The two major incidents of ginger jake or ginger jake like paralysis described in the last slide had a great impact on the toxicology of tri-ortho-cresyl phosphate (TOCP). Together, the adulteration of Jamaica ginger and of cooking oil with TOCP had affected nearly half million of people.

More than a century ago, TOCP was already found to be capable of inducing some form of polyneuritis (Lorot, 1899, as cited by Ecobichon, 1982). Its ability to induce delayed polyneuropathy was not confirmed, however, until after the first outbreak had occurred. The ginger extract samples collected from the victims and from the production sources provided strong evidence linking the delayed neurotoxicity to TOCP. It was this epidemiologic evidence that enabled Maurice Smith and his colleagues at the U.S. National Institutes of Health to focus their attention on TOCP as the prime suspect. After all, not every test species in their animal studies developed the paralysis syndrome when given the suspected gingers or the TOCP solution.

The concern over this type of adverse effects has persisted to this date. For example, the U.S. Environmental Protection Agency (U.S. EPA, 1996) subsequently developed a regulatory guideline specifically for testing delayed neurotoxicity of organophosphates from acute and 28-day exposure. A large number of toxicology studies also have been conducted attempting to reveal the actual mechanism by which TOCP or other organophosphorus esters cause the ginger jake like paralysis (see, e.g., Abou-Donia, 1985; Ecobichon, 1982).