Cocaine, also known as coke, is a strong stimulant mostly used as a
recreational drug. It is commonly snorted, inhaled as smoke, or as
a solution injected into a vein. Mental effects may include loss of
contact with reality, an intense feeling of happiness, or
agitation. Physical symptoms may include a fast heart rate,
sweating, and large pupils. High doses can result in very high
blood pressure or body temperature. Effects begin within seconds
to minutes of use and last between five and ninety minutes. Cocaine
has a small number of accepted medical uses such as numbing and
decreasing bleeding during nasal surgery.
Cocaine is addictive due to its effect on the reward pathway in the
brain. After a short period of use, there is a high risk that
dependence will occur. Its use also increases the risk of stroke,
myocardial infarction, lung problems in those who smoke it, blood
infections, and sudden cardiac death.
Cocaine sold on the
street is commonly mixed with local anesthetics, cornstarch, quinine,
or sugar, which can result in additional toxicity. Following
repeated doses a person may have decreased ability to feel pleasure
and be very physically tired.
Cocaine acts by inhibiting the reuptake of serotonin, norepinephrine,
and dopamine. This results in greater concentrations of these
three neurotransmitters in the brain. It can easily cross the
blood–brain barrier and may lead to the breakdown of the
Cocaine is a naturally occurring substance found in
the coca plant which is mostly grown in South America. In 2013, 419
kilograms were produced legally. It is estimated that the illegal
market for cocaine is 100 to 500 billion USD each year. With
further processing crack cocaine can be produced from cocaine.
After cannabis, cocaine is the most frequently used illegal drug
globally. Between 14 and 21 million people use the drug each
year. Use is highest in North America followed by Europe and South
America. Between one and three percent of people in the developed
world have used cocaine at some point in their life. In 2013
cocaine use directly resulted in 4,300 deaths, up from 2,400 in
1990. The leaves of the coca plant have been used by Peruvians
since ancient times.
Cocaine was first isolated from the leaves in
1860. Since 1961 the international Single Convention on Narcotic
Drugs has required countries to make recreational use of cocaine a
2 Adverse effects
2.4 Dependence and withdrawal
2.5 During pregnancy
4.2.3 Crack cocaine
Coca leaf infusions
4.3.1 N-methyl-pyrrolinium cation
4.3.2 Robert Robinson's acetonedicarboxylate
4.3.3 Reduction of tropinone
4.4 Detection in body fluids
5.2 United States
6.2 Isolation and naming
6.5 Modern usage
7 Society and culture
7.1 Legal status
7.1.2 United States
7.3.3 Trafficking and distribution
220.127.116.11 Caribbean and Mexican routes
18.104.22.168 Chilean route
7.3.4 Sales to consumers
9 See also
12 Further reading
13 External links
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Topical cocaine can be used as a local numbing agent to help with
painful procedures in the mouth or nose. TAC is one such
formulation used for pediatrics.
Cocaine is now predominantly used for nasal and lacrimal duct surgery.
The major disadvantages of this use are cocaine's potential for
cardiovascular toxicity, glaucoma, and pupil dilation. Medicinal
use of cocaine has decreased as other synthetic local anesthetics such
as benzocaine, proparacaine, lidocaine, and tetracaine are now used
more often. If vasoconstriction is desired for a procedure (as it
reduces bleeding), the anesthetic is combined with a vasoconstrictor
such as phenylephrine or epinephrine. 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 before the procedure,
thus performing the dual role of both numbing the area to be
cauterized, and vasoconstriction. Even when used this way, some of the
used cocaine may be absorbed through oral or nasal mucosa and give
systemic effects. An alternative method of
administration for ENT surgery is mixed with adrenaline and sodium
bicarbonate, as Moffett's solution.
Cocaine is a powerful nervous system stimulant. Its effects can
last from fifteen or thirty minutes to an hour. The duration of
cocaine's effects depends on the amount taken and the route of
Cocaine can be in the form of fine white powder,
bitter to the taste. When inhaled or injected, it causes a numbing
Crack cocaine is a smokeable form of cocaine made into small
"rocks" by processing cocaine with sodium bicarbonate (baking soda)
Crack cocaine is referred to as "crack" because of
the crackling sounds it makes when heated.
Cocaine use leads to increases in alertness, feelings of well-being
and euphoria, increased energy and motor activity, and increased
feelings of competence and sexuality.
A spoon containing baking soda, cocaine, and a small amount of water.
Used in a "poor-man's" crack-cocaine production
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
(snorting). Another oral method is to wrap up some cocaine in rolling
paper and swallow (parachute) it.
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 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
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.
Orally administered cocaine takes approximately 30 minutes to
enter the bloodstream. Typically, only a third of an oral dose is
absorbed, although absorption has been shown to reach 60% in
controlled settings. Given the slow rate of absorption, maximum
physiological and psychotropic effects are attained approximately
60 minutes after cocaine is administered by ingestion. While the
onset of these effects is slow, the effects are sustained for
approximately 60 minutes after their peak is attained.[citation
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.
Physiological and psychotropic effects from
nasally insufflated cocaine are sustained for approximately
40–60 minutes after the peak effects are attained.
Coca tea, an infusion of coca leaves, is also a traditional method of
consumption. The tea has often been recommended for travelers in the
Andes to prevent altitude sickness. However, its actual
effectiveness has never been systematically studied. This method
of consumption has been practised for many centuries by the indigenous
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." 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, Georgia, and several
locations on the East Coast of the United States, and the product was
removed from the shelves.
