Sodium hypochlorite
| 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) |
Sodium hypochlorite
International Programme on Chemical Safety
Poisons Information Monograph 495
Chemical
This Monograph contain the following
sections completed: 1, 2, 3, 4.1, 4.2, 5, 7.1, 7.2, 9, 10, 12.1.
1. NAME
1.1 Substance
Sodium hypochlorite
1.2 Group
Chlorine and compounds
Hypochlorite
1.3 Synonyms
Bleach; Hypochlorite de sodium;
Hypochlorous acid, sodium salt;
Liquid bleach; Sodium oxychloride
1.4 Identification numbers
1.4.1 CAS number
7681-52-9
1.4.2 Other numbers
UN/NA Number: 1791
RTECS Number: NH3486300
EU EINECS/ELINCS NUMBER: 231-668-3
1.5 Main brand names, main trade names
1.6 Main manufacturers, main importers
2. SUMMARY
2.1 Main risks and target organs
Sodium hypochlorite solution causes moderate mucosal
irritation, the extent of which depends very much on the
volume ingested, the viscosity and concentration of the
preparation and the duration of contact. Although sodium
hypochlorite solution is alkaline it does not tend to cause
corrosive damage except in large quantities or concentrated
solutions. Sodium hypochlorite may release small amounts of
chlorine and hypochlorous acid when acidified, but usually in
concentrations too small to cause any significant damage.
This release of chlorine often causes problems when bleach is
mixed with an acidic cleaning agent in the home.
Most children who ingest sodium hypochlorite bleach swallow
only small amounts and suffer nothing more than vomiting and
gastrointestinal discomfort. Pulmonary complications, such as
ARDS, usually resulting from aspiration, often contribute to
death. The ingestion of industrial bleaches may pose more of
a risk because of additional chemicals or higher alkalinity.
2.2 Summary of clinical effects
Gastrointestinal irritation, with nausea, vomiting and
diarrhoea, is very common with ingestion of sodium
hypochlorite solution. Haematemesis may occur with
concentrated solutions. Household bleaches are unlikely to
cause severe irritation unless contact is prolonged or the
amount ingested is large. Severe oesophageal damage may occur
from ingestion of bleach, but several reports have concluded
that it is not common.
Corrosive injury of the stomach and hypernatraemia with
hyperchloraemic acidosis have all been reported usually
following large intentional ingestions by adults.
2.3 Diagnosis
Clinical manifestation of mucous irritation of the eyes,
respiratory and gastrointestinal (GI) tract together with the
known hypochlorite exposure are essential. The main toxic
effect is due to release of chlorine gas. pH indicator shows
alkaline reaction in contact with the affected tissues.
2.4 First aid measures and management principles
Ingestion:
Emesis is not recommended because of the risks associated
with re-exposure of the oesophagus to sodium hypochlorite. In
the majority of cases the only treatment necessary is plenty
of fluids, especially milk. Less than 5 mL/kg oral ingestion
of a 7% solution is unlikely to cause severe effects.
Where a concentrated or highly alkaline solution has been
ingested or the quantity swallowed is thought to be large,
nasogastric aspiration of the stomach contents should be
considered. Monitor the pH, sodium and chloride in severe
cases. Give symptomatic and supportive care with intravenous
(IV) fluids for hypotension.
The use of steroids and antibiotics in the management of
corrosive injury is controversial and should be discussed
with a poisons information service. Patients with suspected
corrosive injury will require endoscopic examination to
assess the extent of the damage.
Inhalation (after exposure to chlorine gas):
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.
Please see PIM on Chlorine
Dermal: Wash thoroughly with running water or saline. Treat
as a thermal burn, if necessary.
Please see PIM on Chlorine
Eyes: Irrigate thoroughly for 10 to 15 minutes. Refer to an
ophthalmologist.
