Cocaine

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Advice for firefighters: Wear self contained breathing apparatus for fire fighting if necessary.

Keep container tightly closed in a dry and well-ventilated place.

Cocaine hydrochloride crystals and powder should be stored in well-closed, light-resistant containers; topical solutions of the drug should be stored at 15-30 °C. /Cocaine hydrochloride/

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Contaminated packaging: Dispose of as unused product.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains.

Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Provide appropriate exhaust ventilation at places where dust is formed. Normal measures for preventive fire protection.

Appropriate engineering controls: Avoid contact with skin, eyes and clothing. Wash hands before breaks and immediately after handling the product.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

For more Preventive Measures (Complete) data for Cocaine (6 total), please visit the HSDB record page.

Eye/face protection: Face shield and safety glasses. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).

Skin protection: Handle with gloves.

Body Protection: Complete suit protecting against chemicals. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.

Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face particle respirator type N100 (US) or type P3 (EN 143) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

Cocaine has been measured in its unchanged form in sweat at 33-3579 ng/patch/30 min from heat-induced sweating; 43-3799 ng/wipe and up to 315 ng/patch during one week after nasal doses of 50-126 mg(1). Approximately 1-9% of cocaine passes through the body unchanged, 35-54% is excreted as benzoylecgonine and 32-49% is excreted as ecgonine(2).

The specific treatment of acute cocaine poisoning is the intravenous administration of a short-acting barbiturate or diazepam. Artificial respiration may be necessary. It is important to limit absorption of the drug. If entrance of the drug into circulation can be checked, and respiratory exchange maintained, the prognosis is favorable since cocaine is eliminated fairly rapidly. (L1712)

Substance abuse is a pressing problem with few therapeutic options. The identification of addiction resilience factors is a potential strategy to identify new mechanisms that can be targeted therapeutically. Heparan sulfate (HS) is a linear sulfated polysaccharide that is a component of the cell surface and extracellular matrix. Heparan sulfate modulates the activity and distribution of a set of negatively charged signaling peptides and proteins - known as the HS interactome - by acting as a co-receptor or alternative receptor for growth factors and other signaling peptides and sequestering and localizing them, among other actions. Here, we show that stimulants like cocaine and methamphetamine greatly increase HS content and sulfation levels in the lateral hypothalamus and that HS contributes to the regulation of cocaine seeking and taking. The ability of the HS-binding neuropeptide glial-cell-line-derived neurotrophic factor (GDNF) to increase cocaine intake was potentiated by a deletion that abolished its HS binding. The delivery of heparanase, the endo-beta-D-glucuronidase that degrades HS, accelerated the acquisition of cocaine self-administration and promoted persistent responding during extinction. Altogether, these results indicate that HS is a resilience factor for cocaine abuse and a novel therapeutic target for the treatment of cocaine addiction.

A common combination is heroin and cocaine ("speedball"). Users report an improved euphoria because of the combination, and there is evidence of an interaction because the partial mu opiate agonist buprenorphine reduces cocaine self-administration in animals. Cocaine reduces the signs of opiate withdrawal, and heroin may reduce the irritability seen in chronic cocaine users.

Cocaine and heroin are frequently co-abused by humans, in a combination known as speedball. Recently, chemical interactions between heroin (Her) or its metabolite morphine (Mor) and cocaine (Coc) were described, resulting in the formation of strong adducts. In this work, we evaluated whether combinations of Coc and Her affect the neurotoxicity of these drugs, using rat cortical neurons incubated with Coc, Her, Her followed by Coc (Her+Coc) and Her plus Coc (Her:Coc, 1:1). Neurons exposed to Her, Her+Coc and Her:Coc exhibited a decrease in cell viability, which was more pronounced in neurons exposed to Her and Her+Coc, in comparison with neurons exposed to the mixture (Her:Coc). Cells exposed to the mixture showed increased intracellular calcium and mitochondrial dysfunction, as determined by a decrease in intracellular ATP levels and in mitochondrial membrane potential, displaying both apoptotic and necrotic characteristics. Conversely, a major increase in cytochrome c release, caspase 3-dependent apoptosis, and decreased metabolic neuronal viability were observed upon sequential exposure to Her and Coc. The data show that drug combinations potentiate cortical neurotoxicity and that the mode of co-exposure changes cellular death pathways activated by the drugs, strongly suggesting that chemical interactions occurring in Her:Coc, such as adduct formation, shift cell death mechanisms towards necrosis. Since impairment of the prefrontal cortex is involved in the loss of impulse control observed in drug addicts, the data presented here may contribute to explain the increase in treatment failure observed in speedball abusers.

