Chlorine
| 1. NAME |
| 1.1 Substance |
| 1.2 Group |
| 1.3 Synonyms |
| 1.4 Identification numbers |
| 1.4.1 CAS number |
| 1.4.2 Other numbers |
| 1.5 Main brand names, main trade names |
| 1.6 Main manufacturers, main importers |
| 2. SUMMARY |
| 2.1 Main risks and target organs |
| 2.2 Summary of clinical effects |
| 2.3 Diagnosis |
| 2.4 First aid measures and management principles |
| 3. PHYSICO-CHEMICAL PROPERTIES |
| 3.1 Origin of the substance |
| 3.2 Chemical structure |
| 3.3 Physical properties |
| 3.3.1 Colour |
| 3.3.2 State/Form |
| 3.3.3 Description |
| 3.4 Hazardous characteristics |
| 4. USES |
| 4.1 Uses |
| 4.1.1 Uses |
| 4.1.2 Description |
| 4.2 High risk circumstance of poisoning |
| 4.3 Occupationally exposed populations |
| 5. ROUTES OF EXPOSURE |
| 5.1 Oral |
| 5.2 Inhalation |
| 5.3 Dermal |
| 5.4 Eye |
| 5.5 Parenteral |
| 5.6 Other |
| 6. KINETICS |
| 6.1 Absorption by route of exposure |
| 6.2 Distribution by route of exposure |
| 6.3 Biological half-life by route of exposure |
| 6.4 Metabolism |
| 6.5 Elimination and excretion |
| 7. TOXICOLOGY |
| 7.1 Mode of action |
| 7.2 Toxicity |
| 7.2.1 Human data |
| 7.2.1.1 Adults |
| 7.2.1.2 Children |
| 7.2.2 Relevant animal data |
| 7.2.3 Relevant in vitro data |
| 7.2.4 Workplace standards |
| 7.2.5 Acceptable daily intake (ADI) |
| 7.3 Carcinogenicity |
| 7.4 Teratogenicity |
| 7.5 Mutagenicity |
| 7.6 Interactions |
| 8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS |
| 8.1 Material sampling plan |
| 8.1.1 Sampling and specimen collection |
| 8.1.1.1 Toxicological analyses |
| 8.1.1.2 Biomedical analyses |
| 8.1.1.3 Arterial blood gas analysis |
| 8.1.1.4 Haematological analyses |
| 8.1.1.5 Other (unspecified) analyses |
| 8.1.2 Storage of laboratory samples and specimens |
| 8.1.2.1 Toxicological analyses |
| 8.1.2.2 Biomedical analyses |
| 8.1.2.3 Arterial blood gas analysis |
| 8.1.2.4 Haematological analyses |
| 8.1.2.5 Other (unspecified) analyses |
| 8.1.3 Transport of laboratory samples and specimens |
| 8.1.3.1 Toxicological analyses |
| 8.1.3.2 Biomedical analyses |
| 8.1.3.3 Arterial blood gas analysis |
| 8.1.3.4 Haematological analyses |
| 8.1.3.5 Other (unspecified) analyses |
| 8.2 Toxicological Analyses and Their Interpretation |
| 8.2.1 Tests on toxic ingredient(s) of material |
| 8.2.1.1 Simple Qualitative Test(s) |
| 8.2.1.2 Advanced Qualitative Confirmation Test(s) |
| 8.2.1.3 Simple Quantitative Method(s) |
| 8.2.1.4 Advanced Quantitative Method(s) |
| 8.2.2 Tests for biological specimens |
| 8.2.2.1 Simple Qualitative Test(s) |
| 8.2.2.2 Advanced Qualitative Confirmation Test(s) |
| 8.2.2.3 Simple Quantitative Method(s) |
| 8.2.2.4 Advanced Quantitative Method(s) |
| 8.2.2.5 Other Dedicated Method(s) |
| 8.2.3 Interpretation of toxicological analyses |
| 8.3 Biomedical investigations and their interpretation |
| 8.3.1 Biochemical analysis |
| 8.3.1.1 Blood, plasma or serum |
| 8.3.1.2 Urine |
| 8.3.1.3 Other fluids |
| 8.3.2 Arterial blood gas analyses |
| 8.3.3 Haematological analyses |
| 8.3.4 Interpretation of biomedical investigations |
| 8.4 Other biomedical (diagnostic) investigations and their interpretation |
| 8.5 Overall interpretation of all toxicological analyses and toxicological investigations |
| 8.6 References |
| 9. CLINICAL EFFECTS |
| 9.1 Acute poisoning |
| 9.1.1 Ingestion |
| 9.1.2 Inhalation |
| 9.1.3 Skin exposure |
| 9.1.4 Eye contact |
| 9.1.5 Parenteral exposure |
| 9.1.6 Other |
| 9.2 Chronic poisoning |
| 9.2.1 Ingestion |
| 9.2.2 Inhalation |
| 9.2.3 Skin exposure |
