Articles

Polonium-210 poisoning: a first-hand account

Amit C Nathwani, James F Down, John Goldstone, James Yassin, Paul I Dargan, Andres Virchis, Nick Gent, David Lloyd, John D Harrison

Summary
Background Polonium-210 (²¹⁰Po) gained widespread notoriety after the poisoning and subsequent death of Lancet 2016; 388: 1075–80
Mr Alexander Litvinenko in London, UK, in 2006. Exposure to ²¹⁰Po resulted initially in a clinical course that was Published Online
indistinguishable from infection or exposure to chemical toxins, such as thallium. July 22, 2016
http://dx.doi.org/10.1016/
S0140-6736(16)00144-6
Methods A 43-year-old man presented to his local hospital with acute abdominal pain, diarrhoea, and vomiting, and
Department of Haematology,
was admitted to the hospital because of dehydration and persistent gastrointestinal symptoms. He was initially UCL Cancer Institute, London,
diagnosed with gastroenteritis and treated with antibiotics. Clostridium difficile toxin was subsequently detected in his UK (A C Nathwani MBChB);
stools, which is when he first raised the possibility of being poisoned and revealed his background and former identity, Department of Haematology
(A C Nathwani, A Virchis MBBS)
having been admitted under a new identity with which he had been provided on being granted asylum in the UK.
and Katharine Dormandy
Within 6 days, the patient had developed thrombocytopenia and neutropenia, which was initially thought to be drug Haemophilia Centre and
induced. By 2 weeks, in addition to bone marrow failure, he had evidence of alopecia and mucositis. Thallium Thrombosis Unit
poisoning was suspected and investigated but ultimately dismissed because blood levels of thallium, although raised, (A C Nathwani), Royal Free
London NHS Foundation Trust
were lower than toxic concentrations. The patient continued to deteriorate and within 3 weeks had developed multiple
Hospital, London, UK; National
organ failure requiring ventilation, haemofiltration, and cardiac support, associated with a drop in consciousness. On Health Services Blood and
the 23rd day after he first became ill, he suffered a pulseless electrical activity cardiorespiratory arrest from which he Transplant, Watford, UK
could not be resuscitated and was pronounced dead. (A C Nathwani); Intensive Care
Unit, University College
London Hospitals NHS
Findings Urine analysis using gamma-ray spectroscopy on day 22 showed a characteristic 803 keV photon emission, Foundation Trust, London, UK
raising the possibility of ²¹⁰Po poisoning. Results of confirmatory analysis that became available after the patient’s (J F Down MBBS,
death established the presence of ²¹⁰Po at concentrations about 10⁹-times higher than normal background levels. J Goldstone MBBS,
J Yassin MBBS); Clinical
Post-mortem tissue analyses showed autolysis and retention of ²¹⁰Po at lethal doses in several organs. On the basis Toxicology, Guy’s & St Thomas’
of the measured amounts and tissue distribution of ²¹⁰Po, it was estimated that the patient had ingested several NHS Foundation Trust,
1000 million becquerels (a few GBq), probably as a soluble salt (eg, chloride), which delivered very high and fatal London, UK (P I Dargan MBBS);
radiation doses over a period of a few days. Faculty of Life Sciences and
Medicine, King’s College
London, London, UK
Interpretation Early symptoms of ²¹⁰Po poisoning are indistinguishable from those of a wide range of chemical (P I Dargan); and Public Health
toxins. Hence, the diagnosis can be delayed and even missed without a high degree of suspicion. Although body England, London, UK
surface scanning with a standard Geiger counter was unable to detect the radiation emitted by ²¹⁰Po, an atypical (N Gent MBChB, D Lloyd PhD,
J D Harrison PhD)
clinical course prompted active consideration of poisoning with radioactive material, with the diagnosis ultimately
Correspondence to:
being made with gamma-ray spectroscopy of a urine sample. Dr Amit C Nathwani,
Department of Haematology,
Funding UK NHS, Public Health England, and the UK Department of Health. UCL Cancer Institute, London
WC1E 6BT, UK
[email protected]
Introduction and included review of the patient’s medical records,
Alexander Litvinenko (born Dec 4, 1962) was an officer of clinical course, spectroscopy results, and statements
the Russian secret service who, in 2000, was granted from experts. The hearing concluded on July 31, 2015,
asylum in the UK and is said by his widow to have begun and the final report into the death of Mr Litvinenko was
working as a consultant for the British intelligence published on Jan 21, 2016.
services. On Nov 1, 2006, Mr Litvinenko fell ill and was Following the public hearing, the primary clinicians
admitted to hospital. His illness was later attributed to and toxicology experts involved in the care of
poisoning with polonium-210 (²¹⁰Po), since substantial Mr Litvinenko in 2006 are now free of any restrictions to
amounts of this highly toxic radionuclide were found in describe the clinical aspects of this highly unusual case.
his body by the Health Protection Agency (now In this report, we provide a first-hand account of the
Public Health England). An inquest into Mr Litvinenko’s events leading to the diagnosis of ²¹⁰Po poisoning, as
death was opened and adjourned in November, 2006, due well as the detailed toxico-kinetics of the first documented
to outstanding criminal proceedings. The inquest was case of lethal poisoning with polonium.
subsequently resumed when it became clear that the two
men suspected of his murder could not be extradited Presentation
from Russia. The inquest was suspended in July, 2014, to On Nov 3, 2006, a 43-year-old man named Edwin Carter
allow a public inquiry under the Inquiries Act 2005 to presented to the Accident and Emergency department of
take place. The inquiry’s public hearing commenced at Barnet General Hospital (now part of Royal Free Hospital,
the Royal Courts of Justice in London in January, 2015, London) complaining of abdominal pain, vomiting, and

