DESCRIPTION
PHYSICOCHEMICAL PROPERTIES
Colorless/almost colorless fuming liquid Molecular Weight | 20.01 20.01% degrees C |
pKa | 3.19 3.19% degrees C |
Boiling Point | 112.2 112.2% degrees C |
Solubility | Water: miscible |
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INTERVENTION CRITERIA
Medical assessment in an emergency department is recommended for: - Dermal exposure to any concentration of hydrofluoric acid where calcium gluconate gel has not been given as a first aid procedure, even if asymptomatic - Dermal exposure to any solution of greater than 6% hydrofluoric acid, regardless of whether calcium gluconate gel has been administered - Any patient developing pain, erythema, or swelling at the exposure site at any time following dermal exposure to hydrofluoric acid |
Medical assessment in an emergency department is recommended for: - Any hydrofluoric acid ingestion |
Medical assessment in an emergency department is recommended for: - Symptomatic cases |
Medical assessment in an emergency department is recommended for: - All eye exposures to hydrofluoric acid liquids - All symptomatic eye exposures to hydrofluoric acid vapors |
The patient can be observed at home in the event of: Dermal exposures to: - Solutions of less than 6% hydrofluoric acid, involving very small areas of skin, but where the area has been decontaminated and calcium gluconate gel has been given as a first aid treatment Inhalation: - Where the exposure is via inhalation, serious symptoms are unlikely to develop and medical assessment is unlikely to be required However, if the following symptoms develop the patient should seek medical attention: Dermal: Pain Erythema Edema Inhalation: Mild cough Throat/nasal irritation Dyspnea or breathing difficulty Stridor Wheeze Tachypnea |
If medical observation is required the patient should be monitored for 12 hours following exposure for the onset or worsening of symptoms. If the patient is asymptomatic and has a normal ECG and serum calcium concentration (without calcium administration), they can be: - Discharged into the care of a reliable observer, or - Referred for psychological assessment (if the exposure was intentional) |
Admission to an intensive care environment is recommended: Those developing hypocalcemia following any route of exposure. Dermal - Any patient who requires intraarterial infusion of calcium - Patients with a significant percentage of body surface area affected Ingestion - Any patient ingesting a concentrated hydrofluroic acid solution (>50%) Inhalation - Patients suffering: Dyspnea Breathing difficulty Tachypnea Stridor Wheeze Cyanosis Pulmonary signs |
TREATMENT
TREATMENT SUMMARY
The personal protection and safety of the attending personnel must be considered at all times, during the treatment of patients exposed to hydrofluoric acid. The treatment of all hydrofluoric acid exposures focuses on preventing systemic absorption, evaluating the degree of systemic toxicity and rapidly correcting electrolyte abnormalities. Following systemically toxic doses of hydrofluoric acid, the initial emergency stabilization involves monitoring for and correcting hypocalcemia, which may lead to severe hypotension, seizures or dysrhythmias, if left untreated. Blood pressure and ECG should also be closely monitored and IV access secured immediately. Skin exposures should be decontaminated firstly with water and then treated with calcium gluconate gel. Although gastrointestinal decontamination is not recommended, patients can be given water, or preferably milk, to rinse the mouth out. The mainstay of the supportive care focuses on the prevention and treatment of hypocalcemia. Monitor serum electrolyte levels (particularly calcium and magnesium) for evidence of hypocalcemia and hypomagnesemia. Patients should also be observed for symptoms secondary to the onset of hypocalcemia, i.e. hypotension, seizures or dysrhythmias. Administer IV calcium gluconate to replace calcium, if plasma levels are depleted or in the presence of secondary effects. Correct any hypomagnesemia and/or hyperkalemia using standard procedures. Hyperkalemia and metabolic acidosis may be severe enough to warrant urgent hemodialysis, if not responsive to standard treatment measures. All ocular exposures are potentially severe and will require immediate copious irrigation with water or normal saline for at least 30 minutes. Application of ice packs during any transportation to medical facilities has been suggested. Examination with a slit-lamp microscope and fluorescein stain to assess the injury is recommended for all exposures. The patient should always be referred to an ophthalmologist. |
EMERGENCY STABILIZATION
Ensure Adequate Cardiopulmonary Function |
Ensure the airway is protected if compromised (intubation may be necessary). |
Establish secure intravenous access in ingestions, inhalational exposures, and large dermal exposures (>3% body surface area).
