Ricin is a potent protein toxin derived from the beans of the castor plant (Ricinus communis). Castor beans are ubiquitous worldwide, and the toxin is fairly easily produced. Ricin is therefore a potentially widely available toxin. When inhaled as a small particle aerosol, this toxin may produce pathologic changes within 8 hours and severe respiratory symptoms followed by acute hypoxic respiratory failure in 36-72 hours. When ingested, ricin causes severe gastrointestinal symptoms followed by vascular collapse and death. This toxin may also cause disseminated intravascular coagulation, microcirculatory failure and multiple organ failure if given intravenously in laboratory animals.
TOXIN CHARACTERISTICS
Ricin is actually made up of two hemagglutinins and two toxins. The toxins, RCL III and RCL IV, are dimers of about 66,000 daltons molecular weight. The toxins are made up of two polypeptide chains, an A chain and a B chain, which are joined by a disulfide bond. Ricin can be produced relatively easily and inexpensively in large quantities in a fairly low technology setting. It is of marginal toxicity in terms of its LED50 in comparison to toxins such as botulinum and SEB (incapacitating dose), so an enemy would have to produce it in larger quantities to cover a significant area on the battlefield. This might limit large-scale use of ricin by an adversary. Ricin can be prepared in liquid or crystalline form, or it can be lyophilized to make it a dry powder. It could be disseminated by an enemy as an aerosol, or it could be used as a sabotage, assassination, or terrorist weapon.
MECHANISM OF TOXICITY
Ricin is very toxic to cells. It acts by inhibiting protein synthesis. The B chain binds to cell surface receptors and the toxin-receptor complex is taken into the cell; the A chain has endonuclease activity and extremely low concentrations will inhibit protein synthesis. In rodents, the histopathology of aerosol exposure is characterized by necrotizing airway lesions causing tracheitis, bronchitis, bronchiolitis, and interstitial pneumonia with perivascular and alveolar edema. There is a latent period of 8 hours post-inhalation exposure before histologic lesions are observed in animal models. In rodents, ricin is more toxic by the aerosol route than by other routes of exposure.
There is little toxicity data in humans. The exact cause of morbidity and mortality would be dependent upon the route of exposure. Aerosol exposure in man would be expected to cause acute lung injury, pulmonary edema secondary to increased capillary permeability, and eventual acute hypoxic respiratory failure.