Recent reports on the toxicity and metabolism of 1, 1, 1-trichloroethane are reviewed. Problems studied include transformation of this substance in the body and in the environment, its short and long term toxicities in animal experiments and human experiences, possible teratogenicity and tumorigenicity, and hazards due to contact with the skin and mucosae. Presumable modification of toxicity by inhibitors and other chemicals as well as physical conditions are also briefly discussed.

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We examined the tissue reaction of the oil absorbant particles made of perlite “expanded.” Five milligrams of perlite dust suspended in 5% alcohol was infused intratraheally into lungs of rats, and 12 weeks after the injection tissues from the left lung of the rats were examined pathohistologically. Tissue hydroxyproline in the right lung of each rat was quantitatively determined.
The results are summerized as follows.
Twelve weeks after the injection, some of the alveolar ducts and alveoli were filled with particles of perlite duct, and the wall of these alveoli was thickened in which phagocytes and lymphocytes were observed. Giant cell granulomatous foci and infiltration of numerous mononuclear or rounded cells were found in the interstitium of the intraalveolar septa of the lung. In these foci fibroblast prolifilation was observed, but the replacement to collagen fibers was not so strong. Glallet's cell prolifilation was observed sporadically. The amount of tissue hydroxyproline was estimated to be 3.95±0.59 mg (per dry weight) for the perlite group, 5.62±0.94mg for the quartz sands group and 6.38 ±1.89mg for the kaolin group.
The results suggest that the perticles of perlite “expanded” does not show so strong fibrogenesity to the lung tissue. However, the lung would have shown fibrosis slowly but steadily, if large quantity of particles of perlite had been depositted for a long time in the alveoli.

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