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SECTION 1. CHEMICAL IDENTIFICATION

CHEMINFO Record Number: 47
CCOHS Chemical Name: Hydrofluoric acid

Synonyms:
Aqueous hydrogen fluoride
Fluoric acid
Fluorohydric acid (non-specific name)
HF (non-specific name)
Hyfluoric Acid

Chemical Name French: Acide fluorhydrique
Chemical Name Spanish: ácido fluorhídrico
CAS Registry Number: 7664-39-3
UN/NA Number(s): 1790
RTECS Number(s): MW7875000
EU EINECS/ELINCS Number: 231-634-8 (hydrofluoric acid ...%)
Chemical Family: Mineral acid / inorganic acid / halogenated inorganic acid / hydrogen halide / hydrogen fluoride
Molecular Formula: F-H
Structural Formula: H-F

SECTION 2. DESCRIPTION

Appearance and Odour:
Colourless liquid with a pungent, irritating, penetrating odour. Concentrations above 40% fume in air.(21,35,36)

Odour Threshold:
A range of values have been reported; 0.04-0.14 ppm (0.03-0.11 mg/m3).(3) 0.04 ppm (0.03 mg/m3) (minimum perceptible concentration).(36)

Warning Properties:
GOOD - TLV is more than 10 times the odour threshold.

Composition/Purity:
Hydrogen fluoride is available in anhydrous form (either as a gas or a liquid), or as a solution in water (known as hydrofluoric acid). This CHEMINFO profile reviews the hazards and control information for hydrofluoric acid. For information on the anhydrous form, refer to the CHEMINFO review for hydrogen fluoride. Hydrofluoric acid is primarily available as 50% and 70% hydrogen fluoride solutions in water.(35,37) It is also available as 30%, 40% and 48% solutions.(36) The major impurities are sulfur dioxide, sulfuric acid and hydrofluosilic acid.(35) Hydrofluoric acid is used at dilutions ranging down to 0.5%.(23) It is shipped in bulk in tank cars and tank trucks, mainly as a 70% aqueous solution, with a small amount shipped as a 50% solution.(35,37)

Uses and Occurrences:
Hydrofluoric acid is used in stainless steel pickling operations; in chemical milling; in exotic metal extraction; in quartz purification; in metal coatings; for polishing, etching and frosting glass and enamel; cleaning iron, steel castings, copper and brass; cleaning of stone and brick; removing sand particle from metallic castings; for the acid treatment of oil wells; in the production of elemental fluorine, aluminum fluoride, synthetic cryolite (sodium aluminum fluoride), fluoborates, and fluorinated organics, like aerosol propellants, special-purpose solvents, refrigerants and plastics; in the formulation of atomic-energy feed materials; dissolving of ores; and as an analytical reagent. It is also used in the electronics industry in the engraving, polishing and etching of electronic silicon wafers.(35,37,39,46)
Hydrogen fluoride can be released to the environment by volcanoes and sea salt aerosol, as well as from manufacturing and processing facilities, and welding processes. However, because of its very high reactivity, it is unlikely to remain in its original form for very long.(2,21)


SECTION 3. HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW:
Colourless liquid with a pungent, irritating, penetrating odour. Concentrations above 40% fume in air. Will not burn. Cylinders or tanks may rupture and explode if heated. Highly reactive. Contact with metals, such as iron or steel, slowly releases extremely flammable and potentially explosive hydrogen gas. VERY TOXIC. May be fatal if inhaled, absorbed through the skin or swallowed. CORROSIVE to the nose, throat and respiratory tract. Causes lung injury-effects may be delayed. CORROSIVE to the eyes and skin. Causes severe burns. May cause blindness and permanent scarring. Absorbed fluoride can cause metabolic imbalances with irregular heartbeat, nausea, dizziness, vomiting and seizures. Long-term exposure may cause skeletal fluorosis (weakened bone structure).



POTENTIAL HEALTH EFFECTS

Effects of Short-Term (Acute) Exposure

Inhalation:
Hydrofluoric acid (HF) is extremely toxic by inhalation.
Low concentrations (a few ppm) can cause irritation of the nose, throat, eyes and respiratory tract. Higher concentrations can cause severe burns to the throat, airways and lungs. Absorbed fluoride can cause metabolic imbalances with irregular heartbeat, central nervous system depression, and seizures. Fluid accumulation in the lungs and irregular heartbeat has led to deaths within hours following inhalation and, in some cases, concurrent skin contact with unknown concentrations of HF.(2,21)
With serious exposures, throat irritation, coughing, chest pain, nausea and perhaps some difficulty breathing may be experienced during exposure. These symptoms usually resolve once exposure stops. The victim may feel fine and may even return to work. This latent period can last from 1-24 hours, depending on the extent of the exposure. Within 24-48 hours, the victim may experience a rapidly worsening difficulty in breathing, accompanied by coughing. These symptoms are due to the development of a life-threatening accumulation of fluid in the lungs (pulmonary edema). Severe short-term exposures may result in long- lasting effects such as shortness of breath and pulmonary emphysema (larger than normal air spaces in the lungs which decrease lung efficiency).
Exposure of 24 male volunteers to 0.24 to 6.34 ppm (cited as 0.2 to 5.2 mg/m3) for 1 hour caused upper airway symptoms even at the lowest concentration. Most symptoms disappeared within 4 hours after exposure.(9) Exposure of 19 male volunteers to 0.24-0.73, 0.85-2.92 or 3.05-6.34 ppm (cited as 0.2-0.6, 0.7-2.4 or 2.5-5.2 mg/m3) for 1 hour resulted in inflammatory changes in the airways at concentrations greater than 0.73 ppm.(56) Exposure of 10 male volunteers to 4.02-4.76 ppm (cited as 3.3-3.9 mg/m3) for 1 hour resulted in an immediate nasal inflammatory response in the nose.(57) Following the accidental release of HF into a community, the most commonly reported symptoms were burning throat, headache, and shortness of breath. Nausea, vomiting, and dizziness were commonly reported in those hospitalized. Affects on breathing were detected in lung function tests. A concentration of 10 ppm HF was measured downwind 1-hour after the release.(7)
Five volunteers tolerated average concentrations of 1.4 ppm for 15 days to over 4.2 ppm for 25-50 days (6 hours/day). Up to 2 ppm was reported to have no noticeable effect. At 2.6-4.7 ppm, some discomfort and slight irritation of the nasal passages was reported.(17,21)

