


Cocaine chemical structure

IUPAC name
CAS number
ATC code

N01BC01 ., ., .

Chemical formula {{{chemical_formula}}}
Molecular weight 303.353 g/mol
Bioavailability Oral: 33%[1]
Insufflated: 60[2]–80%[3]
Nasal Spray: 25[4]–43%[1]
Metabolism Hepatic CYP3A4
Elimination half-life 1 hour
Excretion Renal (benzoylecgonine and ecgonine methyl ester)
Pregnancy category C
Legal status {{{legal_status}}}
Routes of administration Topical, Oral, Insufflation, IV, PO

Cocaine (benzoylmethylecgonine) (INN) is a crystalline tropane alkaloid that is obtained from the leaves of the coca plant.[5] The name comes from "coca" in addition to the alkaloid suffix -ine, forming cocaine. It is a stimulant of the central nervous system, an appetite suppressant, and a topical anesthetic. Specifically, it is a serotonin–norepinephrine–dopamine reuptake inhibitor, which mediates functionality of these neurotransmitters as an exogenous catecholamine transporter ligand. Because of the way it affects the mesolimbic reward pathway, cocaine is addictive.[6]



Medical effects[edit | edit source]


Data from The Lancet suggests cocaine is ranked both the 2nd most addictive and the 2nd most harmful of 20 popular recreational drugs.[7]

Cocaine is a powerful nervous system stimulant.[8] Its effects can last from 15–30 minutes to an hour, depending upon the method of ingestion.[9]

Cocaine increases alertness, feelings of well-being and euphoria, energy and motor activity, feelings of competence and sexuality. Athletic performance may be enhanced in sports where sustained attention and endurance is required. Anxiety, paranoia and restlessness are also frequent. With excessive dosage, tremors, convulsions and increased body temperature are observed.[8]

Occasional cocaine use does not typically lead to severe or even minor physical or social problems.[10][11]

Acute[edit | edit source]

Template:Refimprove section

Main article: Cocaine intoxication

With excessive or prolonged use, the drug can cause itching, tachycardia, hallucinations, and paranoid delusions—though the latter two are mostly attributed to extreme sleep deprivation. Overdoses cause tachyarrhythmias and a marked elevation of blood pressure, which can be life-threatening.

Chronic[edit | edit source]

File:Side effects of chronic use of Cocaine.png

Side effects of chronic cocaine use

File:Cocaine hydrochloride CII for medicinal use.jpg

Cocaine hydrochloride

Chronic cocaine intake causes brain cells to adapt functionally to strong imbalances of transmitter levels in order to compensate extremes. Thus, receptors disappear from the cell surface or reappear on it, resulting more or less in an "off" or "working mode" respectively, or they change their susceptibility for binding partners (ligands) – mechanisms called down-/upregulation. However, studies suggest cocaine abusers do not show normal age-related loss of striatal dopamine transporter (DAT) sites, suggesting cocaine has neuroprotective properties for dopamine neurons.[12] The experience of insatiable hunger, aches, insomnia/oversleeping, lethargy, and persistent runny nose are often described as very unpleasant. Depression with suicidal ideation may develop in very heavy users. Finally, a loss of vesicular monoamine transporters, neurofilament proteins, and other morphological changes appear to indicate a long term damage of dopamine neurons. All these effects contribute a rise in tolerance thus requiring a larger dosage to achieve the same effect.[13]

The lack of normal amounts of serotonin and dopamine in the brain is the cause of the dysphoria and depression felt after the initial high. Physical withdrawal is not dangerous, and is in fact restorative. Physiological changes caused by cocaine withdrawal include vivid and unpleasant dreams, insomnia or hypersomnia, increased appetite and psychomotor retardation or agitation.[14]

Physical side effects from chronic smoking of cocaine include hemoptysis, bronchospasm, pruritus, fever, diffuse alveolar infiltrates without effusions, pulmonary and systemic eosinophilia, chest pain, lung trauma, sore throat, asthma, hoarse voice, dyspnea (shortness of breath), and an aching, flu-like syndrome. A common but untrue belief is that the smoking of cocaine chemically breaks down tooth enamel and causes tooth decay. However, cocaine does often cause involuntary tooth grinding, known as bruxism, which can deteriorate tooth enamel and lead to gingivitis.[15] Additionally, stimulants like cocaine, methamphetamine, and even caffeine cause dehydration and dry mouth. Since saliva is an important mechanism in maintaining one's oral pH level, chronic stimulant abusers who do not hydrate sufficiently may experience demineralization of their teeth due to the pH of the tooth surface dropping too low (below 5.5).


Cocaine may also greatly increase this risk of developing rare autoimmune or connective tissue diseases such as lupus, Goodpasture's disease, vasculitis, glomerulonephritis, Stevens–Johnson syndrome and other diseases.[17][18][19][20] It can also cause a wide array of kidney diseases and renal failure.[21][22]

Cocaine abuse doubles both the risks of hemorrhagic and ischemic strokes,[23] as well as increases the risk of other infarctions, such as myocardial infarction.[24]

Addiction[edit | edit source]

Main article: Cocaine dependence


Biosynthesis[edit | edit source]

Main article: Biosynthesis of cocaine

The first synthesis and elucidation of the cocaine molecule was by Richard Willstätter in 1898.[25] Willstätter's synthesis derived cocaine from tropinone. Since then, Robert Robinson and Edward Leete have made significant contributions to the mechanism of the synthesis.

Biosynthesis of N-methyl-pyrrolinium cation[edit | edit source]

File:Biosynthesis of N-methyl-pyrrolinium cation.png

Biosynthesis of N-methyl-pyrrolinium cation

File:Biosynthesis of cocaine.png

Biosynthesis of cocaine

File:Robinson biosynthesis of tropane.png

Robinson biosynthesis of tropane

File:Reduction of tropinone.png

Reduction of tropinone


Biosynthesis of cocaine[edit | edit source]

The additional carbon atoms required for the synthesis of cocaine are derived from acetyl-CoA, by addition of two acetyl-CoA units to the N-methyl-Δ1-pyrrolinium cation.[28] The first addition is a Mannich-like reaction with the enolate anion from acetyl-CoA acting as a nucleophile towards the pyrrolinium cation. The second addition occurs through a Claisen condensation. This produces a racemic mixture of the 2-substituted pyrrolidine, with the retention of the thioester from the Claisen condensation. In formation of tropinone from racemic ethyl [2,3-13C2]4(Nmethyl-2-pyrrolidinyl)-3-oxobutanoate there is no preference for either stereoisomer.[29] In the biosynthesis of cocaine, however, only the (S)-enantiomer can cyclize to form the tropane ring system of cocaine. The stereoselectivity of this reaction was further investigated through study of prochiral methylene hydrogen discrimination.[30] This is due to the extra chiral center at C-2.[31] This process occurs through an oxidation, which regenerates the pyrrolinium cation and formation of an enolate anion, and an intramolecular Mannich reaction. The tropane ring system undergoes hydrolysis, SAM-dependent methylation, and reduction via NADPH for the formation of methylecgonine. The benzoyl moiety required for the formation of the cocaine diester is synthesized from phenylalanine via cinnamic acid.[32] Benzoyl-CoA then combines the two units to form cocaine.

