Sodium Hexafluorosilicate and Fluorosilicic Acid - Review of Toxicological Literature

Sodium Hexafluorosilicate
[CASRN 16893-85-9]
and
Fluorosilicic Acid
[CASRN 16961-83-4]
Review of Toxicological Literature
October 2001
[CASRN 16893-85-9]
and
Fluorosilicic Acid
[CASRN 16961-83-4]
Review of Toxicological Literature
Prepared for
Scott Masten, Ph.D.
National Institute of Environmental Health Sciences
P.O. Box 12233
Research Triangle Park, North Carolina 27709
Contract No. N01-ES-65402
Submitted by
Karen E. Haneke, M.S. (Principal Investigator)
Bonnie L. Carson, M.S. (Co-Principal Investigator)
Integrated Laboratory Systems
P.O. Box 13501
Research Triangle Park, North Carolina 27709
October 2001
Toxicological Summary for Sodium Hexafluorosilicate [16893-85-9] and Fluorosilicic Acid [16961-83-4] 10/01
Executive Summary
Nomination
Sodium hexafluorosilicate and fluorosilicic acid were nominated for toxicological testing based
on their widespread use in water fluoridation and concerns that if they are not completely
dissociated to silica and fluoride in water that persons drinking fluoridated water may be exposed
to compounds that have not been thoroughly tested for toxicity.
Nontoxicological Data
Analysis and Physical-Chemical Properties
Analytical methods for sodium hexafluorosilicate include the lead chlorofluoride method (for
total fluorine) and an ion-specific electrode procedure. The percentage of fluorosilicic acid
content for water supply service application can be determined by the specific-gravity method
and the hydrogen titration method. The American Water Works Association (AWWA) has
specified that fluorosilicic acid contain 20 to 30% active ingredient, a maximum of 1%
hydrofluoric acid, a maximum of 200 mg/kg heavy metals (as lead), and no amounts of soluble
mineral or organic substance capable of causing health effects. Recently, single-column ion
chromatography with conductometric detection and sodium hydroxide-methanol-water eluent
was used for the simultaneous determination of fluorosilicic acid, Ca2+, Mg2+, Al3+, Cl-, and NO3-
and successfully applied to the analysis of mineral water and composite tablets.
When heated to decomposition, sodium hexafluorosilicate releases toxic fumes of hydrogen

fluoride and sodium oxide, while contact with metals releases hydrogen gas. In water, the
compound readily dissociates to sodium ions and hexafluorosilicate ions and then to hydrogen
gas, fluoride ions, and hydrated silica. At the pH of drinking water (6.5-8.5) and at the
concentration usually used for fluoridation (1 mg fluoride/L), the degree of hydrolysis is
essentially 100%. Fluorosilicic acid is a moderately strong acid that can corrode glass and
stoneware. Like its salt, its degree of hydrolysis is essentially 100% in drinking water, and when
reacted with steam or water or when heated to decomposition or highly acidified, toxic and
corrosive fumes of fluorides (e.g., hydrogen fluoride and silicon tetrafluoride) are released. It
also reacts with metals, producing hydrogen gas.
Commercial Availability, Production, and Uses

Sodium hexafluorosilicate is usually commercially available in technical and C.P. grades; it was
formally available in insecticides of up to ~98% purity such as granular baits. A typical product
contains 59.34% fluorine and a maximum of 0.50% each of water moisture, water-insoluble
matter, and heavy metals (as lead). Fluorosilicic acid is commercially available as aqueous
solutions (up to 70%) in technical and C.P. grades. A typical product contains a maximum of
23% of the acid, a minimum of 18.22% fluorine, a maximum of 0.02% heavy metals (as lead),
and <1.00% hydrofluoric acid. Many U.S. producers and suppliers are available for both
compounds (over 20 for each). Bulk producers/suppliers include Lucier Chemical Industries and
Creanova Inc.
Sodium hexafluorosilicate is produced by treating fluorosilicic acid with sodium hydroxide,

sodium carbonate, or sodium chloride; alkalinity is adjusted to avoid the release of the fluoride.
Fluorosilicic acid is mainly produced as a byproduct of the manufacture of phosphate fertilizers
i
where phosphate rock is treated with sulfuric acid. It can also be made by the reaction of sulfuric
acid on barium hexafluorosilicate, apatite, or fluorite (fluorspar).
The latest available figure for U.S. production of sodium hexafluorosilicate is 19,600 metric tons
(43.2 million pounds) in 1984. In that same year, 3000 metric tons (6.61 million pounds) was
imported. In 1995, ten phosphate rock processing plants produced 55,900 metric tons (123
million pounds) of fluorosilicic acid as a byproduct. In 1999, ten plants again reported on the
production of fluorosilicic acid as a byproduct from phosphate rock processing; 69,200 metric
tons (153 million pounds) was produced. This was an almost 3% increase in output from the
previous year.
The major use of sodium hexafluorosilicate and fluorosilicic acid is as fluoridation agents for
drinking water. Sodium hexafluorosilicate has also been used for caries control as part of a
silicophosphate cement, an acidic gel in combination with monocalcium phosphate monohydrate,
and a two-solution fluoride mouth rinse. Both chemicals are also used as a chemical
intermediate (raw material) for aluminum trifluoride, cryolite (Na3AlF6), silicon tetrafluoride,
and other fluorosilicates and have found applications in commercial laundry.
Other applications for sodium hexafluorosilicate include its use in enamels/enamel frits for china
and porcelain, in opalescent glass, metallurgy (aluminum and beryllium), glue, ore flotation,
leather and wood preservatives, and in insecticides and rodenticides. It has been used in the
manufacture of pure silicon, as a gelling agent in the production of molded latex foam, and as a
fluorinating agent in organic synthesis to convert organodichlorophosphorus compounds to the
corresponding organodifluorophosphorus compound. In veterinary practice, external application
of sodium hexafluorosilicate combats lice and mosquitoes on cattle, sheep, swine, and poultry,
and oral administration combats roundworms and possibly whipworms in swine and prevents
dental caries in rats. Apparently, all pesticidal products had their registrations cancelled or they
were discontinued by the early 1990s.
Fluorosilicic acid is used in the tanning of animal hides and skins, in ceramics and glass, in
technical paints, in oil well acidizing, in the manufacture of hydrogen fluoride, for the
sterilization of equipment (e.g., in brewing and bottling establishments and for copper and brass
vehicles), and in electroplating. It is also employed as an impregnating ingredient to preserve
wood and harden masonry and for the removal of mold as well as rust and stain in textiles.
Environmental Occurrence and Persistence

Fluorosilicic acid (30-35%) can readily be recovered in the hydrogen fluoride process from the
silicon tetrafluoride-containing plant vent gases, as well as from wet-process phosphoric acid
plants. In the manufacture of phosphate fertilizer in Central Florida, fluorides and radionuclides
(radium and uranium) are released as toxic pollutants. During the acidulation process, radon gas
can be released and carried into the fluorosilicic acid, while polonium can be captured during the
scrubbing process and combined with fluoride.
For drinking water fluoridation, the maximum use level (MUL) for sodium hexafluorosilicate is
2 mg/L; for fluorosilicic acid, the level is 6 mg/L of a 25% fluorosilicic acid solution. Both
values correspond to a fluoride concentration of 1.2 mg/L, which is below the U.S.
ii
Environmental Protection Agency’s (EPA’s) Maximum Contaminant Level (MCL) of 4.0 mg/L
and the Secondary Maximum Contaminant Level (SMCL) of 2.0 mg/L. The National Sanitation
Foundation (NSF) has established a Maximum Drinking Water Level of 16 mg/L for silicates
and a Maximum Allowable Level (MAL) of 1.2 mg fluoride/L for its certified products used in
drinking water.
Human Exposure
Potential exposure to sodium hexafluorosilicate and fluorosilicic acid is via inhalation and eye
and skin contact. Another route for the former compound is ingestion. Although current data
indicate that silicofluorides are used in over 9200 U.S. water treatment systems, serving over 120
million individuals, exposure via drinking water is expected to be minimal since both compounds
hydrolyze almost completely under these conditions.
In the workplace, exposure to both chemicals is possible during their manufacture,

transportation, or use in water treatment. In the National Institute for Occupational Safety and
Health (NIOSH) 1983 National Occupation Exposure Survey (NOES), 79,556 employees were
potentially exposed to sodium hexafluorosilicate, while 10,867 were potentially exposed to
fluorosilicic acid.
Regulations
Workers treating agricultural products with insecticides such as weevil baits and persons using
roach baits and other insecticidal products containing sodium hexafluorosilicate in the home may
have been exposed by inhalation or the skin, and by hand-to-mouth contact. In the United States,
all pesticide uses of sodium hexafluorosilicate have been cancelled. (It is noted that its use as an
insecticide is currently listed in the 2001 Farm Chemicals Handbook, which does not note
discontinuation of the product Safsan.) Both sodium hexafluorosilicate and fluorosilicic acid are
listed in Section 8(b) of the Toxic Substances Control Act (TSCA; chemical inventory section).
Both are also exempt from reporting under the Inventory Update Rule (i.e., Partial Updating of
the TSCA Inventory Data Base Production and Site Reports [40CFR, Section 710(b)]). The
Occupational Safety and Health Administration (OSHA) and American Conference of
Governmental Industrial Hygienists (ACGIH) have established an eight-hour time-weighted
average (TWA) of 2.5 mg/m3 fluorides, as fluorine, for work place exposure. NIOSH has also
recommended an air exposure level to inorganic fluorides of 2.5 mg F/m3 but as a ten-hour
TWA.
Toxicological Data
Human Data
Chronic exposure to sodium hexafluorosilicate dust at levels above the eight-hour TWA can
result in severe calcification of the ribs, pelvis, and spinal column ligaments; effects on the
enzyme system; pulmonary fibrosis; stiffness; irritation of the eyes, skin, and mucous
membranes; weight loss; anorexia; anemia; cachexia; wasting; and dental effects. Long-term or
repeated exposure to the skin can result in skin rash. A probable oral lethal dose of 50-500
mg/kg, classified as very toxic, has been reported for a 150-pound (70-kg) person receiving
between 1 teaspoon and 1 ounce of sodium hexafluorosilicate. Cases of sodium
hexafluorosilicate ingestion reported symptoms such as acute respiratory failure, ventricular
iii
tachycardia and fibrillation, hypocalcemia, facial numbness, diarrhea, tachycardia, enlarged