Skin Contact:
Hydrofluoric acid is extremely corrosive and can cause very deep and excruciatingly painful burns and tissue loss. Burns from concentrated solutions (greater than 50%) are felt immediately and tissue destruction is readily apparent. Weaker solutions (20-50%) result in burns that are apparent after several hours. Burns from solutions of less than 20% may take up to 24 hours to become apparent. Weak solutions (less than 7%) penetrate deeply before causing tissue damage and surface involvement may be minimal. Pain is greater than expected for the skin involvement and is described as severe deep and throbbing. The severity of hydrofluoric acid burns depends on the concentration of the solution, surface area involved and the duration of exposure. Burns are swollen, hot and painful, then develop white or yellowish areas and blistering, with deep ulceration and destruction of tissue, which tends to heal slowly. Loss of fingers has been reported following untreated skin contact. The severity of the burns and absorption of the acid (with liquefaction necrosis of soft tissue and decalcification and corrosion of the bone) have resulted in permanent scarring, disability and death. In some cases, systemic fluoride toxicity has occurred following skin contact. Absorbed fluoride can cause metabolic imbalances with irregular heartbeat, central nervous system depression, seizures, and deaths.(2,21,25,26,28,31,32,60)
Any serious skin contact may also involve inhalation exposure. There are some reports of serious inhalation effects occurring following significant skin contact.(2,28) See "Inhalation" above for details.

Eye Contact:
Direct contact with hydrofluoric acid can cause severe and irreversible corrosive injury with possible corneal scarring and blindness. The acid penetrates to deep tissue layers and causes severe corrosive injury.(23,34) Very few cases of direct eye contact have been reported in the literature.(21) In one case, a severe splash of hydrofluoric acid on the face resulted in extensive clouding of both corneas.(30) In another case, severe corrosive injury to the eyes was observed, but full recovery occurred by day 35.(21)
The gas can dissolve in the moisture on the surface, forming corrosive hydrofluoric acid. Irritation has been reported with exposure to concentrations as low as 0.24 ppm for 1 hour.

Ingestion:
Hydrofluoric acid is corrosive and can cause severe burning of the mouth, throat and stomach. Perforation of the digestive system may occur. Systemic fluoride toxicity has occurred following ingestion. Absorbed fluoride can cause metabolic imbalances with irregular heartbeat, central nervous system depression, seizures, and deaths. Symptoms such as nausea, vomiting, abdominal pain, reduced heartbeat and blood pressure, shortness of breath have been reported. Several deaths have occurred following accidental or intentional ingestion of hydrofluoric acid. In some cases, death occurred in less than one hour following ingestion.(2,28,33) Ingestion is not a typical route of occupational exposure.

Effects of Long-Term (Chronic) Exposure

The major health hazards of hydrofluoric acid exposure are related to the irritant and corrosive effects experienced during short-term exposures.

FLUOROSIS: Fluoride is a bone seeker, and exposure to excessive amounts will weaken and degenerate the bone structure (osteosclerosis). Early signs of the disease (e.g. denser and thicker bones) may only be detected with x- ray examination. Early symptoms include pain in the joints of the hands, feet, knees and spine and a limited range of joint movement. There may also be heart, nerve, and intestinal problems. In some cases, greyish or chalk-white discolouration and pitting of the teeth may be noted. The disease is called fluorosis. The amount of fluoride stored in the bones usually increases with increasing fluoride intake.(1,3,8) Excess fluoride is removed slowly from the body over a period of years. Skeletal fluorosis may be slowly and partially reversible.(13)
There have been reports of employees with long-term exposure to hydrogen fluoride and/or fluoride dust developing very early signs of fluorosis.(1,2,21) Occupational fluorosis of crippling severity has rarely been seen since the 1930's and 1940's.(11,21) One large study followed 2,258 aluminum workers exposed to fluoride (form not specified, but probably hydrogen fluoride and fluoride dust) for an average of 17.6 years. Exposures ranged up to 2.0 mg HF/m3 (actual measurements and sampling methods not provided). Possible or definite fluorosis was observed in 20.5% of cases. Of these cases, 14% were very early cases of possible fluorosis (multiple joint pains, limited motion in at least two joints or the spine and initial ossification observed on x-rays). Initial fluorosis (Stage 0) was observed in 5.12% of the cases, Stage I fluorosis in 1.0% and Stage II fluorosis in 0.05%. There were no cases of Stage III fluorosis.(10) A study of 107 potroom workers with severe fluoride exposure (2.4 to 6 .0 mg F/m3) for an average of 19.1 years showed that a large percentage (96% of 79 employees x-rayed) had developed varying degrees of skeletal fluorosis, but without physical impairment or noticeable signs or symptoms of the disease.(12)
An extensive review has concluded that the incidence of osteosclerosis is often high in employees exposed to airborne fluoride concentrations of higher than 2.5 mg F/m3 and/or when urinary levels of fluoride exceed 9 mg/L.(1,11) With higher air fluoride concentrations and with long- continued employment, osteosclerosis develops more rapidly, the extent and the degree of abnormality are greater, the stage of osteosclerosis tends to be higher and the percentage of workers showing osteosclerosis is greater.(11)

Lungs/Respiratory System:
It is difficult to draw conclusions regarding the possibility of respiratory effects developing following long-term, low-level HF exposure. Many of the available studies are limited because employees were exposed to other potentially harmful chemicals at the same time. Nevertheless, reviews have concluded that HF exposure less than the occupational exposure limit would not cause lung disease, with the possible exception of increased frequency of upper respiratory infections in aluminum potroom workers.(11,21) Exposure to HF may increase the reactivity of the airways (bronchial hyperreactivity).(20) Increased reactivity of the airways may lead to symptoms such as wheezing and shortness of breath upon exposure to respiratory irritants or cold air.
One study of employees exposed to hydrogen fluoride and fluoride dusts in aluminum smeltering showed respiratory effects (lower forced expiratory volume, increased cough and sputum production) in the highest exposure group (more than 50% of working time spent in potroom).(19) No firm conclusions about the respiratory effects of hydrogen fluoride can be drawn from this study. Actual exposure concentrations are unknown (the employees wore respirators) and there was exposure to other respiratory irritants at the same time.
One study describes inflammation of the upper respiratory tract and nose, progressing to degeneration of the membranes and even perforation of the nasal septum. The exposures were described as "elevated".(11, unconfirmed) There are no further details available.

