Sodium metasilicate
SODIUM METASILICATE
International Programme on Chemical Safety
Poisons Information Monograph 500
Chemical
1. NAME
1.1 Substance
Sodium Metasilicate
1.2 Group
Silicon oxide, sodium compound
1.3 Synonyms
Disodium Metasilicate; Sodium Silicate;
Sodium Metasilicate, 9-hydrate;
Sodium Metasilicate, anhydrous Soluble Glass;
Waterglass
1.4 Identification numbers
1.4.1 CAS number
6834-92-0 (anhydrous)
1.4.2 Other numbers
10213-79-3 (pentahydrate)
13517-24-3 (nonahydrate)
RTECS Number VV9275000 (sodium metasilicate)
(IPCS/CEC,1993).
1.5 Brand names, Trade names
To be completed by each Centre using the monograph.
1.6 Manufacturers, Importers
To be completed by each Centre using the monograph.
2. SUMMARY
2.1 Main risks and target organs
Sodium metasilicate is strongly irritating to the skin,
eyes and respiratory tract. Acute exposures involving the
inhalation of dusts may result in irritation of the
respiratory tract and corrosive damage may result from
contact with mucous membranes. Prolonged exposures can lead
to inflammatory changes and ulcerative problems in the mouth.
Possible bronchial and gastrointestinal problems can occur,
depending upon concentration and duration of exposure.
2.2 Summary of clinical effects
Initial clinical manifestations of acute ingestion can
include dysphagia, drooling, pain and haematemesis. Oral,
oesophageal, and gastric burns may be present. Extensive
mucosal damage leads to fever, tachypnoea, tachycardia,
hypertension, and shock. Acute complications include
aspiration pneumonia, burns of the epiglottis and vocal
cords, and laryngeal obstruction. Acute perforation of the
oesophagus or stomach with mediastinal or peritoneal abscess,
sepsis, and death may occur. Possible longterm sequelae of
acute exposure include oesophageal stricture, squamous cell
oesophageal cancer, vocal cord paralysis, and pyloric
stenosis.
2.3 Diagnosis
Diagnosis is based on a history of exposure to this
corrosive agent and characteristic findings of skin, eye, or
mucosal irritation or redness and the presence of injury to
the gastrointestinal tract. Victims with oral or oesophageal
injury nearly always have drooling or pain on swallowing.
2.4 First-aid measures and management principles
Inhalation: Remove from exposure; give supplemental
oxygen if required. Skin and eyes: Remove all affected
clothing and wash skin and irrigate eyes with copious water
or saline.
Ingestion: Immediately give water or milk to drink if the
patient is able to swallow. The volume administered should
not be so excessive as to cause gastric distension and induce
vomiting. Do not induce emesis or give pH-neutralising
solutions such as dilute vinegar or bicarbonate. If
oesophageal or gastric perforation is suspected, obtain
immediate surgical or endoscopic consultation.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
Fusing silica (sand) with sodium carbonate at 1400°C
produces sodium metasilicate. The various hydrates of sodium
metasilicate, range from the anhydrous to the nonahydrate,
with the anhydrous and the penta- and nonahydrates being the
most common forms (Clayton & Clayton, 1993).
3.2 Chemical structure
Chemical formula: Na2SiO3.nH2O
Relative molecular mass 122.07 anhydrous
212.15 pentahydrate
284.21 nonahydrate
(Clayton & Clayton, 1993).
3.3 Physical properties
3.3.1 Colour
Colourless to white or grayish white
3.3.2 State/Form
Solid-crystals
3.3.3 Description
The anhydrous and the pentahydrate are produced
as amorphous beads, whereas the nonahydrate appears as
efflorescent sticky crystals.
Melting point 1089°C anhydrous
72°C pentahydrate
47.8°C nonahydrate (Clayton & Clayton,
1993).
pH of a 1% aqueous solution is about 13 (Clayton &
Clayton, 1993).
Solubility: The metasilicates are highly water soluble
(Clayton & Clayton, 1993).
Insoluble in alcohol, acid and salt solutions
(Budavari, 1989).
Flammability: Not combustible (IPCS/CEC, 1993).
Stability: Solutions of sodium metasilicate, when
heated or acidified, are hydrolysed to free sodium
ions and silicic acid (Clayton & Clayton, 1993).
3.4 Hazardous characteristics
Corrosiveness: In moist air it is corrosive to metals
like zinc, aluminium, tin and lead, forming hydrogen gas
(IPCS/CEC, 1993).
Reactivity: The substance is a strong base, it reacts
violently with acid (IPCS/CEC, 1993).
4. USES/CIRCUMSTANCES OF POISONING
4.1 Uses
4.1.1 Uses
Soap; detergent; bath/washing product
4.1.2 Description
A major use is as a builder (a material that
enhances or maintains the cleaning efficiency of the
surfactant, principally by inactivating water
hardness) in soaps and detergents. It is also used
extensively as an anti-corrosion agent in boiler-water
feed (Clayton & Clayton, 1993).
4.2 High risk circumstance of poisoning
Unintentional ingestion by children of a dishwashing
detergent directly from the container or of the residue from
an automatic dishwasher soap compartment. Intentional
ingestion.
4.3 Occupationally exposed populations
Factory workers involved in formulation and packaging of
sodium metasilicate or metasilicate containing products.
5. ROUTES OF EXPOSURE
5.1 Oral
Ingestion of this chemical is the most common route of
entry with subsequent corrosive injury of the
gastrointestinal tract being the major concern rather than
systemic absorption as for other toxins.
5.2 Inhalation
Inhalation of dusts of sodium metasilicate may result in
irritation of the respiratory tract and corrosive damage may
result from contact with mucous membranes.
5.3 Dermal
Skin exposure to corrosive agents usually results in
immediate pain and redness. Serious full thickness burns can
occur.
5.4 Eye
Eye exposure to corrosive agents commonly results in
conjunctivitis and lachrymation. Blindness can occur.
5.5 Parenteral
No data available.
5.6 Others
No data available.
6. KINETICS
6.1 Absorption by route of exposure
Radio-labelled 31Si sodium metasilicate, partially
neutralized, was given orally to dogs. It was rapidly
absorbed and excreted in the urine but a significant amount
was retained in the tissues (Clayton & Clayton, 1993).
6.2 Distribution by route of exposure
Radio-labeled 31Si sodium metasilicate, partially
neutralized, was given orally to dogs. It was rapidly
absorbed. A significant amount was retained in the tissues.
These findings are consistent with the recognition that
silicon is an essential trace element for bone formation in
animals (Clayton & Clayton, 1993).
6.3 Biological half-life by route of exposure
No data available
6.4 Metabolism
No data available
6.5 Elimination by route of exposure
Radio-labelled 31Si sodium metasilicate, partially
neutralized, was given orally to dogs. It was rapidly
excreted in the urine (Clayton & Clayton, 1993).
7. TOXICOLOGY
7.1 Mode of Action
Sodium metasilicate is markedly corrosive and
penetrating. Solubilizing reactions occur with protein and
collagen, saponifying effects on lipids and dehydration of
tissues and cells. (Houck et al., 1962). Sodium metasilicate
is highly corrosive due to its buffer capacity, which means
that the high pH is well sustained in the presence of tissue
components that quickly neutralize other alkalis such as
sodium hydroxide (Gosselin et al., 1984).
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
There is no specific toxic oral
dose, because the concentration of corrosive
solutions and the potency of caustic effect
vary widely. The concentration or the pH of
the solution may indicate the potential for
serious injury. The titratable alkalinity is
a better predictor of corrosive effect than
the pH (Olson, 1994). Application to human
skin (250mg sodium metasilicate for 24 hours)
caused a severe reaction (RTECS, 1996).
7.2.1.2 Children
No data available
7.2.2 Relevant animal data
Acute oral toxicity LD50 to rats is 1280 mg/kg
as a 10% aqueous solution. (Clayton & Clayton, 1993).
Acute oral toxicity LD50 to mice is 2400 mg/kg as a
10% aqueous solution. (Clayton & Clayton, 1993). Skin
Irritation (rabbit): Application of 0.5 mL of 10%
sodium metasilicate for 4 hours caused mild irritation
(primary irritation score: erythema 1.11/4; oedema
0.11/4) (ECETOC, 1995). Dogs were fed sodium silicate
in their diet at a dose of 2.4 g/kg per day for 4
weeks. Polydipsia and polyuria were observed in some
animals. Damage to renal tubules was observed in 15/16
dogs. (Clayton & Clayton, 1993). A study of detergent
emesis in 11 dogs by gastric intubation, found that 8
mg/kg as a 10.5% aqueous solution of a sodium silicate
(SiO2:Na2O, 3.2:1) produced emesis in 6 minutes which
continued for up to 33 minutes. (Clayton & Clayton,
1993).
7.2.3 Relevant in vitro data
No data available.