liver, and cramps of the palms, feet, and legs.
The symptoms of inhalation of fluorosilicic acid include burning of the eyes and numbness
around the lips. Symptoms do not necessarily occur immediately; they can appear 24 hours after
exposure. A spill incident of the chemical on an interstate in Florida, covering an area 600 feet
long and 60 feet wide, resulted in the visit of more than 50 people to hospitals. Individuals
complained of skin and respiratory irritation, including burning in the throat, and headaches. A
man riding in a truck with his arm out the window experienced burning on his forearm. The
effects of long-term exposure to fluorosilicic acid are changes in bone, corrosivity of the mucous
membranes (e.g., ulceration of the nose, throat, and bronchial tubes), coughing, shock,
pulmonary edema, fluorosis, coma, and even death. In workers engaged for approximately 30
years in the production of phosphate fertilizers, nine out of the 50 observed workers had
increased bone densities. When swallowed, severe irritation of the lungs, nose, and throat can
occur, as well as severe damage to the throat and stomach. A probable oral lethal dose of 50
5000 mg/kg, classified as very toxic, has been reported for doses between 1 teaspoon and 1
ounce for a 150-pound (70-kg) person; a probable oral lethal dose of 5-50 mg/kg, classified as
extremely toxic, has been reported for doses between 7 drops and 1 teaspoon for the same
individual.
Chemical Disposition, Metabolism, and Toxicokinetics

In a female chemical plant worker who ingested sodium hexafluorosilicate in a suicide attempt,
fluoride levels in serum and fresh urine were 5.130 and 235.60 mg/dm3, respectively, on day 2 of
hospitalization; treatment with calcium compounds (calcium carbonate and calcium
lactogluconate) immediately returned levels to normal. In 50 workers engaged for
approximately 30 years in the production of phosphate fertilizers and exposed to gaseous
fluoride (hydrogen fluoride, silicon tetrafluoride, and fluorosilicic acid), urine fluoride excretion
ranged from 1.0 to 9.6 mg F-/L (controls: 0.3 to 1.2).
In rats fed a diet containing 0.16% sodium hexafluorosilicate supplemented in a corn-soybean

oilmeal-casein ration ad libitum for 22-23 days, the average amounts of fluorine were 94.4 mg in
feces and 91.9 mg in urine. The mean amount of fluorine absorbed was 65.1% and that retained
was 31.0%.
Fluorine concentrations in stomach/rumen contents, urine, and blood serum have been
determined in domestic animals experiencing sodium hexafluorosilicate poisoning. Significantly
elevated levels were initially found, which decreased with time.
Acute Toxicity
In mice, an oral LD50 of 70 mg/kg (0.37 mmol/kg) for sodium hexafluorosilicate was reported.
In rats, oral LD50 values of 125 and 430 mg/kg (0.665 and 2.29 mmol/kg, respectively) were
calculated, while a TDLo of 248 mg/kg (1.32 mmol/kg) was calculated. A subcutaneous LDLo of
70 mg/kg (0.37 mmol/kg) was also reported in the animals. In rabbits, the oral LD50 value was
125 mg/kg (0.665 mmol/kg). In guinea pigs, an LCLo value of 33 mg/kg (0.18 mmol/kg) for
sodium hexafluorosilicate was observed; additionally, an oral LD50 of 200 mg/kg (1.39 mmol/kg)
was reported for fluorosilicic acid.
iv
Sodium Hexafluorosilicate: Mice orally given sodium hexafluorosilicate (70 mg/kg; 0.37
mmol/kg) exhibited toxic effects in the peripheral nerves, sensation, and in behavior. In rats, an
oral dose (248 mg/kg; 1.32 mmol/kg) administered intermittently for one month produced toxic
effects in the kidney, ureter, and/or bladder, as well as musculoskeletal and biochemical effects.
Using guinea pigs, inhalation experiments (13-55 mg/m3 [1.7-7.2 ppm] sodium
hexafluorosilicate in air for ≥6 hours) resulted in pulmonary irritation; the lowest concentration
that caused death was 33 mg/m3 (4.3 ppm).
When sodium hexafluorosilicate (500 mg; 2.66 mmol) was applied to the skin of adult rabbits,
mild irritation occurred. When applied to the eyes (100 mg; 0.532 mmol), severe irritation was
observed; following a four-second rinse, the effect was still severe.
Sodium hexafluorosilicate poisoning has been reported in domestic animals (cattle, sheep, a
horse, and a pigeon). Animals exhibited drowsiness, constipation, loss of appetite, paresis of the
rumen, severe abdominal pain, and diarrhea. Sheep also exhibited grinding of the teeth (an
indication of pain) and frothing at the mouth in most cases of lethal poisoning, while the horse
also had bradycardia. In a study in which sheep were orally administered technical sodium
hexafluorosilicate (25, 50, 200, 1500, and 2000 mg/kg; 0.13, 0.27, 1.06, 7.976, and 10.63
mmol/kg) via stomach tube, the animals exhibited similar symptoms. Animals died 6 days after
administration of 200 mg/kg and 2.5 hours after administration of 2000 mg/kg. When a dairy
herd of 600 animals was acutely poisoned from railcar contamination of feed, 95% of the
animals had decreased neuromuscular transmission. The poisoning resembled calcium depletion.
Fluorosilicic Acid: In rats orally given fluorosilicic acid (430 mg/kg; 2.98 mmol/kg),
somnolence and/or general depressed activity was observed. Other rat studies with fluorosilicic
acid (single oral doses of 215, 464, 1000, and 2100 mg/kg [1.49, 3.22, 6.939, and 14.57
mmol/kg]) led to its classification as "moderately toxic." Percutaneous administration of the
compound (amounts not provided) in rats, guinea pigs, and pigs resulted in continuously
spreading necrosis in the deeper regions of injured skin. Hypocellular necrosis, consisting of
sharp leukocyte demarcations, and edema up to the subcutis were also observed. In rabbits, it
was corrosive to the skin (0.5 mL [4 mol] for 1, 24, or 72 hours) and eyes (0.1 mL [0.8 mol]
instilled into left eye).
Synergistic/Antagonistic Effects
Fluoride, administered in the form of sodium hexafluorosilicate, had a strong affinity for calcium
and magnesium. When orally given to sheep via a stomach tube at doses of 25, 50, 200, 1500,
and 2000 mg/kg, increased changes in serum calcium and magnesium levels were observed at
the two highest doses within 30 minutes after dose administration. At 200 mg/kg, recovery of
both levels occurred after five days. With the 1500 mg/kg dose group, changes in phosphorus
and sugar levels in whole blood were also significantly increased.
Genotoxicity
Sodium hexafluorosilicate was negative in the Salmonella/microsome test (concentrations up to
3600 g/plate, –S9), the micronucleus test on mouse bone marrow (37.2 mg/kg; 0.198
mmol/kg), and in the Bacillus subtilis rec-assay system (0.001-10 M; 188 g/mL-1.9 g/mL).
v
The compound (0.25 mM; 47 g/mL) did not induce sex-linked recessive lethal mutations in
Drosophila.
Other Data
Within one week after beginning work in a foam rubber plant, a 23-year-old man exhibited skin
lesions consisting of "diffuse, poorly delineated, erythematous plaques with lichenoid papules
and large pustules" on his arms, wrists, thighs, and trunk. Although scratch and patch tests with
sodium hexafluorosilicate (2% aqueous) were negative, tests in rabbits (topical application of a
1, 5, 10, and 25% solution) showed the compound to be a pustulogen.
No short-term or subchronic exposure, chronic exposure, cytotoxicity, reproductive toxicity,

