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To see if results in rats, rabbits, and dogs at high dose levels justified extrapolation, the fate of butylated hydroxyanisole in man was studied. Further possible pathways were sought in dogs. Dogs excreted 60% of a 350 mg. per kg. dose unchanged in the feces within 3 days, and the remainder in the urine largely as sulfate conjugates of BHA, ferf-butylhydroquinone, and an unidentified phenol. Little glucuronide was formed. Procedures used for low dose levels in rats were applied to man, where 0.5 to 0.7 mg. per kg. yields in the urine less than 1% of the dose as unchanged BHA, and 27 to 77% as the glucuro-

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Because of a number of cases of peripheral neuropathy that occurred in factory workers employed in a fabric-printing plant in 1973, chronic inhalation experiments have been conducted using the printing-ink solvents methyl n-butyl ketone (MBK) and methyl iso-butyl ketone (MIBK). After four months of intermittent respiratory exposure to 1,300 parts per million (ppm) MBK, all six rats tested developed severe symmetric weakness in the hindlimbs. Morphological studies showed massive focal axonal enlargements containing abnormally large numbers of neurofilaments and dying-back axonal degeneration in peripheral and central nerve fibers. Six rats similarly exposed for five months to 1,500 ppm of MIBK showed minimal distal axonal change, but remained neurologically intact. The principal conclusion of this study is that MBK is a neurotoxin in rats.