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吸入原油蒸气的生物学效应。III. 肺部炎症、细胞毒性和基因表达谱。

Biological effects of inhaled crude oil vapor. III. Pulmonary inflammation, cytotoxicity, and gene expression profile.

机构信息

Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV, USA.

出版信息

Inhal Toxicol. 2023 Jan-Dec;35(9-10):241-253. doi: 10.1080/08958378.2023.2224394. Epub 2023 Jun 18.

Abstract

OBJECTIVE

Workers may be exposed to vapors emitted from crude oil in upstream operations in the oil and gas industry. Although the toxicity of crude oil constituents has been studied, there are very few investigations designed to mimic crude oil vapor (COV) exposures that occur in these operations. The goal of the current investigation was to examine lung injury, inflammation, oxidant generation, and effects on the lung global gene expression profile following a whole-body acute or sub-chronic inhalation exposure to COV.

MATERIALS AND METHODS

To conduct this investigation, rats were subjected to either a whole-body acute (6 hr) or a sub-chronic (28 d) inhalation exposure (6 hr/d × 4 d/wk × 4 wk) to COV (300 ppm; Macondo well surrogate oil). Control rats were exposed to filtered air. One and 28 d after acute exposure, and 1, 28, and 90 d following sub-chronic exposure, bronchoalveolar lavage was performed on the left lung to collect cells and fluid for analyses, the apical right lobe was preserved for histopathology, and the right cardiac and diaphragmatic lobes were processed for gene expression analyses.

RESULTS

No exposure-related changes were identified in histopathology, cytotoxicity, or lavage cell profiles. Changes in lavage fluid cytokines indicative of inflammation, immune function, and endothelial function after sub-chronic exposure were limited and varied over time. Minimal gene expression changes were detected only at the 28 d post-exposure time interval in both the exposure groups.

CONCLUSION

Taken together, the results from this exposure paradigm, including concentration, duration, and exposure chamber parameters, did not indicate significant and toxicologically relevant changes in markers of injury, oxidant generation, inflammation, and gene expression profile in the lung.

摘要

目的

在石油和天然气行业的上游作业中,工人可能会接触到原油散发的蒸气。尽管已经研究了原油成分的毒性,但很少有研究旨在模拟这些作业中发生的原油蒸气(COV)暴露。目前研究的目的是检查全身急性或亚慢性吸入 COV 暴露后肺损伤、炎症、氧化剂生成和对肺全局基因表达谱的影响。

材料和方法

为了进行这项研究,大鼠接受了全身急性(6 小时)或亚慢性(28 天)吸入暴露(6 小时/天×4 天/周×4 周)到 COV(300ppm;Macondo 井替代油)。对照大鼠暴露于过滤空气中。急性暴露后 1 天和 28 天,以及亚慢性暴露后 1、28 和 90 天,对左肺进行支气管肺泡灌洗以收集细胞和液体进行分析,保留右肺尖叶进行组织病理学检查,以及右心和膈叶进行基因表达分析。

结果

在组织病理学、细胞毒性或灌洗细胞谱中没有发现与暴露相关的变化。亚慢性暴露后表明炎症、免疫功能和内皮功能的灌洗液细胞因子变化有限且随时间变化。仅在暴露组的 28 天暴露后时间间隔检测到最小的基因表达变化。

结论

综上所述,包括浓度、持续时间和暴露室参数在内的这种暴露模式的结果并未表明在肺损伤、氧化剂生成、炎症和基因表达谱的标志物中存在显著的、具有毒理学相关性的变化。

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