teratology, carcinogenicity, or initiation/promotion studies were available.
Structure-Activity Relationships
For the same fluorine content, sodium fluoride, sodium hexafluorosilicate, cryolite (Na3AlF6),
and barium sulfate were observed to have the same extent of chronic fluorine intoxication in rats.
Ammonium fluoride, potassium fluoride, barium fluorosilicate, potassium fluorosilicate, and
sodium fluorosilicate exhibited the same acute toxicity as sodium fluoride in the animals.
In a comparative study of absorption and excretion of fluorine in rats fed sodium fluoride,
calcium fluoride, and sodium hexafluorosilicate, the percent fluorine retained was the same for
the two sodium compounds. Several experiments on growing rats orally given 5, 10, 15, 25, and
50 ppm fluorine as sodium fluoride or sodium hexafluorosilicate for 90-100 days found no
differences in the quantity of fluorine deposited and the contents of ash, calcium, and phosphorus
in the incisor teeth, molar teeth, mandibles, and femurs. Furthermore, there were no differences
in the percent of ingested fluorine retained in the body, and a combination of sodium silicate (15
ppm silicon) with sodium fluoride (25 ppm fluorine) did not affect the amount of fluorine
deposited. The growth rate was normal in all rats. A separate study using litters of female
weanling Osborne-Mendel rats that were given 50 ppm fluorine as sodium fluoride or
ammonium fluorosilicate in drinking water for 99 days observed similar results.
vi
Table of Contents
Executive Summary................................................................................................................... i
1.0 Basis for Nomination..................................................................................................... 1
2.0 Introduction................................................................................................................... 1
2.1 Chemical Identification and Analysis ............................................................... 1
2.1.1 Sodium Hexafluorosilicate ..................................................................... 1
2.1.2 Fluorosilicic Acid.................................................................................... 2
2.2 Physical-Chemical Properties ........................................................................... 3
2.3 Commercial Availability.................................................................................... 4
3.0 Production Processes..................................................................................................... 5
4.0 Production and Import Volumes .................................................................................. 5
5.0 Uses ................................................................................................................................ 6
6.0 Environmental Occurrence and Persistence ................................................................ 6
7.0 Human Exposure........................................................................................................... 7
8.0 Regulatory Status .......................................................................................................... 8
9.0 Toxicological Data......................................................................................................... 9
9.1 General Toxicology............................................................................................ 9
9.1.1 Human Data ........................................................................................... 9
9.1.2 Chemical Disposition, Metabolism, and Toxicokinetics ..................... 10
9.1.3 Acute Exposure .................................................................................... 11
9.1.4 Short-term and Subchronic Exposure................................................. 14
9.1.5 Chronic Exposure ................................................................................ 14
9.1.6 Synergistic/Antagonistic Effects .......................................................... 14
9.1.7 Cytotoxicity .......................................................................................... 15
9.2 Reproductive and Teratological Effects.......................................................... 15
9.3 Carcinogenicity ................................................................................................ 15
9.4 Initiation/Promotion Studies ........................................................................... 15
9.5 Anticarcinogenicity.......................................................................................... 15
9.6 Genotoxicity ..................................................................................................... 15
9.7 Cogenotoxicity ................................................................................................. 15
9.8 Antigenotoxicity............................................................................................... 15
9.9 Other Data ....................................................................................................... 15
10.0 Structure-Activity Relationships ................................................................................ 15
vii
11.0 Online Databases and Secondary References ............................................................ 17
11.1 Online Databases ............................................................................................. 17
11.2 Secondary References...................................................................................... 18
12.0 References.................................................................................................................... 19
13.0 References Considered But Not Cited ........................................................................ 23
Acknowledgements ................................................................................................................. 24
Appendix: Units and Abbreviations...................................................................................... 24
Tables:
Table 1 Acute Toxicity Values for Sodium Hexafluorosilicate and
Fluorosilicic Acid ...................................................................................... 11
Table 2 Acute Exposure to Sodium Hexafluorosilicate and Fluorosilicic Acid ... 12
viii
1.0 Basis for Nomination

Sodium hexafluorosilicate and fluorosilicic acid were nominated for toxicological testing based
on their widespread use in water fluoridation and concerns that if they are not completely
dissociated to silica and fluoride in water that persons drinking fluoridated water may be exposed
to compounds that have not been thoroughly tested for toxicity.
2.0 Introduction
[16893-85-9]
F-
F- F-
Si4+
F- F-
F
2 Na+
Fluorosilicic Acid
[16961-83-4]
F-
F- F-
Si4+
F- F-
F
2 H+
2.1 Chemical Identification and Analysis

2.1.1 Sodium Hexafluorosilicate
Sodium hexafluorosilicate ([Na2SiF6]; mol. wt. = 188.06) is also called:
Destruxol applex
Disodium hexafluorosilicatea,b,d
Disodium silicofluoride
Ens-zem weevil bait
ENT 1,501
Fluorosilicate de sodium
Fluosilicate de sodium
Ortho earwig bait
Ortho weevil bait
Prodan
Prodan (pesticide)
PSC Co-Op weevil bait
Safsan
1
Salufer
Silicate (2-), hexafluoro-, disodium (8CI, 9CI)
Silicon sodium fluoridea,b,c
Sodium fluoride silicate
Sodium fluorosilicatea,b
Sodium fluosilicatea,b,e
Sodium hexafluosilicate
Sodium silicofluoridea,b
Sodium silicon fluoridea,b
Super prodan
UN2674 (DOT)
May be written as the following: awithout any appended formula; bwith Na2SiF6 appended in parentheses, cwith SiNa2F6
appended in parentheses, dwith (2-) appended in parentheses, or ewith ACN (accepted common name) appended in parentheses.
Sources: HSDB (2000b); Registry (2000); RTECS (2000); SANSS (2000)

Other CAS Registry Numbers (CASRNs) that have been used for the compound are 1310-02-7,
1344-04-3, 12656-12-1, 39413-34-8, 221174-64-7 (Registry, 2000). CASRNs for the hydrates
are 10213-79-3 (pentahydrate), 15630-83-8 (hexahydrate), 27121-04-6 (octahydrate), and 13517
24-3 (nonahydrate). AOAC (Association of Official Analytical Chemists) Method 945.05 has
been used to detect fluorine as sodium hexafluorosilicate in pesticide formulations (HSDB,
2000b). The chemical composition of sodium hexafluorosilicate used in water supply service
applications can be determined by test procedures specified in AWWA (American Water Works
Association) B702-99 (AWWA, 1999).
2.1.2 Fluorosilicic Acid

Fluorosilicic acide ([H2SiF6]; mol. wt. = 144.11) is also called:
Dihydrogen hexafluorosilicatea,c
FKS
Fluosilicic acida,d (6CI)
Hexafluorosilicic acid
Hexafluorosilicate (2-), dihydrogen
Hexafluosilicic acid
Hydrofluorosilicic acida,e
Hydrofluosilicic acida,d
Hydrogen hexafluorosilicatea,b
Hydrogen hexafluorosilicic
Hydrosilicofluoric acida,e
Sand acida,e
Silicate (2-), hexafluoro-, dihydrogen (8CI, 9CI)
Silicic acid (H2SiF6)
Silicofluoric acida.e
Silicofluoride
Silicon hexafluoride dihydride
UN1778 (DOT)
May be written as the following: awithout any appended formula; bwith H2SiF6 appended in parentheses, cwith (2-) appended in
parentheses, dwith ACN (accepted common name) appended in parentheses, or ewith DOT (Department of Transportation)
appended in parentheses.
Sources: HSDB (2000a); Registry (2000); RTECS (2000); SANSS (2000)
2
Other CASRNs that have been used for the compound are 1309-45-1 and 12672-67-2 (Registry,
2000). Total fluorine in fluorosilicates can be detected by the lead chlorofluoride method. In air,
an ion-specific electrode procedure with a range of 0.05 to 475 mg fluoride/m3 has been used
(HSDB, 2000a). The percentage of fluorosilicic acid content for water supply service
application can be determined by the specific-gravity method and the hydrogen titration method
(specified in AWWA B703-94); the latter is the preferred method, since the former procedure
provides a "very rough estimation." AWWA has specified that fluorosilicic acid must contain 20
to 30% active ingredient, a maximum of 1% hydrofluoric acid, a maximum of 200 mg/kg heavy
metals (as lead), and no amounts of soluble mineral or organic substance that can cause health
effects (AWWA, 2000; HSDB, 2000a). Analyses of tap water treated with silicofluorides (e.g.,
samples from Seattle, WA, San Francisco, CA, and Ft. Collins, CO) have revealed insignificant
lead and arsenic levels (CSDS, 2001). Recently, single-column ion chromatography with
conductometric detection and sodium hydroxide-methanol-water eluent was used for the
simultaneous determination of fluorosilicic acid, Ca2+, Mg2+, Al3+, Cl-, and NO3-; the detection
limit for the anion of the acid was 1.25 x 106 M. It was successfully applied to the analysis of
mineral water and composite tablets (Xu et al., 2001).
2.2 Physical-Chemical Properties

Property Information Reference(s)
Sodium hexafluorosilicate
Physical State white, granular, crystalline, or free-flowing HSDB (2000b)
powder; white hexagonal crystals
Odor odorless
Boiling Point (oC) decomposes at 500 LCI, Ltd. (2000b)
Melting Point (oC) melts at red heat with decomposition HSDB (2000b)
Specific Gravity (g/cm3) 2.7
pH Value neutral (solution in cold water)
3.0-4.5 (1% solution) LCI, Ltd. (2000b)
Water Solubility soluble in cold water (150 parts) and boiling HSDB (2000b)
water (40 parts)
mg/L or g/m 3 at 17.5 ¡C 6,500 Worthing (1987; cited by
Shiu et al., 1990)
mg/L or g/m 3 at 20 ¡C 72,000 Dean (1985; cited by Shiu
et al., 1990)
Insoluble in alcohol (e.g., ethanol) HSDB (2000b)
Fluorosilicic acid
Physical State colorless liquid; white crystals HSDB (2000a)
Odor sour, pungent
Density @ 25 ¡C 1.4634 (60.97% solution)
Boiling Point (oC) decomposes (60.97% solution)
105 (25% solution) LCI, Ltd. (2000a)
Freezing Point (oC) -15.5 (25% solution)
Specific Gravity (g/cm3) 1.234 (25% solution) @ 16 ¡C LCI, Ltd. (2000a)
pH Value 1.2 (1% solution) LCI, Ltd. (undated-a)
Soluble in alkali; cold and hot water HSDB (2000a)
In alkaline medium, fluorosilicate solutions are readily hydrolyzed; in acidic conditions, silicon
tetrafluoride and hydrogen fluoride are released. Thermal decomposition of fluorosilicates
releases gaseous silicon tetrafluoride and forms solid fluoride. When heated to decomposition,
3
sodium hexafluorosilicate releases toxic fumes of hydrogen fluoride and sodium oxide; contact
with metals can release hydrogen gas (HSDB, 2000b; NICNAS, 2001).
Fluorosilicic acid is a moderately strong acid that can corrode glass and stoneware. At about 19
˚C, a 60-70% solution solidifies, forming crystalline dihydrate. A 13.3% solution may be
distilled without decomposition. Fluorosilicic acid is deliquescent that is, it absorbs moisture
from the air and becomes liquid (HSDB, 2000a). It produces toxic and corrosive fumes of
fluorides (e.g., hydrogen fluoride and silicon tetrafluoride) when reacted with water or steam or
when the compound is heated to decomposition or highly acidified with sulfuric acid (HSDB,
2000a; NICNAS, 2001). It also reacts with many metals, producing hydrogen gas (HSDB,
2000a; LCI, Ltd., undated-a).
Aqueous Chemistry
In water, the compound readily dissociates to sodium ions and hexafluorosilicate ions. At the pH
of drinking water (6.5-8.5) and at the concentration usually used for fluoridation (1 mg
fluoride/L), essentially 100% of sodium hexafluorosilicate dissociates to fluoride ions and
hydrated silica (Crosby, 1969; Urbansky and Schock, 2000). In a quasi-constant composition
titration study using high concentrations of hydrogen ion (H+) and calcium ion (Ca2+), the
promoting effect of Ca2+ on the hydrolysis of sodium hexafluorosilicate was observed to be
stronger than the inhibiting effect of H+, thereby causing faster hydrolysis at low pH (Eidelman
and Chow, 1991).
Na2SiF6(aq) + 4 H2O 4 HF(aq) + 2 NaF(aq) + Si(OH)4(aq)
In water, fluorosilicic acid readily hydrolyzes to hydrofluoric acid and various forms of
amorphous and hydrated silica. At the concentration usually used for water fluoridation, 99%
hydrolysis occurs and the pH drops to 4.2. As pH increases, hydrolysis increases. At the pH of
drinking water, the degree of hydrolysis is "essentially 100%" (Crosby, 1969; Urbansky and
Schock, 2000).
H2SiF6(aq) + 4 H2O 6 HF(aq) + Si(OH)4(aq)
2.3 Commercial Availability

