发现联系:人类的乙烯暴露和内源性乙烯氧化物水平
Yu-Sheng Lin1, Kristina A Thayer2,3, Paul White4
1Office of Research and Development, Center for Public Health and Environmental Assessment, Chemical & Pollutant Assessment Division, U.S. Environmental Protection Agency, Washington, DC, USA. Lin.Yu-Sheng@epa.gov.
Journal of exposure science & environmental epidemiology
|November 20, 2025
概括
乙烯氧化物 (EtO) 是一种致癌物. 这项研究发现,在未暴露的个体中,来自乙烯 (ET) 暴露的内部EtO比以前想象的要低,这表明EtO生物标志物的其他来源.
科学领域:
- 环境健康 环境健康
- 毒理学 毒理学 毒理学
- 生物标记分析 生物标记分析
背景情况:
- 乙烯氧化物 (EtO) 是已知的致癌物质,因空气污染和吸烟而暴露.
- 内源性EtO可以从乙烯 (ET) 氧化中形成,这引发了关于ET作为主要来源的疑问,尽管证据有限.
研究的目的:
- 量化总乙烯暴露 (外部和内部) 对未暴露人群内源性乙烯氧化物水平的影响.
- 评估乙烯对氧化乙烯体内负荷和相关生物标志物的贡献.
主要方法:
- 进行了文献审查和药理动力学分析,以评估ET暴露和EtO水平.
- 使用呼吸分析来估计由于其呼气而导致的ET总暴露.
- 通过血红蛋白添加物 (HEV) 评估循环中的EtO作为生物标志物.
主要成果:
- 呼出的ET度差异很大 (0.2-740ppb),在净化空气条件下较低的水平 (0.2-1.2ppb),表明内部ET贡献有限.
- 药物动力学模型预测成年人从内部来源呼出的ET<1-2ppb,增加到16ppb,随着名义环境ET暴露 (15ppb).
- 来自ET的EtO占HEV/g球蛋白<3.5 pmol,明显低于观察到的背景HEV水平,表明HEV的未确定来源.
结论:
- 暴露于乙烯的内源性EtO似乎比以前估计的在未暴露的人群中明显低.
- 这些发现表明,未确定的来源对背景HEV水平作出了重大贡献.
- 进一步的研究,包括方法改进,对于准确的EtO风险评估至关重要,因为它具有致癌潜力.
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