The effect of lung burden on biopersistence and pulmonary effects in rats exposed to potassium octatitanate whiskers by inhalation.

The effect of lung burden on biopersistence and histopathological changes caused by potassium octatitanate whiskers (POW) which is one of the asbestos substitutes were investigated for 1-yr and 4-wk inhalation periods. In the 1-yr inhalation experiment, male Wistar rats were exposed to POW (TW) for 6 h/d, 5 d/wk under the same conditions as a previous study of POW (PT1, JFM fiber) which is made by different manufacturer. The exposure concentration was 1.9 +/- 0.7 mg/m(3) and the mass median aerodynamic diameter (MMAD) and geometric standard deviation (GSD) in the chamber were 1.6 microm and 2.9. Rats were sacrificed at 3 d and 1 yr after the inhalation experiment and TW deposits in the lungs were determined by ICP-AES. Lung burden at 3 d and 1 yr after the inhalation was 2.39 +/- 0.50 mg and 1.37 +/- 0.96 mg, respectively, the deposition fraction was 8.1% and biological half time (BHT) was 15 months. Aggregated dust cells and mild fibrotic changes around these dust cells were observed in the exposed rat lung. These results were almost the same as those obtained in the previous 1-yr PT1 study. In the 4-wk inhalation experiment, to investigate the effect of lung burden on biopersistence and histopathological change, male Wistar rats were exposed to PT1. The exposure concentration was 102 +/- 21 mg/m(3), MMAD (GSD), the geometiric mean length and diameter (GSD) of the PT1 in the chamber were 1.6 microm (3.0), 2.2 microm (1.8) and 0.33 microm (1.5), respectively. Rats were sacrificed at 3 d, 1 wk, and 1, 3, 6 and 12 months after the inhalation experiment. The lung burden of POW at 3 d after 4 wk inhalation was 1.49 +/- 0.19 mg, which was close to the estimated amount of overload. The BHT of the total mass (4.1 months) was not prolonged, but aggregated dust cells were observed in the subpleural region and around the bronchioles and mild fibrotic changes were observed only around the dust cells at one year after the 4-wk inhalation. It is considered that the excessive exposure which impairs the function of alveolar macrophage mediated clearance may cause the aggregation of dust cells and fibrotic changes.