Biological effects of chrysolite after SO2 sorption. iii. effects on the biochemical components of alveolar washing

Our plain-English summary of Biological effects of chrysolite after SO2 sorption. iii. effects on the biochemical components of alveolar washing, by A. Oblin, J.M. Warnet, M.C. Jaurand, et al (British Journal of Experimental Pathology, 1978).

The study

• Authors: A. Oblin, J.M. Warnet, M.C. Jaurand, J. Bignon, J.R. Claude
• Journal: British Journal of Experimental Pathology
• Published: 1978;59(1):32-7
• Cited by: 4 articles, as counted by NIH iCite
• Read it: PubMed · Free full text

Abstract

The short-term effects of chrysotile asbestos before and after SO2 sorption are studied in the rabbit after intratracheal injection of low doses of these pollutants. Chrysotile, as well as SO2-chrysotile, induces an increase in the unsaturated fatty acid content of lung surfactant, which is similar to that observed in the respiratory distress syndrome of the newborn, and an increase in the protein level of pulmonary washings which may be explained by an increase of the permeability of the blood-air barrier. These soluble proteins can interact with the surfacant and thus decrease its tensio-active properites.

In plain English

This animal experiment in rabbits examined short-term changes in fluid washed from the lungs. Two groups received 10 mg of UICC A chrysotile asbestos fibres injected into the windpipe, either plain or after sulphur dioxide (SO2) had been adsorbed onto the fibres. The authors described these as doses similar to those found in the environment. One control group was untreated and another received salt solution. The amounts of lipids, phospholipids and phosphatidylcholine in the lung surfactant did not differ between control and exposed groups. Both chrysotile groups seemed to have more unsaturated fatty acids than untreated rabbits, but the salt-solution controls showed a similar change. Soluble protein in the washings, mainly albumin, was significantly higher in both chrysotile groups than in salt-solution controls, but did not differ from untreated rabbits. The authors noted that their two control groups gave conflicting results. They concluded that the protein rise might reflect a leakier barrier between blood and air spaces, and that these proteins could reduce the surfactant's surface-active properties.

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: animal experiment (short-term, intratracheal injection in rabbits, with two control groups and two exposed groups)
• Who was studied: Rabbits (EC 601 Evic Ceba, France) in four groups: untreated controls, salt-solution (NaCl) controls, chrysotile, and SO2-chrysotile. The total number of animals is not clearly stated. The protein table counts 3 or 4 'groups' of three animals each per arm.
• Exposure: 10 mg of UICC A chrysotile fibres given by intratracheal injection, either before or after SO2 sorption onto the fibres. The authors described the doses as similar to those found in the environment.
• Main results:
  • There was no difference in levels of lipids, phospholipids or phosphatidylcholine in surfactant between the control and experimental groups.
  • Chrysotile and SO2-chrysotile seemed to increase unsaturated fatty acids in surfactant phosphatidylcholine compared with untreated animals. These fatty acid analyses were based on 1 or 2 samples per group.
  • A similar variation in fatty acids was also seen in the NaCl controls compared with untreated animals.
  • Both exposed groups had more soluble protein in the lung washings than NaCl controls, which the authors reported as statistically significant. In the supernatant S2, chrysotile rabbits had 40.27 plus or minus 2.54 mg and SO2-chrysotile rabbits had 44.59 plus or minus 5.24 mg.
  • For comparison, supernatant S2 protein was 26.98 plus or minus 2.80 mg in NaCl controls and 39.36 plus or minus 3.40 mg in untreated controls. The exposed groups showed no variation compared with untreated animals.
  • The major protein component of the washings was albumin.
  • Histological studies in these experiments showed no interstitial reaction and only very slight hyperplasia of type II pneumocytes.
  • The authors stated that the study found no significant differences in phospholipid and protein content of the alveolar lining material in either experimental group.
• The authors' conclusion: The authors concluded that the protein increase in both chrysotile groups might be explained by increased permeability of the blood-air barrier, letting plasma proteins into the air sacs. They suggested these proteins could interact with surfactant and decrease its surface-active properties. They also likened the fatty acid change to that seen in respiratory distress syndrome of the newborn.
• Limitations the authors state:
  • The two control groups gave conflicting results. Protein was higher in untreated animals than in NaCl controls, and unsaturated fatty acid content was lower in NaCl controls than in untreated animals.

Topics

Medical terms in this study, explained in our Lexicon: Chrysotile.

Related studies

• Biological effects of chrysotile after SO2 sorption. II. Effects on alveolar macrophages and red blood cells — M.C. Jaurand, J. Bignon, et al. (1978)
• Biochemical components of bronchoalveolar lavage in early experimental asbestosis of the sheep: phospholipase A2 activity, prostaglandin E2 and proteins — P. Sirois, G. Drapeau, et al. (1983)
• In vitro reactivity of alveolar macrophages and red blood cells with asbestos fibres treated with oxalic acid, sulfur dioxide and benzo-3,4-pyrene — M.C. Jaurand, L. Magne, et al. (1981)
• Leaching of chrysotile asbestos in human lungs. Correlation with in vitro studies using rabbit alveolar macrophages — M.C. Jaurand, J. Bignon, et al. (1977)
• In vitro biodegradation of chrysotile fibres by alveolar macrophages and mesothelial cells in culture: comparison with a pH effect — M.C. Jaurand, A. Gaudichet, et al. (1984)
• Effect of air pollutants on the pulmonary surfactant system — B. Müller, C. Seifart, et al. (1998)

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