Department of Epidemiology, GROW-School for Oncology and Developmental Biology, Maastricht University, Maastricht, The Netherlands.
Crit Rev Toxicol. 2010 Jul;40(6):485-512. doi: 10.3109/10408440903524254.
Since 2002, it is known that the probable human carcinogen acrylamide is present in commonly consumed carbohydrate-rich foods, such as French fries and potato chips. In this review, the authors discuss the body of evidence on acrylamide carcinogenicity from both epidemiological and rodent studies, including variability, strengths and weaknesses, how both types of evidence relate, and possible reasons for discrepancies. In both rats and humans, increased incidences of various cancer types were observed. In rats, increased incidences of mammary gland, thyroid tumors and scrotal mesothelioma were observed in both studies that were performed. In humans, increased risks of ovarian and endometrial cancers, renal cell cancer, estrogen (and progesterone) receptor-positive breast cancer, and oral cavity cancer (the latter in non-smoking women) were observed. Some cancer types were found in both rats and humans, e.g., endometrial cancer (observed in one of the two rat studies), but there are also some inconsistencies. Interestingly, in humans, some indications for inverse associations were observed for lung and bladder cancers in women, and prostate and oro- and hypopharynx cancers in men. These latter observations indicate that genotoxicity may not be the only mechanism by which acrylamide causes cancer. The estimated risks based on the epidemiological studies for the sites for which a positive association was observed were considerably higher than those based on extrapolations from the rat studies. The observed pattern of increased risks in the rat and epidemiological studies and the decreased risks in the epidemiological studies suggests that acrylamide might influence hormonal systems, for which rodents may not be good models.
自 2002 年以来，人们已经知道可能的人类致癌物质丙烯酰胺存在于人们经常食用的富含碳水化合物的食物中，如炸薯条和薯片。在这篇综述中，作者讨论了来自流行病学和啮齿动物研究的丙烯酰胺致癌性证据，包括变异性、优势和弱点、这两种类型的证据如何相关以及差异的可能原因。在大鼠和人类中，观察到各种癌症类型的发病率增加。在大鼠中，在两项研究中都观察到乳腺、甲状腺肿瘤和睪丸间皮瘤的发病率增加。在人类中，观察到卵巢癌和子宫内膜癌、肾癌、雌激素（和孕激素）受体阳性乳腺癌以及口腔癌（非吸烟女性）的风险增加。一些癌症类型在大鼠和人类中都有发现，例如子宫内膜癌（在两项大鼠研究中的一项中观察到），但也存在一些不一致之处。有趣的是，在人类中，一些女性肺癌和膀胱癌以及男性前列腺癌、口咽癌和下咽癌的观察结果表明，遗传毒性可能不是丙烯酰胺致癌的唯一机制。基于流行病学研究观察到阳性关联的部位，估计的风险远高于基于大鼠研究外推的风险。在大鼠和流行病学研究中观察到的风险增加模式以及流行病学研究中风险降低的模式表明，丙烯酰胺可能会影响激素系统，而啮齿动物可能不是研究激素系统的良好模型。
