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吸入原油蒸气的生物学效应。二、肺部效应。

Biological effects of inhaled crude oil vapor. II. Pulmonary effects.

机构信息

Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, United States of America.

Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, United States of America.

出版信息

Toxicol Appl Pharmacol. 2022 Sep 1;450:116154. doi: 10.1016/j.taap.2022.116154. Epub 2022 Jul 5.

Abstract

Workers involved in oil exploration and production in the upstream petroleum industry are exposed to crude oil vapor (COV). COV levels in the proximity of workers during production tank gauging and opening of thief hatches can exceed regulatory standards, and several deaths have occurred after opening thief hatches. There is a paucity of information regarding the effects of COV inhalation in the lung. To address these knowledge gaps, the present hazard identification study was undertaken to investigate the effects of an acute, single inhalation exposure (6 h) or a 28 d sub-chronic exposure (6 h/d × 4 d/wk × 4 wks) to COV (300 ppm; Macondo well surrogate oil) on ventilatory and non-ventilatory functions of the lung in a rat model 1 and 28 d after acute exposure, and 1, 28 and 90 d following sub-chronic exposure. Basal airway resistance was increased 90 d post-sub-chronic exposure, but reactivity to methacholine (MCh) was unaffected. In the isolated, perfused trachea preparation the inhibitory effect of the airway epithelium on reactivity to MCh was increased at 90 d post-exposure. Efferent cholinergic nerve activity regulating airway smooth muscle was unaffected by COV exposure. Acute exposure did not affect basal airway epithelial ion transport, but 28 d after sub-chronic exposure alterations in active (Na and Cl¯) and passive ion transport occurred. COV treatment did not affect lung vascular permeability. The findings indicate that acute and sub-chronic COV inhalation does not appreciably affect ventilatory properties of the rat, but transient changes in airway epithelium occur.

摘要

从事上游石油工业石油勘探和生产的工人会接触到原油蒸气(COV)。在生产罐计量和打开小偷舱口时,工人附近的 COV 水平可能会超过监管标准,并且在打开小偷舱口后已经发生了几起死亡事件。关于 COV 吸入对肺部的影响,信息匮乏。为了解决这些知识空白,进行了本项危害识别研究,以调查单次急性吸入暴露(6 小时)或 28 天亚慢性暴露(6 小时/天×4 天/周×4 周)至 COV(300ppm;马孔多井替代油)对大鼠模型的肺通气和非通气功能的影响。在急性暴露后 1 天和 28 天以及亚慢性暴露后 1、28 和 90 天进行检测。在亚慢性暴露后 90 天,基础气道阻力增加,但对乙酰甲胆碱(MCh)的反应性不受影响。在离体灌注气管准备中,气道上皮对 MCh 反应的抑制作用在暴露后 90 天增加。调节气道平滑肌的传出胆碱能神经活性不受 COV 暴露的影响。急性暴露不会影响基础气道上皮离子转运,但在亚慢性暴露 28 天后,主动(Na 和 Cl¯)和被动离子转运发生改变。COV 处理不会影响肺血管通透性。研究结果表明,急性和亚慢性 COV 吸入不会明显影响大鼠的通气功能,但气道上皮会发生短暂变化。

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