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Clinical Toxicology (2011), 49, 834839

Copyright 2011 Informa Healthcare USA, Inc.


ISSN: 1556-3650 print / 1556-9519 online
DOI: 10.3109/15563650.2011.618456

CRITICAL CARE

A mass cyanide poisoning from pickling bamboo shoots


PENSIRIWAN SANG-A-GAD1, SURIYA GUHARAT2, and WINAI WANANUKUL3
1Department

of Medicine, Ratchaburi Hospital, Ratchaburi Province, Thailand


Provincial Health Office, Ministry of Public Health, Ratchaburi Province, Thailand
3Ramathibodi Poison Center, Department of Medicine, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand
2Ratchaburi

Context. Bamboo shoots contain cyanogenic glycosides named taxiphyllin. Cyanide poisoning from cyanogenic glycosides commonly
occurs following ingestion. However, toxicity caused by inhalation of hydrogen cyanide gas (HCN) produced from pickled shoots has
never been reported. Objective. To describe cyanide poisoning in eight victims who were exposed to HCN produced in a well containing
pickling bamboo shoots. Materials and methods. Due to a series of botched rescue attempts, a total of eight patients entered into a
27 m3 well containing pickled bamboo shoots and immediately lost consciousness. After rescue, two patients developed cardiac arrest,
metabolic acidosis and died. Four other patients suffered metabolic acidosis, but recovered after supportive care. The remaining two
regained consciousness and recovered soon after the event. Ambient air study and cyanide content of bamboo shoots helped confirm the
diagnosis. Results. All patients had high anion gap metabolic acidosis with normal oxygenation. Blood cyanide levels ranged from 2.66
to 3.30 mcg/ml (taken after about 18 h of incident). Ambient air study (21 h after incident) revealed oxygen 20.9%, and sulfur dioxide
19.4 ppm. The instrument was unfortunately not equipped to detect HCN. A simulation study revealed HCN and sulfur dioxide in the
ambient air at 10 ppm and 7.5 ppm, respectively. Cyanide content in the bamboo shoots ranged from 39 to 434 mg/kg in the wet shoots.
Discussion. This series of patients developed sudden onset of alteration of consciousness and metabolic acidosis upon exposure, and
cyanide was confirmed in all victims. The simulation study confirmed the presence of HCN in the ambient air of the well containing
bamboo shoots. Conclusion. We have reported mass acute cyanide poisoning with two fatalities. The source of HCN was unusual as it was
produced from pickling bamboo shoot.
Keywords Metabolic; Heart; CNS/ Psychological

Introduction

and sliced by local farmers. The sliced fresh bamboo shoots


are mixed with salt and sent to the factory in plastic bags.
Then, they are pickled in wells for a month before pickled
shoots are packed and sold in market.
Bamboo is a plant which produces cyanogenic glycosides.2
One of its glycosides is p-hydroxylated mandelonitrile, named
taxiphyllin. The content of hydrogen cyanide (HCN) varies
depending on parts of the shoots and the bamboo species,
ranging from less than 100 to nearly a 1000 mg HCN per kg
of fresh shoot.3,4 When the shoots are disrupted by cutting or
peeling, a glycosidase enzyme in the shoots hydrolyzes the
glycoside and produces HCN, as shown in Fig. 1.46 Usually,
traditional preparations including boiling can reduce the HCN
content in bamboo shoots and make them edible.4,7 Unlike
cases involving the consumption of cassava, no cyanide poisoning has been reported from consuming bamboo shoots.8,9
Moreover, there has been no report of cyanide poisoning by
inhaling HCN gas produced by these cyanogenic glycosides.
The objective of this report was to describe a mass cyanide poisoning in victims who were exposed to HCN gas
produced in a well used for pickling bamboo shoots.

