1. Crack Cocaine
2. What Is The Origin Of Crack Cocaine
3. The History Of Crack Cocaine
4. Where Did Crack Cocaine Come From
5. Who Invented Crack Cocaine
6. Crack Cocaine In The 1980s

Crack cocaine, also known simply as crack or rock, is a free base form of cocaine that can be smoked. Crack offers a short but intense high to smokers. The Manual of Adolescent Substance Abuse Treatment calls it the most addictive form of cocaine.^[1] Crack first saw widespread use as a recreational drug in primarily impoverishedinner city neighborhoods in New York, Philadelphia, Baltimore, Washington, D.C., Los Angeles, and Miami in late 1984 and 1985; its rapid increase in use and availability is sometimes termed as the 'crack epidemic'.^[2]

• 1Physical and chemical properties
• 3Adverse effects
  • 3.1Physiological
  • 3.4Reinforcement disorders
• 5Society and culture
  • 5.4Legal status

Crack could be produced by dissolving powdered cocaine in a mixture of water and ammonia and boiling it down until a solid formed. Broken into smaller chunks, or “rocks,” this solid form could. Crack cocaine is the most popularly used version of cocaine today. Smoking cocaine rocks began in the late 1970’s. Rocking-up cocaine powder and smoking it was originally the method developed so distributors of cocaine could test the purity of the drug before it was purchased from the manufacturers. Crack has destroyed millions of lives since it was first introduced to the streets of America.

Physical and chemical properties

In purer forms, crack rocks appear as off-white nuggets with jagged edges,^[3] with a slightly higher density than candle wax. Purer forms of crack resemble a hard plastic in crystalline form, which is brittle^[3] (pieces snap when they are broken). A crack rock acts as a local anesthetic (see: cocaine), numbing the tongue or mouth only where directly placed. Purer forms of crack will sink in water or melt at the edges when near a flame (crack vaporizes at 90 °C, 194 °F).^[1]

Crack cocaine as sold on the streets may be adulterated or 'cut' with other substances mimicking the appearance of crack cocaine to increase bulk. Use of toxic adulterants such as levamisole^[4] has been documented.^[5]

Synthesis

Sodium bicarbonate (NaHCO₃, common baking soda) is a base used in preparation of crack, although other weak bases may substitute for it.^[6][7] The net reaction when using sodium bicarbonate is

Coc-H⁺Cl⁻ + NaHCO₃ → Coc + H₂O + CO₂ + NaCl

With ammonium bicarbonate:

Coc-H⁺Cl⁻ + NH₄HCO₃ → Coc + NH₄Cl + CO₂ + H₂O

With ammonium carbonate:

2(Coc-H⁺Cl⁻) + (NH₄)₂CO₃ → 2 Coc + 2 NH₄Cl + CO₂ + H₂O

Crack cocaine is frequently purchased already in rock form,^[3] although it is not uncommon for some users to 'wash up' or 'cook' powder cocaine into crack themselves. This process is frequently done with baking soda (sodium bicarbonate), water, and a spoon. Once mixed and heated, the bicarbonate reacts with the hydrochloride of the powder cocaine, forming free base cocaine and carbonic acid (H₂CO₃) in a reversible acid-base reaction. The heating accelerates the degradation of carbonic acid into carbon dioxide (CO₂) and water. Loss of CO₂ prevents the reaction from reversing back to cocaine hydrochloride. Free base cocaine separates as an oily layer, floating on the top of the now leftover aqueous phase. It is at this point that the oil is picked up rapidly, usually with a pin or long thin object. This pulls the oil up and spins it, allowing air to set and dry the oil, and allows the maker to roll the oil into the rock-like shape.

Crack vaporizes near temperature 90 °C (194 °F),^[1] much lower than the cocaine hydrochloride melting point of 190 °C (374 °F).^[1] Whereas cocaine hydrochloride cannot be smoked (burns with no effect),^[1]crack cocaine when smoked allows for quick absorption into the blood stream, and reaches the brain in eight seconds.^[1] Crack cocaine can also be injected intravenously with the same effect as powder cocaine. However, whereas powder cocaine dissolves in water, crack must be dissolved in an acidic solution such as lemon juice or white vinegar, a process that effectively reverses the original conversion of powder cocaine to crack.

Recreational use

Crack cocaine is commonly used as a recreational drug. Effects of crack cocaine include euphoria,^[8] supreme confidence,^[9] loss of appetite,^[8]insomnia,^[8] alertness,^[8] increased energy,^[8] a craving for more cocaine,^[9]and potential paranoia (ending after use).^[8][10]Its initial effect is to release a large amount of dopamine,^[3] a brain chemical inducing feelings of euphoria. The high usually lasts from 5–10 minutes,^[3][8] after which time dopamine levels in the brain plummet, leaving the user feeling depressed and low.^[3] When (powder) cocaine is dissolved and injected, the absorption into the bloodstream is at least as rapid as the absorption of the drug which occurs when crack cocaine is smoked,^[8] and similar euphoria may be experienced.

Adverse effects

Because crack is an illicit drug, users may consume impure or fake ('bunk') drug,^[5] which may pose additional health risks.

