The changing epidemiology of smoking and lung cancer histology
The changing epidemiology of smoking and lung cancer histology
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DOI：
10.2307/3432301
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发表时间：
1995-11-01
影响因子：
10.4
通讯作者：
Muscat, JE
中科院分区：
文献类型：
--
作者：
Wynder, EL;Muscat, JE
1950年，第一次大规模的流行病学研究表明，肺癌与吸烟有关，这一发现随后得到了伦敦皇家医师学院、美国卫生局局长和世界卫生组织的证实。虽然美国的香烟消费量从1965年每个成年人每年约3800支的高点逐渐下降到1993年的约2800支，但肺癌死亡率在男性中达到了74.9/100,000/年的高水平，在女性中达到了28.5。然而，在年轻人群中，男性和女性的肺癌死亡率都在下降。在这篇综述中，我们讨论了近几十年来肺腺癌发病率与肺鳞状细胞癌相比的急剧增长。1950年，这两种主要类型的肺癌在男性中的比例约为1:18；今天大约是1:1.2-1.4。这篇综述讨论了两个概念，这两个概念被认为是在肺癌的组织学类型中起作用的因素。其中一个因素是香烟的平均尼古丁和焦油含量分别从1955年的2.7毫克和38毫克下降到1993年的1.0毫克和13.5毫克。减少烟雾排放的其他主要因素与香烟混合烟草成分的改变和带过滤嘴香烟的普遍接受有关；后者占目前销售的卷烟总量的97%。然而，低含量香烟的吸烟者通过更深入地吸入烟雾和更猛烈地吸烟来补偿尼古丁的低释放；这些吸烟者可能每分钟吸5次烟，吞吐量高达55毫升。在这种情况下，周围肺暴露于更多的烟雾致癌物中，这些致癌物被怀疑会导致肺腺癌。美国卷烟混合烟草成分的重要变化之一是硝酸盐含量显著增加（0.5%至1.2-1.5%），这提高了烟雾中氮氧化物和n -亚硝胺的产量。此外，低产量香烟的消费者吸烟程度越高，烟雾中的n -亚硝胺含量就会增加2至3倍。n -亚硝胺中有4-（甲基亚硝胺）-1-（3-吡啶基）-1-丁酮（NNK），这是一种强效的动物肺癌物质，完全由尼古丁形成。这种器官特异性烟草特异性亚硝胺（TSNA）诱导肺腺癌。所有这些因素，吸烟越剧烈，吸入的烟雾越深，以及低含量香烟烟雾中n -亚硝胺含量的增加，都被认为是近年来吸烟者中肺腺癌急剧增加的主要原因。本综述还讨论了女性吸烟者与男性吸烟者在主要肺癌类型上的差异，以及非裔美国人与白人美国人相比肺癌风险增加的可能潜在因素。虽然预防吸烟相关疾病的唯一可靠方法是放弃吸烟习惯，但对于那些无法做到这一点的人，必须采取措施保护他们。因此，应该考虑制定美国香烟烟雾中焦油含量的上限，类似于西欧已经采取的策略。
In 1950, the first large-scale epidemiological studies demonstrated that lung cancer is causatively associated with cigarette smoking, a finding subsequently confirmed by the Royal College of Physicians in London, the U.S. Surgeon General, and the World Health Organization. Although cigarette consumption has gradually decreased in the United States from a high of about 3800 cigarettes per adult per year in 1965 to about 2800 cigarettes in 1993, death from lung cancer has reached a high among males at the rate of 74.9/100,000/year and among females at the rate of 28.5. However, in the younger cohorts, the lung cancer death rate is decreasing in both men and women. In this overview we discuss the steeper increase during recent decades of lung adenocarcinoma incidence compared with squamous cell carcinoma of the lung. In 1950, the ratio of these two major types of lung cancer in males was about 1:18; today it is about 1:1.2-1.4. This overview discusses two concepts that are regarded as contributors to this charge in the histological types of lung cancer. One factor is the decrease in average nicotine and tar delivery of cigarettes from about 2.7 and 38 mg in 1955 to 1.0 and 13.5 mg in 1993, respectively. Other major factors for the reduced emission of smoke relate to changes in the composition of the cigarette tobacco blend and general acceptance of cigarettes with filter tips; the latter constitute 97% of all cigarettes currently sold. However, smokers of low-yield cigarettes compensate for the low delivery of nicotine by inhaling the smoke more deeply and by smoking more intensely; such smokers may be taking up to 5 puffs/min with puff volumes up to 55 ml. Under these conditions, the peripheral lung is exposed to increased amounts of smoke carcinogens that are suspected to lead to lung adenocarcinoma. Among the important changes in the composition of the tobacco blend of the U.S. cigarette is a significant increase in nitrate content (0.5% to 1.2-1.5%), which raises the yields of nitrogen oxides and N-nitrosamines in the smoke. Furthermore, the more intense smoking by the consumers of low-yield cigarettes increases N-nitrosamines in the smoke 2- to 3-fold. Among the N-nitrosamines is 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a powerful lung carcinogen in animals that is exclusively formed from nicotine. This organ-specific tobaco-specific nitrosamine (TSNA) induces adenocarcinoma of the lung. All of these factors, the more intense smoking, the deeper inhalation of the smoke, and the increased yields of N-nitrosamines in the smoke of low-yield cigarettes, are considered major contributors to the drastic increase in lung adenocarcinoma among cigarette smokers in recent years. This overview also discusses the differences in the major lung cancer types in female compared with male smokers as well as the likely underlying factors for increased lung cancer risk among African Americans compared with that among white Americans. Although the only sure way to prevent smoking-related diseases is giving up the tobacco habit, there must be a measure of protection for those who cannot accomplish this. Therefore, setting upper permissible limits of tar levels for the smoke of U.S. cigarettes, similar to strategies already taken in Western Europe, should be considered.