2-t-butyl-4-methoxyphenol (BHA) and 2,6-di-t-butyl-4-methylphenol (BHT) are widely used antioxidant food additives that are generally recognized as safe by the Food and Drug Administration. Previously reported studies have suggested that the ip LD50 of BHA may be as much as 2 orders of magnitude lower than its oral LD50. Metabolic activation of BHA to reactive intermediates possibly may be responsible for this result and may be related to other reported toxic effects. BHT has been reported to cause haemorrhagic lung damage and possible hepatocarcinogenicity in test animals. The present studies report investigations by electron spin resonance spectroscopy of free radical metabolites of BHA, BHT and related compounds. The primary, unstable phenoxy free radical of BHA has been generated by oxidation with horseradish peroxidase and hydrogen peroxide and detected by ESR spectroscopy. A scheme has been proposed for the peroxidatic oxidation of BHA. The ESR spectrum of the di-BHA dimer, one product of BHA oxidation, has been observed, analyzed, and reported. ESR studies have been extended to other phenol derivatives structurally related to BHA and suspected to be substrates for peroxidase. Similarly it has been found that BHT and structurally related phenols are substrates for peroxidation by horseradish peroxidase and hydrogen peroxide. In agreement with previous chemical and biochemical studies, it has been found that ortho-disubstituted phenols are oxidized to more stable phenoxy radicals than are ortho-monosubstituted phenols. The ESR hyperfine coupling constants for the phenoxy radicals studied are in agreement with those for similar radicals produced by chemical oxidation. Attention has been drawn to the biochemical and toxicological implications of these and related studies of BHA and BHT peroxidation.