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Severe hypotension, seizures or dysrhythmias indicate severe hypocalcemia. Whilst it is preferable to document reduced serum ionized calcium, in the presence of these effects intravenous calcium is warranted even without serum test results. |
Blood pressure ECG Serum ionized calcium Serum electrolytes including: Magnesium Potassium Sodium |
DECONTAMINATION
Decontamination is not recommended. Immediate rinsing out of the mouth with water, or preferably milk, may benefit. Oral fluids should be avoided due to the risk of vomiting, with attendant risks of aspiration and re-exposure of the esophagus to this corrosive substance. Activated charcoal is not indicated as it does not adequately adsorb this substance and will impair visibility if endoscopy is required. Nasogastric aspiration, gastric lavage, and whole bowel irrigation are contraindicated. No benefit has been demonstrated from these procedures, and there is significant risk of perforation during gastric intubation. Emesis is contraindicated due to both risks of re-exposure of the esophagus to the corrosive substance and/or aspiration, and the increased intraluminal pressure produced by emesis. |
Irrigate Skin Immediately |
Remove contaminated clothing or jewelry. Flush the affected area with water as soon as possible. Continue to irrigate until all of the contaminant is removed. Further treatment will then be required to address signs and symptoms. |
The personal protection and safety of the attending personnel must be considered at all times during the treatment of patients. |
Apply Calcium Gluconate Gel |
A 2.5% calcium gluconate gel massage should be performed. Continue massaging into the burned skin for a minimum of 30 minutes and for as long as the pain persists. For digital exposures place the gel in a latex glove and put this on the affected hand. If no gel is available, mix calcium gluconate (10 mL of 10%) with KY jelly (10 g) and apply, or use a calcium or magnesium solution for soaking the affected area. Sometimes pain persists for up to four hours.
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All blisters should be removed and the underlying tissues cleaned. The blister fluid is generally contaminated and it is contraindicated to leave the blisters intact. Removal of nails SHOULD BE AVOIDED if periungual or ungual tissues are involved. Pain at these sites will usually respond well to either intra-arterial or regional intravenous calcium therapy. Any excision of affected tissue should be avoided.
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Immediate copious irrigation with water or normal saline for at least 30 minutes is required. Application of ice packs during any transportation to medical facilities has been suggested. Examination with fluorescein and slit-lamp to assess the injury is recommended for all exposures. The patient should always be referred to an ophthalmologist. Further injury may be reduced with application of a 1% solution of calcium gluconate in saline. This is used to wash the eye for a further 5 to 10 minutes (after the initial immediate irrigation), and thereafter as drops every 2 to 3 hours for 48 to 72 hours, or as long as clinically indicated. |
The personal protection and safety of the attending personnel must be considered at all times during the treatment of patients. |
Remove the patient from the exposure. If respiratory symptoms such as shortness of breath are present, administer oxygen and provide additional support if necessary. |
ANTIDOTE(S)
Calcium gluconate is the antidote for hypocalcemia caused by systemic toxicity and for the treatment of localized dermal burns. Historically other agents including iced quaternary ammonium compounds, magnesium salts, and calcium carbonate have been used, but these were less effective than calcium gluconate in the treatment of burns. |
Intravenous administration of calcium, to prevent the depletion of plasma calcium or to replace it, is one of the mainstays of management. Administration should be considered if a systemically toxic dose is suspected or if symptoms of hypocalcemia occur. When given IV through a peripheral venous catheter, the gluconate salt must be used.
