Gas fatalities

As u group, the lung injurants were used to a larger extent than any other tyi>e of gas and sccuretl the bulk of the gas fatalities in the war. 

Merlani G, Fox M, Oehen HP, Cathomas G, Renner EL, Fattinger K, Schneemann M, Kullak-Ublick GA. Fatal hepatoxicity secondary to nimesulide. Fur J Clin Pharmacol 2001 57(4) 321-6. 

Hazard Very toxic by inhalation, cholinesterase inhibitor, a military nerve gas, fatal dose (man) 0.01 mg/kg. 

Without considering the sources or accuracy of Prentiss data [1660], they will be examined here (initially) as received wisdom. Given this assumption, there are two possible origins for the oft-cited quote that "more than 80% of the gas fatalities of World War I were caused by phosgene". Firstly there is the following statement, taken from Prentiss [1660 p. 674] ... 

Carbonyl chloride, CG, Collongite, D-stoff. Used by Germany as a mixture with chlorine at Nieltje in Flanders on December 19th 1915. 88 tons released 1069 casualties, 129 fatal. 80% of WWI gas fatalities due to phosgene. Colourless gas, bp 8°C with odour variably described as new-mown hay or mouldy hay. Tobacco... 

While the CPE devoted great attention during 1915 to chemical munitions, the spectre of gas weapons soon overshadowed even the horrors of high explosives. At the end of May 1915 and continuing intermittently for several months, the Germans attacked Russian troops near Warsaw with various types of gases. The initial attacks cost more than 1,100 gas fatalities of a total of 9,000 gas casualties. The result was to force the Russians to mobilize their efforts in chemical warfare, both in defensive (gas masks) as well as in offensive (the production and delivery of gases). 

A procedure is installed that requires employees to test for gas before entering the enclosed area. But, supervisors condone employees entering the area without making the required test. Both detection and alarm systems fail. Gas accumulates. An employee enters the area without testing for gas. The result is a toxic gas fatality. 

The most common contaminants in produced gas are carbon dioxide (COj) and hydrogen sulphide (HjS). Both can combine with free water to cause corrosion and H2S is extremely toxic even in very small amounts (less than 0.01% volume can be fatal if inhaled). Because of the equipment required, extraction is performed onshore whenever possible, and providing gas is dehydrated, most pipeline corrosion problems can be avoided. However, if third party pipelines are used it may be necessary to perform some extraction on site prior to evacuation to meet pipeline owner specifications. Extraction of CO2 and H2S is normally performed by absorption in contact towers like those used for dehydration, though other solvents are used instead of glycol. 

Chlorine is a respiratory irritant. The gas irritates the mucus membranes and the liquid burns the skin. As little as 3.5 ppm can be detected as an odor, and 1000 ppm is likely to be fatal after a few deep breaths. In fact, chlorine was used as a war gas in 1915. 

Techniques for handling sodium in commercial-scale appHcations have improved (5,23,98,101,102). Contamination by sodium oxide is kept at a minimum by completely welded constmction and inert gas-pressured transfers. Residual oxide is removed by cold traps or micrometallic filters. Special mechanical pumps or leak-free electromagnetic pumps and meters work well with clean Hquid sodium. Corrosion of stainless or carbon steel equipment is minimi2ed by keeping the oxide content low. The 8-h TWA PEL and ceiling TLV for sodium or sodium oxide or hydroxide smoke exposure is 2 mg/m. There is no defined AID for pure sodium, as even the smallest quantity ingested could potentially cause fatal injury. 

Skin Absorption. Normal skin absorbs HCN slowly. However, 2% HCN in air may cause poisoning in 3 min, 1% is dangerous in 10 min, and 0.05% may produce symptoms after 30 min, even though a gas mask or air mask is worn. Some areas of the body, such as the feet and mucous membranes, are more absorptive than others. Cuts and abrasions absorb cyanide rapidly, and 50 mg of HCN absorbed through the skin can be fatal. 

Toxicology. An excellent review of the toxicity and health assessment of ethylene oxide has been compiled (233). Ethylene oxide (EO) can be relatively toxic as both a Hquid and gas. Inhalation of ethylene oxide ia high concentrations may be fatal. Estimates of lethal ethylene oxide inhalation levels in animals depend on the duration of exposure. The reported 4-h LC q values for rats, mice, and dogs are 1460, 835, and 960 ppm, respectively (234). More recent information (235) indicates that the 1-h LC q in rats is approximately 5000 ppm. 

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