Historians have suggested that US president Andrew Jackson (1767-1845)
experienced lead and mercury poisoning following his therapeutic use of calomel
(mercurous chloride) and sugar of lead (lead acetate). To evaluate these claims,
we performed direct physical measurement of 2 samples of Jackson's hair (1
from 1815, 1 from 1839). Following pretreatment and acid digestion, mercury
was measured using cold vapor generation techniques, while lead levels were
measured by electrothermal atomic absorption spectrophotometry. Mercury levels
of 6.0 and 5.6 ppm were obtained from the 1815 and 1839 hair specimens, respectively.
Lead levels were significantly elevated in both the 1815 sample (mean lead
level, 130.5 ppm) and the 1839 sample (mean lead level, 44 ppm). These results
suggest that Jackson had mercury and lead exposure, the latter compatible
with symptomatic plumbism in the 1815 sample. However, Jackson's death was
probably not due to heavy metal poisoning.
Biographers have concluded that US president Andrew Jackson (1767-1845)
experienced mercury and lead poisoning.1-10
Some have even suggested that heavy metal toxicity contributed to Jackson's
His physicians plied him with calomel (mercurous chloride) and sugar of lead
(lead acetate) prescriptions from the early 19th-century pharmacopoeia. Jackson
also harbored 2 lead bullets, a consequence of his propensity to settle disputes
Jackson exhibited many symptoms and signs compatible with mercury poisoning
and plumbism, including excessive salivation, rapid tooth loss, colic, diarrhea,
pallor, hand tremor, irritability, paranoia, violent mood swings, and probable
chronic renal failure. Because these symptoms also might be attributed to
other causes, we performed direct physical measurement of samples of Jackson's
hair to evaluate whether he had mercury and lead poisoning.
Following Hermitage Board approval, samples of Jackson's hair from 1815
and 1839 were obtained from the collection of The Hermitage: Home of Andrew
Jackson in Nashville, Tenn. Samples were chosen corresponding with periods
of either Jackson's use of calomel and sugar of lead or exhibition of symptoms
compatible with either lead or mercury poisoning. The Hermitage curatorial
staff selected hair samples and forwarded them to the Armed Forces Institute
of Pathology, Washington, DC, for analysis.
The 1815 specimen,
5.1 cm (2 in) in length, was contained in a letter stating "Genl. Jackson's
hair in 1815." This specimen is temporally related to Jackson's use of calomel
and subsequent salivation (sialism) in November 1814. It also postdates the
onset of Jackson's cachexia and dysentery during the War of 1812 and bullet
wounds received during an 1806 duel and an 1813 gunfight.
1839 specimen, 2.5 cm (1 in) in length, was contained in a letter from Andrew
J. Donelson to Felix Grundy. The letter stated that "This hair was cut from
the head of A. Jackson August 22, 1839 by M.C. Bass." Jackson complained of
costiveness (constipation), dysentery, and headaches and continually ingested
calomel during the 1830s.
Hair samples (0.5 mg) were rinsed in
acetone and soaked for 1 to 2 hours in distilled deionized water and mixed
and washed 3 times by ultrasonic cleaning for 1 hour in a solution containing
0.1% Triton TX-100 (Sigma Chemical Co, St Louis, Mo). Analysis of detergent
wash revealed no detectable mercury or lead. Detergent was removed by rinsing
(5 times) with distilled deionized water, and the specimens were dried in
a vacuum oven at 40°C overnight. Each sample was weighed and digested
using 2 mL of 70% nitric acid and 1 mL of 30% hydrogen peroxide. Hair samples
were placed in polyfluoroethylene vessels and acid digested with a microwave
digestion system (MDS 2000, CEM Corporation, Indian Trail, NC) at a controlled
pressure (150 psi) and temperature (110°C). Quality controls consisted
of a blank reagent sample and a control of digested hair, spiked with atomic
absorption standard solutions to yield predetermined concentrations of lead
or mercury. Quality controls were subjected to the same digestion procedure
as the hair specimens. Recovery of both lead and mercury in the spiked solution
was 98% to 105%.
