The n e w e ng l a n d j o u r na l of
Clinical Problem-Solving
From the British Columbia Centre on
Substance Use (S.Y.), and the Depart-
ment of Medicine (S.Y.), the Division of
Hematology (L.C.), the Centre for Health
Education Scholarship (L.C.), and the Di-
vision of Critical Care (J.W.), University of
British Columbia, Vancouver, the Depart-
ment of Emergency Medicine (W.P.) and
the Department of Internal Medicine
Section of Critical Care (J.W.), University
of Manitoba, Winnipeg, and the Depart-
ment of Pathology and Laboratory Medi-
cine, Richmond General Hospital, Rich-
mond, BC (P.W.) — all in Canada.
Address reprint requests to Dr. Young at
the British Columbia Centre on Substance
Use, 400-1045 Howe St., Vancouver, BC
V6Z 2A9, Canada, or at ­samantha​.­young@​
­alumni​.­ubc​.­ca.
N Engl J Med 2020;383:578-83.
DOI: 10.1056/NEJMcps1900799
Copyright © 2020 Massachusetts Medical Society.
578
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Copyright © 2020 Massachusetts Medical Society. All rights reserved.
m e dic i n e
Caren G. Solomon, M.D., M.P.H., Editor
Led Astray
Samantha Young, M.D., Luke Chen, M.D., Wesley Palatnick, M.D.,
Patrick Wong, M.D., and Justin Wong, M.D.​​
In this Journal feature, information about a real patient is presented in stages (boldface type) to an expert
clinician, who responds to the information by sharing relevant background and reasoning with the reader
(regular type). The authors’ commentary follows.
A 34-year-old man presented to a community hospital in Vancouver, Canada, with a
1-month history of constant diffuse abdominal pain, fatigue, and anorexia associ-
ated with a weight loss of 2.7 kg but no fevers or night sweats. He reported constipa-
tion but no diarrhea, melena, or hematochezia. His medical history and travel his-
tory were unremarkable.
The differential diagnosis of subacute, diffuse abdominal pain in a young man is
broad. It includes inflammatory conditions (e.g., Crohn’s disease), cancer, an ob-
struction, a hepatic or biliary pathologic condition, pancreatitis, celiac disease,
adrenal insufficiency, acute intermittent porphyria, infection (e.g., helminthic or
human immunodeficiency virus [HIV]–related), metabolic causes (e.g., hypercal-
cemia or ingestion of toxic substances), and as a diagnosis of exclusion, func-
tional causes.
The patient was from India but had lived in Canada since he was 13 years of age. He
worked at a family-run business and lived with his wife and his parents. His medica-
tions included gabapentin, ibuprofen, and acetaminophen with codeine, all of which
had been prescribed for his recent pain. He reported that he did not use nicotine-
containing products, drink alcohol, or use illicit drugs.
On examination, the patient’s temperature was 36.7°C, the blood pressure
117/73 mm Hg, the pulse 99 beats per minute, the oxygen saturation 99% while he
was breathing ambient air, and the respiratory rate 16 breaths per minute. He ap-
peared thin with conjunctival pallor. The jugular venous pressure was 1 cm above the
sternal angle. The cardiac, respiratory, and neurologic examinations were normal.
There was no palpable lymphadenopathy. The abdominal examination revealed
mild tenderness in the left lower quadrant, with no rebound tenderness, guarding,
ascites, masses, or organomegaly. Bowel sounds were normal.
The patient is afebrile, with no obvious focus of infection. The jugular venous
pressure suggests volume depletion, which could be a manifestation of the condi-
tion that is causing his abdominal pain (e.g., adrenal insufficiency) or a conse-
quence of the pain (e.g., decreased oral intake).
The hemoglobin level was 7.7 g per deciliter, and the hematocrit 25%, with a mean
corpuscular volume of 73 fl. The platelet count was 344,000 per cubic millimeter, and
n engl j med 383;6  nejm.org  August 6, 2020
The New England Journal of Medicine
 Clinical Problem-Solving
10 µm
Figure 1. Peripheral-Blood Smear.
