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Brunka, Z.;  Ryl, J.;  Brushtulli, P.;  Gromala, D.;  Walczak, G.;  Zięba, S.;  Pieśniak, D.;  Anand, J.S.;  Wiergowski, M. Criminal Poisonings. Encyclopedia. Available online: (accessed on 21 June 2024).
Brunka Z,  Ryl J,  Brushtulli P,  Gromala D,  Walczak G,  Zięba S, et al. Criminal Poisonings. Encyclopedia. Available at: Accessed June 21, 2024.
Brunka, Zuzanna, Jan Ryl, Piotr Brushtulli, Daria Gromala, Grzegorz Walczak, Sonia Zięba, Dorota Pieśniak, Jacek Sein Anand, Marek Wiergowski. "Criminal Poisonings" Encyclopedia, (accessed June 21, 2024).
Brunka, Z.,  Ryl, J.,  Brushtulli, P.,  Gromala, D.,  Walczak, G.,  Zięba, S.,  Pieśniak, D.,  Anand, J.S., & Wiergowski, M. (2022, August 24). Criminal Poisonings. In Encyclopedia.
Brunka, Zuzanna, et al. "Criminal Poisonings." Encyclopedia. Web. 24 August, 2022.
Criminal Poisonings

Criminal poisonings are among the least frequently detected crimes in the world. Lack of suspicion of this type of event by police officers and prosecutors, clinical symptoms imitating many somatic diseases and technical difficulties in diagnostics, as well as high research costs make the actual frequency of these events difficult to estimate. The substance used for criminal poisoning is often characterized by: lack of taste, color and smell, delayed action, easy availability and difficulty to detect.

criminal poisoning political intoxication ricin fentanyl

1. Introduction

Toxicology still refers back to the words of Paracelsus, who stated that toxic effect of each substance depends mostly on its dose. Besides the dose, the toxicity is affected by factors reliant directly on the poisonous substance, such as the route and rate of administration, hydro- and lipophilicity, physical state and formulation (e.g., liquid, gas, solid) and the clinical state of the victim, particularly including: age, sex, body mass, comorbidities and genetic predisposition. The poison used in a criminal poisoning should be characterized by such features as: colorlessness, lack of taste and smell, delayed toxic effects, difficulties in detection and easy availability (Table 1) [1].
Table 1. Properties of pharmacologically active substances facilitated criminal poisoning [1][2].
Today, with the development of diagnostic techniques, the chance of revealing various types of criminal poisoning has increased. However, it is worth realizing that at the same time there has also been significant progress in planning criminal activities.

2. Criminal Poisoning Cases

Researchers would like to outline the historical background of politically motivated crime poisonings, with an emphasis primarily on the detection of toxic substances and medical treatment. There are many poisonings in which circumstances are of a political nature but no toxic substances or their metabolites have been detected. One such example is the case of the suspected poisoning of Pyotr Verzilov, Pussy Riot activist [3]. Verzilov fell ill on 11 September 2018 in Moscow. He lost his eyesight and ability to speak, became delirious and lost consciousness. He was hospitalized in Moscow in critical condition and four days later Verzilov was flown to Berlin [4]. Staff of the Berlin Charité hospital believed that, although there were no traces of poison in Verzilov’s system, there was no other explanation for his condition [5].
Table 2 describes selected cases of politically motivated poisonings in the years 1978–2020, with particular emphasis on the circumstances of the event, symptoms of poisoning and the undertaken treatment.
Table 2. Description of political criminal poisonings in the years 1978–2020.
The common feature of the poisoning cases described above was the alleged or proven involvement of secret services in the physical elimination of the political opponents. The symptoms were experienced by the victims almost immediately after poisoning (fentanyl, VX) or a few hours after exposure (ricin, Novichok, polonium 210Po isotope). The following describes the toxicological properties of selected toxic substances used for criminal purposes, as well as the diagnostic methods and the proposed treatment methods.