Physiological

The short-term physiological effects of cocaine include^[8] constricted blood vessels, dilated pupils, and increased temperature, heart rate, and blood pressure. Some users of cocaine report feelings of restlessness, irritability, and anxiety. In rare instances, sudden death can occur on the first use of cocaine or unexpectedly thereafter.^[8] Cocaine-related deaths are often a result of cardiac arrest or seizures followed by respiratory arrest.

Like other forms of cocaine, smoking crack can increase heart rate^[11] and blood pressure, leading to long-term cardiovascular problems. Some research suggests that smoking crack or freebase cocaine has additional health risks compared to other methods of taking cocaine. Many of these issues relate specifically to the release of methylecgonidine and its effect on the heart,^[11] lungs,^[12] and liver.^[13]

• Toxic adulterants: Many substances may have been added in order to expand the weight and volume of a batch, while still appearing to be pure crack. Occasionally, highly toxic substances are used, with a range of corresponding short and long-term health risks. Adulturants used with crack and cocaine include milk powder, sugars such as glucose, starch, caffeine, lidocaine, benzocaine, paracetamol, amphetamine, scopolamine and strychnine.^[14]
• Smoking problems: Any route of administration poses its own set of health risks; in the case of crack cocaine, smoking tends to be more harmful than other routes. Crack users tend to smoke the drug because that has a higher bioavailability than other routes typically used for drugs of abuse such as insufflation.^{[citation needed]} Crack has a melting point of around 90 °C(194 °F),^[1] and the smoke does not remain potent for long. Therefore, crack pipes are generally very short, to minimize the time between evaporating and ingestion (thereby minimizing loss of potency).^{[citation needed]} Having a very hot pipe pressed against the lips often causes cracked and blistered lips, colloquially known as 'crack lip'. The use of 'convenience store crack pipes'^[15] – glass tubes which originally contained small artificial roses – may contribute to this condition. These 4-inch (10-cm) pipes^[15] are not durable and will quickly develop breaks; users may continue to use the pipe even though it has been broken to a shorter length. The hot pipe might burn the lips, tongue, or fingers, especially when passed between people who take hits in rapid succession, causing the short pipe to reach higher temperatures than if used by one person alone.
• Pure or large doses: Because the quality of crack can vary greatly, some people might smoke larger amounts of diluted crack, unaware that a similar amount of a new batch of purer crack could cause an overdose. This can trigger heart problems or cause unconsciousness.
• Pathogens on pipes: When pipes are shared, bacteria or viruses can be transferred from person to person.

Crack lung

In crack users, acute respiratory symptoms have been reported, sometimes termed crack lung. Symptoms include fever, coughing up blood and difficulty breathing.^[16] In the 48-hour period after use, people with these symptoms have also had associated radiographic findings on chest X-ray of fluid in the lungs (pulmonary edema), interstitial pneumonia, diffuse alveolar hemorrhage, and eosinophil infiltration.^[16]

Psychological

Stimulant drug abuse (particularly amphetamine and cocaine) can lead to delusional parasitosis (aka Ekbom's Syndrome: a mistaken belief they are infested with parasites).^[17] For example, excessive cocaine use can lead to formication, nicknamed 'cocaine bugs' or 'coke bugs', where the affected people believe they have, or feel, parasites crawling under their skin.^[17] (Similar delusions may also be associated with high fever or in connection with alcohol withdrawal, sometimes accompanied by visual hallucinations of insects.)^[17]

People experiencing these hallucinations might scratch themselves to the extent of serious skin damage and bleeding, especially when they are delirious.^[10][17]

Paranoia and anxiety are among the most common psychological symptoms of crack cocaine use. Psychosis is more closely associated with smoking crack cocaine than intranasal and intravenous use.^[18]

Pregnancy and nursing

Crack baby is a term for a child born to a mother who used crack cocaine during her pregnancy. The threat that cocaine use during pregnancy poses to the fetus is now considered exaggerated.^[19] Studies show that prenatal cocaine exposure (independent of other effects such as, for example, alcohol, tobacco, or physical environment) has no appreciable effect on childhood growth and development.^[20]However, the official opinion of the National Institute on Drug Abuse of the United States warns about health risks while cautioning against stereotyping:

Many recall that 'crack babies', or babies born to mothers who used crack cocaine while pregnant, were at one time written off by many as a lost generation. They were predicted to suffer from severe, irreversible damage, including reduced intelligence and social skills. It was later found that this was a gross exaggeration. However, the fact that most of these children appear normal should not be over-interpreted as indicating that there is no cause for concern. Using sophisticated technologies, scientists are now finding that exposure to cocaine during fetal development may lead to subtle, yet significant, later deficits in some children, including deficits in some aspects of cognitive performance, information-processing, and attention to tasks—abilities that are important for success in school.^[21]

There are also warnings about the threat of breastfeeding: The March of Dimes said 'it is likely that cocaine will reach the baby through breast milk,' and advises the following regarding cocaine use during pregnancy:

Cocaine use during pregnancy can affect a pregnant woman and her unborn baby in many ways. During the early months of pregnancy, it may increase the risk of miscarriage. Later in pregnancy, it can trigger preterm labor (labor that occurs before 37 weeks of pregnancy) or cause the baby to grow poorly. As a result, cocaine-exposed babies are more likely than unexposed babies to be born with low birthweight (less than 5.5 lb or 2.5 kg). Low-birthweight babies are 20 times more likely to die in their first month of life than normal-weight babies, and face an increased risk of lifelong disabilities such as mental retardation and cerebral palsy. Cocaine-exposed babies also tend to have smaller heads, which generally reflect smaller brains. Some studies suggest that cocaine-exposed babies are at increased risk of birth defects, including urinary-tract defects and, possibly, heart defects. Cocaine also may cause an unborn baby to have a stroke, irreversible brain damage, or a heart attack.^[22]