Bamboo shoots are an ingredient of various popular traditional Thai and Asian cuisines. There are 30 kinds of bamboo
in Thailand, but the shoots of Dendrocalamus aspe, Bambusa
nutans, Bambusa mulfiplex, and Thyrsostachys siamensis are
commonly selected for food.1 The demand for consuming
bamboo shoots occurs year round, but shoots are harvested
only in the early rainy season in Thailand. Therefore, the Thai
people have developed various methods to preserve bamboo
shoots so that they are available for consumption year round.
One of the methods is salt pickling of sliced bamboo shoots.
In the past, pickling bamboo shoots was a home-based industry. The salt pickling process commences by taking fresh
bamboo shoots which are peeled and then sliced into small
thin pieces. The thin pieces are then washed and mixed with
salt and kept in closed containers for at least 30 days before
being ready to eat. Nowadays, demand is increasing and
hence pickled bamboo shoot production is carried out on an
industrial scale. Bamboo shoots are harvested from the forest
Received 23 April 2011; accepted 24 August 2011.

Case Series

Address correspondence to Dr. Winai Wananukul, M.D., Ramathibodi


Poison Center, Department of Medicine, Faculty of Medicine
Ramathibodi Hospital, Mahidol University, Rama 6 Road, Bangkok
10400, Thailand. E-mail: rawwn@mahidol.ac.th

At a bamboo shoot pickling factory located in the central


west of Thailand, Patient 1 (Pt 1) accidentally dropped a 20 kg
834

A mass cyanide poisoning from pickling bamboo shoots 835

Fig. 1. Chemical biotransformation of taxiphyllin in bamboo shoots to generate hydrogen cyanide during the preparation.

bag of fresh sliced bamboo shoots into the bamboo shoot


pickling well. The well had a 27 m3 capacity (3x3x3 m in
size) and partially filled with 20 MT of sliced bamboo shoots.
He jumped into the well to retrieve the bag, but immediately
lost consciousness in the well.
Pt 2 immediately jumped into the well to rescue Pt 1, but
also became unconscious in the well. Other workers saw the
incident and shouted for help.
Pt 3, 4 and 5 jumped into the well to rescue Pt 1 and 2. All
of these patients fell prone and became unconscious.
Pt 6, the factory owner, arrived and saw the incident. He
jumped into the well and also lost consciousness as soon as
he was in the well.
Pt 7 and 8, the owners sons, jumped down to help their
father and they also became unconscious.
Subsequently, other workers wore cloth masks and tied
themselves with ropes and went down to lift the eight patients
out of the well. All were unconscious. A rescue team was
notified and came to transfer these patients to the hospital 30
min after the incident occurred. The initial clinical features
of these patients are summarized in Table 1.
All patients were admitted to the hospital. Laboratory
tests such as blood chemistry, arterial blood gas (ABG) and
chest X-ray were done in most of the patients 30 to 45 min
after arrival at the hospital. Serum lactate was not obtained
because the hospital was not able to perform the test.
Pt 4 and 7 developed cardiac arrest upon arrival in the
emergency room. After cardiopulmonary resuscitation, Pt 4s
chest radiograph showed infiltration of right lower and upper
lung fields which suggested possible aspiration pneumonitis.
Pt 7s chest radiograph showed only basal infiltration and
plate atelectasis. Their chest radiographs did not reveal any
significant pathology that might explain the cause of cardiac
Copyright Informa Healthcare USA, Inc. 2011