Robert Robinson's acetonedicarboxylate[edit | edit source]

The biosynthesis of the tropane alkaloid, however, is still uncertain. Hemscheidt proposes that Robinson's acetonedicarboxylate emerges as a potential intermediate for this reaction.[33] Condensation of N-methylpyrrolinium and acetonedicarboxylate would generate the oxobutyrate. Decarboxylation leads to tropane alkaloid formation.

Reduction of tropinone[edit | edit source]


Pharmacology[edit | edit source]

Appearance[edit | edit source]


A pile of cocaine hydrochloride


A piece of compressed cocaine powder

Cocaine in its purest form is a white, pearly product. Cocaine appearing in powder form is a salt, typically cocaine hydrochloride (CAS 53-21-4). Street market cocaine is frequently adulterated or “cut” with various powdery fillers to increase its weight; the substances most commonly used in this process are baking soda; sugars, such as lactose, dextrose, inositol, and mannitol; and local anesthetics, such as lidocaine or benzocaine, which mimic or add to cocaine's numbing effect on mucous membranes. Cocaine may also be "cut" with other stimulants such as methamphetamine.[36] Adulterated cocaine is often a white, off-white or pinkish powder.


Forms of cocaine[edit | edit source]

Salts[edit | edit source]


Basic[edit | edit source]

Main article: Freebase (chemistry)


Smoking freebase cocaine has the additional effect of releasing methylecgonidine into the user's system due to the pyrolysis of the substance (a side effect which insufflating or injecting powder cocaine does not create). Some research suggests that smoking freebase cocaine can be even more cardiotoxic than other routes of administration[37] because of methylecgonidine's effects on lung tissue[38] and liver tissue.[39]

Pure cocaine is prepared by neutralizing its compounding salt with an alkaline solution which will precipitate to non-polar basic cocaine. It is further refined through aqueous-solvent Liquid-liquid extraction.

Crack cocaine[edit | edit source]

Main article: Crack cocaine
File:Smoking Crack.jpg

A woman smoking crack cocaine


The "freebase" and "crack" forms of cocaine are usually administered by vaporization of the powdered substance into smoke, which is then inhaled.[40] The origin of the name "crack" comes from the "crackling" sound (and hence the onomatopoeic moniker “crack”) that is produced when the cocaine and its impurities (i.e. water, sodium bicarbonate) are heated past the point of vaporization.[41] Pure cocaine base/crack is easy to smoke because it vaporizes smoothly, with little or no decomposition at around 98 degrees Centigrade,[citation needed][dubious] which is below the boiling point of water. The smoke produced from cocaine base is usually described as having a very distinctive, pleasant taste.

In contrast, cocaine hydrochloride does not vaporize until heated to a much higher temperature (about 197 degrees Centigrade), and considerable decomposition/burning occurs at these high temperatures. This effectively destroys some of the cocaine, and yields a sharp, acrid, and foul-tasting smoke.


Coca leaf infusions[edit | edit source]


It has been promoted as an adjuvant for the treatment of cocaine dependence. In one controversial study, coca leaf infusion was used -in addition to counseling- to treat 23 addicted coca-paste smokers in Lima, Peru. Relapses fell from an average of four times per month before treatment with coca tea to one during the treatment. The duration of abstinence increased from an average of 32 days prior to treatment to 217 days during treatment. These results suggest that the administration of coca leaf infusion plus counseling would be an effective method for preventing relapse during treatment for cocaine addiction.[42] Importantly, these results also suggest strongly that the primary pharmacologically active metabolite in coca leaf infusions is actually cocaine and not the secondary alkaloids.


Routes of administration[edit | edit source]

Oral[edit | edit source]

File:Crack Crack.JPG


Many users rub the powder along the gum line, or onto a cigarette filter which is then smoked, which numbs the gums and teeth – hence the colloquial names of "numbies", "gummers" or "cocoa puffs" for this type of administration. This is mostly done with the small amounts of cocaine remaining on a surface after insufflation. Another oral method is to wrap up some cocaine in rolling paper and swallow (parachute) it. This is sometimes called a "snow bomb."

Coca leaf[edit | edit source]

Coca leaves are typically mixed with an alkaline substance (such as lime) and chewed into a wad that is retained in the mouth between gum and cheek (much in the same as chewing tobacco is chewed) and sucked of its juices. The juices are absorbed slowly by the mucous membrane of the inner cheek and by the gastrointestinal tract when swallowed. Alternatively, coca leaves can be infused in liquid and consumed like tea. Ingesting coca leaves generally is an inefficient means of administering cocaine. Advocates of the consumption of the coca leaf state that coca leaf consumption should not be criminalized as it is not actual cocaine, and consequently it is not properly the illicit drug. Because cocaine is hydrolyzed and rendered inactive in the acidic stomach, it is not readily absorbed when ingested alone. Only when mixed with a highly alkaline substance (such as lime) can it be absorbed into the bloodstream through the stomach. The efficiency of absorption of orally administered cocaine is limited by two additional factors. First, the drug is partly catabolized by the liver. Second, capillaries in the mouth and esophagus constrict after contact with the drug, reducing the surface area over which the drug can be absorbed. Nevertheless, cocaine metabolites can be detected in the urine of subjects that have sipped even one cup of coca leaf infusion. Therefore, this is an actual additional form of administration of cocaine, albeit an inefficient one.


Contrary to popular belief, both ingestion and insufflation result in approximately the same proportion of the drug being absorbed: 30 to 60%. Compared to ingestion, the faster absorption of insufflated cocaine results in quicker attainment of maximum drug effects. Snorting cocaine produces maximum physiological effects within 40 minutes and maximum psychotropic effects within 20 minutes, however, a more realistic activation period is closer to 5 to 10 minutes, which is similar to ingestion of cocaine. Physiological and psychotropic effects from nasally insufflated cocaine are sustained for approximately 40–60 minutes after the peak effects are attained.[43]

Mate de coca or coca-leaf infusion is also a traditional method of consumption and is often recommended in coca producing countries, like Peru and Bolivia, to ameliorate some symptoms of altitude sickness. This method of consumption has been practiced for many centuries by the native tribes of South America. One specific purpose of ancient coca leaf consumption was to increase energy and reduce fatigue in messengers who made multi-day quests to other settlements.

In 1986 an article in the Journal of the American Medical Association revealed that U.S. health food stores were selling dried coca leaves to be prepared as an infusion as “Health Inca Tea.”[44] While the packaging claimed it had been "decocainized," no such process had actually taken place. The article stated that drinking two cups of the tea per day gave a mild stimulation, increased heart rate, and mood elevation, and the tea was essentially harmless. Despite this, the DEA seized several shipments in Hawaii, Chicago, Illinois, Georgia, and several locations on the East Coast of the United States, and the product was removed from the shelves.

Insufflation[edit | edit source]

File:Man sniffing.jpg

A man sniffing cocaine

Nasal insufflation (known colloquially as "snorting," "sniffing," or "blowing") is the most common method of ingestion of recreational powdered cocaine in the Western world. The drug coats and is absorbed through the mucous membranes lining the sinuses. When insufflating cocaine, absorption through the nasal membranes is approximately 30–60%, with higher doses leading to increased absorption efficiency. Any material not directly absorbed through the mucous membranes is collected in mucus and swallowed (this "drip" is considered pleasant by some and unpleasant by others). In a study[45] of cocaine users, the average time taken to reach peak subjective effects was 14.6 minutes. Any damage to the inside of the nose is because cocaine highly constricts blood vessels – and therefore blood and oxygen/nutrient flow – to that area. Nosebleeds after cocaine insufflation are due to irritation and damage of mucus membranes by foreign particles and adulterants and not the cocaine itself; as a vasoconstrictor, cocaine acts to reduce bleeding.