Lead was measured by electrothermal atomic absorption
spectrophotometry (Varian Australia Qty Ltd, Mulgrave, Australia) equipped
with a Zeeman background corrector and autosampler accessory (Varian Australia
Qty Ltd). Digested samples were placed in the autosampler cups and analyzed
in duplicate. Electrothermal atomic absorption spectrophotometry was repeated
automatically if the percent relative SD between 2 duplications exceeded 4%.
As a result, all measured lead levels represent at least duplicate sampling
from each individual specimen. The temperature-furnace parameters for electrothermal
atomic absorption spectrophotometry analysis consisted of a drying (250°C
for 30 seconds), charring (450°C for 20 seconds), atomization (2100°C
for 3.1 seconds), and a cleaning (2500°C for 2.8 seconds) temperature.
Lead signal was monitored at a wavelength of 283.3 nm and measured using peak
area mode with a 5-point standard calibration curve. A 0.4% ammonium dihydrogen
phosphate (NH4H2PO4) solution was used as
the chemical modifier to reduce the formation of chemical interferences during
the electrothermal process. The detection limit was determined to be 1 ppb
from 20 consecutive measurements of a blank solution.
was measured with a dedicated mercury analyzer (CETAC M-6000A Analyzer, Cetac
Technologies Inc, Omaha, Neb). The instrument was operated at a wavelength
of 254 nm. The detection limit was 0.05 ppb of mercury and determined by 2
times the SD from 10 consecutive measurements of blank and spiked-hair samples.
Certified standard reference materials from the National Institute of Standards
and Technology were used as quality controls. The recovery of mercury was −98%
to 100% for the standard reference materials. In the spiked-hair samples,
the recovery was 100%. All measurements were correlated with qualitative measurements
obtained with energy-dispersive x-ray microanalysis.
Results of duplicate determinations of Jackson's hair for mercury and
lead are shown in Table 1. Insufficient
material for mercury analysis aborted initial testing of the 1839 hair sample;
however, the duplicate sample provided sufficient material for analysis. Normal
ranges for mercury and lead also appear in Table 1.
Significantly elevated mercury
levels of 6.0 and 5.6 ppm were obtained from the 1815 and 1839 hair specimens,
respectively. These levels were consistent with mercury levels reported among
Japanese dentists exposed to dental amalgam and a variety of populations consuming
These levels are also similar to hair mercury levels reported for the poet
Robert Burns.18 However, neither sample affords
proof of systemic mercurialism. Individuals with symptomatic mercury poisoning
have evinced hair mercury levels of 125 to 649 ppm.15
Hair concentrations higher than 150 ppm have been associated with toxic levels.19
Hair lead levels were significantly elevated
in the 1815 and 1839 samples (Table 1).
The 1815 measurements were elevated by both 19th-century and contemporary
Jackson's 1815 hair lead levels were similar to results observed among Singaporean
battery workers with elevated blood lead levels and mild symptoms of lead
The 1839 hair lead measurement, although significantly lower than the
1815 level, still indicated lead exposure. However, it was below levels expected
in patients with symptomatic plumbism.