Lines of cocaine prepared for insufflation
Nasal insufflation (known colloquially as "snorting", "sniffing", or
"blowing") is a common method of ingestion of recreational powdered
cocaine. The drug coats and is absorbed through the mucous
membranes lining the nasal passages. Cocaine's desired euphoric
effects are delayed when snorted through the nose by about five
minutes. This occurs because cocaine's absorption is slowed by its
constricting effect on the blood vessels of the nose. Insufflation
of cocaine also leads to the longest duration of its effects (60–90
minutes). 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 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
Rolled up banknotes, hollowed-out pens, cut straws, pointed ends of
keys, specialized spoons, long fingernails, and (clean) tampon
applicators are often used to insufflate cocaine. Such devices are
often called "tooters" by users. The cocaine typically is poured onto
a flat, hard surface (such as a mirror, CD case or book) and divided
into "bumps", "lines" or "rails", and then insufflated. The amount
of cocaine in a line varies widely from person to person and occasion
to occasion (the purity of the cocaine is also a factor), but one line
is generally considered to be a single dose and is typically
35 mg (a "bump") to 100 mg (a "rail").[dubious – discuss]
As tolerance builds rapidly in the short-term (hours), many lines are
often snorted to produce greater effects. A 2001
study reported that the sharing of straws used to "snort" cocaine can
spread blood diseases such as hepatitis C.
Drug injection by turning the drug into a solution 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 and audio distortion. This is
colloquially referred to as a "bell ringer". In a study 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 consequences from improperly performed
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 comedians/actors
John Belushi and Chris Farley,
Mitch Hedberg, River Phoenix, grunge singer
Layne Staley and actor
Philip Seymour Hoffman. Experimentally, cocaine injections can be
delivered to animals such as fruit flies to study the mechanisms of
See also: Crack cocaine
Inhalation by smoking cocaine is one of the several ways the drug is
consumed. The onset of cocaine's desired euphoric effects is fastest
with inhaling cocaine and begins after 3–5 seconds. In contrast,
inhalation of cocaine leads to the shortest duration of its effects
(5–15 minutes). The two main ways cocaine is smoked are
freebasing and by using cocaine which has been converted to smokable
Cocaine is smoked by inhaling the vapor produced when
solid cocaine is heated to the point that it sublimates. 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.
of cocaine that occur only when heated/smoked have been shown to
change the effect profile, i.e. anhydroecgonine methyl ester when
co-administered with cocaine increases the dopamine in CPu and NAc
brain regions, and has M1- and M3- receptor affinity.
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. 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 on the side or bottom.[citation
needed] Crack is smoked by placing it at the end of the pipe; a flame
held close to it produces vapor, which is then inhaled by the smoker.
The effects, felt almost immediately after smoking, are very intense
and do not last long – usually 2 to 10 minutes. When
smoked, cocaine is sometimes combined with other drugs, such as
cannabis, often rolled into a joint or blunt. Powdered cocaine is also
sometimes smoked, though heat destroys much of the chemical; smokers
often sprinkle it on cannabis. The language referring
to paraphernalia and practices of smoking cocaine vary, as do the
packaging methods in the street level sale.
Another way users consume cocaine is by making it into a suppository
which they then insert into the anus or vagina. The drug is then
absorbed by the membranes of these body parts. Little research has
been focused on the suppository (anal or vaginal insertion) method of
administration, also known as "plugging". This method of
administration is commonly administered using an oral syringe. Cocaine
can be dissolved in water and withdrawn into an oral syringe which may
then be lubricated and inserted into the anus or vagina before the
plunger is pushed. Anecdotal evidence of its effects is infrequently
discussed, possibly due to social taboos in many cultures. The rectum
and the vaginal canal is where the majority of the drug would be taken
up through the membranes lining its walls.
With excessive or prolonged use, the drug can cause itching, fast
heart rate, hallucinations, and paranoid delusions. Overdoses
cause hyperthermia and a marked elevation of blood pressure, which can
be life-threatening, arrhythmias, and death.
Anxiety, paranoia, and restlessness can also occur, especially during
the comedown. With excessive dosage, tremors, convulsions and
increased body temperature are observed. Severe cardiac adverse
events, particularly sudden cardiac death, become a serious risk at
high doses due to cocaine's blocking effect on cardiac sodium
Timeline of number of yearly U.S. overdose deaths involving
Opioid involvement in cocaine overdose deaths. Red line represents the
number of cocaine deaths that also involved opioids, and the purple
line represents cocaine deaths that did not involve opioids.
Delphic analysis regarding 20 popular recreational drugs based on
Cocaine was ranked the 2nd in dependence and physical
harm and 3rd in social harm.
Side effects of chronic cocaine use
Chronic cocaine intake causes 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 downregulation
and 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. Possible side effects include insatiable hunger, aches,
insomnia/oversleeping, lethargy, and persistent runny nose. 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. 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.
Physiological changes caused by
cocaine withdrawal include vivid and unpleasant dreams, insomnia or
hypersomnia, increased appetite and psychomotor retardation or
Physical side effects from chronic smoking of cocaine include coughing
up blood, bronchospasm, itching, 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.
Cocaine constricts blood
vessels, dilates pupils, and increases body temperature, heart rate,
and blood pressure. It can also cause headaches and gastrointestinal
complications such as abdominal pain and nausea. 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. 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 use also
promotes the formation of blood clots. This increase in blood clot
formation is attributed to cocaine-associated increases in the
activity of plasminogen activator inhibitor, and an increase in the
number, activation, and aggregation of platelets.
Chronic intranasal usage can degrade the cartilage separating the
nostrils (the septum nasi), leading eventually to its complete
disappearance. Due to the absorption of the cocaine from cocaine
hydrochloride, the remaining hydrochloride forms a dilute hydrochloric
Cocaine may also greatly increase this risk of developing rare
autoimmune or connective tissue diseases such as lupus, Goodpasture
syndrome, vasculitis, glomerulonephritis, Stevens–Johnson syndrome,
and other diseases. It can also cause a wide array of
kidney diseases and kidney failure.
Cocaine use leads to an increased risk of hemorrhagic and ischemic
Cocaine use also increases the risk of having a heart
See also: Epigenetics of cocaine addiction
Cocaine addiction occurs through
ΔFosB overexpression in the nucleus
accumbens, which results in altered transcriptional regulation in
neurons within the nucleus accumbens.
ΔFosB levels have been found to increase upon the use of cocaine.
