CAS RN: 75-44-5

Health Effects

    • A) USES: Phosgene, also known as carbonyl chloride, is a colorless irritant gas at room temperature. Historically, it was used in chemical warfare during World War I. Today, it is used in the synthesis of organic compounds such as pharmaceuticals, dyes, resins, and pesticides. Welding material cleaned with chlorinated solvents can produce phosgene gas. It can also be released following the combustion of volatile substances that include organochloride compounds (ie, polyvinyl chloride and isocyanates) found frequently in many household items such as solvents, paint removers, dry cleaning fluids, home and office furnishings, floor coverings and electrical insulation. In low concentrations, its odor is described as resembling freshly cut hay or grass, and at high concentrations the odor can be sharp and suffocating.
    • B) TOXICOLOGY: Phosgene injury caused by inhalation are dependent on phosgene concentration and/or the inhaled dose. Of note, determining the actual dose inhaled is very difficult. Phosgene is a lower respiratory tract irritant. Its low water solubility leads to less upper respiratory tract irritation. It then hydrolyzes in the lungs on contact with water to form hydrochloric acids. Phosgene initiates a cascade of inflammatory cytokines and pulmonary vascular permeability, resulting in gas diffusion abnormalities and pulmonary edema. Cases of high concentration but short-duration exposures may result in initial symptoms but no long-term effects; conversely low concentrations but longer exposures may have no immediate symptoms but result in fatal outcomes.
    • C) EPIDEMIOLOGY: Reports of phosgene poisonings are very rare. However, there has been historical use of phosgene as a chemical weapon and continued concern for this potential use in the future. In addition, fatalities have occurred due to industrial release of phosgene.
      • 1) ROUTES OF EXPOSURE: Inhalation is the most common route of exposure to phosgene and may result in irritant and pulmonary effects. Dermal and/or ocular contact with phosgene gas may cause irritation and reddening of the skin and/or eyes. Severe burns may result from contact with liquid phosgene. Contamination (eg, clothing) of phosgene in solvent solution can lead to significant off-gassing and potentially continuous (ie, inhalation) exposure to the individual or to others (eg, coworkers, first-responders). Ingestion of phosgene is unlikely.
      • 2) MILD TO MODERATE TOXICITY: IRRITANT EFFECTS: Immediate onset of symptoms are usually due to the irritant effects of phosgene. Severity is based on vapor concentrations of the gas and not the exposure dose. Contact with gas concentrations greater than 3 ppm can cause immediate irritation and pain of the mucous membranes (ie, eyes, nose, throat and bronchi). Symptoms may include conjunctivitis, rhinitis, pharyngitis, bronchitis, lacrimation, blepharospasm, conjunctival hyperemia, and upper respiratory tract irritation. Levels greater than 3 ppm causes throat irritation, levels greater than 4 ppm cause eye irritation, and levels of greater than 4.8 ppm can induce cough and chest tightness.
      • 3) SEVERE TOXICITY: PULMONARY EFFECTS: Based on the inhaled dose (not the exposure concentration), severe pulmonary toxicity (including pulmonary edema) may occur. Although signs and symptoms of inhalation exposure can be divided into 3 phases (ie, reflex, latency, terminal), patients may NOT develop distinct phases of exposure or the phases may be clinically unrecognizable.
        • a) REFLEX PHASE: Following inhalation concentrations of greater than 3 ppm, patients develop shallow, rapid breathing due to a vagal reflex action that can cause decreased vital capacity and volume producing mild hypoxemia and mild respiratory acidosis. During this phase, patients can experience pain in the eyes and throat, chest tightness, shortness of breath, wheezing, coughing, hypotension, bradycardia and possible dysrhythmias.
        • b) DELAYED (LATENCY PHASE) EFFECTS: Depending on the inhaled dose (ie, higher exposure doses usually result in a shorter symptom-free period) there can be a symptom free period of up to 48 hours. However, biochemical effects (ie, histologic changes) start immediately after exposure. Following the symptom-free period, symptoms of cough, chest tightness, dyspnea, tachypnea and pulmonary edema can develop. INHALATION DOSE: Inhalation dose of less than 50 ppm-min: no clinical pulmonary effects; 50 to 150 ppm-min: subclinical pulmonary reactions (edema unlikely); 150 ppm-min or above: pulmonary edema probable; 300 ppm-min or above: life-threatening pulmonary edema anticipated. PROGNOSTIC INDICATOR: Generally, the shorter the latency period, the worse the prognosis.
        • c) CLINICAL (TERMINAL PHASE) EFFECTS: Progressive dyspnea, crackles throughout the lung fields and cyanosis are present. Symptoms can include pulmonary edema, cough, choking sensation, tachypnea, and production of foaming bloody sputum. Secondary to severe pulmonary edema, cardiac failure has also occurred.
      • 4) OTHER CLINICAL EFFECTS: Phosgene-induced hypoxia/anoxia and hypotension can cause injury to the heart, brain, kidneys and liver, and metabolic acidosis. Hematologic events (ie, intravascular hemolysis and coagulopathy, leukocytosis) have been associated with very high concentrations of phosgene (ie, greater than 200 ppm).
      • 5) DERMAL EXPOSURE: Severe dermal burns or frostbite may develop from skin exposure. Vapor contact (greater than 3 ppm) with moist or wet skin can produce mild irritation and erythema, however, serious injury has not been reported from this type of exposure. Liquid phosgene can be a frostbite hazard.
      • 6) OCULAR EXPOSURE: Contact with splashed liquid phosgene has produced complete corneal opacification, perforation, and symblepharon in one case. Exposure to phosgene gas has caused conjunctival inflammation.
      • 7) NON-SPECIFIC EFFECTS: Headache, anxiety, and nausea may be reported.
    • A) IARC Carcinogenicity Ratings for CAS75-44-5 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
      • 1) Not Listed
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