Although the mode of action of ricin at the molecular level is known, the mechanisms responsible for the clinical and lethal effects of the toxin are still inadequately understood. Representative animal toxicity data for ricin administered by different routes are shown in Table 1. The variations in the acute toxicity values reported in the literature are mainly due to mixture of the preparations used in the tests (reviewed by Balint, 1974). The symptoms of ricin poisoning manifest slowly, usually 12 hr after administration, and include rather sudden outbursts of convulsions and opisthotonos, followed by paralysis of the respiratory center, eventually leading to death. Fortuitous poisoning is usually due to ingestion of castor beans (for recent examples, see Aslani et al., 2007; Soto-Blanco et al., 2002). Laboratory tests with seeds showed hen to be the most resistant species (the lethal dose was 14 g/kg); sheep and horse were more sensitive (lethal doses were and g/kg, respectively). The toxin is pyrogenic in mammals (Balint, 1993). In the serum of animals treated with ricin, antibodies specific to ricin have repeatedly been detected (see, for example, Griffiths et al., 2007).
Last summer, the dairy industry found itself in the middle of a media flurry over a paper that paints a terrorist scenario about botulinum toxin in milk. The paper, by Dr. Lawrence Wein of Stanford University, described a scenario by which terrorists could poison thousands of people through the . milk supply ( Wein and Liu, 2005 ). Wein’s paper was initially withheld at the government’s request over fears that it could aid attackers; later, the National Academy of Sciences (NAS) published the paper, insisting that it did not put any new information before terrorists.