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Responses to welding fumes: lung injury, inflammation, and the release of tumor necrosis factor-alpha and interleukin-1beta.

Antonini JM; Murthy GG; Brain JD
Exp Lung Res 1997 May; 23(3):205-227
Possible mechanisms by which welding fumes induce lung injury were investigated. Alveolar macrophages recovered by bronchoalveolar lavage (BAL) from untreated male CD/VAF-rats were incubated with samples of fume generated during flux covered manual metal arc welding using stainless steel electrodes (MMA/SS) or gas metal arc welding using mild steel electrodes (GMA/SS) suspended in saline for 30 minutes or 24 hours (hr). The fume concentration was 25 micrograms per milliliter. The effects on macrophage viability were evaluated in macrophages treated for 24hr using the trypan-blue dye test. The effects on the respiratory burst response following priming with lipopolysaccharide were assessed in macrophages treated for 30min. Other male CD/VAF-rats were instilled intratracheally with 0 or 1.00 milligram per 100 gram of the MMA/SS or GMA/SS fume samples. BAL was performed 1, 14, or 35 days later. The effects on lavagate cellularity, albumin, tumor necrosis factor alpha (TNFa), and interleukin-1beta (IL1b) concentrations, and lactate- dehydrogenase (LDH) and beta-n-acetyl-glucosaminidase (NAG) activity were determined. In-vitro, MMA/SS caused a significantly greater loss of macrophage viability than GMA/MS fume, 53 versus 13%. Only 6% of the control macrophages died after 24hr. MMA/SS fume caused a greater increase in the respiratory burst response than GMA/SS fume relative to control cells, 47 versus 29%. In-vivo, both fume samples caused a significant increase in total BAL fluid cellularity by day one. The increase was due primarily to increases in neutrophil counts. Neutrophil counts returned to normal in rats treated with GMA/MS fume at later times, but remained significantly elevated in those treated with MMA/SS fume. Most biochemical parameters of lung injury and release of TNFa and IL1b were significantly increased 1 day after dosing. MMA/SS fumes caused larger increases in these parameters than GMA/MS fume. All biochemical parameters and the levels of TNFa and IL1b returned to the control values by day 14 in GMA/MS fume treated rats. Lavagate albumin, LDH, and NAG levels were still significantly elevated in MMA/SS fume treated rats on day 14, although they returned to the control value by day 35. The authors conclude that MMA/SS fume is more pneumotoxic than GMA/MS fume. The greater toxicity of MMA/SS fume may reflect a greater level of macrophage activation and increased production of reactive oxygen species and secretion of TNFa and IL1b.
NIOSH-Publication; NIOSH-Cooperative-Agreement; Pulmonary-system-disorders; Arc-welding; Metallic-fumes; In-vitro-studies; Lung-cells; In-vivo-studies; Proteins; Laboratory-animals; Lung-disorders; Biochemical-indicators; Enzyme-activity; Author Keywords: interleukin-1ß; lung inflammation; lung macrophages; occupational health; reactive oxygen species; respiratory burst; tumor necrosis factor-alpha; welding fumes
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Journal Article
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Cooperative Agreement
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Source Name
Experimental Lung Research
Performing Organization
Harvard School of Public Health
Page last reviewed: September 2, 2020
Content source: National Institute for Occupational Safety and Health Education and Information Division