Ammonium silicofluoride (Ammonium fluosilicate). TOXNET profile from Hazardous Substances Data Bank.

FLUORIDE ACTION NETWORK PESTICIDE PROJECT

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Ammonium silicofluoride. TOXNET profile from Hazardous Substances Data Bank.

Also known as Ammonium fluosilicate

See for Updates: http://toxnet.nlm.nih.gov/cgi-bin/sis/htmlgen?HSDB

AMMONIUM SILICOFLUORIDE
CASRN: 16919-19-0
For other data, click on the Table of Contents

Human Health Effects:

Human Toxicity Excerpts:

SYMPTOMATOLOGY: A. Ingestion of soluble fluoride salts. 1. Salty or soapy taste, salivation, nausea. Repeated small doses (as in drinking water) may produce no other symptoms, but polyuria and polydipsia have also been reported. 2. Large doses lead promptly to burning or crampy abdominal pain, intense vomiting and diarrhea, often with hematemesis and melena. Dehydration and thirst. 3. Muscle weakness, tremors, and rarely transient epileptiform convulsions, preceded or followed by progressive central nervous depression (lethargy, coma and respiratory arrest, even in the absence of circulatory failure). 4. Shock characterized by pallor, weak and thready pulse (sometimes irregular), shallow unlabored respiration, weak heart sounds, wet cold skin, cyanosis, anuria, dilated pupils, followed almost invariably by death in 2 to 4 hours. 5. Even in the absence of shock, arrhythmias may occur, especially multiple episodes of ventricular fibrillation leading eventually to cardiac arrest. 6. If the victim survives a few hours, paralysis of the muscles of deglutition, carpopedal spasm, and painful spasms of the extremities. 7. Occasionally localized or generalized urticaria. 8. The above signs and symptoms are related to a variety of metabolic disorders that may occur in acute fluoride poisoning, including hypocalcemia, hypomagnesemia, metabolic and/or respiratory acidosis and sometimes hyperkalemia. /Fluoride/
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984.,p. III-190]**PEER REVIEWED**

INITIAL SYMPTOMS FROM INGESTION INCLUDE ... SALIVATION, NAUSEA, ABDOMINAL PAIN, VOMITING, AND DIARRHEA ARE FREQUENT. ... THE PATIENT SHOWS SIGNS OF INCR IRRITABILITY OF THE NERVOUS SYSTEM ... HYPOCALCEMIA & HYPOGLYCEMIA ARE FREQUENT LAB FINDINGS. ... BLOOD PRESSURE FALLS ... DUE TO CENTRAL VASOMOTOR DEPRESSION AS WELL AS DIRECT TOXIC ACTION ON CARDIAC MUSCLE. THE RESPIRATORY CENTER IS FIRST STIMULATED & LATER DEPRESSED. DEATH ... FROM EITHER RESPIRATORY PARALYSIS OR CARDIAC FAILURE. /FLUORIDE SALTS/
[Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996. 1538]**PEER REVIEWED**

... THE MAJOR MANIFESTATIONS OF CHRONIC INGESTION OF EXCESSIVE AMT OF FLUORIDE ARE OSTEOSCLEROSIS & MOTTLED ENAMEL. ... DENSITY AND CALCIFICATION OF BONE ARE INCREASED ... THOUGHT TO REPRESENT THE REPLACEMENT OF HYDROXYAPATITE BY THE DENSER FLUOROAPATITE. /FLUORIDE SALTS/
[Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996. 1539]**PEER REVIEWED**

CHRONIC POISONING: INTAKE OF MORE THAN 6 MG ... /A/ DAY RESULTS IN FLUOROSIS. SYMPTOMS ARE WT LOSS ... ANEMIA, WEAKNESS, GENERAL ILL HEALTH, STIFFNESS OF JOINTS ... ./FLUORIDE/
[Dreisbach, R. H. Handbook of Poisoning. 9th ed. Los Altos, California: Lange Medical Publications, 1977. 207]**PEER REVIEWED**

TOXIC BY INHALATION.
[Hawley, G.G. The Condensed Chemical Dictionary. 10th ed. New York: Van Nostrand Reinhold Co., 1981. 59]**PEER REVIEWED**

Skin, Eye and Respiratory Irritations:

STRONG IRRITANT TO EYES & SKIN.
[Sax, N.I. and R.J. Lewis, Sr. (eds.). Hawley's Condensed Chemical Dictionary. 11th ed. New York: Van Nostrand Reinhold Co., 1987. 67]**PEER REVIEWED**

Drug Warnings:

