1,1,1-trichloroethane (levels unknown) showed evidence of a toxic encephalopathy, with
symptoms similar to those seen after exposure to other solvents. The principal finding at
autopsy of victims of occupational poisoning or solvent abuse has generally been lung
oedema. Repeated, controlled exposures to up to 500 ppm 1,1,1-trichloroethane produced
mild CNS disturbance.
Refs. Stewart RD and Andrews JT JAMA 1966 195 904-906
Stahl CJ et al., J. Forensic Sci. 1969 14 393-397
Hall FB and Hine CH J. Forensic Sci. 1966 11 404-413
Kelafant GA et al., Am. J. Indust. Med. 1994 25 439-446
Stewart RD et al., Arch. Environ. Health 1969 19 467-472
Very few studies have been carried out on workers exposed occupationally to 1,1,1-
trichloroethane for long periods. Multiple studies provide no convincing evidence of
genotoxicity of 1,1,1-trichloroethane itself. No anecdotal accounts suggesting carcinogenicity
in humans have been located, and the solvent gave negative results in 2-year rodent studies.
Under the revised Montreal Protocol, production and use of 1,1,1-trichloroethane are
scheduled to be phased out by the year 2005 by ratifying parties (excluding 10-year
derogations for developing nations), because of its contribution to atmospheric ozone
depletion (ozone-depleting potential 0.15, cf. 0.8-1.0 for fully halogenated CFCs, and short
residence time, but world production is high).
Animal toxicity generally low; not carcinogenic in well-designed studies. No evidence of
reproductive toxicity in adequate studies. Relatively low toxicity in man after acute or
The PDE for 1,1,1-trichloroethane is 15.0 mg/day (limit 1500 ppm). However, note that
production of 1,1,1-trichloroethane is scheduled to be phased out by 2005 under the Montreal
Protocol, because of atmospheric ozone depletion.