Introduction: Hydrofluoric acid (HFA) is commonly used in chemical industries despite reports of acute lethality after occupational accident. We previously confirmed that acute death of rats after HFA aerosol inhalation can be due to pulmonary dysfunction. Although there have been several reports suggesting that respiratory disorders can be improved with specialized emergency procedures over a few days, there are currently no established protocols for emergency procedures for aerosolized HFA inhalation. It is necessary for therapy protocol to establish the experimental animal model about recovery process for the best treatment. The purpose of this study was to elucidate the process of lung recovery in rats exposed to HFA below fatal dose as the model with the occupational accident.
Methods: Rats were divided into four groups: saline (1 h) group (n = 6), saline (48 h) group (n = 6), HFA (1h) group (n = 11), and HFA (48 h) group (n = 11). Rats were intratracheally sprayed with aerosols of HFA (0.36mg/kg) or saline. Blood, bronchoalveolar lavage (BALF) and lung tissue were collected at 1 h or 48 h after HFA administration. Blood gases and BALF were analyzed. The concentrations of F were measured in serum and BALF. The lung tissues were observed by light microscopy. The severities of pathohistological findings were evaluated by semi-quantative gradings in a rat from each group.
Results: All rats exposed to HFA were alive 48 h later. The mean PO2 of the HFA (1 h) group was significantly lower compared with the saline (1 h) group, and mean PO2 of the HFA (48 h) group was higher compared to the HFA (1 h) group. The mean of surfactant protein-D (SP-D) level in BALF in the HFA (1 h) group was significantly lower compared to the saline (1 h) group. The mean values of SP-D and LDH in the HFA (48 h) group were significantly higher than those in the HFA (1 h) group, respectively. Means of F in serum and BALF in the HFA (1 h) group were significantly higher compared to the saline and the HFA (48 h) groups. There were no significant differences in these indices between the HFA (48 h) and saline (48 h) groups. Macroscopic swelling and hemorrhages in the lung were observed bilaterally in both HFA groups. Semi-quantitative grading of pathohistological findings indicated that perivascular and alveolar effusion into alveolar spaces were evident in the HFA (1 h) group and thickened bronchial epithelium and desquamations of bronchial epithelium were evident in the HFA (48 h) group.
Discussion: The dose used in this study was not lethal. No differences between PO2 of the HFA (48 h) group and saline group (48 h) suggested that respiratory function recovered. Reduced F levels in serum and BALF indicated that HFA was rapidly absorbed from lung tissue into blood and metabolized by 48 h after administration. Perivascular and alveolar injury occurred within 1 h and thickened bronchial epithelium and desquamations of bronchial epithelium appeared 48 h later. It was suggested that the lung tissues were in recovery process from the pathohistological findings in 48 h. The experimental model of the HFA inhalation was established in this study. It would be an important step toward a possible treatment for the lung injury exposed to HFA.