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Arsenic and antique copper A potential source for intoxication and development of peripheral neuropathy.

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Arsenic and
Antique Copper:
A Potential Source
for lntoxication
and Development
of Peripheral Neuropathy
H. Royden Jones, Jr, M D
Although arsenic is known for its ubiquitous distribution in
the environment, it is no longer a frequent cause of peripheral neuropathy. Heightened awareness of its toxic potential has led to measures that have decreased the public’s
exposure. Because of its notoriety as a surreptitious means
of committing homicide, when excess quantities of arsenic
appear to be the cause of a patient’s symptoms, suspicion
may inappropriately be directed to other individuals if no
apparent source is found. A case is reported of a patient
with arsenical peripheral neuropathy secondary to leaching
of arsenic from an “antique” copper kettle.
A 42-year-old man presented with increasingly frequent
episodes of sweats, fevers, headaches, unsteadiness, fatigue, blurred vision, and nausea. H e had associated numbness in all four extremities, increasing in degree, occurring on a daily basis. The patient admitted to substantial
chronic alcohol ingestion. Past history was not otherwise
Abnormal findings on examination included a mild static
finger tremor, symmetrical decrease in ankle reflexes, diminution in pinprick and vibration sensation in a stocking
and glove distribution, and alcohol on his breath.
Abnormal laboratory results included serum glutamic
oxaloacetic transaminase, 125 units; 3-hour glucose tolerance test (fasting, 102 mgldl; 1 hour, 277; 2 hour, 239; and
3 hour, 167 mg/dl); and 24-hour urine collection containing 720 p g of arsenic (normal, 20 pg) with concomitant
increased arsenic levels in the hair and nails. Nerve conduction study and needle electromyography demonstrated
a mild axonal neuropathy.
Search for sources of arsenic exposure was unsuccessful
until his wife recalled that he was the only family member
who used an antique copper teakettle. A specimen of Boston water boiled in this kettle contained 200 p g of arsenic
per liter. Concomitantly, water from the same source was
boiled in a modern copper teakettle and had no arsenic.
Six weeks after the patient stopped using this kettle, no
arsenic was detectable in his urine. His symptoms disappeared within ten weeks. None have recurred in a six-year
follow-up period.
In patients with arsenical peripheral neuropathy, sources
such as insecticides or industrial exposure may be apparent.
However, in many patients the origin of the toxin may be
enigmatic [3].
Arsenic has a diffuse natural distribution in soil and
water, especially ocean water. Copper ores contain various
mineral impurities, of which arsenic is the most troublesome [l]. It is speculated that ancient humans became
aware of the toxic properties of arsenic and thus searched
for other copper alloys [41. Modern copper manufacturing
techniques eliminate inorganic arsenic [23. The age of this
patient’s antique kettle could not be determined. Presumably, its copper did not meet modern standards of metallurgic technique.
This case emphasizes the need to consider arsenic as a
cause for peripheral neuropathy in (1) patients with associated intermittent, poorly defined systemic symptoms, including fever, sweats, blurred vision, and recurrent nausea
or vomiting; (2) any patient with a new onset of peripheral
neuropathy, even when other problems such as glucose
intolerance or ethanol excess are present; and ( 3 ) patients
using antique copper kettles that may contain arsenic.
Department of Neurology
Lahey Clinic Medical Center
41 Mall Rd
Burlington, M A 0180.3
Arsenic. Encyclopaedia Britannica 2:478-481, 1967
Baker EL Jr, Hayes CG, Landrigan PJ, et al: A nation-wide survey of heavy metal absorption in children living near primary
copper, lead, and zinc smelters. Am J Epidemiol 106:261-273,
Heyman A, Pfeiffer JB, Willett RW, er al: Peripheral neuropathy caused by arsenic intoxication. N Engl J Med 254:
401-409, 1956
Wertime TA: The beginnings of metallurgy: a new look. Science 182:875-887, 1973
Normal Muscle
Pyruvate Oxidation
in Spinocerebellar
Owen B. Evans, MD
Spinocerebellar degenerations (SCD) are a group of genetic disorders characterized by progressive ataxia and
other neurological dysfunctions. Although the pathophysiology of SCD is unknown, disordered carbohydrate
metabolism and reduced pyruvate dehydrogenase complex (PDHC) activity have been demonstrated in some
patients [3]. The SCD patients were clinically similar to patients with Friedreich’s ataxia, and subsequent work
showed that an altered Michaelis-Menten constant for
lipoamide dehydrogenase, the third component of PDHC,
was the responsible enzyme abnormality 141. Other laboratories have failed to confirm deficient lipoamide dehydroge n a e activity [l, 51. P D H C is a regulatable enzyme that
exists in an active or inactive state, and abnormal pyruvate
oxidation in SCD could result from disordered PDHC reg-
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development, potential, periphery, antiqua, neuropathy, source, arsenic, coppel, intoxication
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