Progressive Lung Injury over a One-Year Period after a Single Inhalation Exposure to Beryllium Sulfate

Abstract

The chronic pulmonary toxicity of beryllium sulfate was examined in rats over a 1-yr period after a single, 1-h exposure. Male rats, exposed in a nose-only inhalation chamber to an aerosol of 4.05 micrograms Be/L, were evaluated for lung toxicity by the methods of bronchoalveolar lavage, lung cell kinetics, and histopathologic analysis. Bronchoalveolar lavage activities for alkaline phosphatase (Alk Pase) and acid phosphatase (Ac Pase) were elevated 3 wk after exposure; lactate dehydrogenase (LDH) and Alk Pase activities peaked 3 months after exposure. Histopathologic analysis revealed progressive focal interstitial pneumonitis with a prominent alveolar component of heteromorphic macrophages, neutrophils, and debris. No increase was noted in the overall labeling index in the alveolar cell population at any of the time points sampled. This study demonstrates the effectiveness of bronchoalveolar lavage fluid analysis in monitoring lung damage over a prolonged period and shows that the pulmonary toxicity of beryllium manifests itself as a progressive lesion from a single 1-h inhalation exposure to BeSO4.

Mechanisms of Granulomatous Lung Disease from Inhaled Beryllium: The Role of Antigenicity in Granuloma Formation*1

“…These data are similar to those reported by others (55,56,58) in which foreign-body type granulomatous inflammation of the lung occured after inhalation exposure of rats to Be materials. In these previous reports, lymphocytes were not a significant component of the lesions, and granuloma formation either did not occur or was limited to that associated with cholesterol cleft formation, an indicator of cell necrosis.…”

Dose–Response Relationships between Inhaled Beryllium Metal and Lung Toxicity in C3H Mice

“…Sendelbach and Witschi (1987) exposed mice for 1 h by inhalation to BeSO 4 , a soluble form of Be, and found indicators of lung damage (LDH, alkaline phosphatase, and albumin) to be markedly elevated within the first few days after exposure, with values returning to control levels by 21 days. Similar patterns were reported in rats exposed to BeSO 4 (Sendelbach and Witschi, 1987), although a chronic elevation of LDH through 1 year after exposure to Be was observed (Sendelbach et al, 1989). Hart et al (1984) exposed rats to an aerosol of Be oxalate that had been briefly heat treated at 560°C in a tube furnace (producing a material of uncertain oxidation state and solubility).…”

“…BALF analyses of rodent responses to Be have been conducted in both mice (Sendelbach and Witschi, 1987) and more commonly in rats (Sanders et al, 1975;Hart et al, 1984;Sendelbach and Witschi, 1987;Sendelbach et al, 1989;Haley FIG. 4.…”

Epidemiological and experimental aspects of metal carcinogenesis: physicochemical properties, kinetics, and the active species.

“…After this initial period of inhibitions phagocytic activity is stimulated by beryllium (72,74). After a single 1-hr inhalation exposure of rats to 4 mg Be/m3 (as BeSO4), the signs of cell deaths and increased phagocytic activity in the bronchoalveolar lavage persisted at least for 1 year (75).…”