title: Comparative pulmonary toxicity of blasting sand and five substitute abrasive blasting agents.
abstract: Blasting sand is used for abrasive blasting, but its inhalation is associated with pulmonary inflammation and fibrosis. Consequently, safer substitute materials for blasting sand are needed. In a previous study from this laboratory, the comparative pulmonary toxicity of five abrasive blasting substitutes and blasting sand was reported. In this study, the pulmonary toxicity of blasting sand was compared to five additional abrasive blasting substitutes: steel grit, copper slag, nickel slag, crushed glass, and olivine. Exposed rats received by intratracheal instillation 10 mg of respirable-size particles of blasting sand or an abrasive blasting substitute, while controls were instilled with vehicle. Pulmonary inflammation, damage, and fibrosis were examined 28 d postexposure. Pulmonary inflammation was monitored by determining bronchoalveolar lavage polymorphonuclear cell counts and alveolar macrophage activation by chemiluminescence. Pulmonary damage was assessed by acellular bronchoalveolar (BAL) fluid serum albumin concentrations and lactate dehydrogenase activities. Histological examination of lung tissue samples was made to assess the severity and distribution of pulmonary fibrosis, alveolitis, and alveolar epithelial cell hypertrophy and hyperplasia. In comparison to blasting sand, olivine exposed rats had higher levels of pulmonary inflammation and damage with a similar level of fibrosis. Steel grit-exposed rats had lower levels of pulmonary inflammation and damage, and did not develop fibrosis. However, steel grit-exposed rats had a level of epithelial cell hypertrophy and hyperplasia similar to blasting sand. The other abrasive blasting substitutes gave a mixed profile of toxicity. The data demonstrate that steel grit produced less acute pulmonary toxicity than blasting sand or any of the other abrasive blasting substitutes. Notwithstanding, the data also suggest that chronic exposure to steel grit may pose a health risk due to its effects on epithelial cell proliferation in the lung.
authors.affiliation: Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, 1095 Willowdale Road, M/S 2015, Morgantown, WV 26505, USA. DPorter@cdc.gov
authors.forename: Dale W
authors.initials: DW
authors.lastname: Porter
authors.forename: Ann F
authors.initials: AF
authors.lastname: Hubbs
authors.forename: Victor A
authors.initials: VA
authors.lastname: Robinson
authors.forename: Lori A
authors.initials: LA
authors.lastname: Battelli
authors.forename: Mark
authors.initials: M
authors.lastname: Greskevitch
authors.forename: Mark
authors.initials: M
authors.lastname: Barger
authors.forename: Douglas
authors.initials: D
authors.lastname: Landsittel
authors.forename: William
authors.initials: W
authors.lastname: Jones
authors.forename: Vincent
authors.initials: V
authors.lastname: Castranova
mesh_terms: D000280:Administration, Inhalation; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid; D016676:Macrophages, Alveolar / Q000187:drug effects* / Q000473:pathology; D008297:Male; D008670:Metals / Q000633:toxicity*; D010316:Particle Size; D011658:Pulmonary Fibrosis / Q000139:chemically induced* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012822:Silicon Dioxide / Q000633:toxicity*
chemical_list: D008670:Metals; D012822:Silicon Dioxide