CBD Drug Interactions

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Summary for UKPID

QUININE

Kathryn Pughe, BSc (Hons) MRPharmS

National Poisons Information Service (Newcastle Centre)

Regional Drug & Therapeutics Centre

This monograph has been produced by staff of a National Poisons

Information Service Centre in the United Kingdom. The work was

commissioned and funded by the UK Departments of Health, and was

designed as a source of detailed information for use by poisons

information centres.

Peer review group: Directors of the UK National Poisons Information

Service.

Summary

Name

quinine sulphate

quinine bisulphate

quinine hydrochloride

quinine dihydrochloride

Chemical group/family

Antimalarials

BNF 5.4.1

Reference number

(CAS) 130-95-0 (anhydrous quinine)

Manufacturer/supplier

(generic)

Cox Arthur H & Co Ltd

Whiddon Valley

Barnstable

North Devon EX32 8NS

Presentation

quinine sulphate 125 mg, 200 mg, 300 mg

quinine bisulphate 200 mg, 300 mg

quinine hydrochloride 300 mg

quinine dihydrochloride 300 mg

produced in various pack sizes e.g. 100,1000

injection 300 mg/ml also available from Martindale

Pharmaceuticals

Physico-chemical properties (Dollery)

6-methoxy-alpha-(5-vinyl-2-quinuclidinyl)-4-quinolone-methanol

Molecular Weight

378.5

pKa

quinuclidinyl group 4.1

quinolone group 8.5

Solubility

in water very low

in alcohol 1 in 1

USES

Indications

prophylaxis and treatment of malaria

prevention of nocturnal muscle cramps

Therapeutic Dosage (BNF)

Adults malaria 300 mg – 600 mg daily

muscle cramps 200 mg – 300 mg daily

Children malaria 30 mg/kg daily

Contraindications

Hypersensitivity to quinine and other cinchona alkaloids.

Concurrent use with cimetidine, amiodarone, digoxin and other

digitalis glycosides.

Therapeutic administration of mefloquine within the preceding 14 days.

Haemoglobinuria

Optic neuritis

Precautions

Caution should be used in patients with history of asthma, serious

heart disease or tinnitus.

Quinine may stimulate pancreatic insulin release and should be used

cautiously in hypoglycaemic persons.

Quinine may cause thrombocytopenia purpura and should be used

cautiously in patients with a history of this reaction, or in highly

sensitive patients.

Pharmacokinetics

Oral absorption >80%

Presystemic metabolism >10%

Volume of distribution (healthy subjects) 1.5 Lkg-1

(severe malaria) 1.2 Lkg-1

Plasma half life

range (healthy subjects) 7 – 11 hr

(severe malaria) 6 – 47 hr

mean (healthy subjects) 8.7 hr

mean (severe malaria) 18.2 hr

Toxicokinetics (Bateman DN et al, 1985)

At toxic levels elimination half life is reported to be 26.5 +/- 5.8

hrs.

Adverse effects

Cinchonism, including tinnitus, headache, hot and flushed skin,

nausea, abdominal pain, rashes, visual disturbances (including

temporary blindness), confusion.

Hypersensitivity reactions including angioedema, blood disorders

(including thrombocytopenia and intravascular coagulation) and acute

renal failure.

Hypoglycaemia (especially after parenteral administration).

Pregnancy

Quinine is used mainly in the treatment of chloroquine resistant

malaria. There have been a large number of case reports of

malformations following quinine ingestion in human pregnancy. Many of

these pregnancies involved large doses of quinine used as an

abortifacient. The most frequently reported abnormality following

quinine exposure during early pregnancy is hypoplasia of the auditory

nerve with resultant deafness. Other major malformations involving

most organ systems have been reported also. However, the Perinatal

Collaborative Study reported no association between first trimester

exposure to quinine and birth defects. In general, there has been no

proven association between quinine at doses used for malarial

prophylaxis and an increased risk of malformations.

Third trimester exposure to quinine does not appear to adversely

effect uterine contractility. However, an increase in insulin

secretion associated with hypoglycaemia has been reported. Therefore,

monitoring of blood or serum glucose levels during quinine therapy is

advisable.

Breast milk

Quinine is excreted into breast milk. Following 300 and 640 mg oral

doses in six patients, milk concentrations varied up to 2.2 mcg/ml,

with an average level of 1 mcg/ml at 3 hours. No adverse effects in

breast fed babies were reported. Quinine is thought to be

compatible with breast feeding (Bennet PN, 1988).

Interactions (BNF)

Anti-arrhythmic plasma concentration of flecainide increased

Antihistamines increased risk of ventricular arrythmias with

astemizole and terfenadine

Cardiac glycosides plasma concentration of digoxin increased –

halve digoxin maintenance dose (includes use

of quinine for cramps)

Ulcer-healing drugs cimetidine inhibits quinine metabolism

(increased plasma quinine concentration)

Other antimalarials Increased risk of arryhthmias with

halofantrine and mefloquine

SUMMARY

Quinine

Type of product: For treatment of malaria and leg cramps.

Quinine salt Tablet size (mg) Quinine base content (mg)

Sulphate 125 103

200 165

300 248

Dihydrochloride 300 246

Hydrochloride 300 246

Toxicity

Highly toxic.

There is a higher risk of visual loss and cardiac complications when

plasma concentrations of quinine exceed 15 mg/l at any stage of

overdosage.

The average fatal dose for an adult is about 8 g although deaths have

been reported from as little as 1.5 g in an adult and 900 mg in a

child.

General features

Quinine causes nausea, vomiting, tremor, tinnitus and deafness.

Visual features

Blurred vision may proceed to complete blindness within a few hours.

As vision is lost the pupils become dilated and unresponsive to light.

Initially only narrowing of the retinal arterioles may be seen on

fundoscopy but after 3 days retinal oedema may appear.

Cardiac features

Tachycardia, dysrhythmias, hypotension and ECG conduction

abnormalities may precede cardiac arrest.

Other features

Oliguria and acute renal failure from intravascular haemolysis. Coma

and convulsions (especially in children)

Management

Monitor cardiac conduction and rhythm.

Supportive measures from coma and convulsions.

Empty the stomach if within 4 hours of ingestion.

Repeated dose oral activated charcoal has been shown to increase

quinine elimination in volunteers, and should therefore be used in

patients.

Severe impairment of vision cannot be treated. The evidence that

stellate ganglion block, retro-bulbar injections or vasodilators are

effective is poor and based on wrong assumptions about the mode of

toxicity of quinine. Discuss with the doctor on call.

Some recovery of vision can be expected but permanent, severe

restriction of the visual fields may occur. Optic atrophy may appear

later.

Methods to enhance elimination of quinine from the body (other than

oral activated charcoal) are of doubtful value. This is particularly

true of forced acid diuresis, exchange transfusion, haemodialysis and

charcoal haemoperfusion. The value or otherwise of resin

haemoperfusion is yet to be demonstrated.

Serious poisoning should be discussed with the doctor on call.

References

Wolf LR et al. Cinchonism: two case reports and review of acute

quinine toxicity and treatment. J Emerg Med 1992;10:295-301.

Schonwald and Shannon M. Unsuspected quinine intoxication presenting

as acute deafness and mutism. Am J Emerg Med 1991;9:318-320.

Canning CR, Hague S. Ocular quinine toxicity. Br J Opthalmol

1988;72:23-26.

Bateman DN. Quinine toxicity. Adv Drug React Ac Pois Rev 1986;4:215-

233.

Dyson EH, et al. Quinine amblopia: is current management appropriate ?

Clin Toxicol 1985-86;23:571-578.

Bateman DN et al. Pharmacokinetics and clinical toxicity of quinine

overdosage: lack of efficacy of techniques intended to enhance

elimination. Q J Med 1985;ns54,no214:125-131.

Murray SB, Jay JL. Loss of sight after self-poisoning with quinine. Br

Med J 1983;287:1700.

EPIDEMIOLOGY OF POISONING

MECHANISM OF ACTION/TOXICITY

Quinine has class 1A antiarrhythmic effects, but is less potent than

its stereoenantiomer quinidine. These effects include sodium channel

blockade, slowed phase o depolarisation, conduction delay and

prolonged repolarisation. Quinine also has alpha agonist action and

may have oxytocic actions.

Range of toxicity (Poisindex)

The adult toxic dose may be as little as 2g, although usually greater

than 3 to 4g.

Toxic Levels

Plasma concentrations over 5 mcg/ml causes cinchonism

Plasma concentrations above 10 mcg/ml are associated with visual

impairment.

Plasma concentrations above 15 mcg/ml are associated with cardiac

arrhythmias.

Fatal Level

Death was reported in a patient with an initial quinine level of 22.2

mcg/ml. A peak level of 17.8 mcg/ml was reported in a fatal case

(Wenstone et al 1989).

FEATURES OF POISONING

Summary

Quinine overdose either intentionally or accidentally has been

reported to result in signs and signs and symptoms including headache,

deafness, tachycardia, depression of atrial, atrioventricular and

ventricular conduction arrhythmias, hypotension, heart failure

syncope, respiratory arrest, paraesthesia, coma and death.

EYES

Visual field constriction may progress to sudden blindness with

non-reactive dilated pupils.

Fixed dilated pupils are seen frequently in children following quinine

overdosage (Grattan-Smith et al,1987).

In addition to cinchonism quinine is thought to have a direct toxic

effect on the retina, causing constricted fields that can progress to

blindness with dilated non reactive pupils (Dyson et al,1985).

Central vision usually recovers first. Complete recovery of vision may

take several months; pupils may remain dilated after recovery of

vision.

Blindness following quinine overdosage is typically delayed in onset

usually for more than 12 hours (Smilkstein et al, 1987).

Plasma concentrations associated with the visual deficits usually

exceed 15mg/l in less than 10 hours post-ingestion and greater than 10

mg/l after 10 hours. However, plasma concentrations appear to be

inadequate to predict the extent of visual deficit.

Ears

Transient tinnitus and eighth bilateral nerve damage have been

observed after overdose.

Deafness and mutism occurred in a 14 year old who ingested

approximately 6.5 to 7.8 g of quinine sulphate. Symptoms lasted for

approximately 3 days (Schonwald & Shannon, 1991).

Cardiovascular

Cardiotoxicity typically appears within 8 hours following ingestion of

quinine, but delayed cardiotoxicity up to 25 hours after ingestion

have been reported (Bodenhamer & Smilkstein, 1993).

Sinoatrial, atrioventricular and His-ventricular depression of

conduction may occur along with ventricular tachycardia and

ventricular fibrillation. Syncope is usually related to transient

torsade de pointes ventricular tachycardia (Bauman et al, 1984).

Hypotension occurs frequently. Heart failure may result. Toxic ECG

abnormalities include prolongation of the PR, QRS and QT intervals. ST

depression and T wave inversion may also occur.

Respiratory

Respiratory depression may occur. Adult respiratory distress syndrome

has been reported in one fatal case (Wenston et al, 1989).

Neurological

Ataxia, paresthesias. Convulsions may follow an overdose.

Central nervous system toxicity seems to be more marked in children

than adults. Children frequently present with seizures following and

overdose (Grattan-Smith et al, 1987).

Gastrointestinal

Nausea and vomiting are common side effects of quinine.

Hepatic

Hepatic granulomas have been reported with quinidine as well as

reversible hypersensitivity-related hepatitis.

Fluid-Electrolyte

Hypokalaemia may occur secondary to quinine induced electrolyte

fluxes. Aggressive treatment is not recommended.

Haematological

Haemolytic anaemia may occur in patients with G6PD deficiency.

Thrombocytopenia (immune mechanism)

Endocrine

Therapeutic use of quinine and overdosage has resulted in severe

hypoglycaemia (Wenstone et al, 1989).

Dermatologic

Photosensitivity reactions may occur

Chronic toxicity

No information

MANAGEMENT

Decontamination

Repeated doses of oral activated charcoal should be started as soon as

possible since their is some evidence that this shortens the half life

which is otherwise about 26 hours after over dosage. 50 – 100g (25g in

children) should be given initially followed by 25 g 2 hourly or 50 g

4 hourly (12g in children). 20ml of lactulose should be given with

each dose of charcoal.

Supportive care

There is no evidence that stellete ganglion block, retro-bulbar

injections or vasodilators are effective. Evidence is based on wrong

assumptions about the mode of toxicity of quinine. They are not

recommended.

Fluid and electrolyte monitoring and repeated evaluations of renal

function should be performed

Monitoring

Monitor vital signs – pulse, blood pressure, respiration

Careful monitoring of ECG and ventilation should be instituted.

Blood for evaluation of plasma quinine level may useful to asses

prognosis

Renal function

Blood gases if patient is unconscious

Blood sugar

Antidotes

There are no effective antidotes

Elimination techniques

Measures to enhance the elimination of quinine have been generally

ineffective (Bateman et al, 1985). The natural history of quinine

amblyopia is such that elimination procedures may not critically alter

its course (Heath,1985).

Forced diuresis has not been found not to produce a sufficiently rapid

reduction in plasma concentration or to have a substantial effect on

visual disturbances. (Bateman DN at al 1985).

Peritoneal dialysis is less effective than normal renal excretion, but

has been used occasionally in patients with renal failure (Markham et

al, 1967).

Haemodialysis, charcoal haemoperfusion and exchange transfusion have

similarly been found to be ineffective in increasing quinine

elimination (Bateman DN et al 1985).

Haemodialysis combined with resin haemoperfusion may be effective in

the treatment of quinine blindness refractory to the usual therapy

(Gibbs JL,1985). However these data have yet to be corroborated

(Bateman DN, 1985).

Investigations

On admission blood should be drawn for a full blood count, blood

sugar, prothrombin time, renal function tests, urinalysis and

electrolytes.

Periodic eye examinations should include visual acuity. Other

techniques that may be used in the longer term assessment of patients

with quinine ambylopia include electroretinography, electrooculogram,

visual evoked potentials, dark adaptations, and colour testing.

Periodic ECGs as indicated.

Management controversies

Most recent evidence has shown that enhancement of elimination of

quinine by forced acid diuresis, peritoneal dialysis, haemodialysis,

charcoal haemoperfusion are ineffective (Bateman DN et al 1985).

The evidence that stellate ganglion block, retro-bulbar injections or

vasodilators are effective is poor and based on wrong assumptions

about the mode of toxicity of quinine. This technique should,

therefore, not be used.

CASE DATA

Bodenhamer & Smilkstein (1993) reported delayed cardiotoxicity

following ingestion of 16.25g of quinine in a 49 year old female.

Symptoms appeared 11.5 hours following ingestion, with conduction

abnormalities, ectopy and torsades de pointes occurring 25 hours after

ingestion.

Notelovitz et al (1970) report a case of a 21 year old female who

ingested 90g of quinine during her 8th week of pregnancy to induce

abortion. The patient subsequently became drowsy with dark red urine

which was positive for blood and albumin. The patient became oliguric

and her blood urea rose to 2080 g/l. The patient was treated with

diuretics, blood transfusion and haemodialysis with improvement and

discharge within 72 hours.

3.Visual damage occurred following overdose of quinine in 2 patients (

a 38 year old male who ingested 2g of quinine and a 60 year old woman

who ingested 4g of quinine). The vision loss was only partially

reversible (Murray & Jay 83). A 26 year old male developed bilateral

loss of vision after ingesting 20 quinine tablets and an unknown

quantity of alcohol (Drake & Hiorns 1994).

A 17 year old man ingested 5 g of quinine and developed deafness

within several hours. Upon presentation he was noted to have broad

complex tachycardia, which normalised over 8 hours. The case was

complicated with hypokalaemia (2.2 mmol/l) and hypoglycaemia (2.7

mmol/l). Later chest x-ray revealed non-cardiogenic pulmonary oedema.

He was treated with antibiotics and inotropic agents. Renal

dysfunction developed on the ninth day and the patient died from

hypoxic cardiac arrest on the twelfth day. Necropsy revealed ARDS. The

peak quinine level was 17.8 mg/l (Wenston et al 1989).

Goldenberg AM & Wexler LF (1988) report a case of a 24 year old man

who ingested 8 g of quinine sulphate in a suicide attempt. The patient

presented within 2 hours and was given a stomach washout. Despite

haemoperfusion which was started 10 hours after ingestion, the patient

suffered a fatal asystolic cardiac arrest.

A case of unsuspected quinine overdose is reported in a 14 year old

girl who presented with symptoms including deafness and mutism

(Schonwald S & Shannon M, 1991). Diagnosis was delayed for

approximately 4 hours because of the absence of an accurate history.

The patient took upto 7.8g of quinine, and the serum level 6-8 hours

postingestion was 4.5mg/L. Hearing gradually returned on the third day

after admission and later that day the patients mutism resolved

spontaneously.

Two cases of acute quinine toxicity are reported by Wolf LR et al

(1992). Both patients presented with acute bilateral blindness. They

also experienced the classic symptoms of sinchinism, including nausea,

vomiting, and tinnitus. Prolongation of the Q-T interval developed in

both patients. Serum quinine levels were 5.3 mg/l and 13 mg/l.

Although their visual acuity improved, both patients has some residual

deficit at follow up.

ANALYSIS

Plasma quinine levels can be performed with a modification of the test

used to measure quinidine levels using high performance liquid

chromatography. (Dyson EH et al 1985 BMJ1985)

Author

Kathryn Pughe, BSc (Hons) MRPharmS

National Poisons Information Service (Newcastle Centre)

Regional Drug & Therapeutics Centre

This monograph was produced by the staff of the Newcastle Centre of

the National Poisons Information Service in the United Kingdom. The

work was commissioned and funded by the UK Departments of Health, and

was designed as a source of detailed information for use by poisons

information centres.

Peer review was undertaken by the Directors of the UK National Poisons

Information Service.

Last updated March 1996

REFERENCES

Bateman DN, Blain PG, Woodhouse KW, Rawlins MD, Dyson H, Heyworth R,

Prescott LF, Proudfoot AT. Q J Med N Ser. 1985;54:125-131.

Bauman JL, Baurenfiend RA, Strasberg B. Torsades de pointes due to

quinidine; observation in 31 patients. Am Heart J 1984;107:4125-4230.

Bennett PN and the WHO Group, Drugs and Human Lactation, Elsevier

1988.

Bodenhamer JE & Smilkstein MJ. Delayed cardiotoxicity following

quinine overdosage: A case report. J Emerg Med. 1993;11:279-285.

British National Formulary. Number 30 (September 1995). British

Medical Association and Royal Pharmaceutical Society.

Drake WM and Hiorns MP. Quinine overdose: review of toxicity and

treatment. Clin Cardiol. 1988;11:726-718.

Dollery C. Therapeutic Drugs. Churchill Livingstone. 1991.

Dyson EH, Proudfoot AT, Prescott LF, Heyworth R. Death and blindness

due to overdose of quinine. Br Med J 1985;291:31-33.

Gibbs JL, Trafford A, Sharpstone P. Quinine amblyopia treated by

combined haemodialysis and activated resin haemoperfusion. Lancet

1985;1:752-753.

Goldenberg AM & Wexler LF. Quinine overdose: review of toxicity and

treatment. Clin Cardiol. 1988;11:716-718.

Grattan-Smith TM, Gillis J, Killham H. Quinine poisoning in children.

Med J Aust. 1987;147:93-95.

Heath A. Resin haemoperfusion for quinine poisoning. Lancet

1985;1:1244.

Markhan TN, Dodson VN, Eckberg DL. Peritoneal dialysis in quinine

sulphate intoxication. JAMA 1967;202:1102-1103.

Murray SB and Jay JL. Loss of sight after self poisoning with quinine.

Br Med J 1983;287:1700.

Notelovitz M. Acute renal failure following quinine poisoning. So Afr

Med J 1970;44:649.

Poisindex System(R), Micromedex, inc, Denver Colorado, Edition Expires

31/3/96.

Schonwald S & Shannon M. Unsuspected quinine intoxication presenting

as acute deafness and mutism. Am J Emerg Med. 1991;9:318-320.

Smilkstein MJ, Kulig KW, Rumack BH. Acute toxic blindness:

Unrecognised quinine poisoning. Ann Emerg Med. 1987;16:98-101.

Wenstone R, Bell ME, Mostafa SM. Fatal adult respiratory distress

syndrome after quinine overdose (letter). Lancet 1989;1:1143-1144

Wolf LR, Otten EJ, Spadafora MP. Cinchonism: Two case reports and

review of acute quinine toxicity and treatment. J Emerg Med.

1992;10:295-301.

See Also:

Quinine (PIM 464)

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Content from Reference Pages:

The following information has been extracted from our CHEMINFO database, which also contains hazard control and regulatory information. [More about…] [Sample Record]

Access the complete CHEMINFO database by contacting CCOHS Client Services.

SECTION 1. CHEMICAL IDENTIFICATION

CHEMINFO Record Number: 768

CCOHS Chemical Name: Jet A

Synonyms:

Aviation kerosene (non-specific name)

Aviation turbine fuel (non-specific name)

Jet Fuel A

Jet A-1

Jet fuel (non-specific name)

Jet Fuel A-1

Jet fuel type A

Turbine engine aviation fuel (non-specific name)

Chemical Name French: Kérosène

Chemical Name Spanish: Queroseno (petroleo)

CAS Registry Number: 8008-20-6

UN/NA Number(s): 1863

RTECS Number(s): SE7548500

EU EINECS/ELINCS Number: 232-366-4

Chemical Family: Mixed hydrocarbons / petroleum hydrocarbons / petroleum hydrocarbon distillate / aviation turbine fuel

Molecular Formula: Complex hydrocarbon mixture

Structural Formula: Complex hydrocarbon mixture

SECTION 2. DESCRIPTION

Appearance and Odour:

Colourless to pale yellow liquid with a kerosene-like or petroleum odour.

Odour Threshold:

Not available; 0.5517 mg/m3 (unspecified kerosene) (23)

Warning Properties:

Information not available for evaluation.

Composition/Purity:

The most important aspect of evaluating the hazards of any petroleum distillate is accurate definition of the material in question. The source of the crude petroleum, the boiling range of the distillate and all of the processing and refining steps influence the composition and hazards of the resulting petroleum distillate. The composition of Jet A is established by the American Society for Testing and Materials (ASTM) in consultation with manufacturers and users. The specifications are based primarily on performance characteristics. There is no standard formula for Jet A. The straight-run kerosene stream is used for aviation fuel production. Jet A and Jet A-1 are mixtures of aliphatic and aromatic hydrocarbons with carbon numbers predominantly in the range of C9-C16 and which meet the requirements of ASTM specification D 1655.(24) Jet A and Jet A-1 only differ in freezing point. According to the specification, the maximum allowed level of aromatic hydrocarbons is 25% (by volume) and 3% naphthalenes (by volume). Total sulfur (0.3% by weight) and mercaptan sulfur (0.003% by weight) are present as impurities. Jet A has a distillation range of less than 205 to 300 deg C (401 to 572 deg F). The physical properties given in this review are either for specific products, from the specification or for straight-run kerosene (CAS 8008-20-6). The specification lists a number of additives that may be used in jet fuels. Typical additives include an antioxidant (e.g. 2,6-di-tert-butylphenol and tert- and tri-tert-butylphenols), a metal deactivator (e.g., N,N- disalicylidene-1,2-propanediamine), an electrical conductivity additive (e.g. Stadis 450), a static inhibitor, a fuel system icing inhibitor (e.g. diethylene glycol monomethyl ether), a corrosion of steel inhibitor, a lubrication improver, a biocide, a fuel lubricity additive, and a thermal stability improver. The presence of additives can contribute significantly to the overall hazards of a particular jet fuel product. Consult the manufacturer/supplier of your specific product for additional information.

Uses and Occurrences:

Used as an commercial aviation fuel.(9,25,26)

SECTION 3. HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW:

Colourless to pale yellow liquid with a kerosene-like or petroleum odour. COMBUSTIBLE LIQUID AND VAPOUR. May accumulate static charge by flow or agitation. Liquid can float on water and may travel to distant locations and/or spread fire. During a fire, irritating and/or toxic gases, such as sulfur and nitrogen oxides, as well as unidentified organic compounds may be generated. High vapour concentrations may cause headache, nausea, dizziness, drowsiness, incoordination and confusion. Aspiration hazard. Swallowing or vomiting may result in aspiration (inhalation of the liquid) into the lungs. May contain hazardous additives.

POTENTIAL HEALTH EFFECTS

Effects of Short-Term (Acute) Exposure

Inhalation:

There is no specific information available for Jet A. Based on comparison to straight-run kerosene, Jet A probably readily forms a vapour at room temperature. Like other petroleum distillates, Jet A can probably cause symptoms of central nervous system (CNS) depression, such as dizziness, headache, nausea, fatigue, vomiting and incoordination. Severe exposures may result in unconsciousness and death.

More than 2/3 of 29 aircraft factory workers exposed to unspecified jet fuels reported that they repeatedly experienced dizziness, respiratory tract symptoms, irregular heart beat, a feeling of pressure on the chest, nausea and/or headache following exposure.(1) Airmen exposed to unspecified jet fuel during fuel cell repair occasionally reported dizziness, headaches and incoordination.(2)

Skin Contact:

Jet A is a very mild skin irritant based on animal information. No human information was located for Jet A. A 24-hour exposure to straight-run kerosene, a major component of jet fuel, has produced moderate to severe irritation in humans.

Animal evidence indicates that Jet A is only minimally absorbed through the skin and harmful effects are not expected by this route of exposure.

Eye Contact:

Jet A is slightly or not irritating to the eyes based on animal information. No human information was located regarding direct eye contact with jet fuels.

Ingestion:

In animal studies, the oral toxicity of Jet A is very low. There are no reported cases of human ingestion of jet fuel, but the accidental ingestion of kerosene, primarily in children, has been frequently reported in the literature. Often in these cases, the kerosene has been aspirated (inhaled into the lungs during ingestion or vomiting). Severe lung damage and deaths have resulted. It is expected that Jet A would also be easily aspirated. Ingestion is not a typical route of occupational exposure.

Effects of Long-Term (Chronic) Exposure

Jet fuels are complex mixtures which can have variable composition (see “Composition/Purity” above). In addition, there is only a small amount of information available about the potential long-term health effects of jet fuels available and often there are serious limitations to the studies. Therefore, it is not possible to draw any firm conclusions about the potential long-term health effects of jet fuels.

SKIN: Repeated skin contact with jet fuels would likely result in dry, cracked, red skin (dermatitis), like kerosene.(3)

EFFECTS ON THE NERVOUS SYSTEM: It is not possible to draw any firm conclusions from the available studies because of the small number of employees studied, poor or no exposure information and the possibility that other exposures could have caused the observed effects.

Studies of a small number of employees (29-30) with long-term exposure to jet fuel concentrations which may have been as high as 3000 ppm reported psychiatric symptoms (e.g. anxiety or mental depression), poorer performance in some psychological tests and reduced sensorimotor speed. These employees also reported significant short-term health effects.(1,4) Another study reported memory problems, fatigue, moodiness, unsteadiness, and headache in 9 employees exposed to jet fuel for 15 to 41 years.(5) Another study showed a relationship between changes in postural balance in 27 subjects and exposure to jet fuels (average duration 12 years).(6)

A case report describes symptoms of polyneuropathy such as pain, tingling and numbness in the feet, legs, hands and arms in a man who had been exposed to jet fuel and other fuels for 30 years. The authors attribute these effects to exposure to n-hexane, a possible component of some jet fuels. Estimated exposure concentrations were up to 100 mg/m3 in the first 10 years, then lower.(7) It is not possible to draw conclusions from this single case report.

EFFECTS ON THE LIVER: It is not clear from the one study available that jet fuel exposure was responsible for the observed effect. In this study, 91 fuel filling attendants exposed to jet fuel showed increased liver metabolism during exposure compared to after summer vacation (unexposed for 2 or 4 weeks). A similar but smaller effect was observed in unexposed office workers.(8) It is not clear from this study that jet fuel exposure was responsible for the observed effect.

Carcinogenicity:

The International Agency for Research on Cancer (IARC) has concluded that there is inadequate evidence for the carcinogenicity of jet fuel in humans.(9)

A study of 2176 employees with long-term exposure to jet fuel, as well as other fuels and chemicals, found no increase in the frequency of cancers even when duration of employment, latency, occupation or type of exposure were considered. This study was limited by the rather short follow-up (10 years).(9,10)

A study of 3726 cancer patients related their exposure to petroleum-derived liquids to the incidence of cancer by specific site. An association was observed between jet fuel exposure and kidney cancer.(9,11) However, this was a very preliminary study and no firm conclusions can be drawn.

Jet fuels have caused skin tumours in animals following dermal application of doses that caused severe skin irritation and ulceration.

The International Agency for Research on Cancer (IARC) has concluded that this chemical is not classifiable as to its carcinogenicity to humans (Group 3).

The American Conference of Governmental Industrial Hygienists (ACGIH) has designated this chemical as an animal carcinogen (A3).

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

Teratogenicity and Embryotoxicity:

There is no human information available. No harmful effects were observed in one animal study.

Reproductive Toxicity:

There is no human or animal information available.

Mutagenicity:

No human studies have been reported. Positive results were obtained in one study using live animals. This study has been criticized for technical errors. Negative results have been obtained in other studies using live animals, cultured mammalian cells without activation and bacteria. Positive results were obtained in cultured mammalian cells with activation.

Toxicologically Synergistic Materials:

There is no information available.

Potential for Accumulation:

There is no information available on the absorption, distribution, metabolism and excretion of Jet A.

SECTION 4. FIRST AID MEASURES

Inhalation:

If symptoms are experienced, remove source of contamination or have victim move to fresh air. If symptoms persist, obtain medical advice.

Skin Contact:

Remove contaminated clothing, shoes and leather goods (e.g. watchbands, belts). Quickly and gently blot or brush away excess chemical. Wash gently and thoroughly with lukewarm, gently flowing water and non-abrasive soap for 5 minutes. Obtain medical advice. Completely decontaminate clothing, shoes and leather goods before re-use or discard.

Eye Contact:

Quickly and gently blot away excess chemical. Immediately flush the contaminated eye(s) with lukewarm, gently flowing water for 5 minutes or until the chemical is removed. If irritation persists, obtain medical advice.

Ingestion:

NEVER give anything by mouth if the victim is rapidly losing consciousness, is unconscious or is convulsing. DO NOT INDUCE VOMITING. If vomiting occurs naturally, have victim lean forward to reduce risk of aspiration. Have victim rinse mouth with water again. Immediately obtain medical attention.

First Aid Comments:

Provide general supportive measures (comfort, warmth, rest).

Consult a doctor and/or the nearest Poison Control Centre for all exposures except minor instances of inhalation or skin contact.

All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.

SECTION 5. FIRE FIGHTING MEASURES

Flash Point:

38 deg C min (100 deg F min) (closed cup) (24); 43-66 deg C (110-150 deg F) (closed cup) (27)

Lower Flammable (Explosive) Limit (LFL/LEL):

Not available

Upper Flammable (Explosive) Limit (UFL/UEL):

Not available

Autoignition (Ignition) Temperature:

Not available

Sensitivity to Mechanical Impact:

Probably not sensitive. Stable compounds.

Sensitivity to Static Charge:

Like straight-run kerosene, Jet A and A-1 probably have low electrical conductivities and therefore can accumulate static charge by flow or agitation.(28) Additives can be added to dissipate charge more rapidly. This is most effective when the fuel electrical conductivity range is 50 to 450 pS/m.(24) Vapours from heated liquid, in the flammable range, can be ignited by a static discharge.(28)

Combustion and Thermal Decomposition Products:

Thermal decomposition products are highly dependent on combustion conditions and the type of additives and impurities present. A complex mixture of airborne material (solid, liquid, and gas) will evolve during heating or burning. Carbon dioxide, carbon monoxide, sulfur and nitrogen oxides, as well as unidentified organic compounds may be formed.

Fire Hazard Summary:

Combustible liquid. Can form explosive mixtures with air, at or above 38 deg C. Liquid can float on water and may travel to distant locations and/or spread fire. During a fire, irritating, toxic and/or hazardous gases, such as sulfur and nitrogen oxides and unidentified organic compounds, may be generated. Vapours may accumulate in confined spaces, resulting in a explosion and toxicity hazard. Containers may rupture violently when exposed to fire or excessive heat for sufficient time.

Extinguishing Media:

Carbon dioxide, dry chemical powder, alcohol foam, polymer foam, water spray or fog.

Fire Fighting Instructions:

Evacuate area and fight fire from a safe distance or a protected location. Approach fire from upwind to avoid hazardous vapours and toxic decomposition products.

Closed containers may rupture violently when exposed to heat of fire. If possible, isolate materials not yet involved in the fire, and move containers from fire area if this can be done without risk, and protect personnel. Otherwise, fire-exposed containers or tanks should be cooled by application of hose streams. Application should begin as soon as possible and should concentrate on any unwetted portions of the container. If it is not possible to cool the containers, use unmanned monitor nozzles and immediately evacuate the area.

Stop leak before attempting to stop the fire. If the leak cannot be stopped, and if there is no risk to the surrounding area, let the fire burn itself out. If a leak or spill has not ignited, use water spray in large quantities to disperse the vapours and to protect personnel attempting to stop a leak. Water spray can also be used to flush spills away from ignition sources. Solid streams of water may be ineffective and spread material. Do not use water to fight the fire, except as a fog.

For a massive fire in a large area, use unmanned hose holder or monitor nozzles; if this is not possible withdraw from fire area and allow fire to burn. Stay away from ends of tanks, but be aware that flying material from ruptured tanks may travel in any direction. Withdraw immediately in case of rising sound from venting safety device or any discolouration of tank due to fire.

Although Jet A and A-1 are only slightly hazardous to health, their decomposition products may be hazardous. Do not enter without wearing specialized protective equipment suitable for the situation. Firefighter’s normal protective equipment (Bunker Gear) may not provide adequate protection. Chemical resistant clothing (e.g. chemical splash suit) and positive pressure self-contained breathing apparatus (MSHA/NIOSH approved or equivalent) may be necessary.

NATIONAL FIRE PROTECTION ASSOCIATION (NFPA) HAZARD IDENTIFICATION

NFPA – Health: 0 – Exposure, under fire conditions, would be no more hazardous than an ordinary combustible material.

NFPA – Flammability: 2 – Must be moderately heated or exposed to relatively high ambient temperatures before ignition can occur.

NFPA – Instability: 0 – Normally stable, even under fire conditions, and not reactive with water.

SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES

Molecular Weight: Complex hydrocarbon mixture

Conversion Factor:

Not available (molecular weight unknown)

Physical State: Liquid

Melting Point: Freezing point: Jet A: -40 max deg C (-40 max deg F); Jet A-1: -47 deg C (- 53 deg C) (24)

Boiling Point: Distillation range: 205-300 deg C (401-572 deg F) (temperature of 10% recovered to final boiling point) (24)

Relative Density (Specific Gravity): 0.755-0.840 at 15 deg C (water = 1) (24)

Solubility in Water: Practically insoluble; approximately 0.5 mg/100 mL (unspecified kerosene)

Solubility in Other Liquids: Soluble in all proportions with many other petroleum solvents.

