This article is about the purified salt form of cocaine. For the vaporized freebase, seeCrack cocaine. For the crude coca leaf extract, seeCocaine paste. For the disguised smuggled form, seeBlack cocaine.
Not to be confused with "Pink cocaine", which typically does not contain cocaine; seeTusi (drug).
Globally, in 2019, cocaine was used by an estimated 20 million people (0.4% of adults aged 15 to 64 years). The highest prevalence of cocaine use was inAustralia andNew Zealand (2.1%), followed byNorth America (2.1%),Western andCentral Europe (1.4%), andSouth andCentral America (1.0%).[58] Since 1961, theSingle Convention on Narcotic Drugs has required countries to make recreational use of cocaine acrime.[59] In the United States, cocaine is regulated as aSchedule II drug under theControlled Substances Act, meaning that it has a high potential for abuse but has an accepted medical use.[60] While rarely used medically today, its accepted uses include serving as a topical local anesthetic for the upperrespiratory tract and as anantihemorrhagic agent to stop bleeding in the mouth, throat, and nasal cavities.[61]
Llipta is used to improve extraction when chewing coca (Museo de la Coca,Cusco, Peru).
It is legal for people to usecoca leaves in theAndean Community, such asPeru andBolivia, and Argentina, where they are chewed, consumed in the form of tea, or are sometimes incorporated into food products.[62] Coca leaves are typically mixed with an alkaline substance (such asslaked lime) and chewed into a wad that is retained in thebuccal pouch (mouth between gum and cheek, much the same aschewing tobacco is chewed) and sucked of its juices. The juices are absorbed slowly by themucous membrane of the inner cheek and by thegastrointestinal tract when swallowed.
Coca herbalinfusion (also referred to ascoca 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 ofPeru andBolivia for many years as a drink havingmedicinal powers. In Peru, theNational 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.[63] The effects of drinking coca tea are mild stimulation and mood lift.[64]
In 1986 an article in theJournal of the American Medical Association revealed that U.S.health food stores were selling dried coca leaves to be prepared as an infusion as "Health Inca Tea". While the packaging claimed it had been "decocainized", no such process had actually taken place. The article stated that drinking two cups of the tea per day gave a mildstimulation, increasedheart rate, andmood elevation, and the tea was essentially harmless.[65]
Mambe or ypadu is made from toasted and ground coca leaves with ashes
Ypadú or ypadu (also known as mambé) is an unrefined, unconcentratedpowder made from toastedcoca leaves and the ash of various other plants. It is traditionally prepared and consumed by indigenous tribes in the Northwest Amazon.[66] Like coca teas consumed inPeru to adapt to sickness induced by high elevation, it has a longethnobotanical history and cultural associations.
Medical
Karl Koller's groundbreaking discovery of cocaine as a local anesthetic is regarded as the second most significant advance in the history of anesthesia. Although cocaine was once widely preferred for topical anesthesia, the search for replacement agents intensified due to rising costs, strict regulations, and its habit-forming potential.[21] Cocaine is not included on theWHO Model List of Essential Medicines; the list formally excludes "cocaine and its combinations" as therapeutic alternatives toophthalmological preparations.[67]
Today, the USDrug Enforcement Administration (DEA) classifies cocaine as aSchedule II drug, recognizing its high potential for abuse but still permitting its limited use for medical purposes. However, currentpharmacoepidemiological trends suggest that cocaine may soon reach the point where, in practical terms, it is no longer used medically in health care as a Schedule II substance. This report may prompt some states (such as North Dakota) and institutions to reconsider whether further efforts to identify alternative agents are needed. As physician boards—but not pharmacy boards—continue to assess knowledge of licit cocaine, attention may shift toward drugs with more contemporary medical use.[21]
Cocaine is rarely prescribed in modern medicine due to its high potential for abuse and significant risk of adverse effects; its use is now almost exclusively limited tohealth facilities for specific diagnostic procedures or surgeries.
Topical
Cocaine is used in medical practice as atopical medication.[21] Because it is not absorbed into the bloodstream in significant amounts when used this way, topical application does not produce the psychoactive effects associated with recreational cocaine use.
Nasal solution cocaine hydrochloride (Goprelto), an ester used for intranasal application, was approved for medical use in the United States in December 2017, and is indicated for the introduction of topical anesthesia of the mucous membranes for diagnostic procedures and surgeries on or through the nasal cavities of adults.[71][2] Cocaine hydrochloride (Numbrino) was approved for medical use in the United States in January 2020.[72][3] Headache andepistaxis are the most frequently reported adverse reactions with Goprelto,[2] while hypertension and tachycardia-includingsinus tachycardia-are most common with Numbrino.[3]
Ophthalmological use
Cocaineeye drops have traditionally been used byneurologists when examining people suspected of havingHorner syndrome. In Horner syndrome,sympathetic innervation to the eye is blocked. In a healthy eye, cocaine stimulates thesympathetic nervous system (SNS) by inhibiting norepinephrine reuptake, causing thepupil to dilate. In patients with Horner syndrome, sympathetic innervation to the eye is disrupted, so the affected pupil does not dilate in response to cocaine and remains constricted, or dilates to a lesser extent than the unaffected eye, which also receives the eye drop test. If both eyes dilate equally, the patient does not have Horner syndrome.[73]
However,apraclonidine has largely replaced cocaine as the first-line pharmacologic agent for the diagnosis of Horner syndrome in routine clinical practice.[74][75][20]
Peruvian flake cocaine on a metal milligramscale tray
Recreational cocaine is typically not taken by mouth due to its poor bioavailability, instead it is usuallysnorted orinjected. Cocaine hydrochloride can also be chemically converted into itsfree base form,crack cocaine, which can be vaporized.[citation needed]
Cocaine is acentral nervous systemstimulant.[76] Its effects can last from 15 minutes to an hour. The duration of cocaine's effects depends on the amount taken and the route of administration.[77] Cocaine can be in the form of fine white powder and has a bitter taste.Crack cocaine is a smokeable form of cocaine made into small "rocks" by processing cocaine withsodium bicarbonate (baking soda) and water.[13][25]
Cocaine use leads to increases in alertness, feelings of well-being andeuphoria, increased energy andmotor activity, and increased feelings of competence andsexuality.[78]
