For definition of Groups, see Preamble Evaluation.
VOL.: 71 (1999) (p. 1027)
N.B. - Summary (but not the evaluation) prepared by the Secretariat after the meeting.
5.1 Exposure data
Exposure to isopropanol may occur in its production, in the production of acetone and during its use as a solvent.
5.2 Human carcinogenicity data
An increased incidence of cancer of the paranasal sinuses and laryngeal cancer was observed in workers at factories where isopropanol was manufactured by the strong-acid process. One case–control study investigated the risk associated with occupational exposure to isopropanol, but for none of the investigated cancer sites was a significant increase in risk observed.
5.3 Animal carcinogenicity data
Isopropanol was tested for carcinogenicity in mice and rats by inhalation exposure. Although no increase in tumours was observed in mice, the study had some limitations in design and adequacy. A slight increase in interstitial cell adenomas of the testis was observed in male rats.
5.4 Other relevant data
Isopropanol is rapidly absorbed from the human gastrointestinal tract, whereas absorption through the skin is slow. It is metabolized by aldehyde dehydrogenase to acetone, but following human exposure, a large proportion is excreted unchanged in expired air and urine. It is a human sensitizer and is irritant to the eyes and rhinopharynx. Isopropanol is a central nervous system depressant and prolonged inhalation exposure of rats can produce degenerative changes in the brain. There is no evidence for genetic toxicity.
There is inadequate evidence for the carcinogenicity of isopropanol in humans.
There is inadequate evidence for the carcinogenicity of isopropanol in experimental animals.
Isopropanol is not classifiable as to its carcinogenicity to humans (Group 3).For definition of the italicized terms, see Preamble Evaluation.
Previous evaluations: Vol. 15 (1977); Suppl. 7 (1987)
See Also: Toxicological Abbreviations