Coefficient of Oil/Water Distribution (Partition Coefficient): Not available; Log P(oct) = 3.3-6+ (straight-run kerosene) (3)

pH Value: Not applicable

Vapour Density: 4.5 (air = 1)

Vapour Pressure: Not available; 1.4 kPa (10.5 mm Hg) at 37.8 deg C (straight-run kerosene) (3)

Saturation Vapour Concentration: Not available; 13820 ppm (1.38%) at 37.8 deg C (straight-run kerosene) (calculated)

Evaporation Rate: Not available

Critical Temperature: Not available

Other Physical Properties:

VISCOSITY-KINEMATIC: 8.0 mm2/s max (8.0 centistokes max) at -20 deg C (24)

NOTE: Some petroleum products are treated with mineral acid or caustic, or both, as part of the refining process. Any residual acid or caustic is not desirable. Neither is likely to be present.

According to specification D 1655, the total acidity of Jet A is 0.1 mg KOH/g max.(24)

SECTION 10. STABILITY AND REACTIVITY

Stability:

According to specification D 1655, commercial jet fuels should be thermally stable at temperature as high as 149 deg C (300 deg F). These fuels have been shown to be stable in storage.(24)

Hazardous Polymerization:

Does not occur.

Incompatibility – Materials to Avoid:

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

STRONG OXIDIZING AGENTS (e.g. peroxides, nitric acid, perchlorates, chlorine and fluorine) – risk of fire and explosion.(28)

Hazardous Decomposition Products:

None reported.

Conditions to Avoid:

Open flames, heat, static discharge, sparks and other ignition sources.

Corrosivity to Metals:

Specific information is not available. According to specification D 1655, Jet A and Jet A-1 must pass the copper strip test (ASTM test method D 130) to ensure that the fuel will not corrode copper or any copper-base alloys.(24) Jet A and Jet A-1 may corrode steel, but corrosion rates are not available.(28) In order to inhibit this corrosion, additives are added to Jet A and Jet A- 1.(24)

SECTION 11. TOXICOLOGICAL INFORMATION

LC50 (rat): greater than 5.0 mg/L (5000 mg/m3) (4-hour exposure) (0/10 deaths) (shale-derived).(12)

LD50 (oral, rat): greater than 20000 mg/kg; cited as 25.0 mL/kg (0/10 deaths) (3,13,14); greater than 5000 mg/kg (0/10 deaths) (shale-derived) (12)

LD50 (dermal, rabbit): greater than 5000 mg/kg (14); greater than 2000 mg/kg (0/10 deaths) (shale-derived) (12)

NOTE: specific gravity is assumed to be 0.8 for conversion purposes.

Eye Irritation:

Jet A is a non-irritant to very mild eye irritant.

Application of 0.1 mL of undiluted shale-derived Jet A was non-irritating in rabbits.(12) In other studies, application of Jet A resulted in minimal or slight irritation in rabbits.(3,13,14)

Skin Irritation:

Jet A is a very mild skin irritant.

In 2 studies, application of 0.5 mL undiluted Jet A, under a cover to intact and abraded skin for 24 hours, caused very mild irritation in rabbits (scored 2/8 and 1.96/8).(13,14) Application of 25 or 79 microL of Jet A, covered and uncovered for 5 or 24 hours to intact skin, caused no or very mild irritation in rabbits. Scores immediately following exposure were: erythema 0/4-1/4; edema: 0/4. Scores were not measured at later times.(32) Application of 0.5 mL of undiluted Jet A derived from shale, under a cover, to intact and damaged skin for 24 hours, produced moderate irritation in rabbits (score 3.4/8).(12) In an unpublished study, application of Jet A-1 for 4 hours caused mild irritation.(3, unconfirmed) No further information was provided.

Effects of Short-Term (Acute) Exposure:

Skin Contact:

Dermal application of 6400 mg/kg/day (cited as 8 mL/kg) to rabbits for 2 weeks resulted in severe skin damage at the treatment sites with depression and weight loss associated with reduced food intake. Deaths were also observed at this dose. Liver, kidney and bladder effects were considered to be secondary to the severe skin irritancy.(3,14)

Effects of Long-Term (Chronic) Exposure:

In general, male rats with long-term inhalation or oral exposure to hydrocarbon fuels develop a dose-related kidney injury that is not observed in females, controls or mice.(15) There is no specific information on this effect for Jet A. Long-term dermal exposures to Jet A have produced severe irritation at the site of application, but no other toxicity.

Skin Contact:

Dermal application of 25 mg shale- or petroleum-derived Jet A to mice three times/week for 2 years produced irritation at days 10-15. Generally, inflammation appeared after the sixth month of treatment. Tissue death occurred shortly before the end of the first year.(16) Application of Jet A to the clipped skin of mice twice/week for 13 weeks resulted in irritation which was concentration and time dependent. The most marked effects, moderate inflammatory and proliferative changes with some ulceration, were observed with undiluted jet fuel applied for 13 weeks. No other significant toxic effects were observed.(17)

Skin Sensitization:

Negative results have been obtained in guinea pigs for both shale- and petroleum-derived Jet A.(3,12-14)

Carcinogenicity:

The International Agency for Research on Cancer (IARC) has concluded that there is inadequate evidence for the carcinogenicity of jet fuels in animals.(9)

A long-term skin painting study with mice exposed to shale- or petroleum- derived Jet A showed an increase in skin tumours.(16) These tumours may have been related to severe irritation at the test site rather than true carcinogenicity. A standard skin painting study with Jet A produced irritation and increased incidence of skin tumours in mice (44%). However, with an intermittent schedule of painting that allowed healing to occur, there was only a 2% tumour incidence.(19)

Teratogenicity, Embryotoxicity and/or Fetotoxicity:

No harmful effects were observed in the offspring when rats were exposed by inhalation to 100 or 400 ppm Jet A on days 6-15 of pregnancy. Eye irritation was observed in the mothers.(18)

Mutagenicity:

Positive results were obtained in rat bone marrow cells following inhalation of 100 ppm for 20 days or 400 ppm for 5 days.(20) This study has been criticized and the results are considered invalid due to technical errors.(22) Negative results were obtained in a dominant lethal assay.(3,21)

Negative results were also obtained in cultured mammalian cells without activation, but positive results were obtained with activation. Negative results have been obtained in bacteria.(3,20,21)

SECTION 16. OTHER INFORMATION

Selected Bibliography:

(1) Knave, B., et al. Long-term exposure to jet fuel: an investigation on occupational exposed workers with special reference to the nervous system. In: Adverse effects of environmental chemicals and psychotropic drugs: neurophysiological and behaviour tests. Vol. 2. Edited by H. J. Zimmerman. Appleton-Century-Crofts, 1978. p. 149-155

(2) Lombardi, A.R., et al. Health hazards encountered in repair of jet aircraft fuel cells. Journal of the American Medical Association. Vol. 164, no. 5 (June 1, 1957). p. 531-533

(3) CONCAWE. Petroleum Products and Health Management Groups. Kerosines/jet fuels. Product dossier no. 94/106. CONCAWE, Apr. 1995

(4) Knave, B., et al. Long-term exposure to jet fuel. II. Cross-sectional epidemiologic investigation on occupationally exposed industrial workers with special reference to the nervous system. Scandinavian Journal of Work, Environment and Health. Vol. 4, no. 1 (Mar. 1978). p. 19-45

(5) Bergholtz, L.M., et al. Audiological findings in solvent exposed workers. Acta Otolaryngologica. Suppl. 412 (1984). p. 109-110

(6) Smith, L.B., et al. Effect of chronic low-level exposure to jet fuel on postural balance of US Air Force Personnel. Journal of Occupational and Environmental Medicine. Vol. 39, no. 7 (July 1997). p. 623-632

(7) Barregard, L., et al. Polyneuropathy possibly caused by 30 years of low exposure to n-hexane. Scandinavian Journal of Work, Environment and Health. Vol. 17, no. 3 (June 1991). p. 205-207

(8) Dossing, M., et al. Jet fuel and liver function. Scandinavian Journal of Work, Environmental and Health. Vol. 11, no. 6 (Dec. 1985). p. 433- 437

(9) International Agency for Research on Cancer. Jet fuel. In: IARC monographs on the evaluation of carcinogenic risks to humans. Vol. 45. Occupational exposures in petroleum refining: crude oil and major petroleum fuels. World Health Organization, 1989. p. 203-218

(10) Selden, A., et al. Mortality and cancer morbidity after exposure to military aircraft fuel. Aviation, Space and Environmental Medicine. Vol. 62, no. 8 (Aug. 1991). p. 789-794

(11) Siemiatycki, J., et al. Associations between several sites of cancer and twelve petroleum-derived liquids: results from a case-referent study in Montreal. Scandinavian Journal of Work, Environment and Health. Vol. 13, no. 6 (Dec. 1987). p. 493-504

(12) Clark, C.R., et al. Comparative acute toxicity of shale and petroleum derived distillates. Toxicology and Industrial Health. Vol. 5, no. 6 (Dec. 1989). p. 1005-1016

(13) The American Petroleum Institute. Jet Fuel A. Journal of American College of Toxicology. Part B, Vol. 1 (1990). p. 30

(14) Beck, L.S., et al. The acute toxicology of selected petroleum hydrocarbons. In: Advances in modern environmental toxicology. Vol. 6. Applied toxicology of petroleum hydrocarbons. Edited by H.N MacFarland, et al. Princeton Scientific Publishers, Inc., 1984. p. 1-16

(15) Bruner, R. Pathologic findings in laboratory animals exposed to hydrocarbon fuels of military interest. In: Advances in modern experimental toxicology. Vol. 7. Renal effects of petroleum hydrocarbons. Edited by M. Mehlman. Princeton Scientific Publishers, Inc., 1984. p. 133-140

(16) Clark, C.R., et al. Comparative dermal carcinogenesis of shale and petroleum-derived distillates. Toxicology and Industrial Health. Vol. 4, no. 1 (Mar. 1988). p. 11-22

(17) Freeman, J.J., et al. A 90-day toxicity study of the effects of petroleum middle distillates on the skin of C3H mice. Toxicology and Industrial Health. Vol. 6, no. 3/4 (May 1990). p. 475-491

(18) Beliles, R.P., et al. Inhalation teratology of jet fuel A, fuel oil and petroleum naphtha in rats. The Toxicology of Petroleum Hydrocarbons. Symposium proceedings. Edited by H.N. MacFarland, et al. American Petroleum Institute, 1982. p. 233-238

(19) Freeman, J.J., et al. Evaluation of the contribution of chronic skin irritation and selected compositional parameters to the tumorigenicity of petroleum middle distillates in mouse skin. Toxicology. Vol. 81, no. 2 (July 28, 1993). p. 103-112

(20) Conaway, C.C., et al. Mutagenicity evaluation of petroleum hydrocarbons. In: Advances in modern environmental toxicology. Vol. 6. Applied toxicology of petroleum hydrocarbons. Edited by H.N MacFarland, et al. Princeton Scientific Publishers, Inc., 1984. p. 89-107

(21) National Toxicology Program. NTP technical report on the toxicology and carcinogenesis of marine diesel fuel and JP-5 navy fuel (CAS 8008-20-6) in B6C3F1 mice (dermal studies). NTP TR 310. US Department of Health and Human Services, Sept. 1986

(22) CanTox Inc. PACE WHMIS classification guidelines: guideline revisions, documentation and update. Petroleum Association for Conservation of the Canadian Environment (PACE), Jan. 1990

(23) Ruth, J.H. Odor thresholds and irritation levels of several chemical substances: a review. American Industrial Hygiene Association Journal. Vol. 47 (Mar. 1985). p. A 147

(24) Strauss, K.H. Aviation turbine fuels. In: Ullmann’s encyclopedia of industrial chemistry. 5th completely revised ed. Vol. A 3. VCH Verlagsgesellschaft, 1985. p. 201-212

(25) Dukek, W.G. Aviation and other gas turbine fuels. In: Kirk-Othmer encyclopedia of chemical technology. 4th ed. Vol. 3. John Wiley and Sons, 1992. p. 788-812

(26) NIOSH pocket guide to chemical hazards. National Institute for occupational Safety and Health, June 1997.

(27) Fire protection guide to hazardous materials. 13th ed. Edited by A.B. Spencer, et al. National Fire Protection Association, 2002. NFPA 325

(28) Pohanish, R.P., et al. Rapid guide to chemical incompatibilities. Van Nostrand Reinhold, 1997. p. 465

(29) European Economic Community. Commission Directive 94/69/EC. Dec. 19, 1994

(30) European Communities. Commission Directive 96/54/EC. Sept. 30, 1996

(31) Forsberg, K., et al. Quick selection guide to chemical protective clothing. 4th ed. Van Nostrand Reinhold, 2002

(32) Monteiro-Riviere, N., et al. Effects of short-term high-dose and low-dose dermal exposure to Jet A, JP-8 and JP-8 + 100 jet fuels. Journal of Applied Toxicology. Vol. 21, no. 6 (Nov. 2001). p. 485-494

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

Review/Preparation Date: 1998-12-30

Revision Indicators:

WHMIS (disclosure list) 1999-02-01

TDG 2002-05-29

TLV-TWA 2003-05-22

TLV basis 2003-05-22

TLV comments 2003-05-22

TLV proposed changes 2003-05-22

Carcinogenicity 2003-05-26

Boiling point 2004-02-19

Resistance of materials for PPE 2004-04-13

Bibliography 2006-03-23

Toxicological info 2006-04-04

Short-term skin contact 2006-04-04

WHMIS health effects 2006-04-04

WHMIS detailed classification 2006-04-04

WHMIS proposed classification 2006-04-04

Emergency overview 2006-04-04

First aid skin 2006-04-04

UN/NA No 2006-04-04

Handling 2006-04-04

Skin protection 2006-04-04

BERYLLIUM CHLORIDE

ICSC: 1354

Date of Peer Review: April 2000

CAS #

7787-47-5

BeCl2

RTECS #

DS2625000

Molecular mass: 79.9

UN #

1566

EC #

004-002-00-2

TYPES OF HAZARD / EXPOSURE

ACUTE HAZARDS / SYMPTOMS

PREVENTION

FIRST AID / FIRE FIGHTING

FIRE

Gives off irritating or toxic fumes (or gases) in a fire.

NO contact with water.

In case of fire in the surroundings: NO water.

EXPLOSION

EXPOSURE

PREVENT DISPERSION OF DUST! AVOID ALL CONTACT!

IN ALL CASES CONSULT A DOCTOR!

Inhalation

Cough. Sore throat. Shortness of breath. Symptoms may be delayed (see Notes).

Closed system and ventilation.

Fresh air, rest. Half-upright position. Refer for medical attention.

Skin

Redness. Pain.

Protective gloves. Protective clothing.

Remove contaminated clothes. Rinse skin with plenty of water or shower. Refer for medical attention.

Eyes

Redness. Pain. Blurred vision.

Face shield or eye protection in combination with breathing protection.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then take to a doctor.

Ingestion

Nausea. Vomiting. Abdominal pain.

Do not eat, drink, or smoke during work. Wash hands before eating.

Rinse mouth. Refer for medical attention.

SPILLAGE DISPOSAL

PACKAGING & LABELLING

Sweep spilled substance into sealable containers; if appropriate, moisten first to prevent dusting. Carefully collect remainder, then remove to safe place. Do NOT let this chemical enter the environment. Chemical protection suit including self-contained breathing apparatus.

Unbreakable packaging; put breakable packaging into closed unbreakable container. Do not transport with food and feedstuffs.

EU Classification

Symbol: T+, N

R: 49-25-26-36/37/38-43-48/23-51/53

S: 53-45-61

Note: [A, E]

UN Classification

UN Hazard Class: 6.1

UN Pack Group: II

EMERGENCY RESPONSE

SAFE STORAGE

Transport Emergency Card: TEC (R)-61GT5-II

Separated from food and feedstuffs. Dry. Well closed.

IPCS

International

Programme on

Chemical Safety

Prepared in the context of cooperation between the International Programme on Chemical Safety and the Commission of the European Communities © IPCS, CEC 2004

SEE IMPORTANT INFORMATION ON BACK

BERYLLIUM CHLORIDE

ICSC: 1354

IMPORTANT DATA

PHYSICAL STATE; APPEARANCE:

COLOURLESS TO YELLOW CRYSTALS

CHEMICAL DANGERS:

The substance decomposes rapidly on contact with water producing hydrogen chloride (see ICSC 0163). Attacks many metals in presence of water.

OCCUPATIONAL EXPOSURE LIMITS:

TLV: (as Be) 0.002 mg/m³ as TWA, 0.01 mg/m³ as STEL; A1 (confirmed human carcinogen); (ACGIH 2004).

MAK: sensitization of respiratory tract and skin (Sah); Carcinogen category: 1; (DFG 2004).

ROUTES OF EXPOSURE:

The substance can be absorbed into the body by inhalation of its aerosol and by ingestion.

INHALATION RISK:

Evaporation at 20°C is negligible; a harmful concentration of airborne particles can, however, be reached quickly when dispersed.

EFFECTS OF SHORT-TERM EXPOSURE:

The substance is severely irritating to the eyes, the skin and the respiratory tract. Inhalation of dust or fumes may cause chemical pneumonitis. The effects may be delayed. Medical observation is indicated. Exposure may result in death.

EFFECTS OF LONG-TERM OR REPEATED EXPOSURE:

Repeated or prolonged contact may cause skin sensitization. Lungs may be affected by repeated or prolonged exposure, resulting in chronic beryllium disease (cough, weight loss, weakness). This substance is carcinogenic to humans.

PHYSICAL PROPERTIES

Boiling point: 520°C

Melting point: 399.2°C

Density: 1.9 g/cm³

Solubility in water, g/100 ml at 20°C: 15.1

ENVIRONMENTAL DATA

The substance is very toxic to aquatic organisms. The substance may cause long-term effects in the aquatic environment.

NOTES

The symptoms of acute pneumonitis following a massive short-term exposure do not become manifest until 3 days. Depending on the degree of exposure, periodic medical examination is suggested. Do NOT take working clothes home.

Card has been partly updated in April 2005. See sections Occupational Exposure Limits, Emergency Response.

ADDITIONAL INFORMATION

LEGAL NOTICE

Neither the CEC nor the IPCS nor any person acting on behalf of the CEC or the IPCS is responsible for the use which might be made of this information

See Also:

Beryllium (EHC 106, 1990)

Beryllium (UK PID)

Beryllium carbonate (ICSC)

Beryllium fluoride (ICSC)

Beryllium nitrate (ICSC)

Beryllium sulfate (ICSC)

SECTION 1. CHEMICAL IDENTIFICATION

CHEMINFO Record Number: 474

CCOHS Chemical Name: Terephthalic acid

Synonyms:

Benzene-1,4-dicarboxylic acid

1,4-Benzenedicarboxylic acid

p-Benzenedicarboxylic acid

1,4-Dicarboxybenzene

p-Dicarboxybenzene

1,4-Phthalic acid

p-Phthalic acid

TPA

Phthalic acid (non-specific name)

Chemical Name French: Acide téréphtalique

Chemical Name Spanish: Acido tereftálico

CAS Registry Number: 100-21-0

RTECS Number(s): WZ0875000

EU EINECS/ELINCS Number: 202-830-0

Chemical Family: Aromatic carboxylic acid / aromatic dicarboxylic acid / benzenecarboxylic acid / benzenedicarboxylic acid / phthalic acid isomer

Molecular Formula: C8-H6-O4

Structural Formula: HO-C(=O)-C6H4-C(=O)-OH

SECTION 2. DESCRIPTION

Appearance and Odour:

White or off-white crystals or powder. Odourless or a slight acetic acid odour.(8,13)

Odour Threshold:

No information was located.

Warning Properties:

Insufficient information for evaluation.

Composition/Purity:

Terephthalic acid is one of three chemical forms (isomers) of benzenedicarboxylic acid (1,4-benzenecarboxylic acid). 1,2-Benzenecarboxylic acid is commonly known as phthalic acid and 1,3-benzenecarboxylic acid as isophthalic acid. For information on these related acids refer to CHEMINFO records 472 and 473 respectively. Terephthalic acid is commercially available as polymer grade (greater than 99.9 weight % pure, exclusive of some residual water) and technical grade (typically greater than 97-98% pure). Impurities include p-toluic acid, 4-formylbenzoic acid, residual water, trace metals and ash (trace metal oxides).(4,14,15)

Uses and Occurrences:

Terephthalic acid is used almost exclusively for the manufacture of saturated polyesters, such as poly(ethylene terephthalate). It is also used in the manufacture of high performance polymers or engineering resins; as the diacid in specialty nylons; in the manufacture of specialty fibres; in the production of terephthalic acid esters, particularly dimethyl terephthalate; as a poultry feed additive; as a reagent for alkali in wool; and in analytical chemistry.(13-15)

SECTION 3. HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW:

White crystals or powder, with a slightly acidic odour. Can burn if strongly heated. COMBUSTIBLE DUST. Can form explosive dust-air mixtures. Essentially non-toxic following short-term exposure.

POTENTIAL HEALTH EFFECTS

Effects of Short-Term (Acute) Exposure

Inhalation:

Dusts and mists from solutions are probably only mildly irritating to the nose, throat and lungs, based on limited animal information. In general, high concentrations of dust may cause coughing and mild, temporary irritation. There is no human information available.

Skin Contact:

Dusts and solutions are probably not irritating to the skin, based on limited animal information. There is no human information available.

Based on animal information, this acid is not absorbed through intact skin.

Eye Contact:

Contact with dusts or mists would probably produce mild irritation, based on unconfirmed animal information. In general, dusts are irritating as “foreign objects”. Some tearing, blinking and mild temporary pain may occur as the solid material is rinsed from the eye by tears. There is no human information available.

Ingestion:

Terephthalic acid is low in acute oral toxicity, based on animal information. Bladder stones have been observed in animal studies following ingestion of high dietary concentrations. These levels of exposure are not relevant to occupational situations. There is no human information available.

Effects of Long-Term (Chronic) Exposure

There is no human information available.

INGESTION: Bladder stones have been observed in animal studies following long- term ingestion of high dietary concentrations. Based on these animal studies, it was concluded that bladder stones could occur if humans absorbed at least 2000 mg/day of terephthalic acid.(1) Such a large dose is not relevant to occupational exposures.

Carcinogenicity:

Bladder and urinary tract cancers have been observed in animal studies following long-term ingestion of high dietary concentrations. However, these effects are considered secondary to the development of bladder stones and the high levels of exposure are not relevant to occupational situations. There is no human information available.

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

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

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

Teratogenicity and Embryotoxicity:

There is no human information available. Terephthalic acid did not cause teratogenic effects, except in the presence of maternal toxicity, in three animal studies.

Reproductive Toxicity:

There is no human information available. Terephthalic acid did not cause harmful effects on reproduction in male or female rats in two animal studies.

Mutagenicity:

There is no human information available. Negative results were obtained in tests using bacteria and cultured mammalian cells.

Toxicologically Synergistic Materials:

There is no information available.

Potential for Accumulation:

Terephthalic acid does not accumulate in the body. In one rat study, it was almost completely excreted in the urine within 24 hours. Only a very small amount was excreted in the feces. No metabolites were found in the expired air or urine, indicating that no metabolism had occurred.(2) In another rat study, it was reported that after single or repeated oral administration of terephthalic acid, the amount excreted after 24 to 48 hours was equally divided between urine and feces. These authors indicated that terephthalic acid was metabolized to water-soluble compounds.(3)

SECTION 4. FIRST AID MEASURES

Inhalation:

No health effects expected. If symptoms develop, remove source of contamination or have victim move to fresh air. If symptoms persists, obtain medical advice immediately.

Skin Contact:

If irritation occurs, gently blot or brush away excess chemical quickly. Wash gently and thoroughly with water and non-abrasive soap. If irritation persists, obtain medical advice immediately. Completely decontaminate clothing, shoes and leather goods before re-use or discard.

Eye Contact:

Do not allow victim to rub eye(s). Let the eye(s) water naturally for a few minutes. Have the victim look right and left, and then up and down. If particle/dust does not dislodge, flush with lukewarm, gently flowing water for 5 minutes or until particle/dust is removed, while holding the eyelid(s) open. If irritation persists, obtain medical attention. DO NOT attempt to manually remove anything stuck to the eye(s).

Ingestion:

If irritation or discomfort occur, obtain medical advice immediately.

First Aid Comments:

All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.

SECTION 5. FIRE FIGHTING MEASURES

Flash Point:

260 deg C (500 deg F) (open cup) (13)

Lower Flammable (Explosive) Limit (LFL/LEL):

Not available

Upper Flammable (Explosive) Limit (UFL/UEL):

Not available

Autoignition (Ignition) Temperature:

496 deg C (925 deg F) (13,20)

Sensitivity to Mechanical Impact:

Not sensitive. Stable material.

Combustion and Thermal Decomposition Products:

Incomplete combustion may also produce acrid smoke and irritating fumes.(13,20)

Flammable Properties:

Specific Hazards Arising from the Chemical:

During a fire, irritating/toxic gases and fumes may be generated.

Extinguishing Media:

Carbon dioxide, dry chemical powder, alcohol foam, polymer foam, water spray or fog.(13,20)

Fire Fighting Instructions:

Evacuate area and fight fire from a safe distance or a protected location. Approach fire from upwind to avoid toxic decomposition products.

Water or foam may cause frothing. The frothing may be violent and could endanger personnel close to the fire. However, a water spray or fog that is carefully applied to the surface of the burning material, preferably with a fine spray or fog nozzle, will cause frothing that will blanket and extinguish the fire. In addition, water spray or fog can be used to prevent dust formation, absorb heat, keep containers cool and protect exposed material. Water spray may be used to flush spills away from ignition sources. Solid streams of water may be ineffective and spread material.

The decomposition products of terephthalic acid may be hazardous to health. Firefighters may enter the area if positive-pressure self-contained breathing apparatus (MSHA/NIOSH approved or equivalent) and full Bunker Gear is worn.

NATIONAL FIRE PROTECTION ASSOCIATION (NFPA) HAZARD IDENTIFICATION

NFPA – Health: 1 – Exposure would cause significant irritation, but only minor residual injury.

NFPA – Flammability: 1 – Must be preheated before ignition can occur.

NFPA – Instability: 0 – Normally stable, even under fire conditions, and not reactive with water.

SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES

Molecular Weight: 166.14

Conversion Factor:

Not applicable

Physical State: Solid

Melting Point: Sublimes at 402 deg C (755.6 deg F) at atmospheric pressure, without melting.(14,15,22) Reported to melt at 427 deg C (800.6 deg F) in a sealed tube.(13,14)

Boiling Point: Sublimes (13,15,22)

Relative Density (Specific Gravity): 1.522 at 25 deg C (water = 1) (14)

Solubility in Water: Practically insoluble (1.7 mg/100 g) at 25 deg C.(14,15)

Solubility in Other Liquids: Soluble in dimethyl sulfoxide, dimethylformamide and alkalies, such as potassium and sodium hydroxide; slightly soluble in cold ethanol, methanol, formic acid and sulfuric acid; very slightly soluble in chloroform, diethyl ether and glacial acetic acid.(13-15,22)

Coefficient of Oil/Water Distribution (Partition Coefficient): Log P(oct) = 1.25; 1.96; 2.0 (measured) (23)

pH Value: 2.16 (saturated solution (0.002% in water)) (calculated) (13)

Vapour Density: Not applicable

Vapour Pressure: Less than 0.0013 kPa (0.01 mm Hg) at 20 deg C (13); 0.067 kPa (0.5 mm Hg) at 120 deg C (13)

Saturation Vapour Concentration: Very low at normal temperatures.

Evaporation Rate: Probably very low at normal temperatures.

Other Physical Properties:

ACIDITY: Weak acid; pKa1 = 3.54 (Ka1 = 2.9 X 10(-4)); pKa2 = 4.46 (Ka2 = 3.5 X 10(-5)) at 25 deg C.(14,15)

NOTE: Very small amounts of terephthalic acid in water are reported to substantially lower the pH of the solution and form a fairly strong acid.(13)

TRIPLE POINT: 427 deg C (800.6 deg F) (14)

SECTION 10. STABILITY AND REACTIVITY

Stability:

Normally stable.(13)

Hazardous Polymerization:

Does not occur

Incompatibility – Materials to Avoid:

STRONG OXIDIZING AGENTS (e.g. perchlorates, peroxides, chlorine) – react violently or explosively. Increased risk of fire and explosion.(13,20)

CONCENTRATED NITRIC ACID – may form explosive mixtures.(24)

ACTIVE METALS (e.g. aluminum or zinc) – may evolve flammable and potentially explosive hydrogen gas.(13)

STRONG BASES (including alkalis such as sodium hydroxide) – react vigorously.(13)

Hazardous Decomposition Products:

None reported

Conditions to Avoid:

Generation of dust, heat, flames, sparks, build-up of static electricity and other ignition sources.

Corrosivity to Metals:

No specific data is available. May be corrosive to some metals in the presence of moisture or water.(13) Saturated solutions of phthalic acid, a closely related acid, produce corrosive effects on cast iron and steel.(25) Acids are generally not corrosive to types 304 and 316 stainless steels, and aluminum is generally resistant to acids at room temperature.(26)

Stability and Reactivity Comments:

Probably attacks some forms of plastics, rubber and coatings.(13)

SECTION 11. TOXICOLOGICAL INFORMATION

LD50 (oral, mouse): greater than 5000 mg/kg (5)

LD50 (dermal, rabbit): greater than 2000 mg/kg (6, unconfirmed)

Eye Irritation:

Mild irritation was observed in rabbits following administration of terephthalic acid in a standard Draize test.(7, unconfirmed) In another test, no eye damage was observed in rabbits following application of 50 mg terephthalic acid.(3)

Skin Irritation:

Application of 0.2 mL of solution of terephthalic acid in water did not produce irritation in rats and was not absorbed through the skin.(3)

Effects of Short-Term (Acute) Exposure:

Inhalation:

No harmful effects were observed in rats following inhalation of very high concentrations (up to 400 mg/m3) terephthalic acid dust for 30 minutes.(8, unconfirmed) Reduced weight gain was observed in rats exposed to 25 mg/m3 for 4 weeks.(6)

Ingestion:

A statistically significant increase in bladder stones and decreased body weight were observed in rats fed very high dietary levels 4-5% (2000-3000 mg/kg/day) terephthalic acid for 2 weeks. These effects were not observed in rats fed 0.5-3% (250-1500 mg/kg/day).(9) Bladder stones were also observed in 50% of young (28 day old) rats fed 4% (4000 mg/kg/day) terephthalic acid for 2 weeks.(10) No adverse effects on the liver or kidney were observed in mice fed 0.5% (750 mg/kg/day) terephthalic acid in the diet for 7 days.(5)

Effects of Long-Term (Chronic) Exposure:

Inhalation:

No harmful effects were observed in rats or guinea pigs following inhalation exposure to 10 mg/m3 terephthalic acid for 6 months.(1)

Ingestion:

A number of studies have been conducted in which bladder stones and evidence of tissue damage to the lining of the bladder (hyperplasia) were observed following long-term ingestion of high dietary concentrations of terephthalic acid.(1)

Carcinogenicity:

Bladder and urinary tract cancers have been observed in rats in two studies following ingestion of high dietary concentrations of terephthalic acid for 2 years. After reviewing these studies and other toxicity data, it was concluded that the carcinogenic effect is secondary to the development of bladder stones.(1) The dose level were very high and are not relevant to occupational exposures.

Teratogenicity, Embryotoxicity and/or Fetotoxicity:

Terephthalic acid has caused effects, but only in the presence of maternal toxicity.