Skin:
A number of studies have commented on the possibility that long-term fluoride exposure may cause certain skin disorders (e.g. dermatitis, rashes). Review of this literature does not reveal an association between long-lasting skin injury and exposures below 2.5 mg F/m3.(11)

Kidneys/Urinary System:
A number of studies have examined the possibility that long-term fluoride exposure may cause kidney effects. Reviews of this literature have concluded that it is unlikely that HF exposure below occupational exposure limits would cause kidney injury.(2,11)

Carcinogenicity:

It is not possible to draw conclusions about the potential carcinogenicity of hydrofluoric acid based on the available information. A number of studies have evaluated occupational groups exposed to fluorides, as well as other chemicals. Excess cancer rates have been reported in some groups with exposure to hydrogen fluoride and fluoride dusts. However, due to the concurrent exposures to other chemicals and other significant study design limitations, it is not possible to draw any specific conclusions about hydrofluoric acid.(1,2)

The International Agency for Research on Cancer (IARC) has not evaluated the carcinogenicity of this chemical.

The American Conference of Governmental Industrial Hygienists (ACGIH) has not assigned a carcinogenicity designation to this chemical.

The US National Toxicology Program (NTP) has not listed this chemical in its report on carcinogens.

Teratogenicity and Embryotoxicity:
Hydrofluoric acid is not expected to cause developmental effects.(2,58) There is no specific human information available. There are insufficient details available to evaluate the one animal study located.

Reproductive Toxicity:
There is no specific human or animal information available for hydrofluoric acid. No conclusions can be drawn about the potential for fluorides to cause reproductive effects.(2)

Mutagenicity:
The available information does not suggest that hydrofluoric acid is mutagenic. In one limited study, positive results (sister chromatid exchanges in peripheral blood lymphocytes) were obtained in a small number of employees exposed to HF and several other chemicals.(18) In general, fluorides are only mutagenic at doses that are highly toxic to cells and whole animals.(2)

Toxicologically Synergistic Materials:
There is no information available.

Potential for Accumulation:
Hydrofluoric acid can enter the body through ingestion, inhalation or skin contact. Absorbed fluoride is either excreted in the urine or taken up by bones and teeth. Fluoride stored in bones and teeth may be eliminated from the body over several years. Fluoride passes through the placenta and occurs in very low concentrations in saliva, sweat and milk.(1,2)


SECTION 4. FIRST AID MEASURES

Inhalation:
Take proper precautions to ensure your own safety before attempting rescue (e.g. wear appropriate protective equipment, use the "buddy" system). Remove source of contamination or move victim to fresh air. If breathing is difficult, trained personnel should administer oxygen and 2.5% calcium gluconate, preferably with a doctor's advice. DO NOT allow victim to move about unnecessarily. Symptoms of pulmonary edema can be delayed up to 48 hours after exposure. If breathing has stopped, trained personnel should begin artificial respiration (AR) or, if the heart has stopped, cardiopulmonary resuscitation (CPR) or automated external defibrillation (AED) immediately. Avoid mouth-to-mouth contact by using mouth guards or shields. Quickly transport victim to an emergency care facility.

Skin Contact:
Avoid direct contact. Wear chemical protective clothing, if necessary. As quickly as possible, remove contaminated clothing, shoes and leather goods (e.g. watchbands, belts). Immediately flush with lukewarm, gently flowing water. Limit flushing with water to 5 minutes if 0.13% benzalkonium chloride (Zephiran(R)) solution or 2.5% calcium gluconate gel is available. If these treatments are not available, continue flushing until medical treatment is available. BENZALKONIUM CHLORIDE: Begin soaking the affected area in iced 0.13% benzalkonium chloride (Zephiran(R)) solution. Use ice cubes, not shaved ice, to prevent frostbite. If immersion is not practical, towels should be soaked with iced 0.13% benzalkonium chloride (Zephiran(R)) solutions and used as compresses for the burned area. Compresses should be changed every 2-4 minutes. Benzalkonium chloride (Zephiran(R)) soaks or compresses should be continued until medical attention is available. CALCIUM GLUCONATE GEL: Wearing chemical protective gloves, start massaging 2.5% calcium gluconate gel into the burn site. Apply gel frequently and massage continuously until medical attention is available. Quickly transport victim to an emergency care facility. Double bag, seal, label and leave contaminated clothing, shoes and leather goods at the scene for safe disposal.

Eye Contact:
Avoid direct contact. Wear chemical protective gloves if necessary. Immediately flush the contaminated eye(s) with lukewarm, gently flowing water for 15-20 minutes, while holding the eyelid(s) open. If a contact lens is present, DO NOT delay irrigation or attempt to remove the lens. Take care not to rinse contaminated water into the unaffected eye. DO NOT use benzalkonium chloride (Zephiran(R)) for eye contact. If sterile 1% calcium gluconate is available, limit water flushing to 5 minutes. Then, use the 1% calcium gluconate solution to repeatedly rinse the eye(s). Immediately transport victim to an emergency care facility. Continue flushing with water, neutral saline or 1% calcium gluconate during transport, if at all possible.

Ingestion:
NEVER give anything by mouth if victim is rapidly losing consciousness, is unconscious or is convulsing. Have victim rinse mouth thoroughly with water. DO NOT INDUCE VOMITING. If vomiting occurs naturally, rinse have victim rinse mouth with water again. Quickly transport victim to an emergency care facility.

First Aid Comments:
Provide general supportive measures (comfort, warmth, rest).
Consult a doctor and/or the nearest Poison Control Centre for all exposures.
Some first aid procedures recommended above require advanced first aid training. Protocols for undertaking advanced procedures must be developed in consultation with a doctor and routinely reviewed.
All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.

NOTE: Burns caused by weak hydrofluoric acid may go unnoticed for several hours. Therefore, first aid procedures must be followed if any contact is suspected.

Note to Physicians:
For more information on first aid procedures and medical advice, refer to references 40, 41, 59 and 61.



SECTION 5. FIRE FIGHTING MEASURES

Flash Point:
Not combustible (does not burn)

Lower Flammable (Explosive) Limit (LFL/LEL):
Not applicable

Upper Flammable (Explosive) Limit (UFL/UEL):
Not applicable

Autoignition (Ignition) Temperature:
Not applicable

Sensitivity to Mechanical Impact:
Not sensitive. Stable material.

Sensitivity to Static Charge:
Will not accumulate static charge. The electrical conductivity of 70% hydrogen fluoride in water is very high and solutions of lower concentration have even higher electrical conductivities.(35) Since it does not burn, hydrofluoric acid will not be ignited by a static discharge.