Each subsequent dose of cocaine continues to increase
with no ceiling of tolerance. Elevated levels of
ΔFosB leads to
increases in brain-derived neurotrophic factor (BDNF) levels, which in
turn increases the number of dendritic branches and spines present on
neurons involved with the nucleus accumbens and prefrontal cortex
areas of the brain. This change can be identified rather quickly, and
may be sustained weeks after the last dose of the drug.
Transgenic mice exhibiting inducible expression of
ΔFosB primarily in
the nucleus accumbens and dorsal striatum exhibit sensitized
behavioural responses to cocaine. They self-administer cocaine at
lower doses than control, but have a greater likelihood of relapse
when the drug is withheld.
ΔFosB increases the expression of
AMPA receptor subunit GluR2 and also decreases expression of
dynorphin, thereby enhancing sensitivity to reward.
Dependence and withdrawal
Cocaine dependence is a form of psychological dependence that develops
from regular cocaine use and produces a withdrawal state with
emotional-motivational deficits upon cessation of cocaine use.
According to a 2005 review, "it is unclear whether prenatal cocaine
exposure is associated with SIDS."
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). The most extensively studied effect of cocaine on the
central nervous system is the blockade of the dopamine transporter
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.
Cocaine's affects certain serotonin (5-HT) receptors; in particular,
it has been shown to antagonize the 5-HT3 receptor, which is a
ligand-gated ion channel. 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. The 5-HT2 receptor
(particularly the subtypes 5-HT2AR, 5-HT2BR and 5-HT2CR) are involved
in the locomotor-activating effects of cocaine.
Cocaine has been demonstrated to bind as to directly stabilize the DAT
transporter on the open outward-facing conformation. Further, cocaine
binds in such a way as to inhibit a hydrogen bond innate to DAT.
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 and how on the transporter the
Sigma receptors are affected by cocaine, as cocaine functions as a
sigma ligand agonist. Further specific receptors it has been
demonstrated to function on are
NMDA and the D1 dopamine receptor.
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. In addition to this
cocaine has some target binding to the site of the Kappa-opioid
receptor as well.
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 and
clock genes in behavioral actions of cocaine.
Cocaine can often cause reduced food intake, many chronic users lose
their appetite and can experience severe malnutrition and significant
Cocaine effects, further, are shown to be potentiated for
the user when used in conjunction with new surroundings and stimuli,
and otherwise novel environs.
Cocaine has a short half life of 0.7-1.5 hours and is extensively
metabolized by cholinesterase enzymes (primarily in the liver and
plasma), 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. If consumed with alcohol, cocaine
combines with alcohol in the liver to form cocaethylene. Studies
have suggested cocaethylene is both more euphoric, and has a higher
cardiovascular toxicity than cocaine by itself.
Depending on liver and kidney function, cocaine metabolites are
detectable in urine.
Benzoylecgonine can be detected in urine within
four hours after cocaine intake and remains detectable in
concentrations greater than 150 ng/mL typically for up to eight
days after cocaine is used. Detection of accumulation of cocaine
metabolites in hair is possible in regular users until the sections of
hair grown during use are cut or fall out.
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.
Street cocaine is often adulterated or "cut" with talc, lactose,
sucrose, glucose, mannitol, inositol, caffeine, procaine,
phencyclidine, phenytoin, lignocaine, strychnine, amphetamine, or
The color of "crack" cocaine depends upon several factors including
the origin of the cocaine used, the method of preparation – with
ammonia or baking soda – and the presence of impurities, but will
generally range from white to a yellowish cream to a light brown. Its
texture will also depend on the adulterants, origin and processing of
the powdered cocaine, and the method of converting the base. It ranges
from a crumbly texture, sometimes extremely oily, to a hard, almost
Cocaine – a tropane alkaloid – is a weakly alkaline compound, and
can therefore combine with acidic compounds to form various salts. The
hydrochloride (HCl) salt of cocaine is by far the most commonly
encountered, although the sulfate (-SO4) and the nitrate (-NO3) are
occasionally seen. Different salts dissolve to a greater or lesser
extent in various solvents – the hydrochloride salt is polar in
character and is quite soluble in water.
Main article: Freebase (chemistry)
As the name implies, "freebase" is the base form of cocaine, as
opposed to the salt form. It is practically insoluble in water whereas
hydrochloride salt is water-soluble.
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 because of methylecgonidine's effects on lung
tissue and liver tissue.
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
Main article: Crack cocaine
A woman smoking crack cocaine
"Rocks" of crack cocaine
Crack is a lower purity form of free-base cocaine that is usually
produced by neutralization of cocaine hydrochloride with a solution of
baking soda (sodium bicarbonate, NaHCO3) and water, producing a very
hard/brittle, off-white-to-brown colored, amorphous material that
contains sodium carbonate, entrapped water, and other by-products as
the main impurities.
The "freebase" and "crack" forms of cocaine are usually administered
by vaporization of the powdered substance into smoke, which is then
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.
Pure cocaine base/crack can be smoked because it vaporizes smoothly,
with little or no decomposition at 98 °C (208 °F),
which is below the boiling point of water.
In contrast, cocaine hydrochloride does not vaporize until heated to a
much higher temperature (about 197 °C), 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.
Smoking or vaporizing cocaine and inhaling it into the lungs produces
an almost immediate "high" that can be very powerful (and addicting)
quite rapidly – this initial crescendo of stimulation is known as a
"rush". While the stimulating effects may last for hours, the euphoric
sensation is very brief, prompting the user to smoke more immediately.