Lines of cocaine prepared for snorting.Contaminated currency such as banknotes might serve as afomite of diseases like hepatitis C[80]
Nasalinsufflation (known colloquially as "snorting", "sniffing", or "blowing") is a common method of ingestion of recreational powdered cocaine.[81] The drug coats and is absorbed through the mucous membranes lining thenasal 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.[13] Insufflation of cocaine also leads to the longest duration of its effects (60–90 minutes).[13] When insufflating cocaine, absorption through the nasal membranes is approximately 30–60%[82]
Snuff spoons, hollowed-outpens, cutstraws, pointed ends of keys,[86] longfingernails orartificial nails, and (clean)tampon applicators are also used to insufflate cocaine. The cocaine typically is poured onto a flat, hard surface and divided into "bumps", "lines", or "rails", and then insufflated.[87] A 2001 study reported that the sharing of straws used to "snort" cocaine can spread blood diseases such ashepatitis C.[88]
Cocaine spoon
Chinese snuff bottle stopper with a spoon
Historically,snuff spoons were used for cocaine in the 20th century, hence the names "cocaine spoon" and "coke spoon". Some local statutes in the US treat spoons that are too small and thus "unsuited for the typical, lawful uses of a spoon" asdrug paraphernalia.[89][90][91]
Injection
Subjective effects not commonly shared with other methods of administration include a ringing in the ears moments after injection (usually when over 120 milligrams) lasting 2 to 5 minutes includingtinnitus 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.[92] The euphoria passes quickly. Aside from the toxic effects of cocaine, there is also the danger of circulatoryemboli from the insoluble substances that may be used to cut the drug. As with all injectedillicit substances, there is a risk of the user contractingblood-borne infections if sterile injecting equipment is not available or used.
Coca paste (paco, basuco, oxi, pasta) is a crudeextract of thecoca leaf which contains 40% to 91%cocaine freebase along with companion coca alkaloids and varying quantities ofbenzoic acid,methanol, andkerosene. The caustic reactions associated with the local application of coca paste prevents its use by oral, intranasal, mucosal, intramuscular, intravenous or subcutaneous routes. Coca paste can only be smoked when combined with a combustible material such as tobacco or cannabis.[93]
Crude cocaine preparation intermediates are marketed as cheaper alternatives to pure cocaine to local markets while the more expensive end product is exported to United States and European markets.Freebase cocaine paste preparations can be smoked. The psychological and physiological effects of thepaco are quite severe.[94][95] Media usually report that it is extremely toxic and addictive.[96][97][98] According to a study by Intercambios, media appear to exaggerate the effects ofpaco. These stereotypes create a sense that nothing can be done to help apaco addict and thus stand in the way of rehabilitation programs.[99]
Powder cocaine (cocaine hydrochloride) must be heated to a high temperature to be smoked (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. Cocaine base/crack can be smoked because it vaporizes with little or no decomposition at 98 °C (208 °F),[100] which is below the boiling point of water.
Cocaine should not be used in individuals with a known allergy orhypersensitivity to the drug or any components of its topical formulation. It is also contraindicated inelderly patients and those with a history of hypertension orcardiovascular disease.[101]
Under the former FDApregnancy category system, cocaine was classified as a Category C drug. Its potential to cause harm to the fetus is not fully known, so it should only be administered to pregnant women if clearly necessary.[101]
Cocaine can act as ateratogen, having various effects on the developing fetus.[102] Some common teratogenic defects caused by cocaine includehydronephrosis,cleft palate,polydactyly, anddown syndrome.[102] Cocaine as a drug has a low molecular weight and high water and lipid solubility which enables it to cross theplacenta and fetal blood-brain barrier.[103] Because cocaine is able to pass through the placenta and enter the fetus, the fetus' circulation can be negatively affected. With restriction of fetal circulation, the development of organs in the fetus can be impacted, even resulting inintestines developing outside of the fetus' body.[102] Cocaine use during pregnancy can also result inobstetric labor complications such as,placental abruption,[104]preterm birth or delivery,uterine rupture,miscarriage, andstillbirth.[102][105] Prenatal cocaine exposure may cause subtle cognitive deficits and lower the chance of above-average IQ by age 4, but supportive caregiving can significantly improve outcomes.[106]
Breastfeeding
Mothers utilizing recreational drugs, such as cocaine, methamphetamines, PCP, and heroin, should notbreastfeed.[107][108]: 13
TheMarch 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 ofmiscarriage. Later in pregnancy, it can triggerpreterm 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 withlow birth weight (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 oflifelong disabilities such as mental retardation andcerebral 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 astroke, irreversiblebrain injury, or amyocardial infarction.[109]
A 2010 study ranking various illegal and legal drugs based on statements by drug-harm experts in the UK. Crack cocaine and cocaine were found to be the third and fifth overall most dangerous drugs respectively.[110]
2007delphic analysis regarding 20 popular recreational drugs based on expert opinion in the UK. Cocaine was ranked the 2nd in dependence and physical harm and 3rd in social harm.[111]
Cardiac complications
Cocaine use can cause serious heart problems like sudden death, heart inflammation,arrhythmias, and heart attacks. It triggers coronary artery spasms, increases blood clot risk, and acceleratesatherosclerosis, especially with long-term use. The severity of heart disease often relates to how long and how often cocaine is used.[112] It can also become a serious risk at high doses due to cocaine's blocking effect on cardiac sodium channels.[113]
Levamisole syndromes
Levamisole is one of the most common adulterants found in illicit cocaine, with studies showing that between 2009 and 2016, 50–70% of all cocaine specimens worldwide contained levamisole, reflecting similar high rates of contamination across North America and Europe.[114] Before trafficking to the United States, the cocaine is frequently adulterated with levamisole.[115] By October 2017, this figure had risen further, with the USDrug Enforcement Administration (DEA) reporting that 87% of seized and analyzed cocaine bricks in the United States contained levamisole, making it the most common adulterant in cocaine at that time.[116]
