Clinical Toxicology of
Commercial Products

ACUTE POISONING (HOME & FARM)

MARION N. GLEASON
Research Assistant in Pharmacology, School of Medicine and Dentistry, The University of Rochester, Rochester, New York.

ROBERT E. GOSSELIN, M.D., Ph.D.Professor of Pharmacology, Dartmouth Medical School, Hanover, New Hampshire.

HAROLD C. HODGE, Ph.D., D.Sc.
Professor of Pharmocology and Toxicology, School of Medicine and Dentistry, The Univerrsity of Rochester, Rochester, New York.

 

THE WILLIAMS & WILKINS CO.

BALTIMORE    1957

 


(pages 143 & 144)

FLUORIDE

   Sodium fluoride (NaF) and sodium fluosilicate (Na2SiF6) are used commonly as insecticides (ant, roach, and beetle powders) and rarely as rodenticides. Sodium fluoride has been used internally as an anthelmintic in swine (never in man) and externally as a delousing powder on poultry and cattle. Cryolite, an insoluble sodium fluoaluminate, is sometimes dusted on vegetable and fruit crops as an insecticide. Although infrequently found outside of laboratories and various industries, HF as a gas (hydrogen fluoride) and as an aqueous solution (hydrofluoric acid) warrants consideration because it is a very hazardous form of fluoride.
   Toxicology: In spite of several fatalities, the lethal dose of sodium fluoride in man is not accurately known. Less than 1 gm. by mouth has caused dangerous poisoning, but the mean lethal dose is probably close to 5 gm., and 8 to 10 gm. are almost certainly lethal in untreated cases. The toxicity of sodium fluosilicate is about the same. Hydrofluoric acid is probably more toxic than sodium fluoride, while cryolite is certainly much less toxic.
   Fluoride is a "general protoplasmic poison." When present as a soluble salt, it is readily absorbed from the alimentary tract. A   2   per cent solution of sodium fluoride kills mucosal cells, and its ingestion leads to a severe hemorrhagic gastroenteritis; in part this corrosiveness is due to a toxic action on mucosal capillaries and is seen even after parenteral administration. Hydrofluoric acid is corrosive even on intact skin, where it causes painful penetrating ulcers which heal slowly.
   The systemic actions of fluoride are presumably related to the inhibition of one or more enzymes controlling cellular glycolysis (and perhaps respiration) and to the binding or precipitation of calcium as CaF2. If death is not prompt, systemic symptoms are many and varied. Severe shock is due not alone to gastrointestinal damage but also to central vasomotor depression and to cardiac disturbances. At least in dogs, fluoride interferes with both the contractile power of the heart and the mechanism of beat, in a way that cannot be ascribed to hypocalcemia. The central nervous system is also poisoned, and perhaps this is responsible for the occasional epileptiform convulsions and eventual respiratory failure. Death is usually due to respiretory arrest or to cardiovascular collapse. The role of calcium binding in these phenomena is not clearly established. Many victims die without overt manifestations of hypocalcemia (e.g., tetany). Nevertheless the repeated administration of soluble calcium salts is appropriate therapy, not only to prevent or correct hypocalcemia but also to attempt the inactivation of the toxic fluoride ion by binding or precipitating it.
Symptomatology:
A. Ingestion of neutral fluorides (e.g., NaF)
1. Salty or soapy taste, salivation, nausea, burning or crampy abdominal pain, vomiting, diarrhea (may be bloody). Dehydration and thirst.
2. Muscle weakness, tremors, and rarely transient epileptiform convulsions, followed by central nervous depression.
3. Shock characterized by pallor, weak and thready pulse (sometimes irregular), shallow unlabored respiration, weak heart tones, wet cold skin, cyanosis, dilated pupils, followed almost invariably by death in 2 to 4 hours.
4. When death is delayed, paralysis of the muscles of deglutition, carpopedal spasm, and spasm of the extremities.
5. Occasionally local or generalized urticaria.
B. Local actions of HF vapor or aqueous solutions.
1. Superficial or deep burns of the skin and mucous membranes of the digestive and/or respiratory tracts. Necrotic ulcers are painful and heal slowly.
2. For symptoms (and treatment) after the inhalation of HF or F2, see Nitrogen Oxides on p. 163.
Treatment:
A. Ingestion of neutral fluorides (e.g., NaF)
1. Start intravenous infusion of glucose in isotonic saline.
2. Inject intravenously 10 ml. of 10 per cent calcium gluconate solution. Repeat in about 1 hour and/or whenever tetany appears.
3. Gentle gastric lavage with lime water or a 1 per cent solution of calcium chloride (saline is a poor substitute but better than nothing). Then give orally several oz. of lime water at frequent intervals; if necessary large quantities of milk may be substituted. Aluminum hydroxide gels should
be exceptionally effective for binding fluoride.
4. Inject intramuscularly 10 ml. of 10 per cent calcium gluconate at 4 to 6 hour intervals until recovery is complete (p. 220).
5. Treat shock vigorously by the administration of saline, plasma, or whole blood (p. 193). Norepinephrine is probably useful. Give oxygen as needed. Keep the patient
warm.
6. Correct dehydration and attempt to maintain a mild diuresis, but discontinue fluids and electrolytes (except calcium) if anuria develops (p. 210).
B. Treatment of HF burns of skin
1. Houston Baker of the Corning Glass Co. recommends the immediate local alpplication of the following solution: boric acid, 1 part; borax, 1 part; water, 30 parts.
2. Dr. E. E. Evens of the DuPont Co. gives the following directions for treating HF burns:
a. Wash thoroughly with clean cold water and apply magnesium oxide paste.
b. Soak the affected area for at least an hour in 70 per cent alcohol and ice. Apply magnesium oxide paste and bandage. Pain developing late may be relieved by infiltrating with 10 per cent calcium gluconate into and around such areas.
c. In extensive burns with blisters, debride completely, cutting away all white raised tissue. Apply magnesium oxide paste for 24 to 48 hours and, if there is no further extension of the burned area, apply a mild ointment. Pressure dressings are satisfactory.
Laboratory:
1. Signs of renal injury may arise as a direct toxic action or as a consequence of shock.
2. Electrocardiograms are desirable.
 
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