No teratogenic effects were observed in offspring following exposure of rats to 1, 5 or 10 mg/m3 terephthalic acid during pregnancy. No harmful effects on the mothers were observed.(11) In another study, decreased body weight of offspring and deaths associated with kidney and bladder stones among young rats were observed following ingestion of 5% in the diet prior to mating, during mating, gestation, lactation and postweaning. These effects were not observed following ingestion of 0.03-2% in the diet. Deaths among fetuses and newborns were observed following ingestion of 2% and 5%, but not at lower doses.(4, unconfirmed) These doses would be expected to cause maternal toxicity. In another study, teratogenic effects (skeletal anomalies) were observed in offspring born to rats exposed to airborne terephthalic acid during pregnancy, however, maternal toxicity was also observed.(4, unconfirmed)

Reproductive Toxicity:

No harmful effects on reproduction were observed in male or female rats following ingestion of 0.03-5% in the diet.(4, unconfirmed) No harmful effects on reproduction were observed in male or female rats fed 0.03-5% terephthalic acid in the diet for 90 days, although there were other (non-reproductive) harmful effects at 2% or 5%.(4, unconfirmed)

SECTION 16. OTHER INFORMATION

Selected Bibliography:

(1) Heck, H.d’A., et al. The induction of bladder stones by terephthalic acid, dimethyl terephthalate and melamin (2,4,6-triamino-s-triazine) and its relevance to risk assessment. Regulatory Toxicology and Pharmacology. Vol. 5, no. 3 (Sept. 1985). p. 294-313

(2) Hoshi, A., et al. Metabolism of terephthalic acid: III. Absorption of terephthalic acid from gastrointestinal tract and detection of its metabolites. Chemical and Pharmaceutical Bulletin. Vol. 15, no. 12 (1967). p. 1979-1984

(3) Moffitt, A.E., et al. Absorption, distribution and excretion of terephthalic acid and dimethyl terephthalate. American Industrial Hygiene Association Journal. Vol. 36, no. 8 (Aug. 1975). p. 633-641

(4) HSDB record for terephthalic acid. Last revision date: 97/02/21

(5) Hoshi, A., et al. Toxicity of terephthalic acid. Chemical and Pharmaceutical Bulletin. Vol. 16, no. 9 (1968). p. 1655-1660

(6) MSDS database record for AMOCO TA-22 (Amoco Chemical Company). Date of MSDS: 1996-04-05

(7) RTECS record for terephthalic acid. Last updated: 9704

(8) Terephthalic acid. In: Documentation of the threshold limit values and biological exposure indices. 6th ed. including 1996 Suppl. American Conference of Governmental Industrial Hygienists, 1996. p. Supplement: Terephthalic acid – 1 to 3

(9) Chin, T.Y., et al. Chemical urolithiasis: 1. Characteristics of bladder stone induction by terephthalic acid and dimethyl terephthalate in weanling Fischer-344 rats. Toxicology and Applied Pharmacology. Vol. 58, no. 2 (Apr. 1981). p. 307-321

(10) Wolkowski-Tyl, R., et al. Effects of selected therpeutic agents on urolithiasis induced by terephthalic acid in the male weanling Fischer 344 rat. Fundamental and Applied Toxicology. Vol. 3, no. 6 (Nov./Dec. 1983). p. 552-558

(11) Ryan, B.M., et al. A segment II inhalation teratology study of terephthalic acid in rats. [Abstract]. Toxicologist. Vol. 10, no. 1 (1990). p. 40

(12) Brooks, A.L., et al. In vitro genotoxicity of dyes present in colored smoke munitions. Environmental and Molecular Mutagenesis. Vol. 13, no. 4 (1989). p. 304-313

(13) Emergency action guide for terephthalic acid. Association of American Railroads, Sept. 1992

(14) Park, C-H, et al. Phthalic acids and other benzenepolycarboxylic acids. In: Kirk-Othmer encyclopedia of chemical technology. 4th ed. Vol. 18. John Wiley and Sons, 1996. p. 991–1043

(15) Sheehan, R.J. Terephthalic acid, dimethyl phthalate and isophthalic acid. In: Ullmann’s encyclopedia of industrial chemistry. 5th completely revised ed. Vol. A 26. VCH Verlagsgesellschaft, 1995. p. 193-204

(16) Fire protection guide to hazardous materials. 13th ed. Edited by A.B. Spencer, et al. National Fire Protection Association, 2002. NFPA 325

(17) Field, P. Dust explosions. Elsevier Scientific Publishing Company, 1982. p. 218

(18) Grossel, S.S. Safety considerations in conveying of bulk solids and powders. Journal of Loss Prevention in the Process Industries. Vol. 1 (Apr. 1988). p. 62-74

(19) Schwab, R.F. Dusts. In: Fire protection handbook. Edited by G.P. McKinnon. 15th edi. National Fire Protection Association, 1981. p. 4-84 to 4-97

(20) The Sigma-Aldrich library of chemical safety data. Ed. II. Vol. 2. Sigma-Aldrich Corporation, 1988. p. 3219D

(21) Field, P. Explosibility assessment of industrial powders and dusts. Building Research Establishment, 1983

(22) Dean, J.A. Lange’s handbook of chemistry. 14th ed. McGraw-Hill, Inc., 1992. p. 1.100

(23) Verschueren, K. Handbook of environmental data on organic chemicals. 3rd ed. Van Nostrand Reinhold, 1996. p. 1652-1653

(24) Urben, P.G., ed. Bretherick’s handbook of reactive chemical hazards. 5th ed. Vol. 1. Butterworth-Heinemann Ltd., 1995. p. 944-945, 1483

(25) Corrosion data survey: metals section. 6th ed. National Association of Corrosion Engineers, 1985. p. 96-16 to 97-16

(26) Elder, G.B. Materials of construction for organic acids. In: Process industries corrosion: the theory and practice. Edited by B.J. Moniz, et al. National Association of Corrosion Engineers, 1986. p. 287-296

(27) Forsberg, K., et al. Quick selection guide to chemical protective clothing. 3rd ed. Van Nostrand Reinhold, 1997

(28) European Commission. Terophthalic acid. IUCLID Dataset. European Chemicals Bureau, Feb. 2000. Available at:

Review/Preparation Date: 1997-12-24

Revision Indicators:

Resistance of materials 1998-02-01

NFPA (health) 2003-04-17

TLV basis 2004-01-04

Bibliography 2006-03-03

Conversion factor 2006-10-05

Vapour density 2006-10-05

LFL/LEL 2006-10-05

UFL/UEL 2006-10-05

COBALT CHLORIDE

SM Bradberry BSc MB MRCP

P Sabatta MSc

JA Vale MD FRCP FRCPE FRCPG FFOM

National Poisons Information Service

This monograph has been produced by staff of a National Poisons

Information Service Centre in the United Kingdom. The work was

commissioned and funded by the UK Departments of Health, and was

designed as a source of detailed information for use by poisons

information centres.

Peer review group: Directors of the UK National Poisons Information

Service.

COBALT CHLORIDE

Toxbase summary

Type of product

Used in inks, varnishes, enamels, fertilizers, feed additives and

humidity indicators.

Toxicity

Cobalt chloride is only moderately toxic by ingestion although a 19

month-old child died some six hours after allegedly drinking only 30

mL (Jacobziner and Raybin, 1961). In another report a six year-old

developed only transient gastrointestinal upset after ingesting 2.5 g

(Mucklow et al, 1990).

Cobalt sensitization may occur following dermal exposure.

Features

Dermal

– Cobalt chloride is a topical irritant and a recognized cause

of occupational contact dermatitis.

– Simultaneous allergies to nickel and cobalt are frequent.

Ocular

– Cobalt chloride is a potential eye irritant but there are no

reports of acute eye toxicity in man.

Ingestion

– There may be no or minimal symptoms after small ingestions.

Nausea, vomiting and/or abdominal pain are likely after more

substantial ingestions (> 100 mg). Concentrated solutions

are acidic (the pH of a 0.2 M solution is 4.6). There is an

early case report of fatal cobalt chloride ingestion (30 mL)

in which autopsy showed a blistered oesophageal mucosa and

partially necrosed gastric mucosa (Jacobziner and Raybin,

1961).

– Transient neutropenia occurred in a six year old child who

ingested 2.5 g (Mucklow et al, 1990).

– In the past congestive cardiomyopathy occurred after the

consumption of large quantities of beer to which cobalt

chloride/cobalt sulphate had been added as a foam stabilizer

and in those receiving oral cobalt chloride therapy as

treatment for anaemia. These presentations are now most

unlikely in the UK.

– Chronic cobalt chloride ingestion has also caused

hypothyroidism (cobalt inhibits the iodination of tyrosine).

Inhalation

– Pulmonary toxicity following chronic cobalt exposure is

associated typically with the hard metal industry in which

elemental cobalt forms a matrix for tungsten carbide.

Symptoms are most prevalent, however, among those working in

‘wet’ processes where cobalt is ionized.

– Hard metal lung disease usually arises after several years

and may manifest as pneumoconiosis (with dyspnoea and cough

secondary to interstitial fibrosis), allergic alveolitis or

occupational asthma.

– Cor pulmonale may complicate hard metal pneumoconiosis.

– There are occasional reports of cobalt cardiomyopathy

following occupational exposure.

Management

Dermal

Removal from exposure is the priority.
Contact dermatitis responds to topical and/or systemic steroids.
There is no confirmed role for topical chelation therapy in

cobalt dermatitis.

Ocular

Irrigate for at least 15 minutes with lukewarm water.
Topical anaesthesia may be required.
Ensure particle removal from conjunctival recesses.
An ophthalmic opinion may be required.

Ingestion

Gastrointestinal decontamination is not necessary. Vomiting will

occur spontaneously following significant ingestions and gastric

lavage is contraindicated following ingestion of acid solutions.

Supportive care is the priority. Replace fluids and electrolytes

as required.

Check the full blood count.
If chronic cobalt ingestion is suspected consider the possibility

of cobalt cardiomyopathy and check thyroid function.

Collect blood and urine for cobalt concentration determination in

symptomatic patients to confirm diagnosis. Cobalt assays are not

widely available. Check with NPIS.

There are no controlled clinical data regarding the use of

chelating agents in cobalt poisoning. Discuss with an NPIS

physician.

Inhalation

Acute inhalation:

Remove from exposure and treat symptomatically.

Chronic inhalation:

Asthmatic symptoms respond to conventional measures.
Established pulmonary fibrosis generally has a poor prognosis.

Some cases have responded to high dose prednisolone (Rolfe et al,

1992) or cyclophosphamide (Balmes, 1987). Discuss with an NPIS

physician.

References

Alexander CS.

Cobalt-beer cardiomyopathy. A clinical and pathologic study of twenty-

eight cases.

Am J Med 1972; 53: 395-417.

Balmes JR.

Respiratory effects of hard-metal dust exposure.

Occup Med 1987; 2: 327-44.

Cugell DW.

The hard metal diseases.

Clin Chest Med 1992; 13: 269-79.

Curtis JR, Goode GC, Herrington J, Urdaneta LE.

Possible cobalt toxicity in maintenance hemodialysis patients after

treatment with cobaltous chloride: a study of blood and tissue cobalt

concentrations in normal subjects and patients with terminal renal

failure.

Clin Nephrol 1976; 5: 61-5.

Jacobziner H, Raybin HW.

Accidental cobalt poisoning.

Arch Pediatr 1961; 78: 200-5.

Manifold IH, Platts MM, Kennedy A.

Cobalt cardiomyopathy in a patient on maintenance haemodialysis.

Br Med J 1978; 2: 1609.

Mucklow ES, Griffin SJ, Delves HT, Suchak B.

Cobalt poisoning in a 6-year-old.

Lancet 1990; 335: 981.

Rolfe MW, Paine R, Davenport RB, Strieter RM.

Hard metal pneumoconiosis and the association of tumor necrosis

factor-alpha.

Am Rev Respir Dis 1992; 146: 1600-2.

Sullivan JF, Egan JD, George RP.

A distinctive myocardiopathy occurring in Omaha, Nebraska: Clinical

aspects.

Ann NY Acad Sci 1969; 156: 526-43.

Substance name

Cobalt (II) chloride

Origin of substance

Prepared commercially in hexahydrate, dihydrate and monohydrate

forms. (DOSE, 1993)

Synonyms

Cobalt dichloride

Cobaltous chloride (DOSE, 1993)

Chemical group

A compound of cobalt, a group VIIIB element.

Reference numbers

CAS 7646-79-9, (DOSE, 1993)

7791-13-1 (hexahydrate)

RTECS GF 9800000 (RTECS, 1997)

UN NIF

HAZCHEM NIF

Physicochemical properties

Chemical structure

CoCl2 (DOSE, 1993)

Molecular weight

129.84 (DOSE, 1993)

Physical state at room temperature

Solid (DOSE, 1993)

Colour

Pale blue, turning pink on exposure to air.

(OHM/TADS, 1997)

Odour

Very slight sharp odour. (CHRIS, 1997)

Viscosity

Forms acid solution in water (0.2 M aqueous solution has pH 4.6).

(MERCK, 1996; OHM/TADS, 1997)

Solubility

450 g/L in water at 7°C

385 g/L in methanol (HSDB, 1997)

Autoignition temperature

Chemical interactions

A mixture of potassium and cobalt chloride is sensitive to

mechanical shock and may cause a violent explosion.

Sodium dispersions will reduce cobalt chloride exothermically,

resulting in a temperature increase of 50°C. Very violent

explosions may occur.

Contact of dust with strong oxidizers may cause fire and

explosion. (HSDB, 1997)

Major products of combustion

Cobalt oxide (HSDB, 1997)

Explosive limits

Flammability

Not flammable (HSDB, 1997)

Boiling point

1049°C (DOSE, 1993)

Density

3.367 at 25°C (DOSE, 1993)

Vapour pressure

5333 Pa at 770°C (DOSE, 1993)

Relative vapour density

Flash point

Reactivity

Cobalt chloride decomposes at 400°C on heating in air.

Cobalt chloride hydrolyzes in aqueous solution.

(HSDB, 1997)

Uses

Invisible ink

Humidity indicator

Glass and porcelain painting

Production of vitamin B12

Fertilizer and feed additive

Stabilizer in beer

Absorbant for poisonous gases and ammonia

(DOSE, 1993)

Hazard/risk classification

NIF

INTRODUCTION AND EPIDEMIOLOGY

Cobalt chloride is a water soluble bivalent cobalt salt. Cobalt

chloride poisoning is now rare with only isolated case reports of

accidental or intentional ingestion, usually from chemistry sets or

crystal growing kits (Jacobziner and Raybin, 1961; Everson et al,

1988; Mucklow et al, 1990).

Outbreaks of cobalt cardiomyopathy occurred in Belgium, Nebraska and

Quebec in the 1960’s among heavy beer drinkers when cobalt

chloride/sulphate was added to beer to act as a foam stabilizer

(Kesteloot et al, 1968). Chronic cobalt intoxication also occurred

when oral cobalt chloride was used to treat anaemia (Duckham and Lee,

1976; Manifold et al, 1978) but this is no longer a licensed

indication in the UK.

Cobalt is an important cause of occupational contact dermatitis and

cobalt chloride is widely used in patch testing. However, reports in

which cobalt chloride specifically is the allergen are rare (Zenorola

et al, 1994).

MECHANISM OF TOXICITY

Cytotoxic hydroxy radicals may form when cobalt ions interact with

reactive oxygen species. Hydroxy radicals may then cause the

production of further free radicals which reduce cellular glutathione

concentrations and NADPH activity. The resulting oxidative stress

leads to DNA and cellular protein damage (Timbrell, 1994).

Cobalt is immunogenic and acts as a hapten in the induction of

bronchial and dermal hypersensitivity (Sjögren et al, 1980). Ionized

cobalt, though not specifically cobalt chloride, is an important

contributing factor in the aetiology of hard metal lung disease.

Evidence for an autoimmune mechanism in this disorder is suggested by

the recurrence of disease in a single transplanted lung despite no

evidence of cobalt in the donated organ (Frost et al, 1993). In cobalt

pneumoconiosis non-respiratory symptoms may be due to cobalt-induced

release of a tumour necrosis factor from sensitized pulmonary

lymphocytes (Rolfe et al, 1992).

In a dog model cobalt myocardial toxicity was characterized by

vacuolation and loss of myofibers (Sandusky et al, 1981a) with

histochemical evidence of severe mitochondrial damage (Sandusky et al,

1981b). Alexander (1972) suggested cobalt depresses mitochondrial

oxygen uptake in the myocardium by complexing with sulphydryl groups

and preventing the oxidation of pyruvate in the citric acid cycle.

Tissue hypoxia is the probable stimulus also of erythropoietin

secretion in cobalt-induced polycythaemia (Taylor and Marks, 1978).

In animal studies, cobalt decreases synthesis of several enzymes

including cellular cytochrome P450 (Timbrell, 1994). Cobalt inhibits

aminolaevulinic acid synthetase and increases the activity of haem

oxygenase which breaks down haem to biliverdin (Taylor and Marks,

1978; Timbrell, 1994).

TOXICOKINETICS

Absorption

Cobalt chloride can be absorbed following ingestion, inhalation and

dermal exposure (Domingo, 1989; Scansetti et al, 1994; Linnainmaa and

Kiilunen, 1997). Cobalt and iron share the same transport mechanism

within the small intestine such that cobalt ingestion competitively

inhibits iron uptake. The extent of intestinal cobalt absorption

depends on the dose with only some 20 per cent of a large ingestion

being absorbed (Domingo, 1989).

Some inhaled cobalt chloride is swallowed following mucociliary

clearance while particles which reach the distant pulmonary tree are

taken up predominantly by macrophages (Taylor and Marks, 1978; Evans

et al, 1993). Systemic uptake is confirmed by increased blood and

urine cobalt concentrations in those occupationally exposed to

cobalt-containing dusts and mists (Della Torre et al, 1990).

Distribution

The normal body burden of cobalt is about 1.1 mg. Approximately 43 per

cent of this is in muscle with some 14 per cent in bone and the

remainder in other soft tissues (Taylor and Marks, 1978; Domingo,

1989).

Excretion

Cobalt which reaches the systemic circulation is eliminated

predominantly in urine with a variable but small amount excreted in

bile (Taylor and Marks, 1978; Domingo, 1989).

Following acute occupational cobalt inhalation urinary elimination is

rapid for the first 24 hours followed by a slower excretion phase

lasting several weeks (Alexandersson, 1988). A small proportion of

retained cobalt has a biological half-life of several years (Elinder

and Friberg, 1986).

CLINICAL FEATURES: ACUTE EXPOSURE

Dermal exposure

Cobalt chloride may cause skin irritation but dermal toxicity is

associated primarily with contact sensitivity (see Chronic exposure).

Ocular exposure

Cobalt chloride causes corneal damage when directly applied to the

eyes of experimental animals (Grant and Schuman, 1993) but there are

no reports of acute eye toxicity in man.

Inhalation

There are no reports of acute cobalt chloride inhalation.

Ingestion

Most reports of cobalt chloride ingestion involve only modest

gastrointestinal upset although Jacobziner and Raybin (1961) described

a fatality in a 19 month-old child (see below).

Gastrointestinal toxicity

Jacobziner and Raybin (1961) reported a 19 month-old child who

ingested approximately 30 mL of a cobalt chloride solution. Vomiting

was induced immediately and gastric lavage performed on arrival at

hospital two hours later. On examination the child was pale and

peripherally cyanosed. The lips and tongue were oedematous. The

clinical condition deteriorated rapidly with death following a cardiac

arrest some six hours post ingestion. Autopsy revealed a blistered

oesophageal mucosa with coagulative necrosis involving one third the

thickness of the gastric mucosa. The precise cause of death was not

clear but these findings suggest the solution was highly concentrated

and corrosive. Cobalt was identified in the liver, kidney, spleen (89

mg total in these organs) and stomach.

A six year-old boy developed nausea, vomiting and abdominal pain after

swallowing a drink to which he had added about 2.5 g cobalt chloride

from a crystal growing set (Mucklow et al, 1990). The whole blood

cobalt concentration some seven hours post ingestion was 241 µg/L

(normal range < 1 µg/L) but he made a full recovery.

Everson et al (1988) reported a 14 year-old female who vomited but was

otherwise asymptomatic following ingestion of approximately 130 mg

cobalt chloride from her brother’s chemistry set. The serum cobalt

concentration 12 hours post ingestion was 78 µg/L.

Haemotoxicity

A six year old boy who ingested 2.5 g cobalt chloride developed a

transient neutropenia (1.7 x 109/L) but recovered fully (Mucklow et

al, 1990).

Neurotoxicity

A 19 month-old child who ingested 30 mL of a cobalt chloride solution

became restless and drowsy within two hours in association with severe

respiratory distress, cyanosis and pallor. He died some six hours

later (Jacobziner and Raybin, 1961). Cerebral oedema was evident at

autopsy.

CLINICAL FEATURES: CHRONIC EXPOSURE

Dermal exposure

Cobalt is a well recognized cause of contact dermatitis (Smith et al,

1975), a delayed hypersensitivity reaction characterized by vesicles,

itchy maculopapular lesions, scaling and/or fissuring (Miyachi et al,

1985; Foussereau and Cavelier, 1988; Illuminati et al, 1988). These

features are seen commonly on the hands, face and neck and sometimes

the eyelids and chest.

Cobalt contact dermatitis primarily occurs following exposure to the

elemental form, which subsequently is ionized in sweat, although there

are situations where cobalt compounds are the primary allergen. For

example, a 71 year-old construction labourer developed contact

dermatitis induced by cobalt and chromium ions present in cement

(Miyachi et al, 1985). Cobalt dermatitis is also described in those

handling or manufacturing rubber. In the rubber industry cobalt is

used as lipid soluble (cobalt naphthenates and stearates) rather than

water soluble salts (Bedello et al, 1984; Foussereau and Cavelier,

1988).

Zenorola et al (1994) described atypical dermatitis in a 23 year-old

plumber. The clinical appearance was highly suggestive of “Ashy

dermatitis” or erythema dyschromicum perstans, a disorder of uncertain

aetiology characterized by asymptomatic, ash-like grey macular

pigmentation of the skin. The patient patch tested positive to cobalt

chloride for which there were several sources in his workplace

including varnishes and paints. However a causative association

between ashy dermatitis and cobalt allergy could not be confirmed.

An initial irritant dermatitis, often involving operations traumatic

to the hand, usually precedes cobalt allergy in industry (Fischer and

Rystedt, 1983a). In addition false positive cobalt patch tests may

occur due to an irritant rather than delayed hypersensitivity response

(Fischer and Rystedt, 1985).

Cobalt chloride is used widely in patch testing (James and Smith,

1975; Munro-Ashman and Miller, 1976; Veien and Svejgaard, 1978;

Schmidt et al, 1980; Rae, 1981; Romaguera et al, 1982; Miyachi et al,

1985; Shirakawa et al 1988; Allenby and Basketter, 1989; Pryce and

King, 1990; Zhang et al, 1991; Castiglioni et al, 1992; Torresani et

al, 1994). Lantinga et al (1984) invited 2800 members of the general

population in a geographically defined area of the Netherlands to be

examined for skin disorders of the hands and forearms. Patch testing

was performed in 141 persons with eczema. Contact allergy was detected

in 50 (35 per cent) of these. Cobalt chloride was the allergen in five

cases with nickel sulphate in 28 and potassium dichromate in nine

cases.

Among 4721 consecutive patients at a patch test clinic, six per cent

had a positive reaction to cobalt chloride (compared to nickel

sensitivity in 18.5 per cent) (Shehade et al, 1991). These authors

emphasized the importance of not reading the patch test before day

four; 69 of 271 (24 per cent) patients with a positive reaction to

cobalt chloride on day four had a negative result on day two.

Simultaneous allergies to nickel and cobalt are frequent (Burden and

Eedy, 1991; Kanerva and Estlander, 1995) and there is some evidence

for a mutual enhancing effect of contact sensitization to one metal in

the presence of the other (Domingo, 1989).

Inhalation

Pulmonary toxicity

Pulmonary toxicity following chronic cobalt exposure is associated

typically with the hard metal (tungsten carbide in a cobalt matrix)

industry (Auchincloss et al, 1992) but similar problems have been

reported in diamond polishers using cobalt-coated discs (Lahaye et al,

1984; Nemery et al, 1990) and in a dental technician (Sherson et al,

1990). Hard metal lung disease is discussed here since employees are

exposed both to elemental and ionized cobalt (the latter in ‘wet’

grinding processes where cobalt is dissolved in machine coolants).

Cugell (1992) suggested ionized cobalt is more likely than elemental

cobalt to cause occupational pulmonary disease although this may not

be true of hard metal asthma (Kusaka et al, 1996a).

There is some debate concerning whether cobalt exposure alone is

sufficient to cause pulmonary fibrosis. In-vitro and animal studies

suggest there is no relationship between cellular cobalt uptake and

cellular toxicity (Lison and Lauwerys, 1994) and cobalt workers

frequently are exposed to several other potential toxins (including

tungsten carbide, iron, silica and diamond) (Swennen et al, 1993).

While Gennart and Lauwerys (1990) observed a significantly increased

incidence (p<0.05) of restrictive spirometry and respiratory symptoms

in workers exposed for more than five years to cobalt dust in a plant

producing diamond-cobalt circular saws compared to non cobalt-exposed

factory workers, Swennen et al (1993) found no difference in

ventilatory performance, lung volumes or carbon monoxide diffusion

capacity between 82 cobalt refinery workers and controls even though

the cobalt workers complained more frequently of wheeze and dyspnoea.

Hard metal pneumoconiosis

Chronic cobalt (and tungsten carbide) inhalation is associated

typically with “hard metal” pneumoconiosis characterized by

interstitial fibrosis (primarily of the lower zones) and a restrictive

ventilatory defect (Bech et al, 1962). Patients usually present with

exertional dyspnoea, cough and sometimes chest tightness (Bech et al,

1962). There may be associated symptoms of fever, weight loss or

general malaise (Coates and Watson, 1971; Balmes, 1987; Migliori et

al, 1994). In one study of 12 tungsten carbide workers the mean

duration of exposure before the onset of respiratory symptoms was 12

years with a range of one month to 28 years (Coates and Watson, 1971).

Inspiratory crackles are the earliest physical sign (Rochat et al,

1987) but finger clubbing, cyanosis and eventually cor pulmonale may

ensue. Chest X-ray findings vary greatly (Cugell et al, 1990) but

usually show increased linear markings and small nodular opacities in

the lower (and mid) zones with later cardiomegaly and features of

pulmonary hypertension (Bech et al, 1962).

Many patients develop a form of pulmonary fibrosis complicated by

atypical intraalveolar giant cells (Davison et al, 1983; Rochat et al,

1987; Cugell, 1992; Frost et al, 1993) which can be demonstrated in

bronchoalveolar lavage fluid (Forni, 1994) and transbronchial biopsies

(Rolfe et al, 1992). Pulmonary eosinophilia is also a feature of hard

metal lung disease (Della Torre et al, 1990). Forni (1994) suggested

that a persistently high bronchoalveolar lavage eosinophil count

despite steroid therapy and cessation of exposure carried an

unfavourable prognosis.

Several fatalities from hard metal pneumoconiosis have been reported

(Della Torre et al, 1990; Figueroa et al, 1992). Nemery et al (1990)

described a 52 year-old diamond polisher who died less than one year

after a diagnosis of interstitial lung disease. He continued work

without specific treatment until three months before death when he

required continuous oxygen and systemic steroids. At autopsy there was

evidence of extensive fibrosis with interstitial giant cells. The lung

cobalt concentration was 2.1 µg/g. The authors suggested that oxygen

therapy may have exacerbated this man’s deterioration via

cobalt-induced hydroxyl free radical formation.

A 37 year-old female developed rapidly progressive pneumoconiosis

after working, without respiratory protection, for seven years in

sharpening and grinding operations with hard metal tools (Della Torre

et al, 1990). There was no response to steroid therapy and she died

from respiratory failure less than one year after presentation.

Interestingly, although the lung cobalt concentration in

bronchoalveolar lavage fluid was increased on presentation (2 µg/L,

reference value 0.6 µg/L) the cobalt concentration at open biopsy four

months later was not raised significantly, supporting the hypothesis

that cobalt-induced lung damage is immunologically mediated rather

than a direct effect.

Allergic alveolitis

An allergic alveolitis has been described in hard-metal workers with

cough, dyspnoea and flu-like symptoms associated with bilateral

crackles, radiographic small nodular infiltrates and a restrictive

lung function defect (Sjögren et al, 1980; Cugell, 1992). These

abnormalities may reverse if exposure ceases but with continued cobalt

inhalation irreversible fibrosis is likely (Cugell, 1992).

Occupational asthma

Hard metal workers may develop occupational asthma with cough, wheeze

and dyspnoea that characteristically improves during week-ends and

holidays (Sprince et al, 1988; Cugell, 1992). Similar symptoms have

been described in diamond workers exposed to cobalt in polishing discs

(Gheysens et al, 1985).

In a study of 703 hard metal workers Kusaka et al (1996a) identified

age (>40 years), atopy and cobalt exposure as risk factors for

asthma. Surprisingly, low airborne cobalt concentrations (below 50

µg/m3) posed a greater risk of hard metal asthma than did higher air

cobalt concentrations (Kusaka et al, 1996a) although the observed

deterioration in ventilatory function seemed to be related to duration

of cobalt exposure (Kusaka et al, 1996b). In this study there was no

significant difference in asthma prevalence between those exposed to

the elemental (dust) or ionized (mist) metal (Kusaka et al, 1996a).

Cobalt asthma is associated in some, but not all, cases with

circulating cobalt-specific IgE and generalized bronchial

hyperresponsiveness (Coates and Watson 1971; Sjögren et al, 1980;

Kusaka et al, 1989; Shirakawa et al, 1989; Cugell, 1992). Respiratory

cross-reactivity between cobalt and nickel has also been described

(Shirakawa et al, 1990).

Cardiovascular toxicity

Patients with fulminant hard metal pneumoconiosis may, after several

years, develop cor pulmonale with clinical and radiological features

of pulmonary hypertension and right heart failure (Bech et al, 1962).

Cobalt cardiomyopathy is associated most frequently with chronic

excess cobalt chloride or cobalt sulphate ingestion (see above) but an

identical syndrome has been reported occasionally in those exposed

occupationally (Barborik and Dusek, 1972; Jarvis et al, 1992).

Kennedy et al (1981) reported fatal cardiogenic shock in a 48 year-old

hard metal worker following routine vagotomy and pyloroplasty for

duodenal ulceration. The patient, who had handled tungsten carbide and

cobalt dust for four years, initially developed signs of

cardiovascular compromise during the operation and gradually

deteriorated without evidence of ischaemic heart disease. At

post-mortem the heart was dilated with extensive myocardial fibrosis

and a myocardial cobalt concentration of 7 µg/g (normal range

0.1-0.4).

There is limited evidence that hard metal workers may develop

electrocardiographic abnormalities and/or impaired left ventricular

function after chronic cobalt exposure (Horowitz et al, 1988; Evans et

al, 1993) but the significance of these studies is uncertain.

Neurotoxicity

Jordan et al (1990) reported significantly impaired attention

(p<0.05) and verbal memory (p<0.001) in 12 hard metal workers

exposed to tungsten carbide and cobalt (as dust and dissolved in an

organic solvent) compared to healthy unexposed controls. However, all

members of the study group had “pulmonary manifestations” of hard

metal disease which may have affected performance.

A patient exposed occupationally (mainly via inhalation) to cobalt

dust for 20 months developed bilateral optic atrophy and bilateral

nerve deafness. Fourteen months after stopping work visual acuity

improved and hearing returned to normal (Meecham and Humphrey, 1991).

Nephrotoxicity

Lechleitner et al (1993) reported Goodpasture’s syndrome in a 26

year-old hard metal worker with severe interstitial lung disease and

fulminant glomerulonephritis. The role of heavy metal exposure in the

aetiology of this case is not known though the authors proposed

cobalt-induced ß-cell activation or exposure of pulmonary basement

membrane antigens as possible disease mechanisms.

Ocular toxicity

Optic atrophy occurring in association with chronic cobalt inhalation

is discussed above (Neurotoxicity).

Ingestion

Dermal toxicity

The administration of disulfiram in the treatment of ethanol abuse has

led to an exacerbation of cobalt dermatitis presumably via

diethyldithiocarbamate (a disulfiram metabolite) chelation and

mobilization of cobalt in a manner similar to that reported in nickel

sensitive subjects (Menné, 1985).

Gastrointestinal toxicity

Gastrointestinal symptoms similar to those occurring after acute

cobalt chloride ingestion have also complicated chronic therapy. A 35

year-old woman with anaemia treated with cobalt chloride 25 mg qds

complained of nausea, vomiting and weight loss in addition to

neurological symptoms (Schirrmacher, 1967).

One of 12 renal failure patients on haemodialysis treated with cobalt

chloride 25-50 mg daily had to discontinue therapy after ten days due

to nausea and constipation. Symptoms resolved on withdrawal of cobalt

supplements (Duckham and Lee, 1976).

Increased serum triglyceride concentrations have been noted in

cobalt-treated anephric patients and although hepatic glucagon

resistance was postulated as the cause this has not been confirmed

(Taylor and Marks, 1978). Cobalt-induced inhibition of lipoprotein

lipase is now thought likely to be relevant (Taylor and Marks, 1978).

Cardiovascular toxicity

Congestive cardiomyopathy has been reported in people who drank large

quantities of beer to which cobalt chloride/sulphate had been added as

a foam stabilizer (Morin et al, 1967; Kesteloot et al, 1968; Sullivan

et al, 1969) and in those receiving oral cobalt chloride therapy

(Manifold et al, 1978).

In a study of 28 cases of cobalt beer cardiomyopathy (Alexander, 1972)

symptoms of cardiac failure were of fairly abrupt onset (mean duration

at presentation 10 weeks) and variable severity with five deaths from

cardiogenic shock and a full physical recovery in only 11 patients.

Cardiomegaly, a pericardial effusion and polycythaemia were present in

the majority with pleural effusion in 11 cases though radiological

evidence of pulmonary oedema “characteristically ….. was absent”.

Profound lactic acidosis was a prominent feature in severe cases.

Electrocardiographic abnormalities included p pulmonale or p mitrale,

axis (usually right) deviation and acute ischaemic changes in the

precordial leads typically associated with increased plasma cardiac

enzyme activities. Electron microscopy of myocardial tissue from these

patients showed extensive myofibril degeneration with abnormal

mitochondria containing electron-dense bodies believed to incorporate

cobalt. It is probable that alcohol and malnutrition contributed to

the cardiotoxicity observed in these and other cases since the

absolute quantities of cobalt ingested often were small (up to 10 mg

daily) (Kesteloot et al, 1968; Alexander, 1972).

Curtis et al (1976) described a haemodialysis patient who died three

months after “a course” of cobalt chloride. At post mortem the

myocardial cobalt concentration was 1.65 µg/g, some 25-80 times

greater than myocardial cobalt concentrations in haemodialysis

patients who had not received cobalt. These authors noted also that

patients treated with oral cobalt chloride had significantly higher

(p=0.001) blood cobalt concentrations than haemodialysis patients who

had not received cobalt. In another report a 17 year-old girl on

maintenance haemodialysis died from rapidly progressive dilated

cardiomyopathy after nine months cobalt chloride therapy (25 mg bd)

for anaemia. At necropsy the myocardial cobalt concentration was 8.9

µg/g (Manifold et al, 1978).

Neurotoxicity

After six months treatment with cobalt chloride 25 mg qds for anaemia

a 35 year-old woman developed limb paraesthesiae, an unsteady gait,

impaired hearing and dizzy spells in addition to nausea, vomiting and

weight loss (Schirrmacher, 1967). Clinical examination confirmed

bilateral nerve deafness, absent ankle reflexes and impaired vibration

sense. All symptoms and signs resolved with four months of cobalt

chloride withdrawal.

A haemodialysis patient developed polyarthralgia and muscle weakness

after three weeks cobalt chloride therapy (25-50 mg daily). Weakness

improved following cobalt withdrawal but polyarthralgia persisted; the

patient died eight months later after renal transplantation failure

(Duckham and Lee, 1976).

Haemotoxicity

Chronic excess cobalt chloride ingestion causes polycythaemia which in

the past led to its use in the treatment of anaemia (Manifold et al,

1978). A 13 month-old child developed persistent anaemia with

polycythaemia and cardiomegaly in addition to hypothyroidism (see

below) and hypertrichosis following treatment of iron deficiency for

one year with a commercial iron-cobalt preparation. At the end of the

treatment period the serum cobalt concentration was 59 µg/L. The

haematological abnormalities and hypothyroidism resolved when the

treatment was stopped, with some improvement in cardiac size and a

fall in the serum cobalt concentration to 6.8 µg/L and 1.4 µg/L at

four and 12 months respectively (Bianchi et al, 1989).

Endocrine toxicity

Cobalt inhibits the iodination of tyrosine and goitre is a recognized

side-effect of cobalt therapy (Schirrmacher, 1967). A four year-old

boy with sickle cell anaemia admitted for tonsillectomy was noted to

have a large goitre. For seven months prior to admission the patient

had taken 60-80 mg cobalt chloride daily. The thyroid gland was

bilaterally and asymmetrically enlarged, firm, nodular, painless and

mobile (Kriss et al, 1955). The goitre disappeared one month after

cobalt chloride withdrawal.

A 13 month-old baby developed clinical and biochemical hypothyroidism

after treatment of iron deficiency for one year with a commercial

iron-cobalt preparation. The endocrine abnormality resolved when

treatment was withdrawn (Bianchi et al, 1989).