A peripheral-blood smear shows microcytosis of red
cells with basophilic stippling (Wright–Giemsa stain).
the white-cell count 11,300 per cubic millimeter,
with 90% polymorphonuclear leukocytes and a
normal eosinophil count. The ferritin level was
316 ng per milliliter (normal range, 15 to 300), the
iron level 184 μg per deciliter (33 μmol per liter)
(normal range, 60 to 150 μg per deciliter [11 to
27 μmol per liter]), the total iron-binding capacity
290 μg per deciliter (52 μmol per liter) (normal
range, 250 to 425 μg per deciliter [45 to 76 μmol
per liter]), and the transferrin saturation 63%
(normal range, 20 to 55). A peripheral-blood
smear showed occasional nucleated red cells,
polychromasia, basophilic stippling, Pappen-
heimer bodies, teardrop cells, and microcytosis
(Fig. 1). The aspartate aminotransferase level was
100 U per liter (normal range, 10 to 38), the
­alanine aminotransferase level 162 U per liter
(normal range, 10 to 80), the γ-glutamyltransfer­
ase level 195 U per liter (normal range, 15 to 80),
and the alkaline phosphatase level 132 U per liter
(normal range, 30 to 135); the bilirubin and lac-
tate dehydrogenase levels were normal. No recent
blood test results were available for comparison.
The results of renal-function tests were normal,
as were the levels of electrolytes, thyrotropin, se-
rum vitamin B12, and C-reactive protein; the inter-
national normalized ratio; and the activated par-
tial-thromboplastin time. Computed tomography
(CT) of the abdomen revealed thickening of the
rectum and sigmoid colon near the hepatic flex-
ure, with a normal-appearing terminal ileum and
no lymphadenopathy.
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The abnormalities noted on CT warrant endo-
scopic investigation. The patient’s microcytic
anemia with nucleated red cells is of interest. A
ferritin level of greater than 200 ng per deciliter,
along with elevated levels of serum iron and
transferrin saturation, are inconsistent with iron
deficiency. The normal C-reactive protein level
makes an inflammatory cause of anemia (i.e.,
anemia of chronic disease) unlikely, although it
does not rule it out. In a patient of South Asian
ancestry, thalassemia should be considered; how-
ever, it would not explain his abdominal pain.
Serum and urine protein electrophoresis, a direct
antiglobulin test, measurement of the haptoglo-
bin level, and measurement of the hemoglobin
level with the use of high-performance liquid
chromatography should be performed. Serologic
tests for HIV and hepatitis A, B, and C viruses
should also be performed, particularly given the
patient’s elevated liver-enzyme levels. It would also
be worthwhile to measure the blood lead level,
since lead poisoning can cause microcytic anemia
with basophilic stippling and abdominal pain.
The patient was admitted to the hospital for fur-
ther investigation. Upper and lower endoscopy
revealed normal-appearing mucosa, with no bleed-
ing or inflammation; random biopsy specimens
of the rectum, terminal ileum, duodenum, and
stomach were obtained. Ultrasonography of the
liver revealed diffuse fatty infiltration. The patient
received morphine, which reduced his pain. He
was discharged home with pantoprazole at a dose
of 40 mg per day; given the presence of microcytic
anemia, the presumptive diagnosis was thalas-
semia, although the results of the hemoglobin
electrophoresis were pending. After discharge,
the gastric-biopsy specimens showed evidence of
Helicobacter pylori infection; despite treatment with
lansoprazole, amoxicillin, and clarithromycin,
the symptoms did not abate. Examinations of the
other biopsy specimens were negative, as was the
test for hemoglobinopathy.
During the next 6 weeks, the patient had three
subsequent visits to the emergency department
for ongoing abdominal pain. He was referred to
a gastroenterologist for a capsule endoscopy; the
results were normal. He was then readmitted to
the hospital; he had lost an additional 11 kg of
weight and had a new headache on the right side
that had lasted 2 to 3 hours, with associated nau-
579
 The n e w e ng l a n d j o u r na l
sea but no photophobia or neck stiffness. He re-
mained afebrile. An additional workup included
serologic testing for hepatitis A, B, and C viruses,
testing for syphilis and HIV infection, serum pro-
tein electrophoresis, lumbar puncture, blood cul-
tures, urine cultures, chest radiography, and
magnetic resonance imaging (MRI) of the head
and spine, all of which were unremarkable. The
patient was seen by a neurologist, a rheumatolo-
gist, and an infectious-disease specialist. He was
ultimately discharged home with an unclear diag-
nosis (with his presentation postulated to be re-
lated to a viral illness), and outpatient follow-up
with a hematologist was planned. He received a
prescription for hydromorphone to be used as
needed for ongoing abdominal pain.