Prior to insufflation, cocaine powder must be divided into very fine particles. Cocaine of high purity breaks into fine dust very easily, except when it is moist (not well stored) and forms "chunks," which reduces the efficiency of nasal absorption.


A study by Bonkovsky and Mehta[47] reported that, just like shared needles, the sharing of straws used to "snort" cocaine can spread blood diseases such as Hepatitis C.

In the United States, as far back as 1992 many of the people sentenced by federal authorities for charges related to powder cocaine were Hispanic American; more Hispanics than non-Hispanic White and non-Hispanic Black people received sentences for crimes related to powder cocaine.[48]

Injection[edit | edit source]

Drug injection provides the highest blood levels of drug in the shortest amount of time. Subjective effects not commonly shared with other methods of administration include a ringing in the ears moments after injection (usually when in excess of 120 milligrams) lasting 2 to 5 minutes including tinnitus & audio distortion. This is colloquially referred to as a "bell ringer".[49] In a study[45] of cocaine users, the average time taken to reach peak subjective effects was 3.1 minutes. The euphoria passes quickly. Aside from the toxic effects of cocaine, there is also danger of circulatory emboli from the insoluble substances that may be used to cut the drug. As with all injected illicit substances, there is a risk of the user contracting blood-borne infections if sterile injecting equipment is not available or used. Additionally, because cocaine is a vasoconstrictor, and usage often entails multiple injections within several hours or less, subsequent injections are progressively more difficult to administer, which in turn may lead to more injection attempts and more sequelae from improperly performed injection.

An injected mixture of cocaine and heroin, known as “speedball” is a particularly dangerous combination, as the converse effects of the drugs actually complement each other, but may also mask the symptoms of an overdose. It has been responsible for numerous deaths, including celebrities such as John Belushi, Chris Farley, Mitch Hedberg, River Phoenix and Layne Staley.


Inhalation[edit | edit source]

See also: Crack cocaine

Inhalation or smoking is one of the several means cocaine is administered. Cocaine is smoked by inhaling the vapor by sublimating solid cocaine by heating.[51] In a 2000 Brookhaven National Laboratory medical department study, based on self reports of 32 abusers who participated in the study,"peak high" was found at mean of 1.4min +/- 0.5 minutes.[45]

Smoking freebase or crack cocaine is most often accomplished using a pipe made from a small glass tube, often taken from "Love roses," small glass tubes with a paper rose that are promoted as romantic gifts.[52] These are sometimes called "stems", "horns", "blasters" and "straight shooters". A small piece of clean heavy copper or occasionally stainless steel scouring pad – often called a "brillo" (actual Brillo pads contain soap, and are not used), or "chore", named for Chore Boy brand copper scouring pads, – serves as a reduction base and flow modulator in which the "rock" can be melted and boiled to vapor. Crack smokers also sometimes smoke through a soda can with small holes in the bottom.




Suppository[edit | edit source]


Physical mechanisms[edit | edit source]


Cocaine binds directly to the DAT1 transporter, inhibiting reuptake with more efficacy than amphetamines which phosphorylate it causing internalization; instead primarily releasing DAT (which cocaine does not do) and only inhibiting its reuptake as a secondary, and much more minor, mode of action than cocaine and in another manner: from the opposite conformation/orientation to DAT.

The pharmacodynamics of cocaine involve the complex relationships of neurotransmitters (inhibiting monoamine uptake in rats with ratios of about: serotonin:dopamine = 2:3, serotonin:norepinephrine = 2:5[53]) The most extensively studied effect of cocaine on the central nervous system is the blockade of the dopamine transporter protein. Dopamine transmitter released during neural signaling is normally recycled via the transporter; i.e., the transporter binds the transmitter and pumps it out of the synaptic cleft back into the presynaptic neuron, where it is taken up into storage vesicles. Cocaine binds tightly at the dopamine transporter forming a complex that blocks the transporter's function. The dopamine transporter can no longer perform its reuptake function, and thus dopamine accumulates in the synaptic cleft. This results in an enhanced and prolonged postsynaptic effect of dopaminergic signaling at dopamine receptors on the receiving neuron. Prolonged exposure to cocaine, as occurs with habitual use, leads to homeostatic dysregulation of normal (i.e. without cocaine) dopaminergic signaling via down-regulation of dopamine receptors and enhanced signal transduction. The decreased dopaminergic signaling after chronic cocaine use may contribute to depressive mood disorders and sensitize this important brain reward circuit to the reinforcing effects of cocaine (for example, enhanced dopaminergic signalling only when cocaine is self-administered). This sensitization contributes to the intractable nature of addiction and relapse.

Dopamine-rich brain regions such as the ventral tegmental area, nucleus accumbens, and prefrontal cortex are frequent targets of cocaine addiction research. Of particular interest is the pathway consisting of dopaminergic neurons originating in the ventral tegmental area that terminate in the nucleus accumbens. This projection may function as a "reward center", in that it seems to show activation in response to drugs of abuse like cocaine in addition to natural rewards like food or sex.[54] While the precise role of dopamine in the subjective experience of reward is highly controversial among neuroscientists, the release of dopamine in the nucleus accumbens is widely considered to be at least partially responsible for cocaine's rewarding effects. This hypothesis is largely based on laboratory data involving rats that are trained to self-administer cocaine. If dopamine antagonists are infused directly into the nucleus accumbens, well-trained rats self-administering cocaine will undergo extinction (i.e. initially increase responding only to stop completely) thereby indicating that cocaine is no longer reinforcing (i.e. rewarding) the drug-seeking behavior.

Cocaine's effects on serotonin (5-hydroxytryptamine, 5-HT) show across multiple serotonin receptors, and is shown to inhibit the re-uptake of 5-HT3 specifically as an important contributor to the effects of cocaine. The overabundance of 5-HT3 receptors in cocaine conditioned rats display this trait, however the exact effect of 5-HT3 in this process is unclear.[55] The 5-HT2 receptor (particularly the subtypes 5-HT2AR, 5-HT2BR and 5-HT2CR) show influence in the evocation of hyperactivity displayed in cocaine use.[56]

In addition to the mechanism shown on the above chart, cocaine has been demonstrated to bind as to directly stabilize the DAT transporter on the open outward-facing conformation whereas other stimulants (namely phenethylamines) stabilize the closed conformation. Further, cocaine binds in such a way as to inhibit a hydrogen bond innate to DAT that otherwise still forms when amphetamine and similar molecules are bound. Cocaine's binding properties are such that it attaches so this hydrogen bond will not form and is blocked from formation due to the tightly locked orientation of the cocaine molecule. Research studies have suggested that the affinity for the transporter is not what is involved in habituation of the substance so much as the conformation and binding properties to where & how on the transporter the molecule binds.[57]

Sigma receptors are affected by cocaine, as cocaine functions as a sigma ligand agonist.[58] Further specific receptors it has been demonstrated to function on are NMDA and the D1 dopamine receptor.[59]

Cocaine also blocks sodium channels, thereby interfering with the propagation of action potentials; thus, like lignocaine and novocaine, it acts as a local anesthetic. It also functions on the binding sites to the dopamine and serotonin sodium dependent transport area as targets as separate mechanisms from its reuptake of those transporters; unique to its local anesthetic value which makes it in a class of functionality different from both its own derived phenyltropanes analogues which have that removed and the amphetamine class of stimulants which as well altogether lack that. In addition to this cocaine has some target binding to the site of the Kappa-opioid receptor as well.[60] Cocaine also causes vasoconstriction, thus reducing bleeding during minor surgical procedures. The locomotor enhancing properties of cocaine may be attributable to its enhancement of dopaminergic transmission from the substantia nigra. Recent research points to an important role of circadian mechanisms[61] and clock genes[62] in behavioral actions of cocaine.