3. Toxicological Properties, Treatment and Diagnostics

The physicochemical and toxicological properties for selected criminal poisons are presented in Table 3 [16]. The most important factors determining the potency of the toxic effect were the dose and route of administration. It is worth noting that there is a very limited amount of data on poisons’ doses that are lethal to humans [17].
Table 3. Selected poisonous substances used for criminal purposes in the years 1978–2020 on a political background, their physicochemical and toxicological properties.
Toxic Substance (CAS) Physicochemical Properties Toxicological Properties Refs.
Lethal/Incapacitating Dose [mg⋅min−1⋅m−3] Time of Death [h]  
White powder.
It can be prepared in liquid/crystalline form.
Lethal dose:
  • p.o. 20–30 mg/kg (rats)
  • p.o. 15–35 mg/kg (mice)
  • p.o. 1–20 mg/kg (human), about 5–10 castor bean seeds
  • i.v. 3 to 5 µg/kg (mice)
  • s.c. 22 µg/kg (mice)
  • aero. 5–15 μg/kg (human)
  • i.m. 0.8 μg/kg (guinea pig)
  • no data on lethal doses in humans
Several dozen hours (with p.o. possible delay in absorption up to 5 days) [16][18][19][20]
Crystal-like solid, moderately water-soluble Lethal dose:
  • i.v. 2.91 mg/kg (mice)
  • p.o. 368 mg/kg (mice)
  • p.o. 18 mg/kg (rats)
  • s.c. 62 mg/kg (mice)
  • s.c. 1.5 mg/kg (rats)
  • no data on lethal doses in humans
Crystalline, colorless solid, soluble in organic solvents, hydrophobic Lethal dose LD50:
  • p.o. 2 μg/kg (guinea pig)
  • p.o. 70 μg/kg (king macaque)
  • p.o. 22–45 μg/kg (rats)
  • p.o. 5051 μg/kg (hamster)
  • no data on lethal doses in humans
From several days to several weeks [16][22][23]
Isotope of polonium 210Po Radioactive metal, soluble in water, forming simple salts in dilute acids Lethal dose LD50:
  • 50 ng (oral suspension)
  • 10 ng (inhalation)
From 2–3 weeks after the onset of symptoms [16][24]
organophosphorus compound VX
Amber to transparent oily liquid, slightly soluble in water Lethal dose (predicted):
  • LCt50 30 (air-cutaneous)
  • LCt50 7 (aerosol)
Incapacitating dose (predicted):
  • ECt50 25 (air-cutaneous)
  • ECt50 10 (aerosol)
A few to several minutes—bronchospasm [16][25][26][27]
organophosphorus compound Novichok
(no clear identification of the compound)
Liquid, fine powder, no details available For A-230 (estimated for human):
LCt50—1.9–3 mg-min/m3
LD50—7.5 × 10−4 − 0.002 g/70 kg body weight
Dla A-232 (estimated for human):
LCt50—7 mg-min/m3
LD50—0.035 g/70 kg body weight
Dla A-234 (estimated for human):
LCt50—7 mg-min/m3
LD50—0.035 g/70 kg body weight

3.1. Ricin

3.1.1. Properties, Metabolic Pathway and Toxic Effects

Ricin is a protein found in a plant called Ricinus communis. It is one of the first lectins detected, i.e., proteins that nonenzymatically attach to membrane sugar receptors. The biological properties of ricin were first described in 1888 by Hermann Stilmark [29]. Ricin is classified as an extremely hazardous substance [30][31]. However, production of the ricin is difficult to legal control because the castor bean plant from which ricin is derived can be grown at home without any special care. In the US, scientists must register it in the Department of Health and Human Services to use ricin and investigators possessing less than 1 g are exempt from regulation [32]. Castor bean seeds, in addition to ricin itself, also contain a homologous but much less toxic agglutinin called RCA120. Ricin is composed of two RTA and RTB protein chains (having 267 and 262 amino acids, respectively), linked by a disulfide bridge. RCA120, in turn, is a protein composed of four chains, 2 RTA and 2 RTB, linked by a disulfide bridge between the A chains. Both compounds show a very high sequence homology of their amino acids. However, ricin is a potential toxic substance, while RCA120 exhibits strong hemagglutinating properties.
The RTB chain is responsible for binding with galactose. The RTB chain is responsible for the entry of ricin into the cell, which is achieved by the production of endosomes. Some of the chains are transported to the Golgi apparatus. Others to the endoplasmic reticulum, in which the RTB is detached from the endosome protein, and the RTA chain itself passes into the cytosol of the cell using the ERAD (ER-associated degradation) pathway. The RTA chain is an enzyme (RNA N-glycosidase) and is responsible for ribosome inactivation (RIP—ribosome inactivating protein). Its action is based on the removal of adenine rRNA from 28S, which prevents the attachment of the translational factor EF2 (elongation factor-2) to the ribosome. In this way, protein synthesis is inhibited, which ultimately leads to cell death [33].
Ricin poisoning is characterized by a delayed onset of symptoms and a slow action with fatal outcome. The lethal dose of ricin depends on the route of its administration (Table 3). The in vivo toxicity of the substance for humans after oral administration is 1–20 mg/kg body weight, while when administered by injection or inhalation, this dose may be slightly lower [34].
After ingestion of the toxin through the alimentary tract, nausea, vomiting, diarrhea and abdominal pain occur. Within about 4–36 h, symptoms may progress, accompanied by: arterial hypertension, renal failure and liver damage.
In the case of inhalation, symptoms usually develop within about 8 h and include: cough, shortness of breath, joint pain and fever. Occasionally, these types of patients suffer from respiratory distress and death.
In the case of injection, local swelling and redness appear at the site of injection of the toxin. The first symptoms of poisoning develop within approx. 6 h. Among them, the dominant ones are: weakness and muscle pain. After the next 24–36 h, symptoms progress, including: nausea, fever and hypotension, as well as multiorgan failure or death.