Reinforcement disorders

Tolerance

An appreciable tolerance to cocaine's high may develop, with many addicts reporting that they seek but fail to achieve as much pleasure as they did from their first experience.^[8] Some users will frequently increase their doses to intensify and prolong the euphoric effects. While tolerance to the high can occur, users might also become more sensitive (drug sensitization) to cocaine's local anesthetic (pain killing) and convulsant (seizure inducing) effects, without increasing the dose taken; this increased sensitivity may explain some deaths occurring after apparent low doses of cocaine.^[8]

Addiction

Crack cocaine is popularly thought to be the most addictive form of cocaine.^[1] However, this claim has been contested: Morgan and Zimmer wrote that available data indicated that '..smoking cocaine by itself does not increase markedly the likelihood of dependence.. The claim that cocaine is much more addictive when smoked must be reexamined.'^[23] They argued that cocaine users who are already prone to abuse are most likely to 'move toward a more efficient mode of ingestion' (that is, smoking).

The intense desire to recapture the initial high is what is so addictive for many users.^[3] On the other hand, Reinarman et al. wrote that the nature of crack addiction depends on the social context in which it is used and the psychological characteristics of users, pointing out that many heavy crack users can go for days or weeks without using the drugs.^[24]

Overdose

A typical response among users is to have another hit of the drug; however, the levels of dopamine in the brain take a long time to replenish themselves, and each hit taken in rapid succession leads to progressively less intense highs.^[3] However, a person might binge for 3 or more days without sleep, while inhaling hits from the pipe.^[10]

Use of cocaine in a binge, during which the drug is taken repeatedly and at increasingly high doses, leads to a state of increasing irritability, restlessness, and paranoia.^[8] This may result in a full-blown paranoid psychosis, in which the individual loses touch with reality and experiences auditory hallucinations.^[8]

Large amounts of crack cocaine (several hundred milligrams or more) intensify the user's high, but may also lead to bizarre, erratic, and violent behavior.^[8] Large amounts can induce tremors, vertigo, muscle twitches, paranoia, or, with repeated doses, a toxic reaction closely resembling amphetamine poisoning.^[8]

Society and culture

Synonyms

atari; base; bazooka; beamers; beemers; bebe; bee-bee; berry; bing; bolo; bomb; boulder; boulders; butter; caine; cane; Casper; Casper the ghost; cavvy; chemical; chewies; cloud; cloud nine; crills; crunch and munch; dip; famous dimes; fan; fish scale; fries; fry; glo; golfball; gravel; grit; hail; hamburger; helper; hubba; ice cube; kangaroo; kibbles and bits; kibbles; krills; lightem; paste; patico; pebbles; pee wee; pony; raw; ready; ready rocks; redi rocks; roca; rock; rooster; rox; Roxanne; scud; Scotty; scramble; scruples; seven-up; sherm; sherms; sleet; snowballs; stones; teeth; tension; top gun; tweak; ultimate; wash; white cloud; work; yahoo; yale; yay; yayoo; yeah-O; yeyo; yeo; yuck.^[25]

Drug combinations

Crack cocaine may be combined with amphetamine ('croack'); tobacco ('coolie'); marijuana ('buddha'; 'caviar'; 'chronic'; 'cocoa puffs'; 'fry daddy'; 'gimmie'; 'gremmie'; 'juice'; 'primo'; 'torpedo'; 'turbo'; 'woolie'; 'woola'); heroin ('moon rock'); and phencyclidine ('clicker'; 'p-funk'; 'spacebase').^[25]

Consumption

Crack smoking ('hitting the pipe'; 'puffing'; 'beaming up (to Scotty)') is commonly performed with utensils such as pipes ('bowl'; 'devil's dick'; 'glass dick'; 'horn'; 'Uzi'); improvised pipes made from a plastic bottle ('Masarati'); water pipes ('bong'; 'hubbly-bubbly'); and laboratory pipettes ('demo').^[25]

Legal status

Cocaine is listed as a Schedule I drug in the United Nations 1961 Single Convention on Narcotic Drugs, making it illegal for non-state-sanctioned production, manufacture, export, import, distribution, trade, use and possession.^[26] In most states (except in the U.S.) crack falls under the same category as cocaine.

Australia

In Australia, crack falls under the same category as cocaine, which is listed as a Schedule 8 controlled drug, indicating that any substances and preparations for therapeutic use under this category have high potential for abuse and addiction. It is permitted for some medical use, but is otherwise outlawed.

Canada

As a Schedule I substance under the Controlled Drugs and Substances Act, crack is not differentiated from cocaine and other coca products. However, the court may weigh the socio-economic factors of crack usage in sentencing. As a guideline, Schedule I drugs carry a maximum 7-year prison sentence for possession for an indictable offense and up to life imprisonment for trafficking and production. A summary conviction on possession carries a $1000–$2000 fine and/or 6 months to a year imprisonment.

United States

In the United States, cocaine is a Schedule II drug under the Controlled Substances Act, indicating that it has a high abuse potential but also carries a medicinal purpose.^[27][28] Under the Controlled Substances Act, crack and cocaine are considered the same drug.

The Anti-Drug Abuse Act of 1986 increased penalties for crack cocaine possession and usage. It mandated a mandatory minimum sentence of five years without parole for possession of five grams of crack; to receive the same sentence with powder cocaine one had to have 500 grams.^[29] This sentencing disparity was reduced from 100-to-1 to 18-to-1 by the Fair Sentencing Act of 2010.

Europe

In the United Kingdom, crack is a Class A drug under the Misuse of Drugs Act 1971. In the Netherlands it is a List 1 drug of the Opium Law.

Political scandals

Rob Ford, the 64th mayor of Toronto, was filmed smoking crack while he was in office. Marion Barry, Mayor of Washington D.C., was filmed smoking crack in 1990 in a sting operation.^[30]

See also

• Cocaine paste ('paco')
• Structurally related chemicals: proparacaine, tetracaine, lidocaine, procaine, hexylcaine, bupivacaine, benoxinate, mepivacaine, prilocaine, etidocaine, benzocaine, chloroprocaine, propoxycaine, dyclonine, dibucaine, and pramoxine.

References

1. ^ ^abcdefghManual of Adolescent Substance Abuse Treatment, Todd Wilk Estroff, M.D., 2001 (306 pages), pp. 44–45, (describes cocaine/crack processing & melting points): p.44 has 'cannot be smoked because..melting point of 190 °C'; p.45 has 'It is the most addictive form of cocaine', webpage: [1], p. 44, at Google Books
2. ^Reinarman, Craig; Levine, Harry G. (1997). 'Crack in Context: America's Latest Demon Drug'. In Reinarman, Craig; Levine, Harry G. (eds.). Crack in America: Demon Drugs and Social Justice. Berkeley, CA: University of California Press.
3. ^ ^abcdefghA.M. Costa Rica, July 2008, Crack rocks offer a short but intense high to smokers.
4. ^Kinzie, Erik (April 2009). 'Levamisole Found in Patients Using Cocaine'. Annals of Emergency Medicine. 53 (4). Retrieved 2009-08-18.
5. ^ ^ab'Officials warn of life-threatening cocaine in area', Stacy O'Brien, Red Deer Advocate, December 2008, webpage: reddeer-officials^{[permanent dead link]}: notes cocaine with the worming medicine levamisole.
6. ^Treadwell, SD; Robinson, TG (June 2007). 'Cocaine use and stroke'. Postgraduate Medical Journal (Review). 83 (980): 389–94. doi:10.1136/pgmj.2006.055970. PMC2600058. PMID17551070.
7. ^'Cocaine Abuse & Addiction'. www1.nyc.gov. City of New York.
8. ^ ^{abcdefghijklmnop}'DEA, Drug Information, Cocaine', United States DOJ Drug Enforcement Administration, 2008, webpage: DEA-cocaineArchived 2008-06-22 at the Wayback Machine.
9. ^ ^abWhite Mischief: A Cultural History of Cocaine, Tim Madge, 2004, ISBN1-56025-370-3, link: [2], p. 18, at Google Books.
10. ^ ^abc 'Life or Meth – CRACK OF THE 90'S', Salt Lake City Police Department, Utah, 2008, PDF file: Methlife-PDFArchived 2007-10-31 at the Wayback Machine.
11. ^ ^abScheidweiler KB, Plessinger MA, Shojaie J, Wood RW, Kwong TC (2003). 'Pharmacokinetics and pharmacodynamics of methylecgonidine, a crack cocaine pyrolyzate'. Journal of Pharmacology and Experimental Therapeutics. 307 (3): 1179–1187. doi:10.1124/jpet.103.055434. PMID14561847. Retrieved 2008-02-24.
12. ^Yang Y, Ke Q, Cai J, Xiao YF, Morgan JP (2001). 'Evidence for cocaine and methylecgonidine stimulation of M(2) muscarinic receptors in cultured human embryonic lung cells'. British Journal of Pharmacology. 132 (2): 451–460. doi:10.1038/sj.bjp.0703819. PMC1572570. PMID11159694.
13. ^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'. Chemical Research in Toxicology. 15 (12): 1543–1548. doi:10.1021/tx0255828. PMID12482236.
14. ^Cole, Claire; Jones, Lisa; McVeigh, Jim; Kicman, Andrew; Syed, Qutub; Belis, Mark A. (2010). Cut: A Guide to Adulturants, Bulkinh Agents and other Contaminants found in Illicit Drugs. Centre for Public Health, Liverpool John Moores University. pp. 6–25.
15. ^ ^abLengel, Allan (April 5, 2006). 'A Rose With Another Name: Crack Pipe'. The Washington Post. Retrieved May 28, 2017.
16. ^ ^abMégarbane, B; Chevillard, L (5 December 2013). 'The large spectrum of pulmonary complications following illicit drug use: features and mechanisms'. Chemico-Biological Interactions. 206 (3): 444–51. doi:10.1016/j.cbi.2013.10.011. PMID24144776.
17. ^ ^abcd 'Delusional Parasitosis', The Bohart Museum of Entomology, 2005, webpage: UCDavis-delusional^{[permanent dead link]}.
18. ^Morton, W. Alexander (August 1999). 'Cocaine and Psychiatric Symptoms'. Primary Care Companion to the Journal of Clinical Psychiatry. 1 (4): 109–113. doi:10.4088/pcc.v01n0403. PMC181074. PMID15014683.
19. ^Okie, Susan (2009-01-27). 'The Epidemic That Wasn't'. The New York Times.
20. ^'Growth, Development, and Behavior in Early Childhood Following Prenatal Cocaine Exposure, Frank et al. 285 (12): 1613 – JAMA'. Jama.ama-assn.org. 2001-03-28. Retrieved 2010-12-22.
21. ^NIDA – Research Report Series – Cocaine Abuse and AddictionArchived September 26, 2007, at the Wayback Machine
22. ^'Street Drugs and pregnancy'. March of Dimes. Retrieved 2009-05-26.
23. ^Morgan, John P.; Zimmer, Lynn (1997). 'Social Pharmacology of Smokeable Cocaine'. In Reinarman, Craig; Levine, Harry G. (eds.). Crack in America: Demon Drugs and Social Justice. Berkeley, Ca.: University of California Press.
24. ^Reinarman, Craig; Waldorf, Dan; Murphy, Sheigla B.; Levine, Harry G. (1997). 'The Contingent Call of the Pipe: Bingeing and Addiction Among Heavy Cocaine Smokers'. In Reinarman, Craig; Levine, Harry G. (eds.). Crack in America: Demon Drugs and Social Justice. Berkeley, Ca.: University of California Press.
25. ^ ^abcTom Dalzell (2009), The Routledge Dictionary of Modern American Slang and Unconventional English, Routledge, ISBN978-0-415-37182-7
26. ^'Single Convention on Narcotic Drugs, 1961'(PDF). International Narcotics Control Board. Archived from the original(PDF) on 2008-05-09. Retrieved 2008-05-01.
27. ^'DEA, Title 21, Section 812'. Usdoj.gov. Archived from the original on 2008-08-22. Retrieved 2008-09-05.
28. ^21 U.S.C.§ 812(b)(2)Retrieved 2008-05-01.
29. ^Sterling, Eric. 'Drug Laws and Snitching: A Primer'. PBS. Retrieved 20 May 2013.
30. ^LaFraniere, Sharon (January 19, 1990). 'Barry Arrested on Cocaine Charges in Undercover FBI, Police Operation'. The Washington Post. p. A1.

Further reading

• Cooper, Edith Fairman, The emergence of crack cocaine abuse, Nova Publishers, 2002

Cocaine, also known as coke, is a strong stimulant most frequently used as a recreational drug.^[10] It is commonly snorted, inhaled as smoke, or dissolved and injected into a vein.^[9] Mental effects may include loss of contact with reality, an intense feeling of happiness, or agitation.^[9] Physical symptoms may include a fast heart rate, sweating, and large pupils.^[9] High doses can result in very high blood pressure or body temperature.^[11] Effects begin within seconds to minutes of use and last between five and ninety minutes.^[9] Cocaine has a small number of accepted medical uses such as numbing and decreasing bleeding during nasal surgery.^[12]

Cocaine is addictive due to its effect on the reward pathway in the brain.^[10] After a short period of use, there is a high risk that dependence will occur.^[10] Its use also increases the risk of stroke, myocardial infarction, lung problems in those who smoke it, blood infections, and sudden cardiac death.^[10][13] Cocaine sold on the street is commonly mixed with local anesthetics, cornstarch, quinine, or sugar, which can result in additional toxicity.^[14] Following repeated doses a person may have decreased ability to feel pleasure and be very physically tired.^[10]

Cocaine acts by inhibiting the reuptake of serotonin, norepinephrine, and dopamine.^[10] This results in greater concentrations of these three neurotransmitters in the brain.^[10] It can easily cross the blood–brain barrier and may lead to the breakdown of the barrier.^[15][16] In 2013, 419 kilograms were produced legally.^[17] It is estimated that the illegal market for cocaine is 100 to US$500 billion each year.^[10] With further processing crack cocaine can be produced from cocaine.^[10]

Cocaine is the second most frequently used illegal drug globally, after cannabis.^[18] Between 14 and 21 million people use the drug each year.^[10] Use is highest in North America followed by Europe and South America.^[10] Between one and three percent of people in the developed world have used cocaine at some point in their life.^[10] In 2013, cocaine use directly resulted in 4,300 deaths, up from 2,400 in 1990.^[19] It is named after the coca plant from which it is isolated.^[9] The leaves of the coca plant have been used by Peruvians since ancient times.^[14] Cocaine was first isolated from the leaves in 1860.^[10] Since 1961, the international Single Convention on Narcotic Drugs has required countries to make recreational use of cocaine a crime.^[20]

• 1Uses
  • 1.2Recreational
• 2Adverse effects
• 3Pharmacology
• 4Chemistry
  • 4.2Forms
  • 4.3Biosynthesis
• 5Usage
• 6History
• 7Society and culture
  • 7.1Legal status
  • 7.3Economics
    • 7.3.3Trafficking and distribution

Uses

Medical

Topical cocaine can be used as a local numbing agent to help with painful procedures in the mouth or nose.^[21]

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.^[21] Medicinal use of cocaine has decreased as other synthetic local anesthetics such as benzocaine, proparacaine, lidocaine, and tetracaine are now used more often.^[21] 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.^{[citation needed]} An alternative method of administration for ENT surgery is mixed with adrenaline and sodium bicarbonate, as Moffett's solution.^{[citation needed]}

Recreational

Cocaine is a powerful nervous system stimulant.^[22] Its effects can last from 15 or 30 minutes to an hour. The duration of cocaine's effects depends on the amount taken and the route of administration.^[23] Cocaine can be in the form of fine white powder, bitter to the taste. When inhaled or injected, it causes a numbing effect. Crack cocaine is a smokeable form of cocaine made into small 'rocks' by processing cocaine with sodium bicarbonate (baking soda) and water.^[9][24] Crack cocaine is referred to as 'crack' because of the crackling sounds it makes when heated.^[9]

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.^[25]

Coca leaves

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 administering cocaine.

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.

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.^[26]

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.^[27] However, its actual effectiveness has never been systematically studied.^[27]

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.'^[28] 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.^{[citation needed]}

Insufflation

Nasal insufflation (known colloquially as 'snorting', 'sniffing', or 'blowing') is a common method of ingestion of recreational powdered cocaine.^[29] 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.^[9] Insufflation of cocaine also leads to the longest duration of its effects (60–90 minutes).^[9] When insufflating cocaine, absorption through the nasal membranes is approximately 30–60%, with higher doses leading to increased absorption efficiency.^{[citation needed]} 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.^[30] 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;^{[citation needed]} as a vasoconstrictor, cocaine acts to reduce bleeding.

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.^[31] 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] As tolerance builds rapidly in the short-term (hours), many lines are often snorted to produce greater effects.^{[citation needed]} A 2001 study reported that the sharing of straws used to 'snort' cocaine can spread blood diseases such as hepatitis C.^[32]Serial killers in the us.

Injection

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 two 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.^[30] 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 injection.^{[citation needed]}

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 cocaine addiction.^[33]

Inhalation

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.^[9] In contrast, inhalation of cocaine leads to the shortest duration of its effects (5–15 minutes).^[9] The two main ways cocaine is smoked are freebasing and by using cocaine which has been converted to smokable 'crack cocaine'. Cocaine is smoked by inhaling the vapor produced when solid cocaine is heated to the point that it sublimates.^[34] 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.^[30]Pyrolysis products 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.^[35]

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.^[36] 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.^[37] 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.^{[citation needed]} The language referring to paraphernalia and practices of smoking cocaine vary, as do the packaging methods in the street level sale.^{[citation needed]}

Suppository

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.^{[citation needed]}

Adverse effects

Acute

With excessive or prolonged use, the drug can cause itching, fast heart rate, hallucinations, and paranoid delusions or sensations of insects crawling on the skin.^[38] Overdoses may cause abnormally high body temperature and a marked elevation of blood pressure, which can be life-threatening,^[38]abnormal heart rhythms,^[39] and death.^[39]

Anxiety, paranoia, and restlessness can also occur, especially during the comedown. With excessive dosage, tremors, convulsions and increased body temperature are observed.^[22] Severe cardiac adverse events, particularly sudden cardiac death, become a serious risk at high doses due to cocaine's blocking effect on cardiac sodium channels.^[39]

• Opioid involvement in cocaine overdose deaths. Green line is cocaine and any opioid (top line in 2017). Gray line is cocaine without any opioids (bottom line in 2017). Yellow line is cocaine and other synthetic opioids (middle line in 2017).^[40]

• Delphic analysis regarding 20 popular recreational drugs based on expert opinion. Cocaine was ranked the 2nd in dependence and physical harm and 3rd in social harm.^[41]

Chronic

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 striataldopamine transporter (DAT) sites, suggesting cocaine has neuroprotective properties for dopamine neurons.^[42] 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.^[43]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 agitation.^[43]

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.^[44] 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.^[9] 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.^[9]

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 acid.^[45]

Cocaine may also greatly increase the risk of developing rare autoimmune or connective tissue diseases such as lupus, Goodpasture syndrome, vasculitis, glomerulonephritis, Stevens–Johnson syndrome, and other diseases.^{[46][47][48][49]} It can also cause a wide array of kidney diseases and kidney failure.^[50][51]

Cocaine use leads to an increased risk of hemorrhagic and ischemic strokes.^[24] Cocaine use also increases the risk of having a heart attack.^[52]

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.^[53] Each subsequent dose of cocaine continues to increase ΔFosB levels 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.^[54] They self-administer cocaine at lower doses than control,^[55] but have a greater likelihood of relapse when the drug is withheld.^[55][56] ΔFosB increases the expression of AMPA receptor subunit GluR2^[54] and also decreases expression of dynorphin, thereby enhancing sensitivity to reward.^[56]

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.