7.2.4 Workplace standards
Not established
7.2.5 Acceptable daily intake (ADI) and other guideline
levels.
Not established
7.3 Carcinogenicity
An increased risk of squamous cell oesophageal cancer is
considered possible following ingestion of corrosive agents
such as sodium metasilicate (Gorman et al., 1992).
7.4 Teratogenicity
No data available.
7.5 Mutagenicity
No data available.
7.6 Interactions
No data available.
8. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
8.1.1.2 Biomedical analyses
8.1.1.3 Arterial blood gas analysis
8.1.1.4 Haematological analyses
8.1.1.5 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation
8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple Qualitative Test(s)
8.2.1.2 Advanced Qualitative Confirmation Test(s)
8.2.1.3 Simple Quantitative Method(s)
8.2.1.4 Advanced Quantitative Method(s)
8.2.2 Tests for biological specimens
8.2.2.1 Simple Qualitative Test(s)
8.2.2.2 Advanced Qualitative Confirmation Test(s)
8.2.2.3 Simple Quantitative Method(s)
8.2.2.4 Advanced Quantitative Method(s)
8.2.2.5 Other Dedicated Method(s)
8.2.3 Interpretation of toxicological analyses
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
8.3.1.1 Blood, plasma or serum
Ancilliary tests that may be useful
include a complete blood count, electrolytes,
creatinine, type and cross for several units
of blood, and a haemocult test for blood in
stool.
8.3.1.2 Urine
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
8.3.3 Haematological analyses
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.4 Interpretation of biomedical investigations
8.4 Other biomedical (diagnostic) investigations and their
interpretation
8.5 Overall interpretation of all toxicological analyses and
toxicological investigations
Sample collection
Not relevant
Biomedical analysis
Ancilliary tests that may be useful include a complete blood
count, electrolytes, creatinine, type and cross for several
units of blood, and a haemocult test for blood in stool.
Toxicological analysis
There are no relevant toxicological analyses for this
chemical. However, the concentration or the pH of the
solution may indicate the potential for serious injury. The
titratable alkalinity is a better predictor of corrosive
effect than the pH (Olson, 1994).
Other investigations
Radiographic studies may demonstrate air in the mediastinum
from oesophageal perforation or free abdominal air from
gastric perforation (Olson, 1994).
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
Ingestion of corrosives can cause oral pain,
dysphagia, drooling, and pain in the throat, chest, or
abdomen. Oesophageal or gastric perforation may
occur, manifested by severe chest or abdominal pain,
signs of peritoneal irritation, or pancreatitis.
Haematemesis and shock may occur. Scarring of the
oeosophagus or stomach may result in permanent
stricture formation and chronic dysphagia. (Olson,
1994).
9.1.2 Inhalation
Acute exposures involving the inhalation of
dusts of sodium metasilicate may result in irritation
of the respiratory tract and corrosive damage may
result from contact with mucous membranes. (Clayton &
Clayton, 1993).
9.1.3 Skin exposure
Skin exposure to corrosive agents usually
results in immediate pain and redness. Serious full
thickness burns can occur (Olson, 1994).
9.1.4 Eye contact
Eye exposure to corrosive agents commonly
results in conjunctivitis and lachrymation. Blindness
can occur. Sodium metasilicate is used with sodium
carbonate in heavy duty alkaline laundry detergents.
In rabbits, this type of detergent causes damage to
the cornea, with opacification, proportional to the
alkalinity of the preparation (Scharpf et al., 1972).
9.1.5 Parenteral exposure
No data available
9.1.6 Other
No data available
9.2 Chronic poisoning
9.2.1 Ingestion
Prolonged exposures can lead to inflammatory
changes and ulcerative problems in the mouth.
Bronchial and gastrointestinal problems may occur,
depending upon concentration, duration and frequency
of exposure (Clayton & Clayton, 1993).
9.2.2 Inhalation
Prolonged and repeated inhalation may lead to
ulceration of respiratory membranes (Clayton &
Clayton, 1993).
9.2.3 Skin exposure
Prolonged and repeated skin exposure with
dilute solutions may lead to dermatitis. (Clayton &
Clayton, 1993).
9.2.4 Eye contact
Irritation and other effects described
following acute exposure are likely to be
seen.
9.2.5 Parenteral exposure
No data available.
9.2.6 Other
No data available.