Food and Environmental Agents: Effect on Breast-Feeding: Reported Sign or Symptom in Infant or Effect on Lactation: Fluorides: None. /from Table 7/
[Report of the American Academy of Pediatrics Committee on Drugs in Pediatrics 93 (1): 142 (1994)]**PEER REVIEWED**

Populations at Special Risk:

Populations that appear to be at increased risk form the effects of fluoride are individuals that suffer for diabetes insipidus or some forms of renal impairment. /Fluoride/
[USEPA, Office of Drinking Water; Criteria Document (Draft): Fluoride p.I-5 (1985)]**PEER REVIEWED**

Emergency Medical Treatment:

Emergency Medical Treatment:

EMT Copyright Disclaimer:

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The following Overview, *** CORROSIVES-ALKALINE ***, is relevant for this HSDB record chemical.

Life Support:

  o   This overview assumes that basic life support measures
      have been instituted.

Clinical Effects:

  SUMMARY OF EXPOSURE
   0.2.1.1 ACUTE EXPOSURE
     o   IRRITANT VS CORROSIVE - Some substances may be
         irritating or corrosive depending on the concentration,
         molarity, and other factors.  In general, serious
         esophageal injury is associated with ingestion of
         products with a pH of 11.5 or higher.
     o   INGESTION - Alkaline corrosive ingestion may produce
         burns to the oropharynx, upper airway, esophagus and
         occasionally stomach.  The absence of visible oral
         burns does NOT reliably exclude the presence of
         esophageal burns.  The presence of stridor, vomiting,
         drooling, and abdominal pain are associated with
         serious esophageal injury in most cases.
      1.  Patients with a history of suicidal intent have a
          higher rate of positive esophagoscopy findings than
          those with accidental ingestion.
      2.  Delayed sequelae of caustic ingestion include
          tracheoesophageal and aortoesophageal fistulae,
          strictures of the mouth, esophagus and stomach, and
          esophageal carcinoma.
     o   INHALATION - Inhalation of alkaline vapors can produce
         upper airway edema, respiratory failure, wheezing,
         pulmonary edema, and pneumonitis.
     o   OCULAR - Ocular exposure can produce severe
         conjunctival irritation and chemosis, corneal
         epithelial defects, limbal ischemia, permanent visual
         loss and in severe cases perforation.
     o   DERMAL - Dermal contact with alkaline corrosives may
         produce pain, redness, irritation or full thickness
         burns.
  HEENT
   0.2.4.1 ACUTE EXPOSURE
     o   Ingestion may result in burns to the lips, tongue, oral
         mucosa, and upper airway.
     o   Alkaline eye exposures produce distortion of cellular
         membranes, loss of corneal, conjunctival and lens
         epithelium and loss of endothelium of the cornea and
         blood vessels.
  CARDIOVASCULAR
   0.2.5.1 ACUTE EXPOSURE
     o   Hypotension and tachycardia are uncommon but may occur
         with severe  GI bleeding or necrosis after ingestion.
  RESPIRATORY
   0.2.6.1 ACUTE EXPOSURE
     o   Stridor, dyspnea, upper airway injury, and pulmonary
         edema, especially following inhalation of vaporized
         caustics, may occur.
  GASTROINTESTINAL
   0.2.8.1 ACUTE EXPOSURE
     o   Burns of the esophagus and less commonly the stomach
         may occur after caustic ingestion; the absence of oral
         mucosal injury does NOT reliably exclude esophageal
         burns.  Patients with stridor, drooling or vomiting are
         more likely to have esophageal burns.
     o   In severe cases gastrointestinal bleeding or perforated
         viscus with mediastinitis or peritonitis may develop.
         Delayed sequelae of burns include strictures,
         obstruction, fistula formation and esophageal
         carcinoma.
  ACID-BASE
   0.2.11.1 ACUTE EXPOSURE
     o   Metabolic acidosis may develop in patients with severe
         burns or shock.
  DERMATOLOGIC
   0.2.14.1 ACUTE EXPOSURE
     o   Severe skin irritation and/or burns may occur.

Laboratory:

  o   Obtain a complete blood count in patients symptomatic
      alkaline corrosive ingestion.  In patients with signs and
      symptoms suggesting severe burns, perforation, or
      bleeding, obtain renal function tests, PT or INR, PTT, and
      type and crossmatch for blood.

