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Cyanide poisoning related deaths, a

four-year experience and review of the
literature
a a b
Maryam Akhgari , Fatemeh Baghdadi & Alireza Kadkhodaei
a
Forensic Toxicology Department, Legal Medicine Research
Center, Legal Medicine Organization, Tehran, Iran
b
Forensic Medicine Department, Legal Medicine Research Center,
Legal Medicine Organization, Tehran, Iran
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poisoning related deaths, a four-year experience and review of the literature, Australian Journal of
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 Australian Journal of Forensic Sciences, 2015
http://dx.doi.org/10.1080/00450618.2015.1045552

Cyanide poisoning related deaths, a four-year experience and review

of the literature
Maryam Akhgaria*, Fatemeh Baghdadia and Alireza Kadkhodaeib
a
Forensic Toxicology Department, Legal Medicine Research Center, Legal Medicine
Organization, Tehran, Iran; bForensic Medicine Department, Legal Medicine Research Center,
Legal Medicine Organization, Tehran, Iran
(Received 3 November 2014; accepted 14 April 2015)
Downloaded by [Maryam Akhgari] at 23:44 03 June 2015

Cyanide has been used as a poison for thousands of years. Symptoms of cyanide
poisoning begin quickly and death occurs within minutes. In this study, we review
52 cyanide poisoning cases in Tehran, Iran, over a four-year interval, from 30
December 2009 to 1 January 2014. Toxicological analysis and post-mortem findings
are discussed. Colour test (Prussian Blue) was used for screening for cyanide with
confirmation using the voltammetry method. The youngest decedent was a 2-month
old girl. Men constituted 76.9% (40) of the total 52 victims. Peak age prevalence of
cases was seen in age groups 21–40 years (32 cases, i.e. 61.5%). Methadone and
opioid alkaloids were the most common drugs detected in biological samples in this
study. A suicide attempt was the main cause of poisoning in 33 cases. The results
showed that cyanide-poisoning-related deaths are among the most public health
problems in Iran. Restricted access to cyanide and stricter buying and selling
controls may reduce intentional self-poisoning with this dangerous substance.
Keywords: cyanide; fatal poisoning; Suicide; forensic toxicology

1. Introduction
Cyanide is a rapidly acting poison. There are many forms of cyanide; they include
gaseous hydrogen cyanide (HCN), sodium and potassium water soluble cyanide salts,
and mercury, copper, gold and silver salts of cyanide that are not easily water-soluble.
In addition, cyanide may be released in the body during metabolism of cyanide-
containing compounds. These cyanogen chemicals include cyanogen chloride and
cyanogen bromide (pulmonary irritant gases), nitriles (R-CN), and sodium nitroprus-
side, which can produce cyanide poisoning during prolonged high dose intravenous
therapy1,2. However; regardless of its origin, hydrogen cyanide (HCN) is the primary
toxic agent3. This toxic substance rapidly enters the blood and circulates throughout the
body. Cyanide inhibits 40 enzymes containing iron, copper or molybdenum. It has an
inhibitory effect on the intracellular electron transport mechanism via irreversible bind-
ing to iron in cytochrome C oxidase (the mithochondrial enzyme responsible for the
last step in cell respiration) and haemoglobin, hence causing intracellular hypoxia with
a shift towards an anaerobic process with energy depletion and cell death1,4,5. Cyanide
affects the functions of a central nervous system (CNS), vascular, pulmonary and
metabolic system3. Humans may be exposed to cyanide from dietary, industrial,