Electrical Conductivity:
7.9 x 10(13) pS/m at 0 deg C (70% HF) (35)

Minimum Ignition Energy:
Not applicable.

Combustion and Thermal Decomposition Products:
Corrosive, very toxic hydrogen fluoride gas.

Flammable Properties:

Specific Hazards Arising from the Chemical:
Contact of HF (particularly in dilute aqueous solutions) with some metals produces extremely flammable and potentially explosive hydrogen gas. A large amount of heat is generated when highly concentrated hydrofluoric acid solutions are diluted with water. Closed containers may rupture violently and suddenly release large amounts of product when exposed to fire or excessive heat for a sufficient period of time.

Extinguishing Media:
Hydrofluoric acid does not burn. Use extinguishing agents compatible with acid and appropriate for fire surrounding hydrofluoric acid containers. The extinguishing medium used depends on the concentration of the acid. Water spray or fog may be used where concentrations below 60% are present. Higher concentrations may react violently with water and a dry agent, e.g. dry chemical powder is recommended. Use water spray to keep fire exposed containers cool.

Extinguishing Media to be Avoided:
DO NOT use water or water-based extinguishers with highly concentrated solutions, since they react violently with water.

Fire Fighting Instructions:
Evacuate area and fight fire from a safe distance or protected location. Approach fire from upwind to avoid corrosive and very toxic hydrogen fluoride gas.
If possible, isolate hydrofluoric acid containers and move them from the fire area if this can be done without risk, and protect personnel. Handle damaged containers with extreme care. Otherwise, fire-exposed containers or tanks should be cooled by application of hose streams and this should begin as soon as possible (within the first several minutes) and should concentrate on any unwetted portions of the container. Water is very effective in knocking down hydrogen fluoride gas escaping from leaking containers of hydrofluoric acid. The resulting water solutions of hydrogen fluoride should be expected to be very corrosive. Dike fire control water for appropriate disposal. However, if water contacts concentrated hydrofluoric acid solutions, a large amount of heat will be generated and there is a danger of violent hydrogen fluoride splashing. DO NOT direct water at open or leaking containers and take precautions not to get water into the containers. Stay away from ends of tanks, but be aware that flying material from ruptured tanks may travel in any direction. Withdraw immediately in case of rising sounds from venting safety device or any discolouration of tanks due to fire.
Containers or tanks should not be approached directly after they have been involved in a fire or heated by exposure, until they have been completely cooled down. After the fire has been extinguished corrosive and toxic atmospheres may linger. Before allowing workers to enter such an area, especially confined areas, check the atmosphere with an appropriate monitoring device while wearing full protective gear.

Protection of Fire Fighters:
Hydrofluoric acid is corrosive and very hazardous to health. Do not enter without wearing specialized protective equipment suitable for the situation. Firefighter's normal protective clothing (Bunker Gear) will not provide adequate protection. A full-body encapsulating chemical protective suit with positive pressure self-contained breathing apparatus (NIOSH approved or equivalent) may be necessary.



NATIONAL FIRE PROTECTION ASSOCIATION (NFPA) HAZARD IDENTIFICATION

NFPA - Health: 4 - Very short exposure could cause death or major residual injury. (hydrogen fluoride)
NFPA - Flammability: 0 - Will not burn under typical fire conditions. (hydrogen fluoride)
NFPA - Instability: 1 - Normally stable, but can become unstable at elevated temperatures and pressures, or may react vigorously, but non-violently with water. (hydrogen fluoride)

SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES

Molecular Weight: Hydrogen fluoride: 20.01 (monomeric form); 55 (at 25 deg C and 101.3 kPa); 74.9 (at 19.5 deg C and 101.3 kPa) See Physical Properties Comments.

Conversion Factor:
1 ppm = 0.82 mg/m3; 1 mg/m3 = 1.22 ppm at 25 deg C (HF monomer) (calculated); 1 ppm = 2.24 mg/m3; 1 mg/m3 = 0.44 ppm at 25 deg C (molecular weight of 55) (calculated); 1 ppm = 3.12 mg/m3; 1 mg/m3 = 0.32 ppm at 20 deg C (molecular weight of 74.9) (calculated); See Physical Properties Comments.

Physical State: Liquid
Melting Point: Varies with concentration; -69 deg C (-92.2 deg F) (70% solution) (35); -37 deg C (-34.6 deg F) (48%) (38)
Boiling Point: Varies with concentration; 66.5 deg C (151.7 deg F) (70% solution) (35); 108.7 deg C (227.7 deg F) (47%) (62); 112.2 deg C (234 deg F) (38.2%) (46,62)
Relative Density (Specific Gravity): Varies with concentration; 1.23 (70% HF); 1.18 (50%) at 20 deg C (water = 1) (35,37)
Solubility in Water: Soluble in all proportions (38,46)
Solubility in Other Liquids: Soluble in ethanol (38); slightly soluble in diethyl ether, benzene, toluene, xylene and tetralin.
Coefficient of Oil/Water Distribution (Partition Coefficient): Log P (oct) = 0.23 (estimated) (47)
pH Value: 1.6 (1M (2%) solution); 1.0 (30%); 0.9 (50%); 0.8 (70%) (calculated)
Acidity: Fairly weak acid; (35,37) Fairly weak acid; (35,37,46)
Dissociation Constant: pKa = 3.19 (Ka = 6.46 x 10(-4)) (35,46)
Viscosity-Dynamic: 0.61 mPa.s (0.61 centipoises) at 25 deg C (70% HF) (35)
Surface Tension: Not available
Vapour Density: 1.86 at 25 deg C (air = 1) (HF gas) (42); {molecular weight of 55; see Physical Properties Comments.}
Vapour Pressure: PARTIAL PRESSURE: 15.72 kPa (117.9 mm Hg) (70%) (38); 1.65 kPa (12.4 mm Hg) (50%); 0.17 kPa (1.27 mm Hg) (30%) at 20 deg C (calculated) (38,63)
Saturation Vapour Concentration: 15520 ppm (15.5%) (70% solution); 16320 ppm (1.63%) (50%); 1670 ppm (0.17%) (30%) at 20 deg C (calculated)
Evaporation Rate: Varies with concentration
Henry's Law Constant: Not available

Physical Properties Comments:
There is an association of anhydrous hydrogen fluoride molecules in the vapour and liquid states at normal room temperatures and pressures. The degree of association is dependent on the temperature. At the boiling point (19.5 deg C) under atmospheric pressure, the average degree of association is 3.74, which corresponds to an average molecular weight of 74.9. At 25 deg C, the mean degree of association is approximately 2.75, corresponding to an average molecular weight of about 55. This molecular association affects certain physical properties, such as boiling point and density. As a result, the actual density of the gas is greater than would be calculated from its monomeric formula.(3,37)


SECTION 10. STABILITY AND REACTIVITY

Stability:
Normally stable. Hydrogen fluoride is one of the most stable diatomic molecules.(35,37)

Hazardous Polymerization:
Hydrogen fluoride tends to associate by means of hydrogen bonds to form polymers in both the liquid and gaseous states.(35,37) This polymerization is not hazardous.

