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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