During pregnancy

Cocaine is known to have a number of deleterious effects during pregnancy. Pregnant people who use cocaine have an elevated risk of placental abruption, a condition where the placenta detaches from the uterus and causes bleeding.^[57] Due to its vasoconstrictive and hypertensive effects, they are also at risk for hemorrhagic stroke and myocardial infarction. Cocaine is also teratogenic, meaning that it can cause birth defects and fetal malformations. In-utero exposure to cocaine is associated with behavioral abnormalities, cognitive impairment, cardiovascular malformations, intrauterine growth restriction, preterm birth, urinary tract malformations, and cleft lip and palate.^[58]

Pharmacology

Pharmacodynamics

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).^[59][10] 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. The increased concentration of dopamine in the synapse activates post-synaptic dopamine receptors, which makes the drug rewarding and promotes the compulsive use of cocaine.^[60]

Cocaine 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.^[61] The 5-HT2 receptor (particularly the subtypes 5-HT2AR, 5-HT2BR and 5-HT2CR) are involved in the locomotor-activating effects of cocaine.^[62]

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 molecule binds.^[63]

Sigma receptors are affected by cocaine, as cocaine functions as a sigma ligand agonist.^[64] Further specific receptors it has been demonstrated to function on are NMDA and the D1 dopamine receptor.^[65]

Cocaine also blocks sodium channels, thereby interfering with the propagation of action potentials;^[66][39] 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.^[67] 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.^{[citation needed]} Recent research points to an important role of circadian mechanisms^[68] and clock genes^[69] 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 weight loss. Cocaine effects, further, are shown to be potentiated for the user when used in conjunction with new surroundings and stimuli, and otherwise novel environs.^[70]

Pharmacokinetics

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.^[9] The metabolism is dominated by hydrolyticester 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.^[9] Further minor metabolites of cocaine include norcocaine, p-hydroxycocaine, m-hydroxycocaine, p-hydroxybenzoylecgonine (pOHBE), and m-hydroxybenzoylecgonine.^[71] If consumed with alcohol, cocaine combines with alcohol in the liver to form cocaethylene.^[9] Studies have suggested cocaethylene is both more euphoric, and has a higher cardiovascular toxicity than cocaine by itself.^[9]

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 cocaine metabolites in hair is possible in regular users until the sections of hair grown during use are cut or fall out.^[72]

Chemistry

Appearance

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 heroin.^{[73][dubious]}

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. It 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 crystalline nature.^{[citation needed]}

Forms

Salts

Cocaine – a tropane alkaloid – is a weakly alkaline compound, and can therefore combine with acidic compounds to form salts. The hydrochloride (HCl) salt of cocaine is by far the most commonly encountered, although the sulfate (SO₄^2-) and the nitrate (NO₃⁻) salts 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.^{[citation needed]}

Base

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.

Crack Cocaine

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^[74] because of methylecgonidine's effects on lung tissue^[75] and liver tissue.^[76]

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.^{[citation needed]}

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 inhaled.^[77]

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.^[78]

Pure cocaine base/crack can be smoked because it vaporizes smoothly, with little or no decomposition at 98 °C (208 °F),^[79] 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

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 Peru and Bolivia for many years as a drink having medicinal powers. In Peru, the National Coca Company, a state-run corporation, sells cocaine-infused teas and other medicinal products and also exports leaves to the U.S. for medicinal use.^[80]

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.^[81] 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 alkaloids.^{[improper synthesis?]} The cocaine metabolite benzoylecgonine can be detected in the urine of people a few hours after drinking one cup of coca leaf infusion.^[82]

Biosynthesis

The first synthesis and elucidation of the cocaine molecule was by Richard Willstätter in 1898.^[83] Willstätter's synthesis derived cocaine from tropinone. Since then, Robert Robinson and Edward Leete have made significant contributions to the mechanism of the synthesis. (-NO₃)

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.^[84] 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.^[85] 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.^[86] This is due to the extra chiral center at C-2.^[87] 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.^[88] Benzoyl-CoA then combines the two units to form cocaine.

N-methyl-pyrrolinium cation

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 Leete.^[89] 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,^[90] 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 N-methyl-Δ¹-pyrrolinium cation.

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.^[91] 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.^[92] 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.^[93]

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.^[94] 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.^[95]

Usage

According to a 2016 United Nations report, England and Wales are the countries with the highest rate of cocaine usage (2.4% of adults in the previous year).^[97] 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 Ireland (1.5%).^[97]

Europe

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 Ireland.

Approximately 17 million Europeans (5.1%) have used cocaine at least once and 3.5 millions (1.1%) in the last year. About 1.9% (2.3 million) of young adults (15–34 years old) have used cocaine in the last year (latest data available as of 2018).^[98]

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.^[99]

In 2014 London had the highest amount of cocaine in its sewage out of 50 European cities.^[100]

United States

Cocaine is the second most popular illegal recreational drug in the United States (behind cannabis)^[101] and the U.S. is the world's largest consumer of cocaine.^[102] 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 from 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.^[103]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.

History

Discovery

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.^[104] There is also evidence that these cultures used a mixture of coca leaves and saliva as an anesthetic for the performance of trepanation.^[105]

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.^[106] But after discovering that these claims were true, they legalized and taxed the leaf, taking 10% off the value of each crop.^[107] In 1569, Spanish botanist Nicolás Monardes described the indigenous peoples' practice of chewing a mixture of tobacco and coca leaves to induce 'great contentment':

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.^[108]

In 1609, PadreBlas 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?^[109]

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 chemists.^{[citation needed]}

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.^[110]

In 1856, 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 in Germany, who then developed an improved purification process.^[111]

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'.^[111][112] Because of its use as a local anesthetic, a suffix '-caine' was later extracted and used to form names of synthetic local anesthetics.

What Is The Origin Of Crack Cocaine

The first synthesis and elucidation of the structure of the cocaine molecule was by Richard Willstätter in 1898.^[83] It was the first biomimetic synthesis of an organic structure recorded in academic chemical literature.^[113][114] The synthesis started from tropinone, a related natural product and took five steps.

