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Case reports

Severe carbon monoxide poisoning from


waterpipe smoking: a public health concern
We believe this is the first Australian report of severe carbon monoxide poisoning caused by waterpipe
use. Carbon monoxide poisoning causes neurological dysfunction and myocardial toxicity, effects that
can be irreversible. Despite a widespread misconception that waterpipes are safer than cigarettes, the
recognised risks of tobacco products also apply to waterpipe use.
Clinical record
A 20-year-old woman was brought by ambulance to the
emergency department of a district hospital after an episode of presyncope. She described symptoms of severe
light-headedness, mild headache and nausea, but denied
experiencing weakness or sensory disturbances. Seizure
activity was not reported. She had used a waterpipe for 1
hour before the onset of symptoms. Although this was her
first hospital presentation with these symptoms, she had
frequently experienced queasiness and light-headedness
after using a waterpipe, which she did on most days of
the week, each session lasting about 45 to 60 minutes. She
denied depression, suicidal ideation, and recent alcohol
or drug use.

Graham RD Jones

The patient appeared lethargic. Her vital signs were


within normal limits: blood pressure, 115/70 mmHg; pulse
rate, 75 beats/min; temperature, 36.7C; Spo2, 98%; and
Glasgow Coma Scale score, 15. Her pupils were dilated
(5 mm), equal and reactive to light. Her cranial nerve,
upper limb and lower limb functions were normal.
There was no nystagmus, nor did she have any cerebellar symptoms. Her chest was clear and her heart sounds
were normal, with no murmurs. Full blood count and
biochemistry and urinalysis data were normal. Severe
carbon monoxide (CO) poisoning was diagnosed on the
basis of the initial venous and arterial blood gas levels
on room air (Box 1). The results of a urinary drug screen
and blood alcohol testing were negative.

Rajesh N Subbiah

High-flow oxygen was administered to the patient, and


she was transferred to our institution. The results of serial

Louis W Wang

MB BS, MM, FRACP1,2,3

Emily YJ He

MB BS, MPH, FRACP4

Debasish Ghosh

MB BS1

Richard O Day

AM, MD, FRACP1,2

MB BS, DPhil, FRCPA1,2

MB BS, PhD, FRACP1,2,3

Cameron J Holloway

DPhil, FRACP, FCSANZ1,2,3


1 St Vincents Hospital,
Sydney, NSW.

1 Initial venous and arterial blood gas levels of the


patient while breathing room air after using a
waterpipe for 1 hour*
Arterial blood

2 St Vincents Clinical School,


University of
New South Wales, Sydney,
NSW.
3 Victor Chang Cardiac
Research Institute,
Sydney, NSW.
4 Lowy Cancer Research
Centre, University of
New South Wales,
Sydney, NSW.

louis.wang@
unsw.edu.au

Venous blood
(at presentation)
Parameter
pH
pO2 (mmHg)
pCO2 (mmHg)
Oxyhaemoglobin

(20 min after


presentation)

Level

RI

Level

RI

7.37

7.327.43

7.43

7.357.45

19

2540

82.3

75105

53

4150

43

3234

35.3% 25%40% 73.6% 95%99%

Carboxyhaemoglobin 25.4%

01.5%

23.9%

RI = reference interval. * Further details in Appendix 1.

doi: 10.5694/mja14.01264

446

MJA 202 (8) 4 May 2015

01.5%

troponin T assessment 3 and 14 hours after presentation


were negative (< 3 ng/L). Her initial electrocardiogram
(ECG) showed a normal sinus rhythm. T wave inversion
was noted in the anteroseptal leads 5 hours after presentation, but had normalised 9 hours after presentation
(Appendix 2). Transthoracic echocardiography showed
that left and right ventricular size and systolic function
were normal, with normal left ventricular wall thickness,
no regional wall motion abnormalities, and normal valve
function. Computed tomography coronary angiography
was performed because of dynamic T wave changes referable to the left anterior descending artery, but showed
that the coronary arteries were normal. The patient was
observed for 24 hours and discharged the next day, and
was advised to abstain from waterpipe use in the future.