In the body, levamisole is converted intoaminorex, a substance withamphetamine-like stimulant effects and a long duration of action.[117] Levamisole-adulterated cocaine is associated with cocaine- and levamisole-inducedvasculitis (CLIV) and cocaine/levamisole-associatedautoimmune syndrome (CLAAS).[118][119]Reagent testing kits can be used to detect the presence of cocaine and levamisole.[120]
Levamisole-induced necrosis syndrome (LINES) is a complication characterized bynecrosis resulting from exposure tolevamisole, a medication with immunomodulatory properties. While LINES can occur with levamisole use alone, most reported cases are associated with the use of cocaine adulterated with levamisole as a cutting agent. This syndrome is marked by skin necrosis, often affecting areas such as the ears, face, and extremities, and is thought to result from levamisole's effects on blood vessels and the immune system.[121]
Cocaine/levamisole-associated syndromes
The skin necrosis associated with levamisole toxicity ranges fromleukocytoclastic vasculitis to occlusivevasculopathy. Several cases of severe agranulocytosis associated with cocaine use have been reported since 2006. With the recently recognized dermal disease, the face and ears are commonly affected, especially the bilateralhelices and cheeks. However, there have also been case reports of involvement of the abdomen, chest, lower buttocks and legs.[122][123]
During the mid-2010s, levamisole was found in most cocaine products available in both the United States and Europe.[124] Levamisole is known to cause an acute condition involving a severe and dangerous lowered white blood cell count, known asagranulocytosis, in cocaine users, and may also accentuate cocaine's effects.[125][126]
Clinical studies have shown that taking levamisole at doses of 50–200 mg per day can lead to agranulocytosis in approximately 0.08–5% of patients.[127]
Cocaine- and levamisole-induced vasculitis (CLIV) is often used as an umbrella term for the vasculitic and necrotic complications seen with levamisole-adulterated cocaine, including both LINES and CLAAS.[118]
Cocaine and levamisole-adulterated cocaine (LAC) can cause cocaine-inducedvasculitis (CIV) that mimics primaryanti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), presenting ascocaine-induced midline destructive lesions, LAC vasculopathy, or CIV. These conditions involve immune activation throughNETosis and ANCA formation, leading totissue damage. Diagnosis is challenging due to symptom overlap and undisclosed drug use, making clinical suspicion and drug history essential for proper management.[128]
Cocaine/levamisole-associated autoimmune syndrome
The broader cocaine/levamisole-associated autoimmune syndrome (CLAAS) includes LINES as a subset and is also common, but LINES is more specifically and frequently cited in the context of street cocaine adulteration.[119]
Levamisole has become a common additive to illicit cocaine. It is thought to intensify the "high" by releasingdopamine in the brain, acts as a bulking agent, and is a difficult adulterant to recognize. Potential risks of levamisole-laced cocaine includeautoimmune disease,neutropenia,arthralgias,retiform purpura, skinnecrosis, andfever.[129]
Mortality
Persons with regular or problematic use of cocaine have a significantly highermortality rate, and are specifically at higher risk of traumatic deaths and deaths attributable to infectious disease.[130] In 2025, the Liberty House Clinic in the United Kingdom noted that chronic cocaine usage in fact had a higher risk of death thanalcoholism.[131]
Neurotoxicity
Cocaine is consideredneurotoxic due to its damaging effects on the brain and nervous system.[132][133][33][134][135][136] Research has shown that both acute and chronic cocaine use can lead to significant reductions in cerebral blood flow, disrupt neurovascular interactions, and impair brain function. These changes are associated withnerve injury, cognitive deficits, and an increased risk of cerebrovascular accidents such as strokes. Brain imaging studies consistently report that individuals who misuse cocaine exhibit structural and functional abnormalities compared to non-users, supporting the classification of cocaine as a neurotoxic substance.[33]
Cocaine use damagesgray matter in brain regions critical for memory, attention, and emotion, leading to cognitive and behavioral impairments. It also disrupts dopamine levels and blood flow, acceleratingbrain aging and causing long-term neurological harm.[137]
Psychiatric symptoms
Cocaine produces a spectrum ofpsychiatric symptoms including agitation, paranoia, anxiety, irritability,psychosis, hallucinations, delusions, violence, as well as suicidal and homicidal thinking.[26][17]
A considerable proportion of cocaine addicts exhibithypomanic personality traits that areego-syntonic with their pattern of cocaine abuse.[138]
Cocaine intoxication mirrors core traits ofnarcissism—both involve a dopamine-driven, compulsive drive for reward. Just as cocaine produces a brief high that temporarily enhances the sense of worth, narcissists rely on externaladmiration to feed an addiction to theirself-esteem, resulting in aself-reinforcing feedback cycle.[139]
The misuse of cocaine has a high correlation withsuicide.[140][141] In those who use cocaine, the risk is greatest during thewithdrawal phase.[142] Cocaine use has been linked to homicide, with up to 31% of homicide victims testing positive for the drug.[26] In 1989 Fulton County, 40% ofhomicide victims had cocaine metabolites, especially Black and firearm victims.[143]
A 2020 study found that men with cocaine use disorder have greater difficulty identifyingemotional expression in female faces, affecting relationships and suggesting a target for intervention.[144] A 2021 study found that cocaine use disorder impairs emotion recognition, especially for happiness and fear, with improvement after long-term abstinence.[145]
Depression is modestly linked to current drug use in cocaine users but does not clearly predict treatment participation or future use.[146] For people who use cocaine, stress and craving can make each other worse. This may help explain why stress can lead torelapse in people trying to stop using cocaine.[147]
Psychosis
Cocaine has a similar potential to induce temporary psychosis[148] with more than half of cocaine abusers reporting at least some psychotic symptoms at some point.[149] Typical symptoms include paranoid delusions that they are being followed and that their drug use is being watched, accompanied by hallucinations that support the delusional beliefs.[149]Delusional parasitosis withformication ('cocaine bugs') is also a fairly common symptom.[150]
Cocaine-induced psychosis showssensitization toward the psychotic effects of the drug. This means that psychosis becomes more severe with repeated intermittent use.[149][151]
Short-term effects
Insufflating (snorting) cocaine commonly causes increasedmucus production due to irritation and inflammation of the nasal passages. This irritation leads to symptoms such as arunny nose,nasal congestion, and excessive or thickened mucus.
