Physical Effects Research Branch, National Institute for Occupational Safety and Health, Morgantown, WV, USA.
Pathology and Physiology Research Branch, National Institute for Occupational Safety and Health, Morgantown, WV, USA.
Inhal Toxicol. 2024 Mar;36(3):189-204. doi: 10.1080/08958378.2024.2327364. Epub 2024 Mar 11.
Inhalation of diesel exhaust (DE) has been shown to be an occupational hazard in the transportation, mining, and gas and oil industries. DE also contributes to air pollution, and therefore, is a health hazard to the general public. Because of its effects on human health, changes have been made to diesel engines to reduce both the amounts of particulate matter and volatile fumes they generate. The goal of the current study was to examine the effects of inhalation of diesel exhaust.
The study presented here specifically examines the effects of exposure to 0.2 and 1.0 mg/m DE or filtered air (6h/d for 4 d) on measures of peripheral and cardio-vascular function, and biomarkers of heart and kidney dysfunction in male rats. A Tier 2 engine used in oil and gas fracking operations was used to generate the diesel exhaust.
Exposure to 0.2 mg/m DE resulted in an increase in blood pressure 1d following the last exposure, and increases in dobutamine-induced cardiac output and stroke volume 1 and 27d after exposure. Changes in peripheral vascular responses to norepinephrine and acetylcholine were minimal as were changes in transcript expression in the heart and kidney. Exposure to 1.0 mg/m DE did not result in major changes in blood pressure, measures of cardiac function, peripheral vascular function or transcript expression.
Based on the results of this study, we suggest that exposure to DE generated by a Tier 2 compliant diesel engine generates acute effects on biomarkers indicative of cardiovascular dysfunction. Recovery occurs quickly with most measures of vascular/cardiovascular function returning to baseline levels by 7d following exposure.
吸入柴油机废气（DE）已被证明是交通运输、采矿、天然气和石油行业的职业危害。DE 还造成空气污染，因此对公众健康构成危害。由于其对人类健康的影响，已经对柴油机进行了改进，以减少其产生的颗粒物和挥发性烟雾的数量。本研究的目的是研究吸入柴油机废气的影响。
本研究专门研究了暴露于 0.2 和 1.0mg/m DE 或过滤空气（6h/d，持续 4d）对雄性大鼠外周和心血管功能以及心脏和肾功能障碍生物标志物的影响。用于石油和天然气压裂作业的二级发动机用于产生柴油机废气。
暴露于 0.2mg/m DE 导致在最后一次暴露后 1 天血压升高，并且在暴露后 1 和 27 天多巴酚丁胺诱导的心输出量和每搏量增加。去甲肾上腺素和乙酰胆碱引起的外周血管反应变化很小，心脏和肾脏的转录表达变化也很小。暴露于 1.0mg/m DE 不会导致血压、心脏功能、外周血管功能或转录表达的重大变化。
根据本研究的结果，我们建议符合二级标准的柴油机产生的 DE 暴露会产生急性心血管功能障碍生物标志物的影响。大多数血管/心血管功能的测量在暴露后 7 天内恢复到基线水平，因此恢复很快。
