The relationship between the chemical structure of organophosphorus esters and their ability to induce delayed neurotoxicity is reviewed. The biochemical target as well as factors affecting the development of organophosphorus ester induced delayed neurotoxicity (OPIDN) are discussed. Specific topics covered include the development of an experimental model of delayed neurotoxicity (with provision for species selectivity, age sensitivity, stages of delayed neurotoxicity in chickens, and factors affecting the development of delayed neurotoxicity), mechanisms of delayed neurotoxicity (as they relate to histopathological studies, cell bodies, central nervous system, peripheral nerves, peripheral sensory nerves, neuromuscular junctions, and muscle), electrophysiological studies, and biochemical studies (including the inhibition of esterases, theory of neurotoxic esterase, significance of inhibition of nonspecific esterases, effect on acid-phosphatase activity, and effect on axoplasmic transport). The site of neurotoxic action is reviewed with specific mention made of chemical structure relationships to delayed neurotoxic activity for aliphatic phosphorus esters, pyrophosphorus esters, aliphatic aromatic phosphorus esters, triaryl phosphate esters, and saligenin cyclic phosphorus esters. A working hypothesis of the mode of action of OPIDN is presented.