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

IF 2 4区 医学 Q4 TOXICOLOGY
Inhalation Toxicology Pub Date : 2023-01-01 Epub Date: 2023-06-18 DOI:10.1080/08958378.2023.2224394
Tina M Sager, Pius Joseph, Christina M Umbright, Ann F Hubbs, Mark Barger, Michael L Kashon, Jeffrey S Fedan, Jenny R Roberts
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引用次数: 0

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 in vivo 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.

吸入原油蒸汽的生物效应。III、 肺部炎症、细胞毒性和基因表达谱。
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排放的蒸汽。尽管已经对原油成分的毒性进行了研究,但很少有旨在模拟这些操作中发生的原油蒸汽(COV)暴露的体内研究。本研究的目的是检查全身急性或亚慢性吸入暴露于新冠病毒后的肺损伤、炎症、氧化剂的产生以及对肺整体基因表达谱的影响。材料和方法:为了进行本研究,大鼠接受全身急性(6 小时)或亚慢性(28天)吸入暴露(6 小时/天 × 4天/周×4周)至COV(300 ppm;马孔多井替代油)。对照大鼠暴露于过滤空气中。急性暴露后1和28天,亚慢性暴露后1、28和90天,对左肺进行支气管肺泡灌洗,收集细胞和液体进行分析,保留右心尖叶进行组织病理学检查,并对右心叶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图谱中未发现与暴露相关的变化。亚慢性暴露后,指示炎症、免疫功能和内皮功能的灌洗液细胞因子的变化是有限的,并且随着时间的推移而变化。在两个暴露组中,仅在暴露后28天的时间间隔检测到最小的基因表达变化。结论:综合来看,这种暴露模式的结果,包括浓度、持续时间和暴露室参数,没有表明肺部损伤、氧化剂生成、炎症和基因表达谱的标志物发生显著和毒理学相关的变化。
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来源期刊
Inhalation Toxicology
Inhalation Toxicology 医学-毒理学
CiteScore
4.10
自引率
4.80%
发文量
38
审稿时长
6-12 weeks
期刊介绍: Inhalation Toxicology is a peer-reviewed publication providing a key forum for the latest accomplishments and advancements in concepts, approaches, and procedures presently being used to evaluate the health risk associated with airborne chemicals. The journal publishes original research, reviews, symposia, and workshop topics involving the respiratory system’s functions in health and disease, the pathogenesis and mechanism of injury, the extrapolation of animal data to humans, the effects of inhaled substances on extra-pulmonary systems, as well as reliable and innovative models for predicting human disease.
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