Oedema caused phosgene

Tlie respiratory system is tlie main target organ for vapour, gas or mist. Readily-soluble cheirticals, e.g. chlorine or phosgene, attack the upper respiratory tract less soluble gases, e.g. oxides of nitrogen, penetrate more deeply into the conducting airways and, in some cases, may cause pulmonary oedema, often after a time delay. 

Phosgene was used as a major CW agent in WW I and was responsible for the greatest number of CW induced mortalities. It causes a lethal pulmonary oedema after an asymptomatic lag phase of up to 24 h. Its specific mechanism of action is unknown, but is assumed to involve reactions with nucleophilic sites on macromolecules. 

Exposure to very high levels of phosgene may lead to death before pulmonary oedema has developed. The cause of this is obscure, although the effect has been recorded in cases of exposure to high levels of other lung-damaging compounds, including chlorine. The hypothesis of reflex inhibition of respiration is often put forward in explanation of this effect. 

Perfluoroisobutene, (CF3)2C=CF2 (bp 7 °C), included in Schedule 2 of the CWC, is also a lung injurant that causes pulmonary oedema. It is a by-product of Teflon production. Like phosgene it is a reactive electrophile. It is not known to have been weaponised but was studied as a potential hydrophobic canister penetrant. ... 

TIC include lung-damaging agents (chlorine and phosgene are both used widely in the chemical industry), perfluoroisobutylene (PFIB) and isocyanates. All these compounds can lead to toxic pulmonary oedema at the alveolar level. In addition, there are many respiratory irritant agents which cause effects on the upper airways such as ammonia and hydrogen chloride and agents such as sulphur dioxide and toluene diisocyanate which cause severe bronchoconstriction. 

The use of phosgene gas by both sides continued for the rest of the war and caused the most fatalities from chemical warfare agents. Because of its lower water solubility compared with chlorine, phosgene was found to be more effective in producing a late onset of pulmonary oedema at lower concentrations. It was therefore more toxic than chlorine. It also caused immediate incapacitation due to its short latency upper respiratory tract actions ( irritant or choking ). 

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