Abstract

269 ISSN 1758-194X 10.2217/CRC.12.32 © 2012 Future Medicine Ltd Colorect. Cancer (2012) 1(4), 269–271 1Division of Epidemiology & Biostatistics, European Institute of Oncology, via Ripamonti 435, 20141 Milan, Italy 2Department of Occupational Health, University of Milan, Milan, Italy *Author for correspondence: Tel.: +39 0257489820; Fax: +39 0257489922; edoardo.botteri@ieo.it Earlier this year the International Agency for Research on Cancer published an extensive re-examination of human carcinogens including tobacco [1]. For the first time the International Agency for Research on Cancer listed the colorectum among the cancer sites for which there is sufficient evidence of a causal association with tobacco. This evaluation was mainly based on the publication of four meta-analyses, which consistently showed a significant association between cigarette smoking and c olorectal cancer (CRC) [2–5]. The largest of the four meta-analyses summarized evidence from 121 independent observational studies, and showed that cigarette smoking increases the incidence of CRC by approximately 18% and its mortality by 25%, corresponding to an absolute excess of 11 CRC cases and six CRC deaths per 100,000 person-years [2]. These results were corroborated by two successive reports from large populationbased prospective cohort studies [6,7]. In the first study from the USA, which followed 184,187 individuals from the Cancer Prevention Study II Nutrition Cohort, the authors reported a 27 and 23% increased risk of developing CRC, respectively, in current and former smokers, as compared with never-smokers [6]. Subsequently, investigators of the European Prospective Investigation into Cancer and Nutrition study, which followed 465,879 individuals, confirmed an increased risk of CRC in smokers, 21% in former and 13% in current smokers, compared with never-smokers [7]. The risk of CRC increases with smoking intensity (cigarettes per day), smoking duration (years of exposure) and lifetime exposure (pack-years) [2,3]. However, the excess risk is modest, approximately 16–17% for an increased consumption of 20 cigarettes per day, 27% for an increase of 35 pack-years or 50% for an increase of 60 pack-years [2,3]. There is also evidence of a nonlinear dose–response relationship between smoking duration and CRC risk, with the risk becoming appreciable only 10 years after the initiation of smoking [2]. Interestingly, consecutive reports from “Tobacco smoking appears to be more strongly associated with an increased risk of cancer developing through the serrated pathway, rather than the traditional adenoma pathway.” EDITORIAL

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