Ocular toxicity

Following treatment of pancytopenia with 73 g oral cobalt chloride

over two and a half years, a patient developed abnormal choroidal

perfusion and optic atrophy. Vision did not deteriorate further

following cessation of therapy (Licht et al, 1972).

MANAGEMENT

Dermal exposure

Removal from exposure is the priority. Most barrier creams do not

prevent the penetration of cobalt chloride through the skin (Fischer

and Rystedt, 1983b) although Fischer and Rystedt (1990) demonstrated

that polyethylene glycol effectively reduced cobalt contact

reactivity. Exacerbations of cobalt contact dermatitis respond to

topical or systemic steroids. The role of chelation therapy in cobalt

contact sensitivity is discussed below.

Ocular exposure

Decontamination with copious lukewarm water (eg via drip tubing) is

the priority. Topical anaesthesia may be necessary, particularly to

ensure removal of particles from the conjunctival recesses. Seek an

ophthalmic opinion if symptoms persist or there are abnormal

examination findings.

Inhalation

Exposure must be discontinued if occupational cobalt lung disease is

suspected or confirmed. Asthmatic symptoms respond to conventional

measures (Pisati and Zedda, 1994). Established pulmonary fibrosis has

a generally poor prognosis although there are reports of substantial

improvement following high dose steroids (prednisolone 60 mg daily

(Rolfe et al, 1992) and/or removal from the workplace (Zanelli et al,

1994). The possibility of cobalt cardiotoxicity should be remembered.

The role of blood and urine cobalt concentration measurements is

discussed below (Medical Surveillance).

Ingestion

Decontamination

Gastric lavage is unlikely to be helpful since if spontaneous vomiting

does not occur the ingestion is almost certainly too small to cause

significant toxicity. Concentrated solutions are acidic and gastric

lavage is contraindicated if corrosive damage is a possibility. There

is no evidence that oral activated charcoal reduces gastrointestinal

cobalt absorption.

Supportive measures

Following acute cobalt chloride ingestion supportive care is usually

all that is required with intravenous fluid replacement if vomiting is

severe. Concentrated solutions are acidic and the possibility of

corrosive damage should be considered. Plasma creatinine, urea and

electrolytes and full blood count should be measured. If chronic

cobalt toxicity is suspected a thorough cardiovascular and

neurological (including fundoscopy) assessment should be undertaken.

Thyroid function tests should be performed. The role of chelation

therapy is discussed below (Antidotes). The presence of cobalt in

blood and urine confirms exposure but blood and urine concentrations

require careful interpretation (see Medical Surveillance) and these

assays are not widely available.

Antidotes

Sodium calciumedetate

Animal studies

Post (1955) observed that rats administered sodium calciumedetate

subcutaneously following intraperitoneal cobalt chloride injection did

not show the polycythaemic response induced in controls (treated with

cobalt only). Subsequent studies (Domingo et al, 1983; Llobet et al,

1985; Llobet et al, 1986) provided further evidence for sodium

calciumedetate as an effective cobalt chelator.

All mice administered intraperitoneal cobalt chloride at doses

approximating to the LD50 – LD95 (0.6-1.8 mmol/kg), immediately

followed by 4.3 mmol/kg intraperitoneal sodium calciumedetate survived

two weeks with significantly increased urine cobalt elimination in the

24 hours post antidote administration (Llobet et al, 1986). Llobet et

al (1988) later demonstrated significantly increased (p<0.05) faecal

but not urinary cobalt elimination during a five day course of

chelation therapy in cobalt-poisoned rats (administration details as

below).

Clinical studies

Topical

Allenby and Basketter (1989) found a positive patch test reaction to

one per cent aqueous cobalt chloride was abolished in five out of six

subjects by the concomitant application of an equimolar sodium

calciumedetate solution.

Systemic

A 14 year-old female who ingested approximately 130 mg cobalt chloride

was asymptomatic but treated with intravenous sodium calciumedetate 1g

tds for three doses on the basis of a raised serum cobalt

concentration (78 µg/L 12 hours post ingestion) (Everson et al, 1988).

No cobalt excretion data were presented. The serum cobalt

concentration had fallen to 7 µg/L 22 hours post ingestion and the

child remained well.

No cobalt was recovered in the urine of a patient with cobalt

cardiomyopathy who received a one week course of sodium calciumedetate

(and penicillamine, doses not stated) but treatment was not instituted

until three years after cobalt ingestion (quantity not stated)

(Alexander, 1972).

DMSA

Animal studies

Aposhian (1983) cited early animal studies published in the Chinese

literature (in 1965) which showed that DMSA 4 mmol/kg (route not

stated) increased threefold the LD50 of cobalt chloride-poisoned

mice.

Four of ten mice administered 1.8 mmol/kg intraperitoneal cobalt

chloride (a dose exceeding the LD95) immediately followed by

intraperitoneal DMSA 3.4 mmol/kg, survived two weeks (Llobet et al,

1986). Under these experimental conditions DMSA was a less effective

cobalt chelator than sodium calciumedetate or DTPA

(diethylenetriamine-pentacetic acid) (see below).

DMSA 1.2 mmol/kg/day intraperitoneally increased urine cobalt

excretion significantly (p<0.01) only on the final (fifth) day of

chelation in rats poisoned with cobalt chloride (0.06 mmol/kg/day

intraperitoneally three days per week for four weeks) (Llobet et al,

1988). In the same study faecal cobalt elimination was increased

significantly during the first four days of chelation therapy (p<0.05

days one, two and four, p<0.01 day three).

DTPA

Animal studies

Llobet et al (1986) reported 70 per cent two week survival in mice

administered intraperitoneal DTPA 3.1 mmol/kg immediately following

intraperitoneal loading with 1.8 mmol/kg cobalt chloride (a dose in

excess of the LD95). In a later study (Llobet et al, 1988) DTPA 1.2

mmol/kg/day significantly (p<0.05) enhanced faecal and urine cobalt

elimination.

Other chelating agents

Animal studies

Intraperitoneal L-histidine 2.7 mmol/kg administered immediately after

oral cobalt chloride (4.2 mmol/kg, approximately the oral LD95)

resulted in 90 per cent seven day survival compared to 15 per cent

survival in animals treated with cobalt chloride only (Domingo et al,

1985a).

Domingo et al (1985b) suggested that N-acetylcysteine (NAC) was

ineffective in reducing experimental cobalt fatalities unless

administered as a cobalt-NAC chelate. However, Llobet et al (1985)

demonstrated that glutathione and NAC (each 3.5 mmol/kg

intraperitoneally) immediately after intraperitoneal cobalt chloride

(0.70 mmol/kg, the LD50) improved survival. In a later study (Llobet

et al, 1988) glutathione and NAC (both 1.2 mmol/kg/day

intraperitoneally) significantly (p<0.05 and p<0.01 respectively)

increased urine and faecal cobalt excretion in cobalt poisoned rats,

with a significant (p<0.05) reduction in the spleen cobalt

concentration compared to controls.

Clinical studies

Topical clioquinol one per cent significantly (p<0.001) reduced patch

test reactions to cobalt in 29 cobalt-sensitive individuals. However

the authors emphasized this chelating agent is not suitable for

regular application since it is itself an allergen (Fischer and

Rystedt, 1990). There is also a risk of systemic uptake if clioquinol

is topically applied chronically. Clioquinol absorption may be

associated with neurological side-effects including peripheral

neuropathy and delirium (Rose, 1986).

Antidotes: Conclusions and recommendations

There are no human controlled data regarding the use of chelating

agents in cobalt(II) poisoning.

Animal studies suggest sodium calciumedetate and DTPA are the

most effective cobalt chelators although NAC and glutathione are

less toxic alternatives.

Following severe cobalt poisoning by ingestion the use of

chelation therapy may be considered; discussion of individual

cases with an NPIS physician is recommended.

There is no evidence that chelation therapy reduces the pulmonary

cobalt burden following chronic inhalation. Moreover, the value

of cobalt chelation my be limited where immunological mechanisms

play an important part in cobalt toxicity.

The role of topical chelating agents in cobalt dermatitis remains

unproven and is likely to be limited by practical difficulties.

Chemotherapy

Balmes (1987) reported a 28 year-old lady with aggressive hard metal

pneumoconiosis unresponsive to prednisolone (40-60 mg daily) who

clinically improved significantly after two months low-dose

cyclophosphamide therapy (25 mg bd).

Haemodialysis

In a patient with uraemic cardiomyopathy and a high serum cobalt

concentration (0.24 ppb), Lins and Pehrsson (1976) reported reduced

cardiac size in association with a fall in the serum cobalt

concentration to 0.07 ppb during haemodialysis. However no cobalt

dialysis clearance data or details of dialysis duration were given.

AT RISK GROUPS

Patients with renal failure are at risk of cobalt toxicity if

administered oral cobalt containing pharmaceuticals (Curtis et al,

1976); these preparations are not available in the UK.

MEDICAL SURVEILLANCE

Regular monitoring of workplace airborne cobalt concentrations (Sala

et al, 1994), strict attention to personal hygiene (Scansetti et al,

1994; Linnainmaa and Kiilunen, 1997) and periodic assessment for

pulmonary or dermatological symptoms are important in the prevention

of cobalt toxicity.

Some studies suggest airborne cobalt concentrations frequently are

underestimated (Auchincloss et al, 1992; Mosconi et al, 1994) and

other workers recently have reported average cobalt airborne

concentrations in a hard metal factory greatly exceeding the

recommended occupational exposure limit (Kumagai et al, 1996).

Furthermore, significant reductions in FEV1 and FVC have been

observed in workers exposed to airborne cobalt concentrations lower

than 50 µg/m3 (Nemery et al, 1992).

Sjögren et al (1980) noted that the development of cobalt contact

dermatitis among hard metal workers often preceded pulmonary disease

and suggested that those with a positive cobalt patch test should be

removed immediately from exposure. However, in another study, only two

of nine hard metal workers sensitive to inhaled cobalt had a positive

cobalt patch test (Kusaka et al, 1986).

Abnormal clinical findings should be investigated conventionally with

particular attention to establishing a temporal relationship to

workplace exposure in those with possible occupational asthma or

alveolitis. The presence of cobalt-specific IgE in plasma or cobalt

particles in bronchoalveolar lavage fluid or lung biopsy tissue may be

useful.

Increased blood and urine cobalt concentrations frequently are

encountered in hard metal workers (Ichikawa et al, 1985; Della Torre

et al, 1990; Stebbins et al, 1992; Linnainmaa and Kiilunen, 1997) but

are more useful as grouped rather than individual data (Sabbioni et

al, 1994) and their significance requires careful interpretation. A

potential role for hair and nail cobalt concentrations as indicators

of chronic exposure has not been substantiated (Della Torre et al,

1990).

In workers exposed to cobalt dust in a plant producing diamond-cobalt

saws urine cobalt concentrations reflected recent rather than

cumulative cobalt exposure (Gennart and Lauwerys, 1990). Lison et al

(1994) concluded that urine and blood cobalt concentrations correlated

reasonably well with recent occupational exposure to soluble forms of

cobalt.

Normal concentrations in biological fluids

In unexposed individuals normal cobalt concentrations are 0.1-1.2 µg/L

in blood (and serum) and 0.1-2.3 µg/L in urine (spot samples)

(Alexandersson, 1988).

OCCUPATIONAL DATA

Maximum exposure limit

Long-term exposure limit (8 hour TWA reference period) 0.1 mg/m3

(Health and Safety Executive, 1997).

OTHER TOXICOLOGICAL DATA

Carcinogenicity

Animal studies suggest cobalt and its compounds are carcinogenic.

While several studies have shown that hard metal workers exhibit

excess lung cancer mortality, there is inadequate evidence for cobalt

or its compounds to be classed as carcinogenic in man (IARC, 1991).

Assessment of human cancer risk is often confounded by simultaneous

tobacco consumption, exposure to nickel and arsenic and small study

population numbers (Mur et al, 1987; Jensen and Tüchsen, 1990).

Mur et al (1987) observed excess lung cancer mortality (standardized

mortality ratio = 4.66) in 1143 workers employed between 1950 and 1980

in a cobalt and sodium producing plant; smoking habits in the study

population were not assessed. A follow-up study from 1981-88 failed to

show a relationship between lung cancer and cobalt exposure (Moulin et

al, 1993).

Lasfargues et al (1994) reported significantly higher lung cancer

mortality among 709 hard metal workers (employed for at least one

year) compared to controls, though the study was too small to be

conclusive.

Reprotoxicity

Cobalt chloride induced hypoxic testicular damage in rats when

administered orally (Mollenhauer et al, 1985). Pedigo and Vernon

(1993) observed reversible infertility in male mice exposed to 400 ppm

cobalt chloride for 10 weeks. Reduced sperm function led to increased

preimplantation embryo loss when these animals were mated.

There are no data confirming human reprotoxicity in association with

cobalt or cobalt compounds although occupational cobalt exposure has

been linked to miscarriages in Finland (Reprotox, 1997; Reprotext,

1997).

Genotoxicity

Cobalt chloride induced gene conversions in the yeast S cerevisiae

(DOSE, 1993).

Kasprzak et al (1994) observed oxidative DNA base damage in renal,

hepatic and pulmonary chromatin of rats after intraperitoneal

injection of cobalt salts.

Fish toxicity

LC50 (96 hr) carp embryo 96 mg/L. Static bioassay in freshwater, pH

7.5, temperature 16°C, water hardness 360 mg/L CaCO3.

The common carp hatching process was impaired by cobalt chloride in a

dose related manner.

Adult giant gourami exposed to 232.8 mg/L for 24, 72 and 96 hr

(freshwater static bioassay, pH 7.5, temperature 23.6°C, water oxygen

content 7.6 mg/L and water hardness 164 mg/L CaCO3) showed blood

pyruvate concentrations increased by 22, 75 and 47 per cent

respectively.

LC50 (96 hr) fathead minnow 48 mg/L; lakewater static bioassay, pH

6.5-8.5, temperature 20°C, water hardness 130 mg/L CaCO3.

LC50 (48 hr) Olyzias latipes 620 ppm (DOSE, 1993).

EC Directive on Drinking Water Quality 80/778/EEC

Chlorides: Maximum admissible concentration 25 mg/L. Concentration

above which effects might occur 200 mg/L (DOSE, 1993).

WHO Guidelines for Drinking Water Quality

NIF

AUTHORS

SM Bradberry BSc MB MRCP

P Sabatta MSc

JA Vale MD FRCP FRCPE FRCPG FFOM

National Poisons Information Service (Birmingham Centre),

This monograph was produced by the staff of the Birmingham Centre of

the National Poisons Information Service in the United Kingdom. The

work was commissioned and funded by the UK Departments of Health, and

was designed as a source of detailed information for use by poisons

information centres.

Date of last revision

28/1/98

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See Also:

Cobalt (II) chloride (ICSC)

SECTION 1. CHEMICAL IDENTIFICATION

CHEMINFO Record Number: 345

CCOHS Chemical Name: Methyl ethyl ketone peroxide

Synonyms:

2-Butanone peroxide

Ethyl methyl ketone peroxide

MEKP

MEK peroxide

Methyl ethyl ketone hydroperoxide

Peroxyde de methylethylcetone

Chemical Name French: Peroxyde de méthyl éthyl cétone

Chemical Name Spanish: Peróxido de metiletilcetona

Trade Name(s):

Butanox LPT

FR 222

Hi-Point 180

Ketonox

Lupersol

Permek N

CAS Registry Number: 1338-23-4

RTECS Number(s): EL9480000 EL9470000 EL9450000

EU EINECS/ELINCS Number: 215-661-2

Chemical Family: Organic peroxide / ketone peroxide / alkanone peroxide

Molecular Formula: C8-H16-O4

SECTION 2. DESCRIPTION

Appearance and Odour:

Colourless liquid with a characteristic odour.

Odour Threshold:

Not available

Warning Properties:

Information not available for evaluation

Composition/Purity:

Commercially available as a mixture of approximately 60% MEKP and 40% diluent to reduce its sensitivity to shock. Diluents may be any combination of dimethyl phthalate, cyclohexanone peroxide or diallyl phthalate. Consult your manufacturer/supplier or Material Safety Data Sheet (MSDS) for complete information on the composition and hazards of the product you are using.

Uses and Occurrences:

Used as a polymerization catalyst in the manufacture of polyester and acrylic resins. Used as a hardening agent for fiberglass reinforced plastics.

SECTION 3. HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW:

Colourless liquid with a characteristic odour. Extreme risk of explosion by shock, friction, flame or other sources of ignition for pure peroxide. OXIDIZER. DANGEROUSLY REACTIVE. May decompose violently. Commercial products, which contain diluents, can form explosive mixtures at, or above, 52-93 deg C. Contact with water or moist air liberates irritating gases. Contents may develop pressure if exposed to water. VERY TOXIC. May be fatal if inhaled, absorbed through the skin or swallowed. CORROSIVE to the eyes, skin and respiratory tract. May cause lung injury–effects may be delayed.

POTENTIAL HEALTH EFFECTS

Effects of Short-Term (Acute) Exposure

Inhalation:

Inhalation of mist or vapour can cause irritation of the nose, sore throat, coughing, shortness of breath and difficulty breathing. In extreme cases, life threatening accumulation of fluid in the lungs (pulmonary edema) may occur. The symptoms of pulmonary edema often do not occur until a few hours have passed, and they are aggravated by physical effort. In some cases, pulmonary edema may be delayed in onset up to 24-72 hours after exposure.

Skin Contact:

MEKP is corrosive. Direct contact with concentrated solutions will cause irritation, redness, pain and blistering. Permanent scarring may result.

MEKP can be absorbed by skin, which can cause certain blood disorders such as hemolytic anemia.(9)

Eye Contact:

Corrosive. Direct contact will cause irritation, redness, pain and blurred vision. Blindness or other permanent damage may result.

Ingestion:

Corrosive. Ingested MEKP can burn the lips, tongue, mouth, throat, esophagus (tube leading to the stomach) and the stomach. Abdominal pain, vomiting and diarrhea can occur. Permanent damage may result. Liver and kidney injury may occur. In extreme cases, death may result.

A man who accidentally ingested a solution of MEKP in dimethyl phthalate died. Symptoms included cardiac arrest, abdominal burns, severe metabolic acidosis, rapid liver failure, muscle disintegration and respiratory insufficiency. Death occurred after 4 days from hepatic coma (coma accompanying advance liver disease).(9)

Ingestion is not a typical route of occupational exposure.

Effects of Long-Term (Chronic) Exposure

Skin:

Repeated skin contact may cause dermatitis (redness, itching, thickening, scaling of skin).

No other health effects have been reported from long-term exposure to MEKP.

Carcinogenicity:

No human information. Animal studies are inconclusive.

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

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

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

Teratogenicity and Embryotoxicity:

No information available.

Reproductive Toxicity:

Information not available

Mutagenicity:

No information available.

Toxicologically Synergistic Materials:

Information not available

Potential for Accumulation:

Probably does not accumulate. Very reactive with human tissues.

SECTION 4. FIRST AID MEASURES

Inhalation:

Remove source of contamination or move victim to fresh air. If breathing is difficult, oxygen may be beneficial if administered by a person trained in its use, preferably on a doctor’s advice. Obtain medical attention immediately. NOTE: Symptoms of pulmonary edema may not become evident until several hours after exposure.

Skin Contact:

Avoid direct contact with this chemical. Wear chemical protective gloves, if necessary. As quickly as possible, flush contaminated area with lukewarm, gently flowing water for at least 20-30 minutes, by the clock. If irritation persists, repeat flushing. DO NOT INTERRUPT FLUSHING. If necessary, keep emergency vehicle waiting. Under running water, remove contaminated clothing, shoes and leather goods (e.g. watchbands, belts). Transport victim to an emergency care facility immediately. Discard contaminated clothing, shoes and leather goods.

Eye Contact:

Avoid direct contact. Wear chemical protective gloves, if necessary. Immediately flush the contaminated eye(s) with lukewarm, gently flowing water for at least 20-30 minutes, by the clock, while holding the eyelid(s) open. Neutral saline solution may be used as soon as it is available. DO NOT INTERRUPT FLUSHING. If necessary, keep emergency vehicle waiting. Take care not to rinse contaminated water into the unaffected eye or onto the face. If irritation persists, repeat flushing. Quickly transport victim to an emergency care facility.

Ingestion:

Never give anything by mouth if victim is rapidly losing consciousness, is unconscious or convulsing. Have victim rinse mouth thoroughly with water. DO NOT INDUCE VOMITING. Have victim drink 240 to 300 mL (8 to 10 oz.) of water to dilute material in stomach. If milk is available, it may be administered AFTER the water is given. If vomiting occurs naturally, rinse mouth and repeat administration of water. Quickly transport victim to an emergency care facility.

First Aid Comments:

Provide general supportive measures (comfort, warmth, rest). Consult a doctor and/or the nearest Poison Control Centre for all exposures except minor instances of inhalation or skin contact.

Some recommendations in the above sections may be considered medical acts in some jurisdictions. These recommendations should be reviewed with a doctor and appropriate delegation of authority obtained, as required.

All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.

SECTION 5. FIRE FIGHTING MEASURES

Flash Point:

None available for pure material. 52-93 deg C (125-200 deg F) (micro open cup) (methyl ethyl ketone peroxide (MEKP) diluted with 40% dimethyl phthalate or other diluents).(5,9) MEKP is commonly sold diluted. The flash point will vary according to the diluent used and its concentration. Consult the manufacturer.

Lower Flammable (Explosive) Limit (LFL/LEL):

No information

Upper Flammable (Explosive) Limit (UFL/UEL):

No information

Autoignition (Ignition) Temperature:

Explosive decomposition occurs at 109 deg C (230 deg F). (MEKP diluted with 40% dimethyl phthalate).(9)

Sensitivity to Mechanical Impact:

Pure MEKP is sensitive to mechanical shock.(5,9)

Sensitivity to Static Charge:

Information not available

Combustion and Thermal Decomposition Products:

Oxygen

Fire Hazard Summary:

Dangerously reactive material. Pure MEKP is sensitive to mechanical or localized thermal shock. May decompose explosively from friction or contamination. Readily capable of detonation, or explosive decomposition, or explosive reaction. Container may explode in heat of fire. May be a combustible liquid. Commercial products, which contain diluents, can form explosive mixtures at, or above 52-93 deg C. During a fire, irritating toxic gases may be generated.

Extinguishing Media:

Small fires: Dry chemical powder, carbon dioxide, water spray or foam. Large fires: Flood fire area with water. MEKP is generally available in a diluent. Use extinguishers suitable for the diluent.

Fire Fighting Instructions:

Use extreme caution since explosive decomposition may occur under fire conditions and heat may rupture containers. Fight fire from a protected, explosion-resistant location or maximum possible distance. Approach fire from upwind to avoid hazardous vapours and toxic decomposition products.

If fire occurs in the vicinity of MEKP, use unmanned monitors and hoseholders to keep cooling streams of water on fire-exposed tanks or containers until well after the fire is out. Use flooding quantities of water. Always stay away from ends of tanks. Withdraw immediately in case of rising sound from venting safety device or any discolouration of tank due to fire.

In an advanced or massive fire, the area should be evacuated; use unmanned hoseholders or monitor nozzles. If this is is not possible, withdraw from fire area and do not attempt to fight the fire.

If a leak or spill has not ignited, use water spray to cool and disperse the vapours. Water spray may also be used to dilute spills to nonflammable mixtures and to flush spills away from ignition sources. Solid streams of water may be ineffective and spread material.

Tanks or drums should not be approached after they have been involved in a fire or heated by exposure, until they have completely cooled down. Clean-up or salvage operations should not be attempted until the MEKP is cooled. After the fire has been extinguished, explosive atmospheres may remain. Before entering area, especially confined spaces, check the atmosphere with an appropriate monitoring device.

Protection of Fire Fighters:

MEKP is very hazardous to health (inhalation and skin absorption/corrosion hazard). Do not enter without wearing specialized protective equipment suitable for the situation. Firefighter’s normal protective clothing (Bunker Gear) will not provide adequate protection. A full-body encapsulating chemical protective suit with positive pressure self-contained breathing apparatus (NIOSH approved or equivalent) may be necessary.

NATIONAL FIRE PROTECTION ASSOCIATION (NFPA) HAZARD IDENTIFICATION

NFPA – Comments:

NFPA has no listing for this chemical in Codes 49 or 325.

SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES

Molecular Weight: 176.22

Conversion Factor:

1 ppm = 7.2 mg/m3; 1 mg/m3 = 0.14 ppm at 25 deg C (calculated)

Physical State: Liquid

Melting Point: Not available

Boiling Point: 118 deg C (244 deg F) (decomposes) (5)

Relative Density (Specific Gravity): 1.12 at 15 deg C (water = 1) (5)

Solubility in Water: Soluble (5)

Solubility in Other Liquids: Very soluble in phthalate esters.

Coefficient of Oil/Water Distribution (Partition Coefficient): Log P(oct) = 0.914 (estimated) (9)

pH Value: Not available

Vapour Density: 6.1 (air = 1)

Vapour Pressure: Not available

Saturation Vapour Concentration: Not available

Evaporation Rate: Not available

Critical Temperature: Not applicable

SECTION 10. STABILITY AND REACTIVITY

Stability:

Unstable. Decomposition can be initiated by heat, sunlight, friction, mechanical shock or contamination. Commercial products are normally stabilized with a diluent such as dimethyl phthalate.

Hazardous Polymerization:

Does not occur

Incompatibility – Materials to Avoid:

Highly reactive. Vigorous decomposition can be stimulated by even trace amounts of a wide variety of contaminants, such as strong acids, bases, metals, alloys, metal salts, sulfur compounds, accelerators, reducing agents and acetone.

Hazardous Decomposition Products:

Oxygen

Conditions to Avoid:

Mechanical shock, friction, heat, sunlight.

Corrosivity to Metals:

Corrosive to copper, brass, mild steel and aluminum alloys.

SECTION 11. TOXICOLOGICAL INFORMATION

NOTE: There is no specific information available for pure MEKP.

LC50 (rat): 200 ppm (4-hour exposure) (60% MEKP, 40% dimethyl phthalate)(1)

LC50 (mouse): 170 ppm (4-hour exposure) (60% MEKP, 40% dimethyl phthalate) (1)

LD50 (oral, rat): 484 mg/kg (60% MEKP, 40% dimethyl phthalate) (1)

LD50 (oral, mouse): 470 mg/kg (probably 60% MEKP, 40% dimethyl phthalate) (7, unconfirmed)

Eye Irritation:

At a concentration of 3% in dimethyl phthalate, MEKP caused severe irritation in rabbits (scored 57/110). The maximum non-irritating concentration was 0.6% in dimethyl phthalate. The dimethyl phthalate did not contribute significantly to the observed effects.(1)

Skin Irritation:

When applied to shaved skin, methyl ethyl ketone peroxide (MEKP) diluted with 40% dimethyl phthalate caused redness, swelling and blisters in rabbits within 2 or 3 days. The maximum non-irritating concentration was 1.5%.(1)

Effects of Long-Term (Chronic) Exposure:

Ingestion:

Rats were given oral doses of MEKP (97 mg/kg) (60% MEKP with 40% dimethyl phthalate) 3 times weekly for 7 weeks. All 5 rats tested died.(1)

Carcinogenicity:

In one study, MEKP (50% solution in dibutyl phthalate) was applied twice weekly for 25 weeks to the skin of twenty mice; no tumours occurred. When a second group of mice was treated for 4 weeks with ultraviolet radiation, a few tumours occurred. Mice treated with UV radiation and then treated as above with MEKP had more tumours. It appears that MEKP was not carcinogenic, but may have had weak “promoting” activity.(4) Mice given a total dose of 7 mg MEKP (route not specified) developed a few tumours, the first of which appeared after 15 months.(8) This study provides very few experimental details. Therefore, no conclusions can be drawn about the possible carcinogenicity of MEKP.

SECTION 16. OTHER INFORMATION

Selected Bibliography:

(1) Floyd, E.P., et al. Toxicity studies of certain organic peroxides and hydroperoxides. Industrial Hygiene Journal. Vol. 19 (June 1958). p. 205-212

(2) Forsberg, K., et al. Quick selection guide to chemical protective clothing. 4th ed. Van Nostrand Reinhold, 2002

(3) Methyl ethyl ketone peroxide. Dangerous Properties of Industrial Materials Report. Vol. 5, no. 4 (July/Aug. 1985). p. 50-55

(4) Logani, M.K., et al. Skin-tumour promoting activity of methyl ethyl ketone peroxide–a potent lipid-peroxidizing agent. Ed. Chem. Toxic. Vol. 22, no. 11 (1984). p. 879-882

(5) Compendium of safety data sheets for research and industrial chemicals. Part I. VCH Publishers, 1985. p. 228-229

(6) Encyclopaedia of occupational health and safety. 3rd rev. ed. Vol. 2. International Labour Organization, 1983. p. 1611-1614

(7) Toxicity in plastic manufacture. Journal of the American Medical Association. Vol. 165, no. 2 (Sept. 14, 1957). p. 201-202

(8) Kotin, Paul, et al. Organic peroxides, hydrogen peroxide, epoxides, and neoplasia. Radiation Research Supplement. Vol. 3 (1963). p. 193-211

(9) HSDB record for 2-butanone peroxide. Last revision date: 92/01/28

(10) NIOSH pocket guide to chemical hazards. NIOSH, June 1994. p. 208-209

(11) Sigma-Aldrich Canada Ltd. URL: http://www.sigma-aldrich.com/saws.nsf/Technical+Library?OpenFrameset

(12) Occupational Safety and Health Administration (OSHA). Methyl Ethyl Ketone Peroxide. In: OSHA Analytical Methods Manual. Revision Date: Oct. 31, 2001. Available at:

(13) National Institute for Occupational Safety and Health (NIOSH). Methyl Ethyl Ketone Peroxide. In: NIOSH Manual of Analytical Methods (NMAM(R)). 4th ed. Edited by M.E. Cassinelli, et al. DHHS (NIOSH) Publication 94-113. Aug. 1994. Available at:

Review/Preparation Date: 1995-11-06

Revision Indicators:

HANDLING AND STORAGE 1995-09-01

Sampling 1996-01-01

EU class 1996-01-01

US transport 1998-03-01

Resistance of materials 1998-06-01

Bibliography 1998-06-01

UN/NA No 2002-12-18

TDG 2002-12-18

First aid skin 2003-05-16

Personal hygiene 2003-05-26

WHMIS detailed classification 2003-10-06

WHMIS proposed classification 2003-10-06

Flash point 2003-10-06

Fire hazard summary 2003-10-06

Emergency overview 2003-10-06

Short-term skin contact 2003-10-06

Handling 2003-10-06

Extinguishing media 2003-10-08

Fire fighting instructions 2003-10-08

Protection of fire fighters 2003-10-08

PEL-C final 2003-11-11

PEL-TWA transitional 2003-11-11

Bibliography 2005-03-16

Passive Sampling Devices 2005-03-16

Sampling/analysis 2005-03-16

1,3-BIS(AMINOMETHYL)BENZENE

1,3-Bis(aminomethyl)benzene (ICSC)

(2-BUTOXYETHOXY)-2-PROPANOL, 1-

1-(2-Butoxyethoxy)-2-Propanol (CHEMINFO)

1,3-BUTADIENE

1,3-butadiene (CHEMINFO)

2-ETHYL-1-BUTANOL

2-ethyl-1-butanol (CHEMINFO)

2-ETHYLHEXYL LACTATE

2-ethylhexyl lactate (CHEMINFO)

2,2′-DIPYRIDYL

2,2′-Dipyridyl (ICSC)

2-METHYL-1-PENTANOL

2-methyl-1-pentanol (CHEMINFO)

ACEPHATE

Acephate (PIM 734)

ACETAL

Acetal (ICSC)

ACETALDEHYDE

Acetaldehyde (CHEMINFO)

Acetaldehyde (EHC 167, 1995)

Acetaldehyde (IARC Summary & Evaluation, Volume 71, 1999)

Acetaldehyde (ICSC)

ACETAMIDE

Acetamide (IARC Summary & Evaluation, Supplement 7, 1987)

Acetamide (IARC Summary & Evaluation, Volume 7, 1974)

Acetamide (ICSC)

ACETIC ACID

Acetic acid (ICSC)

Acetic acid (solutions greater than 10%) (CHEMINFO)

Acetic acid (solutions of 10% or less) (CHEMINFO)

ACETIC ANHYDRIDE

Acetic anhydride (CHEMINFO)

Acetic anhydride (ICSC)

ACETONE

Acetone (CHEMINFO)

Acetone (EHC 207, 1998)

Acetone (ICSC)

ACETONITRILE

Acetonitrile (CHEMINFO)

Acetonitrile (EHC 154, 1993)

Acetonitrile (ICSC)

ACETYLENE

Acetylene (CHEMINFO)

Acetylene (ICSC)

ACETYLOXYBENZOIC ACID, 2-

Acetyloxybenzoic acid, 2- (ICSC)

ACROLEIN

Acrolein (EHC 127, 1991)

Acrolein (IARC Summary & Evaluation, Volume 63, 1995)

Acrolein (ICSC)

ACRYLAMIDE

Acrylamide (EHC 49, 1985)

Acrylamide (IARC Summary & Evaluation, Volume 60, 1994)

Acrylamide (ICSC)

Acrylamide (PIM 652)

Acrylamide solid (CHEMINFO)

Acrylamide solutions (CHEMINFO)

ACRYLIC ACID

Acrylic acid (CHEMINFO)

Acrylic acid (EHC 191, 1997)

Acrylic acid (ICSC)

ACRYLONITRILE

Acrylonitrile (CHEMINFO)

Acrylonitrile (EHC 28, 1983)

Acrylonitrile (IARC Summary & Evaluation, Volume 71, 1999)

Acrylonitrile (ICSC)

ADIPIC ACID

Adipic acid (CHEMINFO)

ALACHLOR

Alachlor (PDS)

ALDICARB

Aldicarb (EHC 121, 1991)

Aldicarb (IARC Summary & Evaluation, Volume 53, 1991)

Aldicarb (ICSC)

Aldicarb (PDS)

ALDRIN

Aldrin (IARC Summary & Evaluation, Supplement 7, 1987)

Aldrin (IARC Summary & Evaluation, Volume 5, 1974)

Aldrin (PDS)

Aldrin (PIM 573)

Aldrin and Dieldrin (EHC 91, 1989)

ALKALIS

Alkalis (Group PIM G012)

ALLETHRIN

Allethrin (ICSC)

Allethrin (UK PID)

Allethrins (EHC 87, 1989)

d-Allethrin (ICSC)

ALLYL PROPYL DISULFIDE

Allyl propyl disulfide (CHEMINFO)

