Lead is a chemical element, which is predominantly mined as lead sulfide (PbS), cerosite (PbCO3), crocoite (PbCrO4), and wulfenite (PbMoO4) .



Synonyms/Trade Names:

C.I. 77575, C.I. Pigment Metal, Glover, Lead Flake, Lead S2, Omaha, Omaha & Grant, Saturnism.


Pb .


Cubic closed packing.

Crystallographic Constants:

1.74 1.74 1.74 90.000 90.000 90.000.

Crystal Group:




Optical Properties:




Powder Diagram:

2.86 2.48 1.49 1.75 (4-686).

Natural Sources:

Lead ores are mined in Australia, Bulgaria, Canada, Mexico, Peru, Russia, and the USA. World production was 3.6×106 tons of lead in 1977.

Medical Importance:

Key Hazards:

Acute and chronic intoxication.

Involved Organs:

Erythrocytes, nervous system, skeleton, kidneys.


Lead intoxication is one of the oldest occupational diseases known. Exposure may occur during mining, heating or usage in chemical industries (colors), metallurgy, batteries, glass and ceramic industries. Exposure to lead has been reported from more than 150 different professions.


France 150
Germany 0.1
Poland 0.05


Lead gases or particles <8 µm enter the alveoli and may be 50-80% absorbed. Mucociliary cleaning induces an enteric uptake of the lead particles. The non-absorbed particles are stored in lung phagosomes and lysosomes. The excretion of the gastroenteric lead is 90% enteric, that of systemic lead 76% renal. The gastrointestinal absorption amounts to 5-10% of the ingested lead in adults, and to 40% in children. Organic lead may be, in addition, absorbed through the skin. Most of the lead is bound to the membrane of erythrocytes and to hemoglobin; a small portion is ionic and free. Lead bound to erythrocytes decreases the activity of delta-aminolevulinic acid dehydrogenase (lead concentration >10 µg/100 ml), the oxidase of coproporphyrinogen, and induces a toxic effect to the capillaries of the central nervous system and cardiac muscles. Lead is stored in all organs, but mainly in the bones (>90%), and replaces Ca. It can be removed by exogenous factors (e.g. fever) from its storage, crosses the placenta and enters the brain. Its toxicity is related to its effects to the cytochrome-P-450 oxidase and the renal tubuli. Lung Diseases: Lead is mutagenic and teratogenic, its cancerogenic potency (lung, gastric and colon carcinoma) has not been confirmed. Lung fibrosis is induced by contaminated silica; compare to silica.

Clinical Presentation:

Acute lead intoxication: gastroenteritis occurs a few hours after intoxication, gastric pain and colics, anuria, hepatomegaly and shock may follow. Chronic intoxication (seldom): non-specific symptoms like colic, arthritis, pale face, weak brown skin, anaemia with anisocytosis, alterations of the central nervous system, peripheral neuropathias, hypertonia, spastic obstipation, liver diseases, endocrine diseases, dementia, basophilic changes of erythrocytes, and impotence. Measurements of the delta-amino-levulinic acid and delta-aminolevulinic acid dehydrogenase in the urine, anaemia, anisocytosis, n-acetyl-ß-Dglucosaminidase and coproporphyrine in the urine are of diagnostic importance. The clinical data of lead intoxication (according to Tsuchiya, 1990) are related to the lead serum levels as follows:
PP : protoporphyrine,
FEP : free erythrocytporphyrine,
ZPP : zinc protoporphyrine,
ALA-D : delta-aminolevulinic acid dehydrogenase. /table
Findings Pbin blood in µg/l
Decreased ALA-D 50-100
Increased PP (FEP, ZPP)
children 150-250 women 200-300 men 250-350
Na+K+AT-paseinhibition 300-400
Increased ALAurine, CPurine 400
Decreased hemoglobin
in children 400 adults 500-600
Decreased nerve velocity 400-500
Minimal brain dysfunction
in children 500-600 adults 600-800
minimal nephropathia
in children 600-700 adults 800


Associated specific findings are not known.

Lung Function:

Usually normal findings.

Bronchoalveolar Lavage:

Usually normal findings.



The lungs are of normal color and consistency.


The alveoli can contain an increased number of macrophages, and collections of brown dust particles may be seen in the lymphatic tissue.


Acute, even severe intoxications have a good Prognosis in children opposite to those of elderly patients.

