Silverman D T, Dunn J A, Hoover R N, Schiffman M, Lillemoe K D, Schoenberg J B, Brown L M, Greenberg R S, Hayes R B, Swanson G M
Division of Cancer Etiology, National Cancer Institute, Bethesda, Md. 20892.
J Natl Cancer Inst. 1994 Oct 19;86(20):1510-6. doi: 10.1093/jnci/86.20.1510.
Cigarette smoking is the most consistently reported risk factor for pancreas cancer, yet the dose-response relationship in many pancreas cancer studies is weak. Because of the poor prognosis for pancreas cancer, many case-control studies have been based largely on interviews with proxy respondents, who are known to report less reliable information on detailed smoking habits than original subjects.
Our purpose was to evaluate cigarette smoking as a risk factor for pancreas cancer based on data obtained only from direct interviews and to estimate the effects of quitting smoking and of switching from nonfiltered to filtered cigarettes on risk. Our objective also was to estimate the contribution of cigarette smoking toward explaining the higher pancreas cancer incidence experienced by black Americans compared with white Americans.
A population-based, case-control study of pancreas cancer was conducted during 1986-1989 in Atlanta, Ga., Detroit, Mich., and 10 counties in New Jersey. Direct interviews were successfully completed with 526 case patients and 2153 control subjects aged 30-79 years, making this the largest population-based, case-control study of pancreas cancer to date based only on direct interviews.
Cigarette smokers had a significant, 70% increased risk of pancreas cancer compared with the risk in nonsmokers. A significant, positive trend in risk with increasing duration smoked was apparent (P < .0001), with long-term (> or = 40 years) smokers experiencing a modest 2.1-fold risk. We also observed a negative trend in risk with increasing years quit smoking. Smokers who quit for more than 10 years experienced about a 30% reduction in risk relative to current smokers; quitters of 10 years or less experienced no risk reduction. Switching from nonfiltered to filtered cigarettes did not appear to decrease risk. Compared with nonsmokers, subjects who smoked only filtered cigarettes had a 50% elevated risk and those who smoked only nonfiltered cigarettes had a 40% elevated risk. The proportion of pancreas cancer attributable to cigarette smoking was 29% in blacks and 26% in whites.
The relationship between cigarette smoking and pancreas cancer risk is likely to be causal, despite the weakness of the dose-response data. Long-term smoking cessation clearly reduces risk, whereas switching from nonfiltered to filtered cigarettes may not be beneficial. Cigarette smoking appears to explain little of the excess pancreas cancer risk experienced by blacks.
Elimination of cigarette smoking would eventually prevent approximately 27% of pancreas cancer, saving 6750 lives in the United States annually.
吸烟是胰腺癌最常被报道的风险因素，但在许多胰腺癌研究中，剂量反应关系并不显著。由于胰腺癌的预后较差，许多病例对照研究很大程度上基于对代理受访者的访谈，而众所周知，代理受访者报告的详细吸烟习惯信息不如原始受试者可靠。
我们的目的是基于仅从直接访谈中获得的数据，评估吸烟作为胰腺癌风险因素的情况，并估计戒烟以及从非过滤嘴香烟改用过滤嘴香烟对风险的影响。我们的目标还包括估计吸烟对解释美国黑人相比白人更高的胰腺癌发病率的贡献。
1986年至1989年期间，在佐治亚州亚特兰大、密歇根州底特律和新泽西州的10个县开展了一项基于人群的胰腺癌病例对照研究。成功对526例病例患者和2153名年龄在30至79岁的对照受试者进行了直接访谈，这使得该研究成为迄今为止仅基于直接访谈的最大规模的基于人群的胰腺癌病例对照研究。
与不吸烟者相比，吸烟者患胰腺癌的风险显著增加70%。随着吸烟持续时间增加，风险呈现出显著的正趋势（P <.0001），长期（≥40年）吸烟者的风险适度增加2.1倍。我们还观察到随着戒烟年限增加，风险呈负趋势。戒烟超过10年的吸烟者相对于当前吸烟者风险降低约30%；戒烟10年或更短时间的吸烟者风险未降低。从非过滤嘴香烟改用过滤嘴香烟似乎并未降低风险。与不吸烟者相比，仅吸过滤嘴香烟的受试者风险升高50%，仅吸非过滤嘴香烟的受试者风险升高40%。吸烟导致的胰腺癌比例在黑人中为29%，在白人中为26%。
尽管剂量反应数据不显著，但吸烟与胰腺癌风险之间的关系可能是因果关系。长期戒烟显然可降低风险，而从非过滤嘴香烟改用过滤嘴香烟可能并无益处。吸烟似乎对黑人中额外的胰腺癌风险解释甚少。
消除吸烟最终可预防约27%的胰腺癌，在美国每年可挽救6750条生命。
