MRC Cancer Unit,Hutchison-MRC Research Centre, University of Cambridge, Hills Road, Cambridge, CB2 0XZ, USA.
Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, The Henry Wellcome Laboratory, Nuffield Building, Crown St., Liverpool, L69 3GE, UK.
Br J Cancer. 2019 Jun;120(12):1099-1104. doi: 10.1038/s41416-019-0467-9. Epub 2019 May 9.
Oesophageal adenocarcinoma has become much more common over the past 50 years, particularly in Britain, with an unexplained male to female ratio of > 4:1. Given the use of asbestos filtration in commercial brewing and reports of its unregulated use in British public houses in the 1970's to clear draught beer "slops", we have assessed the hypothesis that ingested asbestos could be a causative factor for this increased incidence. Importantly, occupational asbestos exposure increases the risk of adenocarcinoma but not squamous cell carcinoma of the oesophagus. The presence of asbestos fibres was consistently reported in filtered beverages including beers in the 1970s and asbestos bodies have been found in gastrointestinal tissue, particularly oesophageal tissue, at autopsy. There is no reported association between the intake of alcohol and oesophageal adenocarcinoma but studies would mostly have missed exposure from draught beer before 1980. Oesophageal adenocarcinoma has some molecular similarities to pleural mesothelioma, a condition that is largely due to inhalation of asbestos fibres, including predominant loss of tumour suppressor genes rather than an increase of classical oncogenic drivers. Trends in incidence of oesophageal adenocarcinoma and mesothelioma are similar, rising rapidly over the past 50 years but now plateauing. Asbestos ingestion, either from beer consumed before around 1980, or from occupational exposure, seems a plausible causative factor for oesophageal adenocarcinoma. If this is indeed the case, its incidence should fall back to a low baseline by around 2050.
食管腺癌在过去 50 年中变得更加普遍，尤其是在英国，其男女比例>4:1，原因不明。鉴于商业酿造中使用石棉过滤以及 20 世纪 70 年代英国酒吧中未经监管使用石棉来清除生啤酒“残液”的报道，我们评估了摄入石棉可能是导致这种发病率增加的一个因素。重要的是，职业性石棉暴露会增加食管腺癌的风险，但不会增加食管鳞癌的风险。在 20 世纪 70 年代，过滤后的饮料（包括啤酒）中都有石棉纤维的存在，尸检中还发现胃肠道组织（特别是食管组织）中有石棉体。目前还没有报告显示摄入酒精与食管腺癌之间存在关联，但在 1980 年之前，这些研究可能大多都忽略了生啤酒暴露。食管腺癌与胸膜间皮瘤有一些分子相似之处，胸膜间皮瘤主要是由于吸入石棉纤维引起的，包括主要的肿瘤抑制基因缺失，而不是经典致癌驱动基因的增加。食管腺癌和间皮瘤的发病率趋势相似，在过去 50 年中迅速上升，但现在已趋于平稳。摄入石棉，无论是来自 1980 年之前饮用的啤酒，还是来自职业暴露，似乎都是食管腺癌的一个合理的致病因素。如果事实确实如此，那么到 2050 年左右，其发病率应该会回落到一个较低的基线。