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Haematological parameters Liver and renal biochemistry

Haemoglobin White blood Neutrophils Lymphocytes Platelets Bilirubin Alanine Urea Creatinine
concentration cells (×10⁹/L) (×10⁹/L) (×10⁹/L) (×10⁹/L) (μmol/L) transaminase (mmol/L) (μmol/L)
(g/L) level (IU/L)
Day 3 201 21·7 19·8 1·0 178 49 16 12·1 101
Day 4 ·· ·· ·· ·· ·· ·· ·· ·· ··
Day 5 149 17·2 16·1 0·6 105 ·· ·· 7·9 76
Day 6 ·· ·· ·· ·· ·· ·· ·· ·· ··
Day 7 130 7·1 6·8 0·1 92 ·· ·· 4·4 79
Day 8 ·· ·· ·· ·· ·· ·· ·· ·· ··
Day 9 129 1·3 1·1 0·0 63 66 50 4·6 76
Day 10 ·· ·· ·· ·· ·· ·· ·· ·· ··
Day 11 136 0·3 0·3 0·0 35 60 92 4·4 90
Day 12 147 0·2 0·1 0·0 21 69 107 ·· ··
Day 13 145 0·1 0·0 0·0 9 76 102 ·· ··
Day 14 113 0·0 0·0 0·0 2* ·· ·· 10 102
Day 15 ·· 0·0 0·0 0·0 17 ·· ·· ·· ··
Day 16 ·· 0·0 0·0 0·0 21 ·· ·· ·· ··
Day 17 ·· 0·0 0·0 0·0 13 ·· ·· ·· ··
Day 18 91 0·1 0·0 0·0 10 153 40 9·2 132
Day 19 84 0·01 0·0 0·0 7 181 34 9·8 133
Day 20 91 0·01 0·0 0·0 15 228 39 11·8 190
Day 21 82 0·05 0·0 0·0 18 242 48 16·6 218
Day 22 90 0·01 0·0 0·0 8 254 54 23·9 286†
Day 23 108 0·02 0·0 0·0 15 158 112 24 353†
Normal levels 120–180 4–11 2·0–7·5 1·0–4·0 150–400 3–20 5–50 3·5–6·5 60–120
(reference range)

*Platelet and plasma transfusions started. †Enzymatic creatinine.

