One of my favorite reads is ProMedMail – ok, I am a nurse I know but they do such a great job for anyone who wants to follow diseases around the world. Today in light of the two ricin letters – one send to President Obama, the other to the Republican Senator from Mississippi, Roger Wicker, it felt appropriate to post some information on ricin. This feels a bit like a flashback to the 2001 anthrax letter scare on Capital Hill doesn’t it?
Ricin is a poison that comes from castor beans and can be found in a powder, a mist, a pellet or dissolved in water. The oil has applications as a purgative, an engine lubricant, and as a component of brake and hydraulic fluid. The industry is no longer active in the United States but the oil is produced in large quantities in other areas of the world. Importantly, the oil, if properly prepared, does not contain the toxin.
One million tons of castor beans are used each year for producing the oil. The waste mash from the oil production process can have as much as 5 percent ricin by weight and is easily and inexpensively isolated via a simple process in a low technology setting using materials easily obtainable. Ricin is easily prepared in liquid or crystalline forms or as a readily aerosolized, lyophilized powder. The toxin is stable and can be poisonous in its native form in the beans.
The clinical presentation of ricin poisoning depends on whether the exposure is parenteral (injection), inhaled, or ingested. In mice, the dose found to be lethal to 50 percent (LD50) of animals was found to be 3-5 microg/kg in inhalation or intravenous exposures and 20-25 microg/kg in intraperitoneal, subcutaneous, or intragastric administration. The time to death in the mice was 60 hours for inhalation, 90 hours for intravenous, and 80-100 hours for the other exposures. It is important to note that there is a variation of as much as 2 logarithms [100-fold] in the microg/kg dose of ricin between animals, with the horse seeming to be the most sensitive and the frog and chicken the least.
The 1st symptoms of toxicity generally occur 6-12 hours after exposure but can occur as early as 3 hours. This is longer than many of the chemical agents affecting the lung and more rapid than infectious agents. In humans, as seemed to have occurred in the Georgi Markov assassination, multiorgan failure occurred with a prominently elevated white blood cell count. [Markov was a Bulgarian communist defector who was killed in London in 2003 by a ricin pellet injected into his leg from a modified umbrella point — see http://edition.cnn.com/2003/WORLD/europe/01/07/terror.poison.bulgarian/index.html.]
As a weapon of bioterrorism, ricin would most likely be dispersed as an aerosol although contamination of food and water supplies is also feasible. Although easily obtained, massive quantities of toxin are necessary to create a large scale effect. Because signs and symptoms are non-specific, detection of an attack would require a high index of suspicion based on clinical and epidemiologic factors. The finding of a geographic cluster of patients with acute lung injury should arouse suspicion of an attack via an aerosolized agent, although the list of potential culprits is extensive and includes chemical as well as biologic agents. Ricin cases do not exhibit mediastinitis, as with anthrax, and they do not demonstrate any response to antibiotic therapy as would be expected with an infectious etiology. Pulmonary edema may develop one to 3 days after ricin exposure, in contrast to staphylococcal enterotoxin B or phosgene where time to development of pulmonary edema is 12 and 6 hours respectively.
There are limited data describing the outcome from an inhalation exposure. In the 1940s, sublethal and accidental exposures were said to have occurred and were manifest 4-8 hours after exposure with fever, cough, shortness of breath, and nausea. Studies in rodents suggest an inhaled ricin aerosol could lead to necrosis of the upper and lower airway, respiratory distress syndrome and respiratory failure. Chest x-ray would be expected to show bilateral infiltrates. In animal studies death occurred in 36 to 72 hours and was dose dependent. In primates, symptoms and time to death were also dose related and associated with alveolar flooding, fibropurulent pneumonia, and necrotizing tracheitis. Death occurred 36 to 48 hours after challenge following a 8-24 hour preclinical period.
The was extracted (citations removed) from: Lutwick LI, Gradon J, Zellen J: Category B Biotoxins. In Lutwick LI, Lutwick SM (eds), Beyond Anthrax: Bioterror – The Weaponization of Infectious Diseases. Springer-Humana, New York, 2009, New York, pp. 181-206: