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Soluble transition metals cause the pro-inflammatory effects of welding fumes in vitro
Jane D McNeilly1, Mathew R Heal, Iain J Beverland
1Respiratory Medicine Unit, ELEGI/Colt Laboratories, University of Edinburgh, Edinburgh EH8 9AG, UK.
Abstract:
Epidemiological studies have consistently reported a higher incidence of respiratory illnesses such as bronchitis, metal fume fever (MFF), and chronic pneumonitis among welders exposed to high concentrations of metal-enriched welding fumes. Here, we studied the molecular toxicology of three different metal-rich welding fumes: NIMROD 182, NIMROD c276, and COBSTEL 6. Fume toxicity in vitro was determined by exposing human type II alveolar epithelial cell line (A549) to whole welding fume, a soluble extract of fume or the "washed" particulate. All whole fumes were significantly toxic to A549 cells at doses >63 microg ml(-1) (TD 50; 42, 25, and 12 microg ml(-1), respectively). NIMROD c276 and COBSTEL 6 fumes increased levels of IL-8 mRNA and protein at 6 h and protein at 24 h, as did the soluble fraction alone, whereas metal chelation of the soluble fraction using chelex beads attenuated the effect. The soluble fraction of all three fumes caused a rapid depletion in intracellular glutathione following 2-h exposure with a rebound increase by 24 h. In addition, both nickel based fumes, NIMROD 182 and NIMROD c276, induced significant reactive oxygen species (ROS) production in A549 cells after 2 h as determined by DCFH fluorescence. ICP analysis confirmed that transition metal concentrations were similar in the whole and soluble fractions of each fume (dominated by Cr), but significantly less in both the washed particles and chelated fractions. These results support the hypothesis that the enhanced pro-inflammatory responses of welding fume particulates are mediated by soluble transition metal components via an oxidative stress mechanism.
Insights
Welding fumes cause respiratory illness. Soluble metal components in fumes trigger inflammation and oxidative stress in lung cells, explaining their toxicity.
Area of Science:
- Environmental Toxicology
- Occupational Health
- In Vitro Toxicology
Background:
- Welders experience higher rates of respiratory illnesses like bronchitis and metal fume fever (MFF).
- Exposure to metal-enriched welding fumes is a significant occupational hazard.
- The specific mechanisms driving welding fume-induced lung injury require further elucidation.
Purpose of the Study:
- To investigate the molecular toxicology of three distinct metal-rich welding fumes (NIMROD 182, NIMROD c276, COBSTEL 6).
- To determine the role of soluble metal components and oxidative stress in welding fume-induced cellular responses.
- To assess the toxicity of whole fume, soluble extracts, and particulate fractions on human alveolar epithelial cells.
Main Methods:
- Exposure of human type II alveolar epithelial cells (A549) to whole welding fume, soluble fume extract, and washed particulate.
- Quantification of cytotoxicity using TD50 values.
- Measurement of IL-8 mRNA and protein levels.
- Assessment of intracellular glutathione depletion and reactive oxygen species (ROS) production.
- Inductively Coupled Plasma (ICP) analysis of metal concentrations.
Main Results:
- All whole fumes exhibited significant toxicity to A549 cells at doses >63 µg/mL.
- NIMROD c276 and COBSTEL 6 fumes, and their soluble fractions, elevated IL-8 levels.
- Metal chelation attenuated the pro-inflammatory effects of the soluble fume fraction.
- Soluble fume fractions rapidly depleted intracellular glutathione.
- Nickel-based fumes induced significant ROS production in A549 cells.
- Soluble fractions and whole fumes contained similar transition metal concentrations (Cr-dominated).
Conclusions:
- The pro-inflammatory effects of welding fumes are primarily mediated by their soluble transition metal components.
- Oxidative stress mechanisms are central to the molecular toxicology of welding fumes.
- Understanding these mechanisms can inform strategies for mitigating occupational respiratory risks in welding.