Sodium hexafluorosilicate is available as granular bait and in technical and C.P. grades. It is
usually commercially available as ~98% pure (HSDB, 2000b). A typical product contains
59.34% fluorine and a maximum of 0.50% each of moisture as water, water-insoluble matter,
and heavy metals (as lead) (LCI, Ltd., 2000b). Chemical producers include Chemtech Products
Inc. (Alorton, IL), IMC-Agrico Company (Faustina, LA), and Kaiser Aluminum and Chemical
Corporation (Mulberry, FL) (SRI Int., 2000). Lucier Chemical Industries produces and ships
sodium hexafluorosilicate in 25-kg bags and 50-pound bags (LCI, Ltd., 2000b). It is supplied by
GFS Chemicals Inc. (Powell, OH) and Spectrum Chemical Manufacturing Corporation
(Gardena, CA) (Chemcyclopedia Online, 2001). Chem Sources (2001) has identified 24
suppliers of the compound; bulk suppliers include Creanova Inc. (Somerset, NJ) and Seal
Chemical Industries (Newport Beach, CA). RIMI Chemicals Company Ltd. formulates the
chemical as the product Safsan (Farm Chem. Handbook, 2001).
4
Fluorosilicic acid is commercially available as aqueous solutions of 5, 10, 15, 20, 25, 30, 34, and
60-70% in technical and C.P. grades (HSDB, 2000a). A typical product contains a minimum of
23% of the acid, a minimum of 18.22% fluorine, a maximum of 0.02% heavy metals (as lead),
and <1.00% hydrofluoric acid (LCI, Ltd., 2000a). It is produced by Cargill Fertilizer, Inc.
(Riverview, FL), Chemtech Products Inc. (Alorton, IL), Farmland Hydro, L.P. (Bartow, FL),
IMC-Agrico Company (Faustina, LA; Nichols, FL; South Pierce, FL; Uncle Sam, LA), PCS
Phosphate Company, Inc. (Aurora, NC), Royster-Clark Inc. (Americus, GA; Florence, AL;
Hartsville, SC), and U.S. Agri-Chemicals Corporation (Fort Meade, FL) (SRI Int., 2000).
Cargill Fertilizer, Inc. produces fluorosilicic acid as a primary nutrient (Farm Chem. Handbook,
2001). Another producer, Lucier Chemical Industries (Jacksonville Beach, FL) ships its product
in tank cars, tank trucks, and drums (LCI, Ltd., 2000a). Chem Sources (2001) has identified 16
suppliers of fluorosilicic acid; bulk suppliers include Creanova Inc. (Somerset, NJ), Fluka
(Milwaukee, WI), and Spectrum Laboratory Products, Inc. (Gardena, CA). Under the name
hydrofluorosilicic acid [56977-47-0], it is supplied by Alfa Aesar/Johnson Matthey (Ward Hill,
MA) and Solvay Fluorides Inc. (St. Louis, MO) (Chemcyclopedia Online, 2001).
3.0 Production Processes

Sodium hexafluorosilicate is produced by the neutralization of fluorosilicic acid with sodium
hydroxide, sodium carbonate, or sodium chloride under vigorous agitation. The amount of the
alkali is controlled so as not to result in the fluoride (HSDB, 2000b).
Fluorosilicic acid is mainly produced as a byproduct of the manufacture of phosphate fertilizers

where phosphate rock, containing fluorides and silica or silicates, is treated with sulfuric acid.
The gases released, hydrogen fluoride and silicon tetrafluoride, are sprayed with water in
condensing towers or drawn into a series of scrubbers and dissolved in water, forming an
aqueous solution of fluorosilicic acid (CSDS, 2001; Farm Chem. Handbook, 2001; NICNAS,
2001). This is the crude form of fluorosilicic acid; the purified form is obtained by distillation of
the crude acid or by reacting pure silica with hydrofluoric acid. The compound can also be made
by the reaction of sulfuric acid on barium hexafluorosilicate (HSDB, 2000a). Furthermore,
fluorosilicic acid is manufactured by the reaction of apatite and/or fluorite (fluorspar) with
sulfuric acid (LCI, Ltd., 2000a). Its production from phosphoric acid producers supplements
fluorspar as a domestic source of fluorine (Miller, 1995, 1999).
4.0 Production and Import Volumes

The latest available figure for U.S. production of sodium hexafluorosilicate is 19,600 metric tons
(43.2 million pounds) in 1984. In that same year, 3000 metric tons (6.61 million pounds) was
imported (HSDB, 2000b).
In 1995, ten phosphate rock processing plants produced 55,900 metric tons (123 million pounds)
of fluorosilicic acid as a byproduct. Of this amount, 45% was used in water fluoridation, directly
or as the sodium salt, while 34% went toward the production of aluminum trifluoride and 20%
went toward other uses (Miller, 1995). In 1999, ten plants again reported on the production of
fluorosilicic acid as a byproduct from phosphate rock processing; 69,200 metric tons (153
million pounds) was produced, and 69,100 metric tons (152 million pounds) was sold or used.
This was an almost 3% increase in output from the previous year. The amount used for water
fluoridation was 34, 900 metric tons (51%), while 19,000 metric tons (27%) was used for
aluminum trifluoride production, and 15,300 metric tons (22%) was used for other uses such as
5
sodium hexafluorosilicate production (Miller, 1999). The latest figures are definitely an increase
compared to the 1975 and 1976 U.S. production of the acid at 30,000 metric tons (66 million
pounds) from phosphoric acid manufacturing. No import data were found (HSDB, 2000a).
5.0 Uses
The major use of sodium hexafluorosilicate and fluorosilicic acid is as fluoridation agents for
drinking water (HSDB, 2000a,b; Urbansky and Schock, 2000). They have been added to water
since the mid-1940s to prevent tooth decay (Chem. Mark. Rep., 2000). Sodium
hexafluorosilicate has also been used for caries control as part of a silicophosphate cement and as
an acidic gel in combination with monocalcium phosphate monohydrate (Jinks et al., 1982 abstr.;
Takagi et al., 1992). As part of a two-solution fluoride mouth rinse, it resulted in enhanced
remineralization of human enamel lesions and root lesions (Takagi et al., 1997; Chow et al.,
2000).
Both chemicals are also used as a chemical intermediate (raw material) for aluminum trifluoride,
cryolite (Na3AlF6), silicon tetrafluoride, and other fluorosilicates (HSDB, 2000a,b). In addition,
they have found applications in commercial laundry; sodium hexafluorosilicate acts as a laundry
souring agent and the acid acts as a neutralizer for alkalis (LCI, Ltd., 2000a,b).
Other applications for sodium hexafluorosilicate include its use in enamels/enamel frits for china
and porcelain, in opalescent glass, metallurgy (aluminum and beryllium), glue, ore flotation,
leather and wood preservatives, and in insecticides and rodenticides (e.g., moth repellent and for
the control of Noctuid larvae [i.e., cotton leafworms, mole crickets, grasshoppers, locusts, crane
flies, earwigs, and sowbugs]) (HSDB, 2000b; LCI, Ltd. 2000b; Farm Chem. Handbook, 2001).
It has been used in the manufacture of pure silicon and as a gelling agent in the Dunlop process
(production of molded latex foam) (HSDB, 2000b). Recently, it has been used in organic
synthesis as a fluorinating agent to convert organodichlorophosphorus compounds to the
corresponding organodifluorophosphorus compound in low to moderate yields (up to 75%)
(Farooq, 1998). In veterinary practice, externally applied sodium hexafluorosilicate has been
used to combat lice and mosquitoes on cattle, sheep, swine, and poultry. It has been given orally
to combat roundworms and possibly whipworms in swine and added to feed (50 ppm) to prevent
dental caries in rats (HSDB, 2000b). Sodium hexafluorosilicate is listed as an oral care agent on
the International Nomenclature of Cosmetic Ingredients inventory established under a European
Commission Directive (96/335/EC) (INCI, 1998).
Fluorosilicic acid is used in the tanning of animal hides and skins, in ceramics and glass (glass
etching), in technical paints, in oil well acidizing, and in the manufacture of hydrogen fluoride.
It is also employed as an impregnating ingredient to preserve wood and harden masonry and for
the removal of mold as well as rust and stain in textiles. It has been used for the sterilization of
equipment (e.g., in brewing and bottling establishments and for copper and brass vehicles) as
well as in electroplating (HSDB, 2000a; LCI, Ltd., 2000a). A typical electrolyte contains 95 g/L
free fluorosilicic acid (King and Ramachandran, 1995). In the electrolytic refining of lead, the
electrolyte contains 33% of the acid (Howe, 1981).
6.0 Environmental Occurrence and Persistence

