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Lead (II) ion

PubChem CID
73212
Structure
Lead (II) ion_small.png
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

1 Structures

1.1 2D Structure

Chemical Structure Depiction
Lead (II) ion.png

1.2 Crystal Structures

2 Names and Identifiers

2.1 Computed Descriptors

2.1.1 IUPAC Name

lead(2+)
Computed by Lexichem TK 2.7.0 (PubChem release 2021.10.14)

2.1.2 InChI

InChI=1S/Pb/q+2
Computed by InChI 1.0.6 (PubChem release 2021.10.14)

2.1.3 InChIKey

RVPVRDXYQKGNMQ-UHFFFAOYSA-N
Computed by InChI 1.0.6 (PubChem release 2021.10.14)

2.1.4 SMILES

[Pb+2]
Computed by OEChem 2.3.0 (PubChem release 2021.10.14)

2.2 Molecular Formula

Pb+2
Computed by PubChem 2.2 (PubChem release 2021.10.14)

2.3 Other Identifiers

2.3.1 CAS

78896-34-1
7439-92-1

2.3.2 ChEBI ID

2.3.3 DSSTox Substance ID

2.3.4 HMDB ID

2.3.5 NCI Thesaurus Code

2.3.6 Wikidata

2.4 Synonyms

2.4.1 Depositor-Supplied Synonyms

3 Chemical and Physical Properties

3.1 Computed Properties

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)

3.2 Experimental Properties

3.2.1 Physical Description

Solid

3.2.2 Melting Point

327.5 °C

5 Chemical Vendors

6 Drug and Medication Information

6.1 Reported Fatal 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.

6.2 Biomarker Information

7 Food Additives and Ingredients

7.1 Associated Foods

8 Pharmacology and Biochemistry

8.1 Metabolism / Metabolites

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

8.2 Biochemical Reactions

9 Use and Manufacturing

9.1 Uses

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

10 Toxicity

10.1 Toxicological Information

10.1.1 Toxicity Summary

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.

10.1.2 Carcinogen Classification

Carcinogen Classification
2B, possibly carcinogenic to humans. (L135)

10.1.3 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)
L21: Wikipedia. Lead poisoning. Last Updated 3 March 2009. http://en.wikipedia.org/wiki/Lead_poisoning

10.1.4 Exposure Routes

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

10.1.5 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)
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

10.1.6 Toxicity Data

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.

10.1.7 Minimum Risk Level

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/

10.1.8 Treatment

Lead poisoning is usually treated with chelation therapy using DMSA, EDTA, or dimercaprol. (L21)
L21: Wikipedia. Lead poisoning. Last Updated 3 March 2009. http://en.wikipedia.org/wiki/Lead_poisoning

11 Associated Disorders and Diseases

12 Literature

12.1 Consolidated References

12.2 Chemical Co-Occurrences in Literature

12.3 Chemical-Gene Co-Occurrences in Literature

12.4 Chemical-Disease Co-Occurrences in Literature

13 Patents

13.1 Depositor-Supplied Patent Identifiers

13.2 Chemical Co-Occurrences in Patents

13.3 Chemical-Disease Co-Occurrences in Patents

13.4 Chemical-Gene Co-Occurrences in Patents

14 Interactions and Pathways

14.1 Protein Bound 3D Structures

14.2 Chemical-Target Interactions

14.3 Pathways

15 Biological Test Results

15.1 BioAssay Results

16 Classification

16.1 ChEBI Ontology

16.2 ChemIDplus

16.3 IUPHAR / BPS Guide to PHARMACOLOGY Target Classification

16.4 NORMAN Suspect List Exchange Classification

16.5 EPA DSSTox Classification

16.6 EPA Substance Registry Services Tree

16.7 MolGenie Organic Chemistry Ontology

17 Information Sources

  1. CAS Common Chemistry
    LICENSE
    The data from CAS Common Chemistry is provided under a CC-BY-NC 4.0 license, unless otherwise stated.
    https://creativecommons.org/licenses/by-nc/4.0/
  2. ChemIDplus
    ChemIDplus Chemical Information Classification
    https://pubchem.ncbi.nlm.nih.gov/source/ChemIDplus
  3. EPA DSSTox
    CompTox Chemicals Dashboard Chemical Lists
    https://comptox.epa.gov/dashboard/chemical-lists/
  4. Human Metabolome Database (HMDB)
    LICENSE
    HMDB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (HMDB) and the original publication (see the HMDB citing page). We ask that users who download significant portions of the database cite the HMDB paper in any resulting publications.
    http://www.hmdb.ca/citing
  5. ChEBI
  6. Toxin and Toxin Target Database (T3DB)
    LICENSE
    T3DB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (T3DB) and the original publication.
    http://www.t3db.ca/downloads
  7. Crystallography Open Database (COD)
    LICENSE
    All data in the COD and the database itself are dedicated to the public domain and licensed under the CC0 License. Users of the data should acknowledge the original authors of the structural data.
    https://creativecommons.org/publicdomain/zero/1.0/
  8. FooDB
    LICENSE
    FooDB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (FooDB) and the original publication.
    https://foodb.ca/about
  9. IUPHAR/BPS Guide to PHARMACOLOGY
    LICENSE
    The Guide to PHARMACOLOGY database is licensed under the Open Data Commons Open Database License (ODbL) https://opendatacommons.org/licenses/odbl/. Its contents are licensed under a Creative Commons Attribution-ShareAlike 4.0 International License (http://creativecommons.org/licenses/by-sa/4.0/)
    https://www.guidetopharmacology.org/about.jsp#license
    Guide to Pharmacology Target Classification
    https://www.guidetopharmacology.org/targets.jsp
  10. MarkerDB
    LICENSE
    This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
    https://markerdb.ca/
  11. NCI Thesaurus (NCIt)
    LICENSE
    Unless otherwise indicated, all text within NCI products is free of copyright and may be reused without our permission. Credit the National Cancer Institute as the source.
    https://www.cancer.gov/policies/copyright-reuse
  12. PubChem Elements
  13. RCSB Protein Data Bank (RCSB PDB)
    LICENSE
    Data files contained in the PDB archive (ftp://ftp.wwpdb.org) are free of all copyright restrictions and made fully and freely available for both non-commercial and commercial use. Users of the data should attribute the original authors of that structural data.
    https://www.rcsb.org/pages/policies
  14. Rhea - Annotated Reactions Database
    LICENSE
    Rhea has chosen to apply the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/). This means that you are free to copy, distribute, display and make commercial use of the database in all legislations, provided you credit (cite) Rhea.
    https://www.rhea-db.org/help/license-disclaimer
  15. Wikidata
  16. PubChem
  17. NORMAN Suspect List Exchange
    LICENSE
    Data: CC-BY 4.0; Code (hosted by ECI, LCSB): Artistic-2.0
    https://creativecommons.org/licenses/by/4.0/
    NORMAN Suspect List Exchange Classification
    https://www.norman-network.com/nds/SLE/
  18. EPA Substance Registry Services
  19. MolGenie
    MolGenie Organic Chemistry Ontology
    https://github.com/MolGenie/ontology/
CONTENTS