Response of bovine alveolar macrophages in vitro to welding fume particles

Our plain-English summary of Response of bovine alveolar macrophages in vitro to welding fume particles, by L.R. White, A.B. Marthinsen, K. Jakobsen, et al (Environmental Health Perspectives, 1983).

The study

• Authors: L.R. White, A.B. Marthinsen, K. Jakobsen, K.B. Eik-Nes
• Journal: Environmental Health Perspectives
• Published: 1983;51:211-5
• Cited by: 16 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Alveolar macrophages (AM) from bovine lungs were exposed in culture to manual metal are (MMA) welding fume particles, chromium (Cr), UICC chrysotile A or anatase for 17-20 hr. All the welding particle samples were more cytotoxic to AM than to anatase. Particles from the welding of mild steel with a rutile-coated electrode were less cytotoxic than those produced with a basic-coated electrode. Particles from the welding of stainless steel were slightly more cytotoxic, and much of this activity was probably due to CrVI. Selective release of N-acetyl-beta-glucosaminidase (beta-NAG) was only detected after exposure of AM to chrysotile. Supplementation of the incubation medium with 10% serum increased the viability of all exposed AM cultures, an effect not produced by serum albumin alone. Incubation of particle samples with dipalmitoyl phosphatidylcholine (DPPC) prior to addition to AM reduced the cytotoxicity of the "rutile" welding particles and of chrysotile.

In plain English

This was a laboratory study using animal cells, not people. Researchers in Trondheim, Norway, collected alveolar macrophages from cow lungs. These are scavenger cells from the lung's air sacs. The researchers exposed the cells in culture for 17-20 hours to three kinds of manual metal arc welding fume particles, to chromium salts, to UICC chrysotile A asbestos, or to titanium dioxide (anatase). Anatase did not harm the cells at doses up to 40 micrograms per mL. All three welding particle types did harm them. Particles from mild steel welding with a rutile-coated electrode were least toxic, and stainless steel welding particles were most toxic. The authors judged that hexavalent chromium, Cr(VI), was the main source of the stainless steel particles' toxicity. Only chrysotile caused selective release of the lysosomal enzyme beta-NAG. Adding 10% calf serum to the medium reduced toxicity in all groups, but serum albumin alone did not. Pre-treating particles with DPPC, the main component of lung surfactant, appeared to reduce the toxicity of chrysotile and of the rutile welding particles. The authors called the DPPC results only preliminary.

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: Laboratory (in vitro) experiment on animal cells in culture
• Who was studied: Alveolar macrophages washed out of cow (bovine) lungs within 1 hour of slaughter, at the Institute of Biophysics, University of Trondheim, Norway. The number of animals is not stated. Experiments were done on at least two occasions in triplicate.
• Exposure: Manual metal arc welding fume particles of three types: stainless steel welded with a rutile basic-coated electrode, and mild steel welded with either a basic-coated or a rutile-coated electrode. Also tested were Cr(VI) and Cr(III) chromium salt solutions, UICC chrysotile A asbestos, and titanium dioxide (99% anatase). Exposure lasted 17-20 hours, at doses up to 40 micrograms of particles per mL of medium.
• Main results:
  • Measured by trypan blue dye exclusion, anatase was not toxic to the cells up to a dose of 40 micrograms per mL. All welding fume particle types were toxic, with viability falling roughly in proportion to dose.
  • Among the welding particles, the rutile particles (mild steel) were the least toxic and the stainless steel particles the most toxic. The basic particles were almost as active as the stainless steel particles.
  • Cr(VI), at concentrations equivalent to those in the stainless steel particles, was toxic to the cells but less so than the whole particles. The authors considered Cr(VI) the main source of the stainless steel particles' toxicity. Cr(III) had no effect on viability at these concentrations.
  • Selective release of the lysosomal enzyme beta-NAG was seen only in cells exposed to chrysotile. It was not seen with any of the welding particles.
  • In this system chrysotile was more toxic to the cells than in most previous studies. The authors attributed this probably to differences in cell type and culture conditions.
  • Adding 10% newborn calf serum to the medium significantly reduced toxicity in all exposure groups. For chrysotile at 40 micrograms per mL, LDH release was 38 ± 4% in serum-free medium and 24 ± 0% with serum (control: 11 ± 3% serum-free). Bovine serum albumin alone did not produce this improvement.
  • Pre-treating particles with DPPC appeared to reduce the toxicity of chrysotile and of the rutile welding particles. For chrysotile, LDH release was 21 ± 3% with DPPC. DPPC did not affect the activity of the stainless steel particles or Cr(VI).
• The authors' conclusion: The authors concluded that in serum-free medium all three welding fume particle types were more toxic to the macrophages than titanium dioxide. Activity increased in the order rutile, then basic, then stainless steel particles.
• Limitations the authors state:
  • The authors called the DPPC results only preliminary because the amount of DPPC adsorbed onto the particles was not measured.
  • Some particle aggregation was present in the DPPC experiments, and particle load in the cells was assessed only by light microscopy. Because of aggregation, no DPPC results were obtained for the basic welding particles.

Topics

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

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

Related studies

• Stimulation of oxidant production in alveolar macrophages by pollutant and latex particles — G.E. Hatch, D.E. Gardner, et al. (1980)
• Cytotoxic effects of quartz and chrysotile asbestos: in vitro interspecies comparison with alveolar macrophages — J. Schimmelpfeng, A. Seidel (1991)
• Interleukin 1 production and accessory cell function of rat alveolar macrophages exposed to mineral dust particles — Y. Oghiso, Y. Kubota (1987)
• Morphologic characterization of alveolar macrophages from subjects with occupational exposure to inorganic particles — T. Takemura, W.N. Rom, et al. (1989)
• 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)

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