Fluoride Action Network


Harmful systemic effects were studied 1 hour after acute sub-lethal exposure to hydrofluoric acid (HFA) in previous study. This study was designed to investigate the early dynamic state of F in blood and urine in rats as a model of accidental occupational exposure to HFA. It was also designed to determine the relationship between the kinetics and harmful effects on kidney. To evaluate the kinetics of F exposure and metabolism, rats received a single intravenous injection of HFA(3.2, 6.4, or 9.6(LD5)mg/kg) or saline. The each volume was 1 ml and the concentrations of HFA were 0.1, 0.2, 0.3%, respectively. Serum ionized fluoride (F) concentrations were determined 0, 5, 10, 30, 60, 120, and 300. Calculating the elimination data of F from serum required two-compartment modeling. Urine was collected for 300 min. urinary parameters were measured to consider the renal injury. T1/2?, AUC0?300 were significantly in 0.3% group longer than 0.1 and 0.2% groups. The total body clearance, V1, V2, Vss, K10 were significantly lower in 0.3% group than 0.1% groups. The pharmacokinetic parameters indicated the retention of F in blood. NAG/Cr and glucose were increased and F clearance, urine volume and excretion of electrolytes were decreased in 0.3% group compared with other groups. Deceased urinary F showed the disorder of F excretion from kidney. Therefore, the metabolism of F was markedly delayed in 0.3%. The kidney is main excretory organ, and also the target organ of F. The glomerular dysfunction and renal tubular injury were caused by HFA exposure. Abnormalities in F kinetics could result from renal dysfunction at a sub-lethal toxic dose. In previous study, the same dose of HFA could also cause electrolyte abnormalities and metabolic acidosis. In conclusion, metabolism of F was mainly disordered by glomerular dysfunction.