1,1,1-Trichloroethane (1,1,1-TE) is a widely used organic solvent which is thought to be relatively safe. The present review is mainly focused on the neurotoxic effects of 1,1,1-TE. Concentrations above 350 ppm are considered capable of negatively conditioning the performance of the exposed person, in particular reaction time and manual abilities. Peripheral neuropathies have also been described. More recently the potential neurotoxicity of 1,1,1-TE has been underscored by animal studies investigating the effects of this substance in neurobehavioral tests and on neurochemical parameters. 1,1,1-TE alters the motor activity in small laboratory rodents. In fixed interval responding in mice, the effects of 1,1,1-TE are qualitatively similar to those of other volatile (ethanol) and non volatile (benzodiazepines and barbiturates) CNS depressants. In addition, in drug discrimination procedures 1,1,1-TE shares discriminative stimulus properties with barbiturates, toluene, halotane, and oxazepam indicating that this solvent has behavioral effects in common with central nervous system depressant drugs. From a neurochemical point of view long-term exposure to 1,1,1-TE induces astrogliosis in the cerebral cortex of gerbils as indicated by an increased concentration of glial fibrillary acidic protein. In addition low dose inhalation of 1,1,1-TE for 3 months decreases DNA concentrations in several brain regions of the gerbil. 1,1,1-TE affects also brain concentrations of cAMP and cGMP as well as calcium ion control, possibly through an action on voltage-dependent calcium channels. It has been also suggested that intermediate metabolites of 1,1,1-TE may give origin to condensation products with dopamine, ultimately impairing dopaminergic transmission. Some of the neurochemical effects of 1,1,1-TE are shared by other chlorinated organic solvents as well as by CNS depressants. The literature analyzed indicates that 1,1,1-TE may exert significant neurotoxic effects suggesting that more caution in its use is needed and that attention should be paid to the possibility of an additive effect of 1,1,1-TE and CNS depressants (ethanol, barbiturates, benzodiazepines and other volatile solvents) giving origin to severe neurotoxicity.
Judging from the human toxiological data reported, 1,1,1-trichloroethane appears to be one of the least toxic members of the
group of chlorinated aliphatic hydrocarbon solvents. This compound is rapidly absorbed through the lungs and the gastrointestinal
tract. Most of it is excreted unchanged via the lungs. The absorption of a toxic quantity results in a functional depression
of the central nervous system which may result in death from respiratory arrest or peripheral vascular collapse. Acute over-exposure
to anesthetic concentrations of the vapour can result in transcient kidney or liver dysfunction. Permanent organic injury
has not been observed following recovery from the anesthetic effects of this solvent.
The diagnosis of exposure to this compound can be made by specifically identifying 1,1,1- trichloroethane in the expired breath
of the exposed person. Comparison of the results of serial breath analyses with available human data affords a means with
which to estimate the magnitude of the chemical exposure.
The pre-employment medical examination of a group of unemployed to be engaged for work in a section of a mechanical industry revealed that the morbidity, quantitatively similar to that of an analogous group of workers who had been working in the plant for over 5 years, was qualitatively different for the prevalence of certain diseases (infectious and parasitic diseases, diseases of the respiratory tract, of the nervous system, of the skin, etc.). The morbidity in the same group of ex unemployed workers, followed up for two working years, resulted higher than that of the control group.