Phosgene
| 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 Physico-chemical 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 circumstances of poisoning |
| 4.3 Occupationally exposed population |
| 5. ROUTES OF EXPOSURE |
| 5.1 Oral |
| 5.2 Inhalation |
| 5.3 Dermal |
| 5.4 Eye |
| 5.5 Parenteral |
| 5.6 Others |
| 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 & 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 & 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 &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 & 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 investigations |
| 8.5 Overall Interpretation |
| 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 contact |
| 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 |
| 9.4.3.2 Peripheral Nervous System |
| 9.4.3.3 Autonomic |
| 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), DATES (INCLUDING UPDATES), COMPLETE ADDRESS(ES) |
PHOSGENE
International Programme on Chemical Safety
Poisons Information Monograph 419
Chemical
1. NAME
1.1 Substance
Phosgene
1.2 Group
Halogenated aliphatic hydrocarbon
1.3 Synonyms
Carbonic Dichloride;
Carbon Dichloride Oxide;
Carbon Oxychloride;
Carbonyl Chloride;
Carbonyl Dichloride;
CG;
Chloroformyl Chloride;
Diphosgene;
Phosgen
1.4 Identification numbers
1.4.1 CAS number
75-44-5
1.4.2 Other numbers
UN No. 1076
NIOSH: SY 5600000
1.5 Main brand names, main trade names
To be added by centre using monograph.
1.6 Main manufacturers, main importers
To be added by centre using monograph.
2. SUMMARY
2.1 Main risks and target organs
Main risk is inhalation of the gas leading to pulmonary
oedema. The main target organ is the lung.
2.2 Summary of clinical effects
The predominant effect is on the lung causing initial
respiratory distress, and ocular burning. Pulmonary (non-
cardiogenic) oedema can develop 8 to 24 hours post exposure
and death is secondary to anoxia. Ocular and dermal exposure
may lead to irritation or burns.
2.3 Diagnosis
The diagnosis is based on history of exposure to
phosgene and/or the occurrence of clinical manifestations of
mucous membrane irritation including cough, ocular
irritation, chest pain, a feeling of suffocation, and
dyspnea. Clinical diagnosis by chest x-ray shows diffuse
interstitial infiltrates and chest sounds reveal bilateral
crackles.
2.4 First aid measures and management principles
Remove subject from exposure, establish and maintain
airway as necessary and administer supplemental oxygen. The
treatment of phosgene poisoning is primarily supportive.
Copious fluids should be used for suspected dermal or eye
exposure. Remove clothing.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
Synthetic production, generally at the site where it is
to be used.
3.2 Chemical structure
Molecular Formula: CCl2O
Molecular Weight: 98.92
Structural Name: Carbonic dichloride
3.3 Physico-chemical properties
3.3.1 Colour
Clear
3.3.2 State/Form
Gas
3.3.3 Description
Suffocating odour similar to newly mown hay
when mixed with air. Slightly soluble in water, in
which it decomposes minimally. Very soluble in
benzene, toluene, acetic acid and most liquid
hydrocarbons (Allen, 1991; American Conference of
Governmental Industrial Hygienists Inc., 1991;
Budavari, 1996).
Condenses at 0°C to a clear fuming liquid.
Boiling Point: 8.3°C
Melting Point: -118°C
Density: 1.37 at 20°C
Vapour density: 3.4
Vapour Pressure: 1215 mm Hg at 20°C
3.4 Hazardous characteristics
May react violently with hexa-fluoro-isopropylidene-
amino-lithium. Forms a shock-sensitive explosive when mixed
with potassium. Reacts with sodium azide to form the
dangerously explosive carbonyl. Dangerous reactions may occur
with aluminium, sodium, lithium, isopropyl alcohol or 2,4-
hexadyn-1,6-diol. Phosgene decomposes to hydrochloric acid
and carbon monoxide in the presence of moisture (water or
steam). It produces toxic fumes when heated to decomposition
(Allen, 1991). Phosgene may be released by photodecomposition
of chlorinated hydrocarbons and also from the reaction of
methylene chloride with heat (Gerritsen & Buschmann, 1960;
English, 1964).
