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Toxins as Weapons of Mass Destruction. Esequiel Barrera, SM (TOX) Biol/Chem Safety Officer UTSWMC at Dallas. Objectives. Examples of toxins potential to be used as a Weapon of Mass Destruction (WMD) Ricin T-2 Mycotoxins. RICIN OVERVIEW.

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Toxins as weapons of mass destruction

Toxins as Weapons of Mass Destruction

Esequiel Barrera, SM (TOX)

Biol/Chem Safety Officer

UTSWMC at Dallas


Examples of toxins potential to be used as a Weapon of Mass Destruction (WMD)


T-2 Mycotoxins

Ricin overview

  • Cytotoxin extracted from Castor Bean (Ricinus communis plant)

  • Protein has a molecular weight 64,000 daltons

  • Worldwide one million tons of castor beans are processed annually in the production of castor oil (waste mash is ~5% ricin by weight)

  • Cancer and autoimmune treatment applications

History and significance
History and Significance

  • Assassination of Bulgarian exile Georgi Markov in London (1978)

  • Minnesota Patriots Council (1994 and 1995)

  • Deborah Green, Kansas (1995)

  • Thomas Leahy, Wisconsin (1997)

  • al Qaeda cell, London (2003)


  • Potent protein and DNA synthesis inhibitor

  • LD50 for mice is 3.0 ug/kg

  • Comparative lethality: LD50 for Botulinum toxin (bacterium) is 0.001 and for VX gas (chemical agent) is 15.0

  • LD50 for humans is uncertain and varies with route of entry (ricin vs ricinine)

Agent characteristics
Agent Characteristics

  • Ricin is environmentally stable with 3 day survival in dry conditions

  • No person to person transmission

  • Lethality is high with death occurring 10-12 days for ricin ingestion and 3-4 days for inhalational exposure


  • Gold Standard technique is enzyme linked immunosorbent assays (ELISA)

    -antigen detection

    -IgG immunoassay

    -IgM immunoassay


  • There is currently no commercial vaccine or prophylactic antitoxin available for human use albeit animal immunization studies have been promising

  • Protective mask and engineering controls are currently the best protection

Inhalational ricin exposure signs and symptoms
Inhalational ricin exposure: Signs and Symptoms

  • 4 to 8 hours: Acute onset of fever, chest tightness, cough, dyspnea, nausea and arthralgias

  • 18-24 hours: Airway necrosis and pulmonary capillary leak leading to pulmonary edema

  • 36-72 hours: severe respiratory distress and death from hypoxemia

Medical sampling
Medical Sampling

  • Early Post-exposure (0-24 h): nasal swabs, induced respiratory secretions for PCR (contaminating castor bean DNA) and Serum for toxin assays

  • Clinical (36-48 h): serum for toxin assay and tissues for immunohistological stain in pathology samples

  • Postmortem (>6 days): Serum for IgM and IgG


  • Ingestional entry: Gastric lavage and cathartics are indicated. Charcoal application is of little value for large molecules such as ricin

  • Inhalation entry: Pulmonary edema treatment and supportive management


  • Ricin inactivation can be accomplished with bleach (1% sodium hypochlorite, 20 min) or autoclave treatment (80C for 10 min)

  • Intact skin surface decontamination use soap and water (dilution).

T 2 mycotoxins overview

  • Trichothecene (T-2) mycotoxins produced by the fungi of genus Fusarium (common grain mold)

  • Extremely stable in the environment

  • Toxin is dermally active causing blisters (minutes to hours after exposure)

History and significance1
History and Significance

  • Shortly after WWII, flour contaminated with Fusarium unknowingly baked into bread and ingested by civilians. Exposed individuals developed a protracted lethal illness called alimentary toxic aleukia (ATA).

  • “Yellow rain” incidents in Laos (1975-81), Kampuchea (1979-81) and Afghanistan (1979-81).

Toxin characteristics
Toxin Characteristics

  • Trichothecene are relatively insoluble in water

  • Compounds are extremely stable to heat and ultraviolet light inactivation

  • Bioactivity retained even after standard autoclaving (inactivation requires 1500 F for 30 minutes)

  • Hypochlorite solution alone does not inactive the toxins

  • Toxin rapidly inhibit protein and nucleic acid synthesis

Clinical features
Clinical Features

  • Routes of exposure: penetration through the skin, inhalation and ingestion.

  • Contaminated clothing can serve as a reservoir for further toxin exposure

  • Early symptoms (minutes after skin exposure): burning skin, redness, tenderness, blistering and progression to skin necrosis with leathery blackening and sloughing of large areas of the skin

  • Pulmonary/tracheobronchial toxicity produces dyspnea, wheezing and cough.

  • Gastrointestinal toxicity causes pain and blood tinged saliva and sputum

  • Death may occur in minutes, hours or days

  • Most common symptoms: vomiting, diarrhea, skin involvement with burning pain, redness, rash or blisters, bleeding and dyspnea.


  • Physical clues yellow, red, green or other pigmented oily liquid

  • Contact with the skin (unlike ricin) forms characteristic symptoms

  • Generally considered odorless (unlike mustard or other vesicant agents)

  • Serum and urine should be collected to be sent to a reference lab for antigen detection (gas liquid chromatography-mass spectrometry technique)

Medical treatment

  • Toxin inactivation requires 0.1M NaOH added to 1% hypochlorite solution for a duration of one hour.

  • No specific antidote or therapeutic regimen is currently available.

  • Exposed individuals: remove clothing, wash skin with soap and water.

  • Standard burn care is indicated for cutaneous involvement

  • Toxin ingestion use superactivated charcoal

  • Aerosol attack: respiratory support may be required, rinse out eyes with saline or water.

  • Prophylaxis: only physical protection of the skin, mucous membranes and airway are the only proven effective methods of protection during an attack.