Chronic systemic mercurialism secondary to calomel use was not a major
factor in Jackson's declining health and death. Given the low levels of mercury
measured in the hair samples, Jackson's calomel use was probably an insignificant
factor in either his renal or his neuropsychiatric symptoms, despite massive
inorganic mercury ingestion. Mercurous ion is poorly absorbed from the gastrointestinal
tract. Conversion to the more soluble mercuric ion is required before intestinal
absorption is possible. Mercury ion in the form of the inorganic salt mercuric
chloride is relatively unabsorbable compared with metallic mercury or mercury
vapors. Causes other than mercury should be identified as the source of Jackson's
most severe complaints. Suggestions that he was slowly poisoned with calomel
Mercurous chloride does, however, have direct corrosive
effects upon the oropharyngeal and gastrointestinal mucosa, so that it provokes
clinical effects without being absorbed or systemically disseminated.19 Excessive salivation is a predictable result of calomel
ingestion and was used as an indicator of a therapeutic dose during the 18th
and 19th centuries. Jackson was familiar with this effect: he mentioned dosing
with ". . . calomel which salivated me."12(p245)
Jackson began to develop rapid progressive dental caries in 1824
and by 1828 all his teeth had been extracted. Many biographers ascribe Jackson's
dental problems in part to his overuse of calomel.2,4
Both Jackson's biographers and his own correspondence document recurrent abdominal
colic, dysentery, and severe diarrhea,1-10
symptoms consistent with calomel use.
The analysis results of
the 1815 hair sample are suggestive of plumbism. Lead's effects are multisystemic,
including central nervous system dysfunction, motor weakness, inhibited heme
synthesis, and intestinal disorders.22 Clinical
evidence for lead poisoning is most compelling for Jackson's intestinal complaints.
His letters contain many graphic references to postprandial intense cramping
abdominal pain associated with "costiveness," Jackson's term for constipation.
He also wrote of bilious colic, a group of symptoms including nausea, severe
abdominal discomfort, griping, headache, and constipation attributed to an
imbalance in bile humors, all consistent with lead colic.
there is no convincing evidence that Jackson developed peripheral neuropathy
from lead exposure, several references suggest this possibility. In numerous
letters, Jackson expressed concern that his handwriting might be illegible
due to "rheumatism in my right wrist."23(p220)
His aide-de-camp, T. L. Butler, signed Jackson's name for him when he could
not sign his own correspondence.23(p65) Dr
May, prior to the Battle of New Orleans, described a paralytic rheumatism
that so disabled Jackson he could barely scrawl his reports.24
Emily Donelson wrote her mother in 1829 that "Uncle . . . complains of pains
in the limbs, particularly in his right hand."25
One possible source of lead poisoning was Jackson's ingestion of sugar
of lead as a therapeutic agent. Sugar of lead was a traditional remedy, widely
used during the Jacksonian era for a variety of purposes, including the control
of bleeding and as a remedy for diarrhea.26,27
Although many writers have commented on Jackson's bath in sugar of lead, administered
by Dr May, and Jackson's use of sugar of lead as an eyewash, transdermal and
transophthalmic absorption of sugar of lead would not have resulted in a significant
More likely candidates
as the source of plumbism are the bullets retained in Jackson's left lung
and left shoulder. Lead poisoning subsequent to lead missile injury is related
to the surface area of the missile (the greater the surface area, the greater
the absorption), the location of the bullet, the presence of synovial fluid,
and the length of time the bullet resides in the body.29
The 1813 bullet wound shattered the left shoulder and contact with synovial
fluid in joint space is highly likely.1(p393)
Bony sequestrum, implying osteomyelitis, was sloughed from this wound in 1814
and presented as a memento to Jackson's wife.
The variation in
Jackson's hair lead levels over time implies a decline in exposure. Dr Thomas
Harris removed the left shoulder bullet in 1832. The bullet was described
as flattened by contusion on bone and hackled on the edge. Jackson reported
improved health following the procedure. The decline in lead levels may also
be attributable to Jackson's recognition of lead's adverse health effects,
which led him to discontinue use of the therapeutic agent. In 1836, Jackson
described sugar of lead as ". . . that potent but pernicious remedy to the
stomach. . . ."23(p439) Lead exposure and its
effects diminished in significance as factors in either Jackson's declining
health or death.
We suspect that Jackson probably died of chronic
renal failure. He first noted the onset of ankle edema in 1829, which progressed
to massive anasarca at the time of his death 16 years later. At the end, Jackson
was "perfect jelly from the toes to the upper part of my abdomen, in any part
of which a finger can be pressed half an inch and the print will remain for
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