Because nicotine increases the levels of dopamine in the brain, many cocaine users find that consumption of tobacco products during cocaine use enhances the euphoria. This, however, may have undesirable consequences, such as uncontrollable chain smoking during cocaine use (even users who do not normally smoke cigarettes have been known to chain smoke when using cocaine), in addition to the detrimental health effects and the additional strain on the cardiovascular system caused by tobacco.


Metabolism and excretion[edit | edit source]

Cocaine is extensively metabolized, primarily in the liver, with only about 1% excreted unchanged in the urine. The metabolism is dominated by hydrolytic ester cleavage, so the eliminated metabolites consist mostly of benzoylecgonine (BE), the major metabolite, and other significant metabolites in lesser amounts such as ecgonine methyl ester (EME) and ecgonine. Further minor metabolites of cocaine include norcocaine, p-hydroxycocaine, m-hydroxycocaine, p-hydroxybenzoylecgonine (pOHBE), and m-hydroxybenzoylecgonine.[64] These do not include metabolites created beyond the standard metabolism of the drug in the human body, like for example by the process of pyrolysis such as is the case with methylecgonidine; or the binding of other exogenous subsumed chemicals in administration concurrently with any constituent cocaine molecule conformation in vivo to be enumerated within the user as a conditionate dependant on tertiary measures to form as a novel metabolite too vast in potential instances to account for beyond the tertiary measure of their otherwise notability.


If consumed with alcohol, cocaine combines with alcohol in the liver to form cocaethylene. Studies have suggested cocaethylene is both more euphorigenic, and has a higher cardiovascular toxicity than cocaine by itself.[65][66][67]

A study in mice has suggested that capsaicin found in pepper spray may interact with cocaine with potentially fatal consequences. The method through which they would interact however, is not known.[68][69]

Detection in biological fluids[edit | edit source]


Cocaine as a local anesthetic[edit | edit source]

Cocaine was historically useful as a topical anesthetic in eye and nasal surgery, although it is now predominantly used for nasal and lacrimal duct surgery. The major disadvantages of this use are cocaine's intense vasoconstrictor activity and potential for cardiovascular toxicity. Cocaine has since been largely replaced in Western medicine by synthetic local anesthetics such as benzocaine, proparacaine, lignocaine/xylocaine/lidocaine, and tetracaine though it remains available for use if specified. If vasoconstriction is desired for a procedure (as it reduces bleeding), the anesthetic is combined with a vasoconstrictor such as phenylephrine or epinephrine. In Australia it is currently prescribed for use as a local anesthetic for conditions such as mouth and lung ulcers. Some ENT specialists occasionally use cocaine within the practice when performing procedures such as nasal cauterization. In this scenario dissolved cocaine is soaked into a ball of cotton wool, which is placed in the nostril for the 10–15 minutes immediately prior to the procedure, thus performing the dual role of both numbing the area to be cauterized and also vasoconstriction. Even when used this way, some of the used cocaine may be absorbed through oral or nasal mucosa and give systemic effects.

In 2005, researchers from Kyoto University Hospital proposed the use of cocaine in conjunction with phenylephrine administered in the form of an eye drop as a diagnostic test for Parkinson's disease.[71]

History[edit | edit source]


Coca leaf[edit | edit source]

File:Folha de coca.jpg

Coca leaf in Bolivia


When the Spanish arrived in South America, most at first ignored aboriginal claims that the leaf gave them strength and energy, and declared the practice of chewing it the work of the Devil. But after discovering that these claims were true, they legalized and taxed the leaf, taking 10% off the value of each crop.[74] In 1569, Nicolás Monardes described the practice of the natives of chewing a mixture of tobacco and coca leaves to induce "great contentment":


In 1609, Padre Blas Valera wrote:


Isolation and naming[edit | edit source]

Although the stimulant and hunger-suppressant properties of coca had been known for many centuries, the isolation of the cocaine alkaloid was not achieved until 1855. Various European scientists had attempted to isolate cocaine, but none had been successful for two reasons: the knowledge of chemistry required was insufficient at the time. [citation needed] Additionally contemporary conditions of sea-shipping from South America could degrade the cocaine in the plant samples available to Europeans. [citation needed]




The first synthesis and elucidation of the structure of the cocaine molecule was by Richard Willstätter in 1898.[25] The synthesis started from tropinone, a related natural product and took five steps.

Medicalization[edit | edit source]


File:Cocaine for kids.gif

Used for dental pain in children


Carl Koller (a close associate of Sigmund Freud, who would write about cocaine later) experimented with cocaine for ophthalmic usage. In an infamous experiment in 1884, he experimented upon himself by applying a cocaine solution to his own eye and then pricking it with pins. His findings were presented to the Heidelberg Ophthalmological Society. Also in 1884, Jellinek demonstrated the effects of cocaine as a respiratory system anesthetic. In 1885, William Halsted demonstrated nerve-block anesthesia,[80] and James Corning demonstrated peridural anesthesia.[81] 1898 saw Heinrich Quincke use cocaine for spinal anesthesia.

Today, cocaine has very limited medical use. See the section Cocaine as a local anesthetic

Popularization[edit | edit source]

Pope Leo XIII purportedly carried a hipflask of the coca-treated Vin Mariani with him, and awarded a Vatican gold medal to Angelo Mariani.[82]









During the mid-1940s, amidst WWII, cocaine was considered for inclusion as an ingredient of a future generation of 'pep pills' for the German military code named D-IX.[85]

Prohibition[edit | edit source]

By the turn of the 20th century, the addictive properties of cocaine had become clear, and perceived problems with cocaine use began to capture public attention in the United States. The dangers of cocaine use became part of a moral panic that was tied to the dominant racial and social anxieties of the day. In 1903, the American Journal of Pharmacy stressed that most cocaine abusers were "bohemians, gamblers, high- and low-class prostitutes, night porters, bell boys, burglars, racketeers, pimps, and casual laborers." In 1914, Dr. Christopher Koch of Pennsylvania's State Pharmacy Board made the racial innuendo explicit, testifying that, “Most of the attacks upon the white women of the South are the direct result of a cocaine-crazed Negro brain." Mass media manufactured an epidemic of cocaine use among African Americans in the Southern United States to play upon racial prejudices of the era, though there is little evidence that such an epidemic actually took place. In the same year, the Harrison Narcotics Tax Act outlawed the sale and distribution of cocaine in the United States. This law incorrectly referred to cocaine as a narcotic, and the misclassification passed into popular culture. As stated above, cocaine is a stimulant, not a narcotic. Although technically illegal for purposes of distribution and use, the distribution, sale and use of cocaine was still legal for registered companies and individuals. Because of the misclassification of cocaine as a narcotic, the debate is still open on whether the government actually enforced these laws strictly. Cocaine was not considered a controlled substance in the United States until 1970, when it was listed in the Controlled Substances Act. Until that point, the use of cocaine was open and rarely prosecuted in the US due to the moral and physical debates commonly discussed.

