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.

The absolute (ARP) and relative refractory period (RRP) of the median sensory nerve was determined in 26 control subjects and 24 alcoholics, nine of whom had symptoms of peripheral neuropathy. Recovery of latency to normal in response to the second stimulus was used to define RRP. A true RRP was calculated by subtracting ARP from measured RRP. Mean ARP for all subjects ranged from 0.75 to 0.80 msec; normal = 0.8 +/- 0.2 msec. The true RRP of control subjects was 2.1 +/- 0.5 msec, and for all alcoholic subjects it was 3.1 +/- 0.5 msec. True RRP for the nine symptomatic alcoholic subjects was 3.6 +/- 0.5 msec and 2.9 +/- 0.4 msec for those who were asymptomatic. Symptomatic and asymptomatic alcoholics differed significantly from one another, as well as from control subjects (P less than 0.001). Routine nerve conduction studies were normal in asymptomatic subjects. Three out of nine symptomatic alcoholics had increases in distal median motor or sensory latency, and three had slight slowing of median nerve conduction velocity. True RRP is more sensitive than routine measures of nerve conduction in the detection of axonal disorders influencing nerve conduction.

No abstract

Physiological and behavioral (conditioned avoidance) responses of male Lonlg-Evans rats were determined during exposure to combustion products produced on thermal degradation of three different polymeric materials. Arterial blood samples were obtained for determination of carboxyhemoglobin (COHb) and acid/base status. Material A produced a syndrome of carbon monoxide (CO)-induced anoxia, the severity of which was a function of the mass of material degraded. Material B produced grand mal seizures despite COHb levels of less than 10%. Material C produced metabolic acidosis and a mild degree of CO-induced anoxia. Loss of avoidance responses occurred at significantly lower CORb levels for materials B and C in comparison to CO alone. Using responses to COHb as a reference, it was possible to detect the presence of other toxicants present in combustion products. Compounds found in smoke in very low concentrations may have a high degree of biological activity and be responsible for impairment of survival responses. We have labeled these compounds "limiting" toxicants. They constitute a significant hazard, which is added to that of CO and anoxia.

Experiments were conducted on male Long-Evans rats instrumented for measurement of vital functions and a conditioned avoidance response. An intra-arterial cannula was used for removal of blood samples. Rats were exposed to combustion products of three polymeric materials. A National Bureau of Standards smoke chamber and a smaller “static” chamber were used for exposures. Material A produced a syndrome of carbon monoxide (CO)-induced anoxia, the severity of which depended only upon the amount of material degraded and not upon the mode of combustion (heat flux, flaming, or nonflaming). Material B produced a syndrome of epilepsy and carboxyhemoglobin levels below 10 percent. Material C produced a metabolic acidosis and mild CO-induced anoxia, the severity of which was related to the amount of material degraded, irrespective of the combustion mode. The combustion products of Materials B and C produced intoxication syndromes distinctly different from the syndrome of CO-induced anoxia produced by Material A. “Limiting” toxicants or substances with high biological activity may be present in combustion products and produce unique intoxication syndromes.