In the hydrogen fluoride process, fluorosilicic acid (30-35%) can readily be recovered from the
silicon tetrafluoride-containing plant vent gases, which are absorbed in water. It can also be
6
recovered from wet-process phosphoric acid plants and then processed to form hydrogen fluoride
(Smith, 1994; Woytek, 1980). In this process, 45-60% gaseous fluorine compounds are
recoverable. The fluorosilicic acid is usually disposed of by converting it into inert and harmless
waste products; usually, neutralization with limestone or milk of lime is done to precipitate the
acid as a mixture of calcium fluoride and silica. However, small amounts of poisonous fluorine
compounds remain in the effluent (Denzinger et al., 1979).
The manufacture of phosphate fertilizer in Central Florida releases not only fluorides as a toxic
pollutant but also radionuclides. Radium wastes come from the filtration systems. Uranium and
its decay-rate products are found in the phosphate rock and fertilizer as well as the byproduct
fluorosilicic acid. During the wet-process procedure, trace amounts of both radium and uranium
are captured in the scrubbers and therefore are in the fluorosilicic acid. During the acidulation
process yielding phosphoric acid, radon gas in the phosphate pebbles can be released and carried
into the fluorosilicic acid, while polonium can be captured during the scrubbing process and then
can combine with fluoride (Glasser, undated).
The Centers for Disease Control (CDC) and EPA recommended levels for fluoride in drinking
water ranges from 0.6-1.2 ppm (CSDS, 2001). For drinking water fluoridation, the maximum
use level (MUL) for sodium hexafluorosilicate is 2 mg/L; for fluorosilicic acid, the level is 6
mg/L of a 25% fluorosilicic acid solution. Both values correspond to a fluoride concentration of
1.2 mg/L, which is below the U.S. Environmental Protection Agency’s (EPA’s) Maximum
Contaminant Level (MCL) of 4.0 mg/L and the Secondary Maximum Contaminant Level
(SMCL) of 2.0 mg/L. Although EPA has no MCL for silicate in drinking water, the National
Sanitation Foundation (NSF) has established a Maximum Drinking Water Level of 16 mg/L for
silicates. For NSF Certified Products used in drinking water, the Maximum Allowable Level
(MAL) for fluoride is 1.2 mg/L; the MUL of the products ranges from 4 to 6.6 mg/L (NSF Int.,
2000a). At its plant in Riverview, FL, Cargill Fertilizer, Inc. had an MUL of 8 mg/L sodium
hexafluorosilicate (equivalent to 1.2 mg/L fluoride) for fluoridation (NSF Int., 2001). While the
majority of 29 manufacturers of fluorosilicic acid had an MUL of 6 mg/L, a level of 6.6 mg/L
was measured at the IMC-Agrico Company plant at Uncle Sam, LA. [The Hydrite Chemical
Company’s MUL was 1.7 mg/L at three plants, while the American Development Corporation
had an MUL of 4 mg/L at two plants] (NSF Int., 2000b).
7.0 Human Exposure

Potential exposure to sodium hexafluorosilicate is via inhalation of dusts, ingestion, and eye and
skin contact (HSDB, 2000b). The main routes of entry of fluorosilicic acid are inhalation and
eye and skin contact (HSDB, 2000a; LCI, Ltd., undated-a).
Exposure to sodium hexafluorosilicate is possible from its use to control crawling insects in
homes and work buildings. The chemical has "high inherent toxicity," and children may ingest
the material from crawling on the floors of treated houses (U.S. EPA, 1999).
In 1992, 5876 U.S. public water suppliers were using fluorosilicic acid and 1635 utilities were
using its sodium salt for water fluoridation, serving greater than 80 and 36 million persons,
respectively (Urbansky and Schock, 2000). Currently, silicofluorides are used in over 9200 U.S.
water treatment systems, serving over 120 million individuals (CSDS, 2001). Exposure via
drinking water is, however, expected to be minimal, since at concentrations used in water
7
fluoridation and at the normal pH of drinking water, both compounds hydrolyze almost
completely (see Section 2.2) (Urbansky and Schock, 2000). At equilibrium, the
hexafluorosilicate remaining in drinking water is estimated to be <<1 parts per trillion (Urbansky
and Schock, 2000). In addition, exposure to impurities in the fluoridating agent is judged to be
of low health risk when properly treated water is ingested. For example, in fluorosilicic acid,
iron and iodine are usually below the levels considered useful as a dietary supplement; the
phosphorus level is reported to be insignificant; and silver is usually <4 parts per septillion in the
fluoridated water (CSDS, 2001).
In the workplace, exposure to both chemicals is possible during their manufacture,

transportation, or use in water treatment (HSDB, 2000a,b). In the NIOSH 1983 National
Occupational Exposure Survey (NOES) of 8057 facilities, 74 industries, and 60 occupations,
79,556 employees were potentially exposed to sodium hexafluorosilicate; the total number of
female employees potentially exposed was 22,185. In the 1983 NOES of 1758 facilities, 19
industries, and 15 occupations, 10,867 employees were potentially exposed to fluorosilicic acid;
the total number of females potentially exposed was 2068 (RTECS, 2000).
8.0 Regulatory Status

Under EPA’s Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA), sodium
hexafluorosilicate as a pesticide was subject to registration or re-registration in 1988 (RTECS,
2000). In August 1995, the act was amended, eliminating fluorosilicate compounds from the
registration list and their sale for pesticide use (40CFR153, Subpart H) (U.S. EPA, 1995). In the
United States, all pesticide uses have been cancelled (U.S. EPA, 1999). The registrations of
insecticide formulations containing 0.18% to 98.5% sodium hexafluorosilicate, some on the
market since the late 1940s, were cancelled in the late 1980s and early 1990s. Target organisms
included roaches, moths, and weevils. Other cancelled fluorosilicate products were formulated
with sodium aluminum fluorosilicate or aluminum fluorosilicate (NPIRS¤, 2001). [It is noted
that the use of sodium hexafluorosilicate as an insecticide is currently listed in the 2001 Farm
Chemicals Handbook (see Section 5.0).] Both sodium hexafluorosilicate and fluorosilicic acid
are listed in Section 8(b) of the Toxic Substances Control Act (TSCA; chemical inventory
section). Both are also exempt from reporting under the Inventory Update Rule (i.e., Partial
Updating of the TSCA Inventory Data Base Production and Site Reports [40CFR, Section
710(b)]) (TSCAINV, 2000). The Occupational Safety and Health Administration (OSHA) and
American Conference of Governmental Industrial Hygienists (ACGIH) have established an
eight-hour time-weighted average (TWA) of 2.5 mg/m3 fluorides, as fluorine. OSHA has
established this Permissible Exposure Limit (PEL) for the general industry (29CFR1910.1000),
construction (29CFR1915.1000), shipyard (29CFR1926.55), and federal contracts (41CFR50
204.50). The ACGIH short-term excursion limit (STEL) recommendation is that excursions in
worker exposure levels may exceed three times the threshold limit value (TLV)-TWA for no
more than 30 minutes during a work day and not exceed five times the TLV-TWA, provided that
the TLV-TWA is not exceeded. ACGIH has listed fluorides, as fluorine, as "A4 not
classifiable as a human carcinogen" (HSDB, 2000b; RTECS, 2000). NIOSH has also
recommended an air exposure level to inorganic fluorides of 2.5 mg F/m3 but as a ten-hour TWA
(RTECS, 2000).
8
9.0 Toxicological Data

9.1 General Toxicology
Chronic ingestion of excessive amounts of fluoride produces osteosclerosis and mottled tooth
enamel. Chronic exposure increases osteoblastic activity as well as the density and calcification
of bone (Gilman et al., 1980; cited by HSDB, 2000a).
9.1.1 Human Data

Chronic exposure to dust at levels above the PEL or TLV can result in severe calcification of the
rib, pelvis, and spinal column ligaments; effects on the enzyme system; pulmonary fibrosis;
stiffness; irritation of the eyes, skin, and mucous membranes; weight loss; anorexia; anemia;
cachexia; wasting; and dental effects. Long-term or repeated exposure to the skin can result in
skin rash (LCI, Ltd., undated-b). Contact with the molten forms of the chemical may cause
severe burns to the skin and eyes (HSDB, 2000b).
The clinical signs and symptoms after ingestion of soluble fluoride salts occur in the following
five stages: (I) salty or soapy taste, salivation, nausea, abdominal pain, vomiting, (bloody)
diarrhea, dehydration, and thirst; (II) muscle weakness, tremors, and in rare instances transient
epileptiform convulsions, which may lead to central nervous depression; (III) shock
characterized by pallor, weak and thready pulse, shortness of breath, weak heart sounds, wet and
cold skin, cyanosis, dilated pupils, followed by death in two to four hours; (IV) when death has
not occurred, paralysis of muscle deglutition, carpopedal spasm, and spasm of extremities; and
(V) occasionally localized or generalized urticaria. A probable oral lethal dose of 50-500 mg/kg,
classified as very toxic, has been reported for a 150-pound (70-kg) person receiving between 1
teaspoon and 1 ounce of the chemical (Gosselin et al., 1976; cited by HSDB, 2000b).
A girl (2.5 years old) who ingested sodium hexafluorosilicate "developed acute respiratory
failure, a prolonged AT interval, ventricular tachycardia and fibrillation, hypokalemia,
hypocalcemia (3 to 4 mg/100 mL), and aspiration pneumonia" (Ellenhorn et al., 1997; cited by
HSDB, 2000b). In a suicide attempt, a female chemical plant worker (32 years old) who
ingested three teaspoons of sodium hexafluorosilicate immediately began vomiting, and then
experienced facial numbness, diarrhea, diaphoresis, muscle spasms, weakness, abdominal pain,
dyspnea, shallow breathing, and cramps of the palms, feet, and legs. Tachycardia and tachypnea
were observed. After 12 hours, generalized weakness and enlargement of the liver continued.
Treatment with calcium compounds (calcium carbonate initially; calcium lactogluconate for ten
days after life-threatening symptoms had diminished) resulted in recovery within 21 days (Dadej
et al., 1987).
Fluorosilicic Acid
Contact with the molten forms of fluorosilicic acid may cause severe burns to the skin and eyes.
It is also extremely corrosive to the respiratory tract (Hawley, 1981; cited by HSDB, 2000a).
The symptoms of inhalation include burning of the eyes and numbness around the lips.
Symptoms do not necessarily occur immediately; they can appear 24 hours after exposure.
9
On the morning of September 6, 1994, a tanker truck spilling 4500 gallons of fluorosilicic acid
on Interstate 4 near Deltona, Florida, covering an area 600 feet long and 60 feet wide, resulted in
the evacuation of approximately 2300 people from their homes into shelters. Later in the day,
fumes were detected in the Deltona Woods neighborhood; because the acid could be carried by
the wind, everyone within a mile radius was evacuated, which included 1,750 people in Orange
County and 500 people in Deltona. More than 50 people went to hospitals, complaining of skin
and respiratory irritation, including burning in the throat, and headaches. An individual riding in
a truck with his arm out the window experienced burning on his forearm (Lancaster, 1994).
The effects of long-term exposure to fluorosilicic acid are changes in bone, corrosivity of the
mucous membranes (e.g., ulceration of the nose, throat, and bronchial tubes), coughing, shock,
pulmonary edema, fluorosis, coma, and even death (LCI, Ltd., undated-a). In a study of 50
workers engaged for approximately 30 years in the production of phosphate fertilizers, the
concentration of gaseous fluoride (hydrogen fluoride, silicon tetrafluoride, and fluorosilicic acid)
ranged from 0.04 to 0.17 mg/m3. Nine workers had increased bone densities (Fabbri et al., 1978;
cited by HSDB, 2000a).
When swallowed, severe irritation of the lungs, nose, and throat can occur, as well as severe
damage to the throat and stomach (LCI, Ltd., undated-a). A probable oral lethal dose of 50-5000
mg/kg, classified as very toxic, has been reported for doses between 1 teaspoon and 1 ounce for a
150-pound (70-kg) person; a probable oral lethal dose of 5-50 mg/kg, classified as extremely
toxic, has been reported for doses between 7 drops and 1 teaspoon for the same individual
(Gosselin et al., 1984; cited by HSDB, 2000a).
9.1.2 Chemical Disposition, Metabolism, and Toxicokinetics

In a female chemical plant worker who ingested sodium hexafluorosilicate (see Section 9.1.1),
fluoride levels in serum and urine (fresh) were 5.130 and 235.60 mg/dm3, respectively, on day 2
of hospitalization. Treatment with calcium compounds (calcium carbonate and calcium
lactogluconate) immediately returned levels to normal. The following day, the levels dropped to
0.399 and 15.39 mg/dm3, respectively; by day 20, the levels were 0.067 and 0.87 mg/dm3,
respectively (Dadej et al., 1987).
In 50 workers engaged for approximately 30 years in the production of phosphate fertilizers and
exposed to gaseous fluoride (hydrogen fluoride, silicon tetrafluoride, and fluorosilicic acid),
urine fluoride excretion ranged from 1.0 to 9.6 mg F-/L (controls: 0.3 to 1.2) (Fabbri et al., 1978;
cited by HSDB, 2000a).
In rats fed a diet containing 0.16% sodium hexafluorosilicate supplemented in a corn-soybean

oilmeal-casein ration ad libitum for 22-23 days, the average amounts of fluorine were 94.4 mg in
feces and 91.9 mg in urine. The mean amount of fluorine absorbed was 65.1% and that retained
was 31.0% (Kick et al., 1935).
From 1965 to 1974, 170 cases of suspected fluorosilicate poisoning were reported in domestic
animals. For positive cases, the animals were poisoned from ingestion of bait, which had not
been disposed of after use. Of these, 27 cases were used in the chemical diagnosis of sodium
hexafluorosilicate poisoning (13 for cattle, 11 for sheep, and 1 each for horse, pigeon, and
concentrate for sheep) (see also Section 9.1.3). In cattle and sheep, measured fluorine
10
concentrations ranged from 120 to 2900 ppm (wet weight) in stomach/rumen contents and up to
75 ppm in urine. In blood serum, 8 and 3 ppm fluorine were determined in one animal from the
groups of poisoned cattle and sheep, respectively (Egyed and Shlosberg, 1975).
When sheep were given sodium hexafluorosilicate via stomach tube (25, 50, 200, 1500, and 2000
mg/kg; 0.13, 0.27, 1.06, 7.976, and 10.63 mmol/kg), blood serum concentrations and urine levels
of fluoride initially significantly increased and then decreased with time. For example, the low
dose group had blood serum concentrations ranging from 0.1-0.165 ppm fluoride prior to
treatment and 4.2 ppm fluoride six hours after dose administration. By day 4, levels dropped to
0.38 ppm fluoride. Corresponding urine levels of fluoride were 1.35-6.75, 175, and 25 ppm,
respectively (Egyed and Shlosberg, 1975).
9.1.3 Acute Exposure
Acute toxicity values for sodium hexafluorosilicate and fluorosilicic acid are presented in Table 1.
The details of selected studies discussed in this section are presented in Table 2.
Table 1. Acute Toxicity Values for Sodium Hexafluorosilicate and Fluorosilicic Acid
Route Species (sex and strain) LCLo/LD50/LDLo/TDLo Reference(s)
oral mouse (sex and strain n.p.) LD50 = 70 mg/kg; 0.37 mmol/kg RTECS (1997)
rat (sex and strain n.p.) LD50 = 125 mg/kg; 0.665 mmol/kg HSDB (2000b)
rat (F, Sprague-Dawley albino LD50 = 430 mg/kg; 2.29 mmol/kg Rhone-Poulenc Inc. (1971)
white)
rat (sex and strain n.p.) TDLo = 248 mg/kg; 1.32 mmol/kg RTECS (1997)
rabbit (sex and strain n.p.) LD50 = 125 mg/kg; 0.665 mmol/kg
s.c. rat (sex and strain n.p.) LDLo = 70 mg/kg; 0.37 mmol/kg
inh guinea pig (sex and strain n.p.) LCLo = 33 mg/kg; 0.18 mmol/kg Patty (1963; cited by
HSDB, 2000b)
Fluorosilicic acid
oral guinea pig (sex and strain n.p.) LD50 = 200 mg/kg; 1.39 mmol/kg LCI, Ltd. (undated-a)
Abbreviations: F = female(s); inh = inhalation; LCLo = lethal concentration low; LD50 = lethal dose for 50% of test
animals; LDLo = lethal dose low; n.p. = not provided; s.c. = subcutaneous(ly); TDLo = toxic dose low
Mice orally given sodium hexafluorosilicate (70 mg/kg; 0.37 mmol/kg) exhibited toxic effects in
the peripheral nerves, sensation, and in behavior. In rats, an oral dose (248 mg/kg; 1.32
mmol/kg) administered intermittently for one month produced toxic effects in the kidney, ureter,
and/or bladder, as well as musculoskeletal and biochemical effects (RTECS, 1997). Using
guinea pigs, inhalation experiments (13-55 mg/m3 [1.7-7.2 ppm] sodium hexafluorosilicate in air
for ≥6 hours) resulted in pulmonary irritation; the lowest concentration that caused death was 33
mg/m3 (4.3 ppm) (Patty, 1963; cited by HSDB, 2000b).
11
Table 2. Acute Exposure to Sodium Hexafluorosilicate and Fluorosilicic Acid

