The problem of organic solvent neurotoxicity was discussed. Recent international conferences devoted to the public health aspects of organic solvent neurotoxicity were described. The toxicokinetics of organic solvents were reviewed. Skin absorption and inhalation are the usual routes of exposure. The rate and extent of skin absorption depends on the duration of exposure, solvent concentration, state of the skin, and solubility properties of the solvent. Absorption through the lung depends on the concentration of the inhaled solvent, its solubility properties, and the pulmonary ventilation rate. Animal studies of organic solvent neurotoxicity have shown that long term exposure to organic solvents causes irreversible changes in the central nervous system (CNS) probably as a result of modifying membranes, altering neurotransmitter balances, and interfering with cell respiration and protein metabolism. Organic solvents such as n-hexane (110543) and methyl-n-butylketone (591786) cause a distal axonopathy consisting of symmetrical distal sensory loss and weakness. The clinical aspects of organic solvent neurotoxicity were reviewed. Workers exposed to organic solvent neurotoxicity typically develop a mild form of chronic toxic encephalopathy characterized by neurobehavioral defects in psychomotor, perceptual, and memory function with frequent disturbances in mood. Epidemiological studies have confirmed the occurrence of dose related CNS dysfunction among individuals who have been chronically exposed to a variety of organic solvents. The studies were limited by their inability to measure precisely exposure intensity. The author concludes that environmental monitoring is necessary to document significant exposures. Engineering controls should be the primary means for reducing occupational exposures.