Incompatibility - Materials to Avoid:

NOTE: Chemical reactions that could result in a hazardous situation (e.g. generation of flammable or toxic chemicals, fire or detonation) are listed here. Many of these reactions can be done safely if specific control measures (e.g. cooling of the reaction) are in place. Although not intended to be complete, an overview of important reactions involving common chemicals is provided to assist in the development of safe work practices.


Hydrofluoric acid is highly reactive.
WATER - a large amount of heat is generated when highly concentrated solutions are diluted with water. Spattering or splashing may occur.(38,48)
METALS (e.g. iron, steel; particularly in the presence of water) - may react to form extremely flammable and potentially explosive hydrogen gas.(35,37,38,49)
ANTIMONY OR ARSENIC CONTAINING METAL ALLOYS - extremely toxic stibine may be released from antimony containing metal alloys and extremely toxic arsine from arsenic containing alloys.(49)
CYANIDES - contact may release toxic and flammable hydrogen cyanide gas.(38)
CYANOGEN FLUORIDE - may polymerize explosively at normal temperatures; may decompose violently at -80 deg C.(49)
SULFIDES - contact may liberate toxic and flammable hydrogen sulfide gas.(38)
SILICON-BEARING MATERIALS (e.g. sand, concrete, glass and ceramics) - contact may generate toxic and irritating silicon tetrafluoride gas.(38)
BISMUTHIC ACID - reacts violently with the evolution of ozonized oxygen.(48,49)
METHANESULFONIC ACID - electrolysis of the mixture produces explosive oxygen difluoride.(49)
FLUORINE GAS - reacts vigorously with a 50% hydrofluoric acid solution and may burst into flame.(48)
NITRIC ACID and LACTIC ACID - mixtures of the 3 acids are unstable and can explode.(48,49)
PROPYLENE GLYCOL and SILVER NITRATE - may form explosive silver fulminate.(49)
SODIUM - reacts with explosive violence.(48,49)
STRONG BASES (e.g. ammonium hydroxide, sodium hydroxide or calcium oxide) - may react very violently.(48,49)
SULFURIC ACID - reaction is violent.(49)
ARSENIC TRIOXIDE or PHOSPHOROUS PENTOXIDE (TETRAPHOSPHORUS DECAOXIDE) - reaction is vigorous.(48,49)

Hazardous Decomposition Products:
None reported

Conditions to Avoid:
High temperatures

Corrosivity to Metals:
Hydrofluoric acid is corrosive to stainless steel (e.g. types 301, 304, 347, 400 series, 17-4PH), aluminum (types 3003, Cast B-356), types 1010 and 1020 carbon steel, metals containing silica (like cast iron, high silicon iron, silicon bronze and silicon copper), nickel-base alloys, Inconel and Incoloy, brass, naval brass, admiralty brass, bronze, aluminum bronze, tantalum, titanium and zirconium, and alloys containing appreciable amounts of tantalum, titanium and zirconium. Concentrated solutions (50%-70%) are corrosive to bronze, copper and lead, but not dilute solutions (40% and lower).(50,51,52) Reaction with iron or steel produces hydrogen, which can lead to embrittlement of the iron or steel (observed with hardened carbon and alloy steels), which can seriously weaken and embrittle the metal.(37,39,52) It is not corrosive to nickel (at temperatures up to 65 deg C), nickel-base alloys, Hastelloy, Monel, nickel-chromium iron alloy, nickel-copper alloy 400 (in absence of air), gold, platinum and silver.(50,51,52)

Corrosivity to Non-Metals:
Hydrofluoric acid attacks plastics, like as acrylonitrile-butadiene-styrene (ABS), chlorinated polyvinyl chloride (CPVC), acetal copolymer, nylon, polyetherether ketone (PEEK), polybutylene and polyethylene terephthalate; bisphenol A polyester; and polyurethane; elastomers, like ethylene-propylene terpolymer (EPT), nitrile Buna-N (NBR), polyurethane, ethylene vinyl acetate and silicone rubbers; coatings, like coal tar epoxy, epoxy polyamide, polyester and vinyl; and glass and silicate ceramics, and leather. Concentrated solutions (70-100%) attack plastics, like polyvinylidene chloride (SARAN) and polyvinyl chloride (PVC); and elastomers, like isoprene, natural rubber and styrene-butadiene (SBR; Buna-S).(50,52,64,65) Plastics, like Teflon (FEP and TFE) and other fluorocarbons, like polyvinylidene fluoride (Kynar), Tefzel and Halar, and reinforced phenolics; and elastomers, like Viton A and other fluorocarbons, like Kalrez and Chemraz, butyl rubber, chlorosulfonated polyethylenene, and natural rubber and neoprene (both up to 70 deg C), are resistant to hydrofluoric acid.(50,52,64,65)


SECTION 11. TOXICOLOGICAL INFORMATION

LC50 (mouse): 170 ppm (4-hour exposure); cited as 342 ppm (1-hour exposure) (5)
LC50 (male, rat): 655 ppm (4-hour exposure); cited as 1307 ppm (1-hour exposure) (4)
LC50 (male, rat): 2042 ppm (30-minute exposure (4)
LC50 (male, rat): 2690 ppm (15-minute exposure) (4)
LC50 (male, rat): 4970 ppm (5-minute exposure) (4)

LD50 (oral, mouse): less than 40 mg/kg (cited as less than 2 mEq/kg; at 40 mg/kg all animals (numbers not reported) died within 2 hours) (61)

Eye Irritation:

Even dilute solutions of hydrofluoric acid are extremely corrosive and destructive to the eyes.

Application of 0.5, 2, 4 and 8% solutions of HF to rabbits produced a characteristic and uniform moderate inflammatory reaction of lining of the eyelids (conjunctiva). This initial inflammation and consequent moderate to marked fluid accumulation resolved within 20-30 days. Application of 0.5% produced burns which resolved in 10 days, while 0.8% produced effects still present at day 65. Application of 20% produced immediate and extensive damage within one hour, with extensive clouding and tissue death.(23) (Note: This report does not provide details on methods used.)

Skin Irritation:

Even dilute solutions of hydrofluoric acid are extremely corrosive.

Application of a 2% solution to rabbits for 1 or 4 hours, under cover, was corrosive. Corrosive effects were not observed following application of 2% for 1 minute. Application of 0.01-2% solutions also proved corrosive following exposure for as little as 5 minutes.(24) Tissue death (necrosis) was observed following application of a 50% solution to male rats for 5 minutes.(29)

Effects of Short-Term (Acute) Exposure:

Hydrofluoric acid (HF) is corrosive to the respiratory tract, causing severe irritation and fluid accumulation in the lungs with deaths. Severe liver and/or kidney injury has been observed in animals exposed to high concentrations. Solutions of HF are quickly absorbed through the skin and cause systemic fluoride toxicity, as well as corrosive effects.

Inhalation:
Rats and guinea pigs with brief inhalation exposures (up to 1 hour) to lethal concentrations showed nose irritation, respiratory distress, general weakness, decreased body weight and some deaths. Inflammation and tissue death in the nasal cavity, skin irritation, and kidney, liver and bone marrow damage were observed, but not statistically evaluated. Lower concentrations produced irritation of the nose and upper respiratory tract. Only very mild signs were seen in rats exposed to 307 ppm for 15 minutes or 103 ppm for 60 minutes.(4) Rats and mice exposed to lethal concentrations showed signs of respiratory distress. Autopsy showed evidence of lung injury.(5) Rabbits and guinea pigs were exposed to 30 to 9800 ppm for 5 minutes to 41 hours. Respiratory tract irritation was noticeable in all animals at all concentrations, but exposures of 60 ppm or lower produced mild effects. As the concentration increased, corrosion of the nasal passages was observed. Animals survived exposures of up to 30 ppm for 41 hours, but exposures to 300 ppm for 2 hours or more were fatal. Autopsy showed lung, heart, liver, spleen and renal injury.(6) In a study designed to maximize delivery of HF to the lower airways (animals were orally cannulated and HF was delivered directly to the middle section of the trachea), female rats were exposed to 135-1764 ppm for 10 minutes. It was determined that the estimated threshold for serious changes was 1357 ppm. It was concluded that a 10-minute exposure of 130 ppm would produce significant irritation, but not serious or irreversible damage in humans.(27)

Skin Contact:
Typical symptoms of short-term fluoride toxicity (e.g. decreased ventilation and movement, loss of coordination and righting reflex, tremor, biochemical changes and slowed heart beat) were observed following the dermal application of 0.5 mL of 50% HF to male rats for 5 minutes. Mortality was approximately 80% within 24 hours following application. Measures were taken to prevent inhalation exposure of gaseous HF.(29) Application of 2% HF for 1-4 hours, under cover, resulted in significant skin absorption.(24)

Ingestion:
Anesthetized mice were given 40, 60 or 80 mg/kg of HF (cited as 2,3 or 4 mEq/kg) by gavage. At 40 mg/kg, mice survived up to 2 hours while at 60 mg/kg all were dead after 1 hour and at 80 mg/kg all were dead in 10 minutes.(61)

Effects of Long-Term (Chronic) Exposure:

Long-term exposure to HF can cause severe irritation and corrosive effects to the respiratory system, including the lungs. Deaths have been observed at 30 ppm for less than 5 weeks. Severe liver and kidney damage has also been observed. Skeletal fluorosis has also been observed in animals exposed to fluorides. These studies are not reviewed here, because the effects are well defined in humans.

Inhalation:
Rats, mice, guinea pigs, rabbits and dogs were exposed to 8.6 or 30 ppm over 5 weeks (166 exposure hours; 29 days exposure). Exposure to 30 ppm was lethal to rats and mice (100% mortality). Autopsy showed lung injury (bleeding and fluid accumulation) in dogs, rabbits and rats exposed to 30 ppm. Rats also showed severe kidney damage (degeneration and necrosis) and bleeding under the skin, particularly around the eyes and on the feet. Ulceration of the scrotum was observed in the dogs. At 30 and 8.6 ppm, increased fluoride content of the bones and teeth was observed. One dog exposed to 8.6 ppm showed localized bleeding in the lung. Otherwise, no significant effects were observed at 8.6 ppm.(15) Rabbits, guinea pigs and monkeys were exposed to 18.5 ppm (cited as 0.0152 mg/L) for 50 days. Two out of three guinea pigs died. Severe lung (bleeding and inflammatory effects) and liver (fatty changes, congestion and necrosis) damage were observed in all guinea pigs. The rabbits also showed lung and liver injury, as well as kidney damage (extensive degeneration and necrosis). The monkeys did not show any significant lung or liver injury, but kidney injury (degenerative and inflammatory changes) was evident.(14)

Teratogenicity, Embryotoxicity and/or Fetotoxicity:
The one study identified cannot be obtained in English and cannot be evaluated.(22)

Mutagenicity:
The available evidence is insufficient to conclude that HF is a mutagen. The only study available for HF using live animals is weak and inconclusive. Negative results were obtained in bacteria and positive results were obtained in a limited study using fruit flies. In general, fluorides have not produced mutagenic effects except in the presence of severe toxicity in cells or whole animals.(2)
Positive results (chromosomal damage in bone marrow cells) were obtained in female rats exposed to 1.22 ppm (cited as 1.0 mg/m3) for 1 month. Negative results were obtained in a dominant lethal test using mice exposed by inhalation to 1.22 ppm (cited as 1.0 mg/m3) for up to 4 weeks.(16) The complete original study is not available in English. Only one concentration was tested and the increased rate of damaged cells was due largely to an increase in hyperploidy, the significance of which is unknown.(2)
Negative results (gene mutation) were obtained for HF (form unspecified) in bacteria.(58, unconfirmed)
Positive results (sex-linked recessive lethality) were obtained in poorly reported studies using fruit flies (Drosophila).(58, unconfirmed)


