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We report the case of a 48-year-old patient who developed acute onset bilateral, peripheral motor dysfunction in the arms and forearms. Clinical history, electromyography and laboratory tests confirmed the diagnosis of peripheral neuropathy caused by lead poisoning from the domestic water supply. The EMG showed axonal alterations. Improvement was observed after treatments with chelating agents and removal of the source of poisoning. This case provides the opportunity to recall the traditional 1889 Dejerine classification of lead-related peripheral neuropathies and is a warning signal that lead poisoning remains a problem in peri-urban areas of developed countries.

A seventy-six-year-old patient developed a bulbar form of amyotrophic lateral sclerosis, after chronic lead intoxication from drinking water. Treatment with 2,3 dimercaptosuccinic acid was administered for six months and had no effect on clinical course. We discuss the imputability of lead as a possible etiological factor.

Several thousands of compounds with a potential reproductive toxicity have been identified in animals, some of them are teratogens. In humans, only a small number of chemicals, administered as drugs, present in the diet, or in the occupational environment are recognized human teratogens. In parallel, about 60% of congenital anomalies have no identified cause and most probably some compounds present in the environment may contribute to certain anomalies. This paper presents a review of published epidemiological studies on the association between occupational exposures and congenital anomalies, focusing more particularly on some groups of compounds or some occupations such as: anaesthetic gases, laboratory work, solvents, pesticides and lead.

A study was performed in 278 people living in a Mexican town with a high lead environmental pollution. Lead blood level was found very high (m:59.7 micrograms/l) and some abnormalities were also found for free erythrocyte Protoporphyrin and ALA dehydratase. A significant dose-response relationship was also found with somatic complaints like loss of appetite, insomnia and headache.

In a patient with occupational plumbism and a normal kidney function, EDTA therapy (1 g/24 h) resulted in a massive lead excretion (15 000 microgram/24 h) together with acute renal failure. A direct nephrotoxic effect of EDTA was excluded: after renal function returned to normal, EDTA could be subsequently readministered at progressively increasing doses (250 mg to 1 g/24 h) without any renal dysfunction. These findings strongly suggest a close relationship between the burden of lead mobilized by EDTA and the acute renal failure. This case can be classified as acute lead nephropathy of which only a few instances have been reported in the literature. The interest of monitoring lead excretion during chelation therapy is particularly emphasized.

Treatment of female mice with high doses of lead from different times of the gestation, induces abortion or retardation of growth of the embryos. When it is given from birth, it provokes important mortality in the youngs and a retardation of the postnatal growth. In most cases, lead administered from the first day of gestation delays slightly the development of the embryo and inhibits its implantation. It seems that a deficiency in the plasmatic progesterone levels is directly implied in this inhibition.

A case of severe lead poisoning with haemolytic anemia, extensive polyneuropathy and arterial hypertension is reported in a patient for whom G-6-P-D deficiency and renal tubular acidosis were discovered. Both traits were present in his family. Incomplete regression of paralysis and persistant biological abnormalities after chelating treatment were demonstrative of heavy saturnine load even though the toxic exposure was brief. The role of the two deficiencies in the mechanism of intoxication is discussed: facilitation of haemolysis by enzymopathy and bone lead redistribution resulting from osteolysis probably due to the tubulopathy. The authors emphasize the fact that thorough and serial biological investigation is essential in the discovery of factors which may precipitate lead poisoning, as well as in the determination of follow-up criteria of efficient toxic epuration with sufficient delay. Typing of the enzyme has led to the identification of a new variant of glucose-6-phosphate dehydrogenase deficiency.

When the litters were 14 days old, wistar rat pups received lead ions. The suckling mother was fed by a powdered laboratory chow containing lead carbonate (1%, 2%, 4%). The intoxication was going on for 3 days to 9 weeks. While lead-fed pups showed a decrease in body-weight gain and in neurologic development, lead ions were without effects on oxygen consumption, ADP-phosphorylation and activity of several enzymes of cerebral mitochondria. On the other hand, the important lead accumulation into cerebral mitochondria was in a straight ratio with lead doses in the feedings. To explain the in vivo data, the effects of lead acetate were investigated in vitro on brain mitochondria of young male wistar rats. Our findings indicate that lead ions alter mitochondrial respiration and ADP-phosphorylation and that inorganic phosphate has a protective effect.

The authors report one case of saturnism with chronic nephropathy. In a 49 years old Caucasian male, the diagnosis was suggested by the following findings. Two acute abdominal crisis associated with a severe increase in blood pressure and a slight but significant elevation in the lead concentration in blood (1 mg/l) and urine (0,42 and 0,60 mg/24 h). The chronic poisoning was explained by the high lead concentration in the drinking water used by the patient. Despite chronic renal failure, a significant lead urinary chelation was obtained after infusion of Edetate calcium disodium (8 mg/24 h). Although E.D.T.A. keep its value for diagnosis this chelating agent is less effective on lead removal than the peritoneal dialysis (15 mg over a 36 hour-period) which appears to be the most useful method for treatment in case of chronic nephropathy.

A 32 year old obese, diabetic and hypertensive woman presented with signs of increasing intracranial pressure: diplopia, partial lateralised Jacksonian seizures followed by alternating post-ictal hemiplegia. She was also anaemic. Investigation revealed lead poisoning and thrombosis of the superior sagittal sinus. She recovered rapidly with heparin and calcium EDTA therapy, except for persistent optic atrophy due to the papilloedema. The authors discuss the relation of lead encephalopathy and dural sinus thrombosis, and the contribution of each condition to this patient's clinical symptoms.