 0.001），表明二氧化硅在周围肺部具有炎症作用。此外，血浆IL-6，脂联素，脂肪酶和抵抗素的浓度升高与二氧化硅暴露显着相关（分别为p = 0.002，p = 0.034，p <0.001和p = 0.048）。结论：总之，测量肺泡一氧化氮浓度以及血浆细胞因子和脂肪因子水平似乎提供了一种现代手段来证明暴露于二氧化硅的炎症作用。这些措施可能有助于发现对二氧化硅颗粒具有显着免疫反应的受试者，因此患矽肺病或与暴露于二氧化硅有关的其他免疫性疾病的风险较高，但仍需要进一步的研究。

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