... Reserpine, dopamine, tricyclic antidepressants, alpha-methyldopa, guanethidine, and monoamine oxidase inhibitors potentiate the adverse effects of cocaine.

For more Interactions (Complete) data for Cocaine (29 total), please visit the HSDB record page.

Cocaine has many serious medical consequences including cardiac arrhythmias, coronary artery spasm and myocardial infarction, cerebrovascular accidents, subarachnoid hemorrhage, seizures, hallucinations, intestinal ischemia, renal infarction, rhabdomyolysis and acute liver injury. Cocaine is a not infrequent cause of sudden “unexplained” death in young adults. Hepatotoxicity usually arises hours to a few days after an acute overdose, generally following or accompanying other major organ involvement. The clinical phenotype of cocaine hepatototoxicity is usually acute hepatic necrosis. Initially, serum aminotransferase and LDH levels are markedly elevated with minimal increase in alkaline phosphatase. The prothrombin time becomes abnormal rapidly and may also reflect disseminated intravascular coagulation (DIC). The serum bilirubin begins to rise after 2 to 3 days. Immunoallergic features and autoantibodies are usually absent. Liver histology usually shows centrolobular (zone 3) necrosis and fatty change, features that resemble ischemic hepatitis or liver injury due to hyperthermia, factors that may partially mediate the hepatotoxic effects of cocaine. In self-limited cases, recovery is rapid and serum aminotransferase levels usually return to normal within 1 to 2 weeks.

TERRESTRIAL FATE: Based on a classification scheme(1), a log Koc value of 2.78(2), indicates that cocaine is expected to have low mobility in soil(SRC). The pKa of cocaine is 8.61(3), indicating that this compound will exist partially in cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization of the cation from moist soil is not expected because cations do not volatilize(SRC). Volatilization of neutral cocaine from moist soil surfaces is not expected(SRC) given an estimated Henry's Law constant of 4.2X10-11 atm-cu m/mole(SRC), based upon its vapor pressure, 1.91X10-7 mm Hg(5), and water solubility, 1800 mg/L(6). Cocaine is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(5). Biodegradation data in soil were not available(SRC, 2017).

AQUATIC FATE: Based on a classification scheme(1), a log Koc value of 2.78(2), indicates that cocaine is expected to adsorb to suspended solids and sediment(SRC). The pKa of cocaine is 8.61 at 15 °C(3), indicating that this compound will exist partially in the in the cation form at pH values of 5 to 9 and, therefore, volatilization from water surfaces of the cation is not expected(SRC). Volatilization from water surfaces of neutral cocaine is not expected(4) based upon an estimated Henry's Law constant of 4.2X10-11 atm-cu m/mole(SRC), derived from its vapor pressure, 1.91X10-7 mm Hg(5), and water solubility, 1800 mg/L(6). Cocaine is not expected to undergo hydrolysis in the environment and has estimated hydrolysis half-lives of 55 and 5.5 years at pH values of 7 and 8, respectively(7). According to a classification scheme(8), an estimated BCF of 15(SRC), from its log Kow of 2.30(9) and a regression-derived equation(10), suggests the potential for bioconcentration in aquatic organisms is low. Biodegradation data in water were not available(SRC, 2017).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), cocaine, which has a vapor pressure of 1.91X10-7 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase cocaine is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 7.3 hours(SRC), calculated from its rate constant of 5.3X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase cocaine may be removed from the air by wet or dry deposition(SRC). Cocaine does not contain chromophores that absorb at wavelengths >290 nm(4) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