Table 1: Progression of the patient’s haematological parameters and hepatic and renal biochemistry after suspected poisoning on day 1

diarrhoea, which had started on Nov 1, 2006 (designated as revealed his previous identity and suggested the possibility
day 1 in the following chronology). On examination, he of being poisoned. He disclosed that before coming to the
appeared dehydrated. He was afebrile and had a normal UK he had been known as Alexander Litvinenko and that
pulse and blood pressure. Abdominal examination he had defected from the Russian Security Service.
revealed epigastric tenderness. In view of the profuse Mr Litvinenko explained that on the day he became ill,
nature of his diarrhoea, a provisional diagnosis of he had met with former Komitet gosudarstvennoy
gastroenteritis, possibly of infective origin, was made. He bezopasnosti (KGB) agents and feared that he had been
was admitted for further investigation and started on poisoned (figure 1, table 1). The patient and his wife asked
intravenous fluids and oral ciprofloxacin 500 mg every medical staff whether poisoning by infection with C difficile
12 h. Investigations showed that serum urea and might have occurred since they had a friend who had been
conjugated bilirubin concentrations were mildly raised at killed in this way. Mr Litvinenko was commenced on oral
12·1 mmol per L and 49 μmol per L, respectively, and metronidazole (400 mg three times daily) but his
creatinine was high at 101 μmol per L, suggesting gastrointestinal symptoms persisted. The working
dehydration. Haemoglobin concentration was 201 g per L diagnosis was of C difficile diarrhoea associated with a
(reference range 120–180 g/L) associated with a leucocytosis possible underlying viral gastroenteritis. By day 9,
(white blood cell count 22 × 10⁹ cells/L; reference range Mr Litvinenko had become neutropenic with a neutrophil
4·0–11·0 × 10⁹ cells/L) and neutrophilia (19·8 × 10⁹ cells/L; count 1·1 × 10⁹ per L (table 1). His platelet count had also
reference range 2·0–7·5 × 10⁹/L; table 1). fallen from normal levels to 63 × 10⁹ per L. The cause of the
cytopenia was unknown but thought to be due to a viral
Clinical course gastroenteritis or a consequence of ciprofloxacin toxicity.
On day 7, Clostridium difficile toxin was identified in the On day 11, his neutrophil count was lower than
patient’s stools by the microbiology department at 0·5 × 10⁹ per L and he had spiked a fever. He was started
Barnet General Hospital. The possibility was raised that empirically on intravenous piperacillin–tazobactam
this finding might have been secondary to ciprofloxacin. (4·5 g every 6 h) to avoid progression to a sepsis syndrome.
When the diagnosis was discussed with the patient, he He was also given one dose of pegylated G-CSF (Neulasta,

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Severe vomiting, Deteriorating Pyrexial despite Dies after third

diarrhoea, and liver function treatment with cardiorespiratory
abdominal pain antibiotics and arrest
G-CSF
Admission to
hospital because
of dehydration
and persistent
gastrointestinal Neutropenia Aplastic bone Deteriorating Generalised
symptoms marrow renal function erythema
Thrombocytopenia

Day 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23

Clostridium difficile Alopecia and Abnormal ECG; Second

toxin positive severe mucositis transferred to cardiorespiratory
intensive care unit arrest
Patient and wife
raise possibility
of poisoning
Persistent fever: Oliguric/anuric;
amphotericin and first cardiorespiratory
aciclovir added arrest

Figure 1: Schematic of clinical milestones following exposure to polonium-210 on day 1

