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| Journal of the New Zealand Medical Association,
05-May-2006, Vol 119 No 1233
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Ayurvedic medicine: patients in peril from plumbism
Johan van Schalkwyk, James Davidson, Barry Palmer, Virginia
Hope
There is a common belief among the public that use of
‘herbal medicine’ is harmless while some medical professionals seem
to regard use of such ‘medicines’ as a fad, like bottled water. Such
assumptions are far from the truth. Various ‘herbal medicines’
present some risk, as is shown by the contamination of preparations with
digitalis,1 and introduction of agents such as corticosteroids,2 ephedrine,
testosterone, and heavy metals.3
We wish to alert the medical community to a substantial
threat to wellbeing posed by a particular form of herbal remedy, namely
Ayurvedic medicine. A recent analysis4 demonstrated the presence of substantial
amounts of heavy metals, predominantly lead, in 20% of Ayurvedic preparations
purchased in the Boston area in the United States. We report eight New Zealand
cases of poisoning due to similar preparations.
Methods and case descriptionsWe examined hospital clinical records, laboratory records,
and records of the Auckland Regional Public Health Service for cases of lead
poisoning associated with ingestion of Ayurvedic ‘herbal’ remedies.
All clinical cases known to the authors were included. We report lead content of
samples of Ayurvedic remedies, where these were obtainable, based on analysis by
an accredited laboratory (Environmental Laboratory Services Ltd, Lower Hutt,
arranged by ESR, Environmental Science and Research Ltd), unless otherwise
specified.
We identified seven cases of lead poisoning associated with
the ingestion of Ayurvedic ‘herbal’ remedies occurring within the
Auckland region of New Zealand between May 1999 and May 2005. We include a
further case from the adjacent Waikato region (Case 7). The cases are reported
in chronological order.
Case 1—A
28-year-old Indian woman presented to Auckland Hospital with epigastric pain and
vomiting. She had been taking a mixture of brown Ayurvedic powders and black
tablets from India to aid her fertility. She had a normocytic anaemia (Hb 87
g/L) and stippled cells were noted on the film. Liver enzymes were slightly
elevated and faecal occult blood was negative. Her whole blood lead
concentration was 4.5 μmol/L (notifiable level >0.72 μmol/L),
necessitating chelation therapy.
One of the unidentified brown powder preparations, taken at
a dose of one teaspoon per day, contained 20% lead by weight (200,000 parts per
million, ppm) and another 13% (130,000 ppm). The tablets contained lead at much
lower levels (20–70 ppm).
Case 2—A
physician at Auckland Hospital notified the Public Health Unit of a case of lead
poisoning in a 38-year-old Indian man who had been taking tablets and using
creamy snuff imported from India as a toothpaste. The patient’s whole
blood lead level was 6.9 μmol/L, an indication for urgent treatment.
The patient received ethylenediaminetetraacetic acid (EDTA)
and dimercaprol. Liver enzymes were slightly elevated. As the patient was
reluctant to take part in any further investigations, no other sources of lead
exposure were identified. Lead content of the tablets (7.8 mg per tablet or 4800
ppm) probably accounted for the poisoning, as lead levels in the
Ipco Creamy Snuff and
Dentobac Creamy Snuff were low (both
<100 ppm)
Case 3—A
48-year-old Indian woman presented to her general practitioner with concerns
about her lead levels following the admission to Auckland Hospital of a friend
taking the same Ayurvedic herbal medicine (a brown tablet) as her. The lead
content of each of these tablets was 7.8 mg. She was taking four tablets daily,
and had done so for 3 months. Her whole blood
lead level had been 2.2 μmol/L, requiring no treatment. There were
no other sources of lead exposure.
Case 4—A
66-year-old female family friend of Case 3 presented to her general practitioner
with concerns about having a raised lead level. She had been taking unidentified
Ayurvedic herbal medicines given to her by the friend and had a blood lead level
of 1.5μmol/L, with no treatment indicated. There were no other sources of
lead exposure.
Case 5—A
30-year-old Indian man who had lived in New Zealand for 2 years presented to
Auckland Hospital with a 5-day history of right upper quadrant colicky abdominal
pain, without any associated diarrhoea or vomiting. Examination revealed mild
right upper quadrant tenderness, no organomegaly, and no signs of neuropathy or
encephalopathy. Blood count showed a normocytic anaemia (Hb 107 g/L) with
basophilic stippling. Liver function tests were abnormal with negative hepatitis
serology. The whole blood lead level was 3.8 μmol/L and urine lead 1.2
μmol/24 h (normal: <0.25 μmol/24 h).
