Risk of occupational exposure to asbestos, silicon and arsenic on pulmonary disorders: Understanding the genetic-epigenetic interplay and future prospects

Our plain-English summary of Risk of occupational exposure to asbestos, silicon and arsenic on pulmonary disorders: Understanding the genetic-epigenetic interplay and future prospects, by P. Bhattacharjee, S. Paul, P. Bhattacharjee (Environmental Research, 2016).

The study

• Authors: P. Bhattacharjee, S. Paul, P. Bhattacharjee
• Journal: Environmental Research
• Published: 2016;147:425-34
• Type of article: Review
• Cited by: 31 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Background: Epidemiological studies suggest strong association of lung disorders with occupational exposure to asbestos, silicon and arsenic. The chronic occupational exposure primarily through inhalation results in adverse outcome on the respiratory tract which may also be fatal. Although several mechanisms have attributed towards these diseases; the molecular pathogenesis is still unknown.

Objective: In this review, we investigated the plausible molecular mechanism based on current research that may identify the genetic and epigenetic susceptibility of respiratory disorders upon such occupational exposures in humans.

Methods: We considered genetic variants and epigenetic alterations associated with pulmonary exposure hazards leading to asbestosis, silicosis and arsenicosis. Our review is stringently based on the literatures available through peer-reviewed articles mostly published in the last 10 years. Relevant search were conducted using keywords like "occupational lung disorders" along with "asbestos", "silicon" and "arsenic".

Results: Till September 2015, pubmed search yielded approximately 780 articles relating to asbestos exposure; 240 articles for silicon exposure and 60 articles for arsenic exposure. Extensive screening for genetic and epigenetic factors identified certain genes and related pathways that are important to determine the susceptibility of an individual towards such occupational exposure.

Conclusion: The link between genotype and phenotype and its association with disease susceptibility is very complex in nature due to several factors like person's environment, lifestyle and nutritional status. The epigenome is dynamic as well as reversible and can be reshaped further by certain dietary components throughout its life. In the present review, we have addressed the role of molecular pathogenesis of occupational lung diseases based on the genetic variability and epigenetic alterations and also attempted to highlight the promising aspect of dietary interventions to counter toxic outcomes upon occupational exposure to asbestos, silicon or arsenic.

Copyright © 2016 Elsevier Inc. All rights reserved.

In plain English

This article was a narrative review, not a new study. The authors reviewed published research, mostly from the previous 10 years, on genetic and epigenetic changes linked to lung disorders from workplace exposure to asbestos, silicon (discussed as crystalline silica) and arsenic. A PubMed search up to September 2015 returned about 780 articles on asbestos, 240 on silicon and 60 on arsenic. Among the findings from other studies, the review cited one linking deletion of the GSTT1 gene to a protective effect on asbestosis, and another linking the CAT-262 TT genotype to increased asbestosis risk. The authors grouped the mechanisms into four: oxidative stress, inflammation, cell cycle regulation, and DNA damage and repair. They also discussed diet as a possible way to counter toxic effects, noting that population studies and randomized trials of this were still very limited. The authors concluded that the link between genes and disease susceptibility is very complex and also depends on a person's environment, lifestyle and nutritional status. They noted that most studies examined one exposure at a time, and that little work has been done on silica-related epigenetic changes in humans.

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 peer-reviewed literature
• Who was studied: Published articles found through a PubMed search up to September 2015: about 780 on asbestos exposure, 240 on silicon exposure and 60 on arsenic exposure
• Exposure: Occupational exposure to asbestos, silicon (crystalline silica) and arsenic, and the related diseases asbestosis, silicosis and arsenicosis
• Main results:
  • The review cited a study (Franko et al., 2007) in which deletion of the GSTT1 gene showed a protective effect on the development of asbestosis
  • The review cited a study (Franko et al., 2008) in which the CAT-262 TT genotype was associated with increased risk of asbestosis
  • The review cited a study (Hiraku et al., 2014) in which 8-nitroguanine, a DNA lesion formed during inflammation, was significantly correlated with total asbestos exposure
  • The review cited a study (Christensen et al., 2009) in which genome-wide methylation profiling of mesothelioma tumors showed a trend of hypermethylation-induced gene silencing in 94% of the CpG sites studied
  • The authors identified four major cellular mechanisms disturbed by asbestos, silicon or arsenic exposure in the development of lung disorders: oxidative stress, inflammatory pathways, cell cycle regulation, and DNA damage and repair
• The authors' conclusion: The authors concluded that the link between genotype, phenotype and disease susceptibility is very complex because of factors such as a person's environment, lifestyle and nutritional status. They also attempted to highlight dietary interventions as a promising way to counter toxic outcomes of these exposures.
• Limitations the authors state:
  • Most published studies examined one toxic exposure at a time, although in real settings the compounds interact in complex ways
  • Compared with asbestos, little work has been done on epigenetic profiles in humans exposed to silica
  • Some silica findings in mice had not yet been verified in humans
  • Dietary compounds had been tested mainly in cell or animal models. Epidemiological studies and randomized trials of nutritional interventions were still very limited: the authors cited a few population-based studies and said no other recent reports were available.

Topics

Medical terms in this study, explained in our Lexicon: Occupational Exposure, Silicosis, Asbestos Exposure, Occupational Lung Disease.

Related studies

• Malignant pleural mesothelioma: newer aspects of carcinogenesis, molecular genetics, and prospects for future therapies — J.S. Donington, D.J. Mew, et al. (1995)
• Arsenic, tobacco smoke, and occupation: associations of multiple agents with lung and bladder cancer — C. Ferreccio, Y. Yuan, et al. (2013)
• Arsenic, asbestos and radon: emerging players in lung tumorigenesis — R. Hubaux, D.D. Becker-Santos, et al. (2012)
• Evidence of arsenic release promoted by disinfection by-products within drinking-water distribution systems — S.S. Andra, K.C. Makris, et al. (2014)
• Silicon: the health benefits of a metalloid — K.R. Martin (2013)
• In vitro activity of silicon carbide whiskers in comparison to other industrial fibers using four cell culture systems — N.F. Johnson, M.D. Hoover, et al. (1992)

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