IDENTIFICATION AND USE: Cocaine is a semi-synthetic drug obtained from ecgonine, a product of the saponification of coca alkaloids. Cocaine freebase and cocaine hydrochloride are white solid crystals. Street cocaine used by addicts can be mixed with amphetamines, anti-histamines, benzocaine, inositol, lactose, lidocaine, mannitol, opioids, phencyclidine, procaine, sugars, tetracaine, and sometimes arsenic, caffeine, quinidine, and even flour or talc. Cocaine hydrochloride has a very limited use for anesthesia. Cocaine is Schedule II Controlled Substance. HUMAN STUDIES: The target organs are central nervous system (CNS) and the cardio-vascular system. Abuse of cocaine leads to strong psychological dependence. In low doses acute intoxication causes euphoria and agitation. Larger doses cause hyperthermia, nausea, vomiting, abdominal pain, chest pain, tachycardia, ventricular arrhythmia, hypertension, extreme anxiety, agitation, hallucination, and mydriasis. These can be followed by CNS depression with irregular respirations, convulsions, coma, cardiac disturbances, collapse and death. Chronic intoxication produces euphoria, agitation psychomotor, suicidal ideation, anorexia, weight loss, hallucinations and mental deterioration. A withdrawal syndrome with severe psychiatric effects can occur (euphoria, depression). Cocaine causes hyperthermia as a result of two mechanisms: the increase in muscular activity and a direct effect on thermal regulatory centers. The visceral effects on liver and kidney are due to dopaminergic action of cocaine, or its metabolites, or to impurities. The abrupt increase intra-alveolar pressure can cause alveolar rupture and pneumomediastinum. Rhabdomyolysis occurs as a result of several different mechanisms: direct effect on muscle and muscle metabolism, tissue ischemia, the effects of drugs taken with cocaine, such as alcohol and heroin. The principle effects of cocaine are the result of its sympathetic action: cocaine prevents the re-uptake of dopamine and noradrenaline, which accumulate and stimulate neuronal receptors. At the same time, the release of serotonin a sedative neurotransmitter, is inhibited. There may also be a direct effect on peripheral organs. Applied locally, cocaine blocks neuronal transmission: this results in a powerful local anesthetic action at the level of sensory nerve terminals. A recent meta-analysis shows an increase in congenital malformation rate in the offspring of cocaine-users, particularly for abnormalities of the limbs, the genito-urinary tract, and the cardiovascular, neurological, and digestive systems. Patients with choline esterase deficiency may develop severe reactions. ANIMAL STUDIES: Rats given a moderate dose of cocaine show increased locomotor activity and stereotypic behavior. These behaviors are thought to be mediated by the mesolimbic and nigrostriatal dopamine pathways, respectively. In rats exposed to continuous cocaine, persistent changes in acetylcholine and GABA receptors in the caudate were observed 30 days after removal of cocaine pellets, suggesting that they were long lasting or permanent. In contrast to continuous cocaine infusion, daily injections of 20 mg of cocaine for 5 days failed to produce neurodegeneration but did result in behavioral sensitization. Studies with animals demonstrate that cocaine is three times as lethal as heroin. Ninety percent of animals with free access to cocaine are dead in three months, while only 30% of those with free access to heroin are dead in the same amount of time. Monkeys with unlimited access to cocaine will choose it over food until they starve. Cocaine-induced hepatotoxicity was encountered while studying sensitization to the stimulant effects of cocaine. The surface of livers from mice that had received four or five daily injections of 20 mg/kg cocaine had an unusual pitted or roughened appearance. It was found that a single injection of 50 mg/kg cocaine could produce severe fatty necrosis of the liver. Cocaine caused a 36% drop in fetal oxygen partial pressure following a 2 mg/kg dose of cocaine to the ewe, simultaneously, it caused a 25% rise in fetal blood pressure. ECOTOXICITY STUDIES: Cyto-genotoxic effects were evidenced in mussels exposed to crack cocaine concentrations ranging from 5 to 500 ug/L. Exposure to cocaine and its metabolites significantly altered the protein profile of zebrafish embryos, modulating the expression of diverse proteins belonging to different functional classes, including cytoskeleton, eye constituents, lipid transport, lipid and energy metabolism, and stress response. Expression of vitellogenins and crystallins was modulated by cocaine and its main metabolites.

/AQUATIC SPECIES/ Our study aimed to evaluate crack cocaine effects in different life stages of the marine mussel Perna perna. For this purpose, fertilization rate, embryo-larval development, lysosomal membrane stability and DNA strand breaks were assessed. Effect concentrations in gametes and in larval development were found after 1h (IC50=23.53 mg/L) and 48h (IC50=16.31 mg/L), respectively. The highest tested concentration showing no acute toxicity (NOEC) was 10 mg/L, while the lowest observed effect concentration (LOEC) was 20 mg/L. NOEC concerning embryo-larval development was 0.625 mg/L, while the LOEC was 1.25 mg/L. Cyto-genotoxic effects were evidenced in mussels exposed to crack cocaine concentrations ranging from 5 to 500 ug/L. Our results report the first data on effects of an illicit drug to marine organisms and should encourage further ecotoxicological studies of these contaminants of emerging concern in coastal ecosystems.

