Manganese and extracellular superoxide dismutase polymorphisms and risk for asbestosis

Our plain-English summary of Manganese and extracellular superoxide dismutase polymorphisms and risk for asbestosis, by A. Franko, M. Dodic-Fikfak, N. Arnerić, et al (Journal of Biomedicine & Biotechnology, 2009).

The study

• Authors: A. Franko, M. Dodic-Fikfak, N. Arnerić, V. Dolzan
• Journal: Journal of Biomedicine & Biotechnology
• Published: 2009;2009:493083
• Cited by: 8 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Manganese and extracellular superoxide dismutases (SOD2 and SOD3) are part of the enzymatic defence against reactive oxygen species, which are involved in the pathogenesis of asbestosis. This study investigates whether SOD2Ala - 9Val and SOD3 Arg213Gly genetic polymorphisms represent risk factors for asbestosis in workers exposed to asbestos. The study included 262 cases with asbestosis and 265 controls with no asbestos-related disease. Cumulative asbestos exposure was calculated for each subject. A real-time PCR assay was introduced for genotyping. Logistic regression analysis was used to assess asbestosis risk. Asbestosis was associated with the homozygous SOD2 - 9Ala/Ala genotype (OR = 1.50, 95% CI 1.01-2.24), whereas the association for the SOD3 Arg/Gly genotype was not significant (OR = 1.63, 95% CI 0.62-4.27). The finding that the SOD2 - 9Ala/Ala genotype increases the risk for asbestosis indicates that, in addition to asbestos exposure, genetic factors may also have a significant influence on the development of asbestosis.

In plain English

This nested case-control study asked whether variants of two antioxidant enzyme genes, SOD2 and SOD3, were linked to asbestosis. It included 262 people with asbestosis and 265 controls with no asbestos-related disease, all of whom had worked at the Salonit Anhovo asbestos cement plant in Anhovo, Slovenia. Each person's cumulative asbestos exposure came from an earlier study. The SOD2 Ala/Ala genotype was found in 29.0% of cases and 21.4% of controls. Compared with the other SOD2 genotypes combined, it was associated with asbestosis (odds ratio 1.50, 95% CI 1.01 to 2.24). After adjustment for cumulative exposure, this odds ratio was 1.48 (95% CI 0.96 to 2.28), which the authors described as not changing considerably. The SOD3 Arg/Gly genotype was more common in cases (4.3%) than in controls (2.7%), but its association with asbestosis was not statistically significant (odds ratio 1.63, 95% CI 0.62 to 4.27). The authors attributed this to a lack of statistical power. The authors concluded that the SOD2 Ala/Ala genotype increases asbestosis risk and that genetic factors may influence the development of asbestosis.

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 logistic regression)
• Who was studied: 262 workers with asbestosis (cases) and 265 workers with no asbestos-related disease (controls), matched on gender and date of birth. They were drawn from a cohort of 2 080 workers presented at the Slovenian State Board for the Recognition of Occupational Asbestos Diseases from 1 January 1998 to 31 December 2003. All had worked at the Salonit Anhovo asbestos cement manufacturing plant in Anhovo, Slovenia.
• Exposure: Occupational asbestos exposure at an asbestos cement plant, expressed as cumulative asbestos exposure (fibres/cm3-years) taken from a previous study; fiber types are not specified in this article. Mean cumulative exposure was 37.67 in cases and 11.23 in controls. The genetic factors studied were the SOD2 Ala -9Val and SOD3 Arg213Gly polymorphisms.
• Main results:
  • The SOD2 Ala/Ala genotype was observed in 29.0% of cases and 21.4% of controls.
  • Odds ratio of asbestosis for SOD2 Ala/Ala versus combined Ala/Val and Val/Val genotypes: 1.50 (95% CI 1.01–2.24).
  • The SOD2 Ala/Ala odds ratio did not change considerably after adjustment for gender, age, smoking and cumulative exposure; adjusted for cumulative exposure it was 1.48 (95% CI 0.96–2.28).
  • SOD3 Arg/Gly genotype in 4.3% of cases and 2.7% of controls; odds ratio of asbestosis versus Arg/Arg 1.63 (95% CI 0.62–4.27), not significant; adjusted for cumulative exposure 2.07 (95% CI 0.72–5.94).
  • No synergistic effect was found between the SOD3 Arg/Gly genotype and cumulative asbestos exposure (OR = 0.61, P = .456).
  • Logarithmically transformed cumulative asbestos exposure gave an odds ratio of asbestosis of 3.21 (95% CI 2.43–4.23); ever/never smoking was not associated with asbestosis (OR = 0.98, 95% CI 0.69–1.39).
• The authors' conclusion: The authors concluded that the SOD2 Ala/Ala genotype increases the risk of asbestosis and that, in addition to asbestos exposure, genetic factors may influence the development of asbestosis.
• Limitations the authors state:
  • The study lacked statistical power to detect a significant difference for the rare SOD3 Arg/Gly genotype.

Topics

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

Medical terms in this study, explained in our Lexicon: Superoxide, Reactive Oxygen Species (ROS), Asbestos Exposure.

Related studies

• Asbestos exposure, manganese superoxide dismutase (MnSOD) genotype, and lung cancer risk — L.I. Wang, D. Neuberg, et al. (2004)
• Polymorphisms of glutathione-S-transferase M1 and manganese superoxide dismutase are associated with the risk of malignant pleural mesothelioma — S. Landi, F. Gemignani, et al. (2007)
• Manganese superoxide dismutase genotypes and asbestos-associated pulmonary disorders — A. Hirvonen, J. Tuimala, et al. (2002)
• Extracellular superoxide dismutase inhibits inflammation by preventing oxidative fragmentation of hyaluronan — F. Gao, J.R. Koenitzer, et al. (2008)
• Manganese superoxide dismutase in healthy human pleural mesothelium and in malignant pleural mesothelioma — K. Kahlos, S. Anttila, et al. (1998)
• Manganese superoxide dismutase in human pleural mesothelioma cell lines — V.L. Kinnula, P. Pietarinen-Runtti, et al. (1996)

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