Modern usage[edit | edit source]



The estimated U.S. cocaine market exceeded $70 billion in street value for the year 2005, exceeding revenues by corporations such as Starbucks.[86][87] There is a tremendous demand for cocaine in the U.S. market, particularly among those who are making incomes affording luxury spending, such as single adults and professionals with discretionary income. Cocaine’s status as a club drug shows its immense popularity among the "party crowd".


It was reported in October 2010 that the use of cocaine in Australia has doubled since monitoring began in 2003.[89]

A problem with illegal cocaine use, especially in the higher volumes used to combat fatigue (rather than increase euphoria) by long-term users, is the risk of ill effects or damage caused by the compounds used in adulteration. Cutting or "stepping on" the drug is commonplace, using compounds which simulate ingestion effects, such as Novocain (procaine) producing temporary anesthaesia as many users believe a strong numbing effect is the result of strong and/or pure cocaine, ephedrine or similar stimulants that are to produce an increased heart rate. The normal adulterants for profit are inactive sugars, usually mannitol, creatine or glucose, so introducing active adulterants gives the illusion of purity and to 'stretch' or make it so a dealer can sell more product than without the adulterants.[citation needed] The adulterant of sugars therefore allows the dealer to sell the product for a higher price because of the illusion of purity and allows to sell more of the product at that higher price, enabling dealers to make a lot of revenue with little cost of the adulterants. Cocaine trading carries large penalties in most jurisdictions, so user deception about purity and consequent high profits for dealers are the norm.[original research?]

A study by the European Monitoring Centre for Drugs and Drug Addiction in 2007 showed that the purity levels for street purchased cocaine was often under 5% and on average under 50% pure.[90]

Society and culture[edit | edit source]

Legal status[edit | edit source]

Main article: Legal status of cocaine

The production, distribution and sale of cocaine products is restricted (and illegal in most contexts) in most countries as regulated by the Single Convention on Narcotic Drugs, and the United Nations Convention Against Illicit Traffic in Narcotic Drugs and Psychotropic Substances. In the United States the manufacture, importation, possession, and distribution of cocaine is additionally regulated by the 1970 Controlled Substances Act.

Some countries, such as Peru and Bolivia permit the cultivation of coca leaf for traditional consumption by the local indigenous population, but nevertheless prohibit the production, sale and consumption of cocaine. In addition, some parts of Europe and Australia allow processed cocaine for medicinal uses only.

Interdiction[edit | edit source]


Illicit trade[edit | edit source]


Production[edit | edit source]

Colombia is the world's leading producer of cocaine.[92] Three-quarters of the world's annual yield of cocaine has been produced in Colombia, both from cocaine base imported from Peru (primarily the Huallaga Valley) and Bolivia, and from locally grown coca. There was a 28% increase from the amount of potentially harvestable coca plants which were grown in Colombia in 1998. This, combined with crop reductions in Bolivia and Peru, made Colombia the nation with the largest area of coca under cultivation after the mid-1990s. Coca grown for traditional purposes by indigenous communities, a use which is still present and is permitted by Colombian laws, only makes up a small fragment of total coca production, most of which is used for the illegal drug trade.

An interview with a coca farmer published in 2003 described a mode of production by acid-base extraction that has changed little since 1905. Roughly 625 pounds of leaves were harvested per hectare, six times per year. The leaves were dried for half a day, then chopped into small pieces with a strimmer and sprinkled with a small amount of powdered cement (replacing sodium carbonate from former times). Several hundred pounds of this mixture was soaked in Template:Convert/USgalTemplate:Convert/test/A of gasoline for a day, then the gasoline was removed and the leaves were pressed for remaining liquid, after which they could be discarded. Then battery acid (weak sulfuric acid) was used, one bucket per 25 kilograms of leaves, to create a phase separation in which the cocaine free base in the gasoline was acidified and extracted into a few buckets of "murky-looking smelly liquid". Once powdered caustic soda was added to this, the cocaine precipitated and could be removed by filtration through a cloth. The resulting material, when dried, was termed pasta and sold by the farmer. The 3750 pound yearly harvest of leaves from a hectare produced Template:Convert/LoffAonDbSoffTemplate:Convert/test/Aon of pasta, approximately 40–60% cocaine. Repeated recrystallization from solvents, producing pasta lavada and eventually crystalline cocaine, were performed at specialized laboratories after the sale.[93]


The cultivation of coca has become an attractive, and in some cases even necessary, economic decision on the part of many growers due to the combination of several factors, including the persistence of worldwide demand, the lack of other employment alternatives, the lower profitability of alternative crops in official crop substitution programs, the eradication-related damages to non-drug farms, and the spread of new strains of the coca plant.

Synthesis[edit | edit source]

Synthetic cocaine would be highly desirable to the illegal drug industry, as it would eliminate the high visibility and low reliability of offshore sources and international smuggling, replacing them with clandestine domestic laboratories, as are common for illicit methamphetamine. However, natural cocaine remains the lowest cost and highest quality supply of cocaine. Actual full synthesis of cocaine is rarely done. Formation of inactive enantiomers (cocaine has 4 chiral centres – 1R,2R,3S,5S – hence a total potential of 16 possible enantiomers and disteroisomers) plus synthetic by-products limits the yield and purity. Names like "synthetic cocaine" and "new cocaine" have been misapplied to phencyclidine (PCP) and various designer drugs.

Trafficking and distribution[edit | edit source]


Cocaine smuggled in a charango, 2008

Organized criminal gangs operating on a large scale dominate the cocaine trade. Most cocaine is grown and processed in South America, particularly in Colombia, Bolivia, Peru, and smuggled into the United States and Europe, the United States being the worlds largest consumer of cocaine,[94] where it is sold at huge markups; usually in the US at $80–$120 for 1 gram, and $250–300 for 3.5 grams (1/8 of an ounce, or an "eight ball").

Caribbean and Mexican routes[edit | edit source]



Chilean route[edit | edit source]


Techniques[edit | edit source]

Cocaine is also carried in small, concealed, kilogram quantities across the border by couriers known as “mules” (or “mulas”), who cross a border either legally, for example, through a port or airport, or illegally elsewhere. The drugs may be strapped to the waist or legs or hidden in bags, or hidden in the body. If the mule gets through without being caught, the gangs will reap most of the profits. If he or she is caught however, gangs will sever all links and the mule will usually stand trial for trafficking alone.