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It is better to document serum ionized calcium level prior to treatment. However, if severe hypocalcemia is suspected and seizures, tetany, life-threatening hypotension or cardiac arrhythmia are present, intravenous calcium is warranted without these results. Untreated hypomagnesemia will render hypocalcemia refractory to therapy. |
Calcium gluconate is indicated for hydrofluoric acid toxicity following: - Hydrofluoric acid ingestions - A burn area greater than 2.5% of body surface area - Development of symptoms indicative of hypocalcemia - Pain persisting more than 30 minutes after commencing continuous calcium gluconate gel massage - Any exposure to high concentration solutions greater than 20% |
Calcium gluconate dose: CHILD: 0.6 to 1.0 mL/kg of 10% solution by slow IV push ADULT: 10 to 30 mL of 10% solution diluted in 150 mL 5% dextrose administered IV over 10 minutes |
Maintenance Calcium Infusion |
Calcium gluconate maintenance infusion dose: CHILD: Dose yet to be established ADULT: Add 100 mL 10% calcium gluconate to 900 mL of 5% dextrose and infuse at 50 mL/h (47 mg calcium ion). Titrate infusion rate against effect - minimum infusion time is 4 to 6 h. Rate should be based on serial (2 to 6 hourly) ionized calcium measurements and resolution of manifestations of hypocalcemia. ECG monitoring is recommended. Importantly any existing abnormalities in magnesium, potassium, and pH must be corrected simultaneously. Untreated hypomagnesemia will make hypocalcemia refractory to therapy. |
Patients receiving digoxin or digoxin-like compounds should be monitored very closely as calcium may precipitate potentially fatal digitalis toxicity. Use of calcium gluconate is preferable to calcium chloride, which is an acidifying salt. Note: calcium gluconate (9% calcium ion) contains one third the calcium content of calcium chloride (27% calcium ion). |
If calcium salts are administered too rapidly, bradycardia, vasodilation, hypotension, dysrhythmias and cardiac arrest may occur.
Calcium chloride can be irritating to veins and may cause tissue destruction if extravasation occurs. It should be administered through central venous access.
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Following dermal exposures to digits specialized approaches to the administration of calcium gluconate should be considered. This is due to the increased success that these specialized approaches offer at enhancing the distribution of calcium gluconate to the affected tissues. If symptoms of hypocalcemia and/or if severe hypotension, seizures or arrhythmia exist, IV calcium gluconate should be administered. The primarily treatment should be with regional intravenous calcium gluconate administered as a Bier’s block; if this fails intra-arterial calcium gluconate should be used. |
ENHANCED ELIMINATION
Hemodialysis can be used to enhance the removal of fluoride ions, but may be more commonly indicated for secondary complications, such as acidosis or acute kidney injury. |
SUPPORTIVE CARE
12 lead ECG Electrolytes Calcium Magnesium Potassium Oxygen saturation Blood gas analysis Pain levels (indicator of success of calcium gluconate gel) Blood pressure Circulatory status Symptoms of gastrointestinal corrosion |
As pain is an indicator to the degree of success of the calcium gluconate treatment, care must be taken when choosing analgesia, so as to not mask any objective measures of pain.
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Systemic analgesia (e.g. intravenous opioids) should not be withheld from patients suffering from painful hydrofluoric acid exposures. Although these may reduce the subjective sensation of pain, they will not mask objective measures of pain such as palpation tenderness. The use of topical and regional anesthetics is controversial in painful digital and dermal hydrofluoric acid exposures. For example, digital nerve block will remove all pain in digital exposures. This will make it difficult to assess whether calcium gluconate therapy to the affected site has been successful in removal of pain.