9.3 Course, prognosis, cause of death
Initial clinical manifestations can include dysphagia,
drooling, pain and haematemesis. Oral, oesophageal, and
gastric burns may be present. Extensive mucosal damage leads
to fever, tachypnoea, tachycardia, hypertension, and shock.
Acute complications include aspiration pneumonia, burns of
the epiglottis and vocal cords, and laryngeal obstruction.
Acute perforation of the oesophagus or stomach with
mediastinitis or peritonitis, sepsis, and death may occur.
Longterm sequelae of acute exposure may include oesophageal
stricture, squamous cell oesophageal cancer, vocal cord
paralysis, and pyloric stenosis (Gorman et al., 1992).
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
Tachycardia, hypertension, and shock may occur
(Gorman et al., 1992).
9.4.2 Respiratory
Irritation of the respiratory tract,
tachypnoea, mucosal damage, aspiration pneumonia.
(Clayton & Clayton, 1993; Gorman et al.,
1992).
9.4.3 Neurological
9.4.3.1 Central Nervous System (CNS)
No data available
9.4.3.2 Peripheral nervous system
No data available
9.4.3.3 Autonomic nervous system
No data available
9.4.3.4 Skeletal and smooth muscle
No data available
9.4.4 Gastrointestinal
Oesophageal and gastric burns may be present.
Acute perforation of the oesophagus or stomach with
mediastinitis or peritonitis and sepsis, may occur.
Longterm sequelae of acute exposure may include
oesophageal stricture, squamous cell oesophageal
cancer, vocal cord paralysis, and pyloric stenosis
(Gorman et al., 1992).
9.4.5 Hepatic
No data available.
9.4.6 Urinary
9.4.6.1 Renal
No human data available. Polydipsia
and polyuria were observed in some dogs fed
sodium silicate in their diet at a dose of
2.4 g/kg per day for 4 weeks. Damage to renal
tubules was observed in 15/16 dogs (Clayton &
Clayton, 1993).
9.4.6.2 Others
No data available.
9.4.7 Endocrine & reproductive systems
Pancreatitis may occur (Olson, 1994).
9.4.8 Dermatological
Skin exposure to corrosive agents usually
results in immediate pain and redness. Serious full
thickness burns can occur (Olson, 1994).
9.4.9 Eye, ears, nose, throat: local effects
Dysphagia, drooling, pain. Burns of the
epiglottis and vocal cords, and laryngeal obstruction.
Possible longterm sequelae of acute exposure include
oesophageal stricture and vocal cord paralysis.
(Gorman et al., 1992). Eye exposure to corrosive
agents commonly results in conjunctivitis and
lachrymation. Blindness can occur. Sodium metasilicate
is used with sodium carbonate in heavy duty alkaline
laundry detergents. In rabbits this type of detergent
causes damage to the cornea, with opacification,
proportional to the alkalinity of the preparation
(Scharpf et al., 1972).
9.4.10 Haematological
No data available
9.4.11 Immunological
No data available.
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
No data available.
9.4.12.2 Fluid & electrolyte disturbances
Dehydration may occur if vomiting
is excesssive.
9.4.12.3 Others
No data available.
9.4.13 Allergic reactions
No data available.
9.4.14 Other clinical effects
No data available.
9.4.15 Special risks
No data available.
9.5 Others
No data available.
9.6 Summary
10. MANAGEMENT
10.1 General principles
Management is essentially symptomatic and supportive.
10.2 Life supportive procedures
Administer oxygen if required. Endotracheal intubation,
tracheostomy for life threatening pharyngeal/ tracheal
oedema. If shock is present administer intravenous fluids.
10.3 Decontamination
Skin: Remove all jewellery and affected clothing and
wash skin with copious water or saline.
Irrigation of the eye with water must be done within 60
seconds to reduce the severity of injury (Scharpf et al.,
1972) measurements of the the aqueous humor in alkali burned
and saline irrigated rabbit eyes it has been reported that
more than 2 hours of irrigation might be needed before the
aqueous humor pH comes down to a desirable level. Testing of
the conjunctival sac with wide range pH paper, every five to
ten minutes in the course of irrigation can be used to obtain
a measure of the rate at which the pH is returning to a
tolerable value, such as pH 8 or 8.5. It may take from 48 to
72 hours before an ocular burn can be properly assessed. The
amount of corneal opacification and perilimbal whitening are
used as the basis to assess the seriousness of the burn.
