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ToxSci Advance Access originally published online on March 31, 2004
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Toxicological Sciences 79, 370-380 (2004)
Toxicological Sciences vol. 79 no. 2 © Society of Toxicology; all rights reserved.

Progression of Lung Inflammation and Damage in Rats After Cessation of Silica Inhalation

Dale W. Porter*,1, Ann F. Hubbs*, Robert Mercer*, Victor A. Robinson*, Dawn Ramsey{dagger}, Jeff McLaurin{dagger}, Amir Khan{dagger}, Lori Battelli*, Kurt Brumbaugh*, Alexander Teass{dagger} and Vincent Castranova*

* National Institute for Occupational Safety and Health, Health Effects Laboratory Division, Morgantown, West Virginia 26505; and {dagger} National Institute for Occupational Safety and Health, Division of Applied Research and Technology, Cincinnati, Ohio 45226

Received November 25, 2003; accepted February 13, 2004

Human epidemiologic studies have found that silicosis may develop or progress even after occupational exposure has ended, suggesting that there is a threshold lung burden above which silica-induced pulmonary disease progresses without further exposure. We previously described the time course of rat pulmonary responses to silica inhalation as biphasic, the initial phase characterized by increased but controlled pulmonary inflammation and damage. However, after a threshold lung burden was exceeded, rapid progression of silica-induced pulmonary disease occurred. To test the hypothesis that there is a threshold lung burden above which silica-induced pulmonary disease progresses without further exposure we initiated a study to investigate the relationship between silica exposure, the initiation and progression of silica-induced pulmonary disease, and recovery. Rats were exposed to silica (15 mg/m3, 6 h/day) for either 20, 40, or 60 days. A portion of the rats from each exposure were maintained without further exposure for 36 days to examine recovery. The major findings of this study are: (1) silica-exposed rats were not in pulmonary overload, and lung silica burden decreased with recovery; (2) pulmonary inflammation, damage and lipidosis increased with recovery for rats exposed to silica for 40 and 60 days, but not 20 days; (3) histopathology revealed changes in silica-induced alveolitis, epithelial hypertrophy and hyperplasia, and alveolar lipoproteinosis consistent with bronchoalveolar lavage (BAL) endpoints; and (4) pulmonary fibrosis developed even when exposure was stopped prior to its initial development.

Key Words: silica inhalation; pulmonary inflammation; silica lung burden; recovery.


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