Blood superoxide dismutase and plasma malondialdehyde among workers exposed to asbestos

Our plain-English summary of Blood superoxide dismutase and plasma malondialdehyde among workers exposed to asbestos, by A.A. Kamal, M. el Khafif, S. Koraah, et al (American Journal of Industrial Medicine, 1992).

The study

• Authors: A.A. Kamal, M. el Khafif, S. Koraah, A. Massoud, J.F. Caillard
• Journal: American Journal of Industrial Medicine
• Published: 1992;21(3):353-61
• Cited by: 14 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Blood superoxide dismutase (SOD) and plasma malondialdehyde (MDA) (an indicator of lipid peroxidation [LPO]) were determined in 97 randomly selected asbestos exposed workers (age range: 25-60 years, mean duration of exposures 19.8 +/- 8.3 years) and in 42 healthy male controls. MDA, SOD, and MDA/SOD ratio in asbestos exposed workers were significantly higher than in controls. Among both the controls and exposed workers neither age nor smoking was related to SOD or MDA levels. SOD was significantly positively correlated with MDA among the exposed workers. Such correlation was not observed among the controls. SOD but not MDA was significantly positively correlated with the duration of exposure to asbestos. Mean levels of SOD or MDA in exposed workers with radiographic signs of lung fibrosis or pleural thickening did not differ significantly from those without such signs. The results confirm the possible involvement of LPO and development of anti-oxidant mechanism(s) of prolonged exposure to asbestos in humans. However, SOD seems not to be the essential anti-asbestos-induced LPO. Relation between these factors and lung fibrosis is still unclear.

In plain English

This study compared blood markers of oxidative damage in 97 randomly selected asbestos-cement pipe workers near Cairo, Egypt, and 42 unexposed construction workers. The factory used 70% chrysotile and 30% crocidolite, and the exposed workers averaged 19.8 years of exposure. The authors measured plasma malondialdehyde (MDA) and blood superoxide dismutase (SOD). MDA is a sign of oxidative damage to fats, called lipid peroxidation. SOD is a protective enzyme. Average MDA, SOD and the MDA-to-SOD ratio were significantly higher in the exposed workers than in the controls. Age and smoking were not related to either marker in either group. Among exposed workers, SOD rose with MDA and, more weakly, with years of exposure. MDA did not rise with years of exposure. Levels did not differ significantly between exposed workers with and without X-ray signs of lung fibrosis or pleural thickening. The authors concluded that the results add evidence for a role of lipid peroxidation in asbestos exposure. They also concluded that SOD does not seem to be the main defense against it, and that the role of lipid peroxidation in lung fibrosis still needs to be determined.

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: Comparison of blood measurements in asbestos-exposed workers and an unexposed control group, measured at one point in time (cross-sectional)
• Who was studied: 97 randomly selected male workers from the Segwart Company asbestos-cement pipe factory in Shobra El Khema, a suburb of Cairo, Egypt, aged 25-60. The comparison group was 42 manual construction workers specializing in reinforced concrete, of similar age and physical activity, with no history of asbestos exposure. Chest X-rays used were from the 1989 periodic medical examination.
• Exposure: Work making asbestos-cement pipes: opening asbestos bales by hand, feeding the mixing machine, transporting and cutting pipes. The asbestos was 70% chrysotile (white asbestos) and 30% crocidolite (blue asbestos). The mean duration of exposure was 19.8 years. Airborne levels in the factory, as reported in a separate earlier study, ranged from 3-20 fibers per cc.
• Main results:
  • Average plasma MDA and blood SOD were significantly higher in the asbestos-exposed workers than in the controls.
  • The mean MDA-to-SOD ratio was 12.953 (SD 7.576) in exposed workers, compared with 10.725 (SD 5.136) in controls, which was significantly higher (p less than 0.05).
  • Among exposed workers, SOD was significantly positively correlated with plasma MDA (r = 0.321, p less than 0.0001) and with duration of exposure (r = 0.198, p less than 0.05). In a multiple regression analysis, SOD was related less to duration of exposure than to MDA.
  • Among controls, there was no significant correlation between MDA and SOD.
  • Among exposed workers, duration of exposure was not correlated with MDA.
  • In both exposed workers and controls, MDA and SOD did not differ significantly between smokers and non-smokers. Age was not significantly correlated with either marker in either group.
  • MDA and SOD did not differ significantly between exposed workers with and without X-ray signs of lung fibrosis (26 with, 71 without, per Figure 3). The same was true for pleural thickening, shown as pleural plaques (33 with, 64 without).
• The authors' conclusion: The authors concluded that the higher MDA and SOD in asbestos-exposed workers provide further evidence for a role of lipid peroxidation in asbestos exposure. They concluded that SOD does not seem to be a principal defense against it, that other antioxidant factors should be investigated, and that the role of lipid peroxidation in asbestos-related lung fibrosis needs to be determined.
• Limitations the authors state:
  • The authors noted that ordinary chest X-rays show only about 25% of each lung unobscured by bone shadows. The absence of X-ray signs therefore does not rule out fibrosis.

Topics

Medical terms in this study, explained in our Lexicon: Superoxide, Fibrosis, Pleural Thickening.

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