arrest. However, they had metabolic acidosis and high anion


gap. These two patients died at 13 and 30 h after admission,
respectively.
Pt 2 developed unconsciousness and pulmonary edema
with severe metabolic acidosis and high anion gap of 33.
ABG revealed combined metabolic and respiratory acidosis.
An electrocardiogram showed acute myocardial ischemia.
Serum CPK and troponin-I were elevated. After supportive
care by respiratory support, the pulmonary edema resolved
and consciousness was recovered within 3 days. He was discharged from the hospital on the 5th day.
Pt 5 and 6 initially developed unconsciousness and needed
respiratory support. Serum electrolytes showed metabolic
acidosis with anion gap of 28.7 and 33.8, respectively. This
supportive care, they recovered quickly and were discharged
from hospital on the 3rd day.
Pt 8 regained consciousness upon arrival at the hospital
but initially complained about chest discomfort and needed
to be intubated. X-ray findings were normal. Serum electrolyte and ABG also showed metabolic acidosis with anion
gap of 27.2. After supportive treatment, Pt 8 was able to be
weaned off the respirator and was discharged on the 3rd day.
Pt 1 and 3 regained consciousness after arrival at the hospital. Their serum electrolytes showed metabolic acidosis
with anion gap of 25.9 and 22.3, respectively. Most of the
illness fully disappeared within one day.
None of the patients received cyanide antidotes because
the diagnosis was made after the surviving patients were
stable. In addition, cyanide antidote was not available at the
hospital.
Table 2 shows that chest X-ray revealed lung abnormalities only in Pt 2, 4 and 7. Pt 2s chest X-ray showed pulmonary edema. The oxygenation in ABG of all patients was

836

P. Sang-A-Gad et al.

Table 1. Summary of clinical features and clinical course of the eight patients.

Pt. No. Age (yrs)

Initial manifestation
at emergency room (1st Day)

1st Day (in the ward)

2nd Day

3rd Day

29

The patient was conscious


and able to followed verbal
command but dyspnea.

He was agitated and


tachycardia.
O2 cannular 3 litre/min was
provided.

Recovered

Discharged

20

The patient was agitated, GCS*:


E1V1M1,
Pupils 5 mm, non-reactive to light
He developed hunger and
developed tonic seizure, and
was intubated.

He remained unconscious with


agitation. Then, he developed
pink frothy sputum, was
sedated and intubated and on
mechanical ventilator

Less agitated

Drowsy

26

The patient was conscious but


felt dizzy

Conscious

Recovered

Discharged

47

The patient was unconscious,


GCS*: E1V1M1
Pupils were dilated and not
reactive to light.
He had cardiac arrested; CPR
was performed for 20 min
with 3 ampoules of adrenalin
and 1 ampoule of sodium
bicarbonate

Unconscious and hypotension

Died 13 hr after
admission

35

The patient was drowsy, GCS*:


E4M1V5
He developed progressive
deterioration of consciousness
and was then intubated.

He was restless and dyspnea.


He was supported with
mechanical ventilation

Able to wean
the respirator

Discharged

57

The patient was unconscious and


showed air hunger, but had
normal lungs sign. Then he
was intubated.

Conscious with a ventilator


support

He was able
to wean the
ventilator

Discharged

30

The patient was unconscious and


had cardiac arrest.
CPR was performed for 10 min
with 5 ampoules of adrenalin,
1 ampoule of atropine and
sodium bicarbonate.

Coma

Coma

Died 30 hr
after
admission

34

The patient was conscious but


agitated and complained of
palpitation and tightness of
chest.
EKG showed sinus tachycardia.
He was intuabted but remained
agitated. Hence, he was
sedated with midazolam and
restrained.

He regained consciousness
and was supported with a
mechanical ventilator.

He was able
to wean the
ventilator.

Discharged

4th Day

Discharged on
5th day

GCS, Glasgow Coma Scale; E, Best eye response; M, Best motor response; V, Best verbal response; E1, No eye open; E4, Eye open spontaneously; M1, No motor
response; V1, No verbal response; V5, Oriented; CPR, Cardiopulmonary resuscitation.

also normal. Both chest X-ray and ABG suggested that the
patients ventilation was not the major cause of the illness.
However, the ABG and electrolytes did show metabolic
acidosis with high anion gap. The elevated anion gap predicted the clinical course for the more severely ill patients.
Asphyxia and anoxia were included in the differential diagnosis. Metabolic acidosis did not resolve soon after oxygen
therapy, suggesting systemic asphyxia rather than simple
asphyxia. According to these lines of evidence, cyanide poisoning was suspected. Blood samples were collected from

the patients for whole blood cyanide level determination 18


h after the incident occurred. Table 2 shows the whole blood
cyanide levels, which shows a correlation with anion gap, as
shown in Fig. 2 (correlation coefficient 0.68). Severe cases
had higher blood cyanide levels than the less severe patients.
Pt 1 and 3, who had the lowest blood cyanide levels and lowest anion gap, recovered from unconsciousness upon arrival
at the hospital and had a mild clinical course. Pt 2, having the
highest blood cyanide level, developed pulmonary edema
and had the longest hospital stay of all the surviving patients.
Clinical Toxicology vol. 49 no. 9 2011

A mass cyanide poisoning from pickling bamboo shoots 837


Table 2. Radiographic findings, mode of oxygen delivery, arterial blood gas, anion gap and cyanide levels of the patients.
Arterial blood gas
Pt. No. Age (yrs)
1
2

29
20

3
4

26
47

5
6
7

35
57
30

34

Chest radiography
Normal
Pulmonary edema without
pleural effusion
Normal
Infiltration of both right
lower and upper lobes,
possible aspiration
pneumonitis
Normal
Normal
Basal lung infiltration with
plate atelectasis
Normal

pH

pCO2
(mmHg)

HCO3
(mEq/l)

pO2
(mmHg)

O2 sat.
(%)

Anion
gap**

Whole blood
cyanide level**
(mcg/ml)

C
VR

7.38
7.02

40
41

24
10

222
93

100
93

25.9
33.0

2.66
3.54

C
VR

7.36
7.11

47
36

26
11

186
263

99
100

22.3
30.0

2.93
NA

BR
BR
BR

7.48
7.29
7.24

20
21
39

15
10
16

393
386
180

100
100
99

28.7
33.8
30.4

2.80
3.15
3.30

BR

7.49

24

18

417

100

27.2

3.02

Mode of O2
delivery*

NA: not available


*Mode of O2: C, Cannular 3 L/min; VR, Volume respirator; BR, Bird respirator.
**Pearson correlation coefficient 0.68, p 0.1.

Blood cyanide levels of Pt 7 who died was ranked second


after that of Pt 2. Unfortunately, Pt 4s blood sample was not
available for cyanide determination because he died before
the diagnosis was made.
All of the survivors were followed up for 7 days after the
incident; all remained well. Blood samples were then collected for cyanide determination; none had detectable cyanide in the blood level.

Environmental study
As soon as the incident occurred, the provincial Surveillance
and Rapid Response Team (SRRT) was notified and the team
immediately reached the scene for investigation on the same
day. They found that there were 10 concrete wells in the
factory. Each was 27 m3, 3x3x3 m in size and partially filled

with sliced bamboo shoots. These wells were in a poorly ventilated plant. Though all wells were equipped with exhaust fans,
they were turned off during the incident. The SRRT found that
the ambient air had a bitter odour and was irritative to noses
and eyes. The team came back with an air analysis instrument
21 h after the incident, and found that the odour was reduced.
The instrument found oxygen 20.9%, carbon dioxide 6 ppm,
sulfur dioxide (SO2) 19.4 ppm, but hydrogen sulfide (H2S) was
not found. Unfortunately, no instrument equipped to detect
HCN was available. The team tested the ambient air toxicity in
the well by putting a chick (Gallus gallus domesticus) into the
well (1.5 m down from the upper edge) and observed seizures
in the chick within 2 to 3 min.
The sliced bamboo shoots and pickling juice in the well
were collected for cyanide (CN) and sulfur dioxide determination. The determination of CN liberated from the bamboo

Fig. 2. Scatters plot between whole blood cyanide levels and anion gap of 7 patients (see colour version of this figure online).
Copyright Informa Healthcare USA, Inc. 2011

838

P. Sang-A-Gad et al.

Table 3. Cyanide content in various samples of wet bamboo shoots.


Cyanide contents
(mg CN/kg bamboo shoots)

Samples
Fresh, unprocessed bamboo shoots
Fresh sliced bamboo shoots
Sliced pickled bamboo shoots left over
for 1 night
Sliced pickled bamboo shoots left over
for 2 nights

266434
248299
39196
141

shoots was done by the ion-selective electrodes method.10


Determination of SO2 was done by modified Rankine
method.11 They found that the cyanide content in sliced
bamboo shoots was 87.4 mg CN/kg of wet shoots and 640
mg CN/liter in the pickling juice. No SO2 was found in the
samples.