Cocaine is highly addictive and has poor bioavailability when taken orally. Individuals often engage in repeated use by either insufflating itintranasally or converting it tocrack cocaine for vaporization. Cocaine's effects last longest when insufflated (60–90 minutes),[13] but the drug itself has a shortbiological half-life of about 0.7–1.5 hours.[160] Repeated use raises the risk of developing "cocaine nose," referring to severe nasal tissue damage from intranasal use, as well as "crack lung," a condition involving lung tissue damage caused by inhaling crack cocaine.
Cocaine use leads to an increased risk of hemorrhagic and ischemicstrokes.[25] Cocaine use also increases the risk of having aheart attack.[161]
Cocaineconstricts 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. Chronic users may lose theirappetite and experience severemalnutrition, leading to beingunderweight.
A 2014 study found that increased cocaine use is linked to greatercognitive impairment, particularly in working memory, while reduced or ceased use can lead to partial or full recovery of cognitive function. These findings suggest that some cocaine-related cognitive deficits are reversible, especially if use begins later in life.[162] A 2018 review found little evidence that chronic cocaine use causes widespread cognitive impairment.[163] Exposure to cocaine may lead to the breakdown of theblood–brain barrier.[164][165]
Cocaine can inducetolerance after a single dose, and repeated use frequently leads to the development ofaddiction and prolongedcraving.[153][168][169] Assessment tools like the Obsessive Compulsive Cocaine Use Scale (OCCUS) may be employed to quantify obsessive and compulsive thoughts related to cocaine consumption.[170][171]
A key mechanism involves the overexpression ofΔFosB in thenucleus accumbens, alteringtranscriptional regulation and reinforcing drug-seeking behavior.[177] Each dose of cocaine raises ΔFosB levels without a known saturation point. This elevation leads to increasedbrain-derived neurotrophic factor (BDNF) levels, which in turn enhancedendritic branching andspine density in neurons of the nucleus accumbens andprefrontal cortex, potentially persisting for weeks after drug cessation.[citation needed] Intransgenic mice engineered to express ΔFosB in the nucleus accumbens anddorsal striatum, heightened behavioral sensitization to cocaine has been observed.[178] These mice self-administer cocaine at lower doses and display a greater propensity forrelapse after withdrawal[179][180] ΔFosB also enhances sensitivity to reward by upregulating theAMPA receptor subunit GluR2[178] and downregulating the expression ofdynorphin.[180]
About 25% of adults withattention deficit hyperactivity disorder (ADHD) use cocaine, and 10% develop a cocaine use disorder during their lifetime. Because cocaine use can worsen health outcomes, adults with ADHD should be screened for cocaine use disorder and referred for treatment if needed.[184]
Cocaine-dependent patients with highneuroticism scores are more likely to experience cocaine-induced psychotic symptoms, regardless of other drug use factors, makingpersonality assessment important for risk identification and patient warning.[185]
Cocainewithdrawal symptoms group into two types: depressive (e.g.,depression, craving, insomnia) and somatic (e.g., increased appetite, fatigue). Depressive symptoms are linked to worse outcomes like longer depression, treatment, and risky behaviors.[32]
Treatment
Because there are no medications with an approvedindication for cocaine use disorder, psychosocial treatments are the current standard. Effective approaches include group and individual counseling,cognitive behavioral therapy (CBT), andmotivational interviewing (MI).Contingency management (CM)—which rewards patients with vouchers for meeting treatment goals—has proven especially effective, particularly for helping patients achieve initialabstinence from cocaine.[186]
Cocaine Anonymous (CA) is atwelve-step program formed in 18 November 1982 for people who seek recovery from drugaddiction. It is patterned very closely afterAlcoholics Anonymous (AA), although the two groups are unaffiliated. While many CA members have been addicted to cocaine, crack, speed or similar substances, CA accepts all who desire freedom from "cocaine and all other mind-altering substances" as members.[187]
Numerous medications have been investigated for use in cocaine dependence, but as of 2015[update], none of them were considered to be effective.[188] Drugs which help to re-stabilize the glutamate system such asN-acetylcysteine have been proposed for the treatment of addiction to cocaine,nicotine, andalcohol.[189] However, none have sufficient evidence or regulatory approval for routine clinical use, so psychosocial interventions remain the mainstay of treatment.[186]
Cocaine nose
"Cocaine nose" redirects here. For the Playboi Carti song, seeCocaine Nose (song).
"Cocaine nose" or "coke nose" are informal terms that refer to nose disorders resulting from repeated or chronic cocaine use.[34][190][191][192]
About 30% of people who had snorted cocaine at least 25 times but less than daily, and 47% of daily users, reported experiencing nasal irritation, crusting or scabbing, and frequent nosebleeds. Cocaine use should be considered as a potential cause of persistent or unexplainedrhinitis, including in adolescent patients.[193]
Because the nose is a prominent facial feature, such visible damage often leads to embarrassment, stigma, and negative reactions from others. As a result, individuals with cocaine-induced nasal damage frequently withdraw from social activities and relationships, leading tosocial isolation. In many cases, this isolation is not just likely but almost inevitable, as affected individuals may feel unable to face the outside world due to the noticeable and sometimes severe changes to their appearance.[194][195]
Nose disorders associated with cocaine nose include:
Chronic intranasal usage can degrade thecartilage separating thenostrils (theseptum nasi), leading eventually to its complete disappearance.[199]
Causes
The cause of "cocaine nose" can be traced to the chemical process that occurs when cocaine hydrochloride is insufflated (snorted). As cocaine is absorbed through thenasal mucosa, the remaining hydrochloride component forms a dilutehydrochloric acid.[199] The short half-life of cocaine,[160] combined with binge use, may expose the nasal tissues to this acidic environment more frequently, increasing the risk of irritation and damage.
