Hoffmann D, Rivenson A, Hecht S S
Naylor Dana Institute for Disease Prevention, American Health Foundation, Valhalla, NY 10595, USA.
Crit Rev Toxicol. 1996;26(2):199-211. doi: 10.3109/10408449609017931.
In the U.S., there has been a steeper rise of the incidence of lung adenocarcinoma than of squamous cell carcinoma of the lung among cigarette smokers. Since 1950, the percentage of all cigarettes sold that had filter tips increased from 0.56 to 92% in 1980 and to 97% in 1990. The tobacco of the filter cigarettes is richer in nitrate than that of the nonfilter cigarettes manufactured in past decades. Because the smoker of cigarettes with lower nicotine yield tends to smoke more intensely and to inhale the smoke more deeply than the smoker of plain cigarettes, the peripheral lung is exposed to higher amounts of nitrogen oxides, nitrosated compounds, and lung-specific smoke carcinogens. It is our working hypothesis that more intense smoking, deeper inhalation of the smoke, and higher smoke delivery of the organ-specific lung carcinogen NNK to the peripheral lung are major contributors to the increased risk of cigarette smokers for lung adenocarcinoma. Bioassay data and biochemical studies in support of this concept are discussed.
在美国，吸烟者中肺腺癌发病率的上升幅度比肺鳞状细胞癌更为显著。自1950年以来，带过滤嘴香烟在所有销售香烟中所占的比例从0.56%增至1980年的92%，并于1990年达到97%。过滤嘴香烟的烟草比过去几十年生产的无过滤嘴香烟含有更多的硝酸盐。由于尼古丁含量较低的香烟吸烟者往往比普通香烟吸烟者吸烟更猛、吸入更深，外周肺暴露于更高剂量的氮氧化物、亚硝化化合物和肺特异性烟雾致癌物中。我们的工作假设是，更猛吸烟、更深吸入烟雾以及器官特异性肺致癌物NNK向外周肺更高的烟雾输送量是吸烟者患肺腺癌风险增加的主要原因。本文讨论了支持这一概念的生物测定数据和生化研究。