The patient continues to have abdominal pain
and progressive weight loss, with no unifying
diagnosis. Quadruple therapy for H. pylori infec-
tion — rather than the triple therapy he received
— is preferable, and eradication should be con-
firmed, although the possible presence of such
an infection still does not explain the clinical
picture of anemia that is not due to iron defi-
ciency. Although α-thalassemia is not yet ruled
out by testing, this disorder would not account
for his abdominal pain or headache. The hepatic
steatosis noted on ultrasonography may explain
his elevated liver-enzyme levels; his history of
alcohol use should be reassessed, and other
metabolic risk factors should be considered. The
absence of fever combined with a normal C-reac-
tive protein level, negative cultures, and normal
findings on cerebrospinal fluid analysis do not
support infectious or inflammatory causes. When
one is faced with a constellation of unexplained
symptoms, it can be helpful to focus on an ob-
jective finding with a limited differential diag-
nosis. Microcytic anemia is one such finding.
Iron deficiency, the most common cause, has
been ruled out, as has thalassemia; the other
conditions that can cause a microcytic anemia
are inflammation, sideroblastic anemia (congeni-
tal or acquired), and lead poisoning. The sidero-
blastic anemias are rare bone marrow disorders
characterized by abnormal iron accumulation in
the mitochondria of erythroid precursors, which
manifest as ring sideroblasts in the bone mar-
row aspirate. Congenital forms such as X-linked
sideroblastic anemia typically manifest in child-
580 n engl j med 383;6
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of m e dic i n e
hood. Acquired sideroblastic anemia can be
caused by alcohol use, medications such as iso-
niazid and linezolid (which the patient has not
received), or copper deficiency, which can be
caused by excess ingestion of zinc or by mal-
absorptive disorders. Given an ongoing unex-
plained microcytic anemia with nucleated red
cells, the blood levels of lead and copper should
be assessed; if the levels are normal, I would
recommend a bone marrow biopsy.
One week later, the patient returned to the hospi-
tal after having a witnessed generalized seizure.
Despite treatment with diazepam and phenytoin,
he had subsequent recurrent seizures with inter-
ictal somnolence that resulted in intubation and
transfer to the intensive care unit. He was afebrile
on presentation. A neurologic examination did
not suggest any focal lesions. CT of the head was
unremarkable. Urine drug screening was positive
only for opioids, a finding that was consistent
with his prescribed medications, and ethanol was
not detected in the serum. His blood tests contin-
ued to indicate microcytic anemia, and he had a
normal C-reactive protein level. His liver-enzyme
levels were now normal.
The trachea was extubated on hospital day 2.
Examination of a bone marrow–biopsy specimen
and bone marrow aspirate showed normal triline-
age hematopoiesis with occasional ringed sidero-
blasts (Fig. 2) and no evidence of myelodysplasia
or a lymphoproliferative disorder. On hospital
10 µm
Figure 2. Bone Marrow Aspirate Smear.
A bone marrow aspirate smear shows ringed sidero-
blasts with iron granules accumulating around the
nuclei of erythroid precursors (Prussian blue stain).
nejm.org August 6, 2020
 Clinical Problem-Solving
day 6, a critically elevated serum level of free pro-
toporphyrin was reported (612.4 μg per deciliter
[10.84 μmol per liter]) (normal range, 15 to 50 μg
per deciliter [0.27 to 0.88 μmol per liter]); this
blood test had been ordered to investigate for por-
phyria.
Acute hepatic porphyrias — the most common
of which is acute intermittent porphyria — can
produce neurovisceral symptoms, such as ab-
dominal pain and seizures, but would not cause
anemia. Acute intermittent porphyria also does
not cause elevated protoporphyrin levels, which
are associated with protoporphyria, a cutaneous
form of porphyria that is not compatible with
this patient’s presentation. Rather, an elevated
free protoporphyrin level can be caused by lead
poisoning, and this now seems to be the likely
diagnosis. Occasional ringed sideroblasts can
also be seen in patients with toxic effects from
exposure to lead. A blood lead level should be
measured, although the patient had had suffi-
cient evidence to warrant this having been per-
formed much earlier in the clinical course.
The elevated serum level of free protoporphyrin,
combined with the patient’s abdominal pain, sei-
zures, and laboratory evidence of microcytic ane-
mia, was considered to be indicative of lead poi-
soning. The blood lead level was markedly
elevated, at 94.4 μg per deciliter (4.6 μmol per li-
ter) (normal value, <5 μg per deciliter [0.2 μmol
per liter]).