Treatment
For people with cocaine abuse, mild symptoms may resolve completely with total abstinence from cocaine, making early involvement of addiction services essential.[200]
Repair may involverhinoplasty, which includes creating a new internal lining with nasolabial flaps and restoring support with costal cartilage grafts.[201]
In 2024, Belgian doctors report a rise in patients needing nose reconstruction due to cocaine use, which damages nasal tissue and cartilage; however, few undergo surgery because it requires at least six months of abstinence from cocaine for proper healing.[202]
Some individuals seekplastic surgery to repair or reconstruct nasal damage caused by cocaine use, although surgical outcomes can be complicated by ongoing tissue loss and poor healing. When nasal damage is too severe for reconstruction, anose prosthesis may be used to restore appearance andquality of life.[194][195]
Death rates from cocaine overdosesUS yearly overdose deaths involving cocaine.[203]
According to theEuropean Union Drugs Agency, the estimated minimum lethal dose is 1.2 grams. However, sensitive individuals have died from as little as 30 milligrams applied to mucous membranes-an amount that is 40 times less than the minimum lethal dose. In contrast, addicts may tolerate doses as high as 5 grams per day.[14]
In 2024, drug-related deaths in England and Wales reached their highest level in three decades, with a notable increase in fatalities involving cocaine and experts urging urgent government intervention to address the crisis. Martin Powell, from the charity Transform, which campaigns for thelegal regulation of drugs, suggested that the recent rise in cocaine-related deaths in the UK may be due to the increased purity of cocaine, leading users to consume it more frequently and alongside other substances.[206]
Alcohol interacts with cocainein vivo to producecocaethylene, another psychoactive substance which may be substantially morecardiotoxic than either cocaine or alcohol by themselves.[207][208] In 2024, a systematic review of human studies concluded that, despite some inconsistencies in the findings, the co-use of cocaine and alcohol poses a significantly greater risk of cardiovascular fatalities compared to cocaine use alone. This elevated risk is largely attributed to the formation of cocaethylene, a unique and toxic metabolite produced only when both substances are consumed together. Cocaethylene is associated with an 18- to 25-fold increased risk of sudden death, as well as a higher incidence of myocardial injury and cardiac arrest, underscoring the serious health risks of simultaneous cocaine and alcohol use.[209]
MAOIs
Monoamine oxidase inhibitors (MAOIs) should not be combined with other psychoactive substances (antidepressants, painkillers, stimulants, including prescribed, OTC and illegally acquired drugs, etc.) except under expert care.[citation needed]
Theopioid epidemic now involves more overdose deaths with both opioids and cocaine, especially among non-Hispanic Blacks who are twice as likely to die from combined opioid-stimulant overdoses compared to non-Hispanic whites. Cocaine-related deaths in Blacks are similar to opioid deaths in whites. Risk factors include young age, education, urban living, mental disorders, and stress. It remains unclear if co-use is intentional. Recent studies expand focus beyond heroin to all opioids, reflecting changing overdose patterns.[210]
Pharmacology
Pharmacokinetics
The extent of absorption of cocaine into thecirculatory system after nasal insufflation is similar to that after oral ingestion. The rate of absorption after nasal insufflation is limited by cocaine-induced vasoconstriction of capillaries in the nasal mucosa. Onset of absorption after oral ingestion is delayed because cocaine is a weak base with apKa of 8.6, and is thus in an ionized form that is poorly absorbed from thegastric acid and easily absorbed from the alkalineduodenum.[12] The rate and extent of absorption from inhalation of cocaine is similar or greater than with intravenous injection, as inhalation provides access directly to thecapillary bed. The delay in absorption after oral ingestion may account for the popular belief that cocaine bioavailability from the stomach is lower than after insufflation. Compared with 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. Physiological and psychotropic effects from nasally insufflated cocaine are sustained for approximately 40–60 minutes after the peak effects are attained.[211]
Cocaine has a short elimination half-life of 0.7–1.5 hours and is extensivelymetabolized byplasma esterases and also by livercholinesterases, with only about 1% excreted unchanged in the urine.[13] The metabolism is dominated byhydrolyticester cleavage, so the eliminated metabolites consist mostly ofbenzoylecgonine (BE), the majormetabolite, and other metabolites in lesser amounts such as ecgonine methyl ester (EME) andecgonine.[216][13] Further minor metabolites of cocaine includenorcocaine, p-hydroxycocaine, m-hydroxycocaine, p-hydroxybenzoylecgonine (pOHBE), and m-hydroxybenzoylecgonine.[217]
Depending onliver andkidney functions, cocaine metabolites are detectable in urine between three and eight days. Generally speakingbenzoylecgonine is eliminated from someone's urine between three and five days. In urine from heavy cocaine users, benzoylecgonine can be detected within four hours after intake and in concentrations greater than 150 ng/mL for up to eight days later.[218]
Detection in the body
Body fluids
Cocaine and its major metabolites may be quantified in blood, plasma, or urine to monitor for use, confirm a diagnosis of poisoning, or assist in the forensic investigation of a traffic or other criminal violation or sudden death. Most commercial cocaineimmunoassay screening tests cross-react appreciably with the major cocaine metabolites, butchromatographic 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.[219]
Hair
Hair analysis can detect cocainemetabolites in regular users until after the sections of hair grown during the period of cocaine use are cut or fall out.[220]
