Toxno Substance Profile
Substance Name

Diethyldimethyl lead
Identification Number: CASRN | 1762-27-2

  Substance Attributes

  • Neurotoxic Properties

    Negative impact on brain and nervous system.

  • Metabolic Interference or Disruption



  • Exposure Produces Health Symptoms



  • CATEGORIES: Industrial/Workplace Toxin | Pollutant | Airborne Pollutant | Synthetic Toxin
  • SUBSTANCE LINEAGE: Organic Compounds | Organometallic Compounds | Organo-post-transition metal compounds | | Organic Post-Transition Metal Compounds
  • SYNONYMS: Diethyldimethyllead | Diethyldimethylplumbane | Dimethyldiethyllead
  • DESCRIPTION: Diethyldimethyl lead is an organolead compound. Lead is a heavy metal and stable element with the symbol Pb and the atomic number 82, existing in metallic, organic, and inorganic forms. It is mainly found in nature as the mineral galena (PbS), cerussite (PbCO3) or anglesite (PbSO4), usually in ore with zinc, silver, or copper. (L21)
  • toxin chemical structure pubchem
  • FORMULA: C6H16Pb
  • LAST UPDATE: 28/04/2018

  Health Associations

Mostly focused on Health Implications of Long Term Exposure to this substance

  • SYMPTOMS: Symptions 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)
  • POSSIBLE HEALTH CONSEQUENCES: 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) | 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)
  • ACTION OF TOXIN: 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) | Lead is known to bind ACBP, which is responsible for the regulation of various processes such as acyl-CoA metabolism, GABA-A/benzodiazepine receptor modulation, steroidogenesis, intestinal cholecystokinin release, and insulin secretion. (A21)
  • TOXIN SITES OF ACTION IN CELL: "Cytoplasm", "Extracellular"
  • Additional Exposure Routes:

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