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Supportive care is dependant on the location of the burn and the concentration of the solution. As pain is an indicator to the degree of success of the calcium gluconate treatment, care must be taken when choosing analgesia, so as to not mask any objective measures of pain. Additional care and procedures are required for digits and problematic areas; for the treatment of these cases refer to the appropriate section. Dermal hydrofluoric acid exposures can readily cause systemic toxicity and must be treated with caution. The treatment of dermal exposures is primarily aimed at reducing the absorption of the hydrofluoric acid and limiting the risk of hypocalcemia. Definitive treatment is required if: - Skin is exposed to hydrofluoric acid concentrations of greater than 20% - Pain persists following 30 minutes of continuous calcium gluconate gel massage - The burn area is greater than 2.5% of body surface area |
Monitor patient closely for: Pain levels (indicator of success of calcium gluconate gel) Symptoms of hypocalcemia Serum electrolytes Calcium Magnesium Potassium |
Gastrointestinal Corrosion |
Prophylactic administration of IV calcium and magnesium has been recommended in those symptomatic following hydrofluoric acid ingestion, due to the rapidity of onset of electrolyte abnormalities. |
Monitor patient closely for: Oropharyngeal, retrosternal chest, or abdominal pain Vomiting Oral burns Dysphagia Drooling Hoarseness or stridor In the absence of any of the above symptoms severe esophageal injury is generally unlikely, whereas the presence of three or more symptoms suggests the possibility of severe esophageal injury. The presence or absence of oral lesions is not a good indicator of the presence of esophageal injury. |
Profound hypocalcemia is a significant complication of hydrofluoric acid toxicity following oral or dermal exposure and may lead to serious cardiovascular toxicity. Untreated hypomagnesemia will render hypocalcemia refractory to therapy. |
Monitor for onset of hypocalcemia with: Observation for signs and symptoms of hypocalcemia Serum ionized calcium Serum electrolytes (hypomagnesemia and hyperkalemia are often also present) |
The interaction of the fluoride ion with intracellular magnesium causes the precipitation of insoluble magnesium salts and leads to hypomagnesemia. Untreated hypomagnesemia will make hypocalcemia refractory to therapy. The serum magnesium concentration should therefore be monitored and, if low, corrected. |
Monitor: Serum magnesium Nausea and vomiting Lethargy, weakness, fatigue Tremor Hyperreflexia |
Manage hypomagnesemia following standard treatment protocols. |
Hyperkalemia related to fluoride-induced cardiotoxicity is an additional complication of toxicity. |
Monitor: Serum potassium Blood gas analysis Renal function and urine output ECG for changes suggestive of hyperkalemia including Peaked T waves (tenting) Flattened P waves Prolonged PR interval (first-degree heart block) Widened QRS complex Deepened S waves and merging S and T waves Idioventricular rhythm Sine-wave formation VF and cardiac arrest |
Metabolic acidosis has been observed following ingestion and dermal exposure. Standard protocols for the management of acidosis should only be considered after adequate replacement of calcium has been achieved. |
Monitor: Blood gases Plasma lactate |
Manage metabolic acidosis following standard treatment protocols. |
Cardiac dysrhythmias are best managed with the intravenous administration of calcium gluconate. |
Monitor: Heart rate/rhythm Blood pressure 12 lead ECG |
Inhalation may lead to respiratory irritation and in more serious cases chemical burns, pulmonary edema and pneumonitis. The use of a nebulized solution of 2.5 to 3% calcium gluconate may be considered, although it is of unproven efficacy. |
Pulmonary edema usually manifests with desaturation, tachypnea, and pulmonary crepitations. Occasionally frothy, pink sputum may be apparent. Monitoring for this condition should include: Chest auscultation Oxygen saturation Blood gas analysis Chest x ray |
Manage pulmonary edema following standard treatment protocols. |
Further injury may be reduced with application of a 1% solution of calcium gluconate in normal (0.9%) saline. This is used to wash the eye for a further 5 to 10 minutes (after the initial immediate irrigation), and thereafter as drops every 2 to 3 hours for 48 to 72 hours, or as long as clinically indicated. The patient should always be referred to an ophthalmologist.
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Examine for: Conjunctivitis Lacrimation Photophobia Pupil abnormality Visual acuity Corneal defect (with fluorescein staining) |
SIGNS AND SYMPTOMS
The onset and severity of symptoms is concentration dependent. Hydrofluoric acid is moderately corrosive by ingestion, inhalation, skin and eye exposure, and can cause systemic toxicity via all routes. Unlike more corrosive acids, it may not cause immediate localized pain and tissue damage when individuals are exposed to concentrations less than 50%. Local symptoms may be delayed and should be monitored for following exposures to low concentration formulations. Systemic symptoms of hypocalcemia, hypomagnesemia, hyperkalemia, pulmonary edema, metabolic acidosis, ventricular dysrhythmias and death may occur following ingestion or large dermal exposures. |
Onset/Duration of Symptoms |
The onset and severity of symptoms may vary depending on the concentration and the route of exposure. Following exposure to low concentration formulations localized symptoms may be delayed, while onset of local and systemic symptoms may be rapid following high concentration exposures. Pain may be delayed and may not be proportional to the size of the visible injury. This may result in delayed triage or medical diagnosis on presentation to hospital. Without appropriate treatment, burns can continue to increase in surface area for 4 to 7 days.
Hydrofluoric acid primarily produces tissue damage by the dissociation of fluoride ions into the tissues. This is a relatively slow process, compared to the corrosive action of other acids. Hypocalcemia, hypomagnesemia and acidosis may occur within 1 to 2 hours following large dermal exposures or ingestions of hydrofluoric acid.
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Hydrofluoric acid is moderately corrosive by ingestion, inhalation, skin and eye exposure. Systemic toxicity can occur from all routes of exposure, but is most likely following ingestions or significant dermal exposures to concentrated formulations.
Following any exposure to hydrofluoric acid systemic toxicity is possible and may be delayed; a cautious approach must be applied in all cases.
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Following an exposure to hydrofluoric acid, mild symptoms are associated with local effects, while moderate or severe symptoms are an indication of systemic toxicity or an exposure to a concentrated formulation. | Mild Hydrofluoric Acid Toxicity | Moderate Hydrofluoric Acid Toxicity | Severe Hydrofluoric Acid Toxicity | Edema Pain Erythema | Blanching Blistering Ulceration Vomiting Necrosis | Decalcification of the bone Cardiac dysrhythmias Metabolic acidosis Hypocalcemia Hepatic damage Cardiac arrest Death |
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ACUTE EFFECTS (ROUTE OF EXPOSURE)
Hydrofluoric acid is only moderately corrosive; unlike more corrosive acids (e.g. hydrochloric or sulfuric acids) it may not cause immediate pain and tissue damage when individuals are exposed to concentrations less than 50%. Higher concentrations may produce early corrosive effects with onset of pain and tissue destruction. Hydrofluoric acid primarily produces tissue damage by the dissociation of fluoride ions into the tissues. Fluoride binds to intracellular divalent cations (calcium and magnesium) resulting in cell death. This is a relatively slow process, compared to the corrosive action of other acids. Consequently, symptoms may not be apparent for several hours when exposure to lower concentrations of hydrofluoric acid occurs. The severity and rapidity of onset of symptoms depends on the hydrofluoric acid concentration, the duration of exposure and the penetrability of the exposed area. Pain may be delayed and may not be proportional to the size of the visible injury. This may result in delayed triage or medical diagnosis on presentation to hospital. Concentrations less than 20% Symptoms may be delayed from to 8 to 24 hours. On presentation to hospital symptoms may not be associated with exposure to hydrofluoric acid by the patient. Pain may appear out of proportion to the presence of clinical signs. Concentrations from 20 to 50% Onset of pain is usually within 30 to 60 minutes. Occasionally, symptoms may be delayed up to 8 hours Concentrations greater than 50% Immediate burning, erythema and rapid tissue damage with onset of pain frequently within 5 to 10 minutes Initial symptoms are usually swelling, erythema and burning pain which either: Resolve gradually or, if the patient has a delayed presentation or is left untreated: Progress to intense pain with gradual tissue destruction characterized by: Erythema Pallor Skin blanching Blistering Bluish-black necrotic appearance Tissue destruction proceeds initially under the dead, toughened, skin. With breakdown of the skin surface, ulceration may extend into the deep tissues. Such lesions will heal slowly and may leave a scar. Decalcification and corrosion of the bone beneath the area of the burn may occur. Without appropriate treatment, burns can continue to increase in surface area for 4 to 7 days. The risk of systemic toxicity following dermal exposure is dependent upon the hydrofluoric acid concentration, the surface area involved, and contact time before decontamination. Effects can include metabolic changes (particularly hypocalcemia, hypomagnesemia, and hyperkalemia), cardiac dysrhythmias and death. Exposures involving the fingers and hands are not generally associated with systemic effects due to the small surface area involved. However, dermal exposure to 70% hydrofluoric acid over 2.5% total body surface has resulted in death. |
Ingestion may result in spontaneous vomiting, abdominal pain, painful necrotic lesions in the upper gastrointestinal tract, hemorrhagic gastritis and possibly pancreatitis.
Systemic effects may include metabolic changes (particularly metabolic acidemia, hypocalcemia and hyperkalemia), cardiac QT-interval prolongation, dysrhythmias, and death. These effects may take some hours to become apparent, especially if the ingested substance contains low fluoride concentrations.
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Eye exposure to liquid hydrofluoric acid can result in severe ocular damage. The onset of clinical signs and symptoms may be delayed. Exposure to fumes at concentrations as low as 5 ppm may cause ocular injury.
The composition of products containing hydrofluoric acid commonly ranges from 1.5 to 40%. In experimental animals, even a 2% solution caused mild persistent corneal stromal edema and vascularization. Mild reversible changes were noted with a 0.5% solution.
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At room temperature, solutions of hydrofluoric acid below 50% should not usually be an inhalation hazard due to limited vaporization. Mucous membrane irritation may result from inhalation of fumes or vapor. Dyspnea, bronchospasm, chemical pneumonitis, pulmonary edema (possibly hemorrhagic), tracheobronchitis and airway obstruction, secondary to laryngeal edema have all been reported following inhalation. Chemical burns to the larynx, trachea and bronchi may also occur.
Following inhalation, systemic effects may also be seen, particularly if treatment is not timely. These can include metabolic changes (particularly hypocalcemia), cardiac dysrhythmias and death.
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Rectal administration has caused colitis and colonic perforation.
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ACUTE EFFECTS (ORGAN SYSTEM)
Eschar Edema Erythema Skin discoloration Blistering Ulceration Necrosis |
Corrosion and decalcification of bone |
Nausea Vomiting Pharyngeal erythema and edema Abdominal pain Hemorrhagic gastritis Hematemesis Gastric necrosis and perforation Pancreatitis Colitis and perforation (rectal administration) |
ECG abnormalities QT prolongation Ventricular dysrhythmias Myocardial damage Cardiac arrest |
Metabolic acidosis Hypocalcemia Hypomagnesemia Hyperkalemia |
Elevated serum aspartate aminotransferase (AST) Elevated serum lactate dehydrogenase (LDH) |
Corneal erosion Corneal opacification Corneal stroma scarring and progressive vascularisation Decreased visual acuity Blindness (severe cases) Glaucoma (sequelae) |
CHRONIC EFFECTS
Chronic ingestion or inhalation can lead to fluorosis.