*Corresponding author. Email: akhgari1349@yahoo.com

© 2015 Australian Academy of Forensic Sciences

 2 M. Akhgari et al.

environmental and other sources2. Exposure to cyanide can occur by ingestion,

inhalation and other dermal or parenteral routes6. Some occupations have ready access
to cyanide. They include chemists, jewellers, people involved in photography, dyeing,
printing and electroplating7−9. Domestic fire is one of the causes of cyanide poisoning.
Wool, silk, plastics, synthetic rubber, polyurethane and acrylonitrile contain both carbon
and nitrogen and can liberate cyanide during combustion under pyrolysing conditions
at high temperature and low oxygen content10,11. There is a ‘knockout effect’ generated
by cyanide in some fires. This effect renders the victim unconscious before the carbon
monoxide has reached a lethal level1. Long-term consumption of cyanide-containing
foods is also a source of cyanide poisoning. The pits of many fruits, such as apricot
and papayas, contain amygdalin. Ingestion of large quantities of these foods may result
in toxicity due to hydrolysis of amygdalin to hydrogen cyanide12.
According to a World Health Organisation (WHO) report there were 873,000 cases
of suicide in the year 2002 among the world population13. Suicidal ingestion is one of
the sources of cyanide poisoning. Although medications remain the most important sub-
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stances involved in completed suicides, successful fatal poisoning with non-pharma-

ceutical substances such as cyanide occurs with some regularity. Inhaled toxins are the
most popular toxins for attempted suicide due to their easy use and rapid action14.
Death usually occurs rapidly when an adequate quantity of cyanide is taken. The capac-
ity of cyanide to act as a fatal substance is described as few seconds after exposure2,15.
There are different criteria for the diagnosis of cyanide poisoning; these include
clinical, biological or analytical investigations10. Three classic features of the autopsy
in cyanide-related death detection are: pink lividity, an odour of ‘bitter almond’,
gastritis and oral/peripheral erosions. Pink lividity is not a specific sign in cyanide-
related deaths and is not always seen in cyanide deaths. There are no reliable autopsy
findings that are diagnostic of cyanide intoxication. The bright pink lividity has been
differentiated from the ‘cherry pink’ lividity of carbon monoxide poisoning. Lividity
may be pink for a variety of non-pathologic reasons, including refrigeration and
putrefaction. One cannot rely upon the lividity to include or exclude cyanide intoxica-
tion as the cause of death. The odour of ‘bitter almonds’ is highly suggestive of
cyanide poisoning6. However its absence does not rule out cyanide poisoning. This
odour is specific for cyanide intoxication and can be detected by 60% of the popula-
tion7,16. The persons involved in transportation, examination of cyanide-poisoned
victims, and forensic toxicology laboratory staff are at risk of poisoning by inhalation
of cyanide gas from the body of victims6. Haemorrhagic mucosa in the stomach can be
seen in oral ingestion of cyanide7.
There are many analytical techniques for toxicological determination of cyanide poi-
soning such as fluorimetry17,18, gas chromatography19−21, visible spectrophotometry22,23
and headspace gas chromatography (HSGC)1.
This study is an investigation of 52 fatalities with cyanide detected in post-mortem
specimens (liver, stomach content, and femoral blood). In all cases the cause of death
was reported by the head office of forensic medicine organisation to be cyanide
intoxication.

2. Materials and methods

In this retrospective study, biological specimens (liver, bile, stomach content, blood and
vitreous humour) collected at autopsy examination of 52 fatal cyanide poisoning cases
admitted to the Forensic Toxicology Laboratory, Legal Medicine Organisation, Tehran,
 Australian Journal of Forensic Sciences 3

Iran, from 30 December, 2009 to 1 January, 2014 were analysed. Diagnosis of cyanide
poisoning was based on the history given by relatives, autopsy examination, hospital
reports and finally toxicological analysis.
Most determination techniques of cyanide are based on acidification of biological
and non-biological samples and liberation of formed hydrocyanic acid (HCN). For
cyanide analysis, liver and stomach content samples were homogenised. Samples were
distilled and pH was adjusted to 2–3 by using tartaric acid (10% W/W). Distillate was
gathered in a tube containing ferrous sulphate (20% W/W)-sodium hydroxide
(10% W/W) and sulphuric acid (10% W/W). Prussian blue reaction was used for
cyanide determination as screening test. Confirmational analysis was performed in a
10 mL electrochemical cell on a Metrohm 757 VA Stand24. All experiments were
carried out at room temperature.

2.1. Other drugs and poisons analysis

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Phosphine (PH3) gas was qualitatively detected by the silver nitrate (AgNO3) impreg-
nated paper test according to the analysis method described by Chugh et al. (1989)25.
Pre-analytical preparation of biological matrices was done by liquid–liquid extrac-
tion (LLE) of urine, blood, liver, bile and stomach content samples. Cleavage of drugs
and metabolites from conjugates, extraction of unknown analytes and clean-up steps
had been done by pH adjustment and use of suitable solvents such as chloroform,
methanol, isopropanol and diethyl ether. For preliminary qualitative analysis, the thin
layer chromatography (TLC) technique was used to screen drugs, poisons, and opioid
alkaloids in biological samples. Samples were analysed with more sensitive and specific
instrumentations. High performance liquid chromatography (HPLC) (Knauer, Germany)
with a diode array detector (DAD) (Knauer DAD 2700, Germany) equipped with a
quaternary pump (Knauer pump 1000, Germany) was used. Analytes were separated
using a Eurospher 100–5 C18 column (250 mm × 4.6 mm). Maximum flow rate and
pressure were 10 mL/min and 400 bar respectively. An Agilent model 7890A gas chro-
matograph (Agilent Technologies, Sdn Bhd, Selangor, Malaysia) fitted with split/split-
less injector and a HP5-MS capillary column (cross-linked 5% methyl phenyl silicone,
30 m length × 0.25 mm ID × 0.25 μm film thickness) was used. The capillary column
was connected to a mass analyser (MS 5975C) (Agilent Technologies) operated by
electron impact (70 eV) in full scan mode (50–550 m/z) with the following parameters:
injector temperature, 250°C; interface temperature, 280°C. The oven temperature was
programmed as follows: initial temperature, 60°C; initial hold, 1 min; temperature pro-
gramme rate, 2°C/min; final temperature, 280°C; final hold, 15 min. Helium carrier gas
was maintained at a constant flow of 1.5 mL/min. Femoral vein blood (containing 1%
W/V sodium fluoride) and vitreous humour needed no preparation prior to analysis for
detection of ethanol and methanol with head space gas chromatography (HSGC). Blood
and vitreous humour alcohol concentrations were routinely determined using a quantita-
tive HSGC (Agilent 6890 N, USA) equipped with a flame ionisation detector (FID).
Headspace injections were performed using an automatic sampler. Analytic separation
was achieved using Agilent 6890 N headspace gas chromatography (HS-GC). The col-
umn used here was DB-ALC1 (30 m × 320 μm × 1.8 μm). The GC was fitted with an
Agilent headspace GC injection system that allowed for automated sample pretreatment
and injection. The sample volume was set to 1000 μL and got incubated at 60°C for
15 min prior to injection. The syringe was heated to 60°C. Loop and transfer lines were
set at 140°C. Identification and quantification of analytes was accomplished using a
 4 M. Akhgari et al.

flame ionisation detector (FID) and the GC injector and detector temperature were set
at 150°C and 300°C. Carboxyhaemoglobin was analysed by a Cecil 9000 spectropho-
tometer. The analysis of heavy metals was done by a Reinsch test. The information
needed in this study was collected from forensic autopsy reports and laboratory analysis
sheets. All data were analysed using Chi-square test SPSS (version 18).

3. Results
During the study period, 52 fatal cyanide poisoning cases were admitted to the Legal
Medicine Organisation, Tehran, Iran. Males represented 76.9% (40) of all the studied
cases. The male-to-female ratio was 10:3. The mean ± SD of the age of cases was
31.8 ± 12.8 and the age range was two months to 67 years. Case history study of dece-
dents showed that the majority of cases (35, 67.3%) had a history of depression. A his-
torical background of drug abuse was reported by relatives in nine of 52 cases. The
toxicological analysis involved one or more drugs or substances detected in biological
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samples (Table 1). One of the cases was a 20-year-old jeweller who used potassium
cyanide for cleaning jewellery. Haemorrhages and erosions of the mucosa of the
respiratory tract, oesophagus and stomach were found in five and a ‘bitter almond’
odour was detected in two decedents at autopsy examination. Twenty-one of the studied
cases showed pink lividity.
Suicide was the reported manner of death in 33 cases, of which 30 cases ingested
cyanide salts intentionally. The manner of death of two cases was homicide. They were
two unwanted infants. No cyanide-poisoning-related death due to fire was reported in
our study. There was no history of depression or suicide attempt in 17 of the decedents
referred for autopsy examination. In addition, these cases had no distinctive autopsy
findings that confirmed cyanide poisoning. All of the liver and stomach content samples
showed positive results for cyanide by Prussian Blue and voltammetry methods. The
linear range of calibration, for measurements at the hanging mercury-drop electrode
(HMDE), was from 0.1 to 2.0 μg cyanide with r = 0.998. The RSD was 1.2% (n = 5)
for 0.4 μg cyanide measured. Detection limits of 7.4 μg/L were calculated. A chro-
matogram obtained from a Metrohm 746 VA trace analyser is shown in Figure 1. The
frequency of incidence according to decedents’ age range is shown in Figure 2.

Table 1. Additional drugs and substances detected with cyanide in biological samples of fatal
cyanide-poisoning related deaths in Tehran, Iran, in a four year study (30 December 2009 to 1
January 2014).

Drug Class Positive Results Number

Prescription Drugs Doxepine 1
Carbamazepine 1
Alprazolam 1
Tramadol 1
Methadone 3
Total 7
Illicit Drugs Opiates 3
Methamphetamine 1
Total 4
Pesticides Aluminium phosphide 1
(Phosphine gas)
Total 1
Total 12
 Australian Journal of Forensic Sciences 5
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Figure 1. Determination of free cyanide in liver and stomach content samples with the 757 VA
Computrace.

4. Discussion
The Legal Medicine Organisation, Tehran, Iran, is the main referral centre for autopsy
examination not only for Tehran province but also for other neighbouring provinces.
The total number of cases referred for post-mortem examination is about 10,000 cases
per year and 37% of these cases are referred for toxicological investigation. An autopsy
is performed in cases of suspicious or sudden death, death due to poisoning, unnatural
death causes, suspicious of medical error and any condition where the doctor cannot
write a death certificate.
The goal of this study was to identify-cyanide-poisoning related deaths in Tehran,
Iran over the last four years. It should be considered that epidemiological data based
on cyanide analysis results are prone to bias. Cyanide has a very short half-life in the
body and is a volatile substance in HCN form, thus cyanide concentrations measured
are sometimes erroneously low in post-mortem samples10. However all stomach content
and liver samples of 52 decedents were tested positive for cyanide by both Prussian
blue and voltammetry methods.
Many studies have reported a high number of suicide attempts by females26,27.
However, other studies point to a higher prevalence of suicide among males26,28,29.
This study, however, only analysed the personal history of completed suicides with one
substance (cyanide) not all other drugs and poisons which caused referral for cause of
death investigation.
There are some important findings in this study. These findings are related to
autopsy findings and toxicological analysis.
 6 M. Akhgari et al.
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Figure 2. Age range distribution of fatal cyanide poisoning related deaths in Tehran, Iran in a
four year study (30 December 2009 to 1 January 2014).

