REF CDHS 'Medical Provider Alert: RICIN' (June 2004/update ...



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California Department of Health Services

June 2004 (minor changes November 2005)

| |Medical Provider Alert: RICIN

AGENT OCCURRENCE: Ricin is a potent glycoprotein toxin derived from beans of the castor plant (Ricinus communis). Although not volatile itself, ricin may be formulated as a powder or an aerosol for intentional airborne dispersal. Castor beans are found worldwide and were grown commercially in California’s San Joaquin Valley for castor oil production until the 1960s. Castor is also an ornamental garden plant. The naturally occurring toxin is fairly easily removed from the mash remaining after castor oil extraction.

TOXIC ACTION: Ricin inactivates ribosomal RNA to block protein synthesis leading to cell death. There is no antitoxin.

ROUTES OF EXPOSURE:

• inhalation of aerosolized powdered ricin or ricin-containing dust

• ingestion of ricin contaminated food or water (oral ricin is poorly absorbed compared to inhaled toxin)

• dermal exposure of abraded skin or mucous membrane contact

(Note: ricin is poorly absorbed through intact skin; may penetrate if mixed with a solvent)

• ricin intoxication cannot be transmitted person to person.

PREVENTING EXPOSURE / PERSONAL PROTECTIVE EQUIPMENT: No commercial antidote or vaccine is currently available (a vaccine is in development, 2004). For staff attending victims not adequately decontaminated by first responders at the scene, the following are recommended: (see the National Institute of Occupational Safety and Health (NIOSH) emergency response card: bt.agent/ricin/erc9009-86-3.asp)

▪ full chemical-resistant suit with gloves, and

▪ eye/face protection such as face shield and goggles.

Remove victim’s potentially contaminated clothing, then wash skin thoroughly with soap and water. Clothing contaminated by aerosolized or powdered ricin should be handled very carefully and bagged as it may present a secondary inhalation or dermal risk to health care providers. After completing patient decontamination tasks, health care personnel should carefully remove all personal protective equipment and shower. Those in contact with the decontaminated patient or his/her personal effects should follow standard precautions and practice good hand hygiene.

METABOLISM: Ricin molecules rapidly attach to any mammalian cell. The toxic side chain is quickly absorbed and once sequestered intracellularly the toxin cannot be removed. Ricin is detoxified intracellularly to ordinary amino acids before being eliminated in urine. Toxin half-life was less than 24 hours in rats following intravenous injection. There is no data on half-life after inhalation or oral exposure in either humans or animals.

ACUTE TOXICITY: Animal data indicates symptoms and pathologic changes are route specific. High dose aerosol exposure causes airway irritation or necrosis, acute lung injury, pulmonary edema secondary to increased capillary permeability and eventual acute hypoxic respiratory failure. Allergic airway disease or asthma exacerbation may occur with lower level repeated exposures. Ingestion causes gastrointestinal hemorrhage and with high exposure causes hepatic, splenic, and renal necrosis. In rodents ricin is 1,000 times more toxic by inhalation than ingestion. Prolonged skin exposure can cause dermatitis or eczema. In mice the lethal dose to 50 percent of the test population (LD50) and time to death are 3 - 5 mcg/kg and 60 hours by inhalation and 20 mg/kg and 85 hours by ingestion. Inhaled doses of 20-40 mcg/kg were lethal in nonhuman primates.

There is a limited amount of toxicity data in humans. An oral dose of less than 5 mg/kg may be fatal in humans. A modified ricin molecule (toxic A-chain bound to tumor-specific antibodies) has been used in cancer immunotherapy clinical trials. Patients commonly experienced flu-like symptoms with fatigue and muscular pain four to six hours post intravenous administration of this low-dose ricin-based pharmaceutical. Ricin is also a potent immunogen and sensitizer. Workers extracting oil from castor beans and receiving repeated exposure to ricin dust experienced asthma exacerbation and allergic reactions including urticaria.

CHRONIC TOXICITY: No human or animal chronic exposure data is available.

CANCER RISK: Ricin has not been evaluated by the International Agency for Research on Cancer (IARC) or the U.S. Environmental Protection Agency (EPA) for carcinogenicity.

EXPOSURE IN PREGNANCY: Ricin is a teratogen in some experimental animals, causing neurologic damage in rodents and chicks. Moderate growth retardation, convulsions, and skeletal malformations occurred in an infant whose mother repeatedly ingested processed castor seeds as a contraceptive. Limited rodent studies also suggest reproductive effects including mid-term abortion.

RISK FOR CHILDREN: Ricin crosses the placenta and is excreted in breast milk.

SIGNS AND SYMPTOMS:

| |Routes of Exposure |

| |Inhalation |Ingestion |Dermal |

|Symptom Latency |3-8 hrs (ricin) |2-3 hrs (ricin) |Variable – solvents promote |

| | |2-3 days (castor beans) |uptake |

|Symptoms – |Weakness, fever, cough, allergy/asthma |Nausea, vomiting, diarrhea, abdominal |Local inflammation or allergy |

|initial |exacerbation, dyspnea, nausea, chest |cramping, GI bleeding |especially if exposure is |

| |tightness, arthralgia | |repeated or prolonged |

|followed in hours by |Sweating, noncardiogenic pulmonary edema, |Fever, headache, pupil dilation, | |

| |cyanosis, hypotension, necrotizing airway |dehydration, hypotension, dyspnea, | |

| |lesions |lethargy | |

|Prognosis |If untreated, can lead to seizures, |Can progress to liver, kidney, |Small particles in the eyes or |

| |respiratory and cardiovascular failure and|circulatory failure and death in 72+ hrs |abraded skin or solvent based |

| |death in 36-72 hrs | |ricin may be lethal |

|Differential (in large |Influenza, Q fever, tularemia, plague, |All major enteric pathogens, ingested |Other allergens |

|number of patients) |Staph enterotoxin B, exposure to |toxins (mushrooms), heavy metals, | |

| |insecticides paraquat or ANTU (alpha |pesticides, arsenic, caustics | |

| |–naphthylthiourea), by-products of Teflon | | |

| |or Kevlar pyrolysis | | |

| | | | |

| |Inhalation |Ingestion |Dermal |

|Rule outs |Anthrax - mediastinal widening (not seen |Rule out enteric pathogens with stool |Rule out other causes of |

|(see CDC Ricin Info for |with ricin) |culture, toxins, iron, arsenic and |urticaria and dermatitis |

|Clinicians: |Phosgene - acute lung injury progresses |caustic chemicals with appropriate | |

|bt.agent/ric|faster, + eye/throat irritation |analyses | |

|in/index.asp) |Nerve agents – cause dyspnea with profuse | | |

| |secretions and miosis | | |

|Supporting Tests |Chest x-ray with bilateral infiltrates, |Neutrophilic leukocytosis (2-5 fold | |

| |arterial hypoxemia, leukocytosis, high |increase), elevated liver function tests,| |

| |protein broncho-alveolar lavage fluid |endoscopy: GI mucosal hemorrhages, | |

| | |ulcerations | |

|Treatment (no antitoxin |Supportive, oxygen, hydration, Positive |Supportive, gastric lavage if ................
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