4. USES
4.1 Uses
4.1.1 Uses
4.1.2 Description
Intermediate in the production of isocyanates,
carbamates, organic carbonates, chloroformates and
related pesticides, dyes, and herbicides. Used as a
chemical weapon (WWI). Prepared from carbon monoxide
and chlorine or nitrosyl chloride; or from oleum and
carbon tetrachloride for use in the polyurethane and
polycarbonate industries (Allen, 1991; American
Conference of Governmental Industrial Hygienists Inc.,
1991; Budavari, 1996).
4.2 High risk circumstances of poisoning
As a result of occupational exposure due to photo-
decomposition of many of the chlorinated organic compounds
such as methylene chloride or carbon tetrachloride. Also when
produced by heat decomposition of many chemicals, as in fires
(Allen, 1991; American Conference of Governmental Industrial
Hygienists Inc., 1991).
4.3 Occupationally exposed population
Workers in the polyurethane or polycarbonate industries
(Allen, 1991). Also chemists, glass workers, welders and
firemen potentially exposed through decomposition of
chlorinated hydrocarbons (Currie et al, 1987). Some risk to
public when using non-inflammable chemical paint removers in
the presence of an open flame (Gerritsen & Buschmann, 1960;
English, 1964).
5. ROUTES OF EXPOSURE
5.1 Oral
Not relevant.
5.2 Inhalation
Phosgene is readily inhaled. Odour is detected at 0.5 to
1 ppm and anosmia (odour fatigue) is seen following chronic
exposure (Allen, 1991). No systemic absorption (Currie et
al., 1987).
5.3 Dermal
Severe skin irritant (Sax & Lewis, 1989).
5.4 Eye
Extremely irritating to the eye, no absorption
occurs.
5.5 Parenteral
Not relevant.
5.6 Others
Not relevant.
6. KINETICS
6.1 Absorption by route of exposure
There is no data available which suggests systemic
absorption other than through the lungs (Richardson &
Gangolli, 1994). Only moderately water soluble therefore
causes lower airway irritation. Intrapulmonary hydrolysis to
HCl and CO2 or Cl2.
6.2 Distribution by route of exposure
No systemic absorption.
6.3 Biological half-life by route of exposure
No data available.
6.4 Metabolism
Literature is conflicting as to the production of either
CO2 (Leikin & Paloucek, 1996) or Cl2, the more frequently
stated metabolite is Cl2 and will be referred to from here
on (Gosselin et al., 1984). Conversion to HCl and Cl2 in
the lower airways which are thought to be the triggers for
resulting pulmonary inflammation and oedema.
6.5 Elimination and excretion
No data available.
7. TOXICOLOGY
7.1 Mode of action
Intrapulmonary conversion to HCl and Cl2 which reacts
readily with the hydroxyl, sulfhydryl and ammonia groups
found in proteins, intermediate metabolites and vitamins
leading to degeneration of the blood-air barrier and
subsequent oedema (Diller, 1980; Leikin & Paloucek,
1996).
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
The LC50 in humans is estimated at
500 to 800 ppm for one minute. Levels of 2 to
5 ppm will induce mild respiratory symptoms,
with prolonged exposure to such levels
considered dangerous. Exposure to levels
greater than 50 ppm are considered massive
and will likely be rapidly fatal
(Parmeggiani, 1983; Ellenhorn & Barceloux,
1988; Olsen, 1994). At doses of 200 ppm
phosgene has been shown to pass through the
blood-air barrier and react with the blood
constituents to cause clotting (Richardson &
Gangolli, 1994).
7.2.1.2 Children
No data available
7.2.2 Relevant animal data
Acute: LC50 in the rat 25 ppm over 20
minutes. Phosgene levels as low as 0.5 ppm for two
hours can cause definite pathological changes in the
rat lung. Pulmonary vasoconstriction and oedema has
been witnessed in rabbits acutely inhaling phosgene.
When dogs inhaled 72 ppm for 30 minutes obvious
emphysema and pulmonary consolidation developed at 4
to 9 days post exposure (American Conference of
Governmental Industrial Hygienists Inc., 1991).
Exposures as low as 0.5 ppm for 120 minutes can cause
detectable changes in alveolar epithelium in the rat
although evidence of lasting damage is limited (Gross
et al, 1965).