| 9.2.4 Eye contact |
| 9.2.5 Parenteral exposure |
| 9.2.6 Other |
| 9.3 Course, prognosis, cause of death |
| 9.4 Systematic description of clinical effects |
| 9.4.1 Cardiovascular |
| 9.4.2 Respiratory |
| 9.4.3 Neurological |
| 9.4.3.1 Central nervous system (CNS) |
| 9.4.3.2 Peripheral nervous system |
| 9.4.3.3 Autonomic nervous system |
| 9.4.3.4 Skeletal and smooth muscle |
| 9.4.4 Gastrointestinal |
| 9.4.5 Hepatic |
| 9.4.6 Urinary |
| 9.4.6.1 Renal |
| 9.4.6.2 Other |
| 9.4.7 Endocrine and reproductive systems |
| 9.4.8 Dermatological |
| 9.4.9 Eye, ear, nose, throat: local effects |
| 9.4.10 Haematological |
| 9.4.11 Immunological |
| 9.4.12 Metabolic |
| 9.4.12.1 Acid-base disturbances |
| 9.4.12.2 Fluid and electrolyte disturbances |
| 9.4.12.3 Others |
| 9.4.13 Allergic reactions |
| 9.4.14 Other clinical effects |
| 9.4.15 Special risks |
| 9.5 Other |
| 9.6 Summary |
| 10. MANAGEMENT |
| 10.1 General principles |
| 10.2 Life supportive procedures and symptomatic/specific treatment |
| 10.3 Decontamination |
| 10.4 Enhanced elimination |
| 10.5 Antidote treatment |
| 10.5.1 Adults |
| 10.5.2 Children |
| 10.6 Management discussion |
| 11. ILLUSTRATIVE CASES |
| 11.1 Case reports from literature |
| 12. Additional information |
| 12.1 Specific preventive measures |
| 12.2 Other |
| 13. REFERENCES |
| 14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES) |
Chlorine
International Programme on Chemical Safety
Poisons Information Monograph 947
Chemical
This Monograph contain the following sections
completed: 1, 2, 3, 4.1, 4.2, 7.2, 9, 10 & 11.
1. NAME
1.1 Substance
Chlorine
1.2 Group
Chlorine and compounds
Group VIIa (17) element
1.3 Synonyms
Chlore; Liquefied chlorine gas;
Molecular chlorine
1.4 Identification numbers
1.4.1 CAS number
7782-50-5
1.4.2 Other numbers
UN/NA number: 1017
RTECS number: FO2100000
EU EINECS/ELINCS number: 231-959-5
1.5 Main brand names, main trade names
1.6 Main manufacturers, main importers
2. SUMMARY
2.1 Main risks and target organs
Chlorine reacts with tissue water to form hydrochloric
and hypochlorous acids, thus a potent irritant of the eyes,
skin and mucous membranes, and respiratory tract. Injury is
proportional to the concentration of the gas, duration of
contact and water content of exposed tissues. Evidence
exists suggesting that patients with pre-existing respiratory
disease may be at greater risk from chlorine exposure. The
extent of the injury depends upon the concentration and
duration of the exposure, as well as the water content of the
tissue involved and the presence of underlying
cardiopulmonary disease.
2.2 Summary of clinical effects
EXPOSURE SYMPTOMS
1 to 3 ppm Mild mucous membrane irritation after 1 hour
5 to 15 ppm Moderate irritation of upper respiratory tract
30 ppm Immediate chest pain, vomiting, and coughing
40 to 60 ppm Toxic pneumonitis and pulmonary oedema
430 ppm Lethal after 30 minutes
1,000 ppm Fatal within a few minutes
Inhalation: Initially: irritation of the eyes, nose and
throat, followed by coughing and wheezing, dyspnoea, sputum
production and chest pain. Larger exposures may lead to
hyperchloraemic acidosis; anoxia may lead to cardiac and/or
respiratory arrest and pulmonary oedema. Following chemical
pneumonitis respiratory distress and chest pain generally
subsides within 72 hours; cough may persist for up to 14
days, however in one case reduced airway flow and mild
hyopoxemia persisted for 14 months.
Dermal: Irritation, pain, erythema, blister and burns.
Liquid chlorine may cause burns on contact.