Discussion
We believe this is the first report in Australia of severe
CO poisoning caused by waterpipe use. A waterpipe,
also known as a hookah, narghile, shisha or goza, is an
apparatus for smoking organic material (often flavoured
or non-flavoured tobacco, although non-tobacco herbal
preparations are also available). Smoke formed by the
heating of organic material is siphoned through water
before being inhaled. Variants of the waterpipe have been
used in the Middle East, Africa and Asia since the 16th
century, and were also popular in Victorian England.
Alice encountered the Caterpillar smoking a hookah on
a mushroom in Alices adventures in Wonderland (Box 2).1
The portrayal by Lewis Carroll of the lethargic, irritable
and forgetful Caterpillar in this classic childrens tale
afforded an astonishingly accurate depiction of the dangerous physiological effects of waterpipe use.
Although longstanding public health initiatives have
reduced overall rates of cigarette smoking, waterpipe use,
especially by young adults, poses an important public
health threat. Despite concerns about the rapid increase
in waterpipe use across the world (prevalence of 6%34%
among Middle Eastern adolescents and 5%17% among
American adolescents),2 its prevalence in Australia is
unclear. The only available study, a survey of 1102 Arabicspeaking residents in south-west Sydney, found that 11.4%
reported current use.3
Two main factors have contributed to its popularity: the
pleasant experience of social pipe smoking, and the ongoing misconception that the passage of smoke through
water before inhalation filters out most toxic substances.

Case reports
2 Alice meets the Caterpillar

From Alices adventures in Wonderland by Lewis Carroll.


Illustration by Sir John Tenniel, 1865.

This erroneous perception of reduced harm when compared with cigarette smoking is reinforced by the availability of herbal (tobacco-free) preparations. Waterpipe
users, however, typically inhale greater amounts of smoke
than cigarette smokers. One session of waterpipe use
exposes the user to the same amount of smoke as 50100
cigarettes.4,5 As a result, waterpipe users are subject to
similar risks of cancer, heart disease, respiratory illness,
pregnancy complications and other smoking-related
health problems.
CO poisoning is also a genuine risk for users, with CO
exposure during waterpipe use being almost nine times
higher than for cigarette smoking, and peak carboxyhaemoglobin levels three times higher.5 Passive exposure
to CO also occurs in hookah lounges, and should be of
concern to pregnant women, as fetuses are particularly
sensitive to low levels of CO. During waterpipe use, CO
is formed from incomplete combustion of charcoal and
organic material owing to the reduced oxygen content
within the waterpipe apparatus and the relatively low
heating temperature. CO binds to haemoglobin with
high affinity (more than 200 times that of oxygen) to form
carboxyhaemoglobin, which shifts the oxyhaemoglobin
dissociation curve markedly to the left, impairing oxygen
delivery throughout the body.6 Due to the high affinity
of CO for haemoglobin, significant carboxyhaemoglobinaemia can develop during even relatively low-level
CO exposure. This reduced oxygen-carrying capacity is
not apparent, however, in the reported values for oxygen

