Manganese superoxide dismutase genotypes and asbestos-associated pulmonary disorders

Our plain-English summary of Manganese superoxide dismutase genotypes and asbestos-associated pulmonary disorders, by A. Hirvonen, J. Tuimala, T. Ollikainen, et al (Cancer Letters, 2002).

The study

• Authors: A. Hirvonen, J. Tuimala, T. Ollikainen, K. Linnainmaa, V. Kinnula
• Journal: Cancer Letters
• Published: 2002;178(1):71-4
• Cited by: 25 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Manganese superoxide dismutase (MnSOD) activity is highly elevated in the biopsies of human asbestos-associated malignant mesothelioma. We therefore examined if polymorphism in the mitochondrial targeting sequence of the MnSOD gene modified individual susceptibility to this malignancy or related asbestos-associated pulmonary disorders. The study population consisted of 124 male Finnish asbestos insulators who were all classified as having been exposed to high levels of asbestos; 63 of the workers had no pulmonary disorders and 61 either had malignant mesothelioma or the non-malignant pulmonary disorders asbestosis and/or pleural plaques. No significant associations were found between the MnSOD genotypes and these ill-health. This study therefore suggest no major modifying role for the MnSOD polymorphism in development of asbestos-associated pulmonary disorders.

In plain English

This Finnish study asked whether a common inherited variation in the gene for manganese superoxide dismutase (MnSOD), an antioxidant enzyme, changed workers' susceptibility to asbestos-related disease. The authors studied 124 male asbestos insulators, all classified as highly exposed. They were drawn from about 1500 construction workers screened at the Finnish Institute of Occupational Health. Of these, 63 had no disorder visible on chest X-ray, 20 had malignant mesothelioma and 41 had asbestosis and/or pleural plaques. Gene types were determined from lymphocyte DNA. Odds ratios were adjusted for age, years of asbestos exposure and smoking. For mesothelioma, workers carrying at least one V version of the gene had an odds ratio of 1.5 (95% CI 0.4–6.7) compared with the AA type, which the authors called far from statistical significance. For asbestosis and/or pleural plaques the odds ratio was 0.6 (95% CI 0.2–1.5), also far from significance. The authors concluded that the variation has no major modifying role. They noted that the reduced sample size lowered statistical power and said the findings need confirming in future studies.

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: Case-control comparison of MnSOD gene types (genotypes) among highly exposed asbestos insulators, using adjusted odds ratios
• Who was studied: 124 male Finnish asbestos insulators selected from about 1500 construction workers in a health screening survey at the Finnish Institute of Occupational Health. 63 had no pulmonary disorders on chest X-ray (controls). 61 were cases: 20 with malignant mesothelioma (admitted to Helsinki University Central Hospital 1985–1993) and 41 with asbestosis and/or pleural plaques.
• Exposure: Work as asbestos insulators, all classified as high asbestos exposure; fiber types not specified. Years of known exposure: 1–10 years (n = 24), 11–20 (n = 18), 21–30 (n = 49), more than 30 (n = 32), not available for one subject. The genetic factor studied was the MnSOD Val/Ala gene variation.
• Main results:
  • All cases (malignant and non-malignant) compared with controls: no clear differences in genotype distributions (odds ratio for V-allele-containing genotypes 0.7, 95% CI 0.3–1.9)
  • Malignant mesothelioma (20 cases): odds ratio 1.5 (95% CI 0.4–6.7) for V-allele-containing genotypes compared with AA; the authors described this as far from statistical significance
  • Malignant mesothelioma by genotype: odds ratio 1.4 (95% CI 0.3–6.3) for AV and 2.0 (95% CI 0.3–11.9) for VV; the trend test showed no significant association (P for trend 0.91)
  • Asbestosis and/or pleural plaques (41 cases): odds ratio 0.6 (95% CI 0.2–1.5) for V-allele-containing genotypes, far from statistical significance
• The authors' conclusion: The authors concluded that the MnSOD polymorphism has no major modifying role in individual risk of developing asbestos-associated pulmonary disorders, and that these first findings remain to be confirmed in future studies.
• Limitations the authors state:
  • Restricting the study to highly exposed insulators reduced the sample size and lowered statistical power
  • There were no other reports on this topic, so the findings need confirmation

Topics

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

Medical terms in this study, explained in our Lexicon: Superoxide, Malignant Mesothelioma, Insulator, Pleural Plaques.

Related studies

• Asbestos exposure, manganese superoxide dismutase (MnSOD) genotype, and lung cancer risk — L.I. Wang, D. Neuberg, et al. (2004)
• Manganese and extracellular superoxide dismutase polymorphisms and risk for asbestosis — A. Franko, M. Dodic-Fikfak, et al. (2009)
• Ultrastructural and chromosomal studies on manganese superoxide dismutase in malignant mesothelioma — V.L. Kinnula, T. Torkkeli, 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 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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