Now that the diagnosis of lead poisoning has
been confirmed, it is important to identify the
source in order to prevent ongoing exposure. A
thorough occupational history should be taken,
as well as an assessment of any potential envi-
ronmental or home exposures. Specific sources
to ask about are Ayurvedic therapies, herbal sup-
plements, and glazed ceramic cookware.
No potential occupational or environmental ex-
posures were identified, and the patient reported
no use of herbal supplements or Ayurvedic medi-
cations and no use of glazed ceramic cookware.
Although the patient had previously reported that
he did not use any illicit drugs, his father dis-
closed that the patient had been using opium. The
patient subsequently divulged the details of his
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substance use. He had begun using opium, which
he had obtained from a customer at his business,
2 years earlier. Before the patient was hospital-
ized, he had been using opium on a daily basis
and had spent approximately $2,000 in Canadian
dollars (approximately $1,500 in U.S. dollars) per
month on opium. He had ingested it orally, with
no intravenous use. His withdrawal symptoms
had included nausea, sweating, and tremors. He
was motivated to stop using opium and to begin
opioid-agonist therapy with buprenorphine–
naloxone.
Stigma often prevents patients from being forth-
coming when asked about their substance use in
a clinical setting. At a minimum, this patient
meets the criteria for a moderate opioid use dis-
order; opioid-agonist therapy with buprenorphine
or methadone is recommended, along with psy-
chosocial treatment, if desired. It is notable that
he had received prescriptions for several opioids,
including codeine and hydromorphone, to treat
his abdominal pain without medical personnel
having knowledge of his opioid use disorder.
Unbeknownst to his treating physicians, these
opioids would have also treated any opioid with-
drawal he was having, although he risked having
toxic effects and an overdose if he continued to
use opium. Opium is the likely source of his lead
poisoning, on the basis of several case reports
of this phenomenon, particularly from the Mid­
dle East.
A sample of the opium was obtained for analysis;
inductively coupled plasma–mass spectrometry
confirmed the presence of lead, at 23 ppm. In
consultation with the local poison control center,
and with no residual changes in mental status,
the patient received chelation therapy with oral
meso 2,3-dimercaptosuccinic acid (succimer) for
18 days. He was discharged home with instruc-
tions to take buprenorphine–naloxone (at a dose
of 4 mg and 1 mg, respectively) and was referred
to community addiction support services.
The patient’s symptoms of abdominal and
musculoskeletal pain, lethargy, and anorexia
abated rapidly, and at a follow-up visit 6 months
later, his blood lead level had dropped to 35.0 μg
per deciliter (1.7 μmol per liter). On follow-
up more than 1 year later, he remained absti-
nent from opium with continued treatment with
581
 The n e w e ng l a n d j o u r na l
buprenorphine–naloxone, and he reported that
he had not had any recurrent seizures since his
previous hospitalization for a witnessed general-
ized seizure.
C om men ta r y
Lead poisoning is a diagnosis that is often over-
looked. Although the typical clinical features of
abdominal pain and weight loss are nonspecific,
a focus on the limited number of causes of micro-
cytic anemia ultimately led to the diagnosis. In
this case, iron-deficiency anemia was initially
considered to be a likely diagnosis, despite the
patient having a serum ferritin level above 200 ng
per milliliter, which made iron deficiency ex-
tremely unlikely.1 The diagnostic errors in this
case stemmed predominantly from faulty knowl-
edge synthesis,2 whereby the clinicians failed to
consider lead poisoning earlier in the clinical
course despite highly suggestive clinical signs
and symptoms, including abdominal pain, micro-
cytic anemia, and basophilic stippling. As a re-
sult, the patient underwent repeated endoscopic
studies and had added complications. Given the
availability, accuracy, and relatively low cost of
serum lead testing, this test should be performed
promptly in patients whose presentation is com-
patible with lead poisoning. Once a high lead
level is documented, the source must be identi-
fied to prevent continued exposure. Lead-con-
taminated opium has led to thousands of cases
of lead poisoning in the Middle East3 and sev-
eral cases in Europe4,5 and Australia.6 This case
highlights the effect of globalized illicit drug
trade, whereby lead poisoning from opium oc-
curred in North America.
Lead poisoning can result from short-term or
long-term exposure, the latter being more com-
mon among adults. This patient’s symptoms are
probably a result of steady exposure over an ex-
tended period of time, although they may have
been exacerbated by larger, short-term ingestions.