Thepharmacodynamics of cocaine involve the complex relationships of neurotransmitters (inhibitingmonoamine uptake in rats with ratios of about:serotonin:dopamine = 2:3, serotonin:norepinephrine = 2:5).[224][17] The most extensively studied effect of cocaine on thecentral nervous system is the blockade of thedopamine transporter protein. Dopamineneurotransmitter 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 thepresynapticneuron, where it is taken up into storagevesicles. 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 thusdopamine accumulates in thesynaptic cleft. The increased concentration of dopamine in the synapse activates post-synaptic dopamine receptors, which makes the drugrewarding and promotes the compulsive use of cocaine.[225]
Cocaine has been demonstrated to bind as to directly stabilize theDAT transporter on the open outward-facing conformation. Further, cocaine binds in such a way as to inhibit ahydrogen 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 the habituation of the substance so much as the conformation and binding properties to where and how on the transporter the molecule binds.[228]
Conflicting findings have challenged the widely accepted view that cocaine functions solely as a reuptake inhibitor. To induce euphoria an intravenous dose of 0.3-0.6 mg/kg of cocaine is required, which blocks 66-70% of DAT in the brain.[229] Re-administering cocaine beyond this threshold does not significantly increase DAT occupancy but still results in an increase of euphoria which cannot be explained by reuptake inhibition alone. This discrepancy is not shared with other dopamine reuptake inhibitors likebupropion,sibutramine,mazindol ortesofensine, which have similar or higher potencies than cocaine as dopamine reuptake inhibitors. Furthermore, a similar response-occupancy discrepancy has been observed withmethylphenidate, which also stabilizes the dopamine transporter in an open outward-facing conformation.[230][231][232] These findings have evoked a hypothesis that cocaine may also function as a so-called "DAT inverse agonist" or "negative allosteric modifier of DAT" resulting in dopaminetransporter reversal, and subsequent dopamine release into the synaptic cleft from the axon terminal in a manner similar to but distinct fromamphetamines.[230]
Sigma receptors are affected by cocaine, as cocaine functions as a sigma ligand agonist.[233] Further specific receptors it has been demonstrated to function on areNMDA and the D1 dopamine receptor.[234]
Cocaine also blockssodium channels, thereby interfering with the propagation ofaction potentials;[235][113] thus, likelignocaine andnovocaine, it acts as a local anesthetic. It also functions on the binding sites to the dopamine and serotoninsodium 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 derivedphenyltropanes analogues which have that removed. In addition to this, cocaine has some target binding to the site of theκ-opioid receptor.[236][unreliable medical source?] Cocaine also causesvasoconstriction, thus reducing bleeding during minor surgical procedures. Recent research points to an important role of circadian mechanisms[237] andclock genes[238] in behavioral actions of cocaine.
Cocaine is known to suppress hunger and appetite by increasing co-localization of sigma σ1R receptors andghrelin GHS-R1acell surface receptors, thereby increasing ghrelin-mediated signaling of satiety[239] and possibly via other effects on appetitive hormones.[240]
Cocaine effects, further, are shown to be potentiated for the user when used in conjunction with new surroundings and stimuli, and otherwise novel environs.[241]
A pile ofmicronized cocaine hydrochlorideA piece of compressed cocaine hydrochloride, commonly used for smuggling
In its purest form, cocaine is a white, pearly powder. As atropane alkaloid, cocaine is a weak base and readily forms salts when combined with acids. The most commonly encountered form is the hydrochloride (HCl) salt, although other salts such as the sulfate (SO42−) and nitrate (NO3−) are occasionally observed. The solubility of these salts varies depending on their polarity; the hydrochloride salt is polar and highly soluble in water.[242]
Synthesis
Total synthesis
The firststructure elucidation andtotal synthesis of the cocaine molecule was accomplished byRichard Willstätter in 1898.[243] Willstätter's synthesis involved constructing the cocaine structure from simpler precursors, notably via the intermediatetropinone. Subsequent significant contributions to understanding the synthetic pathway and stereochemistry were made byRobert Robinson and Edward Leete.
Cocaine contains fourchiral centers (1R, 2R, 3S, and 5S), two of which areconfigurationally dependent, resulting in eight possiblestereoisomers. The formation of inactive stereoisomers, along with various synthetic by-products, limits both the yield and purity of the final product.[244][245]
Although the chemical synthesis of cocaine is technically feasible, it is generally considered impractical due to its high cost, low efficiency, and challenges in stereoselective synthesis compared to extraction from natural plant sources. While domestic clandestine laboratories could theoretically reduce reliance on offshore production and international smuggling—as seen with illicitmethamphetamine—manufacture and synthetic production of cocaine remains rare. Large-scale commercial synthesis has not been explored.[246]
Large-scale biosynthesis of cocaine is unexplored.[246]
The biosynthesis of cocaine has long attracted the attention of biochemists and organic chemists. This interest is partly motivated by the strong physiological effects of cocaine, but a further incentive was the unusualbicyclic structure of the molecule. The biosynthesis can be viewed as occurring in two phases, one phase leading to the N-methylpyrrolinium ring, which is preserved in the final product. The second phase incorporates a C4 unit with formation of the bicyclictropane core.[247]
GMO synthesis
In 2022, aGMO producedN. benthamiana were discovered that were able to produce 25% of the amount of cocaine found in a coca plant.[248]
However, sinceN. benthamiana also naturally containsnicotine, separating the cocaine from nicotine and related alkaloids would be challenging.
Personal cards-including ID cards and driver's licenses-are frequently swabbed by inspectors to detect drug residue, as these items are commonly used to prepare lines of cocaine. Swabbing can reveal traces of cocaine or other illicit substances, providing evidence of recent drug handling or use. This practice may be employed during security checks at border crossings.