(Grant & Schuman, 1993). Ingestion: Immediately give water or
milk to drink if the patient is able to swallow. The volume
administered should not be so excessive as to cause gastric
distension and induce vomiting. Do not induce emesis. Do not
give pH-neutralizing solutions such as dilute vinegar or
bicarbonate. If oesophageal or gastric perforation is
suspected, obtain immediate surgical or endoscopic
consultation. See section 10.7 for discussion of
decontamination controversies.
10.4 Enhanced Elimination
These procedures are not relevant for corrosive agents.
10.5 Antidote treatment
10.5.1 Adults
There is no specific antidote. Do not use
neutralizing agents.
10.5.2 Children
There is no specific antidote. Do not use
neutralizing agents.
10.6 Management discussion
Gastric lavage to remove the corrosive material is
controversial but is probably beneficial in acute liquid
corrosive ingestion. Use a soft flexible tube and lavage
with repeated aliquots of water or saline, frequently
checking the pH of the washings. In general, do not give
activated charcoal as it may interfere with visibility at
endoscopy and is of limited value in adsorbing alkalis
(Olson, 1994). Early positive oesophagoscopies identify those
patients requiring hospital treatment as well as patients
without burns who require no therapy. Oesophagoscopy is
invasive and not without discomfort, cost, and risk. Perform
endoscopy within the first 24 hours in patients with a
history of definite ingestion, or when stridor, dysphagia, or
drooling are present. Do not pass endoscope beyond the first
circumferential burn. If burns are found, follow 10 to 20
days with barium swallow (Gorman et al., 1992; Previtera et
al., 1990; Gaudreault et al., 1983; Crain et al., 1984).
Corticosteroids are not indicated. In the past they were used
in the hope of reducing the incidence of oesophageal
scarring but have since proved ineffective. Moreover,
steroids may be harmful in the patient with perforation by
masking early signs of inflammation and inhibiting resistance
to infection (Olson, 1994). Laparotomy and resection of
necrotic gastrointestinal tract in the event of gastric
necrosis should be considered. (Wu M-H & Lai W-W, 1993). In
cases of ocular exposure, topical mydriatic-cycloplegics
twice daily may be used to guard against the development of
posterior synechiae and ciliary spasm. An ophthalmologist
should be consulted in cases of ocular burns (Grant &
Schuman, 1993).
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
A 16-month-old girl swallowed an unknown amount of
automatic-dishwasher detergent. Immediate symptoms were
coughing and vomiting. She was given milk as a first aid
measure and vomited subsequently. On arrival at a primary
healthcare facility, she appeared to have oral burns only.
However during transfer to a children's hospital for
endoscopic evaluation, she developed severe inspiratory
stridor and marked respiratory distress. Examination under
anaesthesia revealed third-degree burns to the oropharynx,
false vocal cords and upper third of the oesophagus. She
required nasotracheal intubation for three days and was given
hydrocortisone and antibiotics for 10 days. Nine days post
ingestion, she was tolerating a normal diet and was
discharged home on day 11. Forty-four days post ingestion,
she was again admitted to hospital with severe respiratory
distress. A barium-swallow examination showed a marked
stricture of the upper oesophagus and evidence of aspiration.
Further examination revealed supraglottic and pharyngeal
stenosis and a narrow but patent oesophagus. She underwent
the construction of a tracheostomy, a gastrostomy and the
insertion of laryngeal and oesophageal stents. She required
feeding by the gastrostomy for 16 months and experienced 18
admissions to hospital over a period of 2 years for multiple
endoscopic dilatations and bronchoscopies, a supraglottic
laryngectomy, the excision of scar-tissue and, finally, the
construction of a jejunal conduit from the cervical
oesophagus to the pharynx, decannulation of the tracheostomy
and the closure of the gastrostomy. (Kynaston, 1989).
An 11-month-old boy was admitted to hospital following the
ingestion of a small quantity of automatic-dishwashing
detergent. He vomited immediately, his mother washed out his
mouth and gave him water to drink. On examination, he was
crying and was drooling saliva. Extensive burns to the tongue
and buccal cavity were noted, as well as a swollen uvula.
Oesophagoscopy revealed an oedematous epiglottis and non-
circumferential burns to the oesophagus. In view of his
significant pharyngeal burns and the potential for airway
obstruction, he remained intubated for 48 hours. The
oesophagus was stented with a nasogastric tube which was used
for feeding. Steroid and antibiotic therapy was undertaken
for 48 hours. In order to exclude gastric burns, endoscopy
was repeated with a flexible endoscope, and the mucosa was
found to be normal. He was discharged home after 7 days,
taking a normal diet (Kynaston, 1989).