Simulation of the incident


The summary of cyanide content in the bamboo shoots is
shown in Table 3. Fresh un-processed bamboo shoots were
found to have the highest cyanide content ranging from 266
to 434 mg CN/kg bamboo shoots. The content was lower
in the peeled or sliced bamboo shoots, ranging from 248 to
299 mg CN/kg bamboo shoots. After being pickled in the
well for 1 day, the content was down to 39 to 196 mg CN/kg
bamboo shoots.
SRRT conducted an experiment to simulate the incident.
After 2,500 kg and 5,000 kg of the salted sliced bamboo
shoots had been put into the well, HCN and SO2 were
measured in ambient air in the well. HCN levels were 10
ppm and 7.5 ppm, respectively, whereas SO2 level were 6.8
and 7.9 ppm, respectively. In the well where sliced bamboo
shoots were left for one night, HCN and SO2 were 3.55 and
0.6 ppm, respectively (Table 4).
Because of the three pieces of evidence, the compatibility
between the clinical features in presenting patients and cyanide poisoning, detection of cyanide content in the bamboo
shoots, and the presence of HCN in the ambient air of the well,
we therefore postulated that these cases were acute cyanide
poisoning. HCN was produced from sliced bamboo shoots
and accumulated in the poorly ventilated well. Eventually, the
accumulated gas caused cyanide poisoning in this incident.

Discussion
When a group illness occurs, it suggests that the patients may
have been exposed to a causative agent such as a poison.
Table 4. Gas contents of the ambient air in the well at various
conditions.

2,500 kg of pickled bamboo shoots


5,000 kg of pickled bamboo shoots
Pickled bamboo shoots left over for
1 night

Hydrogen
cyanide
(ppm)

Sulfur
dioxide
(ppm)

Oxygen
(%)

10
7.5
3.55

6.8
7.9
0.6

20.5
20.5
20.5

However, this depends on the timing and nature of the group


illness. Another likely alternative explanation for a group illness is infection. Because of the sudden onset of unconsciousness in each worker after jumping into a well, the diagnosis
favored poisoning as the causative agent. Therefore, exposure
to a noxious gas was most compatible with this situation.
Alteration of consciousness could be either due to neurological or cardiovascular disorders. In this case series, there was
only one patient who developed pulmonary edema, and no
dysrhythmia was detected in all patients. Chest X-rays and
ABG showed normal ventilation and oxygenation, suggesting that cardiopulmonary condition might not be the principal
cause of this illness. Therefore, alteration of consciousness
and metabolic acidosis should be attributed to systemic anoxia
which may be caused by either simple asphyxiants or systemic
asphyxiants.1214 As the illness and metabolic acidosis did not
resolve soon after oxygen therapy or respiratory support, simple asphyxia was less likely.15 This hypothesis was supported
by ambient air surveys in the well which showed that the oxygen content was not decreased (Table 4). Therefore, systemic
asphyxiate gases such as HCN, carbon monoxide or hydrogen
sulfide appear to be the culprit in this incident. Because it is
known that bamboo shoots contain cyanogenic glycoside,
taxiphyllin, cyanide poisoning should be suspected. Indeed,
this hypothesis was confirmed by measuring cyanide level in
the blood samples of all available patients and we found high
blood cyanide levels in all samples (Table 2).
Our simulation study found 7.5 to 10 ppm for HCN and
6.8 to 7.9 ppm for SO2 in the ambient air of the well. Patients
exposed to HCN at a level of 1836 ppm will typically suffer slight symptoms such as headache, vertigo, nausea and
vomiting after exposure for several hours. Levels of 110 ppm
or higher are potentially fatal or dangerous to life after 0.51 h
exposure.16 Levels of 620 ppm SO2 cause nasal and conjunctival irritation. The lethal level is 400500 ppm which
may cause airway obstruction and acute lung injuries.17,18 Our
study did confirm that the gases were generated and accumulated in the well. However, the measured levels of both gases
would produce only minimal adverse health consequences.
As SO2 is 2.2 times heavier than air, it would accumulate in
the well longer than HCN and this is a suitable marker of gas
accumulation. Therefore, finding SO2 at 19.4 ppm in the well
21 h after the incident suggested that the level of the gas at
that time would have been much higher. We, therefore, speculated that HCN in the well at the time of the incident would
be quite high as well. Both SO2 and HCN can cause the bitter
odour, and eye and nose irritation reported by some victims
and the SRRT. SO2 contributed to aspiration pneumonitis
in Pt4 and 7. However, the major clinical features of these
victims were metabolic acidosis. No airway abnormality was
found in most of the patients. HCN is typically responsible
for this clinical condition but not SO2. Therefore, HCN toxicity should be considered responsible for this illness, and SO2
would be an additional poison to patients.13
Taxiphyllin [2-(b-D-glucopyranosyloxy)-2-(4-hydroxyphenyl) acetonitrile] is a cyanogenic glycoside found in
bamboo shoots. The content of hydrogen cyanide in bamboo shoots is higher than in cassava with the tips of mature
Clinical Toxicology vol. 49 no. 9 2011

