Trichloroethane Epinephrine

Human death following acute exposure to high 1,1.1-trichloroethane concentrations is usually attributed to either depression of the central nervous system, which results in respiratory arrest (Hall and Hine 1966 Jones and Winter 1983 Stahl et al. 1969). or sensitization of the heart to epinephrine, which results in severe cardiac arrhythmias (Guberan et al. 1976 MacDougall et al. 1987 Travers 1974). The occurrence of death during physical exertion following inhalation of... 

In humans, long-term exposure to high 1,1,1-trichloroethane vapor concentrations can have toxic effects on the heart that persist beyond the period of exposure. While experiments in animals have shown that arrhythmias produced by 1,1,1-trichloroethane and epinephrine quickly subside after the cessation of exposure (Carlson 1981 Clark and Tinston 1973), three human cases involved ventricular arrhythmias that persisted for 2 weeks or more after solvent exposure ended (McLeod et al. 1987 Wright and Strobl 1984). In all 3 cases, the subjects had been exposed repeatedly to high (unspecified) 1,1,1-trichloroethane concentrations. Echocardiograms revealed mild left ventricular dilation in one patient and slightly dilated left atrium in another, as well as impaired left ventricle function in both (McLeod et al. 1987.) Chronic exposure (<250 ppm) to 1,1,1-trichloroethane had no... 

The highest NOAEL values and all reliable LOAEL values for cardiovascular effects in each species and duration category are recorded in Table 2-1 and plotted in Figure 2-1. Cardiovascular effects reported in humans include sensitization of the heart to epinephrine and decreased blood pressure. Both effects were found only after brief exposure to high 1,1,1 -trichloroethane concentrations. 

The acute cardiotoxic effects of 1,1,1-trichloroethane (reduced blood pressure and increased sensitization to epinephrine-induced arrhythmias) appear to be mediated by the compound and not its metabolites (Carlson 1973 Toraason et al. 1990, 1992) and have been associated with the ability of 1,1,1-trichloroethane to interfere with membrane-mediated processes including calcium mobilization during myocardial contraction (Herd et al. 1974 Hoffman et al. 1992 Toraason et al. 

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