Species, Strain, and Chemical Form and Route, Dose, Duration, Results/Comments Reference
Age, Number, and Sex Purity and Observation Period
of Animals
Mouse strain, age, sodium hexafluoro oral; 70 mg/kg (LD50; 0.37 Toxic effects were observed in the peripheral nerves and sensation RTECS* (1997)
number, and sex n.p. silicate, purity n.p. mmol/kg); duration and (flaccid paralysis without anesthesia, generally neuromuscular
observation period n.p. blockage) and in behavior (ataxia and muscle contraction or
spasticity).
Rats, strain, age, number, sodium hexafluoro oral; 248 mg/kg (1.32 Toxic effects in the kidney, ureter, and/or bladder (other changes in RTECS* (1997)
and sex n.p. silicate, purity n.p. mmol/kg) for 30 days urine composition) were observed. Musculoskeletal (other
intermittent; observation changes) and biochemical (enzyme inhibition, induction, or changes
period n.p. in blood or tissue [phosphatases] levels) effects were seen.
Rats, strain, age, number, sodium hexafluoro s.c.; 70 mg/kg (LDLo; 0.37 Fatty liver degeneration and other changes in the liver and toxic RTECS* (1997)
and sex n.p. silicate, purity n.p. mmol/kg); duration and effects in the kidney, ureter, and bladder primarily changes in
observation period n.p. glomeruli were observed.
Guinea pigs, strain, age, sodium silicofluoride inhalation; 13-55 mg/m3 Pulmonary irritation was observed. The lowest concentration that Patty (1963; cited
number, and sex n.p. as dust, purity n.p. (1.2-7.2 ppm) in air for ≥6 caused death when inhaled for 6 h was 33 mg/m3. by HSDB, 2000b)
h; observation period n.p.
Sheep, Awassi breed, 1 technical sodium oral (via stomach tube); 25, With the 25- and 50-mg/kg doses, animals exhibited grinding of Egyed and
to 3-yr-old, 5F hexafluorosilicate, 50, 200, 1500, and 2000 teeth (an indication of pain), dullness, and mild diarrhea. At 200 Shlosberg (1975)
purity n.p. mg/kg (0.13, 0.27, 1.06, mg/kg, additional symptoms were experienced and included
7.976, and 10.63 mmol/kg) staggering and severe diarrhea. Animals died on day 6. With the
suspended in water; duration two higher doses, licking of the lips, kicking of the belly, grinding
and observation period n.p. of the teeth, falling down (after 1.5 h), frothing at the mouth,
congested conjunctiva, protrudation of the tongue, forced and
labored breathing, fever, and increased respiration and heart rates
were observed. Animals died 3 h after administration of 1500
mg/kg and 2.5 h after administration of 2000 mg/kg.
Post-mortem examination showed serous pericardial fluid (few
milliliters), a slightly friable liver, mild edema in the lungs, and
froth in the trachea. Hemorrhages occurred on the spleen and
mucosal folds of the abomasum, and a gelatinous fluid was present
in the colon.
For the 1500 mg/kg-dose group, the change in GOT went from
132% (of pretreatment activity) at 1.5 hours to 230% at 2.5 hours.
For LDH, the change was 158% at death. The serum ICDH change
increased from 168% after one hour to 984% at death.
12
Table 2. Acute Exposure to Sodium Hexafluorosilicate and Fluorosilicic Acid (Continued)

Species, Strain, and Chemical Form and Route, Dose, Duration, Results/Comments Reference
Age, Number, and Sex Purity and Observation Period
of Animals
Fluorosilicic acid
Rats, strain, age, number, fluorosilicic acid, oral; 430 mg/kg (LD50; 2.98 Somnolence and/or general depressed activity was observed. RTECS* (2000)
and sex n.p. purity n.p. mmol/kg); duration and
observation period n.p.
Rats, Sprague-Dawley fluorosilicic acid oral (via stomach tube); With 464 mg/kg, 3 out of 5 rats died; at ≥1000 mg/kg, 100% Rhone-Poulenc Inc.
albino, age n.p., 5F per (~23%, neat), purity single doses of 215, 464, mortality was observed. At ≥464 mg/kg, acute depression was (1971)
dose level n.p. 1000, and 2100 mg/kg observed. Necropsy showed that animals in the low-dose group
(1.49, 3.22, 6.939, and 14.57 were "grossly normal" and that dead rats had massive hemorrhages
mmol/kg) dissolved in in the entire gastrointestinal tract.
water. Animals were
observed for 14 days and
then necropsied.
Rats, guinea pigs, and fluorosilicic acid, percutaneous; amounts, The intact skin was not affected. When areas were injured before Alhassan and Zink
swine tested as a group; purity n.p. duration, and observation application of the acid, necrosis, continuously spreading, occurred (1982; cited by
no other data were period n.p. in the deeper regions. Hypocellular necrosis, consisting of sharp HSDB, 2000a)
provided leukocyte demarcations, and edema up to the subcutis were
observed.
Rabbits, New Zealand, fluorosilicic acid dermal; 0.5 mL (4 mol) to Severe erythema and edema were observed, indicating the material Rhone-Poulenc Inc.
age n.p., 6, sex n.p. (~23%, neat), purity the intact and abraded skin to be a primary irritant. (1971)
n.p. for 1, 24, or 72 h
Rabbits, New Zealand, fluorosilicic acid instillation; 0.1 mL (0.8 Severe and permanent corneal opacity with scar tissue occurred. Rhone-Poulenc Inc.
age n.p., 6, sex n.p. (~23%, neat), purity mol) into the left eye. Eyes (1971)
n.p. were observed at 24, 48, and
72 h following treatment.
Abbreviations: GOT = glutamate oxaloacetate transaminase; h = hour(s); ICDH = isocitric dehydrogenase; LDH = lactate dehydrogenase; n.p. = not provided
*RTECS uses codes for Toxic Effects. For some codes, it is unclear whether the effects occur in all organs (e.g., M02 — KIDNEY, URETER, BLADDER
[Changes primarily in glomeruli]). In these instances, "and/or" has been used.
13
When sodium hexafluorosilicate (500 mg; 2.66 mmol) was applied to the skin of adult rabbits,
mild irritation occurred. When applied to the eyes (100 mg; 0.532 mmol), severe irritation was
observed; following a four-second rinse, the effect was still severe (RTECS, 1997).
Sodium hexafluorosilicate poisoning in domestic animals from the ingestion of bait which had
not been disposed of after use (13 cases for cattle, 11 for sheep, and 1 each for horse, pigeon, and
concentrate for sheep) resulted in drowsiness, constipation, loss of appetite, paresis of the rumen,
severe abdominal pain, and diarrhea. Sheep also exhibited grinding of the teeth (an indication of
pain) and frothing at the mouth in most cases of lethal poisoning, while the horse also had
bradycardia. In an acute study in which sheep were orally administered technical sodium
hexafluorosilicate (25, 50, 200, 1500, and 2000 mg/kg; 0.13, 0.27, 1.06, 7.976, and 10.63
mmol/kg) via stomach tube, the animals exhibited similar symptoms. In addition, with the two
highest doses, falling down (after 1.5 hours), congested conjunctiva, forced and labored
breathing, fever, and increased respiration and heart rates were observed. Animals died 6 days
after administration of 200 mg/kg and 2.5 hours after administration of 2000 mg/kg (Egyed and
Shlosberg, 1975). When a dairy herd of 600 animals was acutely poisoned from railcar
contamination of feed, 95% of the animals had decreased neuromuscular transmission. The
poisoning, which resembled calcium depletion, was effectively treated with calcium gluconate
intravenously (HSDB, 2000b [original source was not cited]).
Fluorosilicic Acid
In rats orally given fluorosilicic acid (430 mg/kg; 2.98 mmol/kg), somnolence and/or general
depressed activity was observed (RTECS, 2000). Other rat studies with fluorosilicic acid (single
oral doses of 215, 464, 1000, and 2100 mg/kg [1.49, 3.22, 6.939, and 14.57 mmol/kg]) led to its
classification as "moderately toxic" (Rhone-Poulenc, Inc., 1971). Percutaneous administration of
the compound (amounts not provided) in rats, guinea pigs, and pigs resulted in continuously
spreading necrosis in the deeper regions of injured skin. Hypocellular necrosis, consisting of
sharp leukocyte demarcations, and edema up to the subcutis were also observed (Alhassan and
Zink, 1982; cited by HSDB, 2000a). In rabbits, it was corrosive to the skin (0.5 mL [4 mol] for
1, 24, or 72 hours) and eyes (0.1 mL [0.8 mol] instilled into left eye) (Rhone-Poulenc Inc., 1971).
9.1.4 Short-term and Subchronic Exposure

No data were available.
9.1.5 Chronic Exposure

9.1.6 Synergistic/Antagonistic Effects

Fluoride, administered in the form of sodium hexafluorosilicate, had a strong affinity for calcium
and magnesium. When orally given to sheep via a stomach tube at doses of 25, 50, 200, 1500,
and 2000 mg/kg, increased changes in serum calcium and magnesium levels were observed at
the two highest doses within 30 minutes after dose administration. At 200 mg/kg, recovery of
both levels occurred after five days. With the 1500 mg/kg dose group, changes in phosphorus
and sugar levels in whole blood were also significantly increased (16% [of pretreatment levels]
at 1.5 hours to 146% at 2.5 hours for phosphorus; 300% to 374%, respectively, for sugar levels)
(Egyed and Shlosberg, 1975).
14
9.1.7 Cytotoxicity
9.2 Reproductive and Teratological Effects

9.3 Carcinogenicity
No studies with sodium hexafluorosilicate or fluorosilicic acid were available. IARC (1987)
concluded that there was inadequate evidence for carcinogenicity to humans and to animals for
inorganic fluorides used in drinking water.
9.4 Initiation/Promotion Studies

9.5 Anticarcinogenicity
9.6 Genotoxicity
Sodium hexafluorosilicate was negative in the Salmonella/microsome test (concentrations up to
3600 g/plate, –S9) and the micronucleus test on mouse bone marrow (37.2 mg/kg; 0.198
mmol/kg) (Gocke et al., 1981). The compound (0.25 mM; 47 g/mL) did not induce sex-linked
recessive lethal mutations in Drosophila (Gocke et al., 1981; IARC, 1987). In the Bacillus
subtilis rec-assay system, sodium hexafluorosilicate (0.001-10 M; 188 g/mL-1.9 g/mL) also
gave negative results (Kada et al., 1980; Kanematsu et al., 1980).
9.7 Cogenotoxicity
9.8 Antigenotoxicity
9.9 Other Data

Within one week after beginning work in a foam rubber plant, a 23-year-old man exhibited skin
lesions consisting of "diffuse, poorly delineated, erythematous plaques with lichenoid papules
and large pustules" on his arms, wrists, thighs, and trunk. Although scratch and patch tests with
sodium hexafluorosilicate (2% aqueous) were negative, animal testing showed the compound to
be a pustulogen. When rabbits received topical application of a 1, 5, 10, and 25% solution of
sodium hexafluorosilicate in petroleum, pustules occurred on normal skin only with the high
concentration, while all concentrations produced pustules on stabbed skin (Dooms-Goossens et
al., 1985).
10.0 Structure-Activity Relationships