3.1.2. First Aid and Treatment

Treatment of ricin poisoning is symptomatic. It includes the intravenous administration of fluids and vasopressors. In case of oral poisoning, it is possible to administer activated charcoal. Gastric lavage is considered only in cases where the intoxicity has occurred no more than one hour earlier.
Currently, the greatest hopes in the postexposure treatment of ricin poisoning are placed in the use of neutralizing antibodies. So far, two preparations for vaccination have been tested: ricin chain deactivated with formaldehyde (ricin toxoid) and deglycosylated ricin. Research using genetic recombination methods has led to the production of the RiVax vaccine.
Animal studies were carried out, including pigs exposed to lethal pulmonary exposure and systemic ricin with the use of anti-ricin F(ab’)2 antibodies of equine origin. It is possible to create postexposure remedies for ricin poisoning in humans [35].

3.1.3. Diagnostics

Diagnosis of ricin poisoning is based on history, identification of ricin in biological fluids or environmental samples. In clinical samples, ricin is difficult to detect due to its strong binding to glycosylated protein. Free ricin (with a molecular weight of 164 Da) is a marker of castor bean consumption [33]. There are analytical methods that enable the identification of ricin in blood, urine and in the vitreous humor of the eye (including ELISA tests, liquid chromatography with LC-MS/MS tandem mass spectrometry). Unfortunately, the level of ricin in body fluids does not have to correlate with the severity of symptoms.

3.2. Fentanyl

3.2.1. Properties, Metabolic Pathway and Toxic Effects

Fentanyl is a synthetic compound that belongs to the opioid family. First opioid substance was isolated in 1806 by Serturner which, as a tribute to the god of sleep Morpheus, was named morphine. Because of Serturner’s strong addiction to this substance that he developed soon after, he managed to describe the consequences of its chronic abuse in great detail. Since the time of their discovery, opioids have come to be an essential drug in everyday practice of medicine, mainly as analgesics. However, due to their strong addictive potential, they have also been used widely as recreational drugs.
Fentanyl is one of the most potent opioids, being a 100 times more potent than morphine. As a strongly lipophilic substance it enters the tissue compartments with ease (especially the central nervous system) and clinically produces an opioid toxidrome with a very characteristic presentation: bradycardia, bradypnea, hypotonia [36]. Fentanyl is controlled psychoactive substance by drug law in many countries (e.g., in UK, US, Netherlands, Poland, Canada) [37] and is also applied in medicine (only by prescription) [38]. However deaths involving synthetic opioids other than methadone (primarily fentanyl) continued to rise in the US in 2015–2020 [39]. In developed countries, the illicit market for the supply of fentanyl and related substances is very large [40].
On a molecular level fentanyl acts as a μ, δ and κ receptor agonist, each of which is coupled with a Gi protein (it causes a decrease in intracellular cAMP levels). Fentanyl’s interaction with an opioid receptor causes a decrease in calcium influx in the presynaptic neuron, which then suppresses the release of neurotransmitters into the synaptic cleft, as well as hyperpolarization of postsynaptic neuron due to potassium ion the efflux. All these effects impede physiological neuronal transmission [41].
The most important organ in fentanyl metabolism is the liver (Figure 1). The first phase of its biotransformation is conducted by CYP3A4, also present in enterocytes, which determines its particularly strong first pass effect. During the second phase fentanyl’s metabolites are being conjugated with the glucuronic acid, after which they are eliminated with the urine.
Figure 1. Fentanyl’s metabolic pathway in humans. Ninety-nine percent of the metabolized fentanyl is converted into norfentanyl. The remaining 1% is converted to despropionyl fentanyl and hydroxyfentanyl.

3.2.2. First Aid and Treatment

In spite of a fairly characteristic clinical presentation of an opioid toxidrome, fentanyl intoxication may be sometimes difficult to diagnose, even for an experienced clinician (Figure 2). The most important steps in the treatment are: securing patient’s airways, administering the antidote—naloxone—and providing ventilation support if needed. Naloxone is administered in fractioned doses, with the first one being usually 0.4 mg. After administering naloxone, the patient’s condition should be monitored closely for 2–3 min, and in the absence of improvement, the dose should be increased in a gradual way. Special care must be taken when administering naloxone in patients with an opioid addiction. Overdosing naloxone in such individuals may cause a severe opioid withdrawal syndrome, which can be life-threatening.
Figure 2. Flowchart describing the management of acute opioid poisoning in an adult (1 Most commonly noninvasive; if the GCS < 8 endotracheal intubation is indicated. 2 If no improvement occurs after 2–3 min the dose can be increased first to 0.5 mg, then, after another 2–3 min, to 2 mg, then to 4 mg, 10 mg, and up to the maximum dose of 15 mg. 3 If securing an i.v. access is impossible, naloxone can be administered i.m. or intranasally. 4 Recommended in absence of contraindications).


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