Diggs Deacqunita L, Huderson Ashley C, Harris Kelly L, Myers Jeremy N, Banks Leah D, Rekhadevi Perumalla V, Niaz Mohammad S, Ramesh Aramandla
Department of Biochemistry & Cancer Biology, Meharry Medical College, Nashville, TN 37208, USA.
J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2011 Oct;29(4):324-57. doi: 10.1080/10590501.2011.629974.
Cancers of the colon are most common in the Western world. In majority of these cases, there is no familial history and sporadic gene damage seems to play an important role in the development of tumors in the colon. Studies have shown that environmental factors, especially diet, play an important role in susceptibility to gastrointestinal (GI) tract cancers. Consequently, environmental chemicals that contaminate food or diet during preparation become important in the development of GI cancers. Polycyclic aromatic hydrocarbons (PAHs) are one such family of ubiquitous environmental toxicants. These pollutants enter the human body through consumption of contaminated food, drinking water, inhalation of cigarette smoke, automobile exhausts, and contaminated air from occupational settings. Among these pathways, dietary intake of PAHs constitutes a major source of exposure in humans. Although many reviews and books on PAHs and their ability to cause toxicity and breast or lung cancer have been published, aspects on contribution of diet, smoking and other factors toward development of digestive tract cancers, and strategies to assess risk from exposure to PAHs have received much less attention. This review, therefore, focuses on dietary intake of PAHs in humans, animal models, and cell cultures used for GI cancer studies along with epidemiological findings. Bioavailability and biotransformation processes, which influence the disposition of PAHs in body and the underlying causative mechanisms of GI cancers, are also discussed. The existing data gaps and scope for future studies is also emphasized. This information is expected to stimulate research on mechanisms of sporadic GI cancers caused by exposure to environmental carcinogens.
结肠癌在西方世界最为常见。在大多数此类病例中,没有家族病史,散发性基因损伤似乎在结肠癌的发生发展中起重要作用。研究表明,环境因素,尤其是饮食,在胃肠道(GI)癌症的易感性方面起着重要作用。因此,在食物制备过程中污染食物或饮食的环境化学物质在胃肠道癌症的发生中变得至关重要。多环芳烃(PAHs)就是这样一类普遍存在的环境毒物。这些污染物通过食用受污染的食物、饮用水、吸入香烟烟雾、汽车尾气以及职业环境中的污染空气进入人体。在这些途径中,通过饮食摄入多环芳烃是人类接触的主要来源。尽管已经发表了许多关于多环芳烃及其导致毒性和乳腺癌或肺癌能力的综述和书籍,但饮食、吸烟和其他因素对消化道癌症发生发展的贡献以及评估多环芳烃暴露风险的策略受到的关注要少得多。因此,本综述重点关注用于胃肠道癌症研究的人类、动物模型和细胞培养物中多环芳烃的饮食摄入情况以及流行病学研究结果。还讨论了生物利用度和生物转化过程,这些过程影响多环芳烃在体内的分布以及胃肠道癌症的潜在致病机制。同时也强调了现有的数据差距和未来研究的范围。这些信息有望激发对由环境致癌物暴露引起的散发性胃肠道癌症机制的研究。