Plasma lipid peroxides among workers exposed to silica or asbestos dusts

Our plain-English summary of Plasma lipid peroxides among workers exposed to silica or asbestos dusts, by A.A. Kamal, A. Gomaa, M. el Khafif, et al (Environmental Research, 1989).

The study

• Authors: A.A. Kamal, A. Gomaa, M. el Khafif, A.S. Hammad
• Journal: Environmental Research
• Published: 1989;49(2):173-80
• Cited by: 87 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Plasma malondialdehyde (MDA) (an indicator of lipid peroxidation) was determined in random samples of workers (age range 25-60 years) exposed to silica dust (n = 31, mean exposure duration 21.3 +/- 8.3 years) or asbestos dust (n = 59, mean exposure duration 15.6 +/- 4.5 years) and in 52 age-matched healthy male controls. MDA levels of both exposed groups were significantly higher than that of the controls and were significantly higher among workers exposed to asbestos than among those exposed to silica dusts. Neither age nor smoking was related to MDA levels among both controls and exposed workers; among the latter group MDA was not significantly correlated with duration of exposure. Mean MDA levels of exposed workers with radiographic signs of lung fibrosis or pleural thickening and of those without such signs were not significantly different, except in the case of asbestos-exposed workers where it was significantly less than that of those without such signs. Differences between mean durations of dust exposure of workers with radiographic signs of lung fibrosis and those without such signs were statistically insignificant. The results suggest the possible involvement of lipid peroxidation on exposure to silica or asbestos dusts in humans and possible development of antioxidant mechanism(s) on prolonged dust exposure and support the opinion that development of pneumoconiosis depends on susceptibility factor(s).

In plain English

This study, done in Egypt from January to March 1988, measured plasma malondialdehyde (MDA), a marker of a kind of oxidative damage called lipid peroxidation. Three groups were tested: 31 randomly selected workers exposed to silica dust at limestone quarries in Suez, 59 workers exposed to asbestos dust at a cement asbestos pipe company near Cairo, and 52 construction workers never exposed to either dust. The article does not say which type of asbestos these workers were exposed to. Average MDA was significantly higher in both exposed groups than in controls, and significantly higher in asbestos-exposed than silica-exposed workers. MDA did not differ significantly between smokers and nonsmokers and was not significantly correlated with age or years of exposure. Among asbestos workers, those with chest X-ray signs of lung fibrosis had significantly lower MDA than those without (11.03 versus 12.90 nmoles/ml), though still significantly higher than controls. In both exposed groups, years of exposure did not differ significantly between workers with and without fibrosis signs. The authors concluded that lipid peroxidation may be implicated in the effects of silica or asbestos dust exposure.

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: Cross-sectional comparison of dust-exposed workers with unexposed controls, using blood tests and existing chest X-rays
• Who was studied: 31 silica-exposed workers from limestone quarries in Suez and 59 asbestos-exposed workers from a cement asbestos pipe company in Shobra El Khema (a suburb of Cairo), Egypt, plus 52 construction-worker controls. Ages ranged from 25 to 60. The study ran January to March 1988.
• Exposure: Silica dust (limestone quarrying) and asbestos dust (cement asbestos pipe manufacture). The article does not state which type of asbestos fiber these workers were exposed to. In the Results, mean exposure duration was 21.25 years (SD 4.56) for silica workers and 15.64 years (SD 8.26) for asbestos workers. No dust measurements were reported.
• Main results:
  • Mean plasma MDA was significantly higher in both the silica-exposed and the asbestos-exposed workers than in the controls.
  • Mean plasma MDA of asbestos-exposed workers was significantly higher than that of silica-exposed workers.
  • In all three groups, MDA did not differ significantly between smokers and nonsmokers (P greater than 0.05) and was not significantly correlated with age.
  • Among asbestos-exposed workers, those with radiographic signs of lung fibrosis (n = 38) had significantly lower MDA than those without (n = 21 in Table 2): 11.03 (SD 2.9) versus 12.90 (SD 2.0) nmoles/ml, t = 2.236, P less than 0.05. The fibrosis group was still significantly higher than the controls (t = 2.833, P less than 0.01).
  • Among silica-exposed workers, MDA did not differ significantly between those with radiographic signs of lung fibrosis (10.7, SD 1.38) and those without (10.05, SD 1.94), t = 1.08.
  • Among asbestos-exposed workers, MDA was lower in those with radiographic signs of pleural thickening (n = 36, 11.11, SD 2.97) than in those without (n = 23, 12.41, SD 2.91), t = 1.68. Pleural thickening was not found among silica workers.
  • MDA was not significantly correlated with duration of exposure in silica workers (r = 0.053) or asbestos workers (r = 0.201).
  • Among asbestos-exposed workers, mean exposure duration did not differ significantly between those with radiographic signs of lung fibrosis (15.07 years) and those without (15.9 years), t = 0.804. The same was true for silica workers (t = 0.96).
• The authors' conclusion: The authors concluded that lipid peroxidation may be implicated in the consequences of exposure to silica or asbestos dusts in humans. They suggested that antioxidant defenses may develop with prolonged exposure, and that developing asbestosis may depend on susceptibility factors rather than on exposure duration.
• Limitations the authors state:
  • The authors stated that the higher MDA rise in asbestos-exposed than in silica-exposed workers is difficult to explain because exposure could not be standardized between the two groups.

Topics

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

Related studies

• Interrelationship between hemolysis and lipid peroxidation of human erythrocytes induced by silicic acid and silicate dusts — S.V. Singh, Q. Rahman (1987)
• Respiratory impairments due to dust exposure: a comparative study among workers exposed to silica, asbestos, and coalmine dust — X. Wang, E. Yano, et al. (1997)
• Respiratory symptoms and functional status in workers exposed to silica, asbestos, and coal mine dusts — X.R. Wang, D.C. Christiani (2000)
• Reduced diffusing capacity as an isolated finding in asbestos- and silica-exposed workers — J.G. Garcia, D.E. Griffith, et al. (1990)
• An update on the detoxification processes for silica particles and asbestos fibers: successess and limitations — M. Gulumian (2005)
• Mortality from lung cancer and respiratory disease among pottery workers exposed to silica and talc — T.L. Thomas, P.A. Stewart (1987)

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