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Weight loss Malaise Nausea Diarrhea Constipation Anemia Leukopenia Weakness Discoloration of teeth Osteosclerosis
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TOXICITY
HUMAN
It is estimated that doses of fluoride in the range of 3 to 5 mg/kg will cause mild to moderate toxicity, while serious toxicity is likely at 5 to 10 mg/kg especially in children. A lethal dose is considered to be approximately 15 mg/kg or more. |
70% hydrofluoric acid exposure to 2.5% body surface area Patient details unknown, calcium level of 2.2 mg/dL (0.54 mmol/L) Death 70% hydrofluoric acid exposure to 25% body surface area Patient details unknown, calcium level of 1.7 mg/dL (0.43 mmol/l), cardiac arrest Death An unknown concentration of hydrofluoric acid exposure to 8% body surface area Patient details unknown, intractable cardiac dysrhythmia Death |
15 mL dose of 9% (1.35 g) hydrofluoric acid Patient details unknown Death Unknown volume of unknown strength (1.5 g) hydrofluoric acid Patient details unknown Death occurred 6.5 hours post ingestion |
LCLo Human | 50 ppm for 30 minutes | TCLo Human | 100 mg/cu meter for 1 minute (nose, eye, and pulmonary effects) |
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Chronic exposure to hydrofluoric acid or hydrogen fluoride can lead to fluorosis. |
ANIMAL
LC50 Inhalation, Rat | 966 ppm966 ppm/1 h |
LC50 Inhalation, Mouse | 342 ppm342 ppm/1 h |
LC50 Inhalation, Guinea pig | 4,327 ppm4,327 ppm/15 min |
LC50 Inhalation, Monkey | 1,774 ppm1,774 ppm/1 h |
LDLo SC, Frog | 112 mg/kg112 mg/kg/ |
LDLo Dermal, Mouse | 500 mg/kg500 mg/kg/ |
LDLo IP, Rat | 25 mg/kg25 mg/kg/ |
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BIOLOGICAL LEVELS - TOXIC
To convert an fluoride concentration expressed in mg/L into umol/L: Multiply the mg/L by 52.6 To convert an fluoride concentration expressed in umol/L into mg/L: Multiply the umol/L by 0.019 |
Normal Serum Concentrations |
Background fluoride levels | < 0.018 mg/L (0.94 umol/L) | Persons on a low fluoride diet | 0.01 mg/L (0.5 umol/L) |
Workers exposed to environmental fluoride levels of 0.9 mg/cu meter | Pre-shift plasma fluoride levels | 0.023 mg/L (1.2 umol/L) | Post-shift plasma fluoride levels | 0.048 mg/L (2.5 umol/L) |
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Toxic Serum Concentrations |
Fluoride levels of 2.6 mg/L (137 umol/L) have produced severe toxicity. Post mortem plasma fluoride concentrations following ingestion of hydrofluoric acid have ranged from 8.3 to 56.2 mg/L (437 to 2,956 umol/L). 100 mL ingestion of an unknown strength hydrofluoric acid solution 33 year old man, serum fluoride level 56.2 mg/L (2,956 umol/L) Death resulted 45 minutes after ingestion |
To convert an calcium concentration expressed in mg/dL into mmol/L: Multiply the mg/dL by 0.2495 To convert an calcium concentration expressed in mmol/L into mg/dL: Multiply the mmol/L by 4.008 Units: 1 dL = 0.1 L 1 ug/L = 0.1 ug/dL 1 ug/dL = 10 ug/L |
Normal Serum Concentrations |
Normal blood calcium levels in adults range from 8.8 to 10.3 mg/dL (2.2 to 2.58 mmol/L). |
TOXIC MECHANISM
Many of the pathophysiological effects of hydrofluoric acid are related to the deep penetration of undissociated hydrofluoric acid through tissues. Following dissociation in the tissues, the free fluoride ions bind to calcium and magnesium cations to form insoluble salts, at a rate that exceeds the ability to mobilize further calcium and magnesium from bone. Fluoride may also inhibit the Na+, K+ ATPase enzyme of cell membranes, leading to potassium efflux from cells (including erythrocytes) producing hyperkalemia, which can contribute further to dysrhythmias. |
IDENTIFICATION
OTHER NAME(S)
| Fluohydric acid | Fluorhydric acid | | Fluoric acid | HF | | HFA | Hydrofluoric acid | | Hydrofluoride | Hydrogen fluoride |
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CODES
CAS NUMBER
Hydrofluoric Acid: 7664-39-3 |
Do Not Archive. This document is current on day of issue,
NZ: 25.May.2022 |