Please see PIM on Chlorine
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
3.2 Chemical structure
Structural formula: Na.OCl
Molecular Weight: 74.4
3.3 Physical properties
3.3.1 Colour
Green to yellow
3.3.2 State/Form
Liquid
3.3.3 Description
Melting Point: -6°C (21 deg F) (5% solution)
Boiling Point: Decomposes above 40°C (104 deg F)
Relative Density (Specific Gravity):About 1.1 (6%
solution);
1.21 (14% solution) (water = 1)
Solubility In Water: Soluble in all proportions
Solubility In Other Liquids: Reacts with many organic
solvents
pH value: Approx. 11
Odour chlorine (bleach) odour
Odour Threshold: Not applicable. Odour is due to
breakdown products such as chlorine.
Composition/Purity: Usually sold in solutions
containing 5 to 15% sodium hypochlorite in water, with
0.25 to 0.35% free alkali (usually NaOH) and 0.5 to
1.5% NaCl. Solutions of up to 40% sodium hypochlorite
in water are available. Solid sodium hypochlorite
(NaOCl.5H2O) is not commercially used.
3.4 Hazardous characteristics
Stability: Sodium hypochlorite solution decomposes
slowly. Decomposition is speeded up by heat (temperatures
above 40 deg C) and light.
Hazardous Decomposition Products: Chlorine, oxygen, sodium
chlorate.
Incompatibility - Materials To Avoid:
Nitrogen Compounds (e.g., ammonia, urea, amines,
isocyanurates) -can form toxic, reactive chloramines.
When hypochlorite is in excess, nitrogen gas is
formed.
Ammonium Salts - form explosive nitrogen trichloride
if acid present.
Acids (especially hydrochloric acid HCl) - release
chlorine gas.
Methanol - can form methyl hypochlorite which can
explode.
Metals - some metals, especially copper, nickel and
cobalt, speed up the decomposition of NaOCl.
Corrosivity to metals: Solutions are corrosive to many
metals.
4. USES
4.1 Uses
4.1.1 Uses
4.1.2 Description
Household sodium hypochlorite bleaches are
solutions of up to 10%, but are most commonly about
5%. They are used as general disinfectants and
bleaching agents. Sodium hypochlorite solutions often
contain other agents, including sodium hydroxide to
maintain a pH-dependent equilibrium between
hypochlorite and chlorine. Industrial bleaches may be
more concentrated (up to 50%).
4.2 High risk circumstance of poisoning
The ingestion of industrial bleaches may pose more of a
risk because of additional chemicals or higher alkalinity.
4.3 Occupationally exposed populations
5. ROUTES OF EXPOSURE
5.1 Oral
Ingestion of the sodium hypochlorite solution can occur.
5.2 Inhalation
Exposure can occur to chlorine gas released from sodium
hypochlorite solution after mixture with acid solutions.
5.3 Dermal
Exposure can occur to chlorine gas released from sodium
hypochlorite solution and to the sodium hypochlorite solution
itself.
5.4 Eye
Exposure can occur to chlorine gas released from sodium
hypochlorite solution and to the sodium hypochlorite solution
itself.
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
Sodium hypochlorite solution and chlorine gas are
corrosive causing tissue necrosis.
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
7.2.1.2 Children
Most children who ingest sodium
hypoochlorite bleach swallow only small
amounts and suffer nothing more than vomiting
and gastrointestinal discomfort (Racioppi et
al., 1994). Pulmonary complications, such as
ARDS, usually resulting from aspiration,
often contribute to death.
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
Gastrointestinal irritation, with nausea,
vomiting, is very common with ingestion of sodium
hypochlorite solution. Haematemesis may occur with
concentrated solutions. Household bleaches are
unlikely to cause severe irritation unless contact is
prolonged or the amount ingested is large. Severe
oesophageal damage may occur, but several reports have
concluded that it is not common (Pike et al., 1963;
Landau and Saunders, 1964).
Corrosive injury of the stomach (Van Rhee and
Beaumont, 1990; Strange et al., 1951) and
hypernatraemia with hyperchloraemic acidosis (Ward and
Routledge, 1988) have all been reported usually
following large intentional (Spiller et al., 1994)
ingestions by adults.
