A case of peripheral neuritis followed exposure to the dimethylamine salt of 2,4-dichlorophenoxyacetic acid. 2,4-D is widely used as a weed killer. In minute doses, plant growth is stimulated; but in concentrations employed in ordinary commercial herbicides, this chemical causes excessive stimulation resulting in death to the plant. Although 2,4-D is usually nontoxic, in 1959, Goldstein, Jones, and Brown reported 3 cases of peripheral neuropathy following exposure to an ester of 2,4-D.1 The neuropathy began shortly after the exposure to the skin; therefore, absorption seemed to be percutaneous. Disability was prolonged, and recovery was incomplete. Prior to this report there had been no evidence of serious toxic effect in humans. However, various toxic reactions had been reported in animals, including renal edema with tubular changes, liver damage, myotonia, stiffness of the extremities, ataxia, lethargy, paralysis, and coma. Goldstein, Jones, and Brown did not describe details of manufacture or purity