Song Min-Ae, Benowitz Neal L, Berman Micah, Brasky Theodore M, Cummings K Michael, Hatsukami Dorothy K, Marian Catalin, O'Connor Richard, Rees Vaughan W, Woroszylo Casper, Shields Peter G
Affiliations of authors: Comprehensive Cancer Center, The Ohio State University and James Cancer Hospital, Columbus, OH (MAS, MB, TMB, CM, PGS); Division of Epidemiology, The Ohio State University College of Public Health, Columbus, OH (MAS, CW); Departments of Medicine and Bioengineering and Therapeutic Sciences, Division of Clinical Pharmacology and Experimental Therapeutics and Center for Tobacco Control Research and Education, University of California, San Francisco, CA (NLB); College of Public Health and Moritz College of Law, The Ohio State University, Columbus, OH (MB); Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina, Charleston, SC (KMC); Tobacco Research Programs and Department of Psychiatry, University of Minnesota, Minneapolis, MN (DH); Biochemistry and Pharmacology Department, Victor Babes University of Medicine and Pharmacy, Timisoara, Romania, (CM); Department of Health Behavior, Roswell Park Cancer Institute, Buffalo, NY (RO); Center for Global Tobacco Control, Department of Social and Behavioral Sciences, Harvard T. H. Chan School of Public Health, Boston, MA (VWR).
J Natl Cancer Inst. 2017 Dec 1;109(12). doi: 10.1093/jnci/djx075.
The 2014 Surgeon General's Report on smoking and health concluded that changing cigarette designs have caused an increase in lung adenocarcinomas, implicating cigarette filter ventilation that lowers smoking machine tar yields. The Food and Drug Administration (FDA) now has the authority to regulate cigarette design if doing so would improve public health. To support a potential regulatory action, two weight-of-evidence reviews were applied for causally relating filter ventilation to lung adenocarcinoma. Published scientific literature (3284 citations) and internal tobacco company documents contributed to causation analysis evidence blocks and the identification of research gaps. Filter ventilation was adopted in the mid-1960s and was initially equated with making a cigarette safer. Since then, lung adenocarcinoma rates paradoxically increased relative to other lung cancer subtypes. Filter ventilation 1) alters tobacco combustion, increasing smoke toxicants; 2) allows for elasticity of use so that smokers inhale more smoke to maintain their nicotine intake; and 3) causes a false perception of lower health risk from "lighter" smoke. Seemingly not supportive of a causal relationship is that human exposure biomarker studies indicate no reduction in exposure, but these do not measure exposure in the lung or utilize known biomarkers of harm. Altered puffing and inhalation may make smoke available to lung cells prone to adenocarcinomas. The analysis strongly suggests that filter ventilation has contributed to the rise in lung adenocarcinomas among smokers. Thus, the FDA should consider regulating its use, up to and including a ban. Herein, we propose a research agenda to support such an effort.
2014年美国卫生局局长关于吸烟与健康的报告得出结论，香烟设计的改变导致肺腺癌发病率上升，这与降低吸烟机焦油产量的香烟过滤嘴通风有关。如果这样做能改善公众健康，美国食品药品监督管理局（FDA）现在有权监管香烟设计。为支持一项潜在的监管行动，进行了两项证据权重评估，以因果关系将过滤嘴通风与肺腺癌联系起来。已发表的科学文献（3284篇引用文献）和烟草公司内部文件为因果关系分析证据库及研究空白的识别做出了贡献。过滤嘴通风在20世纪60年代中期被采用，最初被认为能使香烟更安全。从那时起，相对于其他肺癌亚型，肺腺癌发病率反而出现了上升。过滤嘴通风1）改变烟草燃烧，增加烟雾中的有毒物质；2）允许使用方式具有弹性，使吸烟者吸入更多烟雾以维持尼古丁摄入量；3）导致对“较淡”烟雾的健康风险降低产生错误认知。人类暴露生物标志物研究似乎不支持因果关系，因为这些研究表明暴露没有减少，但它们没有测量肺部的暴露情况，也没有使用已知的危害生物标志物。抽吸和吸入方式的改变可能使烟雾进入易患腺癌的肺细胞。分析强烈表明，过滤嘴通风导致了吸烟者中肺腺癌发病率的上升。因此，FDA应考虑对其使用进行监管，直至包括禁令。在此，我们提出一项研究议程以支持这一努力。
