ビスステアリン酸鉛(II)

Metals -> Organic Acids, Metal Salts

Carcinogens

greater than 450 °F (USCG, 1999)

Flash point > 450 °F

Powdery white solid with a slight fatty odor. Sinks in water. (USCG, 1999)

White solid with slight fatty odor; [CAMEO]

Danger

H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]

P203, P260, P261, P264, P270, P271, P273, P280, P301+P317, P304+P340, P317, P318, P319, P330, P391, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 117 reports by companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Danger

H351: Suspected of causing cancer [Warning Carcinogenicity]

Chemical: Octadecanoic acid, lead(2+) salt

Chemical: Octadecanoic acid, lead salt

Restricted substance: Lead distearate

Restricted substance: Octadecanoic acid, lead(2+) salt, basic

Octadecanoic acid, lead(II) salt: Does not have an individual approval but may be used under an appropriate group standard

Octadecanoic acid, lead salt: Does not have an individual approval but may be used as a component in a product covered by a group standard. It is not approved for use as a chemical in its own right.

IMAP assessments - 1:2 Lead(2+) salts of long-chain carboxylic acids: Environment tier II assessment

IMAP assessments - Lead Salts of Selected Fatty Acids: Human health tier II assessment

INHALATION: Joint and muscle pains, headache, dizziness, and insomnia. Weakness, frequently of extensor muscles of hand and wrist (unilateral or bilateral). Heavy contamination - brain damage. Stupor progressing to coma - with or without convulsion, often death. Excitation, confusion and mania less common. Cerebrospinal pressure may be increased. INGESTION: Abdominal pain, diarrhea, constipation, loss of appetite, muscular weakness, headache, blue line on gums, metallic taste, nausea, and vomiting. (USCG, 1999)

LEAD STEARATE has weak oxidizing or reducing powers. Redox reactions can however still occur. The majority of compounds in this class are slightly soluble or insoluble in water. If soluble in water, then the solutions are usually neither strongly acidic nor strongly basic. These compounds are not water-reactive.

Acute Tox. 4 (100%)

Acute toxicity - category 4

Acute toxicity - category 4

Carcinogenicity - Category 1B

Carcinogenicity - Category 2

Carcinogens

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 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)

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)

Organic lead compounds are not classifiable as to their carcinogenicity to humans (Group 3). To the extent that organic lead compounds are metabolized in part to ionic lead, they are expected to exert the toxicities associated with inorganic lead (Group 2A, probably carcinogenic to humans). (L135)

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)