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Inhalation toxicity of methyl n-amyl ketone (2-heptanone) in rats and monkeys.
Lynch-DW; Lewis-TR; Moorman-WJ; Plotnick-HB; Shuler-RL; Smallwood-AW; Kommineni-C
Toxicol Appl Pharmacol 1981 May; 58(3):341-352
The effect of methyl-n-amyl-ketone (110430) (MAK) on cardiopulmonary function, clinical chemistry, metabolism, and tissue distribution was studied in Sprague-Dawley-rats and Cynomolgus-monkeys. Animals were exposed to mean MAK concentrations of 100 or 1000 parts per million for 6 hours per day for 1, 3, 6, or 10 months for rats, and 10 months for monkeys. Both species tolerated the exposures without overt signs of toxicity. No gross or microscopic exposure related changes in organs and tissues from either species were seen. No effect on dynamic compliance, inspiratory capacity, expiratory flow maximum or diffusion capacity occurred in monkeys. There were no dose related alterations in clinical chemistry. In metabolic studies, MAK was detected in both serum and urine from rats and monkeys exposed to both concentrations of MAK. In tissue distribution studies, carbon-14 labeled MAK accumulated primarily in the liver, followed by kidney, pancreas, and lung. Urinary excretion peaked at 12 hours and remained relatively constant through 48 hours. Fecal excretion through 72 hours represented less than 2 percent of the administration dose. The authors conclude that MAK does not produce cardiopulmonary or clinical chemical changes at the doses studied.
NIOSH-Author; Organic-solvents; Laboratory-animals; Comparative-toxicology; Body-distribution; Cardiopulmonary-function; Biochemistry; Metabolism
Issue of Publication
Toxicology and Applied Pharmacology
Page last reviewed: April 12, 2019
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