Asbestos-Induced Gastrointestinal Cancer: An Update

Our plain-English summary of Asbestos-Induced Gastrointestinal Cancer: An Update, by S.J. Kim, D. Williams, P. Cheresh, et al (Journal of Gastrointestinal & Digestive System, 2013).

The study

• Authors: S.J. Kim, D. Williams, P. Cheresh, D.W. Kamp
• Journal: Journal of Gastrointestinal & Digestive System
• Published: 2013;3(3)
• Cited by: 15 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Asbestos-related diseases, such as malignancies and asbestosis, remain a significant occupational and public health concern. Asbestos is still widely used in many developing countries despite being a recognized carcinogen that has been banned over 50 countries. The prevalence and mortality from asbestos-related diseases continue to pose challenges worldwide. Many countries are now experiencing an epidemic of asbestos-related disease that is the legacy of occupational exposure during the 20th century because of the long latency period (up to 40 years) between initial asbestos exposure and exhibition of disease. However, the gastrointestinal (GI) cancers resulting from asbestos exposure are not as clearly defined. In this review, we summarize some of the recent epidemiology of asbestos-related diseases and then focus on the evidence implicating asbestos in causing GI malignancies. We also briefly review the important new pathogenic information that has emerged over the past several years that may account for asbestos-related gastrointestinal cancers. All types of asbestos fibers have been implicated in the mortality and morbidity from GI malignancies but the collective evidence to date is mixed. Although the molecular basis of GI cancers arising from asbestos exposure is unclear, there have been significant advances in our understanding of mesothelioma and asbestosis that may contribute to the pathophysiology underlying asbestos-induced GI cancers. The emerging new evidence into the pathogenesis of asbestos toxicity is providing insights into the molecular basis for developing novel therapeutic strategies for asbestos-related diseases in future management.

In plain English

This article was a review, not a new study. The authors summarized published epidemiological, animal and laboratory research on whether asbestos causes cancers of the gastrointestinal (GI) tract. A table, adapted from an earlier review, counted published studies with positive or negative findings by fiber type and by category: occupational exposure, ingested water, animal studies, and non-occupational or environmental exposure. The authors reported that all asbestos fiber types had been implicated but that the evidence was mixed. They judged the link strongest for stomach cancer, especially after occupational exposure, though some studies disagreed. They noted that several drinking-water studies suggested no increase in GI cancers. Animal findings were also mixed: rats fed chrysotile showed increased DNA synthesis in the intestine, while lifetime amosite diets in rats and hamsters produced no toxic or neoplastic lesions in the GI tract. The authors noted that IARC had called the stomach cancer evidence limited. They concluded that asbestos appears to minimally increase stomach cancer risk, and possibly other cancers they listed, that the risk appears small, and that the mechanisms need further study.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Narrative review of epidemiological, animal (in vivo) and laboratory (in vitro) studies
• Who was studied: Published studies on asbestos and GI cancers, summarized in a table adapted from an earlier review by Bunderson-Schelvan; the authors state that over 50 publications have examined the question
• Exposure: All asbestos fiber types, as studied through occupational exposure, ingested drinking water, animal feeding experiments and non-occupational exposure
• Main results:
  • Across the studies reviewed, the strongest association with GI cancers was for stomach cancer, but some studies disagreed
  • Stomach cancer after occupational exposure was described as the best validated link
  • Several reviewed reports suggested that drinking-water exposure may not increase GI cancers, including stomach cancer
  • Earlier reviews and meta-analyses had not clarified the relationship between asbestos and GI cancer
  • In a reviewed animal study, increased DNA synthesis was found in the small intestine and colon of rats that ingested chrysotile (5 mg/kg for 2 weeks)
  • In other reviewed animal studies, rats and hamsters fed amosite in their diet for life showed no toxic or neoplastic lesions in the GI tract or mesothelium
  • The authors cited IARC's conclusion that the overall evidence linking asbestos to stomach cancer is limited
• The authors' conclusion: The authors concluded that all forms of asbestos exposure appear to minimally increase the risk of stomach cancer, and possibly other cancers they listed (larynx, esophagus, intestines, colorectal). They added that these effects appear much less robust than the lung effects and that the risk appears small.
• Limitations the authors state:
  • The authors stated that cellular-level studies of how asbestos might cause GI cancer are lacking
  • The authors stated that how asbestos fibers are transported and retained in the GI tract has not been well investigated
  • The authors stated that discrepant drinking-water results may reflect varying asbestos amounts and composition in water, and methodologic differences

Topics

Medical terms in this study, explained in our Lexicon: Occupational Exposure, Latency, Asbestos Exposure, Epidemiology, Mesothelioma.

Related studies

• Asbestos-induced lung diseases: an update — D.W. Kamp (2009)
• Mitochondria-targeted Ogg1 and aconitase-2 prevent oxidant-induced mitochondrial DNA damage in alveolar epithelial cells — S.J. Kim, P. Cheresh, et al. (2014)
• Asbestos-induced alveolar epithelial cell apoptosis. The role of endoplasmic reticulum stress response — D.W. Kamp, G. Liu, et al. (2013)
• Malignant mesothelioma as an oxidative stress-induced cancer: An update — S.H. Chew, S. Toyokuni (2015)
• Asbestos-induced pulmonary fibrosis is augmented in 8-oxoguanine DNA glycosylase knockout mice — P. Cheresh, L. Morales-Nebreda, et al. (2015)
• SIRT3 Overexpression Ameliorates Asbestos-Induced Pulmonary Fibrosis, mt-DNA Damage, and Lung Fibrogenic Monocyte Recruitment — P. Cheresh, S.J. Kim, et al. (2021)

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