Sophisticated drug subs are the latest tool drug runners are using to bring cocaine north from Colombia, it was reported on March 20, 2008. Although the vessels were once viewed as a quirky sideshow in the drug war, they are becoming faster, more seaworthy, and capable of carrying bigger loads of drugs than earlier models, according to those charged with catching them.[96]

Sales to consumers[edit | edit source]


Cocaine adulterated with fruit flavoring

Cocaine is readily available in all major countries' metropolitan areas. According to the Summer 1998 Pulse Check, published by the U.S. Office of National Drug Control Policy, cocaine use had stabilized across the country, with a few increases reported in San Diego, Bridgeport, Miami, and Boston. In the West, cocaine usage was lower, which was thought to be due to a switch to methamphetamine among some users; methamphetamine is cheaper, three and a half times more powerful, lasts 12 to 24 times longer with each dose and is known to cause neurotoxicity while cocaine is not.[97][98] Nevertheless, the number of cocaine users remain high, with a large concentration among urban youth.

In addition to the amounts previously mentioned, cocaine can be sold in "bill sizes": for example, $10 might purchase a "dime bag," a very small amount (0.1–0.15 g) of cocaine. Twenty dollars might purchase 0.15–0.3 g. However, in lower Texas, it is sold cheaper due to it being easier to receive: a dime for $10 is 0.4g, a 20 is 0.8–1.0 gram and a 8-ball (3.5g) is sold for $60 to $80 dollars, depending on the quality and dealer. These amounts and prices are very popular among young people because they are inexpensive and easily concealed on one's body. Quality and price can vary dramatically depending on supply and demand, and on geographic region.[99]


Consumption[edit | edit source]



Cocaine adulterants[edit | edit source]

Template:Refimprove section Cocaine is "cut" with many substances such as:

Usage[edit | edit source]


In the United States[edit | edit source]

General usage[edit | edit source]

Cocaine is the second most popular illegal recreational drug in the U.S. (behind marijuana)[105] and the U.S. is the world's largest consumer of cocaine.[94] Cocaine is commonly used in middle to upper class communities. It is also popular amongst college students, as a party drug. Its users span over different ages, races, and professions. In the 1970s and 1980s, the drug became particularly popular in the disco culture as cocaine usage was very common and popular in many discos such as Studio 54.

The National Household Survey on Drug Abuse (NHSDA) reported in 1999 that cocaine was used by 3.7 million Americans, or 1.7% of the household population age 12 and older. Estimates of the current number of those who use cocaine regularly (at least once per month) vary, but 1.5 million is a widely accepted figure within the research community. In 2001, more Hispanics received sentences for crimes relating to powder cocaine than any other ethnicity while more African Americans were convicted of crimes relating to crack cocaine in the United States.[106]

Although cocaine use had not significantly changed over the six years prior to 1999, the number of first-time users went up from 574,000 in 1991, to 934,000 in 1998 – an increase of 63%. While these numbers indicated that cocaine is still widely present in the United States, its use was significantly less prevalent than during the early 1980s.

Usage among youth[edit | edit source]

The 1999 Monitoring the Future (MTF) survey found the proportion of American students reporting use of powdered cocaine rose during the 1990s. In 1991, 2.3% of eighth-graders stated that they had used cocaine in their lifetime. This figure rose to 4.7% in 1999. For the older grades, increases began in 1992 and continued through the beginning of 1999. Between those years, lifetime use of cocaine went from 3.3% to 7.7% for tenth-graders and from 6.1% to 9.8% for high school seniors. Lifetime use of crack cocaine, according to MTF, also increased among eighth-, tenth-, and twelfth-graders, from an average of 2% in 1991 to 3.9% in 1999.

Perceived risk and disapproval of cocaine and crack use both decreased during the 1990s at all three grade levels. The 1999 NHSDA found the highest rate of monthly cocaine use was for those aged 18–25 at 1.7%, an increase from 1.2% in 1997. Rates declined between 1996 and 1998 for ages 26–34, while rates slightly increased for the 12–17 and 35+ age groups. Studies also show people are experimenting with cocaine at younger ages. NHSDA found a steady decline in the mean age of first use from 23.6 years in 1992 to 20.6 years in 1998.

In Europe[edit | edit source]

General usage[edit | edit source]

Cocaine is the second most popular illegal recreational drug in Europe (behind marijuana). Since the mid-1990s, overall cocaine usage in Europe has been on the rise, but usage rates and attitudes tend to vary between countries. Countries with the highest usage rates are: The United Kingdom, Spain, Italy, and Ireland.


Usage among young adults[edit | edit source]

About 3.5 million or 87.5% of those who have used the drug in the last year are young adults (15–34 years old). Usage is particularly prevalent among this demographic: 4% to 7% of males have used cocaine in the last year in Spain, Denmark, Ireland, Italy, and the United Kingdom. The ratio of male to female users is approximately 3.8:1, but this statistic varies from 1:1 to 13:1 depending on country.[107]

See also[edit | edit source]

References[edit | edit source]