6 mg [Amgen, CA, USA]) to stimulate recovery of the

neutrophil count. By day 13, he had developed alopecia
and mucositis; together with progressive cytopenia, these
signs gave him the appearance of someone who had been
exposed to toxin, chemotherapy, or radiation. Once again
the patient and his wife raised the concern that he might
have been poisoned, stating that many of his symptoms
were similar to those he had learned about during his
training as an agent in the Federal Security Service of
Russia (FSB). Reverse barrier nursing was started and on
toxicological advice from the clinical toxicology unit at
Guy’s & St Thomas’ NHS Foundation Trust, London, UK,
samples were sent to this clinical toxicology unit for a
heavy metal screen. A screen of the patient with a
standard Geiger counter revealed only background values.
On the evening of day 16, the results of the heavy metal Figure 2: Haematoxylin and eosin-stained bone marrow trephine showing
screen showed a slightly increased urine thallium cartilage and adipocytes with very few haemopoietic precursors
concentration (30 nmol/L; normal <10 nmol/L) but this
level was below the toxic concentration (800–1000 nmol/L). On day 18, he was jaundiced with normal alanine
A bone marrow trephine sample taken on day 15 was transaminase levels. Diarrhoea and abdominal pain were
acellular (figure 2). He was therefore transferred on day 17 settling and his oral intake was improving, although he
to the haematology unit at University College London for had haematemesis that evening. On day 19, the rapid
specialist support and treatment of bone marrow failure. assessment team was called because of concerns about
Samples were sent for human leucocyte antigen typing in heart rate irregularity: inverted T-waves were noted on the
case a bone marrow transplant was needed. The patient lateral leads of an electrocardiogram. Troponin T levels
had told staff that the Russians used radioactive thallium were normal. Nevertheless, he was transferred to the
as a poison. However, it was not thought likely that intensive care unit for further monitoring. To mitigate
thallium poisoning was the cause of the patient’s against further heart rhythm abnormalities, serum
deterioration, especially since he had no evidence of potassium was maintained at about 5·5 mmol per L.
peripheral neuropathy, which is a key feature of thallium He remained pyrexial, despite antibiotics. Because of
poisoning. However, in the absence of any other clear raised inflammatory markers (C-reactive protein
cause, we started treatment with oral Prussian blue (ferric 100 mg/mL, erythrocyte sedimentation rate 130 mm/h)
ferrocyanide; 4 g, every 8 h) because of the mildly raised but no evidence of disseminated intravascular coagulation,
urine thallium concentration together with gastro- he was started on systemic antifungal therapy with
intestinal symptoms and alopecia—two clinical features Ambisone (Gilead, CA, USA). Repeat analyses of plasma
that are typically associated with thallium poisoning. and urine showed a normal thallium concentration

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Blood film Radiograph film Activity, Total estimated Model prediction

Bq per g of activity in of total activity
tissue organ or tissue, in organ or
MBq* tissue, MBq†
Muscle (psoas) 1100 72 71‡
Brain 5500 8 ··
Lung 3500 1·8 ··
Spleen 9900 1·5 4·5
Kidney 49 000 15 17
Bile 13 000 3–14 per day 4§
Liver 30 000 54 66
Heart 2500 2¶ ··
Skin 1800 6 35
Blood: day 20 3300 19 25
Blood: day 23 1500 8 23
Urine: day 22 825 per mL 1·3 1·0

Bq=becquerel. MBq=megabecquerel. *Scaled from measurements using data for

organ masses, and blood, urine, and bile volumes.1 †An estimate of intake by
ingestion of 4·4 GBq polonium-210 on day 1, assuming 10% absorption to blood,
was made based on the most reliable measurements (urine, liver, and kidneys)
using a model for the behaviour of polonium-210 in the body2 and the model was
Figure 3: Radiograph film (right image) exposed to the patient’s blood smear then used to calculate the tabulated values. ‡Assuming that the concentration of
(left image) showing opacification (red arrow) in the exposed area of the polonium-210 in muscle is representative of “other” tissues in the model.2 §Based
smear but not in the adjacent area that was covered by a glass coverslip on the assumption that biliary excretion accounts for all faecal excretion.
(blue arrow) ¶Including blood content.

