Studies on the inhalation toxicology of two fiberglasses and amosite asbestos in the Syrian golden hamster. Part II. Results of chronic exposure

Fiberglass (FG) is the largest category of man-made mineral fibers (MMVFs). Many types of FC are manufactured for specific uses-building insulation, a ir handling, filtration, and sound absorption. In the United Slates, >95% o f FG produced is for building insulation. Several inhalation studies in rod ents of FC building insulation have shown no indication of pulmonary fibros is or carcinogenic activity. However, because of increasing use and potenti al for widespread human exposure, a chronic toxicity/carcinogenicity inhala tion study of a typical building insulation FG (MMVF 10a) was conducted in hamsters, which were shown to be highly sensitive to the induction of mesot heliomas with another MMVF. A special-application FG (MMVF 33) and amosite asbestos were used for comparative purposes. Groups of 140 weanling male Sy rian golden hamsters were exposed via nose-only inhalation for 6 h/day, 5 d ays/wk for 78 wk to either filtered air (chamber controls) or MMVF 10a, MMV F 33, or amosite asbestos at 250-300 WHO fibers/cm(3) with two additional a mosite asbestos groups at 25 and 125 WHO fibers/cm(3). They were then held unexposed for 6 wk until similar to 10-20% survival. After 13, 26, 52, and 78 wk, various pulmonary parameters and lung fiber burdens were evaluated. Groups hamsters were removed from exposure at 13 and 52 wk and were held un til 78 wk (recovery groups). Initial lung deposition of long fibers (>20 mu m in length) after a single 6-h exposure was similar for all 3 fibers expo sed to 250-300 fibers/cm(3). MMVF 10a lungs showed inflammation (which regr essed in recovery hamsters) but no pulmonary or pleural fibrosis or neoplas ms. MMVF 33 induced more severe inflammation and mild interstitial and pleu ral fibrosis; by 26 wk that progressed in severity until 52 wk, after which it plateaued. While the inflammatory lesions regressed in the recovery ani mals, pulmonary or pleural fibrosis did not. A single multicentric mesothel ioma was observed at 32 wk. No neoplasms were found in the remainder of the study. Amosite asbestos produced dose-related inflammation and pulmonary a nd pleural fibrosis as early as 13 wk in all 3 exposure levels. The lesions progressed during the course of the study, and at 78 wk severe pulmonary f ibrosis with large areas of consolidation was observed in the highest 2 exp osure groups. Progressive pleural fibrosis with mesothelial hypertrophy and hyperplasia was present in the thoracic wall and diaphragm in most animals and increased with lime in the recovery hamsters. While no pulmonary neopl asms were observed in the amosite exposed hamsters, a large number of mesot heliomas were found; 25 fibers/cm(3), 3.6%; 125 fibers/cm(3), 25.9%; and 25 0 fibers/cm(3), 19.5%. For the 3 fiber types, the severity of the lung and pleural lesions generally paralleled the cumulative fiber burden, especiall y those >20 mu m length, in the lung, thoracic wall, and diaphragm. They al so inversely paralleled the in vitro dissolution rates; that is, the faster the dissolution, the lower were the cumulative lung burdens and the less s evere the effects.