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Phosgene CG

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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Phosgene CG

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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

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