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Name Description
id 3
T3DB ID T3D0002
Name Lead
Class SmallMolecule
Description Lead is a soft and malleable heavy and post-transition metal. Metallic lead has a bluish-white color after being freshly cut, but it soon tarnishes to a dull grayish color when exposed to air. It is the heaviest non-radioactive elemen and has the highest atomic number of all of the stable elements. Lead is used in building construction, lead-acid batteries, bullets and shot, weights, as part of solders, pewters, fusible alloys, and as a radiation shield. It readily forms many lead salts and organo-lead compounds. Lead is one of the oldest known and most widely studied occupational and environmental toxins. Despite intensive study, there is still vigorous debate about the toxic effects of lead, both from low level exposure in the general population owing to environmental pollution and historic use of lead in paint and plumbing and from exposure in the occupational setting. The majority of industries historically associated with high lead exposure have made dramatic advances in their control of occupational exposure. However, cases of unacceptably high exposure and even of frank lead poisoning are still seen, predominantly in the demolition and tank cleaning industries. Nevertheless, in most industries blood lead levels have declined below levels at which signs or symptoms are seen and the current focus of attention is on the subclinical effects of exposure. The significance of some of these effects for the overt health of the workers is often the subject of debate. Inevitably there is pressure to reduce lead exposure in the general population and in working environments, but any legislation must be based on a genuine scientific evaluation of the available evidence. Physiologically, it exists as an ion in the body. Inorganic lead is undoubtedly one of the oldest occupational toxins and evidence of lead poisoning can be found dating back to Roman times. As industrial lead production started at least 5000 years ago, it is likely that outbreaks of lead poisoning occurred from this time. These episodes of poisoning were not limited to lead workers. The general population could be significantly exposed owing to poorly glazed ceramic ware, the use of lead solder in the food canning industry, high levels of lead in drinking water, the use of lead compounds in paint and cosmetics and by deposition on crops and dust from industrial and motor vehicle sources. It was an important cause of morbidity and mortality during the Industrial Revolution and effective formal control of lead workers did not occur until the pioneering occupational health work of Ronald Lane in 1949. At very high blood lead levels, lead is a powerful abortifacient. At lower levels, it has been associated with miscarriages and low birth weights of infants. Predominantly to protect the developing fetus, legislation for lead workers often includes lower exposure criteria for women of reproductive capacity. Studies have shown a slowing of sensory motor reaction time in male lead workers and some disturbance of cognitive function in workers with blood lead levels >40 ug/100 ml. Peripheral motor neuropathy is seen as a result of chronic high-level lead exposure, but there is conflicting, although on the whole convincing, evidence of a reduction in peripheral nerve conduction velocity at lower blood lead levels. The threshold has been suggested to be as low as 30 ug/100 ml, although other studies have not seen effects below a blood lead level of 70 ug/100 ml. Several large epidemiological studies of lead workers have found inconclusive evidence of an association between lead exposure and the incidence of cancer. However, based on closer analysis, the increase did not appear to be related to lead exposure. There was also a small but significant increase in the incidence of lung cancer, but this could have been the result of confounding from cigarette smoking or concurrent arsenic exposure. There is some evidence in humans that there is an association between low-level lead exposure and blood pressure, but the results are inconsistent. Lead appears to reduce the resistance and increase the mortality of experimental animals. It apparently impairs antibody production and decreases immunoglobulin plaque forming cells. There is some evidence for suggesting that workers with blood lead levels between 20 and 85 ug/100 ml may have an increased susceptibility to colds, but a study of lead workers with blood lead levels less than 50 ug/100 ml showed no significant immunological changes. Although it is widely accepted that personal hygiene is the most important determinant of an individual's blood lead level, recent interesting information has shown that certain genetic polymorphisms may also have an impact. The use of most of lead containing chemicals is declining with the gradual demise of the use of lead in gasoline (petrol), but lead naphthenates and lead stearates are still used in stabilizers for plastics and as lead 'soaps'. In fact, the only compound now produced for gasoline/fuel usage is tetraethyl lead. Exposure is only seen during the production, transportation and blending of this substance into gasoline/fuel/petrol and in workers involved in cleaning storage tanks that have contained leaded gasoline (or petrol). It is in this final group, the tank cleaners, where the highest potential morbidity and mortality may be seen. (A7666).