As a result of our overall investigation on these cases, toxicology analysis results

and incomplete history given by relatives, we now routinely check all referred cases for
cyanide.
One of the studied cases was a 20-year-old jeweller who committed suicide with
cyanide. It is important in autopsy examination to consider certain occupations and cir-
cumstances around death. Jewellers, chemists, pharmacists, miners, photographers and
laboratory staff can use cyanide to commit suicide2,7. These occupations have contact
and free access to cyanide and committing suicide with this toxic substance is pre-
dictable and expected by them7. An odour of bitter almonds is described in cyanide
deaths but some individuals cannot detect this smell6,7,17. Cyanide is a corrosive sub-
stance and can deteriorate tissues which it is in contact. Many factors can influence
production of haemorrhagic gastric mucosa; these include the amount of cyanide
ingested and the amount of food in the stomach at the time of cyanide ingestion. The
pink lividity is not pathognomonic of cyanide poisoning and is not always seen in cya-
nide deaths. As other studies have also demonstrated, the pink lividity of cyanide poi-
soning is neither specific nor sensitive for cyanide intoxications7,30−32. Nine cases had
a history of drug abuse; six of them committed suicide with cyanide. This study
includes data on the co-ingestion of prescribed and illicit drugs in cyanide-related
deaths. Traditional poisons such as arsenic, cyanide and parathion were used in earlier
years, but nowadays such poisonings are rare and instead other drugs are more com-
monly detected in crime victims33.
Some studies suggest that alcohol and drug abuse are second only to depression
and other mood disorders when it comes to risk factors for suicide. Substance abuse
and mental disorders often go hand-in-hand in committing suicide34. In our study, most
of the deaths were the result of suicide, mostly by intentional oral ingestion at home.
Only three cases received hospital treatment for cyanide poisoning before death. Sui-
cide is one of the most important social problems in many countries. Cyanides are used
as suicidal and homicidal agents. They can also be potentially used in terrorist attacks2.
Suicide rate analysis is not easy in Iran due to large proportion of deaths from
unknown causes. In accordance with other studies there is a higher prevalence among
 Australian Journal of Forensic Sciences 7

males in this study26,28,29,35,36. In suicide cases, cyanide can be voluntarily ingested in

the form of sodium or potassium salts1,2. There is a case report of homicidal poisoning
by cyanide injection in Sri Lanka. It is important to consider cyanide poisoning in
deaths after injection of an unknown substance, when the patient shows symptoms of
cyanide poisoning such as respiratory depression leading to rapid death37.
From a toxicological point of view, it is important to consider that death from cya-
nide poisoning is rare; however, differential diagnosis of suspicious cases should be
evaluated for the detection of cyanide poisoning. There are numerous methods for the
detection of cyanide in non-biological (water, soil, food, etc.) and biological samples
(blood, urine, saliva, etc.). A common practice for extraction of cyanide from biological
samples is distillation and subsequent analysis of the product with colorimetric and
instrumental methods. The Prussian Blue test is commonly used for the preliminary
testing. It is simple, specific and reliable and can be performed directly on stomach
contents without prior preparation38. Many electrochemical methods have been applied
for the detection of cyanide but few of these methods have been used for cyanide
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analysis in biological samples3,39−41. The basis of a cyanide detection procedure is elec-

trochemical determination of CN– with a dropping mercury electrode. This method
allows determining free cyanide accurately (Metrohm 746 VA trace analyser)25. How-
ever, GC/MS is the preferred conformational method in forensic cases for qualitative
and quantitative analysis for cyanide due to its excellent sensitivity38−42.
A scientific autopsy of all suspicious cases is actually necessary to clarify the cause
of death. Toxicological analysis results and death scene investigation are other factors
to significantly help forensic medicine specialists decide the manner of death. Because
of the importance in clinical, forensic and security applications, cyanide detection is
routinely performed in our forensic toxicology laboratories on biological matrices
obtained from suspicious cases at autopsy examination.
Although the results obtained from this study cannot explain all cyanide poisoning
cases, we hope these results will be used to establish public awareness of the dangers
of cyanide and to restrict the access to lethal substances by government in order to
decrease morbidity and mortality from poisoning by this toxic substance.

Disclosure statement
No potential conflict of interest was reported by the authors.

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