saturation of haemoglobin (Appendix 1), as they are based


on the haemoglobin fraction that can carry oxygen; the
carboxyhaemoglobin fraction is thus excluded from the
calculation of oxygen saturation.
CO poisoning causes myocardial toxicity. Transient ECG
abnormalities, suggestive of myocardial ischaemia, are
relatively common, and are evident in 30% of patients
with moderate to severe CO poisoning.7 This occurs even
in the absence of significant coronary artery disease,
and probably reflects impaired cellular respiration. CO
also acts as an important signalling molecule, capable
of altering the function of various cellular ion channels
important to the cardiac action potential, as well as of
proteins that regulate intracellular calcium levels in
cardiomyocytes.8 CO binding to myoglobin may also
account for impaired left ventricular systolic function,9
with the degree of dysfunction correlated with carboxyhaemoglobin levels and duration of CO exposure.10 Left
ventricular dysfunction is usually transient, with recovery
occurring within 24 hours of CO poisoning. This may
explain the normal left ventricular function seen in this
patients ECG, performed 19 hours after presentation.
Myocardial fibrosis can develop, however, after a single
episode of severe CO poisoning.11 Neurological symptoms
of CO toxicity include headache, dizziness, weakness,
nausea, confusion and anterograde amnesia. In the longer
term, CO poisoning can also cause lesions in the basal
ganglia. Treatment of CO poisoning is largely supportive and involves administration of high-flow oxygen to
hasten the elimination of CO. In severe cases, and where
facilities are available, hyperbaric oxygen therapy can
be considered.
The World Health Organization Framework Convention
on Tobacco Control (2005) recommended better regulation
of waterpipe use, including health warnings on packaging, prohibiting claims of harm reduction and safety,
and banning it in public places, similar to measures currently in place for cigarette smoking.4 In many countries,
including Australia, waterpipe smoking has previously
escaped the strict regulation imposed on other tobacco
products, particularly as tobacco is not always the major
constituent of hookah preparations. Although harm minimisation techniques, such as improving ventilation in
hookah lounges and limiting the duration of smoking sessions, may reduce the risk of severe CO poisoning, public
health measures should focus on encouraging changes
to existing legislation, and on discouraging waterpipe
use, especially among young adults, by highlighting
the health risks.
Acknowledgements: Louis Wang is a recipient of a National Health and Medical
Research Council, National Heart Foundation of Australia and Royal Australasian
College of Physicians Postgraduate Scholarship. Cameron Holloway is a recipient of a
National Heart Foundation of Australia NSW Cardiovascular Research Network Life
Sciences Fellowship.
Competing interests: No relevant disclosures.
Provenance: Not commissioned; externally peer reviewed.

References are available online at www.mja.com.au.

MJA 202 (8) 4 May 2015

447

Case reports
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Carroll L. Alices adventures in Wonderland. London:


Macmillan, 1865.
Maziak W. The global epidemic of waterpipe smoking. Addict
Behav 2011; 36: 1-5.
Carroll T, Poder N, Perusco A. Is concern about waterpipe
tobacco smoking warranted? Aust N Z J Public Health 2008;
32: 181-182.
WHO Study Group on Tobacco Product Regulation. Advisory
note: waterpipe tobacco smoking: health effects, research
needs and recommended actions by regulators. Geneva:
World Health Organization, 2005. http://www.who.int/
tobacco/global_interaction/tobreg/Waterpipe%20
recommendation_Final.pdf (accessed Oct 2014).
Eissenberg T, Shihadeh A. Waterpipe tobacco and cigarette
smoking. Am J Prev Med 2009; 37: 518-523.
Weaver LK. Carbon monoxide poisoning. N Engl J Med 2009;
360: 1217-1225.
Satran D, Henry CR, Adkinson C, et al. Cardiovascular
manifestations of moderate to severe carbon monoxide
poisoning. J Am Coll Cardiol 2005; 45: 1513-1516.
Peers C, Steele DS. Carbon monoxide: a vital signalling
molecule and potent toxin in the myocardium. J Mol Cell
Cardiol 2012; 52: 359-365.
Cramlet SH, Erickson HH, Gorman HA. Ventricular function
following acute carbon monoxide exposure. J Appl Physiol
1975; 39: 482-486.
Kalay N, Ozdogru I, Cetinkaya Y, et al. Cardiovascular effects of
carbon monoxide poisoning. Am J Cardiol 2007; 99: 322-324.
Henry TD, Lesser JR, Satran D. Myocardial fibrosis from severe
carbon monoxide poisoning detected by cardiac magnetic
resonance imaging. Circulation 2008; 118: 792.

MJA 202 (8) 4 May 2015

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