Subchronic: In a study of goats, cats, rabbits,
guinea pigs, rats and mice exposure at 0.8 mg/m3 of
phosgene (5 hours per day for 5 consecutive days)
resulted in pulmonary oedema in 41% of exposed
animals, 4% of the animals developed extensive
pulmonary lesions. Identical exposure times at
4mg/m3 for the same species depressed respiratory
tract ciliary function and caused lung lesions. Guinea
pigs inhaling 10 mg/m3 for 10 minutes/day for 7 days
exhibited tolerance development, however such
tolerance has been shown to trigger chronic effects
such as bronchitis (American Conference of
Governmental Industrial Hygienists Inc., 1991).
7.2.3 Relevant in vitro data
No data available
7.2.4 Workplace standards
TLV-TWA: 0.1 ppm (0.40 mg/m3)
PEL 0.1 ppm
IDLH 2 ppm
(American Conference of Governmental Industrial
Hygienists Inc., 1991)
7.2.5 Acceptable daily intake (ADI)
Not relevant.
7.3 Carcinogenicity
No data available.
7.4 Teratogenicity
No data available.
7.5 Mutagenicity
No data available.
7.6 Interactions
No data available.
8. TOXICOLOGICAL ANALYSES & 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 & 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 &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 & 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 investigations
8.5 Overall Interpretation
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
Not relevant
9.1.2 Inhalation
Moderate exposure results in mild cough, mucous
membrane irritation and ocular irritation. The patient
is generally asymptomatic for 30 minutes to 24 hours
after exposure. Delayed symptoms then occur including:
chest pain, discomfort, thirst, headache, nausea,
increased cough with haemoptysis, cyanosis, a feeling
of suffocation and dyspnoea (Parmeggiani, 1983;
Gosselin et al, 1984; Ellenhorn & Barceloux, 1988;
Olsen 1994; Leikin & Paloucek, 1996).
Clinical diagnosis by chest x-ray shows diffuse
interstitial infiltrates and chest sounds reveal
bilateral crackles (Lim et al, 1996). The patient
develops signs and symptoms secondary to hypoxia and
pulmonary oedema. Death would result from anoxia
(Parmeggiani, 1983).
Massive exposures can result in pulmonary
intravascular haemolysis, thrombus formation and
immediate death due to pulmonary circulation occlusion
(Richardson & Gangolli, 1994).
9.1.3 Skin exposure
Possibility of dermal burning with massive
exposures, some dermal irritation with lower
exposures.
9.1.4 Eye contact
Ocular irritation and severe burning. A case of
severe exposure to liquid phosgene resulted in corneal
opacification.
9.1.5 Parenteral exposure
Not relevant.
9.1.6 Other
No data.
9.2 Chronic poisoning
9.2.1 Ingestion
Not relevant.
9.2.2 Inhalation
Symptoms of cough and shortness of breath are
occasionally persistent (Currie et al., 1987).
Documented cases show return to normal limits of lung
function within a period of weeks, however complete
recovery may take a period of years (English, 1964;
Lim et al., 1996). The inhalation of phosgene may
increase the severity of subsequent viral influenza
(Erlich & Burleson, 1991).
9.2.3 Skin contact
No data available
9.2.4 Eye contact
No data available.
9.2.5 Parenteral exposure
Not relevant.
9.2.6 Other
No data.
9.3 Course, prognosis, cause of death
Following massive exposures there is the possibility of
immediate death due to pulmonary vasculature occlusion.
Moderate exposures present as initial lung irritation,
bronchitis and ocular burning. From 30 minutes to 24 hours
later, the patient can develop chest pain, coughing,
haemoptysis, dyspnea and death due to pulmonary oedema. If
the patient survives 2 to 3 days then the prognosis is good,
with a small chance of permanent lung damage.
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
Hypovolemia, due to pulmonary oedema, leading
to hypotension and tachycardia (Leikin & Paloucek,
1996).
9.4.2 Respiratory
Respiratory distress including chest pain,
increasing cough, haemoptysis, a feeling of
suffocation, dyspnoea and pulmonary oedema. Chest
sounds reveal inspiratory and expiratory crackles.
Chest x-rays show diffuse interstitial infiltrates
(Parmeggiani, 1983; Ellenhorn & Barceloux, 1988;
Richardson & Gangolli, 1994; Lim et al., 1996).
9.4.3 Neurological
9.4.3.1 Central Nervous System
Headache, confusion due to hypoxia.