Eyes: Irritation and conjunctivitis. Liquid chlorine may
cause burns on contact.
2.3 Diagnosis
The specific odour of chlorine, the respiratory, eye and
skin symptoms following exposure make the diagnosis.
Measurement of the air levels of chlorine is of significance
in occupational circumstances and case of accidental release.
2.4 First aid measures and management principles
Care workers must ensure adequate protection to prevent
self-contamination when carrying out decontamination and
medical treatment. Remove contaminated clothing and put in a
sealed bag.
Inhalation:
Patients without immediate symptoms may require no treatment,
but a full physical examination and a record of respiratory
peak flow may be of use in assessing any subsequent
respiratory effects.
Patients with mild effects: require a full physical
examination and peak flow and discharge accordingly, and
advised to return if symptoms recur or develop over the
following 24 to 36 hours.
Patients showing immediate moderate or severe effects: Check
lung function and perform chest x-rays. Oxygen and
bronchodilators (e.g. salbutamol; orally or inhaled) are used
for bronchospasm. Pulmonary oedema should be treated with
Positive End Expiratory Pressure (PEEP), or Constant Positive
Airway Pressure (CPAP). Corticosteroids may inhibit the
inflammatory response and should be considered in severe
cases. Monitor arterial blood gases, treat hyperchloraemic
acidosis.
Patients with pre-existing respiratory disease: assess and
consider admission for at least 24 hours.
Dermal: Wash thoroughly with running water or saline. Treat
as a thermal burn, if necessary.
Eyes: Irrigate thoroughly for 10 to 15 minutes. Refer to
an ophthalmologist.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
3.2 Chemical structure
Chemical formula: Cl2
Structural Formula: Cl-Cl
Molecular weight: 70.906
3.3 Physical properties
3.3.1 Colour
Greenish-yellow
3.3.2 State/Form
Gas
3.3.3 Description
Melting Point: -101°C (-149.8 deg F)
Boiling Point: -34.1°C (-29.3 deg F)
Relative Density (Specific Gravity):
1.467 at 0°C and 368.9 kPa (saturated
liquefied gas)
0.0032 at 0°C (gas) (water = 1)
Solubility In Water: Slightly soluble (0.73 g/100 g
water at 20°C) (reacts)
Solubility In Other Liquids: Very soluble in
dimethylformamide; soluble in benzene, chloroform,
carbon tetrachloride, tetrachloroethane,
chlorobenzene, glacial acetic acid (99.84%), sulfuryl
chloride, phosphoryl chloride, silicon tetrachloride
and metal chlorides, such as chromyl chloride,
titanium tetrachloride and vanadium oxide
chloride.
Vapour Density: 2.48 (air=1) (27,28)
Vapour Pressure: 673.1 kPa (6.64 atm) at 20 deg C;
1427 kPa (14.1 atm.) (27)
pH Value: Not applicable (reacts with water to form an
acidic solution)
Critical Temperature: 144 deg C (291.2 deg F)
Critical Pressure: 7711 kPa (76.1 atm) (27,28)
Conversion Factor:
1 ppm = 2.89 mg/m3; 1 mg/m3 = 0.346 ppm at
25 deg C (calculated)
Appearance and Odour:
Greenish-yellow gas or clear amber liquid (under
pressure) with a pungent suffocating odour.
Lachrymator (gas irritates the eyes and causes tears).
(CCOHS, 1998)
3.4 Hazardous characteristics
Chlorine is shipped in steel cylinders as a compressed
liquefied gas under its own vapour pressure of 598 kPa (86.8
psig or 5.9atm.) at 21.1°C. It is available in a number of
grades having a purity of at least 99.5 wt%. Contaminants
are mainly carbon dioxide, nitrogen, oxygen and water, but
may include traces of chlorinated hydrocarbons, such as
hexachloroethane and hexachlorobenzene, inorganic salts such
as ferric chloride, bromine or iodine (CCOHS, 1998).
4. USES
4.1 Uses
4.1.1 Uses
4.1.2 Description
The major uses of chlorine are in the
manufacture of chlorinated organic chemicals (such as
vinyl chloride monomer, carbontetrachloride,
perchlorethylene, 1,1,1-trichloroethane,
chlorobenzenes, chloroprene and epichlorohydrin),
organic chemicals (such as propylene oxide and
glycols) and chlorinated inorganic chemicals (such as
sodium hypochlorite, hydrochloric acid, hypochlorous
acid, sulfur chlorides, phosphorous chlorides,
titanium chlorides and aluminum chloride) (CCOHS,
1998).