  1. 1.0 1.1 Fattinger K, Benowitz NL, Jones RT, Verotta D (2000). Nasal mucosal versus gastrointestinal absorption of nasally administered cocaine. Eur. J. Clin. Pharmacol. 56 (4): 305–10.
  2. Barnett G, Hawks R, Resnick R (1981). Cocaine pharmacokinetics in humans. J Ethnopharmacol 3 (2–3): 353–66.
  3. Jeffcoat AR, Perez-Reyes M, Hill JM, Sadler BM, Cook CE (1989). Cocaine disposition in humans after intravenous injection, nasal insufflation (snorting), or smoking. Drug Metab. Dispos. 17 (2): 153–9.
  4. Wilkinson P, Van Dyke C, Jatlow P, Barash P, Byck R (1980). Intranasal and oral cocaine kinetics. Clin. Pharmacol. Ther. 27 (3): 386–94.
  6. Fattore L, Piras G, Corda MG, Giorgi O (2009). The Roman high- and low-avoidance rat lines differ in the acquisition, maintenance, extinction, and reinstatement of intravenous cocaine self-administration. Neuropsychopharmacology 34 (5): 1091–101.
  7. PMID 17382831 (PMID 17382831)
  8. 8.0 8.1 World Health Organization (2004). Neuroscience of psychoactive substance use and dependence
  9. World Health Organization (2007). International medical guide for ships
  10. includeonly>Goldacre, Ben. "Cocaine study that got up the nose of the US", Bad Science, The Guardian, June 2008. – re. International study on cocaine executed by the World Health Organization.
  12. (2002) Biological Psychiatry By H. A. H. D'haenen, Johan A. den Boer, Paul Willner, Books.google.com. URL accessed 2010-03-09.
  13. Lowinson, Joyce, H; Ruiz, Pedro. Millman, Robert B. (2004). Substance abuse: a comprehensive textbook, Lippincott Williams & Wilkins; Fourth edition. URL accessed May 9, 2011.
  15. Baigent, Michael (2003). Physical complications of substance abuse: what the psychiatrist needs to know. Curr Opin Psychiatry 16 (3): 291–296.
  16. Pagliaro, Louis; Ann Marie Pagliaro (2004). Pagliaros’ Comprehensive Guide to Drugs and Substances of Abuse, Washington, D.C.: American Pharmacists Association.
  17. Scienceblog.com. URL accessed on 2007-07-10.
  18. Trozak D, Gould W (1984). Cocaine abuse and connective tissue disease. J Am Acad Dermatol 10 (3).
  19. Ramón Peces (1999). Antiglomerular Basement Membrane Antibody-Mediated Glomerulonephritis after Intranasal Cocaine Use. Nephron 81 (4): 434–438.
  20. Moore PM, Richardson B (1998). Neurology of the vasculitides and connective tissue diseases. J. Neurol. Neurosurg. Psychiatr. 65 (1): 10–22.
  21. Jared A. Jaffe (2006). Chronic Nephropathies of Cocaine and Heroin Abuse: A Critical Review. Clinical Journal of the American Society of Nephrology 1 (4): 655–67.
  22. Fokko J. van der Woude (2000). Cocaine use and kidney damage. Nephrology Dialysis Transplantation 15 (3): 299–301.
  23. Susan Jeffrey and Charles Vega. Stimulant Abuse May Increase Stroke Among Young Adults. URL accessed on 2011-02-06.
  24. Vasica G, Tennant CC (2002). Cocaine use and cardiovascular complications. Med. J. Aust. 177 (5): 260–2.
  25. 25.0 25.1 Humphrey AJ, O'Hagan D (2001). Tropane alkaloid biosynthesis. A century old problem unresolved. Nat Prod Rep 18 (5): 494–502.
  26. Leete E, Marion L, Sspenser ID (1954). Biogenesis of hyoscyamine. Nature 174 (4431): 650–1.
  27. Robins RJ, Waltons NJ, Hamill JD, Parr AJ, Rhodes MJ (1991). Strategies for the genetic manipulation of alkaloid-producing pathways in plants. Planta Med. 57 (7 Suppl): S27–35.
  28. Dewick, P. M. (2009). Medicinal Natural Products, Chicester: Wiley-Blackwell.
  29. R. J. Robins, T. W. Abraham, A. J. Parr, J. Eagles and N. J. Walton (1997). The Biosynthesis of Tropane Alkaloids in Datura stramonium: The Identity of the Intermediates between N-Methylpyrrolinium Salt and Tropinone. J. Am. Chem. Soc. 119 (45).
  30. Hoye TR, Bjorklund JA, Koltun DO, Renner MK (2000). N-methylputrescine oxidation during cocaine biosynthesis: study of prochiral methylene hydrogen discrimination using the remote isotope method. Org. Lett. 2 (1): 3–5.
  31. E. Leete, J. A. Bjorklund, M. M. Couladis and S. H. Kim (1991). Late intermediates in the biosynthesis of cocaine: 4-(1-methyl-2-pyrrolidinyl)-3-oxobutanoate and methyl ecgonine. J. Am. Chem. Soc. 113 (24).
  32. E. Leete, J. A. Bjorklund and S. H. Kim (1988). The biosynthesis of the benzoyl moiety of cocaine. Phytochemistry 27 (8).
  33. T. Hemscheidt (2000). Tropane and Related Alkaloids. Top. Curr. Chem. 209.
  34. A. Portsteffen, B. Draeger and A. Nahrstedt (1992). Two tropinone reducing enzymes from Datura stramonium transformed root cultures. Phytochemistry 31 (4).
  35. Boswell HD, Dräger B, McLauchlan WR (1999). Specificities of the enzymes of N-alkyltropane biosynthesis in Brugmansia and Datura. Phytochemistry 52 (5): 871–8.
  36. Psychedelic Chemistry: Cocaine. URL accessed on 2007-07-10.
  37. (2003-10-15) Pharmacokinetics and Pharmacodynamics of Methylecgonidine, a Crack Cocaine Pyrolyzate. Journal of Pharmacology and Experimental Therapeutics 307 (3): 1179–87.
  38. Yang Y, Ke Q, Cai J, Xiao YF, Morgan JP (2001). Evidence for cocaine and methylecgonidine stimulation of M2 muscarinic receptors in cultured human embryonic lung cells. Br. J. Pharmacol. 132 (2): 451–60.
  39. Fandiño AS, Toennes SW, Kauert GF (2002). Studies on hydrolytic and oxidative metabolic pathways of anhydroecgonine methyl ester (methylecgonidine) using microsomal preparations from rat organs. Chem. Res. Toxicol. 15 (12): 1543–8.
  40. "Substances – Cocaine" The Steinhardt School of Culture, Education, and Human Development. Retrieved August 2009.
  41. George, Nelson. "Hip Hop America". 1998. Viking Penguin.(Page 40)
  42. Teobaldo, Llosa (1994). The Standard Low Dose of Oral Cocaine: Used for Treatment of Cocaine Dependence. Substance Abuse 15 (4): 215–220.[dead link]
  43. (1981). Cocaine pharmacokinetics in humans. Journal of ethnopharmacology 3 (2–3): 353–66.; Jones, supra note 19; Wilkinson et al., Van Dyke et al.
  44. Siegel RK, Elsohly MA, Plowman T, Rury PM, Jones RT (January 3, 1986). Cocaine in herbal tea. Journal of the American Medical Association 255 (1).
  45. 45.0 45.1 45.2 Nora D. Volkow (2000). Effects of route of administration on cocaine induced dopamine transporter blockade in the human brain. Life Sciences 67 (12): 1507–1515.
  46. cesar.umd.edu – Cocaine terminology
  47. Bonkovsky HL, Mehta S (2001). Hepatitis C: a review and update. J. Am. Acad. Dermatol. 44 (2): 159–82.
  48. White Powder Cocaine No Longer Just for Yuppies – Summer House. URL accessed on 2011-02-06.
  49. Bell ringer. Urban Dictionary. URL accessed on 2010-03-09.
  50. Dimitrijevic N, Dzitoyeva S, Manev H (2004). An automated assay of the behavioral effects of cocaine injections in adult Drosophila. J Neurosci Methods 137 (2): 181–184.
  51. Appendix B: Production of Cocaine Hydrochloride and Cocaine Base, US Justice Dep.
  52. includeonly>Margaret Reist. "A rose by another name: crack pipe", January 16, 2005. Retrieved on 2009-08-21.
  53. Rothman, et al. "Amphetamine-Type Central Nervous System Stimulants Release Norepinepehrine more Potently than they Release Dopamine and Serotonin." (2001): Synapse 39, 32–41 (Table V. on page 37)