(Leikin & Paloucek, 1996)
9.4.3.2 Peripheral Nervous System
No data
9.4.3.3 Autonomic
No data
9.4.3.4 Skeletal and smooth muscle
No data
9.4.4 Gastrointestinal
Nausea, vomiting.
9.4.5 Hepatic
No data
9.4.6 Urinary
9.4.6.1 Renal
No data
9.4.6.2 Other
No data
9.4.7 Endocrine and reproductive systems
No data
9.4.8 Dermatological
Possibility of dermal irritation and burns with
large exposures (Leikin & Paloucek, 1996).
9.4.9 Eye, ear, nose, throat: local effects
Ocular irritation, corneal burns, sensation of
mucous membrane irritation (Leikin & Paloucek,
1996).
9.4.10 Haematological
Possibility of haemolysis and thrombus
formation with massive exposures leading to occlusion
in the pulmonary vasculature (Richardson & Gangolli,
1994).
9.4.11 Immunological
No data
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
Metabolic acidosis would be
expected as a consequence of severe
hypoxemia.
9.4.12.2 Fluid and electrolyte disturbances
Hypovolemia due to pulmonary oedema
(Leikin & Paloucek, 1996).
9.4.12.3 Others
No data
9.4.13 Allergic reactions
No data
9.4.14 Other clinical effects
No data.
9.4.15 Special risks
Pregnancy: one case of exposure with normal
infant (Gerritsen & Buschmann, 1960).
Breast feeding: no data.
Enzyme Deficiencies: no data.
9.5 Other
No data
9.6 Summary
10. MANAGEMENT
10.1 General principles
Maintain airway and use positive pressure ventilation
if necessary. Assessment of condition is mainly via clinical
presentation and radiographs which show diffuse increased
haziness. Treatment of hypoxia with supplemental with oxygen.
Some sources recommend the use of steroids and antibiotics
(if there are signs of infection), however this remains
controversial (Finkel, 1983). Administer fluids as necessary,
with caution not to worsen the pulmonary oedema (Lim et al.,
1996). Patients displaying immediate symptoms should be
observed for the possibility of delayed pulmonary oedema
(Ellenhorn & Barceloux, 1988).
10.2 Life supportive procedures and symptomatic / specific
treatment
Maintain a clear airway.
Administer oxygen.
Endotracheal intubation and support ventilation using
appropriate mechanical devices may be necessary.
Monitor for 12 to 24 hours for possible delayed-onset
pulmonary oedema.
10.3 Decontamination
Remove victim from exposure and give supplemental
oxygen. Rescuers should wear self-contained breathing
apparatus, and eye and skin protection. The patient should be
transported to a hospital immediately (Olsen, 1994). If
dermal exposure is suspected wash copiously with soap and
water, remove contaminated clothing immediately. Eyes should
be washed with flowing water for at least 15 minutes
(American Conference of Governmental Industrial Hygienists
Inc., 1991; Leikin & Paloucek, 1996).
10.4 Enhanced Elimination
No data.
10.5 Antidote treatment
10.5.1 Adults
No antidote available.
10.5.2 Children
No antidote available.
10.6 Management discussion
Early reports of the effectiveness of methenamine in
treatment of phosgene poisoning have been disproven (Diller,
1980). While this compound has been shown to have protective
effects when administered prior to exposure the
administration post-exposure has no therapeutic benefit.
Drugs disrupting the neutrophil influx associated with the
oxidant pathway in phosgene such as aminophylline and
terbutaline, ibuprofen and colchicine have been shown to
reduce oedema in animal studies (Lazar et al., 1989; Kennedy
et al., 1990; Ghio et al., 1991; Wyatt & Allister,
1995).
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
Gas Tank Leakage: A gas tank leak resulted in the
poisoning of 56 persons. Six cases are documented by Lim et
al. (1996). Symptoms were cough, increased sputum production,
dyspnea, chest tightness and chest pain followed by pulmonary
oedema. Diagnosis was through clinical presentation (for
example, case one demonstrated bilateral inspiratory and
expiratory crackles and increased diffuse haziness in both
lungs on the chest x-ray. WBC were 12.7×103/µL, LDH 409
units. Initial arterial blood gases PaO2 68.9 mmHg, PaCO2
34.7 mmHg, pH 7.392). Treatment involved intubation and
ventilation (started at 8 L/min oxygen, later reduced), drug
treatment was with methylprednisolone, aminophylline and
antibiotics with ventilation controlled by diazepam and
vecuronium (Lim et al., 1996).