/AQUATIC SPECIES/ Illicit drugs have been identified as emerging aquatic pollutants because of their widespread presence in freshwaters and potential toxicity towards aquatic organisms. Among illicit drug residues, cocaine (COC) and its main metabolites, namely benzoylecgonine (BE) and ecgonine methyl ester (EME), are commonly detected in freshwaters worldwide at concentration that can induce diverse adverse effects to non-target organisms. However, the information of toxicity and mechanisms of action (MoA) of these drugs, mainly of COC metabolites, to aquatic species is still fragmentary and inadequate. Thus, this study was aimed at investigating the toxicity of two concentrations (0.3 and 1.0 ug/L) of COC, BE and EME similar to those found in aquatic ecosystems on zebrafish (Danio rerio) embryos at 96 hr post fertilization through a functional proteomics approach. Exposure to COC and both its metabolites significantly altered the protein profile of zebrafish embryos, modulating the expression of diverse proteins belonging to different functional classes, including cytoskeleton, eye constituents, lipid transport, lipid and energy metabolism, and stress response. Expression of vitellogenins and crystallins was modulated by COC and both its main metabolites, while only BE and EME altered proteins related to lipid and energy metabolism, as well as to oxidative stress response. Our data confirmed the potential toxicity of low concentrations of COC, BE and EME, and helped to shed light on their MoA on an aquatic vertebrate during early developmental period.

Schedule II shall consist of the drugs and other substances, by whatever official name, common or usual name, chemical name, or brand name designated, listed in this section. Each drug or substance has been assigned the DEA Controlled Substances Code Number set forth opposite it. ... Unless specifically excepted or unless listed in another schedule, any of the following substances whether produced directly or indirectly by extraction from substances of vegetable origin, or independently by means of chemical synthesis, or by a combination of extraction and chemical synthesis: ... (4) Coca leaves (DEA Code Number: 9040) and any salt, compound, derivative or preparation of coca leaves (including cocaine (DEA Code Number: 9041) and ecgonine (DEA Code Number: 9180) and their salts, isomers, derivatives and salts of isomers and derivatives), and any salt, compound, derivative, or preparation thereof which is chemically equivalent or identical with any of these substances, except that the substances shall not include: (i) decocainized coca leaves or extraction of coca leaves, which extractions do not contain cocaine or ecgonine; or (ii) [123I]ioflupane.

Extracted from the leaves of coca shrubs indigenous to South America; Used as local anesthetic (nasal and ophthalmic) and vasoconstrictor for otolaryngology procedures; [HSDB] Used as a controlled substance in medicine and dentistry, usually as the hydrochloride compound; [Hawley] A popular drug of abuse; [Olson, p. 201]

Cocaine (DEA Code Number: 9041) is a Schedule II controlled substance.

Schedule II Controlled Substance: (A) The drug or other substance has a high potential for abuse; (B) The drug or other substance has a currently accepted medical use in treatment in the United States or a currently accepted medical use with severe restrictions; and (C) Abuse of the drug or other substances may lead to severe psychological or physical dependence.

Anesthetics, Local; Vasoconstrictor Agents; Dopamine Uptake Inhibitors

MEDICATION

Cocaine (KOE-kane) is a local anesthetic. It is applied to certain areas of the body (for example, the nose, mouth, or throat) to cause loss of feeling. This allows some kinds of examinations or surgery to be done without causing pain. (L1505)

The purity of crack is generally higher, but depends not only on the purity of the cocaine used in its manufacture, but also on the method of production. Common adulterants of cocaine are phenacetin, lignocaine, benzocaine, procaine, caffeine, paracetamol and sugars. Some of these may be removed in the production of crack. Occasionally, unusual additives have been reported, such as atropine, diltiazem and other pharmaceutical substances. The free base constitutes 89% of the hydrochloride salt.

... The National Household Survey in 1992 indicated that approximately 22.6 million people have tried cocaine, five million within the last year before the survey (down from 12 million in 1985 and 8 million in 1988), and 1.3 million used it at least once within the month before the survey. ... The number of people who have used cocaine in the last 30 days /was/ 5.8 million in 1985 and 1.6 million in 1990 to 1.3 million in 1992. ... The number of people using cocaine on a daily or weekly basis is rising. Of the current three million regular users, about 500,000 use crack (freebase cocaine).