Treatment Overview:

  ORAL EXPOSURE
    o   MUCOSAL DECONTAMINATION:  If no respiratory compromise
        is present, dilute immediately with milk or water; no
        more than 8 ounces in adults and 4 ounces in children.
    o   GASTRIC DECONTAMINATION:  Ipecac contraindicated.
        Consider insertion of a small, flexible nasogastric or
        orogastric tube to suction gastric contents after recent
        large ingestions; the risk of further mucosal injury
        must be weighed against potential benefits.
    B.  NEUTRALIZATION - Is contraindicated.
    o   Keep patient NPO following mucosal decontamination until
        after endoscopy consultation.
XB    E.  ENDOSCOPY:  Perform within 24 hours to evaluate for
        burns in adults with deliberate ingestion or any signs
        or symptoms attributable to ingestion, and in children
        with stridor, vomiting, or drooling.  Consider endoscopy
        in children with dysphagia, refusal to swallow,
        significant oral burns, or abdominal pain.  If burns are
        found, follow 10 to 20 days later with barium swallow or
        esophagram.
XB    F.  PHARMACOLOGIC TREATMENT:  Corticosteroids are
        controversial.  Consider use in second degree burns
        within 48 hours of ingestion in patients without
        gastrointestinal bleeding or evidence of perforation.
        Antibiotics are indicated for suspected perforation or
        infection and in patients receiving corticosteroids.
XB    G.  SURGICAL OPTIONS:  Initially, if severe esophageal burns
        are found a string may be placed in the stomach to
        facilitate later dilation.  Insertion of a specialized
        nasogastric tube after confirmation of a circumferential
        burn may prevent strictures.  Dilation is indicated
        after 2 to 4 weeks if strictures are confirmed; if
        unsuccessful, either colonic intraposition or gastric
        tube placement may be performed.  Consider early
        laparotomy in patients with severe esophageal and/or
        gastric burns.
  INHALATION EXPOSURE
    o   DECONTAMINATION:  Move patient from the toxic
        environment to fresh air and administer oxygen as
        necessary.  Monitor for respiratory distress.  If cough
        or difficulty in breathing develops, evaluate for
        hypoxia, respiratory tract irritation, bronchitis, or
        pneumonitis.
    o   Manage airway aggressively as upper airway edema may
        develop.
    o   Administer 100% humidified supplemental oxygen, perform
        endotracheal  intubation and provide assisted
        ventilation as required.  Administer inhaled  beta
        adrenergic agonists if bronchospasm develops.  Exposed
        skin and eyes  should be flushed with copious amounts of
        water.
  EYE EXPOSURE
    o   HOME IRRIGATION - Exposed eyes should be irrigated with
        copious amounts of water for at least 30 minutes.  An
        examination should always be performed.  Ophthalmologic
        consultation should be obtained.
    o   MEDICAL FACILITY:  Irrigate with sterile 0.9% saline for
        at least  an hour or until the cul-de-sacs are free of
        particulate matter and  returned to neutrality (confirm
        with pH paper).
    o   EYE ASSESSMENT:  The extent of eye injury (degree of
        corneal  opacification and perilimbal whitening) may not
        be apparent for  48 to 72 hours after the burn.
    o   EYE DAMAGE TREATMENT:  If ocular damage is minor,
        topical mydriatics, antibiotics and systemic analgesics
        may be sufficient.   For grade 3 to 4 injuries one or
        more of the following may be  considered, only with
        ophthalmologic consultation:  acetazolamide,  timolol,
        topical steroids, ascorbate, citrate, EDTA, cysteine,
        NAC,  penicillamine, tetracycline, or soft contact
        lenses.
  DERMAL EXPOSURE
    o   Remove contaminated clothes.  Irrigate exposed skin with
        copious amounts of water for at least 15 minutes or
        longer, depending on concentration, amount and duration
        of exposure to the chemical.  A physician may need to
        examine the area if irritation or pain persist.

Range of Toxicity:

  o   LIQUID CORROSIVES - With highly concentrated liquids (30%
      sodium hydroxide) esophageal burns may occur in up to 100%
      of patients, even after accidental  ingestion.
  o   More recent series of caustic ingestions (mixed liquid and
      solid) in children report incidences of significant
      esophageal burns from 5% to 35%.  Adults with deliberate
      ingestions are more likely to develop significant
      esophageal burns (30% to 80%).
  o   LOW PHOSPHATE DETERGENTS and electric dishwasher soaps may
      result in oral and esophageal burns.

[Rumack BH: POISINDEX(R) Information System. Micromedex, Inc., Englewood, CO, 2001; CCIS Volume 110, edition exp November, 2001. Hall AH & Rumack BH (Eds):TOMES(R) Information System. Micromedex, Inc., Englewood, CO, 2001; CCIS Volume 110, edition exp November, 2001.] **PEER REVIEWED**