The History Of
Lead part 1
by Christopher Winder
This is the first of a
series of articles by Dr. Winder on the history of lead Reprinted with
permission, from his book "The Developmental Neurotoxicity of Lead"
MTP Press 1984.
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The
Middle Ages
Following the fall of Rome
in the fourth century, the use of lead declined in Europe and remained at a low
level for about 600 years. After the ninth century lead began to be mined in
Eastern Germany (the lead-rich regions of Spain were not accessible as they
were in Moslem possession). It is known that white lead was used in England in
the thirteenth century as there is reference to its use in the Close rolls of
Edward I (1274). The practice of adulterating wine with lead and its salts had
become widespread, and was banned by the Papal Bull in 1498. Nevertheless, this
continued and epidemics of lead colic were by no means infrequent. These were
known as poitou colic, the entrapado of Spain, the huttenkatze of Germany, the
bellain of Derbyshire and the dry bellyache of the New World. Periodic
outbreaks of what are now seen to be lead colic included Poitou colic (1592),
Devonshire colic (1793), West India dry gripes (1786), Jamaica dry bellyache
(1786) and Madrid colic (1796). Poitou colic, or 'colica pictonum' was
described by Francois Citois in 1616 who thought it was due to unripe grapes.
However, it was long afterwards discovered (Tronchin, 1757) to be lead colic.
In England Devonshire
colic was described by John Huxham (1739), but its true cause was not ascertained. This
was left to Sir George Baker (1767) who demonstrated that the cider of Devon
contained lead, while that of other areas did not. This was due to the common
practice of lining cider presses with lead which subsequently dissolved into
the mixture. He was responsible for the abandonment of this practice, and thus
for the disappearance of the colic. In France, Tronchin (1757) also discovered
many wines were able to dissolve the glaze of storage jars, which were
compounded with litharge. He demonstrated that a type of colic known as
'bellon', which was associated with such wines, was caused by lead.
In the New World, a law
was passed in Massachusetts in 1742 to prevent the distilling of wine in lead
heads or pipes (McCord, 1953). This was not heeded further south, and 'West
India dry gripe' was first described by Thomas Cadwalder. This was an account
of lead poisoning from the habitual consumption of Jamaica rum distilled
through leaden pipes (Cadwalder, 1745). In Jamaica itself, John Hunter (1788)
described the same 'dry bellyache' in the garrison and indicated the same
causes. Even today, lead poisoning can be found in alcoholics who drink
'moonshine' distilled through lead apparatus.
Lead was still being used
medically and in the early part of the nineteenth century for its action on the
blood. Salts of lead were found to be haemostatic and were used for the
treatment of ulcers because of their ability to coagulate albuminous material.
Until recently, lead compounds could be found in the British Pharmacopoeia, including
'lead and opium solution' (a mixture of Goulard's water and laudanum) and
'Diachylon' Plasters, which use lead oxide as a base. However, the 1980 B.P.
does not list any lead or lead containing preparations.
Throughout history, lead
was used for water and sewage piping. As was mentioned by Vitruvius and Pliny,
this practice was not good public health. In modem times, the continued use of
lead in plumbing - does not appear to be based on ignorance of its toxicity. In
an address to the fourth National Quarantine and Sanitary Convention in 1860,
Jacob Bigelow (1786-1879) noted 'but where shall we fly to escape from east
winds and dog days, from lead pipes for water contrived to kill everybody
except the animalcules.' Today lead piping is still present in older houses,
although in decreasing quantity as these are gradually cleared. In the
construction of new buildings, lead has at last been replaced (by copper) about
2000 years after its ill effects were first noted.
These uses and abuses made
many physicians aware of the nature of lead poisoning. Grisolle (1836), and
Burton (1840) recognized the well-known blue line on the gums, now called the
Burtonian line. This line is a layer of reduced lead sulphate particles that
stain the epithelial cells of the gums. Interestingly, the Burtonian line is
not a specific marker of lead poisoning, and it is seen in other conditions. A
blue line may also be seen around the anus.
The best description of
lead poisoning was made by Tanquerel des Planches (1839) who published his work
on 1217 cases of lead poisoning in Paris (translated Dana, 1848). This work is
the classic in the field, and his studies were so complete that later
investigators have added little to the clinical knowledge of symptoms and signs
of the disease, as summarized below from a present day clinical source (Price,
1978). Devergie and Hervy (1838) used some of the post mortem material from this
study to show that lead was present in the tissues of individuals dying of lead
intoxication as, for example, following chelation therapy. The histological
features found at autopsy were also briefly mentioned. These were expanded by later
workers (Kussmaul and Maier, 1872; von Monakow,1880).
Clinical features of lead intoxication in man
Acute poisoning
This usually follows
intense short-term exposure, but may represent an exacerbation of a chronic
intoxication as, for example, following chelation therapy. The initial symptoms
include a metallic taste in the mouth, vomiting, colic and the passage of black
stools. Circulatory collapse may occur, and encephalopathy is a well recognized
feature. Sequelae include hepatitis, renal failure and anaemia. Residual
neurological disorder is frequent.
Chronic poisoning
The features of frank lead
poisoning include haemopoietic, gastrointestinal, renal, and neurological
involvement.
Haemopoietic: lead
inhibits haem production, giving rise to the excretion of D-amino laevulinic
acid and coproporphyrin III. Features of anaemia include pallor, a reduction of
haemoglobin with the occurrence of punctate basophilia in erythrocytes and an
increase in reticulocyte count.
Gastrointestinal: the main
symptom is colic. In some cases it may be so severe as to be mistaken for an
acute abdominal emergency.
Renal: renal tubular
damage may produce a Fanconi syndrome (with aminoaciduria and glycosuria), and
hypertension has been described as a sequel of lead induced renal damage.
Peripheral neuropathy:
wrist drop, due to radial nerve involvement, is a classic manifestation of
chronic lead neurotoxicity. Clinical and experimental studies support the view
that lead induces peripheral nerve lesions.
Central nervous system:
the manifestations of
saturnine encephalopathy include headache, irritability,
insomnia,
apprehension, confusion, nightmares and fits. High exposure levels (at least
200 µg Pb/100 ml in children and 500 µg Pb/100 ml in adults) are usually found.
Recovery from encephalopathy is often incomplete, and residual neurological
damage is frequent.
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