Arsenic, asbestos and radon: emerging players in lung tumorigenesis

Our plain-English summary of Arsenic, asbestos and radon: emerging players in lung tumorigenesis, by R. Hubaux, D.D. Becker-Santos, K.S. Enfield, et al (Environmental Health, 2012).

The study

• Authors: R. Hubaux, D.D. Becker-Santos, K.S. Enfield, S. Lam, W.L. Lam, V.D. Martinez
• Journal: Environmental Health
• Published: 2012;11:89
• Type of article: Review
• Cited by: 67 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

The cause of lung cancer is generally attributed to tobacco smoking. However lung cancer in never smokers accounts for 10 to 25% of all lung cancer cases. Arsenic, asbestos and radon are three prominent non-tobacco carcinogens strongly associated with lung cancer. Exposure to these agents can lead to genetic and epigenetic alterations in tumor genomes, impacting genes and pathways involved in lung cancer development. Moreover, these agents not only exhibit unique mechanisms in causing genomic alterations, but also exert deleterious effects through common mechanisms, such as oxidative stress, commonly associated with carcinogenesis. This article provides a comprehensive review of arsenic, asbestos, and radon induced molecular mechanisms responsible for the generation of genetic and epigenetic alterations in lung cancer. A better understanding of the mode of action of these carcinogens will facilitate the prevention and management of lung cancer related to such environmental hazards.

In plain English

This article was a narrative review, not an original study. The authors gathered published human, animal and cell-line research on how three non-tobacco carcinogens, arsenic, asbestos and radon, may cause genetic and epigenetic changes leading to lung cancer. For asbestos, the review cited earlier work linking chrysotile, amosite, anthophyllite and mixed fibers containing crocidolite to a high incidence of lung cancer. One cited study reported a relative risk of lung cancer more than 3 times higher in exposed than non-exposed people after controlling for smoking. The review described proposed mechanisms: reactive oxygen species (higher with iron-rich fibers such as crocidolite and amosite), chronic inflammation, and interference with cell division. It also listed reported gene changes, such as deletions at the P16/CDKN2A locus. The authors noted that only a few studies have directly tied such changes to a specific carcinogen, and that KRAS and TP53 mutations have not been conclusively linked to asbestos. The authors concluded that each agent may cause its own set of changes, which could help in developing diagnosis and treatment.

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 published literature on molecular mechanisms of arsenic-, asbestos- and radon-induced lung cancer; no original data
• Who was studied: No study population of its own; the authors collected published human, animal (rat, mouse) and cell-line studies. Some cited studies included smokers only. No search method or number of studies reviewed is given.
• Exposure: Arsenic (mainly via drinking water), asbestos (chrysotile, amosite, anthophyllite and mixed fibers containing crocidolite) and radon (radioactive gas and its decay products)
• Main results:
  • The review cited an earlier study (the Netherlands cohort study) reporting that the relative risk of lung cancer was more than 3 times higher for asbestos-exposed than non-exposed individuals after controlling for smoking
  • The review cited earlier sources stating that asbestos fibers, except crocidolite, cause at least twice as many lung cancer deaths as asbestos-related mesothelioma, and that the two cancers combined cause nearly 10,000 deaths per year in the United States
  • According to the cited literature, asbestos fibers with high iron content, such as crocidolite and amosite, can generate higher levels of reactive oxygen species
  • A cited study found a higher frequency of P16/CDKN2A deletions in asbestos-exposed non-small cell lung cancer cases than in unexposed cases
  • A cited study identified an asbestos-associated microRNA pattern in lung cancer (the authors' table marks this study as smokers only)
  • A cited cell study detected changes at chromosomes 5, 8 and 19 in human bronchial epithelial cells transformed by chrysotile asbestos
• The authors' conclusion: The authors concluded that, while sharing a few carcinogenic mechanisms, each agent may induce specific sets of alterations that might affect tumor behavior and offer opportunities for diagnosis and treatment
• Limitations the authors state:
  • The authors stated that only a few studies have directly linked specific genetic alterations with specific environmental carcinogens
  • The authors stated that KRAS and TP53 mutations have not been conclusively associated with asbestos exposure
  • The authors stated that direct asbestos mutagenicity, as a proposed mode of action, requires further study

Topics

The National Library of Medicine indexes this study under subjects our site covers: Lung cancer.

Medical terms in this study, explained in our Lexicon: Tumorigenesis, Lung Cancer, Oxidative Stress, Carcinogenesis.

Related studies

• Arsenic, tobacco smoke, and occupation: associations of multiple agents with lung and bladder cancer — C. Ferreccio, Y. Yuan, et al. (2013)
• Risk of occupational exposure to asbestos, silicon and arsenic on pulmonary disorders: Understanding the genetic-epigenetic interplay and future prospects — P. Bhattacharjee, S. Paul, et al. (2016)
• Evidence of arsenic release promoted by disinfection by-products within drinking-water distribution systems — S.S. Andra, K.C. Makris, et al. (2014)
• Occupation and lung cancer in nonsmokers — J.S. Neuberger, R.W. Field (2003)
• Case-control study on lung cancer and residential radon in western Germany — L. Kreienbrock, M. Kreuzer, et al. (2001)
• Residential radon exposure and lung cancer--an epidemiological study of Norwegian municipalities — K. Magnus, A. Engeland, et al. (1994)

Browse more research in Environmental Health, or return to medical research.