Table 2: Measurements of polonium-210 in post-mortem samples and

(<10 nmol/L). By this stage, his conjugated bilirubin level model predictions of organ content and excretion
was high (230 μmol/L). During the following 2 days
(days 20–22) his renal function deteriorated rapidly
(table 1). An abdominal ultrasound scan showed that the ventricles with no evidence of tamponade or valvular
liver, spleen, and kidneys were of normal size and pathology. Oesophageal Doppler showed a stroke volume
appearance, with no evidence of obstruction. of 40 mL (normal stroke volume is 70 mL) despite high
The possibility of chemotherapeutic agents causing doses of epinephrine (2·0 μg/kg per min). For the next
mucositis and bone marrow failure was considered but 16 h the patient remained unstable and required inotropes,
dismissed because covert administration at the doses continuous veno-venous haemofiltration, and full
necessary to cause rapid multi-organ failure would have mechanical ventilation. On day 23, Mr Litvinenko suffered
been difficult. A search for a radiotoxin was pursued along a third pulseless electrical activity cardiac arrest and was
several lines. Exposure of the patient’s blood smear on a pronounced dead. Results of the day 22 urine sample
glass slide to a radiograph film on day 22 showed that the became available shortly after the patient’s death and
radiograph film exposed to parts of the blood smear not showed the presence of 825 becquerel (Bq) per mL of
covered by a glass coverslip developed opacity (figure 3), ²¹⁰Po, consistent with polonium poisoning.
which is consistent with the presence of a radioactive
substance in the blood. Later that day, gamma-ray Post-mortem results
spectrometry measurements on a urine sample from the A post-mortem examination was done by a consultant
patient showed a characteristic 803 keV photon emission, forensic pathologist on day 31 in the presence of a
raising the possibility of polonium-210 (²¹⁰Po) poisoning. radiation protection officer. Precautions to avoid radiation
Further urine and blood samples were sent for exposure included the wearing of protective suits, gloves
confirmatory spectrometric analysis. However, the taped at the wrists, and large battery-operated plastic
patient’s condition deteriorated rapidly that day with the hoods into which filtered air was piped. Key gross
onset of a florid macular skin rash, abdominal distension, macroscopic findings were the presence of blood-tinged
progressive metabolic acidosis, and oliguria. He became fibrinous pericarditis, a pleural effusion associated with
hypothermic (35·5°C) and progressed to cardiogenic bilateral congestion of the lungs, gross ascites, and
shock with an associated acute drop in consciousness. generalised tissue autolysis of most organs, although the
This was followed rapidly by a pulseless electrical activity brain looked normal. Because of continuing autolysis of
cardiorespiratory arrest. He was resuscitated successfully tissues resulting from their ²¹⁰Po content, and the
but was dependent on escalating doses of epinephrine, hazardous nature of the tissue samples, microscopy of
and had a further pulseless electrical activity cardiac arrest the internal organs was not done and further analyses
2 h later. Echocardiography showed poorly contracting were limited to studies of the biodistribution of ²¹⁰Po

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using gamma-ray spectrometry. The results were used to

Cumulative dose (Gy)
estimate total organ concentrations of ²¹⁰Po at the time of
death. As table 2 shows, ²¹⁰Po was retained in all organs Red bone Gut Liver Kidneys Spleen Skin Testes
marrow
and tissues, with the highest activity in the liver
(30 MBq/g) and kidney (49 MBq/g), consistent with 1 day after intake 0·8 0·2 5·0 8·1 2·9 0·6 0·8

