Pneumotoxicity and pulmonary clearance of different welding fumes after intratracheal instillation in the rat.
The objectives of this study were to compare different welding fumes in regard to their potential to elicit lung inflammation or injury and to examine possible mechanisms whereby welding fumes may damage the lungs. Fume was collected on filters from conventional spray [mild steel (MS-SPRAY) or stainless steel (SS-SPRAY) electrode wire] or pulsed current [mild steel (MS-PULSE) electrode wire] gas-shielded metal arc welding. Rats were given one of the three welding fume samples by intratracheal instillation (1.0 mg/100 g body wt). Other rats received a relatively inert dust (iron oxide), a pneumotoxic dust (crystalline silica), or a vehicle control (saline). Bronchoalveolar lavage (BAL) was performed 1, 7, 14, and 35 days postinstillation, and indicators of pulmonary damage [cellular differential, albumin, as well as, tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), lactate dehydrogenase, and beta-n-acetyl glucosaminidase release] were assessed. One day postinstillation, some evidence of lung inflammation (more neutrophils) was observed for all particle groups, while increased BAL TNF-alpha and IL-1 beta were observed only in the SS-SPRAY and silica groups. By 14 days, lungs appeared normal among the MS-SPRAY, MS-PULSE, and iron oxide groups. At 14 and 35 days postinstillation, elevated pulmonary responses persisted for the animals exposed to silica and the SS-SPRAY welding fume. By 35 days, however, the SS-SPRAY group approached control levels, while the injury induced by silica increased. Using magnetometric estimates of welding fumes, we observed that MS-SPRAY fume was cleared from the lungs at a faster rate than the SS-SPRAY particles. We have demonstrated that the SS-SPRAY fume has more pneumotoxicity than MS fumes. This difference may reflect a greater retention of the SS-SPRAY particles in the lungs and different elemental composition of the fume. The SS-SPRAY fume also had enhanced release of TNF-alpha and IL-1 beta from lung cells soon after fume instillation. In contrast, we saw no influence of the power supply on particle size, composition, or toxicity.
Antonini
J M
JM
Department of Environmental Health, Harvard University School of Public Health, Boston, Massachusetts 02115, USA.
Krishna Murthy
G G
GG
Rogers
R A
RA
Albert
R
R
Ulrich
G D
GD
Brain
J D
JD
D000393:Air Pollutants / Q000493:pharmacokinetics / Q000633:toxicity*; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D004391:Dust / Q000009:adverse effects*; D008168:Lung / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D008657:Metabolic Clearance Rate; D051381:Rats; D012822:Silicon Dioxide / Q000493:pharmacokinetics / Q000633:toxicity*; D013232:Steel / Q000493:pharmacokinetics / Q000633:toxicity*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014896:Welding
D000393:Air Pollutants; D004391:Dust; D014409:Tumor Necrosis Factor-alpha; D013232:Steel; D012822:Silicon Dioxide