Additional Diseases:



Lead arsenate and chromate have a carcinogenic potency. In the USA, cases of industrial lead intoxications have to be reported to the Occupational Safety and Health Administration.


search Pubmed for Lead

Alessio L, Foa V: Lead. In: Commission of the European Community (Ed): Human biological monitoring of industrial chemicals series. Brussels (1983)
Blot WJ: Lung cancer and occupational exposures. In: M Mizell, P Correa (Eds): Lung cancer: causes and prevention. Verlag Chemie Int, Weinheim (1984) 47-64
Cardenas A, Roels H, Bernard AM, Barbon R, Buchet JP, Lauwerys RR: Markers of early renal changes induced by industrial pollutants. Br J Ind Med 50 (1993) 28-36
Gerhardsson L, Chettle DR, Englyst V, Nordberg GF, Nyhlin H, Scott MS, Todd AC, Vesterberg: Kidney effects in long term exposed lead smelter workers. Br J Ind Med 49 (1992) 186-192
Graziano JH, Blum C: Lead exposure from lead crystal. Lancet 337 (1991) 141-142
Graves AB, Van Duijn CM, Chandra V, Fratiglioni L, Heyman A, Jorm AF, Kokmen E, Kondo K: Occupational exposures to solvents and lead as risk factors for Alzheimer’s disease: a collobarative re-analysis of case-control studies. Int J Epidemiol 20 (1991) 258-261
Hodgkins DG, Robins TG, Hinkamp DL, Schork MA, Krebs WH: A longitudinal study of the relation of lead in blood to lead in air concentrations among battery workers. Br J Ind Med 49 (1992) 241-248
Hudak A, Nary M, Süveges E: Clinical relevance of urinary delta-amonolevulinic acid/logarithm of creatine ratio in screening for occupational lead exposure. Am J Ind Med 21 (1992) 673-680
IARC: Overall evaluations of carcinogenicity: an updating of IARC monographs volumes 1 to 42. IARC Mono Eval Carcinog Risk Human Suppl 7 (1987)
IARC: Cancer: causes, occurrence and control. IARC Sci Publ 100 (1990) 1
Ichiba M, Tomokuni K, Mori K: Erythrocyte nucleotides in lead workers. Int Arch Occup Environ Health 63 (1992) 419-421
Konietzko J, Dupuis H: Handbuch der Arbeitsmedizin. Ecomed, Landsberg (1990)
Lerda D: Study of sperm chracteristics in persons occupationally exposed to lead. Am J Ind Med 22 (1992) 567-571
Lewis RJ: Carcinogenically active chemicals. Van Nostrand Reinhold, New York (1991)
Masjedi MR, Estinah N, Bahadori M, Alavi M, Spince NL: Pulmonary complications in lead miners. Chest 96 (1989) 18-21
Ronnebeack L, Hansson E: Chronic encephalopathies induced by mercury or lead: aspects of underlying cellular and molecular mechanisms. Br J Ind Med 49 (1992) 233-240
Stollery BT, Broadbent DE, Banks HA, Lee WR: Short term prospective study of cognitive functioning in lead workers. Brit J Ind Med 48 (1991) 739-749
Takebayashi T, Omae K, Hoso da K, Satoh T, Hamaguchi T , Sakurai H: Ev aluation of delta-aminolevulinic acid in blood of workers exposed to lead. Br J Ind Med 50 (1993) 49-54
Tell I, Sommervaille LJ, Nilsson U, Bensryd I, Schütz A, Chettle DR, Scott MC, Skerfving S: Chelated lead and bone lead. Scand J Work Environ Health 18 (1992) 113-119
Tsuchiya E: Lead. In: L Friberg, GF Nordberg, VB Vouk (Eds): Handbook on the toxicology of metals. Elsevier, Amsterdan, New York (1990)
Ulenbelt P, Lumens MEGL, Geron HMA, Herber RFM: An inverse air to lead blood relation: the impact of air-stream helmets. Int Arch Occup Environ Health 63 (1991) 89-95
Valentin H, Lehnert G, Petry H, Weber G, Wittgens H, Woitowitz HJ: Arbeitsmedizin Vol 2. Thieme, Stuttgart (1985)
Wilson JD, Braunwald E, Isselbach KJ, Petersdorf RJ, Martin JB, Fauci AS, Root RK: Harrison’s principles of internal medicine, 12th Edition. McGraw Hill, New York (1991)
Wirth W, Gloxhuber C: Toxikologie. Thieme, Stuttgart (1985)