published data on the biodistribution of ²¹⁰Po.2–4 The 2 days after intake 1·8 0·4 11 18 6·4 1·3 1·9
lower concentration of ²¹⁰Po in lung tissue (3·5 MBq/g) 3 days after intake 2·7 0·6 17 27 9·9 2·0 2·9
was consistent with intake by ingestion. On the 4 days after intake 3·6 0·8 22 36 13 2·8 4·1
assumption of ²¹⁰Po ingestion on day 1 with 10% being 5 days after intake 4·5 1·1 28 44 16 3·6 5·2
absorbed into the systemic circulation, the concentrations 10 days after intake 8·7 2·0 51 80 31 7·9 12
of ²¹⁰Po measured in the liver, kidneys, and urine were 15 days after intake 12 2·8 70 110 44 13 19
used to estimate intake as 4400 MBq (4·4 GBq)2,4 20 days after intake 16 3·5 86 130 55 18 26
We estimated the cumulative radiation doses to the 22 days after intake 17 3·7 92 140 59 20 29
organs of a reference 70 kg adult man over 22 days
GBq=gigabecquerels. 1 Bq=1 dissociation per second (releasing one alpha particle per second, with associated low-yield
following the ingestion of 4·4 GBq of ²¹⁰Po (table 3). [10–⁵] gamma rays). 1 Gy=1 joule per kg.
Radiation doses causing lethal damage to body organs are
Table 3: Cumulative doses to organs or tissues of a reference adult man after ingestion of 4·4 GBq of
generally quantified in terms of the lethal dose of acute
polonium-210, assuming 10% absorption to blood
gamma radiation estimated to kill 50% of people exposed
in this way (lethal dose 50 [LD50] values), with
corresponding LD0–LD100 ranges. Doses necessary to 803 keV gamma rays. It has a half-life of 138 days and high
cause prodromal symptoms of vomiting and diarrhoea specific activity, so that a very small mass corresponds to a
are expressed as effective doses (however, it should be high amount of radioactivity. Human beings are constantly
noted that LD and effective dose [ED] are toxicological exposed to ²¹⁰Po, which occurs at low concentrations in the
terms and ED should not to be confused with the environment as part of the uranium decay chain. However,
radiation protection quantity of effective dose). When annual intake from natural sources is about 10⁸ times less
estimating values for ²¹⁰Po, it was necessary to take than the intake estimated in our patient at around 4 GBq.
account of the reduced effectiveness of protracted Polonium is used in various industrial processes and as
irradiation and the greater damage caused per Gy by a power supply in small satellites, but its manufacture
alpha particles compared with gamma rays (ie, the relative requires sophisticated equipment. It is, therefore, not
biological effectiveness for alpha particles is >1). Taking widely available, but it is an effective poison. It forms
account of dose protraction and assuming a relative water-soluble, colourless salts that are readily absorbed
biological effectiveness of 2, the ED0 and ED50 values for across biological membranes, becoming widely dis-
vomiting and diarrhoea were estimated to be about tributed in body organs and tissues where the alpha
0·6–0·8 Gy and 7 Gy, respectively.4 Therefore, our particles deliver a large amount of energy to surrounding
estimated dose rate to all regions of the gut of about cells, causing cell death and organ damage. Early
0·2 Gy per day for the first few days after intake (table 3) symptoms of ²¹⁰Po poisoning are indistinguishable from
does not seem to be sufficient to cause the prodromal those of a wide range of chemical toxins. Therefore, the
symptoms the patient experienced. However, the model diagnosis can be delayed and even missed without a high
might have underestimated gut doses, especially since degree of suspicion. Furthermore, ²¹⁰Po can be transported
data from animals suggest that a proportion of ingested easily and safely without detection because its high-energy
²¹⁰Po is retained in the gastric and intestinal mucosa.4 alpha particles have a short range and can be blocked by
Alternatively, these symptoms might have been caused by quite a thin barrier, such as the skin, and the associated
or compounded by infection with C difficile or a gamma-ray emissions are very low yield. Hence, the
cumulative radiation dose delivered by the radiotoxin in Geiger counter used in this case was unable to detect the
the gut lumen as well as that absorbed into the radiation emitted by ²¹⁰Po. Alpha-particle spectroscopy is
bloodstream. By contrast, the estimated dose to the red the best way to test for radiotoxins such as ²¹⁰Po that emit
bone marrow was about 6 Gy after 1 week, rising to 17 Gy alpha particles. However, these devices are not readily
after 22 days. The estimated radiation doses to the liver available in most hospitals.
and kidneys were also very high—about 5 Gy to the liver Reports of ²¹⁰Po poisoning in human beings are scarce;
and 9 Gy to the kidneys per day over the first few days and a Russian accident case involving inhalation of an aerosol
reaching 92 Gy and 140 Gy, respectively, after 22 days. of ²¹⁰Po at a dose of about 530 MBq ²¹⁰Po resulted in death
in 13 days.4,5 However, the timecourse of rapid clinical
Discussion deterioration observed in our patient, resulting in death
Polonium-210 is a naturally occurring radioactive element within 23 days, is consistent with animal data for several
that was discovered in 1898 by Marie Curie. It decays to mammalian species.4 Aside from the gastrointestinal tract,
stable lead-206 by emitting one alpha particle, with the bone marrow was one of the first organ systems to be
occasional excitation in the nucleus and emission of damaged. From an initial neutrophilia, a feature of acute

