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Phosgene - Overview. Phosgene (CG), carbonyl chloride:A colorless gas at ambient temperaturesEasily liquefied under pressure Boiling point is 8.2?CFour times the density of airOdor similar to decaying fruit, fresh-cut grass or moldy hay1.5 ppm (mg/m3) odor thresholdConcentrations of 0.4 ppm c
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1. Phosgene (CG)
2. Phosgene - Overview Phosgene (CG), carbonyl chloride:
A colorless gas at ambient temperatures
Easily liquefied under pressure
Boiling point is 8.2C
Four times the density of air
Odor similar to decaying fruit, fresh-cut grass or moldy hay
1.5 ppm (mg/m3) odor threshold
Concentrations of 0.4 ppm can be detected by trained workers
3. Toxicity Primary route of exposure is inhalation
High concentrations cause skin irritation and eye injury
Degree of injury = concentration and duration of acute exposure
LCt50 ~ 3200 mgmin/m3
4. Toxicity Eyes, nose, throat irritated at 3-4 ppm
Lung damage at > 30 ppmmin
Pulmonary edema at > 150 ppmmin
Dosages > 30 ppmmin
Secondary asymptomatic phase follows
Lasting 24 -48 hours
5. Protective Equipment Respirator with appropriate filters
Chemical protective clothing advised in high concentration spills
6. Detection Techniques for air concentrations
Passive dosimetry
Manual and automated colorimetry
Infrared spectroscopy
Ultraviolet spectrophotometry
Paper tape monitors detect 5 gm3
No automated field detectors available
7. Decontamination Remove victim from exposure
Flush skin and eyes with water for 15-20 minutes
Liquid phosgene
Remove contaminated clothing / footwear
Thaw affected area with lukewarm water
8. Signs and Symptoms Action mode not fully understood
May inhibit enzymes or produce HCl in the alveoli
Alveolar and capillary wall reaction
9. Signs and Symptoms Action mode not fully understood
Carbonyl group (C=O)
Acylation reactions with amino (-NH2), hydroxyl (-OH), or sulfhydryl (-SH) groups
Alveolar-capillary membrane
Lead to capillary leakage
Irritation of ocular, nasal, and central airway may be due to HCl
10. Signs and Symptoms Concentrations > 3 ppm
Burning and watering of the eyes
Sore or scratchy throat, dry cough, choking, nausea, headache, chest tightness
Erythema of oral and pharyngeal mucus membranes at higher concentrations
11. Signs and Symptoms Early symptoms may not indicate severe lung injury
Sustained exposures may result in pulmonary edema 12 - 16 hours later
12. Signs and Symptoms Phosgene passes the blood-air barrier at concentrations > 200 ppm causing
Hemolysis in the pulmonary capillaries
Congestion by red cell fragments
Stoppage of capillary circulation
In minutes acute cor pulmonale results in death
13. Signs and Symptoms Trachea and bronchi appear normal
Damage to the bronchiolar epithelium
Narrowing of the lumen develops
Lengthening of the respiratory cycle
Moist rales in lungs indicate pulmonary edema
Preceded by damage to the bronchiolar epithelium
14. Signs and Symptoms As the edema progresses
Increasing discomfort, apprehension, dyspnea
Frothy sputum develops
Rales and rhonchi are audible over the chest
15. Signs and Symptoms Development of shock-like symptoms
Maximum effects within 12 - 24 hours
Terminal clinical phase of lethal dose
Extreme distress ensues with intolerable dyspnea, until respiration ceases
16. Signs and Symptoms Blood becomes viscous and coagulates easily
Methemoglobin levels increase
Cyanosis
Reduced arterial blood pressure with tachycardia
Metabolic acidosis and compensatory hyperventilation
17. Signs and Symptoms Arterial blood gases = significant hypoxia
Contact with liquid phosgene may cause burns or frostbite
18. Treatment Primarily supportive care
Warmth and forced bed rest
Important to differentiate between early irritant symptoms and edema
Early edema may be detected by chest x-ray, before evident clinical signs, using 50-80 kilovolts
19. Treatment Irritation typically precedes edema
48 hour patient observation
Pulmonary edema will be apparent
Onset of edema in 2 to 6 hours predictive of severe injury
20. Treatment Delay and/or minimize the pulmonary edema and reduce hypoxia
Positive airway pressure intermittent positive pressure breathing (IPPB)
Positive end-expiratory pressure (PEEP) mask
Intubation is critical
Provide adequate oxygenation
21. Treatment Elevation of the pCO2 > 45 mm Hg suggests bronchospasm is likely cause of hypercarbia
Use bronchodilators
Add steroids immediately for patients with prior history
Efficacy of steroids is unproven
Give steroid doses by IV or inhalation
Methylprednisolone, 700-1000 mg in divided doses on day one then tapered
22. Treatment Use sedatives cautiously
Withhold until adequate oxygenation is assured
Barbiturates, atropine, antihistamines and analeptics are all contraindicated
Antibiotics for documented pulmonary infection
23. Long-Term Medical Sequelae Pulmonary function studies and chest x-ray
Performed at 2 - 3 month follow-up exam
Good prognosis
Continuing shortness of breath and physical limitations
24. Long-Term Medical Sequelae Smoking and pre-existing COPD worsen chances of full recovery
Does not appear to be mutagenic
Insufficient data on carcinogenicity
25. Environmental Sequelae Phosgene very persistent in atmosphere
Half-life in atmosphere estimated at 113 years at sea level
Minimal water solubility and vapor pressure allow it to rapidly hydrolyze in water
26. Summary Colorless gas at ambient temperatures
Potential terrorist use
Disruption and fear
Inhalation is primary exposure route
27. Summary Eye / pharyngeal irritation at 3 - 4 ppm
Lung damage at > 30 ppmmin
Pulmonary edema at > 150 ppmmin
Treatment is primarily supportive
Ventilation, oxygenation, general pulmonary care
Good prognosis for most survivors