ALUMINIUM & SALTS

Aluminium (CHEMINFO)

Aluminium (EHC 194, 1997)

Aluminium nitrate (CHEMINFO)

Aluminium phosphate, tribasic (CHEMINFO)

ALUMINIUM CHLORIDE

Aluminium chloride hexahydrate (CHEMINFO)

Aluminium chloride solutions (CHEMINFO)

Aluminium chloride, anhydrous (CHEMINFO)

Aluminium chloride, (anhydrous) (ICSC)

ALUMINIUM HYDROXIDE

Aluminium hydroxide (CHEMINFO)

ALUMINIUM OXIDE

Aluminum oxide (UK PID)

ALUMIUM SULFATE

Aluminum sulfate (UK PID)

Aluminum sulfate octadecahydrate (CHEMINFO)

Aluminum sulfate, anhydrous (CHEMINFO)

AMITROLE

Amitrole (EHC 158, 1994)

Amitrole (IARC Summary & Evaluation, Supplement 7, 1987)

Amitrole (IARC Summary & Evaluation, Volume 41, 1986)

Amitrole (IARC Summary & Evaluation, Volume 7, 1974)

Amitrole (ICSC)

Amitrole (PDS)

Amitrole (PIM 648)

AMMONIA

Ammonia (anhydrous) (ICSC)

Ammonia (EHC 54, 1986)

Ammonia, anhydrous (CHEMINFO)

AMMONIUM BISULFIDE

Ammonium bisulfide (ICSC)

AMMONIUM CHLORIDE

Ammonium chloride (CHEMINFO)

AMMONIUM FORMATE

Ammonium formate (CHEMINFO)

AMMONIUM FLUORIDE

Ammonium fluoride (ICSC)

AMMONIUM HYDROXIDE

Ammonium hydroxide (CHEMINFO)

Ammonium hydroxide (ICSC)

AMMONIUM NITRATE

Ammonium nitrate (PIM 964)

AMYL ACETATE

Isoamyl acetate (CHEMINFO)

Isoamyl acetate (ICSC)

n-Amyl acetate (CHEMINFO)

n-Amyl acetate (ICSC)

sec-Amyl acetate (CHEMINFO)

sec-Amyl acetate (ICSC)

Amyl acetate, mixed isomers (CHEMINFO)

AMYLAMINE (MIXED ISOMERS)

Amylamine (mixed isomers) (CHEMINFO)

ANILINE

Aniline (CHEMINFO)

Aniline (IARC Summary & Evaluation, Supplement 7, 1987)

Aniline (IARC Summary & Evaluation, Volume 4, 1974)

Aniline (ICSC)

ANISIDINE

m-Anisidine (ICSC)

Anisidine (ICSC)

ANTIMONY

Antimony (ICSC)

Antimony (UK PID)

ANTIMONY III TRICHLORIDE

Antimony III trichloride (UK PID)

Antimony trichloride (ICSC)

ANTIMONY PENTACHLORIDE

Antimony pentachloride (UK PID)

ANTIMONY TRIOXIDE

Antimony trioxide (UK PID)

Antimony trioxide (ICSC)

ANTIMONY TRISULPHIDE

Antimony trisulphide (UK PID)

ARGON LIQUID

Argon liquid (CHEMINFO)

Argon (ICSC)

ARSENIC

Arsenic (EHC 18, 1981)

Arsenic (Group PIM G042)

Arsenic (ICSC)

Arsenic and arsenic compounds (second edition) (EHC 224, 2001)

ARSENIC ACID

Arsenic acid (UK PID)

ARSENIC DISULPHIDE

Arsenic disulphide (UK PID)

ARSENIC TRIOXIDE

Arsenic trioxide (UK PID)

ARSENIC TRISULPHIDE

Arsenic trisulphide (UK PID)

ARSENOUS TRICHLORIDE

Arsenous trichloride (ICSC)

ARSINE

Arsine (ICSC)

Arsine (PIM 044)

ASBESTOS

Asbestos (EHC 53, 1986)

Asbestos (IARC Summary & Evaluation, Supplement 7, 1987)

Asbestos (IARC Summary & Evaluation, Volume 14, 1977)

Asbestos (IARC Summary & Evaluation, Volume 2, 1973)

ASPHALT

Asphalt (ICSC)

ATRAZINE

Atrazine (IARC Summary & Evaluation, Volume 53, 1991)

Atrazine (IARC Summary & Evaluation, Volume 73, 1999)

Atrazine (PIM 837)

Atrazine (PDS)

AZAMETHIPHOS

Azamethiphos (PIM 738)

AZINPHOS ETHYL

Azinphos ethyl (PIM 054)

Azinphos-Ethyl (PDS)

AZINPHOS METHYL

Azinphos methyl (PDS)

Azinphos methyl (PIM 739)

AZOBIS

Azobis (isobutyronitrile) (ICSC)

BARIUM

Barium (EHC 107, 1990)

Barium and salts (Group PIM G004F, French)

BARIUM CHLORATE

Barium chlorate (ICSC)

BARIUM NITRATE

Barium nitrate (ICSC)

BENDIOCARB

Bendiocarb (PDS)

BENOMYL

Benomyl (EHC 148, 1993)

Benomyl (ICSC)

Benomyl (PDS)

BENSULIDE

Bensulide (ICSC)

BENZALDEHYDE

Benzaldehyde (CHEMINFO)

BENZENE

Benzene (CHEMINFO)

Benzene (EHC 150, 1993)

Benzene (IARC Summary & Evaluation, Supplement 7, 1987)

Benzene (IARC Summary & Evaluation, Volume 29, 1982)

Benzene (IARC Summary & Evaluation, Volume 7, 1974)

Benzene (ICSC)

Benzene (PIM 063)

BENZENE ARSONIC ACID

Benzene arsonic acid (ICSC)

BENZIDINE

Benzidine (CHEMINFO)

Benzidine (IARC Summary & Evaluation, Supplement 7, 1987)

Benzidine (IARC Summary & Evaluation, Volume 1, 1972)

BENZOIC ACID

Benzoic acid (CHEMINFO)

BENZOPYRENE

Benzo(a)pyrene (CHEMINFO)

BENZO(a)FLUORENE

Benzo(a)fluorene (ICSC)

BENZOYL CHLORIDE

Benzoyl chloride (ICSC)

BENZYL ALCOHOL

Benzyl alcohol (CHEMINFO)

BENZYL CHLOROFORMATE

Benzyl chloroformate (ICSC)

BERYLLIUM

Beryllium (EHC 106, 1990)

Beryllium (UK PID)

Beryllium carbonate(ICSC)

Beryllium chloride (ICSC)

Beryllium fluoride (ICSC)

Beryllium nitrate (ICSC)

Beryllium sulfate (ICSC)

BIFENTHRIN

Bifenthrin (UK PID)

BIOALLETHRIN

Bioallethrin (ICSC)

Bioallethrin (UK PID)

S-Bioallethrin (ICSC)

BIORESMETHRIN

Bioresmethrin (ICSC)

Bioresmethrin (UK PID)

BIS(HYDROXYLAMINE) SULFATE

Bis(hydroxylamine)sulfate (ICSC)

BIS(TRIBUTYLTIN)OXIDE

Bis(tributyltin)oxide (PDS)

BISMUTH

Bismuth (UK PID)

BISPHENOL A DIGLYCIDYL ETHER

Bisphenol A diglycidyl ether (CHEMINFO)

BITOLUENE DIISOCYANATE

Bitoluene diisocyanate (CHEMINFO)

BRODIFACOUM

Brodifacoum (PDS)

Brodifacoum (PIM 077)

BROMACIL

Bromacil (ICSC)

BROMADIOLONE

Bromadiolone (PDS)

BROMINATED DIPHENYL ETHERS

Brominated diphenylethers (EHC 162, 1994)

BROMINE

Bromine (ICSC)

Bromine (PIM 080)

BROMOFORM

Bromoform (CHEMINFO)

Bromoform (IARC Summary & Evaluation, Volume 52, 1991)

Bromoform (IARC Summary & Evaluation, Volume 71, 1999)

Bromoform (ICSC)

BROMOPHOS

Bromophos (PDS)

Bromophos (PIM 742)

BROMOPHOS ETHYL

Bromophos ethyl (PIM 743)

BRUCINE

Brucine (PIM 082)

BUTANE

Butane (PIM 945)

Isobutane (CHEMINFO)

n-Butane (CHEMINFO)

Butane (ICSC)

BUTANOL

Butanols-four isomers (EHC 65, 1987)

Isobutyl alcohol (CHEMINFO)

n-Butyl alcohol (CHEMINFO)

2-butanol alcohol (CHEMINFO)

tert-Butanol (CHEMINFO)

1-Butanol (ICSC)

2-Butanol (ICSC)

tert-Butanol (ICSC)

BUTOXYETHANOL

2-Butoxyethanol (CHEMINFO)

2-Butoxyethanol (ICSC)

BUTOXYETHYL ACETATE

2-Butoxyethyl acetate (ICSC)

BUTYLPHENOL

O-sec-butylphenol (ICSC)

BUTYL ACETATE

2-Butyl acetate (CHEMINFO)

Isobutyl acetate (CHEMINFO)

n-Butyl acetate (CHEMINFO)

tert-Butyl acetate (CHEMINFO)

tert-Butyl acetate (ICSC)

Isobutyl acetate (ICSC)

n-Butyl acetate (ICSC)

sec-Butyl acetate (ICSC)

BUTYL ACRYLATE

Butyl acrylate (ICSC)

BUTYL CHLORIDE

Isobutyl chloride (ICSC)

BUTYL ISOCYANATE

Isobutyl isocyanate (CHEMINFO)

n-Butyl isocyanate (CHEMINFO)

tert-Butyl isocyanate (CHEMINFO)

BUTYL LACTATE

Butyl lactate (CHEMINFO)

BUTYRIC ACID

Butyric acid (CHEMINFO)

Isobutyric acid (CHEMINFO)

BUTYRIC ANHYDRIDE

Isobutyric anhydride (CHEMINFO)

Butyric anhydride (CHEMINFO)

BUTYRONITRILE, N-

Butyronitrile, n- (ICSC)

CADMIUM

Cadmium (EHC 134, 1992)

Cadmium (ICSC)

Cadmium (PIM 089)

Cadmium – environmental aspects (EHC 135, 1992)

CADMIUM ACETATE

Cadmium acetate (ICSC)

CADMIUM CHLORIDE

Cadmium chloride (ICSC)

CADUSAFOS

Cadusafos (PIM 746)

CALCIUM ACETATE

Calcium acetate (CHEMINFO)

Calcium acetate (ICSC)

CALCIUM CYANIDE

Calcium cyanide (CHEMINFO)

CALCIUM FORMATE

Calcium formate (CHEMINFO)

CALCIUM HYDROXIDE

Calcium hydroxide (CHEMINFO)

Calcium hydroxide (ICSC)

Calcium hydroxide (PIM 138)

CALCIUM HYPOCHLORITE

Calcium hypochlorite (CHEMINFO)

CALCIUM NITRATE

Calcium nitrate (PIM 962)

Calcium nitrate (ICSC)

CALCIUM NITRITE

Calcium nitrite (PIM 958)

CALCIUM OXIDE

Calcium oxide (CHEMINFO)

Calcium oxide (ICSC)

CALCIUM PROPIONATE

Calcium propionate (CHEMINFO)

CALCIUM STEARATE

Calcium stearate (ICSC)

CAMPHECHLOR

Camphechlor (EHC 45, 1984)

Camphechlor (PDS)

CAMPHOR

Camphor (ICSC)

CAPROLACTAM

Caprolactam (ICSC)

CAPTAFOL

Captafol (IARC Summary & Evaluation, Volume 53, 1991)

Captafol (ICSC)

Captafol (PIM 097)

CAPTAN

Captan (IARC Summary & Evaluation, Volume 30, 1983)

Captan (ICSC)

Captan (PDS)

Captan (PIM 098)

CARBADOX

Carbadox (ICSC)

CARBAMATE PESTICIDES

Carbamate pesticides: a general introduction (EHC 64, 1986)

CARBARYL

Carbaryl (EHC 153, 1994)

Carbaryl (IARC Summary & Evaluation, Volume 12, 1976)

Carbaryl (ICSC)

Carbaryl (PDS)

Carbaryl (PIM 147)

CARBENDAZIM

Carbendazim (EHC 149, 1993)

Carbendazim (PDS)

CARBOFURAN

Carbofuran (ICSC)

Carbofuran (PDS)

CARBON DIOXIDE

Carbon dioxide (ICSC)

Carbon dioxide gas (CHEMINFO)

Carbon dioxide solid (CHEMINFO)

CARBON DISULFIDE

Carbon disulfide (CHEMINFO)

Carbon disulfide (EHC 10, 1979)

Carbon disulfide (ICSC)

Carbon disulfide (PIM 102)

CARBON MONOXIDE

Carbon monoxide (CHEMINFO)

Carbon monoxide (EHC 13, 1979)

Carbon monoxide (Second Edition) (EHC 213, 1999)

Carbon monoxide (ICSC)

CARBON TETRACHLORIDE

Carbon tetrachloride (CHEMINFO)

Carbon tetrachloride (EHC 208, 1999)

Carbon tetrachloride (IARC Summary & Evaluation, Volume 71, 1999)

Carbon tetrachloride (ICSC)

CARBONYL FLUORIDE

Carbonyl fluoride (ICSC)

CARBOPHENYTHION

Carbophenythion (PIM 747)

CASTOR OIL

Castor oil (ICSC)

CHLOROACETOPHENONE

2-Chloroacetophenone (ICSC)

CHLOROBENZENE

Chlorobenzene (ICSC)

CHLOROBENZILATE

Chlorobenzilate (ICSC)

CHLOROBENZYLIDENEMALONONITRILE

o-Chlorobenzylidenemalononitrile (ICSC)

CHLORO-1-NITROBENZENE

2-Chloro-1-nitrobenzene (ICSC)

CHLORDANE

Chlordane (EHC 34, 1984)

Chlordane (PDS)

Chlordane (PIM 574)

CHLORDECONE

Chlordecone (EHC 43, 1984)

Chlordecone (IARC Summary & Evaluation, Volume 20, 1979)

Chlordecone (ICSC)

CHLORODIFLUOROMETHANE

Chlorodifluoromethane (CHEMINFO)

CHLORDIMEFORM

Chlordimeform (EHC 199, 1997)

Chlordimeform (IARC Summary & Evaluation, Volume 30, 1983)

Chlordimeform hydrochloride (ICSC)

CHLORODIPHENYLARSINE

Chlorodiphenylarsine (ICSC)

CHLORENDIC ACID

Chlorendic acid (IARC Summary & Evaluation, Volume 48, 1990)

Chlorendic acid and anhydride (EHC 185, 1996)

CHLORINE

Chlorine (CHEMINFO)

Chlorine (ICSC)

Chlorine (PIM 947)

Chlorine and hydrogen chloride (EHC 21, 1982)

CHLORINE DIOXIDE

Chlorine dioxide (CHEMINFO)

CHLORMEPHOS

Chlormephos (PIM 750)

CHLOROBENZENE

Chlorobenzene (CHEMINFO)

Chlorobenzene (ICSC)

CHLOROETHANOL

Chloroethanol, 2- (ICSC)

CHLOROFORM

Chloroform (CHEMINFO)

Chloroform (EHC 163, 1994)

Chloroform (IARC Summary & Evaluation, Supplement 7, 1987)

Chloroform (IARC Summary & Evaluation, Volume 1, 1972)

Chloroform (IARC Summary & Evaluation, Volume 20, 1979)

Chloroform (ICSC)

Chloroform (PIM 121)

CHLOROPHACINONE

Chlorophacinone (PDS)

CHLOROPICRIN

Chloropicrin (CHEMINFO)

CHLOROSULFONIC ACID

Chlorosulfonic acid (CHEMINFO)

CHLOROTHALONIL

Chlorothalonil (EHC)

Chlorothalonil (IARC Summary & Evaluation, Volume 30, 1983)

Chlorothalonil (IARC Summary & Evaluation, Volume 73, 1999)

CHLOROTOLUENE

Chlorotoluene, 2- (ICSC)

CHLORPHOXIM

Chlorphoxim (PDS)

Chlorphoxim (PIM 751)

CHLORPROPHAM

Chlorpropham (ICSC)

CHLORPYRIFOS

Chlorpyrifos (PDS)

Chlorpyrifos (PIM 752)

CHLORPYRIFOS METHYL

Chlorpyrifos methyl (PDS)

Chlorpyrifos methyl (PIM 753)

CHLORTHIOPHOS

Chlorthiophos (PIM 860)

CHLORVINPHOS

Chlorvinphos (PIM 587)

CHROMIUM

Chromium (CHEMINFO)

Chromium (EHC 61, 1988)

Chromium (ICSC)

CHROMIUM (III) HYDROXIDE HYDRATE

Chromium (iii) hydroxide hydrate (ICSC)

CHROMYL CHLORIDE

Chromyl chloride (ICSC)

CISMETHRIN

Cismethrin (ICSC)

CITRIC ACID

Citric acid (CHEMINFO)

COAL-TAR PITCH

Coal-tar pitch (ICSC)

COBALT

Cobalt (ICSC)

Cobalt (UK PID)

Cobalt (ICSC)

COBALT CARBONYL

Cobalt Carbonyl (ICSC)

COBALT (II) CHLORIDE

Cobalt (II) chloride (ICSC)

Cobalt chloride (UK PID)

COBALT (III) OXIDE

Cobalt (III) oxide (ICSC)

COBALT SULFIDE

Cobalt Sulfide (ICSC)

COBALT SULPHATE

Cobalt sulphate (UK PID)

Cobalt sulphate (ICSC)

COPPER AND COPPER SALTS

Copper & copper salts (Group PIM G002)

Copper (EHC 200, 1998)

Copper (ICSC)

Copper(II) arsenite (ICSC)

Copper (UK PID)

COPPER CARBONATE

Copper carbonate (UK PID)

COPPER CHLORIDE

Copper chloride (UK PID)

COPPER NAPHTHENATE

Copper naphthenate (ICSC)

COPPER SULFATE

Copper sulfate (UK PID)

Copper sulfate(II), pentahydrate (ICSC)

COUMAPHOS

Coumaphos (PIM 755)

COUMARIN

Coumarin (ICSC)

CREOSOTE

Creosote (ICSC)

CRESOL

Cresol, mixed isomers (CHEMINFO)

Cresols (EHC 168, 1995)

CROTONALDEHYDE

Crotonaldehyde (ICSC)

CROTOXYPHOS

Crotoxyphos (PIM 756)

CRUFOMATE

Crufomate (PIM 757)

Crufomate (ICSC)

CYANAZINE

Cyanazine (PIM 948)

CYANIDES

Cyanides (Group PIM G003)

CYANOFENPHOS

Cyanofenphos (PIM 583)

CYANOGEN

Cyanogen (CHEMINFO)

Cyanogen (ICSC)

CYANOPHOS

Cyanophos (PIM 758)

CYANURIC ACID

Cyanuric acid (CHEMINFO)

CYCLOHEXANE

Cyclohexane (CHEMINFO)

CYCLOHEXANETHIOL

Cyclohexanethiol (ICSC)

CYCLOHEXANONE

Cyclohexanone (CHEMINFO)

Cyclohexanone (IARC Summary & Evaluation, Volume 47, 1989)

Cyclohexanone (IARC Summary & Evaluation, Volume 71, 1999)

Cyclohexanone (ICSC)

CYCLOHEXYLAMINE

Cyclohexylamine (ICSC)

CYCLOHEXYL ACETATE

Cyclohexyl acetate (CHEMINFO)

CYCLOHEXYL ISOCYANATE

Cyclohexyl isocyanate (CHEMINFO)

Cyclohexyl isocyanate (ICSC)

CYFLUTHRIN

Cyfluthrin (UK PID)

CYHALOTHRIN

Cyhalothrin (EHC 99, 1990)

Cyhalothrin (UK PID)

Lambda-cyhalothrin (UK PID)

CYPERMETHRIN

Alpha-cypermethrin (UK PID)

Cypermethrin (EHC 82, 1989)

Cypermethrin (ICSC)

Cypermethrin (PDS)

Cypermethrin (PIM 163)

Cypermethrin (UK PID)

D, 2,4-

2,4-Dichlorophenoxyacetic acid (2,4-D) (EHC 29, 1984)

D, 2,4- (PDS)

DDT & ANALOGUES

DDT (PDS)

DDT (PIM 127)

DDT (ICSC)

DDT and its derivatives: environmental aspects (EHC 83, 1989)

DECANE

Decane, n- (CHEMINFO)

DECANETHIOL

Decanethiol, 1- (ICSC)

DECENE

Decene, 1- (ICSC)

DECYL ACRYLATE, N-

Decyl acrylate, n- (ICSC)

DEET

DEET (PDS)

DEET (PIM 170)

DELTAMETHRIN

Deltamethrin (EHC 97, 1990)

Deltamethrin (IARC Summary & Evaluation, Volume 53, 1991)

Deltamethrin (ICSC)

Deltamethrin (PDS)

Deltamethrin (UK PID)

DEMEPHION

Demephion (PIM 867)

DEMETON

Demeton (PDS)

Demeton (PIM 759)

Demeton (ICSC)

DEMETON-METHYL

Demeton-methyl (ICSC)

DEMETON-S-METHYL

Demeton-s-methyl (PDS)

Demeton-s-methyl (PIM 760)

DEMETON-S-METHYLSULPHON

Demeton-S-methylsulphon (PIM 761)

DHTDMAC

Dhtdmac (with 15% isopropanol)

DI(2-ETHYLHEXYL) PHTHALATE

Di(2-ethylhexyl) phthalate (ICSC)

DI-N-BUTYLTIN OXIDE

Di-n-butyltin oxide (CHEMINFO)

Di-n-butyltin oxide (ICSC)

DI-N-HEPTYL PHTHALATE

Di-n-heptyl phthalate (ICSC)

DIALIFOS

Dialifos (PIM 762)

DIALLYL ETHER

Diallyl ether (ICSC)

DIALLYL PHTHALATE

Diallyl phthalate (ICSC)

DIAMINOTOLUENE

Diaminotoluenes (EHC 74, 1987)

DIAMYLAMINE (MIXED ISOMERS)

Diamylamine (mixed isomers) (CHEMINFO)

DIAZINON

Diazinon (ICSC)

Diazinon (PDS)

Diazinon (PIM 182)

DIBENZOPYRENE

Dibenzo (a,e) pyrene (CHEMINFO)

DIBROMO-3-CHLOROPROPANE

1,2-Dibromo-3-chloropropane (ICSC)

DIBROMODIFLUOROMETHANE

Dibromodifluoromethane (ICSC)

DIBROMOETHANE

1,2-Dibromoethane (EHC 177, 1996)

DIBUTYL PHTHALATE

Di-n-butyl phthalate (EHC 189, 1997)

Dibutyl phthalate (CHEMINFO)

Dibutyl phthalate (ICSC)

DIBUTYLTINDICHLORIDE

Dibutyltindichloride (PIM 586)

DICHLOBENIL

Dichlobenil (ICSC)

DICHLOFENTHION

Dichlofenthion (PIM 763)

DICHLOROBENZENE

1,4-Dichlorobenzene (CHEMINFO)

1,4-,Dichlorobenzene (ICSC)

1,2-,Dichlorobenzene (ICSC)

DICHLOROETHANE, 1,2-

1,2-Dichloroethane (EHC 62,1987)

1,2-Dichloroethane (IARC Summary & Evaluation, Volume 71, 1999)

1,2-Dichloroethane (ICSC)

DICHLOROETHYLENE, 1,2-

Dichloroethylene, 1,2- (ICSC)

DICHLOROISOPROPYL ETHER

Dichloroisopropyl ether (ICSC)

DICHLOROPROPENE

1,3-Dichloropropene (PIM 025)

1,3-Dichloropropene, 1,2-dichloropropane and mixtures (EHC 146, 1993)

DICHLOROPROPIONIC ACID

Dichloropropionic acid, 2,2- (ICSC)

DICHLORVOS

Dichlorvos (EHC 79, 1988)

Dichlorvos (IARC Summary & Evaluation, Volume 53, 1991)

Dichlorvos (ICSC)

Dichlorvos (PDS)

Dichlorvos (PIM 185)

DICOFOL

Dicofol (PDS)

Dicofol (ICSC)

DICROTOPHOS

Dicrotophos (PIM 764)

DICYCLOHEXYL PHTHALATE

Dicyclohexyl phthalate (ICSC)

DIELDRIN

Dieldrin (IARC Summary & Evaluation, Supplement 7, 1987)

Dieldrin (IARC Summary & Evaluation, Volume 5, 1974)

Dieldrin (PDS)

Dieldrin (PIM 575)

DIESEL

Diesel fuel and exhaust emissions (EHC 171, 1996)

DIETHNOLAMINE

Diethanolamine (ICSC)

DIETHYL ETHER

Diethyl ether (CHEMINFO)

Diethyl ether (ICSC)

DIETHYL PHTHALATE

Diethyl phthalate (ICSC)

DIETHYLENE GLYCOL

Diethylene glycol (ICSC)

DIETHYLENE GLYCOL DIETHYL ETHER

Diethylene glycol diethyl ether (ICSC)

DIETHYLENE GLYCOL DINITRATE

Diethylene glycol dinitrate (ICSC)

DIETHYLENE GLYCOL DIVINYL ETHER

Diethylene glycol divinyl ether (CHEMINFO)

DIETHYLENE GLYCOL ETHYL VINYL ETHER

Diethylene glycol ethyl vinyl ether (CHEMINFO)

DIETHYLENE GLYCOL MONOBUTYL ETHER ACETATE

Diethylene glycol monobutyl ether acetate (ICSC)

DIETHYLENE GLYCOL MONOBUTYL ETHER

Diethylene glycol monobutyl ether (CHEMINFO)

Diethylene glycol monobutyl ether (ICSC)

DIETHYLENE GLYCOL MONOETHYL ETHER

Diethylene glycol monoethyl ether (CHEMINFO)

Diethylene glycol monoethyl ether (ICSC)

DIETHYLENE GLYCOL MONOMETHYL ETHER

Diethylene glycol monomethyl ether (CHEMINFO)

Diethylene glycol monomethyl ether (ICSC)

DIETHYLENE GLYCOL N-HEXYL ETHER

Diethylene glycol n-hexyl ether (CHEMINFO)

DIETHYLHEXYL PHTHALATE

Diethylhexyl phthalate (EHC 131, 1992)

DIFLUBENZURON

Diflubenzuron (EHC)

Diflubenzuron (PDS)

DIGLYCIDYL ETHER OF BISPHENOL A-BASED EPOXY RESINS

Diglycidyl ether of bisphenol A-based epoxy resins, low molecular weight liquids (CHEMINFO)

Diglycidyl ether of bisphenol A-based epoxy resins, low molecular weight solids (CHEMINFO)

Diglycidyl ether of bisphenol A-based epoxy resins, medium to high molecular weight solids (CHEMINFO)

DIISOBUTYLAMINE

Diisobutylamine (ICSC)

DIISOBUTYL KETONE

Diisobutyl ketone (CHEMINFO)

DIISONONYL PHTHALATE

Diisononyl phthlate (ICSC)

DIISOOCTYL PHTHALATE

Diisooctyl phthalate (ICSC)

DIMEFOX

Dimefox (PIM 868)

DIMETHOATE

Dimethoate (EHC 90, 1989)

Dimethoate (PDS)

Dimethoate (PIM 388)

DIMETHYL-4,4′-METHYLENEBIS(CYCLOHEXYLAMINE)

2,2′-Dimethyl-4,4′-methylenebis(cyclohexylamine) (ICSC)

DIMETHYLCYCLOHEXYLAMINE

Dimethylcyclohexylamine, n,n- (ICSC)

DIMETHYLDIOCTADECYLAMMONIUM CHLORIDE

Dimethyldioctadecylammonium chloride (ICSC)

DIMETHYLAMINE (AQUEOUS SOLUTION)

Dimethylamine (aqueous solution) (ICSC)

DIMETHYLAMINE

Dimethylamine (ICSC)

DIMETHYL ETHER

Dimethyl ether (ICSC)

DIMETHYL MERCURY

Dimethyl mercury (ICSC)

DIMETHYL PHTHALATE

Dimethyl phthalate (ICSC)

DIMETHYL SULFATE

Dimethyl sulfate (EHC 48, 1985)

DIMETHYL SULFIDE

Dimethyl sulfide (CHEMINFO)

DIMETHYL SULFOXIDE

Dimethyl sulfoxide (CHEMINFO)

DIMETHYLCYCLOHEXANE

Dimethylcyclohexane, Trans-1,4- (CHEMINFO)

DIMETHYLFORMAMIDE

Dimethylformamide (EHC 114, 1991)

Dimethylformamide (IARC Summary & Evaluation, Volume 71, 1999)

DIMETHYLPENTANE

2,4-Dimethylpentane (CHEMINFO)

3,3-Dimethylpentane (CHEMINFO)

DNOC

Dinitro-ortho-cresol (EHC 220, 2000)

DINITRO-O-CRESOL

Dinitro-o-cresol (ICSC)

DINITRO-ORTHO-CRESOL

Dinitro-ortho-cresol (EHC 220, 2000)

DINITROPHENOL

2,4-Dinitrophenol (>15% H2O) (ICSC)

DIOXABENZOFOS

Dioxabenzofos (PIM 768)

DIOXANE

1,4-Dioxane (CHEMINFO)

1,4-Dioxane (ICSC)

DIOXATHION

Dioxathion (PIM 769)

DIPROPYLENE GLYCOL MONOETHYL ETHER

Dipropylene glycol monoethyl ether (CHEMINFO)

DIPROPYLENE GLYCOL MONOMETHYL ETHER

Dipropylene glycol monomethyl ether (CHEMINFO)

DIQUAT

Diquat (PDS)

Diquat (PIM 580F, French)

Paraquat and diquat (EHC 39, 1984)

Diquat dibromide (ICSC)

DISULFOTON

Disulfoton (PDS)

Disulfoton (PIM 770)

Disulfoton (ICSC)

DITALMIFOS

Ditalmifos (PIM 869)

DITHIOCARBAMATES

Dithiocarbamates pesticides, ethylenethiourea, and propylenethiourea: a general introduction (EHC 78, 1988)

Dithiocarbamates (PDS)

DODECANE

n-Dodecane (CHEMINFO)

DODECYL BENZENESULFONIC ACID

Dodecyl benzenesulfonic acid (ICSC)

DODECYLBENZENE

Dodecylbenzene (ICSC)

DODECANOIC ACID

n-Dodecanoic acid (CHEMINFO)

DOMOIC ACID

Domoic Acid (PIM 670)

EDIFENPHOS

Edifenphos (PIM 771)

ENDOSULFAN

Endosulfan (EHC 40, 1984)

Endosulfan (PDS)

Endosulfan (PIM 576)

ENDRIN

Endrin (EHC 130, 1992)

Endrin (IARC Summary & Evaluation, Volume 5, 1974)

Endrin (PDS)

EPBP

EPBP (PIM 870)

EPICHLOROHYDRIN

Epichlorohydrin (EHC 33, 1984)

Epichlorohydrin (IARC Summary & Evaluation, Volume 71, 1999)

Epichlorohydrin (ICSC)

EPN

EPN (PIM 772)

ESFENVALERATE

Esfenvalerate (UK PID)

Esfenvalerate (ICSC)

ESP

ESP (PIM 871)

ETHANE

Ethane (CHEMINFO)

Ethane (Liquidfied gas) (ICSC)

ETHANOL

Ethanol (Cheminfo)

Ethanol (ICSC)

ETHANOLAMINE

Ethanolamine (CHEMINFO)

Ethanolamine (ICSC)

ETHION

Ethion (PIM 773)

ETHOPROPHOS

Ethoprophos (PDS)

Ethoprophos (PIM 774)

ETHOXYETHANOL

2-Ethoxyethanol (CHEMINFO)

2-Ethoxyethanol (ICSC)

ETHOXYETHYL ACETATE

2-Ethoxyethyl acetate (CHEMINFO)

2-Ethoxyethyl acetate (ICSC)

ETHYL ACETATE

Ethyl acetate (CHEMINFO)

ETHYL ACETOACETATE

Ethyl acetoacetate (CHEMINFO)

ETHYL ACRYLATE

Ethyl acrylate (CHEMINFO)

Ethyl acrylate (IARC Summary & Evaluation, Volume 39, 1986)

Ethyl acrylate (IARC Summary & Evaluation, Volume 71, 1999)

Ethyl acrylate (ICSC)

ETHYL CHLOROACETATE

Ethyl chloroacetate (ICSC)

ETHYL FORMATE

Ethyl formate (CHEMINFO)

ETHYL IODIDE

Ethyl iodide (ICSC)

ETHYL ISOCYANATE

Ethyl isocyanate (CHEMINFO)

ETHYL METHACRYLATE

Ethyl methacrylate (ICSC)

ETHYL PROPIONATE

Ethyl propionate (CHEMINFO)

ETHYLAMINE

Ethylamine (ICSC)

ETHYLAMINE (50-70% AQUEOUS SOLUTION)

Ethylamine (50-70% aqueous solution) (ICSC)

ETHYLBENZENE

Ethylbenzene (CHEMINFO)

Ethylbenzene (EHC)

ETHYLENE

Ethylene (CHEMINFO)

Ethylene (IARC Summary & Evaluation, Volume 60, 1994)

ETHYLENE CYANOHYDRIN

Ethylene cyanohydrin (ICSC)

ETHYLENEDIAMINE

Ethylenediamine (ICSC)

ETHYLENEIMINE

Ethyleneimine (ICSC)

ETHYLMORPHOLINE

n-Ethylmorpholine (ICSC)

ETHYLENE GLYCOL

Ethylene glycol (CHEMINFO)

Ethylene glycol (ICSC)

Ethylene glycol (PIM 227F)

Ethylene glycol (PIM 227)

ETHYLENE GLYCOL DIACETATE

Ethylene glycol diacetate (CHEMINFO)

ETHYLENE GLYCOL DIBUTYL ETHER

Ethylene glycol dibutyl ether (ICSC)

ETHYLENE GLYCOL DIMETHACRYLATE

Ethylene glycol dimethacrylate (ICSC)

ETHYLENE GLYCOL MONOPHENYL ETHER

Ethylene glycol monophenyl ether (ICSC)

ETHYLENE GLYCOL MONOPROPYL ETHER

Ethylene glycol monopropyl ether (ICSC)

ETHYLENE OXIDE

Ethylene oxide (CHEMINFO)

Ethylene oxide (EHC 55, 1985)

Ethylene oxide (IARC Summary & Evaluation, Volume 60, 1994)

