The use of blasting (silica) sand in abrasive blasting has been associated with pulmonary disease. Therefore, a need exists for the identification of less toxic substitutes. We assessed the toxicity of several abrasive blasting substitutes and compared the pulmonary effects to those caused by two blasting sands. Rats received a single 10 mg dose of either nickel slag, copper slag, crushed glass, olivine, steel grit, or two blasting sands with PBS as the vehicle (control) by intratracheal (IT) instillation. At four weeks post-IT, the right lung lobe was lavaged to isolate bronchoalveolar lavage (BAL) cells and acellular BAL fluid (BALF); the left lung lobe was inflated with 10% neutral buffered formalin and processed for histopathology. Pulmonary inflammation was monitored by measuring BAL polymorphonuclear leukocytes (PMN) and alveolar macrophage (AM) chemiluminesence (CL). Cytotoxicity was measured by analysis of acellular BALF lacate dehydrogenase (LDH) activity and albumin (ALB) concentration. Examination of the data indicates that in comparison to PBS-exposed rats, all the materials except steel grit caused elevated PMNs, AM CL, and BALF LDH and albumin. Comparing the substitutes to the blasting sands showed that olivine was the most potent. With the exception of steel grit, all the other substitutes exhibited similar potency to that of blasting sand. Preliminary data indicates that steel grit was substantially less reactive than the blasting sands, causing a response similar to PBS-exposed rats. At four weeks post-exposure, these data indicate that except for steel grit these abrasive blasting substitutes did not appear to be less toxic in rats than blasting sands.
The Toxicologist. Society of Toxicology 40th Annual Meeting, March 25-29, 2001, San Francisco, California