SECTION 16. OTHER INFORMATION

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(3) Teitelbaum, D.T. The Halogens. In: Patty's toxicology. 5th ed. Edited by E. Bingham, et al. Vol. 3. (Chpt. 48). John Wiley and Sons, 2001
(4) Rosenholtz, M.J., et al. A toxicopathologic study in animals after brief single exposures to hydrogen fluoride. American Industrial Hygiene Association Journal. Vol. 24 (May-June 1963). p. 253-261
(5) Wohlslagel, J., et al. Toxicity of solid rocket motor exhaust: effects of HCl, HF and alumina on rodents. Journal of Combustion Toxicology. Vol. 3, no. 1 (Feb. 1976). p. 61-70
(6) Machle, W., et al. The effects of the inhalation of hydrogen fluoride. I. The response following exposure to high concentrations. Journal of Industrial Hygiene and Toxicology. Vol. 16, no. 2 (Mar. 1934). p. 129-145
(7) Wing, J.S., et al. Acute health effects in a community after a release of hydrofluoric acid. Archives of Environmental Health. Vol. 46, no. 3 (May/June 1991). p. 155-160
(8) Gupta, B.N. Occupational diseases of teeth. Journal of the Society of Occupational Medicine. Vol. 40 (1990). p. 149-152
(9) Lund, K., et al. Exposure to hydrogen fluoride: an experimental study in humans of concentrations of fluoride in plasma, symptoms and lung function. Occupational and Environmental Medicine. Vol. 54, no. 1 (1997). p. 32-37
(10) Czerwinski, E., et al. Bone and joint pathology in fluoride-exposed workers. Archives of Environmental Health. Vol. 43, no. 5 (Sept./Oct. 1988). p. 340-343
(11) Hodge, H.C., et al. Occupational fluoride exposure. Journal of Occupational Medicine. Vol. 19, no. 1 (Jan. 1977). p. 12-39
(12) Kaltreider, N.L., et al. Health survey of aluminum workers with special reference to fluoride exposure. Journal of Occupational Medicine. Vol. 14, no. 7 (July 1972). p. 531-541
(13) Grandjean, P., et al. Reversibility of skeletal fluorosis. British Journal of Industrial Medicine. Vol. 40, no. 4 (1983). p. 456-461
(14) Machle, W., et al. The effects of the inhalation of hydrogen fluoride. II. The response following exposure to low concentration. Journal of Industrial Hygiene. Vol. 17, no. 5 (Sept. 1935). p. 223-229
(15) Stokinger, H.E. Toxicity following inhalation of fluorine and hydrogen fluoride. In: Pharmacology and toxicology of uranium compounds. Edited by C. Voegtlin, et al. McGraw-Hill Book Company, Inc., 1949. p. 1021-1057
(16) Voroshilin, S.I., et al. Mutagenic effect of hydrogen fluoride on animals. Cytology and Genetics. (Tsitologiya i Genetika). (Translation of Tables and Conclusions). Vol. 9, pt. 1 (1975). p. 40
(17) Largent, E.J. The Metabolism of fluorides in man. American Medical Association Archives of Industrial Health. Vol. 21 (Apr. 1960). p. 318-323
(18) Meng, A., et al. Sister-chromatid exchanges in lymphocytes of workers at a phosphate fertilizer factory. Mutation Research. Vol. 334, no. 2 (1995). p. 243-246
(19) Chan-Yeung, M., et al. Epidemiologic health study of workers in an aluminum smelter in British Columbia. Effects on the respiratory system. American Review of Respiratory Diseases. Vol. 127 (1983). p. 465-469
(20) Saric, M., et al. The role of atopy in potroom workers' asthma. American Journal of Industrial Medicine. Vol. 9, no. 3 (1986). p. 239-242
(21) US National Institute for Occupational Safety and Health (NIOSH). Criteria for a recommended standard: occupational exposure to hydrogen fluoride. US Department of Health, Education, and Welfare, Mar. 1976
(22) MDL Information Systems, Inc. Hydrofluoric acid. Last updated: 2003-02. In: Registry of Toxic Effects of Chemical Substances (RTECS(R)). [CD-ROM]. Canadian Centre for Occupational Health and Safety (CCOHS). Also available at: <ccinfoweb.ccohs.ca/rtecs/search.html>
(23) McCulley, J.P., et al. Hydrofluoric acid burns of the eye. Journal of Occupational Medicine. Vol. 25, no. 6 (June 1983). p. 447-450
(24) Derelanko, M.J., et al. Acute dermal toxicity of dilute hydrofluoric acid. Journal of Toxicology - Cutaneous and Ocular Toxicology. Vol. 4, no. 2 (1985). p. 73-85
(25) Bertolini, J.C. Hydrofluoric acid: a review of toxicity. The Journal of Emergency Medicine. Vol. 10, no. 2 (1992). p. 163-168
(26) Shewmake, S.W., et al. Hydrofluoric acid burns. a report of a case and review of the literature. Archives of Dermatology. Vol. 115 (May 1979). p. 593-596
(27) Dalbey, W., et al. Acute effects of 10-minute exposure to hydrogen fluoride in rats and derivation of a short-term exposure limit for humans. Regulatory Toxicology and Pharmacology. Vol. 27, no. 3 (1998). p. 207-216
(28) Caravati, E.M. Acute hydrofluoric acid exposure. American Journal of Emergency Medicine. Vol. 6, no. 2 (Mar. 1988). p. 143-150
(29) Kono, K., et al. Acute toxicity of hydrogen fluoride skin injuries. In: Proceedings of the Asia- Pacific Symposium on Environmental and Occupational Toxicology. No. 8, Singapore, 1988. p. 381-388
(30) Watson, A.A., et al. Accidental death due to inhalation of hydrofluoric acid. Medicine, Science and the Law. Vol. 13, no. 4 (Oct. 1973). p. 277-279
(31) Tepperman, P.B. Fatality due to acute systemic fluoride poisoning following a hydrofluoric acid skin burn: case report. Journal of Occupational Medicine. Vol. 22, no. 10 (Oct. 1980). p. 691-692
(32) Schmidt, C.W., et al. Erosions of the skin by hydrofluoric acid: an overview of 68 cases. (English translation of Flussaureveratzungen der Haut: Ubsesicht uber 68 Falle.) (CCOHS Translation Series; no. 107). Das Deutsche Gesundheitswesen. Vol. 33, no 16 (1978). p. 761- 766
(33) Kao, W.-F., et al. Ingestion of low-concentration hydrofluoric acid: an insidious and potentially fatal poisoning. Annals of Emergency Medicine. Vol. 34, no. 1 (July 1999). p. 35-41