It is also widely used as a bleaching agent in the
manufacture of pulp and paper; in bleaching textiles
and fabrics; in the manufacture of pesticides,
herbicides, refrigerants, propellants, household and
commercial bleaches, detergents for automatic
dishwashers, antifreeze, antiknock compounds,
plastics, synthetic rubbers, adhesives and
pharmaceuticals; for drinking and swimming water
purification; sanitation of industrial and sewage
wastes; and in the degassing of aluminum metal (CCOHS,
1998).
4.2 High risk circumstance of poisoning
Household exposures: The mixing of household cleaning
agents (for example bleach and acids) may liberate chlorine
gas.
Environmental exposures: spills and traffic accidents.
4.3 Occupationally exposed populations
5. ROUTES OF EXPOSURE
5.1 Oral
Chlorine exists as a liquid under pressure.
5.2 Inhalation
Main route of exposure to chlorine.
5.3 Dermal
Chlorine gas and liquid exposure can lead to dermal
irritation and burns.
5.4 Eye
Chlorine gas and liquid exposure can lead to ocular
irritation and burns.
5.5 Parenteral
Unknown.
5.6 Other
Unknown.
6. KINETICS
6.1 Absorption by route of exposure
6.2 Distribution by route of exposure
6.3 Biological half-life by route of exposure
6.4 Metabolism
6.5 Elimination and excretion
7. TOXICOLOGY
7.1 Mode of action
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
7.2.1.2 Children
7.2.2 Relevant animal data
7.2.3 Relevant in vitro data
7.2.4 Workplace standards
7.2.5 Acceptable daily intake (ADI)
7.3 Carcinogenicity
7.4 Teratogenicity
7.5 Mutagenicity
7.6 Interactions
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
8.1.1.2 Biomedical analyses
8.1.1.3 Arterial blood gas analysis
8.1.1.4 Haematological analyses
8.1.1.5 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation
8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple Qualitative Test(s)
8.2.1.2 Advanced Qualitative Confirmation Test(s)
8.2.1.3 Simple Quantitative Method(s)
8.2.1.4 Advanced Quantitative Method(s)
8.2.2 Tests for biological specimens
8.2.2.1 Simple Qualitative Test(s)
8.2.2.2 Advanced Qualitative Confirmation Test(s)
8.2.2.3 Simple Quantitative Method(s)
8.2.2.4 Advanced Quantitative Method(s)
8.2.2.5 Other Dedicated Method(s)
8.2.3 Interpretation of toxicological analyses
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
8.3.1.1 Blood, plasma or serum
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.1.2 Urine
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
8.3.3 Haematological analyses
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.4 Interpretation of biomedical investigations
8.4 Other biomedical (diagnostic) investigations and their
interpretation
8.5 Overall interpretation of all toxicological analyses and
toxicological investigations
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
9.1.2 Inhalation
EXPOSURE SYMPTOMS
1 to 3 ppm Mild mucous membrane irritation after
1 hour
5 to 15 ppm Moderate irritation of upper
respiratory tract
30 ppm Immediate chest pain, vomiting, and
coughing
40 to 60 ppm Toxic pneumonitis and pulmonary oedema
430 ppm Lethal after 30 minutes
1,000 ppm Fatal within a few minutes
Initially: irritation of the eyes, nose and throat,
followed by coughing and wheezing, dyspnoea, sputum
production and chest pain. Larger exposures may lead
to hyperchloraemic acidosis; anoxia may lead to
cardiac and/or respiratory arrest and pulmonary
oedema. Following chemical pneumonitis respiratory
distress and chest pain generally subsides within 72
hours; cough may persist for up to 14 days, however in
one case reduced airway flow and mild hyopoxemia
persisted for 14 months.
9.1.3 Skin exposure
Irritation, pain, erythema, blister and burns.
Liquid chlorine may cause burns on contact.
9.1.4 Eye contact
Irritation and conjunctivitis. Liquid chlorine
may cause burns on contact.
