Preston-Martin S
University of Southern California School of Medicine, Los Angeles 90033.
Crit Rev Toxicol. 1991;21(4):295-8. doi: 10.3109/10408449109017915.
Considerable evidence exists that TSNA may cause cancer in humans. Strong evidence suggests that the NNN and NNK in snuff are at least partially responsible for the excess of oral cancer among snuff dippers. Tobacco smoke, because it is a combustion product, is a far more complex matrix than is smokeless tobacco. Nonetheless, NNK is well established as a lung carcinogen in laboratory animals at levels similar to those experienced by heavy smokers. Although the epidemiology of the smoking/lung cancer association has been studied extensively and is well established as a causal relationship, few attempts have been made to determine the effective constituents in tobacco smoke, much less to quantify them and to reduce their levels in consumer products. More work is needed to determine TSNA uptake in smokers and users of smokeless tobacco and to determine the factors involved in the possible endogenous formation of TSNA and in their metabolic activation or inhibition of their formation. Exploratory work is in progress with various biological markers that may prove useful in quantifying the levels of TSNA exposure in humans. Epidemiologic evidence indicates that in addition to tobacco use other factors are causally related to the development of cancers of the oral cavity, lung and esophagus and that these factors (e.g., radon exposure in uranium miners who smoke) can act synergistically. Experimental investigation of some of these synergistic effects may prove to be a step in the direction of determining the proportion of various cancers that are likely to be attributable to various causes and ultimately to the various constituents of tobacco exposure.
有大量证据表明烟草特有亚硝胺（TSNA）可能会导致人类患癌。有力证据表明，鼻烟中的亚硝基去甲烟碱（NNN）和亚硝基新烟碱（NNK）至少是导致鼻烟使用者口腔癌高发的部分原因。烟草烟雾作为一种燃烧产物，其成分远比无烟烟草复杂。尽管如此，在实验动物中，NNK作为一种肺癌致癌物已得到充分证实，其在动物体内的含量与重度吸烟者体内的含量相当。虽然吸烟与肺癌关联的流行病学已得到广泛研究，且二者的因果关系也已确立，但几乎没有人尝试确定烟草烟雾中的有效成分，更不用说对其进行量化以及降低消费品中的这些成分含量了。需要开展更多工作来确定吸烟者和无烟烟草使用者体内TSNA的摄入量，并确定可能参与TSNA内源性形成、代谢激活或形成抑制的相关因素。目前正在对各种生物标志物进行探索性研究，这些标志物可能有助于量化人类TSNA暴露水平。流行病学证据表明，除了烟草使用外，其他因素也与口腔癌、肺癌和食管癌的发生存在因果关系，而且这些因素（例如，吸烟的铀矿工人接触氡）可能会产生协同作用。对其中一些协同效应进行实验研究，可能是朝着确定各种癌症中可能归因于各种原因以及最终归因于烟草暴露各种成分的比例迈出的一步。