Medicalization

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.^[115]

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,^[116] and James Leonard Corning demonstrated peridural anesthesia.^[117] 1898 saw Heinrich Quincke use cocaine for spinal anesthesia.

Popularization

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 return to 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 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:^[119]

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.^[120]

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.'

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 laborers.^[121]

In 1909, 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.^[122]

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.^[123]

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'.^{[124][125][126][127]} In addition the pace of modern society − such as in finance − gives many the incentive to make use of the drug.^[124]

Modern usage

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.^{[citation needed][when?]}

Cocaine use is prevalent across all socioeconomic strata, including age, demographics, economic, social, political, religious, and livelihood.^{[citation needed]}

The estimated U.S. cocaine market exceeded US$70 billion in street value for the year 2005, exceeding revenues by corporations such as Starbucks.^[128][129] 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'.^{[citation needed]}

In 1995 the World Health Organization (WHO) and the United Nations Interregional 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 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 conflictedwith 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.^[130]

In October 2010 it was reported that the use of cocaine in Australia has doubled since monitoring began in 2003.^[131]

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 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.^[132]

Society and culture

Legal status

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 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.^[133] The provisions as to how much a coca farmer can yield annually is protected by laws such as the Bolivian Cato accord.^[134] In addition, some parts of Europe, the United States, and Australia allow processed cocaine for medicinal uses only.

Australia

Cocaine is a Schedule 8 prohibited substance in Australia under the Poisons Standard (July 2016).^[135] 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 dependence.^[135]

In 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.^[136]

United States

The US federal government instituted a national labeling requirement for cocaine and cocaine-containing products through the Pure Food and Drug Act of 1906.^[137] 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.^[138] 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 a 1915 editorial in the journal American Medicine to remark that 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.'^[139] The Harrison Act left manufacturers of cocaine untouched so long as they met certain purity and labeling standards.^[140] Despite that cocaine was typically illegal to sell and legal outlets were rarer, the quantities of legal cocaine produced declined very little.^[140] Legal cocaine quantities did not decrease until the Jones–Miller Act of 1922 put serious restrictions on cocaine manufactures.^[140]

Interdiction

In 2004, according to the United Nations, 589 tonnes of cocaine were seized globally by law enforcement authorities. Colombia seized 188 t, the United States 166 t, Europe 79 t, Peru 14 t, Bolivia 9 t, and the rest of the world 133 t.^[141]

Economics

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 needed]}

Production

Colombia is as of 2019 the world's largest cocaine producer, with production more than tripling since 2013.^[142][143] 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.^{[citation needed]}

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.^[144]

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 plantations.^{[citation needed]}

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 needed]}

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.^[146][147]

Synthesis

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 stereoisomers (cocaine has 4 chiral centres – 1R, 2R, 3S, and 5S, 2 of them dependent, hence a total potential of 8 possible stereoisomers) plus synthetic by-products limits the yield and purity.^{[citation needed]}Names like 'synthetic cocaine' and 'new cocaine' have been misapplied to phencyclidine (PCP) and various designer drugs.^{[citation needed]}

Trafficking and distribution

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,^[102] 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').^[148]

Caribbean and Mexican routes

As of 2005, cocaine shipments from South America transported through Mexico or 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.–Mexico border. 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.–Mexico border. Sixty-five percent of cocaine enters the United States through Mexico, and the vast majority of the rest enters through Florida.^{[149][page needed]} As of 2015, 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.^[150]

Cocaine traffickers from Colombia and 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.^{[citation needed]}

Chilean route

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 than in Peru and Bolivia, the final destination is usually Europe, especially Spain where drug dealing networks exist among South American immigrants.^{[citation needed]}

Techniques

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.^{[citation needed]}

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 populations.^{[citation needed]}

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.^[151]

Sales to consumers

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.^[152][153] 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 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.^{[citation needed]} 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.^[154]

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.^[155]

Consumption

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%.^[156] It is estimated that 1.5 million people in the United States used cocaine in 2010 down from 2.4 million in 2006.^[9] Conversely, cocaine use appears to be increasing in Europe with the highest prevalences in Spain, the United Kingdom, Italy, and Ireland.^[9]

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'.^[157]

The History Of Crack Cocaine

Research

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.^[158]

See also

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Bibliography

• Gootenberg P, ed. (1999). Cocaine: Global Histories. London: Routledge. ISBN978-0-203-02646-5.
• Madge T (2001). White Mischief: A Cultural History of Cocaine. Edinburgh: Mainstream Publishing Company. ISBN978-1-84018-405-1.
• Spillane JF (2000). Cocaine: From Medical Marvel to Modern Menace in the United States, 1884–1920. Baltimore and London: The Johns Hopkins University Press. ISBN978-0-8018-6230-4.

Further reading

Where Did Crack Cocaine Come From

• Feiling T (2009). The Candy Machine: How Cocaine Took Over the World. London: Penguin. ISBN978-0-14-103446-1.

External links

Who Invented Crack Cocaine

• Erowid – Cocaine Information — A collection of data about cocaine including dose, effects, chemistry, legal status, images and more.
• Cocaine Market Data and Value-Havocscope Black Markets at the Wayback Machine (archived 23 March 2011) Data on cocaine trafficking worldwide.

Crack Cocaine In The 1980s