He had a past history of infertility and azoospermia and had
been taking two to three Ayurvedic fertility pills for a month preceding his
symptoms. No occupational or other source of lead could be identified. He
underwent chelation therapy and required repeated courses of EDTA infusions. No
tablets were available for analysis.
Case 6—A
51-year-old Indian man presented to Auckland Hospital with a 2-week history of
colicky abdominal pain associated with diarrhoea. There was a background history
of type 2 diabetes for which he had been taking metformin and Ayurvedic
Jambrulin tablets. He had a normocytic
anaemia (Hb 100 g/L) and stippled cells were seen on the film. The whole blood
lead level was 6.7 μmol/L and urine lead was 16.5 μmol/day. Blood
cadmium, urine mercury, and arsenic were all normal. He was treated with oral
dimercaptosuccinic acid (DMSA) chelation therapy resulting in a stable reduction
of levels to 1.5 μmol/L. Analysis of his Ayurvedic tablets showed that each
contained approximately 10 mg of lead (16,000 ppm, unaccredited laboratory). The
recommended dose on the bottle was four tablets daily.
Case 7—A
31-year-old Indian woman who had lived in New Zealand for 10 years presented
several times to her general practitioner with complaints of fatigue, nausea,
weight loss, abdominal pains, and diarrhoea. She was referred for an upper
gastrointestinal (GI) endoscopy, which was normal. Several months later she
again presented with abdominal pain and diarrhoea. A positive faecal occult
blood test led to a lower GI endoscopy, which was normal.
Three months later, she again presented to the Emergency
Department with abdominal pain associated with colic, nausea, vomiting, and no
bowel movement for 6 days. On examination, she had abdominal distension with
tenderness and guarding in right iliac fossa. She had been taking paroxetine,
paracetamol/dextropropoxyphene, and tramadol, as well as Ayurvedic medicinal
powders. There was no exposure to heavy metals apart from Ayurvedic
medicines.
She was anaemic (Hb 105 g/L) and the blood film showed
basophilic stippling, Cabot rings, nucleated red blood cells, occasional red
cell fragments, and target cells. She was hyponatraemic (Na 113 mmol/L) and had
elevated liver enzymes.
An abdominal X-ray suggested small bowel obstruction with no
bowel gas beyond the sigmoid colon. Computerised tomography of the abdomen
showed dilated large and small bowel to the level of the distal sigmoid.
Possible diagnoses considered were atypical sigmoid volvulus and stricture, and
laparotomy was planned but held off as her pain improved.
The patient’s pain settled after sigmoidoscopy, and no
mechanical obstruction was found. The whole blood lead level was 3.5
μmol/L. The abnormal sodium and liver function tests improved spontaneously
and she subsequently underwent EDTA chelation therapy.
Case 8—A
53-year-old woman pharmacist of Indian origin presented with lower leg oedema
for 2 months, followed by a 3-week history of mainly left-sided abdominal pain
of a constant character, accompanied by nausea. She had also been feeling very
tired but attributed this to stress. Examination revealed pallor, and a definite
lead line on the gums. No motor weakness or other neurological deficits were
present.
She had been taking six black
Chandraprabhavati
(‘Chandrapradhavate’) tablets per day for several months. These had
been prescribed for her in India. A normocytic anaemia (Hb 72 g/L) was present
and basophilic stippling was noted. The whole blood lead was 5.3 μmol/L.
She was treated with a blood transfusion and oral DMSA chelation therapy. The
Chandraprabhavati tablets each
contained 11 mg of lead (12,400 ppm).
DiscussionBy way of the Internet, there is universal public exposure
to the Ayurvedic contention that, administered correctly, ‘bhasmas’
(carefully extracted ashes) containing lead or mercury have beneficial
therapeutic effects. Indeed, recent webpages still assert the safety of such
bhasmas.5,6 This belief is irreconcilable with Western
toxicology.