ANewsbeat investigation found that "cocaine torches" used by UK police to detect cocaine use are ineffective on typical street cocaine, as independent lab tests showed they fail to make the drugfluoresce. Experts and drug charities criticized the devices, warning they can give false positives and waste resources, while police forces defended their use as a deterrent. The manufacturer says the torches only work on much purer forms of cocaine than are found on the street.[249][250]
Cocaine may be detected by law enforcement using theScott reagent. The test can easily generatefalse positives for common substances and must be confirmed with a laboratory test.[251][252]
Approximate cocaine purity can be determined using 1 mL 2% cupric sulfate pentahydrate in dilute HCl, 1 mL 2% potassium thiocyanate and 2 mL ofchloroform. The shade of brown shown by the chloroform is proportional to the cocaine content. This test is not cross sensitive to heroin, methamphetamine,benzocaine, procaine and a number of other drugs but other chemicals could cause false positives.[253]
Both thepharmaceutical supply chain and theillicit supply chain obtain cocaine from coca cultivated in Latin America, but they operate under very different controls and oversight. In Peru, for example, legal coca cultivation is monopolized by the state companyNational Coca Company (ENACO), yet approximately 90% of coca leaves produced in the country are diverted to illegal actors for cocaine manufacturing.[254] As a result, these illicit coca crops are a primary target of ongoing government-ledcoca eradication efforts.[255]
Cocaine is sometimes referred to on the street as blow, coca, coke, crank, flake, snow, or soda cot. Slang terms for free base cocaine include crack or rock.[257]
Fishscale cocaine, fromfish +scale, is named for its shiny, yellowish flakes that resemble fish scales—distinct from the dull white appearance of standard cocaine powder.
Some countries, such as Bolivia, Colombia, and Peru, permit the cultivation of coca leaf for traditional consumption by the localindigenous population, but nevertheless, prohibit the production, sale, and consumption of cocaine.[258] The provisions as to how much a coca farmer can yield annually is protected by laws such as the Bolivian Cato accord.[259] In addition, some parts of Europe, the United States, and Australia allow processed cocaine for medicinal uses only.
Australia
Cocaine is a Schedule 8 controlled drug in Australia under thePoisons Standard.[260] It is the second most popular illicit recreational drug in Australiabehind cannabis.[261]
InWestern 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.[262]
PresidentGeorge H. W. Bush holds up a bag ofcrack cocaine during his Address to the Nation on National Drug Control Strategy on 5 September 1989.
The US federal government instituted a nationaldrug labelling requirement for cocaine and cocaine-containing products through thePure Food and Drug Act of 1906.[263]: 37 The next important federal regulation was theHarrison 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 it set up a regulatory and licensing regime.[264] 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 journalAmerican 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."[265] The Harrison Act left manufacturers of cocaine untouched so long as they met certain purity and labeling standards.[263]: 40 Despite that cocaine was typically illegal to sell and legal outlets were rarer, the quantities of legal cocaine produced declined very little.[263]: 40 Legal cocaine quantities did not decrease until theJones–Miller Act of 1922 put serious restrictions on cocaine manufactures.[263]: 40
Before the early 1900s, newspapers primarily portrayed addiction (rather than violence or crime) as the main problem caused by cocaine use, and depicted cocaine users as upper or middle classWhite people. In 1914, The New York Times published an article titled "Negro Cocaine 'Fiends' Are a New Southern Menace," portrayingBlack people who used cocaine as dangerous and able to withstand wounds that would normally be fatal.[266] TheAnti-Drug Abuse Act of 1986 mandated the same prison sentences for distributing 500 grams of powdered cocaine and just 5 grams of crack cocaine.[267] In theNational Survey on Drug Use and Health, white respondents reported a higher rate of powdered cocaine use, and Black respondents reported a higher rate of crack cocaine use.[268]
Prevalence and trends
Cocaine production, seizures, and use all reached record levels in 2023, making it the world's fastest-growing illicit drug market. Seizures rose by 68% from 2019 to 2023, while the number of users increased from 17 million in 2013 to 25 million in 2023, according to the UNODCWorld Drug Report 2025.[43]
The report further states that Western Europe's cocaine market is rapidly expanding, resulting in increased violence driven by traffickers, including organized criminal groups from the Western Balkans. Concurrently, record levels of cocaine production have enabled traffickers to enter new markets across Asia and Africa, reflecting the expanding global reach of cocaine trafficking.[41]
The U.S. is the world's largest consumer of cocaine,[269] while South America, as a continent, ranks third in terms of consumer market size.[18] Europe ranks cocaine as the second most commonly used illicit drug.[270]
Cocaine is among the most widely consumedrecreational stimulants worldwide.[24]
Impact
Impact of illicit cocaine
Impact on impoverished communities
In countries where cocaine is illicitly produced, an intermediate product known as cocaine paste—often referred to as "poor man's cocaine"—is frequently smoked in impoverished communities. This substance is favored in these areas primarily because it is inexpensive and more accessible than refined cocaine. However, the use of cocaine paste poses severe health risks. During its production, various toxic chemicals are used to extract coca alkaloids from the coca leaves. Many of these hazardous substances, such as solvents and acids, remain in the paste after processing. When the paste is smoked, individuals are exposed not only to the addictive effects of the drug itself but also to the dangerous residual chemicals, which can cause significant harm to the lungs, nervous system, and overall health. This combination of affordability, accessibility, and toxicity makes cocaine paste particularly damaging to vulnerable populations in cocaine-producing regions.[22][93][94][95]
Most of the world's cocaine is produced in South America, particularly in theAndean region.[271] The environmental destruction caused by the production of cocaine has been well documented, with reports made the UN and other government bodies.[272] Due to the illegal nature ofcoca production, farmers make little effort in soil conservation and sustainability practices as seen in the high mobility and short life of coca plots in Colombia.[271]