Coca leaf infusions
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Coca herbal infusion (also referred to as coca tea) is used in
coca-leaf producing countries much as any herbal medicinal infusion
would elsewhere in the world. The free and legal commercialization of
dried coca leaves under the form of filtration bags to be used as
"coca tea" has been actively promoted by the governments of
Bolivia for many years as a drink having medicinal powers. Visitors to
the city of
Cuzco in Peru, and
La Paz in
Bolivia are greeted with the
offering of coca leaf infusions (prepared in teapots with whole coca
leaves) purportedly to help the newly arrived traveler overcome the
malaise of high altitude sickness. The effects of drinking coca tea
are a mild stimulation and mood lift. It does not produce any
significant numbing of the mouth nor does it give a rush like snorting
cocaine. In order to prevent the demonization of this product, its
promoters publicize the unproven concept that much of the effect of
the ingestion of coca leaf infusion would come from the secondary
alkaloids, as being not only quantitatively different from pure
cocaine but also qualitatively different.
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. Importantly, these results also suggest strongly
that the primary pharmacologically active metabolite in coca leaf
infusions is actually cocaine and not the secondary
The cocaine metabolite benzoylecgonine can be detected in the urine of
people a few hours after drinking one cup of coca leaf infusion.
Biosynthesis of cocaine
Biosynthesis of N-methyl-pyrrolinium cation
Biosynthesis of cocaine
Robinson biosynthesis of tropane
Reduction of tropinone
The first synthesis and elucidation of the cocaine molecule was by
Richard Willstätter in 1898. Willstätter's synthesis derived
cocaine from tropinone. Since then, Robert Robinson and Edward Leete
have made significant contributions to the mechanism of the synthesis.
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. 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. 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. This is due to the extra chiral center at C-2.
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. Benzoyl-CoA then combines the two units to form
The biosynthesis begins with L-Glutamine, which is derived to
L-ornithine in plants. The major contribution of L-ornithine and
L-arginine as a precursor to the tropane ring was confirmed by Edward
Ornithine then undergoes a pyridoxal phosphate-dependent
decarboxylation to form putrescine. In animals, however, the urea
cycle derives putrescine from ornithine. L-ornithine is converted to
L-arginine, which is then decarboxylated via PLP to form agmatine.
Hydrolysis of the imine derives N-carbamoylputrescine followed with
hydrolysis of the urea to form putrescine. The separate pathways of
converting ornithine to putrescine in plants and animals have
converged. A SAM-dependent N-methylation of putrescine gives the
N-methylputrescine product, which then undergoes oxidative deamination
by the action of diamine oxidase to yield the aminoaldehyde. Schiff
base formation confirms the biosynthesis of the
Robert Robinson's acetonedicarboxylate
The biosynthesis of the tropane alkaloid, however, is still uncertain.
Hemscheidt proposes that Robinson's acetonedicarboxylate emerges as a
potential intermediate for this reaction. Condensation of
N-methylpyrrolinium and acetonedicarboxylate would generate the
oxobutyrate. Decarboxylation leads to tropane alkaloid formation.
Reduction of tropinone
The reduction of tropinone is mediated by NADPH-dependent reductase
enzymes, which have been characterized in multiple plant species.
These plant species all contain two types of the reductase enzymes,
tropinone reductase I and tropinone reductase II. TRI produces tropine
and TRII produces pseudotropine. Due to differing kinetic and
pH/activity characteristics of the enzymes and by the 25-fold higher
activity of TRI over TRII, the majority of the tropinone reduction is
from TRI to form tropine.
Detection in body fluids
Cocaine and its major metabolites may be quantified in blood, plasma,
or urine to monitor for abuse, confirm a diagnosis of poisoning, or
assist in the forensic investigation of a traffic or other criminal
violation or a sudden death. Most commercial cocaine immunoassay
screening tests cross-react appreciably with the major cocaine
metabolites, but chromatographic techniques can easily distinguish and
separately measure each of these substances. When interpreting the
results of a test, it is important to consider the cocaine usage
history of the individual, since a chronic user can develop tolerance
to doses that would incapacitate a cocaine-naive individual, and the
chronic user often has high baseline values of the metabolites in his
system. Cautious interpretation of testing results may allow a
distinction between passive or active usage, and between smoking
versus other routes of administration. In 2011, researchers at
John Jay College of Criminal Justice reported that dietary zinc
supplements can mask the presence of cocaine and other drugs in urine.
Similar claims have been made in web forums on that topic.
Main article: List of countries by prevalence of cocaine use
Global estimates of illegal drug users in 2014
(in millions of users)
According to a 2016
United Nations report,
England and Wales
England and Wales are the
countries with the highest rate of cocaine usage (2.4% of adults in
the previous year). Other countries where the usage rate meets or
exceeds 1.5% are
Spain and Scotland (2.2%), the United States (2.1%),
Australia (2.1%), Uruguay (1.8%), Brazil (1.75%), Chile (1.73%), the
Netherlands (1.5%) and
Cocaine is the second most popular illegal recreational drug in Europe
(behind cannabis). Since the mid-1990s, overall cocaine usage in
Europe has been on the rise, but usage rates and attitudes tend to
vary between countries. European countries with the highest usage
rates are the United Kingdom, Spain, Italy, and the Republic of
Approximately 12 million Europeans (3.6%) have used cocaine at least
once, 4 million (1.2%) in the last year, and 2 million in the last
About 3.5 million or 87.5% of those who have used the drug in the last
year[when?] 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, Republic of 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.
In 2014 London had the highest amount of cocaine in its sewage out of
50 European cities.
Cocaine in the United States
Cocaine is the second most popular illegal recreational drug in the
United States (behind cannabis) and the U.S. is the world's
largest consumer of cocaine.
Cocaine is commonly used in middle to
upper-class communities and is known as a "rich man's drug". It is
also popular amongst college students, as a party drug. A study
throughout the entire United States has reported that around 48
percent of people who graduated high school in 1979 have used cocaine
recreationally during some point in their lifetime, compared to
approximately 20 percent of students who graduated between the years
of 1980 and 1995. 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.