Categories "Cigarette Toxin", "Household Toxin", "Industrial/Workplace Toxin", "Pollutant", "Airborne Pollutant", "Food Toxin", "Natural Toxin"
Types "Inorganic Compound", "Metal", "Lead Compound", "Pollutant", "Food Toxin", "Metabolite", "Cigarette Toxin", "Household Toxin", "Industrial/Workplace Toxin", "Natural Compound"
Synonyms "Lead (II) cation", "Lead ion", "Lead ion (Pb2+)", "Lead(2+)", "Lead(2+) ion", "Lead(II)", "Pb", "Pb(2+)", "Pb2+", "Plumbum"
CAS Number 7439-92-1
Chemical Formula Pb
Average Molecular Mass 207.20
Monoisotopic Mass 207.98
IUPAC Name ?²-lead(2+) ion
Traditional Name ?²-lead(2+) ion
SMILES [Pb++]
InChI Identifier InChI=1S/Pb/q+2
InChI Key InChIKey=RVPVRDXYQKGNMQ-UHFFFAOYSA-N
Kingdom Inorganic Compounds
Super Class Homogeneous Metal Compounds
Class Homogeneous Post-transition Metal Compounds
Sub Class
Direct Parent Homogeneous Post-transition Metal Compounds
Alternate Parents "Inorganic Cations"
Geometric Description Acyclic Compounds
Substituents "Inorganic Cation", "Acyclic Compound", "Homogeneous Post-Transition Metal"
Descriptors "monoatomic dication (ChEBI)", "divalent metal cation (ChEBI)", "lead cation (ChEBI)", "a cation (MetaCyc)"
Status Detected and Quantified
Origin Exogenous
Cellular Locations "Cytoplasm", "Extracellular"
Biofluids "Blood", "Cerebrospinal Fluid (CSF)", "Saliva", "Urine"
Tissues
Pathways
State Solid
Appearance Bluish-white metallic solid, turns grey when exposed to air.
Melting Point 327.5°C
Boiling Point 1740 °C
Solubility
LogP
Route of Exposure Oral (L136) ; inhalation (L136) ; dermal (L136)
Mechanism of Toxicity Lead mimics other biologically important metals, such as zinc, calcium, and iron, competing as cofactors for many of their respective enzymatic reactions. For example, lead has been shown to competitively inhibit calcium's binding of calmodulin, interferring with neurotransmitter release. It exhibits similar competitive inhibition at the NMDA receptor and protein kinase C, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Lead also affects the nervous system by impairing regulation of dopamine synthesis and blocking evoked release of acetylcholine. However, it's main mechanism of action occurs by inhibiting delta-aminolevulinic acid dehydratase, an enzyme vital in the biosynthesis of heme, which is a necesssary cofactor of hemoglobin. (T4, A20, A22, L136)
Metabolism Lead is absorbed following inhalation, oral, and dermal exposure. It is then distributed mainly to the bones and red blood cells. In the blood lead may be found bound to serum albumin or the metal-binding protein metallothionein. Organic lead is metabolized by cytochrome P-450 enzymes, whereas inorganic lead forms complexes with delta-aminolevulinic acid dehydratase. Lead is excreted mainly in the urine and faeces. (L136)
Toxicity At blood lead levels between 25 and 60 ?g/dL, neuropsychiatric effects such as delayed reaction times, irritability, and difficulty concentrating, as well as slowed motor nerve conduction and headache can occur. Anemia may appear at blood lead levels higher than 50 ?g/dL. In adults, Abdominal colic, involving paroxysms of pain, may appear at blood lead levels greater than 80 ?g/dL.
Lethal Dose 714 mg/kg of lead acetate (i.e., about 450 mg/kg of lead) is the lethal oral dose. An oral dose of 450 mg Pb/kg is equivalent to a 70-kg worker being exposed to 21,000 mg Pb/m3 for 30 minutes, assuming a breathing rate of 50 L/minute and 100% absorption.
Carcinogenicity 2B, possibly carcinogenic to humans. (L135)
Uses/Sources Lead is used extensively in building construction and can also be found in batteries, ammunition, non-Western cosmetics, solder, and pipes. Old paints and ceramic products may also contain lead, though recent legislation has banned its use. (L136)
Minimum Risk Level Chronic Inhalation: 0.05 mg/m3 (L134)
Health Effects Lead is a neurotoxin and has been known to cause brain damage and reduced cognitive capacity, especially in children. Lead exposure can result in nephropathy, as well as blood disorders such as high blood pressure and anemia. Lead also exhibits reproductive toxicity and can results in miscarriages and reduced sperm production. (L21)
Symptoms Symptoms of chronic lead poisoning include reduced cognitive abilities, nausea, abdominal pain, irritability, insomnia, metal taste in the mouth, excess lethargy or hyperactivity, chest pain, headache and, in extreme cases, seizures, comas, and death. There are also associated gastrointestinal problems, such as constipation, diarrhea, vomiting, poor appetite, weight loss, which are common in acute poisoning. (A2, L21)
Treatment Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (L21)
DrugBank ID
HMDB ID HMDB04628
PubChem Compound ID 73212
ChEMBL ID
ChemSpider ID 65967
KEGG Compound ID C06696
UniProt ID 0
OMIM ID 150500
ChEBI ID 49807
BioCyc ID CPD-527
CTD ID D007854
Stitch ID Lead
PDB ID PB
ACToR ID 6472
Wikipedia Link http://en.wikipedia.org/wiki/Lead
Creation Date 2009-03-06 18:57:54
Update Date 2014-12-24 20:20:50