9.1.2 Inhalation
Chlorine gas released from sodium hypochlorite
causes burning in the throat and coughing. High levels
of exposure can lead to swelling and obstruction of
the airway. In serious cases noncardiogenic pulmonary
oedema can occur.
Please see PIM on Chlorine
9.1.3 Skin exposure
Exposure to high concentrated solutions can
result in serious corrosive burns.
Please see PIM on Chlorine
9.1.4 Eye contact
Exposure to high concentrated solutions can
result in serious corrosive burns.
Please see PIM on Chlorine
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
Ingestion:
Emesis is not recommended because of the risks associated
with re-exposure of the oesophagus to the bleach. In the
majority of cases the only treatment necessary is plenty of
fluids, especially milk. Less than 5 mL/kg oral ingestion of
a 7% solution is unlikely to cause severe effects.
Where a concentrated or highly alkaline solution has been
ingested or the quantity swallowed is thought to be large,
nasogastric aspiration of the stomach contents should be
considered. Monitor the pH, sodium and chloride in severe
cases. Symptomatic and supportive care with intravenous (IV)
fluids for hypotension.
The use of steroids and antibiotics in the management of
corrosive injury is controversial and should be discussed
with a poisons information service. Patients with suspected
corrosive injury will require endoscopic examination to
assess the extent of the damage.
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.
Please see PIM on Chlorine
Dermal: Wash thoroughly with running water or saline. Treat
as a thermal burn, if necessary.
Please see PIM on Chlorine
Eyes: Irrigate thoroughly for 10 to 15 minutes. Refer to an
ophthalmologist.
Please see PIM on Chlorine
10.2 Life supportive procedures and symptomatic/specific
treatment
See section 10.1
10.3 Decontamination
Emesis is not recommended because of the risks
associated with re-exposure of the oesophagus to the
bleach.
10.4 Enhanced elimination
Not applicable.
10.5 Antidote treatment
10.5.1 Adults
No specific antidote available.
10.5.2 Children
No specific antidote available.
10.6 Management discussion
The use of steroids and antibiotics in the management
of corrosive injury is controversial and should be discussed
with a poisons information service. Patients with suspected
corrosive injury will require endoscopic examination to
assess the extent of the damage.
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
12. Additional information
12.1 Specific preventive measures
Rescuers, first-aid personnel and medical professionals
should use appropriate protective clothing/gloves and where
necessary employ respiratory protection.
12.2 Other
13. REFERENCES
Landau GD and Saunders WH. (1964) The effect of chlorine
bleach on the esophagus. Arch Otolaryngol 80:174-176
Pike DG, Peabody JW, Davis EW and Lyons WS. (1963) A re-evaluation
of the dangers of Clorox ingestion. J Pediatr 63 (2):303-305
Racioppi F, Daskaleros PA, Besbelli N, Borges A, Deraemaeker C,
Magalini SI, Martinez Arrieta R, Pulce C, Ruggerone ML and Vlachos
P. (1994) Household bleaches based on sodium hypochlorite: review
of toxicology and poison control center experience. Fd Chem
Toxicol 32 (9):845-861
Spiller HA, Ross MP and Nichols GR. (1994) Fatal caustic ingestion
of sodium hypochlorite bleach with associated
hypernatremic-hyperchloremic acidosis (abstract 139). Vet Hum
Toxicol 36 (4):373
Strange DC, Finneran JC, Shumacker HB and Bowman DE. (1951)
Corrosive injury of the stomach. Report of a case caused by
ingestion of Clorox and experimental study of injurious effects.
Arch Surg 62:350-357
Van Rhee F and Beaumont DM. (1990) Gastric stricture complicating
oral ingestion of bleach. Br J Clin Pract 44 (11):681-682
Ward MJ and Routledge PA. (1988) Hypernatraemia and
hyperchloraemic acidosis after bleach ingestion.Hum Toxicol
7:37-38
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: December, 1997
Review: As for author. 1997
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)