Pathogenicity of a special-purpose glass microfiber (E glass) relative to another glass microfiber and amosite asbestos

Citation
Rt. Cullen et al., Pathogenicity of a special-purpose glass microfiber (E glass) relative to another glass microfiber and amosite asbestos, INHAL TOXIC, 12(10), 2000, pp. 959-977
Citations number
39
Categorie Soggetti
Pharmacology & Toxicology
Journal title
INHALATION TOXICOLOGY
ISSN journal
08958378 → ACNP
Volume
12
Issue
10
Year of publication
2000
Pages
959 - 977
Database
ISI
SICI code
0895-8378(200010)12:10<959:POASGM>2.0.ZU;2-M
Abstract
This article describes the activity of an E-glass microfiber (104E) during chronic inhalation and intraperitoneal injection studies in rats. Results a re compared with another microfiber of similar dissolution rate (k(dis)), c ode 100/475, and the more durable amosite asbestos, both of which we had pr eviously used in similar experiments (Davis et al., 1996). Rats were expose d to aerosol concentrations of 1000 fibers (longer than 5 mu m)/ ml, as mea sured by optical microscopy, for 7 h/day, 5 days/wk. Subgroups of rats were followed for mean lung burden, early and late signs of fibrosis, and tumor incidence. At the end of 12 mo of exposure, the mean number of 104E fibers of all lengths in the lungs was approximately double that for amosite but two-thirds of that for 100/475. For fibers longer than 15 mu m, the mean 10 4E burden was similar to that for the amosite and more than twice that of t he 100/475. After a 12-mo recovery period, the retained lung burdens (of fi bers of all lengths) were approximately 30% of those at 12 mo for both micr ofibers, and somewhat higher (approximately 44%) for amosite. Amosite and 1 00/475 fibers longer than 15 mu m were more persistent in the lungs than 10 4E fibers. The chemical composition of 104E fibers did not appear to have b een significantly altered by up to 24 mo of residence in lung tissue, where as the composition of 100/475 was substantially altered over the same time period. From the inhalation study, out of the pathology sub-group of 43 ani mals exposed to 104E microfibers, 10 had lung tumors (7 carcinoma, 3 adenom a) and 2 had mesotheliomas, whereas in 42 rats exposed to amosite asbestos, there were 16 lung tumors (7 carcinoma, 9 adenoma) and 2 mesotheliomas. Th e 104E- and amosite-treated animals had similar levels of fibrosis. In cont rast, 38 animals treated with 100/475 had little fibrosis, 4 lung tumors (a denomas), and no mesotheliomas. The greater pathogenicity of the 104E fiber s, compared to 100/475 fibers, might be partly explained by the greater num bers of long fibers retained in the lung after 12 mo of inhalation. However , we speculate that modification of surface properties by extensive selecti ve leaching of some glass components reduces the toxic potential of 100/475 . In a parallel intraperitoneal injection study, 104E caused considerably m ore mesotheliomas (21 rats out of 24) than 100/475 (8 rats out of 24). In a ddition, 104E appeared to be more active than amosite asbestos, since mesot heliomas appeared much more quickly in the 104E- treated animals. In conclu sion, we have shown that two microfiber types, 100/475 and 104E, of similar dissolution rates, had markedly different pathogenicity in rats. We believ e that this contrast is only partly due to differences in numbers of long f ibers and that differences in surface properties of the fibers, possibly du e to proportionately greater leaching of 100/475 fibers, play an important role.