ETHYLHEXANOIC ACID

2-Ethylhexanoic acid (CHEMINFO)

ETHYLHEXYL ACETATE

2-Ethylhexyl acetate (CHEMINFO)

ETHYLHEXYL ACRYLATE

2-Ethylhexyl acrylate (ICSC)

ETRIMFOS

Etrimfos (PIM 775)

FAMPHUR

Famphur (PIM 776)

FENAMIPHOS

Fenamiphos (PDS)

Fenamiphos (PIM 777)

FENCHLORPHOS

Fenchlorphos (PIM 778)

FENITROTHION

Fenitrothion (EHC 133, 1992)

Fenitrothion (PDS)

Fenitrothion (PIM 659)

FENPROPATHRIN

Fenpropathrin (UK PID)

FENSULFOTHION

Fensulfothion (PIM 779)

Fensulfothion (ICSC)

FENTHION

Fenthion (PDS)

Fenthion (PIM 780)

FENVALERATE

Fenvalerate (EHC 95, 1990)

Fenvalerate (IARC Summary & Evaluation, Volume 53, 1991)

Fenvalerate (ICSC)

Fenvalerate (UK PID)

Fenvalerate (PDS)

FERRIC CHLORIDE

Ferric chloride (anhydrous) (ICSC)

FERROCENE

Ferrocene (ICSC)

FIPRONIL

Fipronil (ICSC)

FLAME RETARDANTS

Flame retardants (EHC 218, 2000)

Flame retardants: A general introduction (EHC 192, 1997)

FLUMETHRIN

Flumethrin (UK PID)

FLUOROACETAMIDE

Fluoroacetamide (ICSC)

FLUORIDES

Fluorine and fluorides (EHC 36, 1984)

Fluorides (EHC 227, 2002)

Aluminum (anhydrous) fluoride (ICSC)

Calcium fluoride (ICSC)

Fluorine (ICSC)

FLUTOLANIL

Flutolanil (ICSC)

FONOFOS

Fonofos (PIM 781)

FORMALDEHYDE

Formaldehyde gas (CHEMINFO)

Formaldehyde solutions (CHEMINFO)

Formaldehyde (EHC 89, 1989)

Formaldehyde (IARC Summary & Evaluation, Volume 62)

Formaldehyde (ICSC)

FORMAMIDE

Formamide (CHEMINFO)

FORMIC ACID

Formic acid (CHEMINFO)

Formic acid (ICSC)

FORMOTHION

Formothion (PIM 782)

FOSMETHILAN

Fosmethilan (PIM 872)

FURFURYL ALCOHOL

Furfuryl alcohol (CHEMINFO)

GASOLINE

Gasoline (CHEMINFO)

Gasoline (ICSC)

Gasoline (IARC Summary & Evaluation, Volume 45, 1989)

GLYCERYL MONOSTEARATE

Glyceryl monostearate (CHEMINFO)

GLYCIDYL TRIMETHYL AMMONIUM CHLORIDE

Glycidyl trimethyl ammonium chloride (PIM 953)

GLYCOLONITRILE

Glycolonitrile (ICSC)

GLYPHOSATE

Glyphosate (EHC 159, 1994)

Glyphosate (ICSC)

Glyphosate (PDS)

GLYOXAL (40% SOLUTION)

Glyoxal (ICSC)

GOLD SALTS

Gold salts (UK PID)

PETROLEUM DISTILLATE

Solvent-dewaxed, heavy paraffinic petroleum distillate (severe solvent-refining or severe hydrotreatment) (CHEMINFO)

Solvent-dewaxed heavy paraffinic petroleum distillate (no/mild solvent-refining or no/mild hydrotreatment) (CHEMINFO)

Solvent-refined, heavy paraffinic petroleum distillate (severely solvent-refined) (CHEMINFO)

Solvent-refined heavy paraffinic petroleum distillate (mildly solvent-refined) (CHEMINFO)

Hydrotreated, heavy paraffinic petroleum distillate (severely hydrotreated) (CHEMINFO)

Hydrotreated, heavy paraffinic petroleum distillate (mildly hydrotreated) (CHEMINFO)

Distillates, petroleum, solvent-refined light naphthenic (ICSC)

Distillates, petroleum, solvent-refined heavy paraffinic (ICSC)

HELIUM

Helium (CHEMINFO)

Helium (ICSC)

HEPTACHLOR

Heptachlor (EHC 38, 1984)

Heptachlor (PDS)

Heptachlor (PIM 578)

Heptachlor (ICSC)

HEPTANE

n-Heptane (CHEMINFO)

HEPTANOL, 1-

1-Heptanol (CHEMINFO)

1-Heptanol (ICSC)

HEPTANOL, 2-

2-Heptanol (ICSC)

HEPTENOPHOS

Heptenophos (PIM 786)

HEXANETHIOL

Hexanethiol, n- (ICSC)

HEXACHLOROBENZENE (HCB)

Hexachlorobenzene (EHC 195, 1997)

Hexachlorobenzene (PDS)

Hexachlorobenzene (PIM 256)

HEXACHLOROBUTADIENE

Hexachlorobutadiene (EHC 156, 1994)

Hexachlorobutadiene (IARC Summary & Evaluation, Volume 20, 1979)

Hexachlorobutadiene (IARC Summary & Evaluation, Volume 73, 1999)

HEXACHLOROCYCLOHEXANE

Alpha- and beta-hexachlorocyclohexanes (EHC 123, 1992)

Hexachlorocyclohexane (IARC Summary & Evaluation, Volume 20, 1979)

Hexachlorocyclohexane (Mixed Isomers) (PIM 257)

HEXACHLOROCYCLOPENTADIENE

Hexachlorocyclopentadiene (EHC 120, 1991)

HEXANE, n-

n-Hexane (CHEMINFO)

n-Hexane (EHC 122, 1991)

n-Hexane (ICSC)

n-Hexane (PIM 368)

HEXANOL, 1-

Hexanol, 1- (CHEMINFO)

Hexanol, 1- (ICSC)

HEXYL ISOCYANATE

Hexyl isocyanate (CHEMINFO)

HEXYLENE GLYCOL

Hexylene glycol (ICSC)

HYDRAZINE

Hydrazine (EHC 68, 1987)

Hydrazine (IARC Summary & Evaluation, Volume 71, 1999)

HYDROCHLORIC ACID

Hydrochloric acid (CHEMINFO)

Hydrochloric acid (IARC Summary & Evaluation, Volume 54, 1992)

HYDROCYANIC ACID SOLUTIONS

Hydrocyanic acid solutions (CHEMINFO)

HYDROFLUORIC ACID

Hydrofluoric acid (CHEMINFO)

HYDROGEN

Hydrogen gas (CHEMINFO)

HYDROGEN CHLORIDE

Hydrogen chloride (ICSC)

HYDROGEN CYANIDE

Hydrogen canide (PIM 693)

Hydrogen cyanide (CHEMINFO)

Hydrogen cyanide, liquified (ICSC)

HYDROGEN FLUORIDE

Hydrogen fluoride (ICSC)

Hydrogen fluoride (PIM 268)

Hydrogen fluoride (CHEMINFO)

HYDROGEN PEROXIDE

Hydrogen peroxide (IARC Summary & Evaluation, Volume 71, 1999)

Hydrogen peroxide (ICSC)

Hydrogen peroxide (PIM 946)

Hydrogen peroxide solutinos of 20% to less than 35% (CHEMINFO)

Hydrogen peroxide solutions of 35% and greater (CHEMINFO)

Hydrogen peroxide solutions of 8% to less than 20% (CHEMINFO)

Hydrogen peroxide solutions of less than 8% (CHEMINFO)

HYDROGEN SULPHIDE

Hydrogen sulfide (EHC 19, 1981)

Hydrogen sulphide (CHEMINFO)

Hydrogen sulphide (ICSC)

HYDROTREATED KEROSENE

Hydrotreated kerosene (CHEMINFO)

HYDROQUINONE

Hydroquinone (CHEMINFO)

Hydroquinone (EHC 157, 1994)

Hydroquinone (ICSC)

IMIDACLOPRID

Imidacloprid (ICSC)

IODOFORM

Iodoform (CHEMINFO)

IOXYNIL

Ioxynil (ICSC)

ISAZOFOS

Isazofos (PIM 790)

ISOBENZAN

Isobenzan (EHC 129, 1991)

ISOBUTANOLAMINE

Isobutanolamine (ICSC)

Isobutylamine (ICSC)

ISOFENPHOS

Isofenphos (PIM 791)

ISOHEPTANE

Isoheptane (ICSC)

ISOPHORONE

Isophorone (CHEMINFO)

Isophorone (EHC 174, 1995)

Isophorone (ICSC)

ISOPROPYL ALCOHOL

Isopropyl alcohol (PIM 290)

ISOPROPYL CHLOROFORMATE

Isopropyl chloroformate (ICSC)

ISOPROPYL LACTATE

Isopropyl lactate (CHEMINFO)

ISOTHIOATE

Isothioate (PIM 792)

ISOXATHION

Isoxathion (PIM 793)

JET FUEL

Jet A (CHEMINFO)

Jet B (CHEMINFO)

Jet Fuel (IARC Summary & Evaluation, Volume 45, 1989)

JP-4 (CHEMINFO)

JP-5 (CHEMINFO)

JP-8 (CHEMINFO)

JODFENPHOS

Jodfenphos (PDS)

Jodfenphos (PIM 873)

KELEVAN

Kelevan (EHC 66, 1986)

KEROSENE

Kerosene, deodorized (CHEMINFO)

Kerosene, hydrodesulfurized (CHEMINFO)

Kerosene, straight-run (CHEMINFO)

LACTIC ACID

Lactic Acid (CHEMINFO)

Ethyl lactate (CHEMINFO)

LEAD

Lead (UK PID)

Lead arsenate (ICSC)

Lead carbonate (ICSC)

Lead dioxide (ICSC)

Lead nitrate (ICSC)

Lead tetroxide (ICSC)

Lead(II) arsenite (ICSC)

LEAD ACETATE

Lead acetate (CHEMINFO)

LEAD CHROMATE

Lead chromate (ICSC)

LEAD, INORGANIC

Lead, inorganic (CHEMINFO)

Lead, inorganic (EHC 165, 1995)

Lead, inorganic (ICSC)

Lead, inorganic (PIM 301)

LEAD, ORGANIC

Lead, organic (PIM 302)

LEAD(II) OXIDE

Lead (II) oxide (ICSC)

LEPTOPHOS

Leptophos (PDS)

Leptophos (PIM 304)

LIMONENE

d,l-Limoene (CHEMINFO)

d-Limonene (CHEMINFO)

l-Limonene (CHEMINFO)

d-Limonene (ICSC)

LINDANE

Lindane (EHC 124, 1991)

Lindane (ICSC)

Lindane (PDS)

Lindane (PIM 859)

LINOLEIC ACID

Linoleic acid (CHEMINFO)

LITHIUM

Lithium (CHEMINFO)

LITHIUM CARBONATE

Lithium carbonate (CHEMINFO)

LITHIUM CHLORIDE

Lithium chloride (CHEMINFO)

LITHIUM HYDROXIDE

Lithium hydroxide (CHEMINFO)

LITHIUM HYPOCHLORITE

Lithium hypochlorite (CHEMINFO)

MAGNESIUM ACETATE

Magnesium acetate (CHEMINFO)

MAGNESIUM FORMATE

Magnesium formate (CHEMINFO)

MAGNESIUM NITRATE

Magnesium nitrate (PIM 963)

Magnesium nitrate (ICSC)

MAGNESIUM NITRITE

Magnesium nitrite (PIM 959)

MALATHION

Malathion (IARC Summary & Evaluation, Volume 30, 1983)

Malathion (ICSC)

Malathion (PIM 695)

MALEIC ACID

Maleic acid (CHEMINFO)

MALEIC ANHYDRIDE

Maleic anhydride molten liquid (CHEMINFO)

Maleic anhydride solid (CHEMINFO)

Maleic anhydride (ICSC)

MALONONITRILE

Malononitrile (ICSC)

MANCOZEB

Mancozeb (ICSC)

MANEB

Maneb (IARC Summary & Evaluation, Volume 12, 1976)

Maneb (ICSC)

MANGANESE

Manganese (EHC 17, 1981)

Manganese (ICSC)

MANGANESE DIOXIDE

Mnganese dioxide (ICSC)

MCPA

MCPA (IARC Summary & Evaluation, Volume 30, 1983)

MCPA (ICSC)

MENAZON

Menazon (PIM 795)

MEPHOSFOLAN

Mephosfolan (PIM 796)

MERCURY

Mercury, inorganic (CHEMINFO)

Mercury, inorganic (EHC 118, 1991)

Mercury (UK PID)

Mercury (ICSC)

MERCURIC CHLORIDE

Mercuric chloride (ICSC)

METALDEHYDE

Metaldehyde (PIM 332)

Metaldehyde (PDS)

METHACRIFOS

Methacrifos (PIM 797)

METHAMIDOPHOS

Methamidophos (ICSC)

Methamidophos (PIM 798)

METHANE

Methane (ICSC)

Methane (CHEMINFO)

METHANOL

Methanol (CHEMINFO)

Methanol (EHC 196, 1997)

Methanol (ICSC)

Methanol (PIM 335)

METHIDATHION

Methidathion (PIM 799)

METHOMYL

Methomyl (EHC 178, 1996)

Methomyl (ICSC)

Methomyl (PDS)

METHOPRENE

Methoprene (PDS)

METHOXYCHLOR

Methoxychlor (IARC Summary & Evaluation, Volume 20, 1979)

Methoxychlor (IARC Summary & Evaluation, Volume 5, 1974)

Methoxychlor (PDS)

Methoxychlor (ICSC)

METHOXYETHANOL

2-Methoxyethanol (CHEMINFO)

2-Methoxyethanol (ICSC)

2-Methoxyethanol, 2-ethoxyethanol, and their acetates (EHC 115, 1990)

METHOXYETHYL ACETATE

2-Methoxyethyl acetate (CHEMINFO)

2-Methoxyethyl acetate (ICSC)

METHOXYETHYLMERCURY CHLORIDE, 2-

2-Methoxyethylmercury Chloride (PDS)

METHYL ACETATE

Methyl acetate (CHEMINFO)

METHYL ACRYLATE

Methyl acrylate (CHEMINFO)

Methyl acrylate (IARC Summary & Evaluation, Volume 39, 1986)

Methyl acrylate (IARC Summary & Evaluation, Volume 71, 1999)

Methyl acrylate (ICSC)

METHYL BROMIDE

Methyl bromide (CHEMINFO)

Methyl bromide (EHC 166, 1995)

Methyl bromide (IARC Summary & Evaluation, Volume 71, 1999)

Methyl bromide (PDS)

Methyl bromide (PIM 340)

METHYL CHLORIDE

Methyl chloride (IARC Summary & Evaluation, Volume 71, 1999)

Methyl chloride (ICSC)

Methyl chloride (PIM 339)

METHYL ETHYL KETONE

Methyl ethyl ketone (CHEMINFO)

Methyl ethyl ketone (EHC 143, 1992)

Methyl ethyl ketone (ICSC)

METHYL ETHYL KETONE PEROXIDE

Methyl ethyl ketone peroxide (CHEMINFO)

METHYL FORMATE

Methyl formate (CHEMINFO)

METHYL IODIDE

Methyl iodide (CHEMINFO)

Methyl iodide (ICSC)

Methyl iodide (IARC Summary & Evaluation, Volume 15, 1977)

Methyl iodide (IARC Summary & Evaluation, Volume 41, 1986)

Methyl iodide (IARC Summary & Evaluation, Volume 71, 1999)

Methyl iodide (PIM 341F, French)

METHYL ISOBUTYL KETONE

Methyl isobutyl ketone (CHEMINFO)

Methyl isobutyl ketone (EHC 117, 1990)

Methyl isobutyl ketone (ICSC)

METHYL ISOCYANATE

Methyl isocyanate (CHEMINFO)

Methyl isocyanate (ICSC)

METHYL LACTATE

Methyl lactate (CHEMINFO)

METHYL MERCAPTAN

Methyl mercaptan (ICSC)

METHYL METHACRYLATE

Methyl methacrylate (CHEMINFO)

Methyl methacrylate (IARC Summary & Evaluation, Volume 60, 1994)

Methyl methacrylate (ICSC)

METHYL TERT-BUTYL ETHER

Methyl tert-butyl ether (CHEMINFO)

METHYL VINYL KETONE

Methyl vinyl ketone (CHEMINFO)

Methyl vinyl ketone (ICSC)

METHYLACETOACETATE

Methylacetoacetate (ICSC)

METHYLAMINE

Methylamine (ICSC)

Methylamine (40% aqueous solution) (ICSC)

Methylamine, anhydrous (CHEMINFO)

Methylamine, solutions (CHEMINFO)

METHYLENE BROMIDE

Methylene bromide (CHEMINFO)

METHYLENE CHLORIDE

Methylene chloride (CHEMINFO)

Methylene chloride (EHC 32, 1984, 1st edition)

Methylene chloride (ICSC)

Methylene chloride (PIM 343)

METHYLENE IODIDE

Methylene iodide (CHEMINFO)

METHYLMERCURY

Methylmercury (EHC 101, 1990)

MEVINPHOS

Mevinphos (PDS)

Mevinphos (PIM 348)

MICHLER’S KETONE

Michler’s ketone (CHEMINFO)

MIREX

Mirex (EHC 44, 1984)

Mirex (IARC Summary & Evaluation, Volume 20, 1979)

Mirex (IARC Summary & Evaluation, Volume 5, 1974)

MONOCHLOROACETIC ACID

Monochloroacetic acid (ICSC)

Monochloroacetic acid (PIM 352)

Monochloroacetic acid solid (CHEMINFO)

Monochloroacetic acid solutions (CHEMINFO)

MONOCROTOPHOS

Monocrotophos (ICSC)

Monocrotophos (PIM 800)

MORPHOLINE

Morpholine (CHEMINFO)

Morpholine (EHC 179, 1996)

Morpholine (IARC Summary & Evaluation, Volume 47, 1989)

Morpholine (IARC Summary & Evaluation, Volume 71, 1999)

MUSTARD GAS

Mustard gas (IARC Summary & Evaluation, Volume 9, 1975)

Mustard gas (IARC Summary & Evaluation, Supplement7, 1987)

Mustard gas (PIM 354)

NALED

Naled (PDS)

Naled (PIM 555)

Naled (ICSC)

NAPHTHA

High flash aromatic naphtha (CHEMINFO)

Medium aliphatic solvent naphtha (petroleum) (ICSC)

NAPHTHALENE

Naphthalene (CHEMINFO)

Naphthalene (PIM 363)

Naphthalene (ICSC)

NAPHTHYLAMINE, 2-

Naphthylamine, 2- (ICSC)

NEOHEXANE

Neohexane (CHEMINFO)

NEON

Neon gas (CHEMINFO)

Neon liquid (CHEMINFO)

NICKEL

Nickel (EHC 108, 1991)

Nickel (ICSC)

NICKEL CARBONYL

Nickel carbonyl (UK PID)

NICKEL CHLORIDE

Nickel Chloride (UK PID)

NICKEL OXIDE

Nickel oxide (UK PID)

NICKEL SULPHATE

Nickel sulphate (UK PID)

Nickel(II) sulphate (ICSC)

NICLOSAMIDE

Niclosamide (PDS)

NICOTINE

Nicotine (PIM 373)

NITRATES & NITRITES

Nitrates and nitrites (Group PIM G016)

Nitrates, nitrites and N-nitroso compounds (EHC 5, 1978)

NITRIC ACID

Nitric acid (CHEMINFO)

Nitric acid (ICSC)

NITRIC OXIDE

Nitric oxide (PIM 528)

Nitric oxide (ICSC)

NITRILOTRIACETIC ACID

Nitrilotriacetic acid trisodium salt monohydrate (ICSC)

Nitrilotriacetic acid trisodium salt (ICSC)

Nitrilotriacetic acid (ICSC)

NITROBENZENE

Nitrobenzene (IARC Summary & Evaluation, Volume 65, 1996)

Nitrobenzene (ICSC)

Nitrobenzene (EHC 230, 2003)

NITROFEN

Nitrofen (PDS)

NITROGEN

Nitrogen, gas (CHEMINFO)

Nitrogen, liquid (CHEMINFO)

Nitrogen (compressed gas) (ICSC)

Nitrogen (liquified) (ICSC)

NITROGEN DIOXIDE

Nitrogen dioxide (CHEMINFO)

Nitrogen dioxide (ICSC)

Nitrogen dioxide (PIM 736)

NITROGEN OXIDES

Nitrogen oxides (Group PIM G017)

Nitrogen Oxides (Second Edition) (EHC)

Oxides of nitrogen (EHC 4, 1977)

NITROGEN PENTOXIDE

Nitrogen pentoxide (PIM 283)

NITROGLYCERIN

Nitroglycerin (ICSC)

NITROMETHANE

Nitromethane (CHEMINFO)

NITRO-AND NITRO-OXY-POLYCYCLIC AROMATIC HYDROCARBONS

Nitro-and nitro-oxy-polycyclic aromatic hydrocarbons (EHC 229, 2003)

NITRONAPHTHALENE

Nitronaphthalene, 2- (ICSC)

NITROPHENOL

p-Nitrophenol (ICSC)

NITROPROPANE

2-Nitropropane (CHEMINFO)

2-Nitropropane (EHC 138, 1992)

2-Nitropropane (ICSC)

NITROSODIPHENYLAMINE

Nitrosodiphenylamine, n- (ICSC)

NITROUS OXIDE

Nitrous oxide (CHEMINFO)

Nitrous oxide (ICSC)

NONANE

n-Nonane (CHEMINFO)

NONYL PHENOL (MIXED ISOMERS)

Nonyl phenol (mixed isomers) (ICSC)

OCTAMETHYLCYCLOTETRASILOXANE

Octamethylcyclotetrasiloxane (ICSC)

OCTANE

n-Octane (CHEMINFO)

OCTANOL, 1-

1-Octanol (CHEMINFO)

1-Octanol (ICSC)

OCTANOL, 2-

2-Octanol (ICSC)

OCTANOIC ACID

n-Octanoic Acid (CHEMINFO)

OCTYL ACETATE

n-Octyl acetate (CHEMINFO)

OCTYL MERCAPTAN

n-Octyl mercaptan (ICSC)

tert-Octyl mercaptan (ICSC)

OLEIC ACID

Oleic acid (CHEMINFO)

OMETHOATE

Omethoate (PIM 542)

ORGANOPHOSPHATES

Organophophorus insecticides: a general introduction (EHC 63, 1986)

Organophosphorous pesticides (Group PIM G001)

OXALIC ACID

Oxalic acid (CHEMINFO)

OXAMYL

Oxamyl (PDS)

OXYDEMETON METHYL

Oxydemeton methyl (PIM 532)

OZONE

Ozone (CHEMINFO)

Ozone (ICSC)

PALLADIUM

Palladium (EHC 226, 2002)

PALMITIC ACID

Palmitic acid (CHEMINFO)

PARAFFINS

Chlorinated paraffins (EHC)

PARAFFIN WAX

Paraffin wax (ICSC)

PARAQUAT

Paraquat (ICSC)

Paraquat (PDS)

Paraquat (PIM 399)

Paraquat and diquat (EHC 39, 1984)

PARATHION

Parathion (IARC Summary & Evaluation, Volume 30, 1983)

Parathion (ICSC)

Parathion (PDS)

Parathion (PIM 400)

PARATHION ETHYL

Parathion ethyl (PIM 526)

PARATHION METHYL

Methyl parathion (EHC 145, 1992)

Methyl parathion (ICSC)

Parathion methyl (PIM 666)

Parathion-Methyl (PDS)

PCB & PBB

Polybrominated biphenyls (EHC 152, 1994)

Polychlorinated biphenyls and terphenyls (EHC 140, 1992, 2nd edition)

PCDD & PCDF

Polychlorinated dibenzo-p-dioxins and dibenzofurans (EHC 88, 1989)

PENTACHLOROBENZENE

Pentachlorobenzene (ICSC)

PENTACHLOROETHANE

Pentachloroethane (ICSC)

PENTACHLOROPHENOL (PCP)

Pentachlorophenol (EHC 71, 1987)

Pentachlorophenol (ICSC)

Pentachlorophenol (PIM 405)

PENTACHLOROPHENOL SODIUM

Pentachlorophenol sodium (ICSC)

PENTANE

Isopentane (CHEMINFO)

n-Pentane (CHEMINFO)

PENTASODIUM TRIPHOSPHATE

Pentasodium triphosphate (ICSC)

PERCHLORIC ACID

Perchloric acid solutions greater than 72.5% (CHEMINFO)

Perchloric acid solutions 72.5% and less (CHEMINFO)

PERFLUOROISOBUTYLENE

Perfluoroisobutylene (ICSC)

PERMETHRIN

Permethrin (EHC 94, 1990)

Permethrin (IARC Summary & Evaluation, Volume 53, 1991)

Permethrin (ICSC)

Permethrin (PDS)

Permethrin (UK PID)

PHENOL

Phenol (CHEMINFO)

Phenol (EHC 161, 1994)

Phenol (IARC Summary & Evaluation, Volume 71, 1999)

Phenol (ICSC)

Phenol (PIM 412)

PHENOLPHTHALEIN

Phenolphthalein (CHEMINFO)

PHENOTHRIN

d-Phenothrin (EHC 96, 1990)

d-Phenothrin (PDS)

d-Phenothrin (UK PID)

PHENTHOATE

Phenthoate (PIM 486)

PHENYL-1,4-BENZENEDIAMINE

N-phenyl-1,4-benzenediamine (ICSC)

PHENYL-BETA-NAPHTHYLAMINE

Phenyl-beta-naphthylamine (ICSC)

PHENYLENEDIAMINE

Phenylenediamine (ICSC)

PHENYLPHOSPHINE

Phenylphosphine (ICSC)

PHORATE

Phorate (PDS)

Phorate (PIM 039)

PHOSALONE

Phosalone (PIM 634)

PHOSGENE

Phosgene (CHEMINFO)

Phosgene (EHC 193, 1997)

Phosgene (ICSC)

Phosgene (PIM 419)

PHOSMET

Phosmet (PIM 168)

PHOSPHAMIDON

Phosphamidon (ICSC)

Phosphamidon (PDS)

Phosphamidon (PIM 454)

PHOSPHINE

Phospine (CHEMINFO)

PHOSPHINE & PHOSPHIDES

Phosphine (ICSC)

Phosphine (PDS)

Phosphine (PIM 865)

Phosphine and selected metal phosphides (EHC 73, 1988)

PHOSPHOLAN

Phospholan (PIM 874)

PHOSPHORIC ACID

Phosphoric acid (UK PID)

Phosphoric acid solutions (CHEMINFO)

PHOSPHOROUS PENTOXIDE

Phosphorous pentoxide (CHEMINFO)

PHOSPHORUS

Phosphorus (yellow)(ICSC)

PHOSPHORUS TRICHLORIDE

Phosphorus trichloride (UK PID)

PHOXIM

Phoxim (PDS)

Phoxim (PIM 452)

PHTHALIC ACID

Isophthalic acid (CHEMINFO)

Phthalic acid (CHEMINFO)

PHTHALIC ANHYDRIDE

Phthalic anhydride molten liquid (CHEMINFO)

Phthalic anhydride solid (CHEMINFO)

Phthalic anhydride (ICSC)

PICRIC ACID

Picric acid, wetted with not less than 30% water (CHEMINFO)

Picric acid, dry or wetted with less than 30% water (CHEMINFO)

PINACOLYL ALCOHOL

Pinacolyl Alcohol (PIM 981)

PINDONE

Pindone (ICSC)

PIPERAZINE (ANHYDROUS)

Piperazine (anhydrous) (ICSC)

PIPERIDINE

Piperidine (ICSC)

PIRIMIPHOS ETHYL

Pirimiphos ethyl (PIM 360)

PIRIMIPHOS METHYL

Pirimiphos methyl (PDS)

Pirimiphos methyl (PIM 361)

PLATINIUM

Platinium (ICSC)

POLYALKYLENE GLYCOL MONOBUTYL ETHER

Polyalkylene glycol monobutyl ether, molecular weight 1230 (CHEMINFO)

Polyalkylene glycol monobutyl ether, molecular weight 1590 (CHEMINFO)

Polyalkylene glycol monobutyl ether, molecular weight 2660 (CHEMINFO)

Polyalkylene glycol monobutyl ether, molecular weight 270 (CHEMINFO)

Polyalkylene glycol monobutyl ether, molecular weight 3380 (CHEMINFO)

Polyalkylene glycol monobutyl ether, molecular weight 4000 (CHEMINFO)

Polyalkylene glycol monobutyl ether, molecular weight 520 (CHEMINFO)

Polyalkylene glycol monobutyl ether, molecular weight 750 (CHEMINFO)

Polyalkylene glycol monobutyl ether, molecular weight 970 (CHEMINFO)

POLYDIMETHYLSILOXANE

Polydimethylsiloxane (ICSC)

POLYETHYLENE

Polyethylene, low density (CHEMINFO)

Polyethylene, high density (CHEMINFO)

POLYETHYLENE GLYCOL

Polyethylene glycol (200-600) (ICSC)

POLYPROPYLENE GLYCOL MONOMETHYL ETHER

Polypropylene glycol monomethyl ether (CHEMINFO)

POLYSTYRENE

Polystyrene (ICSC)

PORTLAND CEMENT

Portland cement (ICSC)

POTASSIUM ACID OXALATE

Potassium acid oxalate (CHEMINFO)

POTASSIUM AMYL XANTHATE

Potassium amyl xanthate (CHEMINFO)

POTASSIUM BROMATE

Potassium bromate (ICSC)

POTASSIUM CHLORATE

Potassium chlorate (ICSC)

POTASSIUM CHLORIDE

Potassium chloride (ICSC)

POTASSIUM CYANIDE

Potassium cyanide (CHEMINFO)

Potassium cyanide (ICSC)

Potassium cyanide (PIM 955)

POTASSIUM ETHYL XANTHATE

Potassium ethyl xanthate (CHEMINFO)

POTASSIUM FERRICYANIDE

Potassium ferricyanide (ICSC)

POTASSIUM FORMATE

Potassium formate (CHEMINFO)

POTASSIUM HYDROXIDE

Potassium hydroxide (ICSC)

Potassium hydroxide (PIM 717)

Potassium hydroxide solid (CHEMINFO)

Potassium hydroxide solutions (CHEMINFO)

POTASSIUM ISOAMYL XANTHATE

Potassium isoamyl xanthate (CHEMINFO)

POTASSIUM ISOBUTYL XANTHATE

Potassium isobutyl xanthate (CHEMINFO)

POTASSIUM ISPROPYL XANTHATE

Potassium ispropyl xanthate (CHEMINFO)

POTASSIUM NITRATE

Potassium nitrate (PIM 961)

POTASSIUM NITRITE

Potassium nitrite (PIM 957)

POTASSIUM N-BUTYL XANTHATE

Potassium n-butyl xanthate (CHEMINFO)

POTASSIUM OXALATE

Potassium oxalate (CHEMINFO)

POTASSIUM OXIDE

Potassium oxide (ICSC)

POTASSIUM PERCHLORATE

Potassium perchlorate (ICSC)

POTASSIUM PERMANGANATE

Potassium permanganate (PIM 409)

Potassium permanganate (ICSC)

POTASSIUM PERSULFATE

Potassium persulfate (ICSC)

POTASSIUM SULFATE

Potassium sulfate (ICSC)

POTASSIUM THIOCYANATE

Potassium thiocyanate (ICSC)

POVIDONE-IODINE

Povidone-iodine (ICSC)

PROFENOFOS

Profenofos (PIM 350)

PROPACHLOR

Propachlor (EHC 147, 1993)

Propachlor (PDS)

PROPANE

Propane (CHEMINFO)

Propane (ICSC)

PROPANIL

Propanil (PIM 440)

PROPANOL

1-Propanol (CHEMINFO)

1-Propanol (EHC 102, 1990)

2-Propanol (CHEMINFO)

2-Propanol (EHC 103, 1990)

Isopropyl alcohol (ICSC)

PROPAPHOS

Propaphos (PIM 590)

PROPETAMPHOS

Propetamphos (PIM 023)

PROPIONALDEHYDE

Propionaldehyde (ICSC)

PROPIONIC ACID

Propionic acid (CHEMINFO)

PROPOXUR

Propoxur (ICSC)

Propoxur (PDS)

PROPYL ACETATE

Isopropyl acetate (CHEMINFO)

n-Propyl acetate (CHEMINFO)

PROPYL ISOCYANATE

Isopropyl isocyanate (CHEMINFO)

n-Propyl isocyanate (CHEMINFO)

PROPYL NITRATE

n-Propyl nitrate (ICSC)

PROPYLENE GLYCOL

1,2-Propylene glycol (CHEMINFO)

Propylene glycol (ICSC)

Propylene glycol (PIM 443)

PROPYLENE GLYCOL DIACETATE

Propylene glycol diacetate (CHEMINFO)

PROPYLENE GLYCOL MONO-N-BUTYL ETHER

Propylene glycol mono-n-butyl ether (CHEMINFO)

PROPYLENE GLYCOL MONOETHYL ETHER

Propylene glycol monoethyl ether (CHEMINFO)

PROPYLENE GLYCOL MONOMETHYL ETHER

Propylene glycol monomethyl ether (CHEMINFO)

PROPYLENE GLYCOL MONOMETHYL ETHER ACETATE

Propylene glycol monomethyl ether acetate (CHEMINFO)

PROPYLENE GLYCOL N-MONOPROPYL ETHER

Propylene glycol n-monopropyl ether (CHEMINFO)

PROPYLENE GLYCOL PHENYL ETHER

Propylene glycol phenyl ether (CHEMINFO)

PROPYLENE OXIDE

Propylene oxide (EHC 56, 1985)

Propylene oxide (IARC Summary & Evaluation, Volume 60, 1994)

PROTHIOFOS

Prothiofos (PIM 024)

PROTHOATE

Prothoate (PIM 596)

PYRACLOFOS

Pyraclofos (PIM 076)

PYRENE

Pyrene (ICSC)

PYRETHRINS

Pyrethrins (PDS)

Pyrethrin (Group PIM G026)

PYRETHROIDS

Pyrethroids (UK PID)

PYRENE

Pyrene (ICSC)

PYRETHRUM

Pyrethrum (ICSC)

PYRIDAPHENTHION

Pyridaphenthion (PIM 087)

PYRROLIZIDINE ALKALOIDS

Pyrrolizidine alkaloids (EHC 80, 1988)

QUATERNARY AMMONIUM

Quaternary ammonium (Group PIM G022)

QUINALPHOS

Quinalphos (PIM 462)

QUINTOZENE

Quintozene (EHC 41, 1984)