Coca leaf in Bolivia
For over a thousand years South American indigenous peoples have
chewed the leaves of Erythroxylon coca, a plant that contains vital
nutrients as well as numerous alkaloids, including cocaine. The coca
leaf was, and still is, chewed almost universally by some indigenous
communities. The remains of coca leaves have been found with ancient
Peruvian mummies, and pottery from the time period depicts humans with
bulged cheeks, indicating the presence of something on which they are
chewing. There is also evidence that these cultures used a mixture
of coca leaves and saliva as an anesthetic for the performance of
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. In 1569,
Nicolás Monardes described the indigenous peoples' practice of
chewing a mixture of tobacco and coca leaves to induce "great
When they wished to make themselves drunk and out of judgment they
chewed a mixture of tobacco and coca leaves which make them go as they
were out of their wittes.
In 1609, Padre
Blas Valera wrote:
Coca protects the body from many ailments, and our doctors use it in
powdered form to reduce the swelling of wounds, to strengthen broken
bones, to expel cold from the body or prevent it from entering, and to
cure rotten wounds or sores that are full of maggots. And if it does
so much for outward ailments, will not its singular virtue have even
greater effect in the entrails of those who eat it?
Isolation and naming
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] and contemporary conditions of sea-shipping from South America
could degrade the cocaine in the plant samples available to European
The cocaine alkaloid was first isolated by the German chemist
Friedrich Gaedcke in 1855. Gaedcke named the alkaloid "erythroxyline",
and published a description in the journal Archiv der Pharmazie.
Friedrich Wöhler asked Dr. Carl Scherzer, a scientist aboard
the Novara (an Austrian frigate sent by Emperor Franz Joseph to circle
the globe), to bring him a large amount of coca leaves from South
America. In 1859, the ship finished its travels and Wöhler received a
trunk full of coca. Wöhler passed on the leaves to Albert Niemann, a
Ph.D. student at the
University of Göttingen
University of Göttingen in Germany, who then
developed an improved purification process.
Niemann described every step he took to isolate cocaine in his
dissertation titled Über eine neue organische Base in den
Cocablättern (On a New Organic Base in the
Coca Leaves), which was
published in 1860—it earned him his Ph.D. and is now in the British
Library. He wrote of the alkaloid's "colourless transparent prisms"
and said that "Its solutions have an alkaline reaction, a bitter
taste, promote the flow of saliva and leave a peculiar numbness,
followed by a sense of cold when applied to the tongue." Niemann named
the alkaloid "cocaine" from "coca" (from Quechua "cuca") + suffix
"ine". Because of its use as a local anesthetic, a suffix
"-caine" was later extracted and used to form names of synthetic local
The first synthesis and elucidation of the structure of the cocaine
molecule was by
Richard Willstätter in 1898. It was the first
biomimetic synthesis of an organic structure recorded in academic
chemical literature. The synthesis started from tropinone, a
related natural product and took five steps.
Cocaine toothache drops", 1885 advertisement of cocaine for dental
pain in children
Advertisement in the January 1896 issue of
McClure's Magazine for
Cocaine "for the hair".
With the discovery of this new alkaloid, Western medicine was quick to
exploit the possible uses of this plant.
In 1879, Vassili von Anrep, of the University of Würzburg, devised an
experiment to demonstrate the analgesic properties of the newly
discovered alkaloid. He prepared two separate jars, one containing a
cocaine-salt solution, with the other containing merely salt water. He
then submerged a frog's legs into the two jars, one leg in the
treatment and one in the control solution, and proceeded to stimulate
the legs in several different ways. The leg that had been immersed in
the cocaine solution reacted very differently from the leg that had
been immersed in salt water.
Karl 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, and
James Leonard Corning
James Leonard Corning demonstrated
peridural anesthesia. 1898 saw
Heinrich Quincke use cocaine for
Today, cocaine has a very limited medical use.
Pope Leo XIII
Pope Leo XIII purportedly carried a hip flask of the coca-treated Vin
Mariani with him, and awarded a Vatican gold medal to Angelo
In 1859, an Italian doctor, Paolo Mantegazza, returned from Peru,
where he had witnessed first-hand the use of coca by the local
indigenous peoples. He proceeded to experiment on himself and upon his
Milan he wrote a paper in which he described the effects. In
this paper he declared coca and cocaine (at the time they were assumed
to be the same) as being useful medicinally, in the treatment of "a
furred tongue in the morning, flatulence, and whitening of the teeth."
A chemist named Angelo Mariani who read Mantegazza's paper became
immediately intrigued with coca and its economic potential. In 1863,
Mariani started marketing a wine called Vin Mariani, which had been
treated with coca leaves, to become cocawine. The ethanol in wine
acted as a solvent and extracted the cocaine from the coca leaves,
altering the drink's effect. It contained 6 mg cocaine per ounce
of wine, but
Vin Mariani which was to be exported contained
7.2 mg per ounce, to compete with the higher cocaine content of
similar drinks in the United States. A "pinch of coca leaves" was
included in John Styth Pemberton's original 1886 recipe for Coca-Cola,
though the company began using decocainized leaves in 1906 when the
Pure Food and Drug Act
Pure Food and Drug Act was passed.
In 1879 cocaine began to be used to treat morphine addiction. Cocaine
was introduced into clinical use as a local anesthetic in Germany in
1884, about the same time as
Sigmund Freud published his work Über
Coca, in which he wrote that cocaine causes:
Exhilaration and lasting euphoria, which in no way differs from the
normal euphoria of the healthy person. You perceive an increase of
self-control and possess more vitality and capacity for work. In other
words, you are simply normal, and it is soon hard to believe you are
under the influence of any drug. Long intensive physical work is
performed without any fatigue. This result is enjoyed without any of
the unpleasant after-effects that follow exhilaration brought about by
alcoholic beverages. No craving for the further use of cocaine appears
after the first, or even after repeated taking of the drug.
In 1885 the U.S. manufacturer
Parke-Davis sold cocaine in various
forms, including cigarettes, powder, and even a cocaine mixture that
could be injected directly into the user's veins with the included
needle. The company promised that its cocaine products would "supply
the place of food, make the coward brave, the silent eloquent and
render the sufferer insensitive to pain."
