The products from nonflaming combustion of wood and a trimethylol-propane-based rigid-urethane foam that was not fire-retarded produced elevated carboxyhemoglobin levels but no abnormal neurological effects. However, when this type of foam contained a reactive phosphate fire retardant, the combustion products caused grand mal seizures and death in rats. The toxic combustion product responsible for the seizures has been identified as 4-ethyl-1-phospha-2,6,7-trioxabicyclo(2.2.2.)octane-1-oxide.

A mathematical model is described for the intoxication of rats by carbon monoxide which is a function of carbon monoxide concentration, time of ex posure and respiratory minute volume, the latter being dependent upon the con centration of an irritant, hydrogen chloride. Predictions of the model, which were verified experimentally, led to the conclusion that the overall effect of the presence of HCI on intoxication of rats by CO is relatively minor and appears to lie in a "window" of about 400 to 1000 ppm HCI and within a range of CO con centrations up to about 4000 ppm. The predominant effect is, therefore, on in capacitating rather than lethal conditions when modest time frames are in volved.

This paper, the third in a series of publications on the modeling of tox icological effects of fire gases, addresses the quantification of post-exposure lethality of rats from exposure to hydrogen chloride atmospheres. Experimental L(Ct)50 values for HCl varied from about 80,000 ppm-min (5-minute exposure to 16,000 ppm) to about 170,000 ppm-min (60-minute exposure to 2800 ppm). Rele vant data involving non-human primate exposures are cited, which suggest the comparability of the rat and the primate for the purpose of assessing lethal doses of HCl.

Small-scale smoke toxicity tests were performed on polyvinylchloride-based electrical nonmetallic tubing (PVC/ENT) using the National Bureau of Standards (NBS) protocol for nonflaming combustion. An LC 50 of 28.5 mg/L ( & p l u s m n ; 9.25) was determined, placing PVC/ENT smoke in a toxicity category comparable to smoke from wood.Four large-scale tests were conducted in a 21,734-L room (8 x 12 × 8 ft). In tests involving 18 to 30 linear in. of PVC/ENT with and without fuelcontributing heat sources, it was learned that: a) 30 in. of PVC/ENT developed a 3.3-mg/L smoke concentration and an insufficient HCl concentration to cause death or significant symptoms in test animals (rats) and b) in the presence of a relatively small fire (5-lb wood crib), heat and carbon monoxide became lifelimiting prior to HCl. In additional tests involving approximately 60 in. of PVC/ENT degraded under 2.5 Watts/cm 2 heat flux, a smoke concentration of 7.6 mg/L was developed. Animal fatalities in these tests were shown to be from heat stress rather than smoke inhalation. The measurable percents of theoretical yield of HCl in small-scale tests ranged from 64 to 96 percent and in large-scale tests from 23 to 50 percent. The reasons for these differences are discussed.

A comprehensive and critical review of the state-of-the-art of biological assays acceptable in combustion toxicology evidenced the following: