· Carbonyl chloride, Carbon oxychloride, Chloroformyl chloride.
· Colourless gas, heavier than air, with an odour of freshly-cut hay. At high concentrations, the gas has an odour described as suffocating, strong, stifling, or pungent. Below 0–8.30C or when compressed, phosgene condenses to a colourless to light yellow, non-combustible, highly toxic, fuming/volatile liquid that produces poisonous vapour and sinks in water.
■■ High temperature decomposition of chlorinated hydrocar-bons such as carbon tetrachloride, chloroform, and methy-lene chloride yields phosgene.
■■ Phosgene and chlorine may be formed by burning poly-styrene.
■■ Solvents, paint removers (when exposed to heat) yield phosgene.
■■ Phosgene is used as an intermediate in the manufacture of industrial chemicals such as isocyanates (e.g. toluene diisocyanate, polymethylene polyphenylisocyanate, etc.) and their derivatives (polyurethane and polycarbonate resins), carbamates, and chloroformates.
■■ Phosgene is used in the manufacture of insecticides, herbi-cides, and pharmaceuticals (especially barbiturates).
In concentrations of 3 to 5 ppm, irritation of the eyes, throat and upper respiratory tract are noted. Total dose (concentration in ppm multiplied by time of exposure in minutes) determines the risk of pulmonary oedema. A cumulative dose of 50 ppm min can result in delayed pulmonary oedema; a dose of 150 ppm × min will probably result in pulmonary oedema, and a dose of 300 ppm × min is likely to be fatal. Exposure to 25 ppm is extremely dangerous and greater than 50 ppm may be rapidly fatal.
Phosgene is hydrolysed in the body to hydrochloric acid which produces a systemic inflamatory response. It also stimulates the synthesis of lipoxygenase-derived leukotrienes causing pulmonary oedema. Further, phosgene increases pulmonary vascular permeability, leading to increased fluid accumulation in the interstitial and alveolar compartments. The ability of the lymphatics to clear the excess fluid is exceeded, resulting in gas diffusion abnormalities and pulmonary oedema.
Phosgene gas has low water solubility and thus can be deeply inhaled into the lung before an individual is aware of significant exposure.
· Stage I: Coughing, choking, lacrimation, nausea, vomiting,headache, conjunctivitis, rhinitis, pharyngitis, bronchitis, and upper respiratory tract irritation may occur after expo-sure to concentrations exceeding 3 to 5 ppm. Brief exposure to 50 ppm or greater may be rapidly fatal. Eye irritation is not a significant warning property. Exposures to 2 ppm may not cause eye irritation, but can result in significant, delayed respiratory effects.
· Stage II: Symptom-free interval lasting from half an hour upto 1 to 2 days.
· Stage III: Progressive pulmonary oedema sets in with rapid, shallow respiration, cyanosis, and painful, parox- ysmal cough producing frothy whitish or yellowish liquid. Hypoxia, hypovolaemia, and circulatory failure may lead to death. It is generally felt that if the victim survives 24 to 48 hours, the prognosis will be favourable. However, patients who survive exposure with pulmonary oedema may have persistent complaints of exertional dyspnoea and reduced exercise capacity and abnormal pulmonary function tests for months.
· Severe dermal burns or frostbite may develop following skin exposure to the liquefied material.
Pulmonary fibrosis and emphysema may
develop after chronic exposure.
There is no specific method of diagnosis. Chest X-ray may reveal incipient toxic pulmonary oedema much earlier than overt clinical manifestations.
· Plasma phosgene levels are not clinically useful.
· Monitor arterial blood gases and/or pulse oximetry,pulmonary function tests, and chest X-ray in patients with significant exposure.
· Serial chest X-rays are recommended if significant exposure is suspected as effects may be delayed.
· Monitor fluid balance if pulmonary oedema is developing.
· Rest and warmth (especially important during the latent stage).
· Humidified oxygen, intermittent positive pressure ventila-tion (IPPV), positive end-expiratory pressure (PEEP), etc.
· Codeine phosphate for cough (30 to 60 mg).
· Diuretics in combination with PEEP may help to ameliorate interstitial oedema.
· Steroid therapy: Steroids used soon after exposure maylessen the severity of pulmonary oedema. Betamethasone valerate, beclomethasone dipropionate, or dexamethasone sodium phosphate is generally recommended. The initial dose is five times that conventionally used in asthma, followed by about half the dose for 12 hours, and then standard asthma dosages for the subsequent 72 hours. Systemic therapy can be started simultaneously with methyl prednisolone 2 grams IV or IM., followed by the same dose 12th hourly for upto 5 days. Alternatively, 1000 mg pred-nisolone can be given IV on the first day followed by 800 mg/day for the next 2 days, 700 mg/day for 2 more days, and then progressively reducing the dosage quickly.
· One proposed regimen for preventing pulmonary oedema in adults is as follows:
o Ibuprofen 800 mg (at least one dose).
o Methylprednisolone 1 gram intravenously (or equiva-lent corticosteroid), or dexamethasone phosphate 10 mg aerosol (may be less effective than IV administration).
o Aminophylline 5 mg/kg loading dose followed by 1 mg/kg every 8 to 12 hours to maintain a serum level of 10 to 20 mcg/ml.
o Terbutaline 0.25 mg subcutaneously.
o N-acetylcysteine 10 ml of a 20% solution aerosolised.
o Oxygen as needed.
· Antibiotic and antifungal treatment may be necessary if steroids are used.
· Adrenaline can be used for the relief of acute bronchial spasm.
· Massive pulmonary oedema is the most striking feature.
Phosgene was used as part of chemical warfare during World War I. Prepared for the first time in 1812, phosgene had a large scale presence in World War I as an asphyxiant war gas. The first chemical agent of warfare in modern times was chlorine, used by the German army at Ypres in 1915 against the Allies. Shortly thereafter, the Germans began mixing the chlorine with phosgene, or deployed phosgene alone as a weapon. Phosgene, together with arsenicals, blister agents, and mustard gas (also introduced during World War I) have been estimated to be responsible for approxi-mately 1.3 million casualties during the war, including at least 90,000 fatalities. By the time World War I concluded, mustard gas was the most widely used, but phosgene caused the most deaths.
Today most cases are due to accidental occupational exposure.
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