9.1.5 Parenteral exposure
9.1.6 Other
9.2 Chronic poisoning
9.2.1 Ingestion
9.2.2 Inhalation
9.2.3 Skin exposure
9.2.4 Eye contact
9.2.5 Parenteral exposure
9.2.6 Other
9.3 Course, prognosis, cause of death
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
9.4.2 Respiratory
9.4.3 Neurological
9.4.3.1 Central nervous system (CNS)
9.4.3.2 Peripheral nervous system
9.4.3.3 Autonomic nervous system
9.4.3.4 Skeletal and smooth muscle
9.4.4 Gastrointestinal
9.4.5 Hepatic
9.4.6 Urinary
9.4.6.1 Renal
9.4.6.2 Other
9.4.7 Endocrine and reproductive systems
9.4.8 Dermatological
9.4.9 Eye, ear, nose, throat: local effects
9.4.10 Haematological
9.4.11 Immunological
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
9.4.12.2 Fluid and electrolyte disturbances
9.4.12.3 Others
9.4.13 Allergic reactions
9.4.14 Other clinical effects
9.4.15 Special risks
9.5 Other
9.6 Summary
10. MANAGEMENT
10.1 General principles
Care workers must ensure adequate protection to prevent
self-contamination when carrying out decontamination and
medical treatment. Remove contaminated clothing and put in a
sealed bag.
Inhalation:
Patients without immediate symptoms may require no treatment,
but a full physical examination and a record of respiratory
peak flow may be of use in assessing any subsequent
respiratory effects.
Patients with mild effects: require a full physical
examination and peak flow and discharge accordingly, and
advised to return if symptoms recur or develop over the
following 24 to 36 hours.
Patients showing immediate moderate or severe effects: Check
lung function and perform chest x-rays. Oxygen and
bronchodilators (e.g. salbutamol; orally or inhaled) are used
for bronchospasm. Pulmonary oedema should be treated with
Positive End Expiratory Pressure (PEEP), or Constant Positive
Airway Pressure (CPAP). Corticosteroids may inhibit the
inflammatory response and should be considered in severe
cases. Monitor arterial blood gases, treat hyperchloraemic
acidosis.
Patients with pre-existing respiratory disease: assess and
consider admission for at least 24 hours.
Dermal: Wash thoroughly with running water or saline. Treat
as a thermal burn, if necessary.
Eyes: Irrigate thoroughly for 10 to 15 minutes. Refer to
an ophthalmologist.
10.2 Life supportive procedures and symptomatic/specific treatment
See section 10.1
10.3 Decontamination
See section 10.1
10.4 Enhanced elimination
See section 10.1
10.5 Antidote treatment
10.5.1 Adults
No antidote available.
10.5.2 Children
No antidote available.
10.6 Management discussion
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
The effcts of chronic exposure to chlorine amongst
workers at a pulpmill have been reported by Bherer et al.
(1994). Persistent respiratory symptoms, bronchial
obstruction and bronchial hyper-responsiveness were observed
in 82%, 23% and 41 % of the workers respectively at 18 to 24
months after exposure ended.
The clinical effects of acute exposure to chlorine gas
inhalation has been reviewed by Williams (1997).
Acute exposure to chlorine in schoolchildren from swimming
pools resulted from accidental maintenance procedures (Sexton
and Pronchik, 1998). 13 children at two separate pools were
treated with beta agonists and humidifies oxygen, with 5
being admitted to hospital.
12. Additional information
12.1 Specific preventive measures
Care workers must ensure adequate protection to prevent
self-contamination when carrying out decontamination and
medical treatment.
12.2 Other
The following references may be useful:
Green TC (1997) Out of the blue and into the pink. A new
litmus test for chlorine gas exposure. Med J Aust
167(11-12):651
Myers SJ (1997) Chlorine inhalation in a pediatric patient. J
Emerg Nurs 23(6):583-585.
13. REFERENCES
Bherer L, Cushman R, Couteau JP, Quevillon M, Cote G,
Bourbeau J, LœArcheveque J, Cartier A, & Malo JL (1994) Survey of
construction workers repeatedly exposed to chlorine over a three
to six month peroid in a pulpmill: II. Follow up of affected
workers by questionnaire, spirometry, and assessmenrt of bronchial
responsiveness 18 to 24 months after exposure ended. Occup Environ
Med 51(4):225-228.
CCOHS (1998) CHEMINFO Record Chlorine (No. 85). IPCS INTOX CD-ROM
Issue 98-1. Canadian Centre for Occupational Health and Safety,
Hamilton Canada.
Sexton JD & Pronchik DJ (1998) Chlorine inhalation: the big
picture. J Toxicol Clin Toxicol 36(1-2):87-93
Williams JG (1997) Inhalation of chlorine gas. Postgrad Med J
73(865): 697-700.
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Author: Medical Toxicology Unit,
Guy's and St Thomas' Trust
Avonley Road, London SE14 5ER, UK
Date: March, 1996
Review: As for author. 1996
Peer review: INTOX meeting, March 1998, London, UK
(Members of group: Drs G. Allridge, L.
Lubomovir, R. Turk, C. Alonso, S. de Ben, K.
Hartigan-Go, N. Bates)
Editor: Dr M.Ruse (September, 1998)