Petroleum products—petrol, kerosene, and diesel—composed of volatile organic constituents contribute to air pollution. Exposure of gas station attendants (GSAs) to petroleum products fumes (PPFs) may account for occupation‐related predisposition to respiratory toxicity and disease pathogenesis. We simulated GSA exposure to PPF inhalation and examined their effect on oxido‐inflammatory responses, toxicity, and histopathological alterations in rat lungs, following 8‐hours daily exposure for 60 and 90 days. Reactive oxygen and nitrogen species (RONS), oxidative stress and inflammatory biomarkers, namely: superoxide dismutase (SOD), reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione‐S‐transferase (GST), TNF‐α, IL‐1β, xanthine oxidase (XO), nitric oxide (NO) activity were evaluated. Besides, histopathological examination of the lungs and trachea of exposed rats, PPF exposure resulted in significant (P < .05) increases in RONS, biomarkers of oxidative stress, pro‐inflammation cytokines, and reduced (P < .05) GSH levels in rats, secondary to histopathological alteration in lungs and trachea cytoarchitecture examined in an exposure‐duration‐dependent manner. We conclude, therefore, that the observed biochemical and histological changes create a microenvironment that is permissive to diseases pathogenesis of the respiratory system via oxido‐inflammatory mechanistic pathways.

中文翻译：

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暴露于石油产品烟雾的大鼠肺部的氧化炎症反应和组织学改变

石油产品（汽油、煤油和柴油）由挥发性有机成分组成，会造成空气污染。加油站服务员（GSA）接触石油产品烟雾（PPF）可能是职业相关的呼吸道毒性和疾病发病机制的原因。我们模拟 GSA 暴露于 PPF 吸入，并检查其在每天暴露 8 小时、持续 60 和 90 天后对大鼠肺部氧化炎症反应、毒性和组织病理学改变的影响。活性氧和氮（RONS）、氧化应激和炎症生物标志物，即：超氧化物歧化酶（SOD）、还原型谷胱甘肽（GSH）、谷胱甘肽过氧化物酶（GPx）、谷胱甘肽-S-转移酶（GST）、TNF-α、IL-评估了1β、黄嘌呤氧化酶（XO）、一氧化氮（NO）活性。此外，对暴露大鼠的肺部和气管进行组织病理学检查，PPF 暴露导致大鼠 RONS、氧化应激生物标志物、促炎症细胞因子显着增加 (P < .05)，并降低 (P < .05) GSH 水平，继发于以暴露持续时间依赖性方式检查的肺和气管细胞结构的组织病理学改变。因此，我们得出的结论是，观察到的生化和组织学变化创造了一个微环境，允许通过氧化炎症机制途径导致呼吸系统疾病发病。