12. ADDITIONAL INFORMATION
12.1 Specific preventive measures
Containers of dishwashing powders and similar
preparations containing sodium metasilicate should be
appropriately labelled and fitted with child resistant
closures. Standard industrial hygiene procedures should be
employed to keep workplace exposure levels to an acceptable
amount. Respiratory protection should be available.
Protective clothing and gloves should be worn to prevent skin
contact. Eye protection, goggles and face shield should be
used. Emergency wash facilities, particularly for eyes,
should be available.
12.2 Other
Not relevant
13. REFERENCES
Budavari S (1989) The Merck Index, An encyclopedia of chemicals,
drugs and biologicals, eleventh edition Merck & Co., Inc.
Clayton GD & Clayton FE (1993) Patty's Industrial Hygiene and
Toxicology, 4th ed. New York, John Wiley & Sons Inc., Volume II,
Part A Toxicology 776-778.
Crain EF, Gershel JC & Mezey AP (1984) Caustic Ingestions. Am J
Dis Child, 138:863-865.
Gorman RL, Khin-Maung-Gyi MT, Klein-Schwartz W, Oderda GM, Benson
B, Litovitz T, McCormick M, McElwee N, Spiller H & Krenzelok E
(1992) Initial symptoms as predictors of esophageal injury in
alkaline corrosive ingestions Am J Emerg Med, 10:189-194.
ECETOC (1995) Technical Report no. 66. Skin irritation and
corrosion. Reference Chemicals Data Bank.
Gaudreault P, Parent M, McGuigan MA (1983) Predictability of
esophageal injury from signs and symptoms: a study of caustic
ingestion in 378 children. Pediatrics 71:767-770.
Gosselin RE, Smith RP & Hodge HC (1984) Clinical Toxicology of
Commercial Products, Fifth edition, Williams & Wilkins,
Grant WM & Schuman (1993) Toxicology of the eye: effects on the
eyes and visual system from chemicals and drugs, metals and
minerals, plants, toxins, and venoms: also systemic side effects
from eye medications Fourth edition Charles C Thomas Publisher,
Springfield Illinois USA.
Houck JC, DeAngelo L & Jacob RA (1962) The dermal chemical
response to alkali injury. Surgery, 51:503-507.
IPCS/CEC (1993) ICSC # 0359 Sodium Metasilicate, anhydrous.
Kynaston JA, Patrick MK, Shepherd RW, Raivadera PV & Cleghorn GJ
(1989) The hazards of automatic-dishwasher detergent. Med J Aust,
151(1):5-7.
Olson KR (1994) Poisoning and Drug overdose, 2nd edition, Appleton
& Lange, Norfolk, Connecticut.
Previtera C, Giusti F & Guglielmi M (1990) Predictive value of
visible lesions (cheeks, lips, oropharynx) in suspected caustic
ingestion: may endoscopy reasonably be ommitted in completely
negative pediatric patients? Pediatr Emerg Care 6:176-178.
RTECS (1996) National Institute for Occupational Safety and
Health, Canadian Centre for Occupational Health and Safety Issue
96-2.
Scharpf Jr LG, Hill ID & Kelby RE (1972) Relative eye injury
potential of heavy duty phosphate and non-phoshate laundry
detergents Food Cosmet Toxicol, 10:829-837.
Winter M & Ellis M (1986) Automatic dishwashing detergents: their
pH, ingredients and a retrospective look, Vet Hum Toxicol,
28(6):536-5.
Wu M-H & Lai W-W (1993) Surgical management of extensive corrosive
injuries of the alimentary tract. Surg Gynecol Obstet 177:12-16.
14. AUTHOR(S),ETC.
Authors: Dr Wayne A Temple
National Toxicology Group
Dunedin School of Medicine
University of Otago
Box 913
Dunedin
New Zealand
Phone: 64-3-4797244
Fax: 64-3-4770509
E-mail: wtemple@gandalf.otago.ac.nz
Nerida A Smith
School of Pharmacy
University of Otago
Box 913
Dunedin
New Zealand
Phone: 64-3-4797239
Fax: 64-3-4770509
E-mail: nerida.smith@stonebow.otago.ac.nz
Reviewer: Dr Lindsay Murray,
Prince of Wales Hospital,
Randwick,
NSW,
Australia
Peer Review: Intox-9, Cardiff, September 1996 (A Borges, A Brown,
R Ferner, M Hanafy, L Murray, MO Rambourg, W Temple).
Editor: Dr M. Ruse (October, 1997)