One of the major implications of cocaine production isdeforestation as large areas of forest are cleared for coca cultivation. The UNODC approximated that 97,622 hectares ofprimary forest were cleared for coca cultivation during 2001–2004 in the Andean region.[271] This further causeshabitat destruction, especially inbiodiversity hotspots, areas rich in a variety of species. Such areas are chosen for coca cultivation due to their remote locations, minimising chances of detection.[273] Deforestation impactssoil erosion which further inhibits the survival of native species.[271]
The use ofpesticides can also severely affect the environment. Farmers are able to use unregulated and highly toxic pesticides due to the clandestine nature of drug production.[273] The use of such pesticides can have both direct and indirect effects on the ecosystem. Where lethal levels of exposure directly cause the death of fauna, which is further carried up thefood chain where secondary feeders who consume the poisoned animals are also impacted. Furthermore, non-lethal levels of exposure can also cause weaker immune system development and neurological issues, further increasing mortality rates.[273]
Impact of illicit cocaine trade
Cocaine is extremely expensive on the black market, with prices rising sharply at each distribution level—often more than its weight in gold.[274]
Latin America
Drug war policies in Latin America and the Caribbean have led to more violence, higher incarceration rates, health crises, and deeper poverty, while undermining trust in institutions and worsening inequality. There is increasing support for shifting toward drug policies that focus on sustainable development and human rights instead of punitive measures.[42]
In December 2000, Dutch journalistMarjon van Royen found that "because the chemical is sprayed in Colombia from planes on inhabited areas, there have been consistent health complaints [in humans]. Burning eyes, dizziness and respiratory problems being most frequently reported." In some areas, 80 percent of the children of the indigenous community fell sick with skin rashes, fever, diarrhoea and eye infections.[278] Because the glyphosate is sprayed from the air, there is a much higher chance of human error when spraying suspected illegal coca plantations. In many cases the wrong fields are sprayed, resulting in not only a total loss of the farmer's crop- but the loss of that field altogether as nothing will grow where the herbicide has been sprayed.[279] Though official documentation of the health effects of glyphosate spraying in Colombia are virtually non-existent, neighbouring Ecuador has conducted studies to determine the cause of mysterious illnesses amongst people living along the border of Colombia and has since demanded that no aerial sprayings occur within 10 km of the border because of the damages caused to the people, animals and environment in that area.[279] In 2015, Colombia announced a ban on using glyphosate in these programs due to concerns about human toxicity of the chemical.[280]
Impact of interdiction
The Consolidated Counterdrug Database (CCDB) is a U.S. government dataset created in the 1990s that compiles vetted data on cocaine trafficking and seizures in theWestern Hemisphere "transit zone," involving 26 U.S. agencies and 20 foreign partners. It provides a highly reliable, conservative record of cocaine movements and interdiction efforts, revealing that despite large seizures, interdiction captures only a small fraction of trafficking events and has minimal impact on U.S. cocaine prices. The CCDB challenges optimistic views of drug interdiction effectiveness and underscores the need for new policy approaches, yet remains underutilized in research despite being unclassified.[281]
Research
Cocainehaptens are chemically modified derivatives of cocaine that retain key immunogenic features, allowing them to be attached to carrier proteins such askeyhole limpet hemocyanin orbovine serum albumin. This enables the immune system to recognize cocaine and produce anti-cocaine antibodies, which can bind cocaine in the bloodstream and prevent it from reaching the brain, thereby blocking its psychoactive effects.[282][283][284]
Coca tea has been explored as a supportive treatment for cocaine dependence. A study inLima, Peru, found that using coca leaf infusion along with counseling reduced relapse rates and significantly increased the duration of abstinence among addicted individuals, suggesting that this approach may help prevent relapse during treatment.[286]
Recent research has also examined the use of prescription psychostimulants for cocaine dependence, following theSelf-Medication Hypothesis. This hypothesis suggests that some individuals use cocaine to address underlying neurochemical or psychological issues. While some studies indicate that psychostimulant therapy may reduce cocaine use and cravings, the evidence is mixed and further research is needed.[287]
In animal studies, nicotine exposure inmice increases the likelihood of later cocaine use, with clear molecular changes in the brain.[288] These findings mirror humanepidemiological data showing a link between nicotine use and increased risk of later cannabis and cocaine use, as well as other substances.[289][290] Similarly, in rats, alcohol consumption raises the probability of later cocaine addiction and is associated with changes in the brain's reward system.[291][292] Human studies also show that alcohol use increases the risk of transitioning from cocaine use to addiction.[293][294]
Experimentally, cocaine injections can be delivered to animals such asfruit flies to study the mechanisms of cocaine addiction.[295]
TA-CD is avaccine developed by the Xenova Group and designed to negate the effects of cocaine, making it suitable for use in treatment of addiction. It is created by combiningnorcocaine with inactivatedcholera toxin.[297]
Coca leaves have been used by indigenous South Americans for thousands of years, both as a stimulant and for medicinal purposes.[298]
When theSpanish arrived in South America, they initially banned coca but soon legalized and taxed it after seeing its importance to local labor.[299] The active ingredient, cocaine, was first isolated in 1855 byFriedrich Gaedcke and later refined byAlbert Niemann, who named it "cocaine."[300][301][302] In the late 1800s, cocaine became popular in Western medicine as a local anesthetic and was widely used in various products, including drinks and remedies.[303] andJames Leonard Corning demonstratedperidural anesthesia.[304] However, due to its toxic effects and potential for abuse, safer alternatives eventually replaced it in medical practice.[19]
Large-scale coca cultivation and cocaine production occurred in Taiwan Asia, inTaiwan (then known as Formosa) andJava (today part of Indonesia) beforeWorld War II.[46][47]
Since the 1980s, the cocaine trade was dominated by centralized, hierarchicaldrug cartels such asMedellín andCali, along with their successors and earlyFARC factions. By the early 2000s, this model fragmented into a diverse network of global trafficking links, allowing South American cocaine production to easily supply markets in Europe, Africa, Asia, and Oceania through various routes.[305]
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