At levels of 14-16 ppm fluorine, sodium fluoride, sodium hexafluorosilicate, and cryolite
(Na3AlF6) had the same extent of chronic fluorine intoxication in rats (De Eds and Thomas,
1933-1934; cited by McClure, 1950). At 40 and 80 ppm, the chronic toxicity (observations on
growth rate, fecundity, mortality, tooth development, pathology, and disease) of barium
fluorosilicate and cryolite in rats was "substantially the same as that of sodium fluoride for the
same fluorine content" (Smyth and Smyth, 1932; cited by McClure, 1950). At 14 ppm fluorine,
15
ammonium fluoride, potassium fluoride, barium fluorosilicate, potassium fluorosilicate, and

sodium fluorosilicate exhibited the same acute toxicity as sodium fluoride in the animals (Smith
and Leverton, 1934; cited by McClure, 1950).
In a comparative study of absorption and excretion of fluorine in rats fed sodium fluoride,
calcium fluoride, and sodium hexafluorosilicate, the percent fluorine retained was the same for
the two sodium compounds (Kick et al., 1935 [see Section 9.1.2 for details regarding sodium
hexafluorosilicate]). Several experiments on growing rats orally given 5, 10, 15, 25, and 50 ppm
fluorine as sodium fluoride or sodium hexafluorosilicate for 90-100 days found no differences in
the quantity of fluorine deposited and the contents of ash, calcium, and phosphorus in the incisor
teeth, molar teeth, mandibles, and femurs. Furthermore, there were no differences in the percent
of ingested fluorine retained in the body, and a combination of sodium silicate (15 ppm silicon)
with sodium fluoride (25 ppm fluorine) did not affect the amount of fluorine deposited. The
growth rate was normal in all rats (McClure, 1950).
In a separate study, litters of female weanling Osborne-Mendel rats were given 50 ppm fluorine
as sodium fluoride or ammonium fluorosilicate in drinking water for 99 days. The cariostatic
effect was similar for the two compounds i.e., both inhibited caries to the same extent. There
were no differences in the amounts of fluorine and ash deposited in the molars, incisors,
mandibles, and femurs. There were no differences in growth rate and in the production of incisor
striations (Zipkin and McClure, 1954).
16
11.0 Online Databases and Secondary References

11.1 Online Databases
Chemical Information System Files
SANSS (Structure and Nomenclature Search System)
TSCAINV (Toxic Substances Control Act Inventory)
TSCATS (Toxic Substances Control Act Test Submissions)
National Library of Medicine Databases
EMIC and EMICBACK (Environmental Mutagen Information Center)
STN International Files

AGRICOLA EMBASE NTIS
BIOSIS HSDB PROMT
CA LIFESCI Registry
CABA MEDLINE RTECS
CANCERLIT NIOSHTIC TOXLINE
TOXLINE includes the following subfiles:

Toxicity Bibliography TOXBIB
International Labor Office CIS
Hazardous Materials Technical Center HMTC
Environmental Mutagen Information Center File EMIC
Environmental Teratology Information Center File (continued after ETIC
1989 by DART)
Toxicology Document and Data Depository NTIS
Toxicological Research Projects CRISP
NIOSHTIC¤ NIOSH
Pesticides Abstracts PESTAB
Poisonous Plants Bibliography PPBIB
Aneuploidy ANEUPL
Epidemiology Information System EPIDEM
Toxic Substances Control Act Test Submissions TSCATS
Toxicological Aspects of Environmental Health BIOSIS
International Pharmaceutical Abstracts IPA
Federal Research in Progress FEDRIP
Developmental and Reproductive Toxicology DART
In-House Databases
CPI Electronic Publishing Federal Databases on CD
Current Contents on Diskette¤
The Merck Index, 1996, on CD-ROM
17
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23
Acknowledgements
Support to the National Toxicology Program for the preparation of Sodium Hexafluorosilicate
[CASRN 16893-85-9] and Fluorosilicic Acid [CASRN 16961-83-4] Review of Toxicological
Literature was provided by Integrated Laboratory Systems, Inc., through NIEHS Contract
Number N01-ES-65402. Contributors included: Karen E. Haneke, M.S. (Principal Investigator);
Bonnie L. Carson, M.S. (Co-Principal Investigator); and Claudine A. Gregorio, M.A.
Appendix: Units and Abbreviations

°C = degrees Celsius
µg/L = microgram(s) per liter
µg/m3 = microgram(s) per cubic meter
µg/mL = microgram(s) per milliliter
µM = micromolar
ACGIH = American Conference of Governmental Industrial Hygienists
AOAC = Association of Official Analytical Chemists
AWWA = American Water Works Association
bw = body weight
C.P. = Commercially Pure
CSDS = Colorado Springs Dental Society
EPA = Environmental Protection Agency
F = female(s)
FIFRA = Federal Insecticide, Fungicide, and Rodenticide Act
g = gram(s)
g/mL = gram(s) per milliliter
h = hour(s)
HSDB = Hazardous Substances Data Bank
IARC = International Agency for Research on Cancer
i.p. = intraperitoneal(ly)
kg = kilogram(s)
L = liter(s)
LC50 = lethal concentration for 50% of test animals
LCLo = lethal concentration low
24
LD50 = lethal dose for 50% of test animals

LDLo = lethal dose low
M = male(s)
MAL = Maximum Allowable Level
MCL = Maximum Contaminant Level
MUL = maximum use level
mg/kg = milligram(s) per kilogram
mg/m3 = milligram(s) per cubic meter
mg/mL = milligram(s) per milliliter
min = minute(s)
mL/kg = milliliter(s) per kilogram
mm = millimeter(s)
mM = millimolar
mmol = millimole(s)
mmol/kg = millimoles per kilogram
mo = month(s)
mol = mole(s)
mol. wt. = molecular weight
NICNAS = National Industrial Chemicals Notification and Assessment Scheme
NIOSH = National Institute for Occupational Safety and Health
NSF = National Sanitation Foundation
NOES = National Occupational Exposure Survey
NOHS = National Occupational Hazard Survey
n.p. = not provided
OSHA = Occupational Safety and Health Administration
PEL = permissible exposure limit
ppb = parts per billion
ppm = parts per million
p.o. = peroral(ly), per os
REL = relative exposure limit
RTECS = Registry of Toxic Effects of Chemical Substances
s.c. = subcutaneous(ly)
25
SMCL = Secondary Maximum Contaminant Level

STEL = short-term exposure limit
TDLo = toxic dose low
TLV = threshold limit value
TSCA = Toxic Substances Control Act
TWA = time-weighted average
wk = week(s)
yr = year(s)
26

Sodium Hexafluorosilicate and Fluorosilicic Acid - Review of Toxicological Literature

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Sodium Hexafluorosilicate

Review of Toxicological Literature

Review of Toxicological Literature

National Institute of Environmental Health Sciences

P.O. Box 12233

Research Triangle Park, North Carolina 27709

Contract No. N01-ES-65402

Bonnie L. Carson, M.S. (Co-Principal Investigator)

Integrated Laboratory Systems

P.O. Box 13501

Research Triangle Park, North Carolina 27709

When heated to decomposition, sodium hexafluorosilicate releases toxic fumes of hydrogen

Commercial Availability, Production, and Uses

Sodium hexafluorosilicate is produced by treating fluorosilicic acid with sodium hydroxide,

Environmental Occurrence and Persistence

In the workplace, exposure to both chemicals is possible during their manufacture,

tachycardia and fibrillation, hypocalcemia, facial numbness, diarrhea, tachycardia, enlarged

Chemical Disposition, Metabolism, and Toxicokinetics

In rats fed a diet containing 0.16% sodium hexafluorosilicate supplemented in a corn-soybean

No short-term or subchronic exposure, chronic exposure, cytotoxicity, reproductive toxicity,

1.0 Basis for Nomination..................................................................................................... 1

2.1 Chemical Identification and Analysis ............................................................... 1

2.1.1 Sodium Hexafluorosilicate ..................................................................... 1

2.1.2 Fluorosilicic Acid.................................................................................... 2

2.2 Physical-Chemical Properties ........................................................................... 3

2.3 Commercial Availability.................................................................................... 4

3.0 Production Processes..................................................................................................... 5

4.0 Production and Import Volumes .................................................................................. 5

5.0 Uses ................................................................................................................................ 6

6.0 Environmental Occurrence and Persistence ................................................................ 6

7.0 Human Exposure........................................................................................................... 7

8.0 Regulatory Status .......................................................................................................... 8

9.0 Toxicological Data......................................................................................................... 9

9.1 General Toxicology............................................................................................ 9

9.1.1 Human Data ........................................................................................... 9

9.1.2 Chemical Disposition, Metabolism, and Toxicokinetics ..................... 10

9.1.3 Acute Exposure .................................................................................... 11

9.1.4 Short-term and Subchronic Exposure................................................. 14

9.1.5 Chronic Exposure ................................................................................ 14

9.1.6 Synergistic/Antagonistic Effects .......................................................... 14

9.1.7 Cytotoxicity .......................................................................................... 15

9.2 Reproductive and Teratological Effects.......................................................... 15

9.3 Carcinogenicity ................................................................................................ 15

9.4 Initiation/Promotion Studies ........................................................................... 15

9.6 Genotoxicity ..................................................................................................... 15

9.7 Cogenotoxicity ................................................................................................. 15

9.9 Other Data ....................................................................................................... 15

10.0 Structure-Activity Relationships ................................................................................ 15

11.1 Online Databases ............................................................................................. 17

11.2 Secondary References...................................................................................... 18

13.0 References Considered But Not Cited ........................................................................ 23

Appendix: Units and Abbreviations...................................................................................... 24

Table 1 Acute Toxicity Values for Sodium Hexafluorosilicate and

Fluorosilicic Acid ...................................................................................... 11

Table 2 Acute Exposure to Sodium Hexafluorosilicate and Fluorosilicic Acid ... 12

1.0 Basis for Nomination

2.1 Chemical Identification and Analysis

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Ortho earwig bait