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Chem Res Toxicol. 2020 Apr 20;33(4):999-1009. doi: 10.1021/acs.chemrestox.0c00036. Epub 2020 Mar 27.
3
Air pollutants disrupt iron homeostasis to impact oxidant generation, biological effects, and tissue injury.空气污染物破坏铁稳态,影响氧化剂生成、生物学效应和组织损伤。
Free Radic Biol Med. 2020 May 1;151:38-55. doi: 10.1016/j.freeradbiomed.2020.02.007. Epub 2020 Feb 21.
4
Ambient Ozone Pollution and Daily Mortality: A Nationwide Study in 272 Chinese Cities.环境臭氧污染与每日死亡率:一项在中国272个城市开展的全国性研究。
Environ Health Perspect. 2017 Nov 21;125(11):117006. doi: 10.1289/EHP1849.
5
Air Pollution and Mortality in the Medicare Population.医疗保险人群中的空气污染与死亡率
N Engl J Med. 2017 Jun 29;376(26):2513-2522. doi: 10.1056/NEJMoa1702747.
6
Comparison of lung damage in mice exposed to black carbon particles and 1,4-naphthoquinone coated black carbon particles.比较暴露于黑碳颗粒和 1,4-萘醌包覆黑碳颗粒的小鼠肺部损伤。
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9
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Environ Health Perspect. 2015 Nov;123(11):1180-6. doi: 10.1289/ehp.1409276. Epub 2015 Nov 1.
10
Wood Smoke Particle Sequesters Cell Iron to Impact a Biological Effect.木烟颗粒螯合细胞铁以影响生物学效应。
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臭氧与炭黑反应生成类似富里酸的物质,并增加炎症效应。

Ozone Reacts With Carbon Black to Produce a Fulvic Acid-Like Substance and Increase an Inflammatory Effect.

机构信息

138030US Environmental Protection Agency, Research Triangle Park, NC, USA.

Atmospheric and Oceanic Sciences, 8783University of California at Los Angeles, Los Angeles, CA, USA.

出版信息

Toxicol Pathol. 2020 Oct;48(7):887-898. doi: 10.1177/0192623320961017. Epub 2020 Sep 25.

DOI:10.1177/0192623320961017
PMID:32975498
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7810358/
Abstract

Exposure to ambient ozone has been associated with increased human mortality. Ozone exposure can introduce oxygen-containing functional groups in particulate matter (PM) effecting a greater capacity of the particle for metal complexation and inflammatory effect. We tested the postulate that (1) a fulvic acid-like substance can be produced through a reaction of a carbonaceous particle with high concentrations of ozone and (2) such a fulvic acid-like substance included in the PM can initiate inflammatory effects following exposure of respiratory epithelial (BEAS-2B) cells and an animal model (male Wistar Kyoto rats). Carbon black (CB) was exposed for 72 hours to either filtered air (CB-Air) or approximately 100 ppm ozone (CB-O). Carbon black exposure to high levels of ozone produced water-soluble, fluorescent organic material. Iron import by BEAS-2B cells at 4 and 24 hours was not induced by incubations with CB-Air but was increased following coexposures of CB-O with ferric ammonium citrate. In contrast to CB-Air, exposure of BEAS-2B cells and rats to CB-O for 24 hours increased expression of pro-inflammatory cytokines and lung injury, respectively. It is concluded that inflammatory effects of carbonaceous particles on cells can potentially result from (1) an inclusion of a fulvic acid-like substance after reaction with ozone and (2) changes in iron homeostasis following such exposure.

摘要

暴露于环境臭氧会增加人类死亡率。臭氧暴露会在颗粒物(PM)中引入含氧官能团,从而增加颗粒物与金属络合和产生炎症的能力。我们验证了以下假设:(1)富里酸样物质可以通过碳质颗粒与高浓度臭氧反应产生;(2)PM 中包含的这种富里酸样物质会在暴露于呼吸上皮(BEAS-2B)细胞和动物模型(雄性 Wistar Kyoto 大鼠)后引发炎症反应。将炭黑(CB)暴露于过滤空气(CB-Air)或约 100ppm 臭氧(CB-O)中 72 小时。CB 暴露于高水平臭氧会产生水溶性、荧光有机物质。在孵育过程中,用 CB-Air 孵育 BEAS-2B 细胞 4 小时和 24 小时均不会诱导铁摄取,但在用柠檬酸铁铵共暴露 CB-O 后,铁摄取增加。与 CB-Air 相比,暴露于 CB-O 24 小时的 BEAS-2B 细胞和大鼠分别增加了促炎细胞因子的表达和肺损伤。结论是,碳质颗粒对细胞的炎症作用可能源自(1)与臭氧反应后包含富里酸样物质,以及(2)这种暴露后铁稳态的改变。