Ricin inhalation

Unlike all other routes of exposure, the gross pathological changes caused by ricin inhalation are observed almost exclusively in the respiratory tract, and are generally characterized by a diffuse pulmonary edema with multifocal areas of necrosis and inflammation (Griffiths et al., 1995a Doebler et al., 1996 Poli et al., 1996 Vogel et al., 1996 Wilhelmsen and Pitt, 1996 Brown and White, 1997 Wilhelmsen, 2000). 

Documented cases of human poisoning by ricin aerosol exposure are unknown. Cautious inferences may be drawn from observations of NHP exposed to ricin under controlled laboratory settings. Human toxicity from ricin inhalation would be expected to occur after a latency period of 24—72 h that may be characterized by loss of appetite and listlessness. Based on extrapolation from NHP studies, other signs and symptoms expected in humans after ricin inhalation may include listlessness, high fever, dyspnea, and coughing or bloody sputum that is delayed for 4—8 h after exposure, as well as bilateral abnormalities on chest radiographs, arterial hypoxemia, neutrophilic leukocytosis, and elevated protein levels in bronchial aspirates (Balint, 1974 Wilhelmsen and Pitt, 1996 Franz and Jaax, 1997). 

Confirmation of ricin inhalational intoxication would most likely be through enzyme-linked immunosorbent assay analysis of a swab sample from the nasal mucosa ricin can be identified by this method for at least 24 hours after the challenge.49 Because ricin is extremely immunogenic, individuals surviving a ricin attack would likely... 

Abrin, a potent toxin, is extracted from the seeds of the rosary pea (Abrus precatorius). Due to its easy availability and preparation, this toxin is an attractive option for weap-onizing in poor countries, and thus has also been included in the Sch ule 1 of the CWC. The mechanism of action of abrin is very similar to that of ricin however, in mice, abrin is 75 times more toxic than that of ricin (0.04 pg/ kg for abrin is equivalent to 3pg/kg of ricin). Similar to ricin, inhalation of abrin is found to be more toxic than ingestion. However, abrin ingestion has reported to be toxic to the liver, unlike ricin. At the cellular level, abrin is a potent toxalbumin known to cause cell death by inhibiting protein synthesis (namely, type 2 ribosomal inhibitory protein). Further, abrin is also known to induce endothelial cell damage leading to an increase in cell permeability, fluid and protein leakage, and tissue edema. 

Caution Ricin is extremely toxic to cells and acts by inhibiting protein synthesis. After aerosol exposure, signs and symptoms would depend on the dose inhaled. Humans can be expected to develop severe lung inflammation with progressive cough, dyspnea, cyanosis, and pulmonary edema. 

Ricin No vaccine available Inhalation supportive therapy G-l gastric lavage, superactivated charcoal, cathartics ... 

Symptoms of abrin inhalation are similar to ricin exposure. Initial symptoms of abrin poisoning by inhalation may occur within 8 h of exposure. Symptoms include respiratory distress, fever, cough, nausea, and tightness in the chest. Heavy sweating may follow as well as pulmonary edema. Finally, low blood pressure and respiratory failure may occur, leading to death (Ellenhom and Barceloux, 1997 Kortepeter and Parker, 1999 Eitzen et al., 2001). 

Differential diagnosis of ricin exposure shows early inhalational ricin poisoning and will have primarily respiratory signs and symptoms, whereas ingested ricin will probably present early with gastrointestinal symptoms. 

Candidate vaccines under development are immunogenic and confer protection against lethal aerosol exposures. Recent animal studies have shown that either active immunization or passive prophylaxis may be effective against intravenous or intraperitoneal intoxication with ricin (Poh et al, 1994). In the case of inhalational exposure, active immunization or prophylactic administration of aerosolized specific anti-ricin antibody may also be effective (Poli et al, 1994). Unfortunately, these applications may not be clinically available since they are still under investigation. 

Funatsu, G., Funatsu, M. (1970). Isolation and chemical properties of various types of ricin. Jpn. J. Med. Sci. Biol. 23 342-4 Gareth, D., Griffiths, G.D., Rice, P., Allenby, A.C., Bailey, S.C., Upshall, D.G. (1995). Inhalation toxicology and histopa-thology of ricin and abrin toxins. Inhal. Toxicol. 7 269-88 Gill, D.M. (1982). Bacterial toxins a table of lethal amounts. Microbiol. Rev. 46 86-94. 

Roy, C.J., Hale, M., Hartings, J.M., Pitt, L., Duniho, S. (2003). Impact of inhalation exposure modality and particle size on the respiratory deposition of ricin in BALB/c mice. Inhal. Toxicol. 5 619-38. 

Wilhehnsen, C.L., Pitt, M.L. (1996). Lesions of acute inhaled lethal ricin intoxication in rhesus monkeys. Vet. Pathol. 33 296-302. 

Griffiths, G.D., Phillips, G.J., Holley, J. (2007). Inhalation toxicology of ricin preparations animal models, prophylactic and therapeutic approaches to protection. Inhal Toxicol. 19(10) 873-87. 

Possible routes of exposure include cutaneous, mucosal, gastrointestinal, inhalation, and parenteral (intravenous or intramuscular). Gastrointestinal exposures are usually accidental and occur most commonly when castor (ricin) or jequirty (abrin) beans are chewed or swallowed. Cutaneous exposures are limited primarily to castor beans, which are unusually allergenic and may cause severe cutaneous hypersensitivity and systemic allergic reactions. Inhalation and parenteral exposures are generally limited to intentional, usually malicious, exposures. 

In addition to symptoms and physical findings, diagnostic clues for inhalational exposure may include bilateral pulmonary infiltrates on chest X-ray, arterial hypoxemia, neutrophilic leukocytosis and a bronchial aspirate rich in protein compared to plasma, characteristic of high permeability pulmonary edema (39). Unlike many biologic agents, ricin intoxication wonld progress despite treatment with antibiotics. 

Laboratory testing for ricin is limited, especially for inhalational exposures. The two common methods that can detect ricin in blood or other body fluids are the radioimmunoassay and the enzyme-linked immunosorbent assay (ELISA). Because ricin binds quickly and the body metabolizes it efficiently before excretion, the length of time necessary for these tests limits their usefulness for inhalation exposures (35). Besides testing body fluids, the CDC and member LRN state public health laboratories have a time-resolved fluorescence immunoassay that can test preparations of suspected ricin-containing substances and environmental specimens for the presence of ricin (40). 

Movement of the biological material ricin with soil-size fractions are shown in Figures 4.6 and 4.7. Studies on peanut (Arachis hypogaea) seed lectin show similar results (Zartman et al. 2005). These lectin data are similar in distribution to published values (Ravi et al. 2004). The inhalation of dust generated from ricin-contami-nated soils could pose a serious hazard to war fighters. Work of A. H. Corwin cited in Lamanna (1961) stated that ricin particles with a median diameter of 2 /(ui are 2.75 times as toxic as particles with a maximal particle size of 4.2 pm. 

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