In this 1904 advice column from the Tacoma Times, "Madame Falloppe"
recommended that cold sores be treated with a solution of borax,
cocaine, and morphine.
By the late Victorian era, cocaine use had appeared as a vice in
literature. For example, it was injected by Arthur Conan Doyle's
fictional Sherlock Holmes, generally to offset the boredom he felt
when he was not working on a case.
In early 20th-century Memphis, Tennessee, cocaine was sold in
neighborhood drugstores on Beale Street, costing five or ten cents for
a small boxful. Stevedores along the Mississippi River used the drug
as a stimulant, and white employers encouraged its use by black
Ernest Shackleton took "Forced March" brand cocaine tablets
to Antarctica, as did
Captain Scott a year later on his ill-fated
journey to the South Pole.
During the mid-1940s, amidst World War II, cocaine was considered for
inclusion as an ingredient of a future generation of 'pep pills' for
the German military, code named D-IX.
In modern popular culture references to the drug are prevalent, in it
the drug has a glamorous image associated with the rich, famous and
powerful with it also making users to "feel rich and
beautiful". In addition the pace of modern society
− such as in finance − gives many the incentive to make use of the
Women purchase cocaine capsules in Berlin, 1924
Marion Barry captured on a surveillance camera smoking
crack cocaine during a sting operation by the
FBI and D.C. Police.
In many countries, cocaine is a popular recreational drug. In the
United States, the development of "crack" cocaine introduced the
substance to a generally poorer inner-city market. Use of the powder
form has stayed relatively constant, experiencing a new height of use
during the late 1990s and early 2000s in the U.S., and has become much
more popular in the last few years in the UK.[when?]
Cocaine use is prevalent across all socioeconomic strata, including
age, demographics, economic, social, political, religious, and
The estimated U.S. cocaine market exceeded US$70 billion in street
value for the year 2005, exceeding revenues by corporations such as
Starbucks. 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".
In 1995 the
World Health Organization
World Health Organization (WHO) and the United Nations
Crime and Justice Research Institute (UNICRI) announced
in a press release the publication of the results of the largest
global study on cocaine use ever undertaken. However, a decision by an
American representative in the
World Health Assembly
World Health Assembly banned the
publication of the study, because it seemed to make a case for the
positive uses of cocaine. An excerpt of the report strongly conflicted
with accepted paradigms, for example "that occasional cocaine use does
not typically lead to severe or even minor physical or social
problems." In the sixth meeting of the B committee, the US
representative threatened that "If World Health Organization
activities relating to drugs failed to reinforce proven drug control
approaches, funds for the relevant programs should be curtailed". This
led to the decision to discontinue publication. A part of the study
was recuperated and published in 2010, including profiles of cocaine
use in 20 countries, but are unavailable as of 2015[update].
In October 2010 it was reported that the use of cocaine in Australia
has doubled since monitoring began in 2003.
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. The adulterant of sugars allows the
dealer to sell the product for a higher price because of the illusion
of purity and allows sale of more of the product at that higher price,
enabling dealers to significantly increase revenue with little
additional cost for the adulterants. A 2007 study by the European
Monitoring Centre for Drugs and Drug
Addiction showed that the purity
levels for street purchased cocaine was often under 5% and on average
under 50% pure.
Society and culture
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 are additionally
regulated by the 1970 Controlled Substances Act.
Some countries, such as
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. The provisions as to how much a coca
farmer can yield annually is protected by laws such as the Bolivian
Cato accord. In addition, some parts of Europe and Australia
allow processed cocaine for medicinal uses only.
Cocaine is a Schedule 8 prohibited substance in Australia under the
Poisons Standard (July 2016). A schedule 8 substance is a
controlled Drug – Substances which should be available for use but
require restriction of manufacture, supply, distribution, possession
and use to reduce abuse, misuse and physical or psychological
Western Australia under the Misuse of Drugs Act 1981 4.0g of
cocaine is the amount of prohibited drugs determining a court of
trial, 2.0g is the amount of cocaine required for the presumption of
intention to sell or supply and 28.0g is the amount of cocaine
required for purposes of drug trafficking.
Cocaine in the United States
The US federal government instituted a national labeling requirement
for cocaine and cocaine-containing products through the Food and Drug
Act of 1906. The next important federal regulation was the
Harrison Narcotics Tax Act of 1914. While this act is often seen as
the start of prohibition, the act itself was not actually a
prohibition on cocaine, but instead set up a regulatory and licensing
regime. The Harrison Act did not recognize addiction as a
treatable condition and therefore the therapeutic use of cocaine,
heroin or morphine to such individuals was outlawed – leading
the Journal of American Medicine to remark, "[the addict] is denied
the medical care he urgently needs, open, above-board sources from
which he formerly obtained his drug supply are closed to him, and he
is driven to the underworld where he can get his drug, but of course,
surreptitiously and in violation of the law." The Harrison Act
left manufacturers of cocaine untouched so long as they met certain
purity and labeling standards. Despite that cocaine was typically
illegal to sell and legal outlets were rarer, the quantities of legal
cocaine produced declined very little. Legal cocaine quantities
did not decrease until the Jones–Miller Act of 1922 put serious
restrictions on cocaine manufactures.
In 2004, according to the United Nations, 589 tonnes of cocaine were
seized globally by law enforcement authorities.
188 t, the United States 166 t, Europe 79 t, Peru
Bolivia 9 t, and the rest of the world 133 t.
Because of the drug's potential for addiction and overdose, cocaine is
generally treated as a "hard drug", with severe penalties for
possession and trafficking. Demand remains high, and consequently,
black market cocaine is quite expensive. Unprocessed cocaine, such as
coca leaves, are occasionally purchased and sold, but this is
exceedingly rare as it is much easier and more profitable to conceal
and smuggle it in powdered form. The scale of the market is immense:
770 tonnes times $100 per gram retail = up to $77 billion.[citation
Colombia was the world's leading producer of
cocaine. Three-quarters of the world's annual yield of
cocaine has been produced in Colombia, both from cocaine base imported
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
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 is 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.[citation
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 (283 kg) 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 string trimmer and sprinkled with a small
amount of powdered cement (replacing sodium carbonate from former
times). Several hundred pounds of this mixture were soaked in 50 US
gallons (190 L) 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 55 lb (25 kg) 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 6 lb (2.5 kg) 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.
Attempts to eradicate coca fields through the use of defoliants have
devastated part of the farming economy in some coca growing regions of
Colombia, and strains appear to have been developed that are more
resistant or immune to their use. Whether these strains are natural
mutations or the product of human tampering is unclear. These strains
have also shown to be more potent than those previously grown,
increasing profits for the drug cartels responsible for the exporting
of cocaine. Although production fell temporarily, coca crops rebounded
in numerous smaller fields in Colombia, rather than the larger
The cultivation of coca has become an attractive economic decision for
many growers due to the combination of several factors, including 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, the spread of new
strains of the coca plant due to persistent worldwide demand.[citation
Estimated Andean region coca cultivation and potential pure cocaine
Net cultivation km2 (sq mi)
Potential pure cocaine production (tonnes)
The latest estimate provided by the U.S. authorities on the annual
production of cocaine in
Colombia refers to 290 metric tons. As of the
end of 2011, the seizure operations of
Colombian cocaine carried out
in different countries have totaled 351.8 metric tons of cocaine, i.e.
121.3% of Colombia's annual production according to the U.S.
Department of State's estimates. 
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, and 5S – hence a total potential of 16
possible enantiomers and diastereoisomers) 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
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 world's largest
consumer of cocaine, where it is sold at huge markups; usually in
the US at $80–120 for 1 gram, and $250–300 for 3.5 grams
(⅛ of an ounce, or an "eight ball").
Caribbean and Mexican routes
As of 2005[update], cocaine shipments from South America transported
Central America were generally moved over land or by
air to staging sites in northern Mexico. The cocaine is then broken
down into smaller loads for smuggling across the U.S.–
The primary cocaine importation points in the United States have been
in Arizona, southern California, southern Florida, and Texas.
Typically, land vehicles are driven across the U.S.–
Sixty-five percent of cocaine enters the United States through Mexico,
and the vast majority of the rest enters through
Florida.[page needed] As of 2015[update], the Sinaloa Cartel
is the most active drug cartel involved in smuggling illicit drugs
like cocaine into the United States and trafficking them throughout
the United States.
Cocaine traffickers from
Mexico have established a
labyrinth of smuggling routes throughout the Caribbean, the Bahama
Island chain, and South Florida. They often hire traffickers from
Mexico or the
Dominican Republic to transport the drug using a variety
of smuggling techniques to U.S. markets. These include airdrops of 500
to 700 kg (1,100 to 1,500 lb) in the
Bahama Islands or off
the coast of Puerto Rico, mid-ocean boat-to-boat transfers of 500 to
2,000 kg (1,100 to 4,400 lb), and the commercial shipment of
tonnes of cocaine through the port of Miami.
Another route of cocaine traffic goes through Chile, which is
primarily used for cocaine produced in
Bolivia since the nearest
seaports lie in northern Chile. The arid Bolivia–Chile border is
easily crossed by 4×4 vehicles that then head to the seaports of
Iquique and Antofagasta. While the price of cocaine is higher in Chile
Peru and Bolivia, the final destination is usually Europe,
Spain where drug dealing networks exist among South
American immigrants.
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.
Bulk cargo ships are also used to smuggle cocaine to staging sites in
the western Caribbean–Gulf of
Mexico area. These vessels are
typically 150–250-foot (50–80 m) coastal freighters that
carry an average cocaine load of approximately 2.5 tonnes. Commercial
fishing vessels are also used for smuggling operations. In areas with
a high volume of recreational traffic, smugglers use the same types of
vessels, such as go-fast boats, as those used by the local
Sophisticated drug subs are the latest tool drug runners are using to
bring cocaine north from Colombia, it was reported on 20 March 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.
Sales to consumers
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, and lasts 12–24 times longer with each
dose. 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": As of 2007[update] 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
0.4 g, a 20 is 0.8–1.0 g and an 8-ball (3.5 g) is sold for $60
to $80, 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
In 2008, the European Monitoring Centre for Drugs and Drug Addiction
reports that the typical retail price of cocaine varied between €50
and €75 per gram in most European countries, although Cyprus,
Romania, Sweden and Turkey reported much higher values.
World annual cocaine consumption, as of 2000, stood at around 600
tonnes, with the United States consuming around 300 t, 50% of the
total, Europe about 150 t, 25% of the total, and the rest of the world
the remaining 150 t or 25%. It is estimated that 1.5 million
people in the United States used cocaine in 2010 down from 2.4 million
in 2006. Conversely, cocaine use appears to be increasing in
Europe with the highest prevalences in Spain, the United Kingdom,
Italy, and Ireland.
The 2010 UN
World Drug Report concluded that "it appears that the
North American cocaine market has declined in value from US$47 billion
in 1998 to US$38 billion in 2008. Between 2006 and 2008, the value of
the market remained basically stable".
In 2005, researchers 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.
Cocaine and amphetamine regulated transcript
Crack cocaine § Crack lung
Legal status of cocaine
List of cocaine analogues
Pre-Columbian trans-oceanic evidence for cocaine in ancient Egypt
Prenatal cocaine exposure
Route 36, cocaine bar in Bolivia
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Wikiquote has quotations related to: Cocaine
Wikimedia Commons has media related to Cocaine.
Look up cocaine in Wiktionary, the free dictionary.
"A look at the Evidence for
Cocaine in Mummies". Archived from the
original on 22 August 2013. Retrieved 2010-04-18.
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Cocaine Information — A collection of data about cocaine
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Slang Dictionary for Cocaine.
