Pryor W A
Biodynamics Institute, Louisiana State University, Baton Rouge 70803-1800.
Free Radic Biol Med. 1992 Dec;13(6):659-76. doi: 10.1016/0891-5849(92)90040-n.
This review compares and contrasts the chemistry of cigarette smoke, wood smoke, and the smoke from plastics and building materials that is inhaled by persons trapped in fires. Cigarette smoke produces cancer, emphysema, and other diseases after a delay of years. Acute exposure to smoke in a fire can produce a loss of lung function and death after a delay of days or weeks. Tobacco smoke and the smoke inhaled in a burning building have some similarities from a chemical viewpoint. For example, both contain high concentrations of CO and other combustion products. In addition, both contain high concentrations of free radicals, and our laboratory has studied these free radicals, largely by electron spin resonance (ESR) methods, for about 15 years. This article reviews what is known about the radicals present in these different types of smokes and soots and tars and summarizes the evidence that suggests these radicals could be involved in cigarette-induced pathology and smoke-inhalation deaths. The combustion of all organic materials produces radicals, but (with the exception of the smoke from perfluoropolymers) the radicals that are detected by ESR methods (and thus the radicals that would reach the lungs) are not those that arise in the combustion process. Rather they arise from chemical reactions that occur in the smoke itself. Thus, a knowledge of the chemistry of the smoke is necessary to understand the nature of the radicals formed. Even materials as similar as cigarettes and wood (cellulose) produce smoke that contains radicals with very different lifetimes and chemical characteristics, and mechanistic rationales for this are discussed. Cigarette tar contains a semiquinone radical that is infinitely stable and can be directly observed by ESR. Aqueous extracts of cigarette tar, which contain this radical, reduce oxygen to superoxide and thus produce both hydrogen peroxide and the hydroxyl radical. These solutions both oxidize alpha-1-proteinase inhibitor (a1PI) and nick DNA. Because of the potential role of radicals in smoke-inhalation injury, we suggest that antioxidant therapy (such as use of an inhaler for persons brought out of a burning building) might prove efficacious.
本综述比较并对比了香烟烟雾、木材烟雾以及火灾中被困人员吸入的塑料和建筑材料产生的烟雾的化学性质。香烟烟雾会在数年的延迟后引发癌症、肺气肿和其他疾病。火灾中急性接触烟雾会在数天或数周的延迟后导致肺功能丧失和死亡。从化学角度来看，烟草烟雾和燃烧建筑物中吸入的烟雾有一些相似之处。例如，两者都含有高浓度的一氧化碳和其他燃烧产物。此外，两者都含有高浓度的自由基，我们实验室已经用电子自旋共振（ESR）方法对这些自由基进行了大约15年的研究。本文回顾了关于这些不同类型的烟雾、煤烟和焦油中存在的自由基的已知信息，并总结了表明这些自由基可能与香烟诱发的病理学和烟雾吸入死亡有关的证据。所有有机材料的燃烧都会产生自由基，但（全氟聚合物烟雾除外）通过ESR方法检测到的自由基（因此会到达肺部的自由基）并非燃烧过程中产生的自由基。相反，它们源于烟雾本身发生的化学反应。因此，了解烟雾的化学性质对于理解所形成自由基的性质是必要的。即使是像香烟和木材（纤维素）这样相似的材料，产生的烟雾中所含自由基的寿命和化学特性也截然不同，本文对此进行了机理分析。香烟焦油含有一种无限稳定的半醌自由基，可通过ESR直接观察到。含有这种自由基的香烟焦油的水提取物将氧气还原为超氧化物，从而产生过氧化氢和羟基自由基。这些溶液既能氧化α-1-蛋白酶抑制剂（a1PI），又能切割DNA。由于自由基在烟雾吸入损伤中可能发挥的作用，我们建议抗氧化疗法（如为从燃烧建筑物中救出的人员使用吸入器）可能会被证明是有效的。
