Simultaneous gas chromatographic determination of four toxic gases generally present in combustion atmospheres.

The measurement of combustion gases produced by burning aircraft cabin materials poses a continuing limitation for smoke toxicity research. Because toxic effects of gases depend on both their concentrations and the duration of exposure, frequent atmosphere sampling is necessary to define the gas concentration-exposure time curve. A gas chromatographic (GC) method was developed for the simultaneous analyses of carbon monoxide (CO), hydrogen sulfide (H2S), sulfur dioxide (SO2), and hydrogen cyanide (HCN). The method used an MTI M200 dual-column gas chromatograph equipped with 4-m molecular sieve-5A and 8-m PoraPlot-U wall-coated capillary columns and two low-volume, high-sensitivity thermal conductivity detectors. Detectability (in parts per million [ppm]) and retention times (in seconds) for the gases were as follows: CO, 100 ppm, 28 s; H2S, 50 ppm, 26 s; SO2, 125 ppm, 76 s; and HCN, 60 ppm, 108 s. The method was effective for determining these gases in mixtures and in the combustion atmospheres generated by burning wool (CO, HCN, and H2S) and modacrylic fabrics (CO and HCN). Common atmospheric gaseous or combustion products (oxygen, carbon dioxide, nitrogen, water vapor, and other volatiles) did not interfere with the analyses. However, filtration of the combustion atmospheres was necessary to prevent restriction of the GC sampling inlet by smoke particulates. The speed, sensitivity, and selectivity of this method make it suitable for smoke toxicity research and for evaluating performance of passenger protective breathing equipment. Also, this method can potentially be modified to analyze these gases when they are liberated from biosamples.

Exposures to carbon monoxide, hydrogen cyanide and their mixtures: interrelationship between gas exposure concentration, time to incapacitation, carboxyhemoglobin and blood cyanide in rats.

Carbon monoxide (CO) and hydrogen cyanide (HCN) are generated during aircraft interior fires in sufficient amounts to incapacitate cabin occupants. For typical post-crash and in-flight fires, minimum protection periods of 5 and 35 min, respectively, have been suggested for breathing devices to protect the occupants from smoke. Relationships of blood carboxyhemoglobin (COHb) and cyanide (CN-) levels to incapacitation have not been well defined for these gases. Therefore, time to incapacitation (ti) and blood COHb and CN- at incapacitation were examined in rats exposed to CO (5706 ppm for 5-min ti; 1902 ppm for 35-min ti), HCN (184 ppm for 5-min ti; 64 ppm for 35-min ti) and their mixtures (equipotent concentrations of each gas that produced 5- and 35-min ti). Blood CO and HCN uptakes were evaluated at the two concentrations of each gas. With either gas, variation in ti was higher for the 35-min ti than the 5-min ti The COHb level reached a plateau prior to incapacitation at both CO concentrations, and COHb levels at the 5- and 35-min ti were different from each other. Blood CN- increased as a function of both HCN concentration and exposure time, but CN- at the 5-min ti was half of the 35-min ti CN- level. The HCN uptake at the high concentration was about three times that at the low concentration. In the high concentration CO-HCN mixture, ti was shortened from 5 to 2.6 min; COHb dropped from 81 to 55% and blood CN- from 2.3 to 1.1 microgram ml(-1). At the low-concentration CO-HCN mixture, where ti was reduced from 35 to 11.1 min, COHb decreased from 71 to 61% and blood CN- from 4.2 to 1.1 microgram ml(-1). Any alteration in the uptake of either gas by the presence of the other was minimal. Our findings suggest that specific levels of blood COHb and CN- cannot be correlated directly with the incapacitation onset and that postmortem blood COHb and CN- levels should be evaluated carefully in fire victims.

Comparison of toxicity rankings of six aircraft cabin polymers by lethality and by incapacitation in rats.

Polymeric aircraft cabin materials have the potential to produce toxic gases in fires. Lethality (LC50) in animal models is a standard index to rank polymers on the basis of their combustion toxicity. However, the use of times-to-incapacitation (ti) may be more realistic for predicting relative escape times from a fire. Therefore, LC50 and ti for polymers, polyamide (I), polystyrene (II), Nylon 6/6 (III), polysulfone (IV), polyethylene (V) and chlorinated polyethylene (VI), of different chemical classes were determined and compared. Male rats, 12/fuel loading, were exposed to the pyrolysis products from selected weights of each polymer for 30 min in a 265-L combustion/exposure system, and LC50 values were determined following a 14-d observation period. For each polymer, ti was measured at 16 g and at its respective LC50 using the inability of rats (n greater than or equal to 12) to walk in rotating cages as a criterion for incapacitation. LC50 (45.7-87.5 mg/L) of the polymers had the order of I less than II approximately III less than IV less than V less than VI, while their ti (6.6-21.1 min) at 16 g (60 mg/L) had the order of III approximately I less than V approximately II less than VI less than IV. Based on ti at LC50, polymers were grouped into III & V; I, II & VI; and IV. LC50 and ti did not exhibit the same relative toxic hazard rankings for these polymers; ti were also not equal at the LC50 concentrations. These findings demonstrate the possible involvement of different mechanisms of action for the combustion products of these polymers at the selected end points.

The protective effects of ethylestrenol against acute poisoning by organophosphorus cholinesterase inhibitors in rats.

Pretreatment of rats with 10 mg of ethylestrenol (17alpha-ethylestr-4-en-17beta-ol) by force feeding twice daily for three days and once on the fourth day decreased the severity of parathion (0,0-diethyl 0-4-nitrophenyl phosphorothioate) toxicity and caused a 150% increase in the parathion LD50 in male animals. It decreased by 51% cholinesterase inhibition in the brain caused by i.p. injection of 2 mg of parathion/kg body weight but not that of an equitoxic dose (0.5 mg/kg) of its active metabolite, paraoxon (0,0-diethyl 0-4-nitrophenyl phosphate). It decreased by 29% cholinesterase inhibition in plasma following i.p. administration of parathion but caused only a 16% decrease in cholinesterase inhibition following administration of the equitoxic dose of paraoxon. It did not protect against brain cholinesterase inhibition by 4 mg/kg of parathion given i.v.; however, brain parathion levels were 16% lower in rats pretreated with ethylestrenol than in control rats. It increased the rate of inactivation of both parathion and paraoxon by liver microsomal enzyme preparations. Thus enzyme induction seems to account for the protection afforded by ethylestrenol to toxicity following poisoning by organophosphates.

Comparison of protective effects of ethylestrenol, norbolethone, and spironolactone against lethality from acute doses of parathion and paraoxon in female rats.

Protection against the toxicity of parathion (increased LD50) was provided by preadministered ethylestrenol and, to a lesser extent, by norbolethone and spironlactone. Ethylestrenol and norbolethone also offered protection against paraoxon toxicity. With ethylestrenol and spironolactone, the protection against parathion lethality was greater than that against paraoxon lethality.