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Hydrogen chloride (HC1) is a relatively common component of fire effluents about which there has been much speculation and controversy. The studies reported here represent a continuation of efforts to clarify the role o f HC1 in combustion toxicology. Studies with rodent exposures have shown that at low concentrations of HC1, sensory irritation causes a decrease in respiratory minute volume, with somewhat slower loading of C0 and a delay in toxicological effects. At much higher HC1 concentrations, pulmonary irritant effects are observed leading to post exposure lethality. An empirical analysis of data for mixtures of HC1 and CO suggests that exposure doses leading to lethality may be additive. The lethal toxic potency (LCs0) of PVC smoke may be largely, but not entirely, accounted for by the HC1 produced. However, PVC smoke exhibited a greater incidence of early post exposure deaths. The early deaths, which may be partially attributable to a combined effect of C0 and HC1, may also be linked to the pattern of respiratory penetration by the smoke.