The purpose of presenting this first case study here is at least three-fold. Although as mentioned in Slide 8, tri-ortho-cresyl phosphate (TOCP) has relatively low acute toxicity and widely used in industry, the compound is a potent neurotoxin if abused. Ironically, even after the Jamaica ginger epidemic in the United States was over, there were still numerous outbreaks involving TOCP contained in mineral oils and fat substitutes that were deliberately used for cooking (Ecobichon, 1982).

Available toxicologic investigations and epidemiologic studies all have pointed to the fact that only the ortho isomer of tricresylphosphate is a strong inducer of delayed polyneuropathy in humans and some mammals. These observations suggest that, like some other adverse effects (such as those of thalidomide discussed in the last lecture), delayed neurotoxicity is extremely specific to chemical structure. Because TOCP is a strong inducer of delayed neuropathy, it is not a relatively potent inhibitor of the acetylcholinesterase enzyme. This fact was also confirmed by the numerous epidemiologic studies that were conducted to investigate the TOCP-related poisonings.

Finally, this case study shows that, like in many other incidents, it was epidemiologic evidence that had facilitated as well as advanced the toxicology of TOCP.