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radiation injury,6 the neutrophil count fell rapidly over a future would need a high degree of clinical suspicion and
2-week period. The LD50 for the bone marrow was investment in sensitive detection instrumentation by
estimated to be about 3 Gy, with an LD0–LD100 range of hospitals. However, such cases would remain untreatable
1–4 Gy. Our calculations indicate that the LD100 value for without research into effective antidotes that reduce levels
the red bone marrow was exceeded after 5 days (table 3), and biodistribution of ²¹⁰Po, and limit the extent of organ
causing irreversible damage to the haemopoietic stem cell damage. Nevertheless, early diagnosis of poisoning with
and stromal compartments.4 At substantially lower doses radiotoxin is important to maximise the potential for
of ²¹⁰Po, transplanted progenitor cells might provide effective treatment and enable appropriate precautions to
transient support but animal data suggest that death in be taken to protect hospital staff.
such a setting can occur later, mainly as a consequence of Contributors
radiation damage to the kidneys.7 Similarly, the estimated ACN, NG, DL, and JDH collated all the data and prepared the first draft
LD50 value for acute kidney damage was 6 Gy, with a of the report. ACN provided the University College London Hospital
clinical data for the patient. JFD, JG, JY, and ACN provided the data
corresponding value for liver failure of 8 Gy. Our estimates relating to the intensive treatment unit management of the patient.
of the cumulative dose delivered to the kidney and liver PID provided toxicology input. JDH provided the polonium-210
were 44 and 28 Gy, respectively, at day 5. Hence, the wide biodistribution and dosimetry data. AV provided data from the initial
distribution of ²¹⁰Po probably resulted in the delivery of management of the patient in Barnet General Hospital.
lethal radiation doses to several organs early after intake. Declaration of interests
Several chelating agents have been assessed in animal We declare no competing interests.
models of ²¹⁰Po poisoning to reduce organ retention Acknowledgments
and enhance excretion.8,9 Unithiol (sodium 2,3-dimer- This work was supported by the UK NHS, Public Health England, and
the UK Department of Health. We thank the staff of Public Health
captopropane-1-sulphonate) has been used in children England (formerly of the Health Protection Agency) for polonium-210
accidentally exposed to ²¹⁰Po in the former Soviet Union10 measurements and dose calculations. We are grateful to Mike Holland
and has recently been given to two individuals thought to for his assistance with the writing and formating of the final report.
have been exposed at around the same time as The high global media coverage and unique circumstances of this case
preclude the customary patient anonymity. This report has been
Mr Litvinenko: both survived, but both had received published with the agreement of the patient’s relatives.
much lower doses of ²¹⁰Po than our patient. Animal data
References
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