A mass cyanide poisoning from pickling bamboo shoots 839


bamboo shoots having the highest cyanide content within
the plant.24 An enzyme, glycosidase, in bamboo shoots is
activated as soon as the shoots are disrupted and hydrolyzes
taxiphyllin to glucose and hydroxybenzaldehyde cyanohydrin. Eventually, hydroxybenzaldehyde cyanohydrin decomposes to hydroxybenzaldehyde and hydrogen cyanide.7 This
reaction is shown in Fig. 1. Previous studies and this case
series have demonstrated that the cyanide content in the
bamboo shoot varies depending on species of the bamboo
and sources of the bamboo shoots.2 In the process of preparing the pickling bamboo shoots, such as peeling and slicing, the glycosidase is activated and produces HCN. If the
sliced bamboo shoots are stored, the cyanide content would
decrease over time.4 Indeed, our simulation revealed the
association between time and HCN content in the shoots
(Table 3). At the same time, the cyanide produced by this
reaction was demonstrated to be HCN (Table 4). However,
we could not demonstrate a dose-concentration association
between the amount of sliced bamboo shoots in the well and
the level of HCN in ambient air of the well.
Our findings are subjected to limitations. First, since it was
an unexpected incident, a comprehensive prospective clinical data collection during the initial phase was not possible.
Some laboratory tests, such as serum lactate, were not available in the local hospital. Thus, some crucial information
was unattainable. Second, the whole blood cyanide levels of
the patients on the first day were found to be relatively high
in contrast to their clinical severity and outcome, though all
of them did not receive any specific antidotes. This discrepancy warrants further investigation.
Taken together, we postulated that a large amount of the
fresh sliced bamboo shoots collected from the well could
produce a significant amount of HCN. As the well was not
adequately ventilated, HCN accumulated and caused serious
cyanide poisoning to the exposed patients. This report of eight
cyanide-poisoned patients with two fatalities is an unusual one,
because most incidents of cyanide poisoning are due to smoke
inhalation.1922 Cyanide poisoning from cyanogenic glycosides
is usually caused by ingesting the glycosides.8,9,22 Factories
that use plant matter containing cyanogenic glycosides for
food production should be made aware of the risk of poisoning.
They should provide appropriate workplace protection such as
engineering control to ensure that the pickling vats are well ventilated, personal protective equipment and employee training
for normal work and rescue should be implemented. Finally,
periodic hazard surveillance in the workplace for this kind of
industry should include air monitoring for HCN and SO2, so as
to minimize potential toxic exposure.

Acknowledgement
The authors wish to express sincere thanks to Professor
Amnuay Thithapandha and Dr. Frank J Gonzalez for their
help with the English editing of this article.

Declaration of interest
The authors have no conflicts of interests.
Copyright Informa Healthcare USA, Inc. 2011

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