Quintozene (ICSC)

RESMETHRIN

Resmethrin (ICSC)

Resmethrin (UK PID)

Resmethrins (EHC 92, 1989)

Resmethrins (PDS)

RESORCINOL

Resorcinol (ICSC)

ROSIN

Rosin (ICSC)

ROTENONE

Rotenone (PIM 474)

Rotenone (ICSC)

SCHRADAN

Schradan (PIM 875)

SELENIUM

Selenium (EHC 58, 1986)

Selenium (ICSC)

Selenium (PIM 483)

SELENIUM HEXAFLUORIDE

Selenium hexafluoride (UK PID)

SIMAZINE

Simazine (IARC Summary & Evaluation, Volume 53, 1991)

Simazine (IARC Summary & Evaluation, Volume 73, 1999)

Simazine (PIM 949)

SODIUM ARSENATE

Sodium arsenate (ICSC)

Sodium arsenate (UK PID)

SODIUM ARSENITE

Sodium arsenite (UK PID)

SODIUM BENZOATE

Sodium benzoate (CHEMINFO)

SODIUM BICARBONATE

Sodium bicarbonate (ICSC)

SODIUM BORATE

Sodium borate, decahydrate (ICSC)

SODIUM CARBONATE

Sodium carbonate (CHEMINFO)

SODIUM CHLORATE

Sodium chlorate (CHEMINFO)

Sodium chlorate (ICSC)

SODIUM CHLOROACETATE

Sodium chloroacetate (ICSC)

SODIUM CHLORITE

Sodium chlorite (CHEMINFO)

SODIUM CITRATE ANHYDROUS

Sodium citrate, anhydrous (ICSC)

SODIUM DICHROMATE

Sodium dichromate (anhydrous) (ICSC)

SODIUM CITRATE DIHYDRATE

Sodium citrate dihydrate (ICSC)

SODIUM CITRATE PENTAHYDRATE

Sodium citrate pentahydrate (ICSC)

SODIUM CYANIDE

Sodium cyanide (PIM 718)

Sodium cyanide (ICSC)

SODIUM DISULFITE

Sodium disulfite (ICSC)

SODIUM ETHANOLATE

Sodium ethanolate (ICSC)

SODIUM ETHYL XANTHATE

Sodium ethyl xanthate (CHEMINFO)

SODIUM FLUORACETATE

Sodium Fluoroacetate (PDS)

Sodium Fluoroacetate (PIM 494)

SODIUM FLUORIDE

Sodium fluoride (ICSC)

SODIUM FORMATE

Sodium formate (CHEMINFO)

SODIUM HYDROXIDE

Sodium hydroxide (ICSC)

Sodium hydroxide (PIM 719)

Sodium hydroxide (UK PID)

Sodium hydroxide solid (CHEMINFO)

Sodium hydroxide solutions (CHEMINFO)

SODIUM HYPOCHLORITE

Sodium hypochlorite solutions (CHEMINFO)

Sodium hypochlorite (PIM 495)

SODIUM ISOAMYL XANTHATE

Sodium isoamyl xanthate (CHEMINFO)

SODIUM ISOBUTYL XANTHATE

Sodium isobutyl xanthate (CHEMINFO)

SODIUM ISOPROPYL XANTHATE

Sodium isopropyl xanthate (CHEMINFO)

SODIUM LAURYL SULFATE

Sodium lauryl sulfate (CHEMINFO)

SODIUM METASILICATE

Sodium metasilicate (PIM 500)

Sodium metasilicate, anhydrous (ICSC)

SODIUM N-BUTYL XANTHATE

Sodium n-butyl xanthate (CHEMINFO)

SODIUM NITRATE

Sodium nitrate (PIM 960)

SODIUM NITRITE

Sodium Nitrite (PIM 956)

SODIUM OXALATE

Sodium oxalate (CHEMINFO)

SODIUM PROPIONATE

Sodium propionate (CHEMINFO)

SODIUM SEC-BUTYL XANTHATE

Sodium sec-butyl xanthate (CHEMINFO)

SODIUM SESQUICARBONATE DIHYDRATE

Sodium sesquicarbonate dihydrate (ICSC)

SODIUM STEARATE

Sodium stearate (CHEMINFO)

SODIUM XYLENESULFONATE

Sodium xylenesulfonate (ICSC)

SODIUM SULFIDE

Sodium sulfide (anhydrous) (ICSC)

SORBITOL

d-Sorbitol (ICSC)

SORBIC ACID

Sorbic acid (CHEMINFO)

SPINOSAD

Spinosad (ICSC)

STANNIC OXIDE

Stannic oxide (ICSC)

STANNOUS CHLORIDE

Stannous chloride (anhydrous) (ICSC)

Stannous chloride dihydrate (ICSC)

STANNOUS FLUORIDE

Stannous fluoride (ICSC)

STANNOUS OXIDE

Stannous oxide (ICSC)

STEARALKONIUM CHLORIDE

Stearalkonium chloride (PIM 954)

STEARIC ACID

Stearic acid (CHEMINFO)

STODDARD SOLVENT

Stoddard solvent (ICSC)

STRONTIUM CHROMATE

Strontium chromate (ICSC)

STRYCHNINE

Strychnine (ICSC)

Strychnine (PIM 507)

STRYCHNINE SULFATE

Strychnine sulfate (ICSC)

STYRENE

Styrene (CHEMINFO)

Styrene (EHC 26, 1983)

Styrene (IARC Summary & Evaluation, Volume 60, 1994)

Styrene (ICSC)

Styrene (PIM 509)

SUCROSE

Sucrose (ICSC)

SULFAMIC ACID

Sulphamic acid (ICSC)

SULFOTEP

Sulfotep (PIM 108)

SULFUR DIOXIDE

Sulfur dioxide (CHEMINFO)

Sulphur dioxide (ICSC)

SULFUR HEXAFLUORIDE

Sulfur hexafluoride (CHEMINFO)

SULFUR OXIDES

Sulfur oxides and suspended particulate matter (EHC 8, 1979)

SULFUR TETRAFLUORIDE

Sulfur tetrafluoride (ICSC)

SULFURIC ACID

Sulfuric acid (CHEMINFO)

Sulfuric acid (ICSC)

Oleum (ICSC)

SULFUR TRIOXIDE

Sulfur trioxide (ICSC)

SULPROFOS

Sulprofos (PIM 112)

Sulprofos (ICSC)

T, 2,4,5-

2,4,5-T (PDS)

TAU-FLUVALINATE

Tau-fluvalinate (UK PID)

TBPP

Tris- and bis(2,3-dibromopropyl) phosphate (EHC 173, 1995)

TECNAZENE

Tecnazene (EHC 42, 1984)

TEFLUTHRIN

Tefluthrin (UK PID)

TELLURIUM

Tellurium (UK PID)

TELLURIUM HEXAFLUORIDE

Tellurium hexafluoride (UK PID)

TEMEPHOS

Temephos (ICSC)

Temephos (PDS)

Temephos (PIM 129)

TEPP

TEPP (PIM 602)

TEPP (ICSC)

TERBUFOS

Terbufos (PIM 605)

TEREPHTHALIC ACID

Terephthalic acid (CHEMINFO)

Terephthalic acid (ICSC)

TERPHENYL

Terphenyl, o- (ICSC)

TETRACHLOROBENZENE

Tetrachlorobenzene, 1,2,4,5- (ICSC)

TETRACHLOROETHYLENE

Tetrachloroethylene (CHEMINFO)

Tetrachloroethylene (EHC 31, 1984)

Tetrachloroethylene (IARC Summary & Evaluation, Volume 63, 1995)

Tetrachloroethylene (UK PID)

Tetrachloroethylene (ICSC)

TETRACHLORVINPHOS

Tetrachlorvinphos (PIM 876)

TETRADIFON

Tetradifon (EHC 67, 1986)

TETRAETHYL LEAD

Tetraethyl lead (ICSC)

TETRAHYDROFURAN

Tetrahydrofuran (CHEMINFO)

TETRAMETHRIN

Tetramethrin (EHC 98, 1990)

Tetramethrin (ICSC)

Tetramethrin (UK PID)

TETRAMETHYLAMMONIUM CHLORIDE

Tetramethylammonium chloride (ICSC)

TETRAMETHYLENE DISULFOTETRAMINE

Tetramethylene disulfotetramine (PIM 982)

TETRANITROMETHANE

Tetranitromethane (ICSC)

TEXANOL

Texanol (ICSC)

THALLIUM

Thallium (EHC 182, 1996)

Thallium (PIM 525)

Thallium metal (ICSC)

THALLIUM SULFATE

Thallium Sulfate (PDS)

THIOCARBAMATES

Thiocarbamates pesticides (EHC 76, 1988)

THIODIGLYCOL

Thiodiglycol (PIM 980)

THIOMETON

Thimeton (PDS)

Thiometon (PIM 165)

THIONAZIN

Thionazin (PIM 207)

THIONYL CHLORIDE

Thionyl chloride (ICSC)

TIN

Tin and organotin compounds (EHC 15, 1980)

TITANIUM TETRACHLORIDE

Titanium tetrachloride (ICSC)

TOBACCO

Tobacco (EHC 211, 1999)

TOLIDINE

Tolidine, o- (ICSC)

TOLUENE

Toluene (CHEMINFO)

Toluene (EHC 52, 1986)

Toluene (IARC Summary & Evaluation, Volume 71, 1999)

Toluene (ICSC)

TOLUENE-DIISOCYANATE

2,4-Toluene diisocyanate (ICSC)

Toluene-2,6-diisocyanate (ICSC)

Toluene diisocyanate (65:35 mixture) (CHEMINFO)

Toluene diisocyanate (80:20 mixture) (CHEMINFO)

Toluene diisocyanate (UK PID)

Toluene diisocyanates (EHC 75, 1987)

Toluene-2,4-diisocyanate (CHEMINFO)

Toluene-2,4-diisocyanate (TDI) (PIM 534)

Toluene-2,6-diisocyanate (CHEMINFO)

TRIAMYLAMINE (MIXED ISOMERS)

Triamylamine (mixed isomers) (CHEMINFO)

TRIAZINE HERBICIDES

Triazine herbicides (Group PIM G013)

TRIAZOPHOS

Triazophos (PIM 461)

TRIBUTYL PHOSPHATE

Tributyl phosphate (CHEMINFO)

Tributyl phosphate (EHC 112, 1991)

TRIBUTYLAMINE

Tributylamine (ICSC)

TRIBUTYLTIN

Tributyltin compounds (EHC 116, 1990)

Tributyltin compounds (Group PIM G018)

Tributyltin oxide (ICSC)

TRICHLORFON

Trichlorfon (EHC 132, 1992)

Trichlorfon (IARC Summary & Evaluation, Volume 30, 1983)

Trichlorfon (PDS)

Trichlorfon (PIM 539)

TRICHLOROACETIC ACID

Trichloroacetic acid (IARC Summary & Evaluation, Volume 63, 1995)

Trichloroacetic acid (IARC Summary & Evaluation, Volume 84, 2004)

Trichloroacetic acid solid (CHEMINFO)

Trichloroacetic acid solutions (CHEMINFO)

TRICHLOROBENZENE

1,2,3-Trichlorobenzene (CHEMINFO)

1,2,3-Trichlorobenzene (ICSC)

1,2,4-Trichlorobenzene (ICSC)

1,3,5-,Trichlorobenzene (ICSC)

TRICHLOROMETHANESULFENYL CHLORIDE

Trichloromethanesulfenyl chloride (ICSC)

TRICHLORONAPHTHALENE

Trichloronaphthalene (ICSC)

TRICHLOROETHANE

1,1,1-Trichloroethane (CHEMINFO)

1,1,1-Trichloroethane (EHC 136, 1992)

1,1,1-Trichloroethane (ICSC)

1,1,1-Trichloroethane (PIM 540)

1,1,1-trichloroethane (UK PID)

1,1,2-Trichloroethane (CHEMINFO)

1,1,2-Trichloroethane (ICSC)

TRICHLOROETHYLENE

Trichloroethylene (CHEMINFO)

Trichloroethylene (EHC 50, 1985)

Trichloroethylene (IARC Summary & Evaluation, Volume 63, 1995)

Trichloroethylene (ICSC)

TRICHLOROSILANE

Trichlorosilane (ICSC)

TRICHLOROISOCYANURIC ACID

Trichloroisocyanuric acid (CHEMINFO)

TRICHLOROPROPANE

1,2,3-Trichloropropane (ICSC)

TRICRESYL PHOSPHATE

Tricresyl phosphate (EHC 110, 1991)

TRIETHANOLMINE

Triethanolamine (ICSC)

TRIETHOXYSILANE

Triethoxysilane (ICSC)

TRIETHYLAMINE

Triethylamine (ICSC)

TRIMETHYLAMINE

Trimethylamine (ICSC)

Trimethylamine (40% aqueous solution) (ICSC)

TRIETHYLENE GLYCOL MONOBUTYL ETHER

Triethylene glycol monobutyl ether (ICSC)

TRIETHYLENE GLYCOL MONOETHYL ETHER

Triethylene glycol monoethyl ether (ICSC)

TRIETHYLTIN

Triethyltin (PIM 588)

TRIETRAZINE

Trietrazine (PIM 950)

TRIMELLITIC ACID

Trimellitic acid (ICSC)

TRIMETHYLTIN

Trimethyltin compounds (Group PIM G019)

TRINEXAPAC-ETHYL

Trinexapac-ethyl (ICSC)

TRIPHENYLTIN ACETATE

Triphenyltin acetate (PIM 589)

TRIPROPYLENE GLYCOL MONOETHYL ETHER

Tripropylene glycol monoethyl ether (CHEMINFO)

TRIPROPYLENE GLYCOL MONOMETHYL ETHER

Tripropylene glycol monomethyl ether (CHEMINFO)

TRISODIUM PHOSPHATE

Trisodium phosphate (CHEMINFO)

TURPENTINE

Turpentine (CHEMINFO)

UNDECANE

n-Undecane (CHEMINFO)

UNDECANOIC ACID

Undecanoic acid (CHEMINFO)

VALERIC ACID

Isovaleric acid (CHEMINFO)

n-Valeric acid (CHEMINFO)

VAMIDOTHION

Vamidothion (PIM 313)

VINYL CHLORIDE

Vinyl chloride (CHEMINFO)

Vinyl chloride (EHC 215, 1999)

Vinyl chloride (IARC Summary & Evaluation, Supplement 7, 1987)

Vinyl chloride (IARC Summary & Evaluation, Volume 7, 1974)

Vinyl chloride (ICSC)

Vinyl chloride (PIM 558)

VINYLIDENE CHLORIDE

Vinylidene chloride (EHC 100, 1990)

Vinylidene chloride (IARC Summary & Evaluation, Volume 71, 1999)

Vinylidene chloride (ICSC)

VINYL TOLUENE

3-Vinyl toluene (ICSC)

WARFARIN

Warfarin (ICSC)

Warfarin (PDS)

Warfarin (PIM 563)

WHITE SPIRIT

Stoddard solvent (CHEMINFO)

White Spirit (Stoddard Solvent) (EHC)

XYLENE

m-Xylene (CHEMINFO)

m-Xylene (ICSC)

Mixed xylenes (CHEMINFO)

o-Xylene (CHEMINFO)

o-Xylene (ICSC)

p-Xylene (CHEMINFO)

Xylene (IARC Summary & Evaluation, Volume 71, 1999)

Xylene (PIM 565)

Xylenes (EHC 190, 1997)

XYLENOL, 2,4-

Xylenol, 2,4- (ICSC)

ZINC

Zinc metal (CHEMINFO)

Zinc (UK PID)

Zinc and salts (Group PIM G020)

Zinc (EHC 221, 2001)

ZINC CHLORIDE

Zinc chloride (CHEMINFO)

Zinc chloride (UK PID)

ZINC NAPHTHENATE

Zinc naphthenate (CHEMINFO)

ZINC OXIDE

Zinc oxide (CHEMINFO)

Zinc oxide (ICSC)

Zinc oxide (UK PID)

ZINC PHOSPHIDE

Zinc phosphide (PDS)

ZINC POWDER

Zinc powder(CHEMINFO)

Zinc powder (ICSC)

ZINC STEARATE

Zinc stearate (CHEMINFO)

ZINC SULFATE

Zinc sulfate (CHEMINFO)

Zinc sulfate heptahydrate (ICSC)

Zinc sulphate (UK PID)

ZINEB

Zineb (IARC Summary & Evaluation, Volume 12, 1976)

Zineb (ICSC)

ZIRAM

Ziram (IARC Summary & Evaluation, Volume 53, 1991)

Ziram (ICSC)

Ziram (PDS)

ZIRCONIUM

Zirconium (UK PID)

Zirconium (ICSC)

New ICSCs yet to be categorized:

(2,4,5-TRICHLOROPHENOXY) ACETIC ACID (ICSC)

1,1,1,2-TETRAFLUOROETHANE (ICSC)

1,1,1-TRIMETHYLOLPROPANE (ICSC)

1,1,2,2-TETRACHLOROETHANE (ICSC)

1,1,2-TRICHLORO-1,2,2-TRIFLUOROETHANE (ICSC)

1,1-DICHLOROETHANE (ICSC)

1,1-DICHLOROPROPANE (ICSC)

1,1-DIMETHYLHYDRAZINE (ICSC)

1,2,3-TRIMETHYLBENZENE (ICSC)

1,2,4-TRIAZOLE (ICSC)

1,2,4-TRIMETHYLBENZENE (ICSC)

1,2-DICHLOROPROPANE (ICSC)

1,2-DINITROBENZENE (ICSC)

1,2-DIPHENYLHYDRAZINE (ICSC)

1,3,5-TRIMETHYLBENZENE (ICSC)

1,3-BUTADIENE (ICSC)

1,3-DINITROBENZENE (ICSC)

1,4-BENZENEDIAMINE DIHYDROCHLORIDE (ICSC)

1,4-DINITROBENZENE (ICSC)

1,5-NAPHTHALENEDIAMINE (ICSC)

1,5-NAPHTHALENEDIOL (ICSC)

1-CHLORO-1-NITROPROPANE (ICSC)

1-CHLORO-2,4-DINITROBENZENE (ICSC)

1-CHLOROETHANE (ICSC)

1-DECANOL (ICSC)

1-DODECANETHIOL (ICSC)

1-METHYLCYCLOHEXANOL (ICSC)

1-OCTADECANOL (ICSC)

1-VINYL-2-PYRROLIDONE (ICSC)

2,2,4-TRIMETHYLPENTANE (ICSC)

2,3,4,6-TETRACHLOROPHENOL (ICSC)

2,3,4-TRICHLOROPHENOL (ICSC)

2,3,5-TRICHLOROPHENOL (ICSC)

2,3,6-TRICHLOROPHENOL (ICSC)

2,3,7,8-TETRACHLORODIBENZO-p-DIOXIN (ICSC)

2,3-DICHLOROANILINE (ICSC)

2,3-DINITROTOLUENE (ICSC)

2,4,6-TRIBROMOPHENOL (ICSC)

2,4,6-TRINITROTOLUENE (ICSC)

2,4-D (ICSC)

2,4-DIAMINOANISOLE (ICSC)

2,4-DICHLOROANILINE (ICSC)

2,4-DINITROTOLUENE (ICSC)

2,4-TOLUENEDIAMINE (ICSC)

2,5-DICHLOROPHENOL (ICSC)

2,6-DI-TERT-BUTYLPHENOL (ICSC)

2,6-DICHLOROANILINE (ICSC)

2,6-DINITROTOLUENE (ICSC)

2-AMINOANTHRAQUINONE (ICSC)

2-AMINOPHENOL (ICSC)

2-AMINOPYRIDINE (ICSC)

2-CHLOROACETAMIDE (ICSC)

2-CHLOROANILINE (ICSC)

2-DIETHYLAMINOETHANOL (ICSC)

2-DIMETHYLAMINOETHANOL (ICSC)

2-ETHYLHEXANOIC ACID (ICSC)

2-ETHYLHEXANOL (ICSC)

2-ETHYLHEXYL METHACRYLATE (ICSC)

2-MERCAPTOIMIDAZOLINE (ICSC)

2-METHOXY-2-METHYLBUTANE (ICSC)

2-METHYLCYCLOHEXANOL (ICSC)

2-METHYLHEPTANE (ICSC)

2-METHYLPENTANE (ICSC)

2-N-DIBUTYLAMINOETHANOL (ICSC)

2-NAPHTHOL (ICSC)

2-NITROPHENOL (ICSC)

2-VINYL TOLUENE (ICSC)

3,4-DINITROTOLUENE (ICSC)

3,5-DICHLOROPHENOL (ICSC)

3-CHLOROANILINE (ICSC)

3-METHYLCYCLOHEXANOL (ICSC)

3-METHYLPENTANE (ICSC)

4,4′-OXYBIS(BENZENESULPHONYL HYDRAZIDE) (ICSC)

4-CHLORO-m-CRESOL (ICSC)

4-DIMETHYLAMINOAZOBENZENE (ICSC)

4-METHOXY-4-METHYL-2-PENTANONE (ICSC)

4-METHOXYPHENOL (ICSC)

4-METHYLCYCLOHEXANOL (ICSC)

4-NITROBIPHENYL (ICSC)

4-VINYL TOLUENE (ICSC)

4-VINYLCYCLOHEXENE (ICSC)

5-ETHYLIDENE-2-NORBORNENE (stabilized) (ICSC)

5-METHYL-3-HEPTANONE (ICSC)

ACETONE CYANOHYDRIN (ICSC)

ACETYL BROMIDE (ICSC)

ADIPONITRILE (ICSC)

ALACHLOR (ICSC)

ALLYL ALCOHOL (ICSC)

ALLYL GLYCIDYL ETHER (ICSC)

ALLYL ISOTHIOCYANATE (ICSC)

ALLYL PROPYL DISULFIDE (ICSC)

ALUMINIUM PHOSPHIDE (ICSC)

ALUMINUM HYDROXIDE (ICSC)

AMINOCARB (ICSC)

AMITRAZ (ICSC)

AMMONIUM DICHROMATE (ICSC)

AMMONIUM NITRATE (ICSC)

AMMONIUM VANADIUM OXIDE (ICSC)

ANTHRAQUINONE (ICSC)

ANTIMONY PENTAFLUORIDE (ICSC)

ARSENIC ACID (80% in water) (ICSC)

ARSENIC PENTOXIDE (ICSC)

ARSENIC TRIOXIDE (ICSC)

ASCORBIC ACID (ICSC)

ATRAZINE (ICSC)

ATTAPULGITE (ICSC)

AZODICARBONAMIDE (ICSC)

BARIUM ACETATE (ICSC)

BARIUM CHLORIDE, DIHYDRATE (ICSC)

BARIUM CHLORIDE (ICSC)

BARIUM OXIDE (ICSC)

BARIUM SULFATE (ICSC)

BENTONITE (ICSC)

BENZ(a)ANTHRACENE (ICSC)

BENZAL CHLORIDE (ICSC)

BENZENESULFONIC ACID (ICSC)

BENZENETHIOL (ICSC)

BENZETHONIUM CHLORIDE (ICSC)

BENZIDINE (ICSC)

BENZO(a)PYRENE (ICSC)

BENZO(b)FLUORANTHENE (ICSC)

BENZO(k)FLUORANTHENE (ICSC)

BENZOFURAN (ICSC)

BENZOTRICHLORIDE (ICSC)

BENZYL ACETATE (ICSC)

BENZYL ALCOHOL (ICSC)

BENZYL CHLORIDE (ICSC)

BERYLLIUM (ICSC)

BIPHENYL (ICSC)

BIS(2-CHLOROETHYL) ETHER (ICSC)

BISPHENOL A (ICSC)

BORON BROMIDE (ICSC)

BORON TRIFLUORIDE (ICSC)

BROMINE PENTAFLUORIDE (ICSC)

BROMOACETONE (ICSC)

BROMOCHLOROMETHANE (ICSC)

BROMOETHANE (ICSC)

BUTYL BENZYL PHTHALATE (ICSC)

BUTYLENE OXIDE (STABILIZED) (ICSC)

BUTYRALDEHYDE (ICSC)

C10-13 ALKYLBENZENESULFONIC ACID, SODIUM SALT (ICSC)

CADMIUM OXIDE (ICSC)

CAFFEINE (ICSC)

CALCIUM ARSENATE (ICSC)

CALCIUM BROMIDE (ICSC)

CALCIUM CARBIDE (ICSC)

CALCIUM HYPOCHLORITE (ICSC)

CALCIUM POLYSULFIDE (ICSC)

CALCIUM SILICATE (non-fibrous, less than 1% crystalline silica) (ICSC)

CALCIUM SULFATE (ANHYDROUS) (ICSC)

CARBENDAZIM (ICSC)

CARBON BLACK (ICSC)

CARBON TETRABROMIDE (ICSC)

CARBOPHENOTHION (ICSC)

CATECHOL (ICSC)

CHLORAMINE-T (ICSC)

CHLORDANE (TECHNICAL PRODUCT) (ICSC)

CHLORDIMEFORM (ICSC)

CHLORFENVINPHOS (ICSC)

CHLORINE DIOXIDE (ICSC)

CHLORINE TRIFLUORIDE (ICSC)

CHLOROACETALDEHYDE (40% SOLUTION) (ICSC)

CHLOROMETHYL METHYL ETHER (ICSC)

CHLOROTHALONIL (ICSC)

CHLOROTOLURON (ICSC)

CHLOROTRIFLUOROMETHANE (ICSC)

CHLORPYRIFOS (ICSC)

CHOLINE CHLORIDE (ICSC)

CHROMIUM(III) NITRATE NONAHYDRATE (ICSC)

CHRYSOTILE (ICSC)

CITRIC ACID, MONOHYDRATE (ICSC)

COPPER (I) OXIDE (ICSC)

COPPER (II) ORTHOARSENATE (ICSC)

COUMAPHOS (ICSC)

CROTONIC ACID (ICSC)

CRYOLITE (ICSC)

CUMENE HYDROPEROXIDE (ICSC)

CUMENE (ICSC)

CYANAMIDE (ICSC)

CYANAZINE (ICSC)

CYANOGEN BROMIDE (ICSC)

CYCLOHEXANE (ICSC)

CYCLOHEXANOL (ICSC)

CYCLOHEXIMIDE (ICSC)

CYCLOHEXYL ACETATE (ICSC)

CYCLOPENTANE (ICSC)

CYCLOPENTANONE (ICSC)

CYCLOTETRAMETHYLENE TETRANITRAMINE (ICSC)

DECABORANE (ICSC)

DECAHYDRONAPHTHALENE (cis/trans isomer mixture) (ICSC)

DECANE (ICSC)

DEMETON-O-METHYL (ICSC)

DEMETON-S-METHYL (ICSC)

DI(2,3-EPOXYPROPYL)ETHER (ICSC)

DIACETONE ALCOHOL (ICSC)

DIAMMONIUM HYDROGEN ARSENATE (ICSC)

DIAZOMETHANE (ICSC)

DIBENZO(a,h)ANTHRACENE (ICSC)

DIBROMOMETHANE (ICSC)

DIBUTYL PHOSPHATE (ICSC)

DICAMBA (ICSC)

DICHLOROACETIC ACID (ICSC)

DICHLOROMONOFLUOROMETHANE (ICSC)

DICHLOROSILANE (ICSC)

DICHLOROTETRAFLUOROETHANE (ICSC)

DICYANDIAMIDE (ICSC)

DICYCLOHEXYLAMINE (ICSC)

DICYCLOPENTADIENE (ICSC)

DIETHYL SUCCINATE (ICSC)

DIETHYLAMINE (ICSC)

DIETHYLENE GLYCOL DIMETHYL ETHER (ICSC)

DIETHYLENETRIAMINE (ICSC)

DIISOBUTYL KETONE (ICSC)

DIKETENE (ICSC)

DIMETHYL CARBONATE (ICSC)

DIMETHYL DISULFIDE (ICSC)

DIMETHYL HYDROGEN PHOSPHITE (ICSC)

DIMETHYL SULFATE (ICSC)

DIMETHYL SULPHOXIDE (ICSC)

DIMETHYL TEREPHTHALATE (ICSC)

DINITROBENZENE (mixed isomers) (ICSC)

DINITROTOLUENE (MIXED ISOMERS) (ICSC)

DINOSEB (ICSC)

DIPHENAMID (ICSC)

DIPHENYLAMINE (ICSC)

DIPHENYLOL PROPANE DIGLYCIDYL ETHER (ICSC)

DISUL-SODIUM (ICSC)

DODECANOYL PEROXIDE (ICSC)

DODECYLAMINE (ICSC)

EPTC (ICSC)

ETHYL 2-CYANOACRYLATE (ICSC)

ETHYL CARBAMATE (ICSC)

ETHYLBENZENE (ICSC)

ETHYLENE DIBROMIDE (ICSC)

ETHYLENE GLYCOL DIETHYL ETHER (ICSC)

ETHYLENE GLYCOL DIMETHYL ETHER (ICSC)

ETHYLENE GLYCOL ISOPROPYL ETHER (ICSC)

ETHYLENE OXIDE (ICSC)

ETHYLENE (ICSC)

FENCHLORPHOS (ICSC)

FENTHION (ICSC)

FERROUS OXIDE (ICSC)

FLOCOUMAFEN (ICSC)

FLUOROBORIC ACID (ICSC)

FLUOROSILICIC ACID (ICSC)

FLUOROSULFONIC ACID (ICSC)

FOLPET (ICSC)

FONOFOS (ICSC)

FURFURAL (ICSC)

GLUTARALDEHYDE (50% SOLUTION) (ICSC)

GLUTARALDEHYDE (ICSC)

GLYCIDOL (ICSC)

GUANIDINE NITRATE (ICSC)

HEXACHLOROBENZENE (ICSC)

HEXACHLOROCYCLOPENTADIENE (ICSC)

HEXACHLOROETHANE (ICSC)

HEXACHLORONAPHTHALENE (ICSC)

HEXACHLOROPHENE (ICSC)

HEXAMETHYLENE DIISOCYANATE (ICSC)

HEXAMETHYLENEDIAMINE (ICSC)

HEXAMETHYLENETETRAMINE (ICSC)

HEXAMETHYLPHOSPHORIC TRIAMIDE (ICSC)

HYDRAZINE (ICSC)

HYDROGEN BROMIDE (ICSC)

HYDROGEN IODIDE (ICSC)

HYDROGEN SELENIDE (ICSC)

HYDROXYLAMINE HYDROCHLORIDE (ICSC)

HYDROXYLAMINE (ICSC)

INDENO(1,2,3-cd)PYRENE (ICSC)

INDIUM TRICHLORIDE (ICSC)

IODINE CYANIDE (ICSC)

IRON (III)-o-ARSENITE, PENTAHYDRATE (ICSC)

IRON PENTACARBONYL (ICSC)

ISOBUTANOL (ICSC)

ISOBUTYL CHLOROFORMATE (ICSC)

ISOPENTANE (ICSC)

ISOPHORONE DIISOCYANATE (ICSC)

ISOPHTHALIC ACID (ICSC)

ISOPROPYL GLYCIDYL ETHER (ICSC)

KAOLIN (ICSC)

LAMBDA-CYHALOTHRIN (ICSC)

LEAD ACETATE (ICSC)

LINURON (ICSC)

MAGNESIUM (PELLETS) (ICSC)

MAGNESIUM (POWDER) (ICSC)

MAGNESIUM ARSENATE (ICSC)

MANGANESE OXIDE (ICSC)

MANGANESE SULPHATE MONOHYDRATE (ICSC)

MECOPROP (ICSC)

METHACRYLIC ACID (ICSC)

METHACRYLONITRILE (ICSC)

METHYL 2-CYANOACRYLATE (ICSC)

METHYL ACETATE (ICSC)

METHYL BROMIDE (ICSC)

METHYL CHLOROACETATE (ICSC)

METHYL ETHYL KETONE PEROXIDE (Technical product) (ICSC)

METHYL FORMATE (ICSC)

METHYL HYDRAZINE (ICSC)

METHYL ISOAMYL KETONE (ICSC)

METHYL ISOBUTYL CARBINOL (ICSC)

METHYLAL (ICSC)

METHYLARSONIC ACID (ICSC)

METHYLCHLOROSILANE (ICSC)

METHYLCYCLOHEXANOL (MIXED ISOMERS) (ICSC)

METHYLENE BISPHENYL ISOCYANATE (ICSC)

METRIBUZIN (ICSC)

N,N’-DIPHENYL-para-PHENYLENEDIAMINE (ICSC)

N,N-DIETHYLANILINE (ICSC)

N,N-DIMETHYL-p-TOLUIDINE (ICSC)

N,N-DIMETHYLACETAMIDE (ICSC)

N,N-DIMETHYLFORMAMIDE (ICSC)

N-METHYL DIETHANOLAMINE (ICSC)

N-METHYL-2-PYRROLIDONE (ICSC)

NAPHTHALENE 1,5-DIISOCYANATE (ICSC)

NICKEL CARBONATE (ICSC)

NICKEL SULFIDE (ICSC)

NITROCELLULOSE (less than 12.6% nitrogen ) (ICSC)

NITROGEN TRIFLUORIDE (ICSC)

NITROSYL CHLORIDE (ICSC)

OCTACHLORONAPHTHALENE (ICSC)

OCTADECYLAMINE (ICSC)

OXYGEN (LIQUEFIED) (ICSC)

OXYGEN DIFLUORIDE (ICSC)

OXYGEN (ICSC)

PENTABROMODIPHENYL ETHER (Technical product) (ICSC)

PENTABROMOPHENOL (ICSC)

PENTACHLORONAPHTHALENE (ICSC)

PENTAERYTHRITOL TETRANITRATE (ICSC)

PERACETIC ACID (stabilized) (ICSC)

PERCHLORYL FLUORIDE (ICSC)

PERFLUOROOCTANOIC ACID (ICSC)

PERLITE (ICSC)

PETROLEUM SULFONATE, SODIUM SALT (ICSC)

PHENYL CHLOROFORMATE (ICSC)

PHENYL GLYCIDYL ETHER (ICSC)

PHENYL ISOCYANATE (ICSC)

PHENYLHYDRAZINE (ICSC)

PHORATE (ICSC)

PHOSPHORIC ACID (ICSC)

PHOSPHORUS OXYCHLORIDE (ICSC)

PHOSPHORUS PENTACHLORIDE (ICSC)

PHOSPHORUS PENTOXIDE (ICSC)

PHOSPHORUS TRICHLORIDE (ICSC)

PICLORAM (ICSC)

PICRIC ACID (ICSC)

PIGMENT RED 53, BARIUM SALT (2:1) (ICSC)

PLATINUM TETRACHLORIDE (ICSC)

POLYVINYL CHLORIDE (ICSC)

POTASSIUM ARSENATE (ICSC)