(34) Grant, W.M., et al. Toxicology of the eye. 4th ed. Charles C. Thomas, 1993. p. 788-791
(35) Smith, R. A. Fluorine compounds, inorganic, hydrogen. In: Kirk-Othmer encyclopedia of chemical technology. John Wiley and Sons, 2005. Available at: <www.mrw.interscience.wiley.com/kirk/kirk_search_fs.html> {Subscription required}
(36) Odor thresholds for chemicals with established occupational health standards. American Industrial Hygiene Association, 1989. p. 20,61
(37) Aigueperse, J, et al. Fluorine compounds, inorganic: hydrofluoric acid. In: Ullmann's encyclopedia of industrial chemistry. 7th ed. John Wiley and Sons, 2005. Available at: <www.mrw.interscience.wiley.com/ueic/ueic_search_fs.html> {Subscription required}
(38) Emergency action guide for hydrofluoric acid. Association of American Railroads, Mar. 1995
(39) Hydrofluoric acid and hydrogen fluoride. In: Handbook of corrosion data. 2nd ed. Edited by B.D. Craig, et al. ASM International, 1995. p. 437-457
(40) Segal, E.B. First aid for a unique acid: hydrofluoric acid. Chemical Health and Safety. Vol. 7, no. 1 (Jan./Feb. 2000). p. 18-23. Also available at: <www.adpub.com/ctimes/features3/hydrofluoric.cfm>
(41) Wilkes, G.J. Hydrofluoric acid burns. Available at: <www.emedicine.com/emerg/topic804.htm>
(42) Braker, W., et al. Hydrogen fluoride. In: Matheson gas data book. 6th ed. Matheson Gas Products, 1980. p. 391-397
(43) Hydrogen fluoride. In: NIOSH pocket guide to chemical hazards. National Institute for Occupational Safety and Health, June 1997
(44) Forsberg, K., et al. Quick selection guide to chemical protective clothing. 4th ed. Van Nostrand Reinhold, 2002
(45) Emergency response planning guidelines. AIHA Journal. Vol. 56, no. 3 (1995). p. 297
(46) Hydrofluoric acid. The Merck index: an encyclopedia of chemicals, drugs and biologicals. Edited by M.J. O'Neil, et al. 13th ed. Merck and Company, 2001. p. 856
(47) Syracuse Research Corporation. Interactive LogKow (KowWin) Database Demo. Date unknown. Available at: <syrres.com/esc/kowdemo.htm>
(48) Fire protection guide to hazardous materials. 13th ed. Edited by A.B. Spencer, et al. National Fire Protection Association, 2002. NFPA 49
(49) Bretherick's reactive chemical hazards database. [CD-ROM]. 6th ed. Version 3.0. Edited by P.G. Urben. Butterworth-Heinemann Ltd., 1999
(50) Schweitzer, P.A. Corrosion resistance tables: metals, nonmetals, coatings, mortars, plastics, elastomers and linings, and fabrics. 4th ed. Part B, E-O. Marcel Dekker, Inc., 1995. p. 1497-1524
(51) Pruett, K.M. Chemical resistance guide to metals and alloys: a guide to chemical resistance of metals and alloys. Compass Publications, 1995. p. 170-181
{52) NACE Technical Practices Committee. Materials for receiving, handling and storing hydrofluoric acid. Item no. 54201. NACE publication 5A171 (1983 revision). Materials Performance. Vol. 22, no. 11 (Nov. 1983). p. 9-12
(53) European Communities (EC). Commission Directive 2000/32/EC. May 19, 2000
(54) Occupational Safety and Health Administration (OSHA). Fluoride (HF and F) in Workplace Atmospheres. In: OSHA Analytical Methods Manual. Revision Date: Dec. 14, 2001. Available at: <www.osha-slc.gov/dts/sltc/methods/toc>
(55) National Institute for Occupational Safety and Health (NIOSH). Hydrogen Fluoride. In: NIOSH Manual of Analytical Methods (NMAM(R)). 4th ed. Edited by M.E. Cassinelli, et al. DHHS (NIOSH) Publication 94-113 (Aug. 1994). Available at: <www.cdc.gov/niosh/nmam/nmammenu.html>
(56) Lund, K., et al. Increased CD3 positive cells in bronchoalveolar lavage fluid after hydrogen fluoride inhalation. Scandinavian Journal of Work Environment and Health. Vol. 25, no. 4 (1999). p. 326-334
(57) Lund, K., et al. Human exposure to hydrogen fluoride induces acute neutrophilic, eicosanoid and antioxidant changes in nasal lavage fluid. Inhalation Toxicology. Vol. 14, no. 2 (2002). p. 119-132
(58) European Union Risk Assessment Report. Hydrogen fluoride. Edited by B.G. Hansen, et al. EUR 19729. European Chemicals Bureau. 1st Priority List. Vol. 8. 2001
(59) Recommended medical treatment for hydrofluoric acid exposure. Honeywell, May 2000. Available at: <www.honeywell.com/sites/sm/chemicals/hfacid/>
(60) DiLuigi, K. Hydrofluoric acid burns. American Journal of Nursing. Vol. 101, no. 6 (June 2001). p. 24AAA-24DDD
(61) Heard, K., et al. Oral decontamination with calcium or magnesium salts does not improve survival following hydrofluoric acid ingestion. Journal of Toxicology. Vol. 41, no. 6 (2003). p. 789-792
(62) Munter, P.A., et al. Hydrofluoric acid-water and hydrofluoric acid-hydrofluorosilicic acid-water. Industrial and Engineering Chemistry. Vol. 39, no. 3 (Mar. 1947). p. 427-431
(63) Munter, P.A., et al. Partial pressure measurements on the system hydrogen fluoride-water. Industrial and Engineering Chemistry. Vol. 41, no. 7 (July 1949). p. 1504-1508
(64) Pruett, K.M. Chemical resistance guide for plastics: a guide to chemical resistance of engineering thermoplastics, fluoroplastics, fibers and thermoset resins. Compass Publications, 2000. p. 242-253
(65) Pruett, K.M. Chemical resistance guide for elastomers II: a guide to chemical resistance of rubber and elastomeric compounds. Compass Publications, 1994. p. C-188 to C-193

Information on chemicals reviewed in the CHEMINFO database is drawn from a number of publicly available sources. A list of general references used to compile CHEMINFO records is available in the database Help.


Review/Preparation Date: 2007-04-10



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