Asbestosis and catalase genetic polymorphism

Our plain-English summary of Asbestosis and catalase genetic polymorphism, by A. Franko, V. Dolzan, N. Arnerić, et al (Arhiv Za Higijenu Rada I Toksikologiju, 2008).

The study

• Authors: A. Franko, V. Dolzan, N. Arnerić, M. Dodic-Fikfak
• Journal: Arhiv Za Higijenu Rada I Toksikologiju
• Published: 2008;59(4):233-40
• Cited by: 12 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Catalase (CAT) is part of the enzymatic defense system against reactive oxygen species (ROS), known to be involved in the pathogenesis of asbestosis. This study investigates whether CAT -262 C>T genetic polymorphism influences the risk of asbestosis in workers occupationally exposed to asbestos.The nested case-control study included 262 cases with asbestosis and 265 controls with no asbestos-related disease. Data on cumulative asbestos exposure and smoking were available. A real-time PCR assay was introduced for genotyping CAT -262 C>T promoter polymorphism.A slightly elevated risk of asbestosis was observed in subjects with the CAT -262 TT genotype compared to others (OR=1.36, CI 0.70-2.62). This risk did not change substantially after adjustment by sex, age, and smoking, but the involvement of cumulative asbestos exposure changed the OR to 1.91 (CI 0.93-3.91). These findings indicate that the CAT -262 TT genotype may be slightly associated with an increased risk of asbestosis. No synergistic effect was found between cumulative asbestos exposure and the CAT -262 TT genotype, but cumulative asbestos exposure acted as a confounder. These results are an important contribution to understanding the interactions between genetic and environmental factors that may modify the risk of asbestosis.

In plain English

This nested case-control study looked at whether a common variant in the catalase gene was linked to asbestosis. Catalase is an enzyme that breaks down hydrogen peroxide. The workers had all been employed at the Salonit Anhovo asbestos-cement plant in Slovenia. They came from 2,080 asbestos-exposed workers seen by a board for occupational asbestos diseases from 1998 to 2003. The study compared 262 workers with asbestosis and 265 with no asbestos-related disease. The TT form of the variant (CAT -262 TT) was found in 22 of 256 genotyped cases and 17 of 262 genotyped controls. Workers with TT had an odds ratio for asbestosis of 1.36 (CI 0.70-2.62) compared with the other genotypes. After accounting for cumulative asbestos exposure, it was 1.91 (CI 0.93-3.91). The authors called these results statistically insignificant. Cumulative asbestos exposure was associated with asbestosis (OR 3.21, CI 2.43-4.23), while the authors observed no association with ever versus never smoking (OR 0.98, CI 0.69-1.39). No combined (synergistic) effect of genotype and exposure was found. The authors concluded that the TT genotype may be associated with an increased risk of asbestosis and that larger studies are needed.

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: Nested case-control study (genetic association study using real-time PCR genotyping)
• Who was studied: 262 workers with asbestosis (cases) and 265 workers with no asbestos-related disease (controls). They were drawn from a cohort of 2,080 asbestos-exposed workers presented at the Slovenian Board for the Recognition of Occupational Asbestos Diseases between 1 January 1998 and 31 December 2003. Of 356 cases and 356 controls originally selected, some refused, died, or developed a malignant disease. Controls were matched to cases by age and sex. All had worked at the Salonit Anhovo asbestos-cement plant. Diagnoses followed the Helsinki Criteria and the American Thoracic Society proposal.
• Exposure: Occupational asbestos exposure at an asbestos-cement manufacturing plant (cement production, asbestos-cement pipes, corrugated sheets). Exposure was measured as cumulative asbestos exposure, with data taken from a previous study. Mean cumulative exposure was 37.67 fibres/cm3-years (SD 86.43) in cases and 11.23 fibres/cm3-years (SD 23.47) in controls. This article does not name the fiber types. The genetic factor studied was the CAT -262 C>T promoter polymorphism.
• Main results:
  • The CAT -262 TT genotype was found in 22 cases (8.6% of 256 genotyped) and 17 controls (6.5% of 262 genotyped). CT was found in 107 cases and 105 controls, and CC in 127 cases and 140 controls.
  • Unadjusted odds ratio of asbestosis for the TT genotype compared with the CT and CC genotypes combined: 1.36 (CI 0.70-2.62).
  • Adjusting for sex, age, or smoking did not change the TT odds ratio substantially (1.34, 1.31, 1.37). Adjusting for cumulative asbestos exposure changed it to 1.91 (CI 0.93-3.91), which the authors interpreted as a confounding effect.
  • Other genotype comparisons gave these odds ratios: TT versus CT, 1.27 (CI 0.64-2.53); TT versus CC, 1.43 (CI 0.73-2.81); CT versus CC, 1.12 (CI 0.78-1.61).
  • Cumulative asbestos exposure was positively associated with asbestosis (OR 3.21, CI 2.43-4.23).
  • The authors observed no association between asbestosis and smoking assessed as ever versus never (OR 0.98, CI 0.69-1.39).
  • A test for a combined (synergistic) effect of the TT genotype and cumulative asbestos exposure gave an OR of 1.76 with a p value of 0.369, which the authors interpreted as no synergistic effect.
• The authors' conclusion: The authors concluded that the CAT -262 TT genotype may be associated with an increased risk of asbestosis. They said further studies with more subjects, including studies of the link between CAT genotype and catalase activity, are needed to clarify this.
• Limitations the authors state:
  • The authors acknowledged that the results were not statistically significant.
  • About 26% of the originally selected cases and controls were excluded because they died, developed cancer, or declined to take part. The authors stated that participants and excluded subjects did not differ in cumulative asbestos exposure or cancer diagnosis.
  • The authors noted that this and other enzyme polymorphisms may have a combined effect that has yet to be shown.

Topics

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

Medical terms in this study, explained in our Lexicon: Reactive Oxygen Species (ROS), nested case-control study, Asbestos Exposure, Synergistic Effect.

Related studies

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• Inducible nitric oxide synthase genetic polymorphism and risk of asbestosis — A. Franko, M. Dodič-Fikfak, et al. (2011)
• Glutathione S-transferases GSTM1 and GSTT1 polymorphisms and asbestosis — A. Franko, M. Dodic-Fikfak, et al. (2007)
• Manganese and extracellular superoxide dismutase polymorphisms and risk for asbestosis — A. Franko, M. Dodic-Fikfak, et al. (2009)
• Inhibition of lung injury, inflammation, and interstitial pulmonary fibrosis by polyethylene glycol-conjugated catalase in a rapid inhalation model of asbestosis — B.T. Mossman, J.P. Marsh, et al. (1990)
• Polymorphisms in oxidative stress-related genes are not associated with prostate cancer risk in heavy smokers — J.Y. Choi, M.L. Neuhouser, et al. (2007)

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