Pregnant Woman Exposed Through Use Of Paint Stripper: The
phosgene exposure of a pregnant woman through the reaction of
fumes from non-inflammable chemical paint remover, containing
methylene chloride, to phosgene by a kerosene stove was
reported by Gerritsen & Buschmann (1960). She reported chest
tightness, blood-stained sputum and later dyspnea and
cyanosis. A chest x-ray revealed diffuse opacities and she
was treated with oxygen, antibiotics and cortisone. She
recovered and later gave birth to a healthy child.
Welding: A welder using an argon shielded electric arc in
an atmosphere containing tricholoroethylene developed
symptoms of breathlessness followed by pulmonary oedema 12
hours post-exposure. He was dyspneic 10 days later (Sjogren
et al, 1991).
12. ADDITIONAL INFORMATION
12.1 Specific preventive measures
Phosgene should be used only in a well ventilated, non-
combustible area. It should never be stored with water.
Ensure that storage cylinders remain cool. All environs
should have absorption facilities. Sodium hydroxide or
anhydrous ammonia can be used to neutralise phosgene.
Phosgene at concentrations similar to the TLV can be detected
by an indicator paper colour change from yellow to deep
orange (indicator paper: paper soaked in alcoholic or carbon
tetrachloride solution containing equal parts of p-dimethyl-
amino-benzaldehyde and colourless diphenylamine and dried).
Transporters should avoid throwing or dropping cylinders and
precautions should be taken to prevent them falling. Most
industries (such as the dye industry) have interior
regulations for working with this highly toxic gas.
(Parmeggiani, 1983; American Conference of Governmental
Industrial Hygienists Inc. 1991; Richardson and Gangolli,
1994).
12.2 Other
No data
13. REFERENCES
Allen R (1991) Chemical data safety sheets Volume 4b - Toxic
chemicals m-z, Royal Society of Chemistry, Rochester
American Conference of Governmental Industrial Hygienists Inc.
(1991) Documentation of the Threshold Limit Values and Biological
Exposure Indices, Volume II, 6th edition, Cincinnati
Budavari S ed. (1996) The Merck Index. An encyclopaedia of
chemicals, drugs and biologicals, 12th edition, New Jersey, Merck
and Co.
Currie W, Hatch G & Frosolong M (1987) Pulmonary Alterations in
Rats Due to Acute Phosgene Inhalation, Fundamental and Applied
Toxicology, 8:107-114
Diller W (1980) The Methenamine Misunderstanding in the Therapy of
Phosgene Poisoning, Archives of Toxicology, 46:199-206
Ellenhorn M & Barceloux D ed. (1988) Medical Toxicology -
Diagnosis and Treatment of Human Poisonings, New York, Elsevier
Publishing
English J (1964) A Case of Probable Phosgene Poisoning, British
Journal of Medicine, 1:38
Erlich J & Burleson G (1991) Enhanced and prolonged Pulmonary
Influenza Virus Infection Following Phosgene Inhalation, Journal
of Toxicology and Environmental Health, Abstract, 34(2):259-273
Finkel A ed. (1983) Hamilton and Hodges Industrial Toxicology, 4th
edition, Massachusetts, John Wright Publishing
Gerritsen W & Buschmann C (1960) Phosgene Poisoning Caused by the
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14. AUTHOR(S), REVIEWER(S), DATES (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Author: Belinda Bray
National Toxicology Group
Adams Building
Otago Medical School
Dunedin. NEW ZEALAND
Phone: (03) 479 1200
E-mail: belinda.bray@stonebow.otago.ac.nz
Date: 1996
Reviewer: MO Rambourg Schepens
Centre Anti-Poisons de Champagne Ardenne
Centre Hospitalier Universitaire
F-51092 REIMS Cedex FRANCE
E-mail: marie-odile.rambourg@wanadoo.fr
Date: July 1997
Peer review: INTOX-10 Meeting, Rio, Brazil September 3rd 1997
(Drs M Kowalczyk, L Lubomirov, R Mc Keown, J Szajewski, W Watson)
Finalization/Edition: Drs MO Rambourg Schepens & M Ruse
October 1997