  54. Spanagel R, Weiss F (1999). The dopamine hypothesis of reward: past and current status. Trends Neurosci. 22 (11): 521–7.
  55. Carta M, Allan AM, Partridge LD, Valenzuela CF (2003). Cocaine inhibits 5-HT3 receptor function in neurons from transgenic mice overexpressing the receptor. Eur. J. Pharmacol. 459 (2–3): 167–9.
  56. Filip M, Bubar MJ, Cunningham KA (2004). Contribution of serotonin (5-hydroxytryptamine; 5-HT) 5-HT2 receptor subtypes to the hyperlocomotor effects of cocaine: acute and chronic pharmacological analyses. J. Pharmacol. Exp. Ther. 310 (3): 1246–54.
  57. Beuming T (2008). The binding sites for cocaine and dopamine in the dopamine transporter overlap. Nature Neuroscience 11 (7): 780–9.
  58. Sigma Receptors Play Role In Cocaine-induced Suppression Of Immune System. Sciencedaily.com. URL accessed on 2010-03-09.
  59. Lluch J, Rodríguez-Arias M, Aguilar MA, Miñarro J (2005). Role of dopamine and glutamate receptors in cocaine-induced social effects in isolated and grouped male OF1 mice. Pharmacol. Biochem. Behav. 82 (3): 478–87.
  60. Drugbank website "drug card", "(DB00907)" for Cocaine: Giving ten targets of the molecule in vivo, including dopamine/serotonin sodium channel affinity & K-opioid affinity. Drugbank.ca. URL accessed on 2010-03-09.
  62. McClung C, Sidiropoulou K, Vitaterna M, Takahashi J, White F, Cooper D, Nestler E (2005). Regulation of dopaminergic transmission and cocaine reward by the Clock gene. Proc Natl Acad Sci USA 102 (26): 9377–81.
  63. Carey RJ, Damianopoulos EN, Shanahan AB (2008). Cocaine effects on behavioral responding to a novel object placed in a familiar environment. Pharmacol. Biochem. Behav. 88 (3): 265–71.
  64. Kolbrich EA, Barnes AJ, Gorelick DA, Boyd SJ, Cone EJ, Huestis MA (2006). Major and minor metabolites of cocaine in human plasma following controlled subcutaneous cocaine administration. J Anal Toxicol 30 (8): 501–10.
  65. Wilson LD, Jeromin J, Garvey L, Dorbandt A (2001). Cocaine, ethanol, and cocaethylene cardiotoxity in an animal model of cocaine and ethanol abuse. Acad Emerg Med 8 (3): 211–22.
  66. Pan WJ, Hedaya MA (1999). Cocaine and alcohol interactions in the rat: effect of cocaine and alcohol pretreatments on cocaine pharmacokinetics and pharmacodynamics. J Pharm Sci 88 (12): 1266–74.
  67. Hayase T, Yamamoto Y, Yamamoto K (1999). Role of cocaethylene in toxic symptoms due to repeated subcutaneous cocaine administration modified by oral doses of ethanol. J Toxicol Sci 24 (3): 227–35.
  68. includeonly>Barley, Shanta. "Cocaine and pepper spray – a lethal mix?", New Scientist, 13 November 2009. Retrieved on 2009-11-14.
  69. Mendelson, John E. (October 2, 2009). Capsaicin, an active ingredient in pepper sprays, increases the lethality of cocaine. Forensic Toxicology.
  70. R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 9th edition, Biomedical Publications, Seal Beach, CA, 2011, pp. 390–394.
  71. Sawada, H. (2005-02-23). Cocaine and Phenylephrine Eye Drop Test for Parkinson Disease. JAMA the Journal of the American Medical Association 293 (8): 932–4.
  72. Altman AJ, Albert DM, Fournier GA (1985). Cocaine's use in ophthalmology: our 100-year heritage. Surv Ophthalmol 29 (4): 300–6.
  73. Gay GR, Inaba DS, Sheppard CW, Newmeyer JA (1975). Cocaine: history, epidemiology, human pharmacology, and treatment. a perspective on a new debut for an old girl. Clin. Toxicol. 8 (2): 149–78.
  74. includeonly>"Drug that spans the ages: The history of cocaine", The Independent (UK), 2006. Retrieved on 2010-04-30.
  75. Monardes, Nicholas; Translated into English by J. Frampton (1925). Joyfull Newes out of the Newe Founde Worlde, New York, NY: Alfred Knopf.
  76. F. Gaedcke (1855). Ueber das Erythroxylin, dargestellt aus den Blättern des in Südamerika cultivirten Strauches Erythroxylon Coca. Archiv der Pharmazie 132 (2): 141–150.
  77. 77.0 77.1 Albert Niemann (1860). Ueber eine neue organische Base in den Cocablättern. Archiv der Pharmazie 153 (2): 129–256.
  78. Template:OEtymD
  79. Yentis SM, Vlassakov KV (1999). Vassily von Anrep, forgotten pioneer of regional anesthesia. Anesthesiology 90 (3): 890–5.
  80. Halsted W (1885). Practical comments on the use and abuse of cocaine. New York Medical Journal 42: 294–295.
  81. Corning JL (1885). An experimental study. New York Medical Journal 42.
  82. Experience Vin Mariani today | Grupo Mariani S.A. Cocanaturally.com. URL accessed on 2011-01-15.
  84. Streatfeild, Dominic (2003). Cocaine: An Unauthorized Biography, Picador.
  85. Jeevan Vasagar: cocaine-based "wonder drug" tested on concentration camp inmates. Amphetamines.com. URL accessed on 2011-01-15.
  86. Apple Sanity – Fetish – Blow: War on Drugs VS. Cocaine. Web.archive.org. URL accessed on 2011-11-13.
  87. Cocaine Market. Havocscope.com. URL accessed on 2010-03-09.[dead link]
  88. WHO/UNICRI (1995). WHO Cocaine Project.[dead link]
  89. includeonly>"Cocaine use doubles in a decade", Sydney Morning Herald, 15 October 2010. Retrieved on 19 October 2010.
  90. EMCDDA (2007). EMCDDA Retail Cocaine Purity Study.
  91. (2006) "Cocaine: Seizures, 1998–2003" World Drug Report 2006 (PDF), New York: United Nations.
  92. Colombia. CIA World Factbook
  93. Dominic Streatfeild (2003). Cocaine: An Unauthorized Biography, Macmillan.
  94. 94.0 94.1 Field Listing – Illicit drugs (by country). Cia.gov. URL accessed on 2011-01-15.
  95. Jacobson, Robert. "Illegal Drugs: America's Anguish". Farmington Hills, MI: Thomson Gale, 2006
  96. includeonly>"Coast Guard hunts drug-running semi-subs", CNN, 2008-03-20. Retrieved on 2008-03-20.
  97. Meth Info | The Meth Project[dead link]
  98. Drugs of Abuse | City of Denison Iowa. Denisonia.com. URL accessed on 2011-11-13.
  99. "Pricing powder", The Economist, June 28, 2007, Prices: USA around $110/g, Israel/ Germany/ Britain around $46/g, Colombia $2/g, New Zealand recordbreaking $714.30/g.
  100. European Monitoring Centre for Drugs and Drug Addiction (2008). Annual report: the state of the drugs problem in Europe, Luxembourg: Office for Official Publications of the European Communities.
  101. The Cocaine Threat: A Hemispheric Perspective (PDF), United States Department of Defense. [dead link]
  102. United Nations (June 2010). World Drug Report 2010, United Nations Publications.
  103. (2009). Agranulocytosis associated with cocaine use – four States, March 2008 – November 2009. MMWR Morb. Mortal. Wkly. Rep. 58 (49): 1381–5.
  104. 104.0 104.1 (2007) World Drug Report 2007 (PDF), New York: United Nations., p243.
  105. erowid.org. URL accessed on 2007-07-10.
  106. RJHresearch.com[dead link]
  107. (2008) The State of the Drugs Problem in Europe 2008 (PDF), 58–62, Luxembourg: European Monitoring Centre for Drugs and Drug Addiction.

Further reading[edit | edit source]

  • Feiling, Tom, The Candy Machine: How Cocaine Took Over the World, Penguin, 2009 (published in the United States as Cocaine Nation: How the White Trade Took Over the World. Pegasus Books, 2010)

External links[edit | edit source]

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