... Most addicts are male, under the age of 40, and use multiple drugs (75%). ... Eighty-four percent of persons diagnosed with cocaine dependence also met the criteria for alcohol dependence. A history of marijuana use was reported by 98% of cocaine addicts.

Annual /cocaine/ drug use in young adults age 18-25: 8.1% (1974), 7.0% (1976), 10.2% (1977), 19.6% (1979), 18.8% (1982), 16.3% (1985), 12.1% (1988), and 7.5% (1990) /From table/

Annual /cocaine/ drug use in adults age 26 and over: 0.6% (1976), 0.9% (1977), 2.0% (1979), 3.8% (1982), 4.2% (1985), 2.7% (1988), and 2.4% (1990) /From table/

For more Consumption Patterns (Complete) data for Cocaine (7 total), please visit the HSDB record page.

Crack is manufactured from cocaine hydrochloride by one of two main methods: either microwaving a wet mixture with sodium bicarbonate or by adding alkali to a hot saturated solution of cocaine and allowing the denser base to settle and solidify.

Free base is made by dissolving cocaine salt in an aqueous alkaline solution and then extracting the free base form with a solvent such as ether.

Dried coca leaves contain up to 1% cocaine. They are processed into cocaine hydrochloride in clandestine laboratories. The leaves are moistened with lime water or other alkali and extracted with kerosene (paraffin). The dissolved cocaine is extracted from the kerosene with sulfuric acid to produce an aqueous solution of cocaine sulfate. This solution is neutralised with lime, causing cocaine base (coca paste) to precipitate. Coca paste is redissolved in sulfuric acid and potassium permanganate is added to destroy cinnamoylcocaine and other impurities. The filtered solution is again treated with alkali to precipitate the free base, which is dissolved in acetone or other solvents. Concentrated hydrochloric acid is added to the solution, causing cocaine hydrochloride to settle out as a solid residue.

Extracted from the leaves of several South American shrubs of the genus Erythroxylon, especially E. coca.

Topical, solution 4% Cocaine Hydrochloride Topical Solution (C-II); 10% Cocaine Hydrochloride Topical Solution (C-II). /Cocaine hydrochloride/

Common street names include: Coca, Coke, Crack, Flake, Snow, and Soda Cot.

Cocaine is usually distributed as a white, crystalline powder. Cocaine is often diluted ("cut") with a variety of substances, the most common of which are sugars and local anesthetics. It is "cut" to stretch the amount of the product and increase profits for dealers. In contrast, cocaine base (crack) looks like small, irregularly shaped chunks (or "rocks") of a whitish solid.

Cocaine purchased on the street may contain adulterant drugs such as lidocaine or benzocaine or stimulants such as caffeine, methamphetamine, ephedrine, and phencyclidine. Most illicit cocaine in the United States is adulterated with levamisole, an antiparasitic drug that can cause agranulocytosis.

For more Formulations/Preparations (Complete) data for Cocaine (14 total), please visit the HSDB record page.

The cocaine manufacturing process takes place in remote jungle labs where the raw product undergoes a series of chemical transformations. Colombia produces about 90 percent of the cocaine powder reaching the United States. Most of the cocaine entering the United States comes through Mexico.

Crack is cocaine hydrochloride powder that has been processed to form a rock crystal that is then usually smoked.

Cocaine is one of at least 14 alkaloids extracted from the leaves of two coca shrubs indigenous to South America. ... The small leaves (5 cm) /of Erythroxylum coca/, which contain between 0.5% & 2.0% (avg 1%) cocaine, are harvested in March, June, & November. This plant is the main source of illicit cocaine trade. The leaves are soaked in gasoline drums containing alkali, sulfuric acid, kerosene, & other solvents. Later, the fluid & leaves are discarded, leaving a thick brown paste (coca paste) which is sold to clandestine laboratories. There the paste is refined into white crystalline powder containing cocaine hydrochloride.

Sterile oily solutions are prepared aseptically. In the preparation of oily solutions of cocaine only a mild degree of heat should be used.

For more General Manufacturing Information (Complete) data for Cocaine (15 total), please visit the HSDB record page.