From the point of view of Western science, even minuscule quantities of
lead have potential for harm, including irreversible brain damage, and are of
absolutely no therapeutic benefit.7
Substantial scientific literature documents these harmful
effects in adults and in particular, in the developing human. Severe congenital
lead poisoning has been reported in an infant born to a woman who had taken
Ayurvedic preparations during pregnancy.8
All medical practitioners should be aware of lead poisoning
caused by Ayurvedic preparations, now a common cause of lead poisoning in the
Auckland region. A single case has recently been reported from Christchurch, New
Zealand.9 Use of complementary medicines is common and reports of celebrities
taking Ayurvedic remedies may increase their use.10 Symptomatic lead poisoning
may be difficult to identify without a high index of suspicion. Medical
histories for all age groups should now include a specific enquiry about the use
of complementary, herbal, or traditional medicines.
The lead content of Ayurvedic medications used by the
patients described is clearly such that consumption of even small quantities
would result in intake exceeding the ‘provisional tolerable
weekly intake’ (PTWI) of the
Joint FAO/WHO Expert Committee on Food Additives, set in 1999 at 25
micrograms/kg body weight.11 For example, consumption by a 70 kg adult of a
single tablet containing 8 mg of lead
exceeds the PTWI by a factor of over four! Moreover, in view of the consumption
of Ayurvedic medication with therapeutic intent, as well as the toxicity
described, it is debatable whether such remedies should be regarded solely as
‘food additives’.
The cases we report are likely to be just the tip of the
iceberg—individuals who have taken Ayurvedic preparations and present with
abdominal pain, anaemia, or other features of lead poisoning should have
appropriate determination of blood lead levels to exclude such poisoning. This
is especially important because symptomatic lead poisoning can be effectively
treated, with a substantial scientific rationale for such treatment.12 Where
possible, samples of the Ayurvedic remedy should be obtained, and the name and
origin clearly documented (This was not possible in several of the cases
reported here.)
Lead poisoning is a notifiable disease and the local public
health unit should be notified immediately so that a thorough investigation of
potential risk factors can be undertaken and preparations can be sent to an
accredited laboratory for confirmation of the presence of lead or other
contaminants. Ayurvedic or other herbal preparations may not be the sole sources
of exposure to lead and other sources, such as storage containers, lead paint
dust, and occupational exposures must also be investigated.
Many authorities would not treat asymptomatic lead poisoning
with a whole blood lead level under approximately 2.5 micromol/L, but where
there are any concerns, the case should be discussed with a toxicologist or
physician with experience in the management of lead poisoning. Therapy should be
tailored to the individual patient, but in many cases (such as Case 6 and Case 8
here) oral therapy with dimercaptosuccinic acid (DMSA) is an efficacious,
cost-effective, and convenient option.
Discontinuation of Ayurvedic preparations is advised in all
cases of suspected lead poisoning until the absence of lead in those
preparations can be demonstrated. In one of the cases reported, the patient was
not advised to discontinue her Ayurvedic medication following discharge from
hospital, and poisoning did not cease until the public health officer
investigated the raised lead level and advised her as follows:
Lead
poisoning is often deceptive, and poisoning following the consumption of
Ayurvedic preparations may go undetected for some time. We recommend extreme
caution in the use of preparations of unknown quality or origin especially in
children, pregnant women, women of child-bearing age, and those with chronic
diseases such as diabetes.
Author information:
Johan van Schalkwyk, Perioperative Physician, Departments of Medicine
& Anaesthesia, Auckland City Hospital; James S Davidson, Clinical Head,
Chemical Pathology, Labplus, Auckland City Hospital; Barry Palmer, Scientist,
Chemical Pathology, Labplus, Auckland City Hospital; Virginia Hope, Public
Health Medicine Specialist, Medical Officer of Health, Auckland Regional Public
Health Service and Senior Lecturer, School of Public Health, University of
Auckland; Auckland
Acknowledgements: We
thank Dr Jamie Maddox for case details; physicians who contributed to the care
of the patients in this report; Priya Pratapsingh (Pharmacist) for comments on
the manuscript; and Ramu Beesabathini and John Whitmore (Health Protection
Officers) for fieldwork and documentation.
Correspondence: Dr
JM van Schalkwyk, Auckland City Hospital, P/Bag 92024, Auckland 1. Fax: (09) 307
2814; email: johanvs@adhb.govt.nz
References:
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