Harmful effects and acute lethal toxicity of intravenous administration of low concentrations of hydrofluoric acid in rats.
The acute toxicity of hydrofluoric acid (HFA) was investigated in a 24-h lethal dose study of intravenous infusion in rats. The lethal dose lowest (LDLo) and LD50 were 13.1 and 17.4 mg/kg, respectively. Harmful systemic effects were also studied 1 h after acute sublethal exposure to HFA. The maximum dose was set at 9.6 mg/kg (LD5). Rats were injected with HFA (1.6, 3.2, 6.4 or 9.6 mg/kg), saline, sodium fluoride (NaF) or HCl solution. NaF and HCl solution concentrations corresponded to the F- and H+ concentrations of 9.6 mg/kg HFA. Blood urea nitrogen (BUN) and Cr were significantly increased in response to HFA concentrations greater than 3.2mg/kg. Acute glomerular dysfunction also occurred at HFA concentrations greater than 3.2 mg/kg. HCO3- and base excess (BE) were significantly decreased in the 6.4 and 9.6 mg/kg groups. Ca2+ was significantly decreased, and K+ was increased in the 9.6 mg/kg group. BUN was significantly increased in the NaF and HFA groups and was increased in the HFA group compared with that in the NaF group. Cr was significantly increased in the HFA group only. HCO3- and BE were significantly decreased in the NaF and HFA groups and were increased in the HFA group compared with values in the NaF group. Ca2+ was significantly decreased in the NaF and HFA groups, and K+ was significantly increased in the NaF and HFA groups. F- exposure directly affected serum electrolytes. Mortality was thought to be due to cardiac arrhythmia resulting from hypocalcemia and hyperkalemia. Metabolic acidosis and renal failure were more severe in response to HFA exposure than in response to NaF exposure because of more free F-, which has strong cytotoxicity, in the HFA group than in the NaF group. Lethal effects of HFA are promoted by exposure routes such as inhalation that cause rapid absorption into the body. Even low exposure to HFA can cause acute renal dysfunction, electrolyte abnormalities and metabolic acidosis. These complications result in a poor prognosis.
Mitsui
Go
G
Department of Hygiene and Public Health, Osaka Medical College, 2-7, Daigakumachi, Takatsuki City, Osaka 569-8686, Japan. go.mitsui-107@nifty.com
Dote
Tomotaro
T
Adachi
Kazuya
K
Dote
Emi
E
Fujimoto
Keiichi
K
Shimbo
Yukari
Y
Fujihara
Michiko
M
Shimizu
Hiroyasu
H
Usuda
Kan
K
Kono
Koichi
K
D000141:Acidosis, Renal Tubular / Q000139:chemically induced; D000142:Acidosis, Respiratory / Q000139:chemically induced; D058186:Acute Kidney Injury / Q000139:chemically induced*; D000704:Analysis of Variance; D000818:Animals; D004305:Dose-Response Relationship, Drug; D006858:Hydrofluoric Acid / Q000008:administration & dosage / Q000633:toxicity*; D006947:Hyperkalemia / Q000139:chemically induced*; D006996:Hypocalcemia / Q000139:chemically induced*; D007262:Infusions, Intravenous; D007668:Kidney / Q000187:drug effects / Q000293:injuries*; D007928:Lethal Dose 50; D008099:Liver / Q000187:drug effects / Q000293:injuries*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014882:Water-Electrolyte Balance / Q000187:drug effects
D006858:Hydrofluoric Acid