Lead affects numerous organ systems; common
symptoms and signs include gastrointestinal dis-
comfort, constipation, and altered mental status,
although the presentation is variable and depends
on the duration of exposure. Features common­
ly seen on physical examination that are consis-
tent with lead poisoning include bluish pigmen-
tation at the gum line (termed “lead lines”);
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of m e dic i n e
hypertension, seen in patients with long-term
exposure; and peripheral neuropathy, seen in pa-
tients who have had either short-term or long-
term exposure — although none of these signs
are particularly sensitive for lead poisoning.5,7,8
Anemia typically manifests at a blood lead level
of greater than 50 μg per deciliter (2.4 μmol per
liter).7 Severe encephalopathy, which can include
the occurrence of seizures, characteristically
occurs at a very high blood lead level (>100 μg
per deciliter [4.8 μmol per liter] in adults); in
this patient, seizure occurred at a slightly lower
blood lead level (94.4 μg per deciliter), but it is
presumed to be attributable to lead, in the ab-
sence of an alternative explanation.9 With long-
term low-level exposure, neurologic manifesta-
tions may be more insidious and can include
memory impairment and irritability.7 Mild long-
term elevations of the blood lead level (>10 μg
per deciliter [0.5 μmol per liter]) are associated
with an increased risk of cardiovascular disease,
renal dysfunction, and neurocognitive effects,
highlighting the need to avoid even low-level
exposure.8-11 Basophilic stippling of erythrocytes
is a characteristic finding in cases of lead poi-
soning, but it can also be associated with arsenic
poisoning, sideroblastic anemia, myelodysplastic
syndrome, thalassemia, and other conditions.12
Chelation therapy with succimer or calcium
disodium EDTA is indicated for patients with a
blood lead level above 80 μg per deciliter
(3.9 μmol per liter), as in this case. Depending
on the duration of lead exposure and symptoms,
such therapy may also be indicated for patients
with lower blood lead levels; involvement of a
toxicologist or an occupational and environmen-
tal medicine physician is useful in decision mak-
ing. Once chelation therapy is initiated, patients
are monitored closely for potential side effects,
including hepatic and renal impairment, as well
as transiently worsening symptoms due to the
mobilization of lead from tissue and bone into
the blood. The magnitude of reduction in symp-
toms is variable; such changes may occur over
the course of several weeks or substantially lon-
ger (more than a year). Given that the removal of
lead from the central nervous system is a slow
process, neurocognitive effects may resolve slow­
ly and incompletely, and there is concern that
cumulative lead exposure may accelerate age-
related cognitive decline.10
 Clinical Problem-Solving

In Iran and other Middle Eastern countries,
numerous cases of lead poisoning from lead-
contaminated opium have been reported.3 Dur-
ing an 18-month period from 2016 to 2017, more
than 4000 persons across two large hospitals in
Tehran were treated for lead poisoning resulting
from ingestion of opium.3 The concentration of
lead found in the opium sample tested in this
case, 23 ppm, is within the range of concentra-
tions reported in other cases of opium ingestion,
in which concentrations ranged from 1.8 to
3200 ppm.13,14 The reason for lead contamination
in opium is not known, but two leading hypoth-
eses are that lead is added to increase the
weight, thereby increasing profit, or that it re-
sults from the manufacturing process.
The majority of the world’s 10,500 tons of illicit
opium supply comes from Afghanistan.15 The
percentage of illicit opium that is contaminated
with lead is unclear, but the number of cases of
lead poisoning from opium appears to be in-
creasing. Further research is needed to identify
the prevalence of lead-contaminated opium in the
illicit drug supply in North America.
Once the diagnosis of lead poisoning is es-
tablished, the source of lead is often revealed
from an occupational history, review of medica-
tion, or examination of cookware for leaded
glazes.12 In the case of lead-containing opium,
patients may not disclose their substance use or
may not be aware of the possibility of opium as
a potential source. A heightened awareness
among practitioners and physicians is needed to
make the diagnosis and to connect the patient
with addiction services.
No potential conflict of interest relevant to this article was
reported.
Disclosure forms provided by the authors are available with
the full text of this article at NEJM.org.
We thank Dr. Morris Pudek and Dr. Benjamin Jung for their
analysis of the opium sample, Dr. Karen Ung for her input re-
garding the bone marrow biopsy and peripheral-blood smears,
and Dr. Robert Mitchell for his advice on an earlier version of
the manuscript.

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