POTASSIUM ARSENITE (ICSC)

POTASSIUM CARBONATE (ANHYDROUS) (ICSC)

POTASSIUM DICHROMATE (ICSC)

POTASSIUM DIHYDROGEN PHOSPHATE (ICSC)

POTASSIUM HEXAFLUOROSILICATE (ICSC)

POTASSIUM HYDROGEN SULFATE (ICSC)

POTASSIUM METABISULFITE (ICSC)

PROPARGYL ALCOHOL (ICSC)

PROPAZINE (ICSC)

PROPIONIC ANHYDRIDE (ICSC)

PROPIONITRILE (ICSC)

PROPYLENE GLYCOL DINITRATE (ICSC)

PROPYLENE GLYCOL n-BUTYL ETHER (ICSC)

PROPYLENE OXIDE (ICSC)

PROPYLENEIMINE (ICSC)

PYROGALLIC ACID (ICSC)

PYRROLIDINE (ICSC)

RESORCINOL DIGLYCIDYL ETHER (ICSC)

RHODIUM TRICHLORIDE, TRIHYDRATE (ICSC)

RHODIUM (ICSC)

SALICYLIC ACID, METHYL ESTER (ICSC)

SELENIOUS ACID (ICSC)

SELENIUM DIOXIDE (ICSC)

SELENIUM HEXAFLUORIDE (ICSC)

SELENIUM TRIOXIDE (ICSC)

SIMAZINE (ICSC)

SODIUM ARSENATE DIBASIC (ICSC)

SODIUM ARSENITE (ICSC)

SODIUM BROMATE (ICSC)

SODIUM CHROMATE (ICSC)

SODIUM DICHLOROISOCYANURATE (ICSC)

SODIUM HEXAFLUOROSILICATE (ICSC)

SODIUM IODIDE (ANHYDROUS) (ICSC)

SODIUM MOLYBDATE (ICSC)

SODIUM PERCHLORATE (ICSC)

SODIUM PEROXIDE (ICSC)

SODIUM PERSULFATE (ICSC)

SODIUM SELENITE (ICSC)

SODIUM SULFATE (ICSC)

SODIUM SULFITE (ICSC)

SODIUM THIOCYANATE (ICSC)

SULFANILIC ACID (ICSC)

SULFOTEP (ICSC)

SULFUR MUSTARD (ICSC)

SULPHUR HEXAFLUORIDE (ICSC)

SULPHURYL CHLORIDE (ICSC)

TALC (SILICA AND FIBRE FREE) (ICSC)

TANTALUM (ICSC)

TETRACHLORONAPHTHALENE (ICSC)

TETRAETHYL SILICATE (ICSC)

TETRAFLUOROMETHANE (ICSC)

TETRAFLUOROSILANE (ICSC)

TETRAHYDROFURAN (ICSC)

TETRAHYDROTHIOPHENE (ICSC)

TETRAMETHYL LEAD (ICSC)

TETRAMETHYL SUCCINONITRILE (ICSC)

THALLIUM CARBONATE (ICSC)

THALLIUM SULFATE (ICSC)

THEOPHYLLINE (ICSC)

THIOACETAMIDE (ICSC)

THIODIGLYCOL (ICSC)

THIOUREA (ICSC)

THORIUM (ICSC)

TRI-ALLATE (ICSC)

TRIBUTYL PHOSPHATE (ICSC)

TRICHLOROACETIC ACID (ICSC)

TRICHLORPHON (ICSC)

TRIETHYLENE GLYCOL DIMETHYL ETHER (ICSC)

TRIETHYLENETETRAMINE (ICSC)

TRIFLUOROCHLOROETHYLENE (ICSC)

TRIFLURALIN (ICSC)

TRIISOPROPANOLAMINE (ICSC)

TRIMETHYL BENZENE (MIXED ISOMERS) (ICSC)

TRIMETHYL PHOSPHATE (ICSC)

TRIMETHYL PHOSPHITE (ICSC)

TRIPHENYL PHOSPHITE (ICSC)

TRIPHENYLAMINE (ICSC)

TRIPHENYLPHOSPHINE (ICSC)

TRIPHENYLTIN HYDROXIDE (ICSC)

TUNGSTEN (powder) (ICSC)

TUNGSTEN CARBIDE (ICSC)

URANIUM DIOXIDE (ICSC)

URANIUM HEXAFLUORIDE (ICSC)

UREA AMMONIUM NITRATE (ICSC)

VANADIUM PENTOXIDE (ICSC)

VINYL ACETATE (MONOMER) (ICSC)

VINYL FLUORIDE (ICSC)

VINYL TOLUENE (MIXED ISOMERS) (ICSC)

VINYLIDENE FLUORIDE (ICSC)

XYLIDINE (MIXED ISOMERS) (ICSC)

ZINC CHLORIDE (ICSC)

ZINC SULFIDE (ICSC)

alpha-METHYL STYRENE (ICSC)

bis(CHLOROMETHYL) ETHER (ICSC)

cis-2-BUTENE (ICSC)

d-PHENOTHRIN (ICSC)

iso-PHTHALONITRILE (ICSC)

m-CHLOROPHENOL (ICSC)

m-CRESOL (ICSC)

m-NITROTOLUENE (ICSC)

m-PHENYLENEDIAMINE (ICSC)

meta-TOLUIDINE (ICSC)

n-BUTENE (ICSC)

n-BUTYL CHLOROFORMATE (ICSC)

n-BUTYL ETHER (ICSC)

n-BUTYL GLYCIDYL ETHER (ICSC)

n-BUTYLAMINE (ICSC)

n-HEPTANE (ICSC)

n-PROPYL CHLOROFORMATE (ICSC)

o-CHLOROBENZALDEHYDE (ICSC)

o-CRESYL GLYCIDYL ETHER (ICSC)

o-DIANISIDINE (ICSC)

o-DIETHYLBENZENE (ICSC)

o-NITROTOLUENE (ICSC)

o-PHENYLPHENOL (ICSC)

o-TOLUENESULFONAMIDE (ICSC)

ortho-TOLUIDINE (ICSC)

p-BENZOQUINONE (ICSC)

p-CHLOROBENZOIC ACID (ICSC)

p-NITROTOLUENE (ICSC)

p-OCTYLPHENOL (ICSC)

p-TOLUENESULFONAMIDE (ICSC)

para-CRESIDINE (ICSC)

para-TOLUIDINE (ICSC)

para-tert-BUTYLPHENOL (ICSC)

sec-BUTYLAMINE (ICSC)

sec-HEXYL ACETATE (ICSC)

tert-BUTYL CHROMATE (ICSC)

trans-2-BUTENE (ICSC)

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Supplementary Documents

SECTION 1. CHEMICAL IDENTIFICATION

CHEMINFO Record Number: 714

CCOHS Chemical Name: Sulfur dioxide

Synonyms:

Bisulfite

SO2

Sulfurous acid anhydride

Sulfurous anhydride

Sulfurous oxide

Sulfur oxide

Sulphur dioxide

Chemical Name French: Dioxyde de soufre

CAS Registry Number: 7446-09-5

UN/NA Number(s): 1079

RTECS Number(s): WS4550000

EU EINECS/ELINCS Number: 231-195-2

Chemical Family: Sulfur and compounds / inorganic sulfur compound / oxide / dioxide / inorganic gas

Molecular Formula: SO2

Structural Formula: O=S=O

SECTION 2. DESCRIPTION

Appearance and Odour:

Colourless gas with a pungent, irritating odour similar to burning sulfur. Colourless liquid below -10 deg C (14 deg F).

Odour Threshold:

3 to 5 ppm (detection) (12,13); 1 to 3 ppm (detection) (5)

Warning Properties:

Not reliable: odour threshold is about the same magnitude as TLV.

Composition/Purity:

Available as a liquefied compressed gas. The anhydrous grade has a minimum purity of 99.98%.

Uses and Occurrences:

Its major use is a captive intermediate in the production of sulfuric acid. In the pulp and paper industry, sulfur dioxide is used to produce other chemicals such as chlorine dioxide and sodium hyposulfite and is also used in the bleaching of pulp. In food processing, sulfur dioxide is used for fumigating, preserving, bleaching and steeping. It is also used to reduce residual chlorine in potable water, treated sewage and industrial effluent, as an oxygen scavenger, a selective extraction solvent and as a catalyst in chemical processes. In the presence of a catalyst (e.g. nitrogen compounds), sulfur dioxide can be oxidized to sulfuric acid. Occurs as a by-product during the burning (combustion) of sulfur containing organic compounds (e.g. coal). A common component of air pollution, it is a major contributor to acid rain.

SECTION 3. HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW:

Colourless gas with a pungent, irritating odour similar to burning sulfur. Colourless liquid below -10 deg C. Will not burn. COMPRESSED GAS. Cylinders or tanks may rupture and explode if heated. VERY TOXIC. May be fatal if inhaled. CORROSIVE to the eyes, skin and respiratory tract. Causes lung injury– effects may be delayed. May cause blindness. May cause permanent scarring. May cause frostbite.

Important New Information:

NOTE: The evaluation of this chemical as a chronic toxicity hazard is under review. For additional information, contact the CHEMINFO team.

POTENTIAL HEALTH EFFECTS

Effects of Short-Term (Acute) Exposure

Inhalation:

Sulfur dioxide (SO2) is a gas, which is corrosive to the respiratory tract. Most inhaled SO2 only penetrates as far as the nose and throat with minimal amounts reaching the lungs unless the person is breathing heavily, breathing only through the mouth or the concentration of SO2 is high.

Sensitivity varies among people, however, short exposure (1-6 hours) to concentrations as low as 1 ppm may produce a reversible decrease in lung function.(9) A 10 to 30 minute exposure to concentrations as low as 5 ppm has produced constriction of the bronchiole tubes. Only one of eleven volunteers showed any effects at 1 ppm.(23) A 20-minute exposure to 8 ppm has produced reddening of the throat and mild nose and throat irritation.(24,25) About 20 ppm is objectionably irritating, although people have been reported to work in concentrations exceeding 20 ppm. 500 ppm is so objectionable that a person cannot inhale a single deep breath.(9) In severe cases where very high concentrations of SO2 have been produced in closed spaces, SO2 has caused severe airways obstruction, hypoxemia (insufficient oxygenation of the blood), pulmonary edema (a life threatening accumulation of fluid in the lungs), and death in minutes.(7,26,27) The effects of pulmonary edema include coughing and shortness of breath which can be delayed until hours or days after the exposure. These symptoms are aggravated by physical exertion. As a result of severe exposures, permanent lung injury may occur.(26,27)

Skin Contact:

The gas will react with moisture on the skin and can cause severe irritation or corrosive injury if the concentration is high or exposure is prolonged. Corrosive materials are capable of causing burns and blistering.

Liquid SO2 may cause burns due to freezing.(2) Symptoms of mild frostbite include numbness, prickling and itching in the affected area. The skin may become white or yellow. Blistering, necrosis (dead skin) and gangrene may develop in severe cases.

Eye Contact:

Volunteers exposed to 5.4 ppm SO2 experienced mild irritation, while 9.1 ppm cause moderate to severe irritation.(31) At 8-12 ppm, smarting of the eyes and lachrymation (tears) began. There is strong irritation at 50 ppm.(30) In severe cases, (very high concentrations in confined spaces), SO2 has caused temporary corneal burns.(27) Liquid SO2 can burn the eye and permanently affect vision. Injury from contact with liquid SO2 may not be immediately noticed by the victim because SO2 damages the nerves of the eye. Any eye contact should be treated as very serious.(30)

Ingestion:

Not applicable. Ingestion of gaseous or liquid SO2 is highly unlikely.

Effects of Long-Term (Chronic) Exposure

Lungs/Respiratory System:

Several human studies have shown that repeated exposure to low levels of SO2 (below 5 ppm) has caused permanent pulmonary impairment. This effect is probably due to repeated episodes of bronchoconstriction.(15) One study has found a decrease in lung function in smelter workers exposed for over 1 year to 1-2.5 ppm SO2. No effect was seen in the same study in workers exposed to less than 1 ppm.(32) In another study, a high incidence of respiratory symptoms was reported in workers exposed to 20-30 ppm for an average of 4 years. Workers exposed to daily average values of 5 ppm SO2 (with occasional peaks of 53 ppm) had a much higher incidence of chronic bronchitis than controls.(18)

There are numerous studies on the potential effects of SO2 as a component of air pollution.(9) These studies are difficult to interpret because of confounding factors and uncertainty about exposure concentrations.

Skin:

There are two case reports of individuals developing skin eruptions after repeated inhalation of high concentrations. In later tests, it was found that as little as a 30-minute exposure to 10 ppm SO2 or a 1-hour exposure to 4 ppm SO2 could produce the skin eruptions. The eruptions disappeared after removal from exposure. These particular reactions are probably rare as there are no other reports of this type of reaction.(5)

Carcinogenicity:

Several epidemiological studies have examined the possibility that sulfur dioxide may cause cancers such as lung cancer, stomach cancer or brain tumours. In all of the studies, there were uncontrolled confounding factors, such as concurrent exposure to other chemicals. The International Agency for Cancer (IARC) has reviewed these studies and concluded there is inadequate evidence for carcinogenicity in humans. However, there is limited evidence of carcinogenicity in animals.(18)

The International Agency for Research on Cancer (IARC) has concluded that this chemical is not classifiable as to its carcinogenicity to humans (Group 3).

The American Conference of Governmental Industrial Hygienists (ACGIH) has designated this chemical as not classifiable as a human carcinogen (A4).

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

Teratogenicity and Embryotoxicity:

No human information is available. In animal studies, no teratogenic effects were observed. However, slight fetotoxicity such as reduced birth weight and functional deficits have been reported at doses which were probably toxic to the mother.

Reproductive Toxicity:

A number of epidemiological studies have suggested that exposure to SO2 may be related to adverse reproductive effects. However, it is not clear that SO2 caused the effects observed in any of these studies.(18) There are no relevant results from animal studies.

Mutagenicity:

Conflicting results have been reported in tests on cultured human lymphocytes (white blood cells) taken from workers exposed to sulfur dioxide over several years. In all of the studies, there were serious confounding factors such as exposure to other chemicals and poorly defined control groups.(18)

Toxicologically Synergistic Materials:

Insufficient information is available. Human studies have examined the effect of exposure to SO2 along with other irritating gases such as ozone and nitrogen dioxide. No conclusive evidence of synergistic action has been seen in humans. In animal studies, it has been reported that exposure to SO2 along with soluble particles such as ferrous iron and manganese and vanadium increases the toxic action of SO2.(9)

Potential for Accumulation:

SO2 may enter the body by the respiratory tract or following dilution in saliva. Most studies in both man and animals have indicated that 40-90% or more of inhaled SO2 is absorbed in the moist upper respiratory tract. SO2 is quickly converted to sulfurous acid upon contact with moist mucous membranes. Inhaled SO2 is only slowly removed from the respiratory tract. After absorption in the blood stream, the sulfurous acid is widely distributed throughout the body, quickly converted to sulfite and bisulfite, which in turn is oxidized to sulfate and excreted in the urine.(9,14,18)

SECTION 4. FIRST AID MEASURES

Inhalation:

Take proper precautions to ensure your own safety before attempting rescue (e.g. wear appropriate protective equipment, use the buddy system). Remove source of contamination or move victim to fresh air. If breathing is difficult, oxygen may be beneficial if administered by trained personnel, preferably on a doctor’s advice. DO NOT allow victim to move about unnecessarily. Symptoms of pulmonary edema can be delayed up to 48 hours after exposure. Immediately transport victim to an emergency care facility.

Skin Contact:

GAS: Take measures to prevent skin contact. If irritation occurs, flush contaminated area with lukewarm, gently running water for at least 5 minutes. If irritation persists, obtain medical attention immediately. LIQUID: Avoid direct contact. Wear chemical protective clothing, if necessary. Quickly remove victim from source of contamination and briefly flush with lukewarm, gently flowing water until the chemical is removed. DO NOT attempt to rewarm the affected area on site. DO NOT rub area or apply dry heat. Gently remove clothing or jewelry that may restrict circulation. Carefully cut around clothing that sticks to the skin and remove the rest of the garment. Loosely cover the affected area with a sterile dressing. DO NOT allow victim to drink alcohol or smoke. Quickly transport victim to an emergency care facility.

Eye Contact:

Avoid direct contact. Wear chemical protective gloves, if necessary. Remove source of contamination or move victim to fresh air. Immediately flush the contaminated eye(s) with lukewarm, gently flowing water for at least 5 minutes for the gas (20 minutes for the liquid) or until the chemical is removed, while holding the eyelid(s) open. Take care not to rinse contaminated water into the unaffected eye or onto the face. Quickly transport victim to an emergency care facility.

Ingestion:

Ingestion is not an applicable route of exposure for gases.

First Aid Comments:

Provide general supportive measures (comfort, warmth, rest).

Consult a doctor and/or the nearest Poison Control Centre for all exposures except under minor instances of inhalation or skin contact. Some recommendations in the above sections may be considered medical acts in some jurisdictions. These recommendations should be reviewed with a doctor and appropriate delegation of authority obtained, as required. All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.

SECTION 5. FIRE FIGHTING MEASURES

Flash Point:

Not applicable (not combustible)

Lower Flammable (Explosive) Limit (LFL/LEL):

Not applicable

Upper Flammable (Explosive) Limit (UFL/UEL):

Not applicable

Autoignition (Ignition) Temperature:

Not applicable

Sensitivity to Mechanical Impact:

Not available

Sensitivity to Static Charge:

Not applicable

Combustion and Thermal Decomposition Products:

None formed

Fire Hazard Summary:

Non-flammable gas. However, heat from a surrounding fire can rupture cylinders, causing a dangerous explosion and the release of toxic sulfur dioxide gas. Cylinders have fusible metal plugs which melt at 165 deg F, releasing SO2.

Extinguishing Media:

Non-flammable gas. Use extinguishing media appropriate for surrounding fire.

Fire Fighting Instructions:

Sulfur dioxide (SO2) is not combustible. Use extinguishing media suitable for the surrounding fire. In an advanced or massive fire, evacuate area and fight fire from a safe distance or a protected location. Approach fire from upwind to avoid SO2. If fire occurs in the vicinity of SO2, use unmanned monitors and hoseholders to keep cooling streams of water on fire-exposed cylinders or tanks until well after the fire is out. If possible, isolate materials not yet involved in the fire and protect personnel. Move containers from fire area if this can be done without risk.

Tanks or cylinders should not be approached directly after they have been involved in a fire until they have completely cooled down.

Protection of Fire Fighters:

SO2 is extremely hazardous to health (inhalation and skin corrosion hazard). Do not enter without wearing specialized protective equipment suitable for the situation. Firefighter’s normal protective clothing (Bunker Gear) will not provide adequate protection. A full-body encapsulating chemical protective suit with positive pressure self-contained breathing apparatus (NIOSH approved or equivalent) may be necessary.

NATIONAL FIRE PROTECTION ASSOCIATION (NFPA) HAZARD IDENTIFICATION

NFPA – Health: 3 – Short exposure could cause serious temporary or residual injury.

NFPA – Flammability: 0 – Will not burn under typical fire conditions.

NFPA – Instability: 0 – Normally stable, even under fire conditions, and not reactive with water.

SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES

Molecular Weight: 64.06

Conversion Factor:

1 ppm = 2.61 mg/m3; 1 mg/m3 = 0.38 ppm at 25 deg C (calculated)

Physical State: Gas

Melting Point: -72.7 deg C (-99 deg F) (5,18)

Boiling Point: -10 deg C (14 deg F) (2,5,13)

Relative Density (Specific Gravity): Not applicable (gas)

Solubility in Water: Very soluble (11.28 g/100 mL at 20 deg C) (2)

Solubility in Other Liquids: Not applicable. In water, sulfur dioxide is rapidly converted (hydrated) to sulfurous acid which is a dibasic acid (pH less than 3) (14,18) Soluble in acetone and other ketones, methanol, ethanol, acetic acid, diethyl ether, chloroform and sulfuric acid (5)

Coefficient of Oil/Water Distribution (Partition Coefficient): Not applicable (gas)

pH Value: Not applicable. In water, SO2 is rapidly converted to sulfurous acid (pH less than 3) (14,18)

Vapour Density: 2.26 (air = 1) (2)

Vapour Pressure: 339 kPa (2543 mm Hg) at 21.1 deg C (2)

Vapour Pressure at 50 deg C: 770 kPa (7.6 atm) (5800 mm Hg) (estimated from graph) (2b)

Saturation Vapour Concentration: Not applicable (gas)

Evaporation Rate: Not applicable (gas)

Critical Temperature: 157.6 deg C (315.7 deg F) (2)

Critical Pressure: 7884 kPa (2)

SECTION 10. STABILITY AND REACTIVITY

Stability:

SO2 is extremely stable to heat, even up to 2000 deg C. Complex reactions of SO2 occur in the atmosphere. SO2 gas and its aqueous forms are oxidized to sulfuric and sulfates which contribute to air pollution.(18)

Hazardous Polymerization:

Does not occur

Incompatibility – Materials to Avoid:

BASES (e.g. sodium hydroxide) – Violent reactions can occur.

CHLORATES (e.g. potassium chlorate) – Above 60 deg C, contact with SO2 can produce chlorine dioxide which can flash and explode. Solutions of SO2 in ethanol or ether can cause an explosion on contact with potassium chlorate at ambient temperature.(10,16)

FLUORINE – Contact can produce an explosion.(10,16)

INTERHALOGENS (e.g. bromine pentafluoride, chlorine trifluoride) – Contact can be violent and ignite or produce an explosion.(10,16)

POWDERED METALS – Finely divided (pyrophoric) chromium incandesces in SO2; pyrophoric manganese burns brilliantly on heating in gas; powdered aluminum burns in the vapour of SO2; molten sodium reacts violently with dry gas or liquid; cold sodium and moist gas react vigorously.(10,16)

METAL OXIDES (e.g. cesium oxide, stannous (tin) oxide) – Will ignite and glow on heating in the gas.(10,16)

METAL ACETYLIDES (e.g. monocesium acetylide, monopotassium acetylide) – Will ignite and glow in unheated gas.(10)

SODIUM HYDRIDE – Reacts explosively on contact, unless diluted with hydrogen.(10)

CESIUM AZIDE – Ignites on contact at ambient temperature.(10)

SILVER AZIDE – Mixtures become explosive at elevated temperatures.(10)

DIETHYL ZINC – Addition to liquid SO2 at -15 deg C leads to an explosive reaction.(10)

Hazardous Decomposition Products:

Forms an acid solution (sulfurous acid) upon contact with moisture

Conditions to Avoid:

Moisture

Corrosivity to Metals:

Anhydrous SO2 is non-corrosive to steel and other common metals. However, in the presence of moisture (water), it can corrode aluminum, steel and most common metals.(2,13)

Stability and Reactivity Comments:

In some cases, SO2 behaves as both a reducing and oxidizing agent (metals such as tin, iron and magnesium burn in SO2 to form mixed sulfides and oxides).(2)

SECTION 11. TOXICOLOGICAL INFORMATION

LC50 (rat): 2520 ppm (1-hour exposure) (1)

LC50 (mouse, male): 3000 ppm (30-minute exposure) (1)

Eye Irritation:

Temporary clouding of eyes was seen in rabbits, guinea pigs and mice exposed for 4 hours to 400 ppm. Very severe eye injury in rabbits was produced by a 5-second exposure to a stream of pure sulfur dioxide (SO2).(30)

Effects of Short-Term (Acute) Exposure:

Inhalation:

Most studies indicate that high concentrations of SO2 affect the mechanics of respiration. A dose- related narrowing of the bronchiole tubes leading to the bronchoconstriction (increased airway resistance) was seen in guinea pigs exposed to concentrations of 0.2-100 ppm (0.6-260 mg/m3) for 1 hour.(9) Exposure of male mice for up to 72 hours to concentrations around 10 ppm (26 mg/m3) produced nasal cavity injury (e.g. runny nose, ciliary loss, fluid accumulation and tissue death). The effects became more severe as exposure time was increased. Less severe effects were seen in the trachea and lungs.(12) Other studies have not reported any effects after 1 to 2-hour exposure to concentrations of less than 1 ppm (2.6 mg/m3).(9)

Effects of Long-Term (Chronic) Exposure:

Inhalation:

Exposure to 5 ppm for 225 days produced pulmonary function changes in dogs.(15) Increased swelling, secretions and reddening of the trachea, as well as decreased tracheal mucosal flow was seen in dogs exposed intermittently to 1 ppm for 12 months. There was no apparent effect on pulmonary function.(20) No adverse effects were seen in guinea pigs exposed for 22 hrs/day, 7 days/week for 52 weeks to concentrations of 0.13-5.72 ppm.(21) No adverse effects were seen in monkeys exposed for 78 weeks to 0.14-1.28 ppm.(22)

Respiratory Sensitization:

Exposure to 4.3 ppm SO2 8 hours/day for 5 days has enhanced allergic sensitization to inhaled ovalbumin (a known allergen) in guinea pigs. Further research has shown that this effect can be blocked if the animals are pre-treated with anti-inflammatory drugs.(3)

Carcinogenicity:

500 ppm SO2 was inhaled by mice (35 male, 30 female) 5 minutes/day, 5 days/week for life. Female mice showed a statistically significant increase in lung tumours. Male mice did not. There are a number of design problems with this study, for example, only one dose group and the small number of animals. The International Agency for Research on Cancer (IARC) concluded there is limited evidence for carcinogenicity in experimental animals.(18) A number of studies have investigated the possibility that SO2 can act as a cocarcinogen (promotes the carcinogenicity of other chemicals). However, these studies have been questioned because of design problems such as too few animals for statistically significant results. Therefore, there is no conclusive evidence that SO2 is a cocarcinogen.(4,18)

Teratogenicity, Embryotoxicity and/or Fetotoxicity:

Slight signs of fetotoxicity (reduced birth weight and delayed righting reflex) were seen in mice exposed to 32, 65, 125 or 250 ppm.(11,18) The authors reported no maternal toxicity. However, other studies indicated that these doses would cause significant irritation. Slight embryotoxicity (decreased fetal body weight, delayed bone development) was seen when pregnant mice were exposed to 25 ppm during days 6-15 of pregnancy. Slight embryotoxicity (minor bone variations) was also seen when pregnant rabbits were exposed to 70 ppm during days 6-15 of pregnancy. Mild maternal toxicity was seen in the pregnant mice and rabbits.(28)

Reproductive Toxicity:

In one study, there was a significant reduction in testes weight in rats whose ability to metabolize SO2 was severely compromised.(19) These results are not relevant to normal exposure situations. In a Russian study, exposure of female rats to 1.9 ppm (4.97 mg/m3) for 12 hours/day for 3 months affected the female reproductive cycle. It returned to normal within 7 months after exposure.(18) There are not enough details available to evaluate this study.

Mutagenicity:

SO2 did not induce sister chromatid exchange (SCE), chromosomal aberrations or micronucleus formation in the bone marrow of mice or Chinese hamsters in in-vivo tests.(18)

SO2 induced morphological transformation of Syrian hamster embryo cells (in-vitro).(18) Bisulfite induced both transformation and SCE, but not gene mutation, chromosomal aberrations or DNA repair synthesis in cultured mammalian cells.(14,18) SO2 and its aqueous forms gave both positive and negative results in bacterial tests.(18)

Toxicological Synergisms:

The presence of soluble particles such as ferrous iron, manganese and vanadium has increased the toxic action of inhaled SO2. It has been suggested that this may be due to conversion of SO2 to sulfurous acid by moisture, the oxidation of SO2 to sulfuric acid by catalytic metal ions, or the deeper penetration of SO2 into the lungs because of the particles.(4,9)

SECTION 16. OTHER INFORMATION

Selected Bibliography:

(1) RTECS record for sulfur dioxide. Last updated 9306

(2a) Braker, W., et al. Matheson gas data book. 6th ed. Matheson, 1980. p. 641-648

(2b) Yaws, C.L. Matheson gas data book. 7th ed. McGraw-Hill, 2001. p. 598

(3) Riedel, F., et al. SO2-Induced enhancement of inhalative allergic sensitization: inhibition by anti-inflammatory treatment. Int Arch Allergy Immunol. Vol. 98 (1992). p. 386-391

(4) Mehlman, M.A. Current toxicological information as the basis for sulfur oxide standards. Environmental Health Perspectives. Vol. 52 (1983). p. 261-266

(5) Sulfur dioxide (Hygienic Guide Series). American Industrial Hygiene Association, n.d.

(6) NIOSH pocket guide to chemical hazards. NIOSH, June 1994. p. 288-289

(7) Rabinovitch, S., et al. Clinical and laboratory features of acute sulfur dioxide inhalation poisoning : two-year follow-up (case report). American Review of Respiratory Disease. Vol. 139, no. 2 (Feb. 1989). p. 556-558

(8) Sulfur dioxide. In : Documentation of the threshold limit values and biological exposure indices. 5th ed. ACGIH, 1987. p. 542-543

(9) Ericsson, G. Health effects of sulfur oxides and particulate matter in ambient air. Scandinavian Journal of Work, Environment and Health. Vol. 9, Supplement 3 (1983)

(10) Bretherick, L. Bretherick’s handbook of reactive chemical hazards. 4th ed. Butterworths, 1990. p. 1414-1415

(11) Singh, J. Neonatal development altered by maternal sulfur dioxide exposure. NeuroToxicology. Vol. 10 (1989). p. 523-527

(12) Giddens, W.E., et al. Effects of sulfur dioxide on the nasal mucosa of mice. Archives of Environmental Health. Vol. 25 (1972). p. 166-173

(13) Handbook of compressed gases. 2nd ed. Van Nostrand Reinhold Company, 1981. p. 441-449

(14) Shapiro, R. Genetic effects of bisulfite (sulfur dioxide). Mutation Research. Vol. 39 (1977). p. 149-175

(15) Sulfur Dioxide. Air contaminants Final Rule (29 CFR Part 1910). Federal Register. Vol. 54, no. 12. January 19, 1989. p. 2524-2526

(16) Fire protection guide to hazardous materials. 13th ed. Edited by A.B. Spencer, et al. National Fire Protection Association, 2002. NFPA 49; NFPA 491

(17) Forsberg, K., et al. Quick selection guide to chemical protective clothing. 4th ed. Van Nostrand Reinhold, 2002

(19) Gunnison, A.F., et al. Distribution, metabolism and toxicity of inhaled sulfur dioxide and endogenously generated sulfite in the respiratory tract of normal and sulfite oxidase- deficient rats. Journal of Toxicology and Environmental Health. Vol. 21 (1987). p. 141-162

(20) Hirsch, J.A., et al. Tracheal mucous transport in beagles after long-term exposure to 1 ppm sulfur dioxide. Archives of Environmental Health. Vol. 30 (May 1975). p. 249-253

(21) Alarie, Y., et al. Long-term continuous exposure of guinea pigs to sulfur dioxide. Archives of Environmental Health. Vol. 24 (Dec. 1970). p. 769-777

(22) Alarie, Y., et al. Long-term continuous exposure to sulfur dioxide in cynomolgus monkeys. Archives of Environmental Health. Vol. 24 (Feb. 1972). p. 115-127

(23) Frank, N.R., et al. Effects of acute controlled exposure to SO2 on respiratory mechanics in healthy male adults. Journal of Applied Physiology. Vol. 17 (Mar. 1962). p. 252-258

(24) Sandstrom, T., et al. Is the short term limit value for sulphur dioxide exposure safe? Effects of controlled chamber exposure investigated with bronchoalveolar lavage. British Journal of Industrial Medicine. Vol. 46 (1989). p. 200-203

(25) Sandstrom, T., et al. Cell response in bronchoalveolar lavage fluid after exposure to sulfur dioxide : a time-response study. American Review of Respiratory Disease. Vol. 140, no. 6 (Dec. 1989). p. 1828-1831

(26) Galea, M. Fatal sulfur dioxide inhalation. Canadian Medical Association Journal. Vol. 91 (Aug. 1964). p. 345-347

(27) Charan, N.B., et al. Pulmonary injuries associated with acute sulfur dioxide inhalation. American Review of Respiratory Disease. Vol. 119, no. 4 (Apr. 1979). p. 555-560

(28) Murray, F.J., et al. Teratogenic potential of sulfur dioxide and carbon monoxide in mice and rabbits. In : Developmental toxicology of energy-related pollutants. Proceedings of the Seventeenth Annual Hanford Biology Symposium : held in Richland, Washington, October 17-19, 1977. p. 469-478

(29) Air sampling instruments for evaluation of atmospheric contaminants. 7th ed. ACGIH, 1989. p. 474-476, 507-581

(30) Grant, W.M. Toxicology of the eye. 3rd ed. Charles C. Thomas, 1986. p. 862-865

(31) Hine, C.H., et al. Eye irritation from air pollution. Journal of the Air Pollution Control Association. Vol 10, no. 1 (Feb. 1960). p. 17-20

(32) Smith, T.J., et al. Pulmonary impairment from chronic exposure to sulfur dioxide in a smelter. American Review of Respiratory Disease. Vol. 116 (1977). p. 31-39

(33) Emergency response planning guidelines. AIHA Journal. Vol. 56, no. 3, 1995. p. 297

(34) Safety Equipment Institute. Certified Product List, May 1996. SEI, Arlington, Virginia, USA

(35) European Communities (EC). Commission Directive 2001/59/EC. Aug. 6, 2001

Review/Preparation Date: 1993-11-09

Revision Indicators:

EU number 1996-06-01

Sampling 1996-06-01

Respiratory guidelines 1996-06-01

TLV-TWA 1996-09-01

TLV comments 1996-09-01

US transport 1998-03-01

Resistance of materials 1998-05-01

EU classification 2002-02-11

EU Safety 1998-11-01

EU comments 2002-02-11

EU risks 2002-02-11

TDG 2002-05-27

WHMIS detailed classification 2002-06-07

WHMIS proposed classification 2002-06-07

WHMIS health effects 2002-06-07

Corrosivity to metals 2002-06-12

Emergency overview 2002-06-12

First aid eye 2002-06-12

Handling 2002-06-14

Storage 2002-06-14

US transport 2002-12-04

Carcinogenicity 2002-12-23

WHMIS classification comments 2003-05-13

Important New Information 2003-05-13

Chemical Name French 2003-05-13

Short-term inhalation 2003-06-02

Short-term skin contact 2003-06-02

PEL-TWA final 2003-10-30

PEL-STEL final 2003-10-30

PEL final comments 2003-10-30

PEL transitional comments 2003-10-30

Resistance of materials for PPE 2004-03-28

Bibliography 2006-01-18

Vapour pressure at 50 deg C 2006-01-18

Relative density 2006-09-28

TLV-TWA 2007-03-06

TLV proposed changes 2007-03-06