DEF, commonly known as tribufos, is classified as an organophosphate compound primarily used as a cotton defoliant. This compound is known to cause severe neurotoxic effects attributed to cholinesterase inhibition. While skin contact is the major route of exposure to DEF, it is also readily absorbed from oral route of exposure. Tribufos residues in food and drinking water do not pose risk concerns. The late acute effects of DEF are largely attributed to n-butyl mercaptan, an important breakdown product of DEF. The most common clinical manifestations of DEF toxicity in humans include lacrimation, salivation, nausea, vomiting, headache, giddiness, diarrhea, pupillary constriction, tremors, convulsion, and delayed neuropathic effects. Rhinorrhea and sensation of tightness in chest are common in inhalation exposure. Blurring or dimness of vision, miosis, ciliary muscle spasm, loss of accommodation and ocular pain, and mydriasis may occur. Loss of muscle coordination, slurring of speech, fasciculations and twitching of muscles of tongue and eyelids, and generalized profound weakness. The deteriorating effects of DEF on cellular genomic functions account for both carcinogenic and mutagenic properties of DEF. Physically, DEF is a colorless to pale-yellow liquid. It is completely miscible with n-hexane, toluene, and 2-propanol. While this organophosphate compound is not significantly volatile, its major degradation product, n-butyl mercaptan, is volatile and responsible for its characteristic skunk-like odor near sites of application. DEF is likely to be carcinogenic to humans at high doses, whereas it is not likely to be carcinogenic to humans at low doses. Airway protection along with administration of either atropine sulfate (intravenous or intramuscular), pralidoxine, or glycopyrolate is probably the best antidote to deal with DEF poisoning. © 2014 Elsevier Inc. All rights reserved.