Biology Laboratory, Beijing Third Class Tobacco Supervision Station, No. 99, WANSHENG South Street, Tongzhou Dis., Beijing 101121, China.
National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, No. 29 Nanwei Road, Xicheng District, Beijing 100050, China.
Toxicol Lett. 2020 Oct 1;331:200-207. doi: 10.1016/j.toxlet.2020.06.017. Epub 2020 Jun 20.
Harmful and potential harmful chemicals (HPHCs) and oxidative stress of macrophages are major factors responsible for smoking-caused chronic respiratory diseases. However, comparisons of HPHCs among heat not burn (HnB) product and ultra-light cigarette and their induced oxidative stress of macrophages have not been investigated.
The study detected HPHCs deliveries from HnB and ultra-light and measured their induced oxidative stress of macrophages cultured at air-liquid interface (ALI).
Total particulate matter, tar and 28 chemicals delivered from HnB, ultra-light and 3R4F cigarettes were determined. Mouse mononuclear macrophages at ALI were exposed to the aerosol of three tobacco products. Cell viability was measured by MTT assay. Reduced glutathione was detected by colorimetry method. Reactive oxygen species (ROS) was determined by fluorescence method.
The results showed levels of 26 common HPHCs from both HnB product and ultra-light cigarette were less than that from 3R4F cigarette. HnB product delivered formaldehyde, acetaldehyde, propanal, butyraldehyde and crotonaldehyde more than ultra-light cigarette. The levels of 21 HPHCs were lower in the HnB product compared to the ultra-light cigarette. At the same exposure dose and time, the order of cell viability induced by aerosol of that was HnB > ultra-light > 3R4F, the order of content of intracellular reduced glutathione induced by aerosol of that was HnB > ultra-light > 3R4F. It showed no significant difference of ROS level between ultra-light and HnB in each designed exposure dose. HnB induced more ROS than ultra-light cigarette in each designed exposure time.
Conclusively, most HPHCs from HnB were lower than that from ultra-light, while certain harmful chemicals were higher than ultra-light, e.g., carbonyl compounds. HnB-induced oxidative stress of macrophages is less than ultra-light cigarette.
有害和潜在有害化学物质（HPHCs）以及巨噬细胞的氧化应激是导致吸烟引起的慢性呼吸道疾病的主要因素。然而，热不燃烧（HnB）产品和超低焦油卷烟中的 HPHCs 及其诱导的巨噬细胞氧化应激尚未进行比较。
本研究检测了 HnB 和超低焦油卷烟中 HPHCs 的释放情况，并测量了它们在气液界面（ALI）培养的巨噬细胞中诱导的氧化应激。
测定了 HnB、超低焦油和 3R4F 卷烟释放的总颗粒物、焦油和 28 种化学物质。将 ALI 上的单核巨噬细胞暴露于三种烟草产品的气溶胶中。通过 MTT 测定法测量细胞活力。通过比色法检测还原型谷胱甘肽。通过荧光法测定活性氧（ROS）。
结果表明，HnB 产品和超低焦油卷烟中的 26 种常见 HPHCs 水平均低于 3R4F 卷烟。HnB 产品释放的甲醛、乙醛、丙醛、丁醛和巴豆醛多于超低焦油卷烟。与超低焦油卷烟相比，HnB 产品中 21 种 HPHCs 水平较低。在相同的暴露剂量和时间下，气溶胶诱导的细胞活力顺序为 HnB > 超低焦油 > 3R4F，气溶胶诱导的细胞内还原型谷胱甘肽含量顺序为 HnB > 超低焦油 > 3R4F。在每个设计的暴露剂量下，超轻和 HnB 之间的 ROS 水平没有显著差异。在每个设计的暴露时间内，HnB 诱导的 ROS 水平均高于超低焦油卷烟。
总之，HnB 中的大多数 HPHCs 低于超低焦油，而某些有害化学物质高于超低焦油，例如羰基化合物。HnB 诱导的巨噬细胞氧化应激低于超低焦油卷烟。
