Lead (II) ion
PubChem CID
73212
Structure
Molecular Formula
Synonyms
- Lead(2+)
- Lead (II) ion
- Lead(2+) ion
- Lead, ion (Pb2+)
- 14280-50-3
Molecular Weight
207 g/mol
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Element Name
Dates
- Create:2004-09-16
- Modify:2024-12-28
Description
Lead(2+) is a lead cation, a divalent metal cation and a monoatomic dication. It has a role as a cofactor.
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).
A7666: Gidlow DA: Lead toxicity. Occup Med (Lond). 2004 Mar;54(2):76-81. PMID:15020724
Chemical Structure Depiction
COD records with this CID as component
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- (the list is too long and has been truncated)
lead(2+)
Computed by Lexichem TK 2.7.0 (PubChem release 2021.10.14)
InChI=1S/Pb/q+2
Computed by InChI 1.0.6 (PubChem release 2021.10.14)
RVPVRDXYQKGNMQ-UHFFFAOYSA-N
Computed by InChI 1.0.6 (PubChem release 2021.10.14)
[Pb+2]
Computed by OEChem 2.3.0 (PubChem release 2021.10.14)
Pb+2
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
Property Value
Reference
Property Name
Molecular Weight
Property Value
207 g/mol
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
Hydrogen Bond Donor Count
Property Value
0
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Hydrogen Bond Acceptor Count
Property Value
0
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Rotatable Bond Count
Property Value
0
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Exact Mass
Property Value
207.97665 Da
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
Monoisotopic Mass
Property Value
207.97665 Da
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
Topological Polar Surface Area
Property Value
0Ų
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Heavy Atom Count
Property Value
1
Reference
Computed by PubChem
Property Name
Formal Charge
Property Value
2
Reference
Computed by PubChem
Property Name
Complexity
Property Value
0
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Isotope Atom Count
Property Value
0
Reference
Computed by PubChem
Property Name
Defined Atom Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Undefined Atom Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Defined Bond Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Undefined Bond Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Covalently-Bonded Unit Count
Property Value
1
Reference
Computed by PubChem
Property Name
Compound Is Canonicalized
Property Value
Yes
Reference
Computed by PubChem (release 2021.10.14)
Solid
327.5 °C
Follow these links to do a live 2D search or do a live 3D search for this compound, sorted by annotation score. This section is deprecated (see here for details), but these live search links provide equivalent functionality to the table that was previously shown here.
Same Connectivity Count
Mixtures, Components, and Neutralized Forms Count
Similar Compounds (2D)
Similar Conformers (3D)
Same Count
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.
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)
L136: ATSDR - Agency for Toxic Substances and Disease Registry (2007). Toxicological profile for lead. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). http://www.atsdr.cdc.gov/toxprofiles/tp13.html
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)
L136: ATSDR - Agency for Toxic Substances and Disease Registry (2007). Toxicological profile for lead. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). http://www.atsdr.cdc.gov/toxprofiles/tp13.html
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)
A20: Gill KD, Gupta V, Sandhir R: Ca2+/calmodulin-mediated neurotransmitter release and neurobehavioural deficits following lead exposure. Cell Biochem Funct. 2003 Dec;21(4):345-53. PMID:14624473
A22: Hashemzadeh-Gargari H, Guilarte TR: Divalent cations modulate N-methyl-D-aspartate receptor function at the glycine site. J Pharmacol Exp Ther. 1999 Sep;290(3):1356-62. PMID:10454514
L136: ATSDR - Agency for Toxic Substances and Disease Registry (2007). Toxicological profile for lead. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). http://www.atsdr.cdc.gov/toxprofiles/tp13.html
T4: Ellenhorn MJ and Barceloux DG (1988). Diagnosis and treatment of human poisoning. Medical Toxicology. New York, New York: Elsevier Science Publishing Company, Inc.
Carcinogen Classification
2B, possibly carcinogenic to humans. (L135)
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)
L21: Wikipedia. Lead poisoning. Last Updated 3 March 2009. http://en.wikipedia.org/wiki/Lead_poisoning
Oral (L136) ; inhalation (L136) ; dermal (L136)
L136: ATSDR - Agency for Toxic Substances and Disease Registry (2007). Toxicological profile for lead. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). http://www.atsdr.cdc.gov/toxprofiles/tp13.html
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)
A2: Needleman HL, Schell A, Bellinger D, Leviton A, Allred EN: The long-term effects of exposure to low doses of lead in childhood. An 11-year follow-up report. N Engl J Med. 1990 Jan 11;322(2):83-8. PMID:2294437
L21: Wikipedia. Lead poisoning. Last Updated 3 March 2009. http://en.wikipedia.org/wiki/Lead_poisoning
At blood lead levels between 25 and 60 μg/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 μg/dL. In adults, Abdominal colic, involving paroxysms of pain, may appear at blood lead levels greater than 80 μg/dL.
Chronic Inhalation: 0.05 mg/m3 (L134)
L134: ATSDR - Agency for Toxic Substances and Disease Registry (2001). Minimal Risk Levels (MRLs) for Hazardous Substances. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). http://www.atsdr.cdc.gov/mrls/
L21: Wikipedia. Lead poisoning. Last Updated 3 March 2009. http://en.wikipedia.org/wiki/Lead_poisoning
Disease
References
Disease
Alzheimer's disease
References
Disease
Multiple sclerosis
References
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- EPA DSSToxLead(2+) ionhttps://comptox.epa.gov/dashboard/DTXSID10872437CompTox Chemicals Dashboard Chemical Listshttps://comptox.epa.gov/dashboard/chemical-lists/
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