Cocaine content of plants
Cocaine – The History and the Risks at h2g2
Cocaine Frequently Asked Questions
U.S. National Library of Medicine: Drug Information
Portal – Cocaine
Cocaine Market Data and Value-Havocscope Black Markets at the Wayback
Machine (archived 23 March 2011) Data on cocaine trafficking
Recreational drug use
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Psilocybin / Psilocin
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Opioid receptor agonists (opioids) (e.g., morphine, heroin,
hydrocodone, oxycodone, opium, kratom)
α2δ subunit-containing voltage-dependent calcium channels blockers
(gabapentinoids) (e.g., gabapentin, pregabalin, phenibut)
AMPA receptor antagonists (e.g., perampanel)
CB1 receptor agonists (cannabinoids) (e.g., THC, cannabis)
Dopamine receptor agonists (e.g., levodopa)
Dopamine releasing agents (e.g., amphetamine, methamphetamine, MDMA,
Dopamine reuptake inhibitors (e.g., cocaine, methylphenidate)
GABAA receptor positive allosteric modulators (e.g., barbiturates,
benzodiazepines, carbamates, ethanol (alcohol) (alcoholic drink),
inhalants, nonbenzodiazepines, quinazolinones)
GHB (sodium oxybate) and analogues
Glucocorticoids (corticosteroids) (e.g., dexamethasone, prednisone)
nACh receptor agonists (e.g., nicotine, tobacco, arecoline, areca nut)
Nitric oxide prodrugs (e.g., alkyl nitrites (poppers))
NMDA receptor antagonists (e.g., DXM, ketamine, methoxetamine, nitrous
oxide, phencyclidine, inhalants)
Orexin receptor antagonists (e.g., suvorexant)
Recreational drug use
Amphetamine (Dextroamphetamine, Levoamphetamine)
DOPA (Dextrodopa, Levodopa)
Fenfluramine (Dexfenfluramine, Levofenfluramine)
Methamphetamine (Dextromethamphetamine, Levomethamphetamine)
CFT (WIN 35,428)
Troparil (β-CPT, WIN 35,065-2)
ATC code: N06B
Local anesthetics (primarily sodium channel blockers) (N01B)
Esters by acid
ArCO2- (not para-amino or Ph)
Bupivacaine# / Levobupivacaine / Ropivacaine
Lidocaine / prilocaine
Anesthetic / vasoconstrictor
‡Withdrawn from market
§Never to phase III
Plants / animals
Atropa belladonna (belladonna)
Datura innoxia (thorn-apple)
Datura metel (devil's trumpet)
Hyoscyamus niger (henbane)
Mandragora officinarum (mandrake)
Ion channel modulators
L-type-selective: Dihydropyridines: Amlodipine
Diltiazem derivatives: Clentiazem
Siratiazem; Phenylalkylamines: Anipamil
Verapamil; Others: AH-1058
Leconotide (ω-conotoxin CVID)
Ziconotide (ω-conotoxin MVIIA)
P-type-selective: ω-Agatoxin IVA
Non-selective: ω-Agatoxin TK
α2δ subunit-selective (gabapentinoids): 4-Methylpregabalin
L-type-selective: Bay K8644
hERG (KCNH2, Kv11.1)-specific: Ajmaline
KCNQ (Kv7)-specific: Linopirdine
Spooky toxin (SsTx)
KCNQ (Kv7)-specific: Flupirtine
GIRK-specific: ML-297 (VU0456810)
BKCa-specific: Flufenamic acid
Antiarrhythmics (class I): Ajmaline
Local anesthetics: pFBT
Bupivacaine (Levobupivacaine, Ropivacaine)
Atracotoxins (Robustoxin, Versutoxin)
See here instead.
See also: Receptor/signaling modulators • Transient receptor
potential channel modulators
Monoamine reuptake inhibitors
Selective norepinephrine reuptake inhibitors: Amedalin
Norepinephrine–dopamine reuptake inhibitors: Amineptine
Serotonin–norepinephrine reuptake inhibitors: Atomoxetine
Serotonin–norepinephrine–dopamine reuptake inhibitors:
Tropanes (e.g., cocaine)
Tricyclic antidepressants: Amitriptyline
Tetracyclic antidepressants: Amoxapine
Others: Antihistamines (e.g., brompheniramine, chlorphenamine,
Antipsychotics (e.g., loxapine, ziprasidone)
Arylcyclohexylamines (e.g., ketamine, phencyclidine)
Opioids (e.g., desmetramadol, methadone, pethidine (meperidine),
tapentadol, tramadol, levorphanol)
Selective serotonin reuptake inhibitors: Alaproclate
Selective serotonin reuptake inhibitors and serotonin receptor
Serotonin–norepinephrine reuptake inhibitors: Atomoxetine
Serotonin–norepinephrine–dopamine reuptake inhibitors:
Tropanes (e.g., cocaine)
Tricyclic antidepressants: Amitriptyline
Antihistamines (e.g., brompheniramine, chlorphenamine, dimenhydrinate,
diphenhydramine, mepyramine (pyrilamine), pheniramine, tripelennamine)
Antipsychotics (e.g., loxapine, ziprasidone)
Arylcyclohexylamines (e.g., 3-MeO-PCP, esketamine, ketamine,
Opioids (e.g., dextropropoxyphene, methadone, pethidine (meperidine),
levorphanol, tapentadol, tramadol)
Amphetamines (e.g., amphetamine, methamphetamine, MDMA)
DAT enhancers: Luteolin
DAT modulators: Agonist-like: SoRI-9804
SoRI-20040; Antagonist-like: SoRI-20041
See also: Receptor/signaling modulators •
Monoamine releasing agents
• Adrenergics • Dopaminergics • Serotonergics • Monoamine
metabolism modulators •
Sigma receptor modulators
Dehydroepiandrosterone (DHEA) (prasterone)
Dehydroepiandrosterone sulfate (DHEA-S) (prasterone sulfate)
Allosteric modulators: Phenytoin; Positive: Methylphenylpiracetam
Siramesine (Lu 28-179)
Allosteric modulators: SKF-83959
Hypericin (St. John's wort)
See also: Receptor/signaling modulators