Editing Cocaine (section)

== Adverse effects ==
{{For|harm caused by the freebase form|Crack cocaine#Adverse effects}}
{{See also|Cocaine#Lacing}}

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| HarmCausedByDrugsTable.svg
 | 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.<ref>{{Cite journal | vauthors = Nutt DJ, King LA, Phillips LD | title = Drug harms in the UK: a multicriteria decision analysis | journal = Lancet | volume = 376 | issue = 9752 | pages = 1558–65 | date = November 2010 | pmid = 21036393 | doi = 10.1016/S0140-6736(10)61462-6 | s2cid = 5667719 | citeseerx = 10.1.1.690.1283 }}</ref>
| Rational harm assessment of drugs bar plot.svg
 | 2007 [[Delphi method|delphic 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.<ref name="Lancet">{{Cite journal|vauthors = Nutt D, King LA, Saulsbury W, Blakemore C|title = Development of a rational scale to assess the harm of drugs of potential misuse|journal = Lancet|volume = 369|issue = 9566|pages = 1047–53|date = March 2007|pmid = 17382831|doi = 10.1016/S0140-6736(07)60464-4|s2cid = 5903121|author-link4 = Colin Blakemore|author-link1 = David Nutt }}</ref>
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Cocaine is considered [[neurotoxic]] due to its damaging effects on the brain and nervous system. 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 with [[nerve 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.<ref>{{cite journal | vauthors = Clare K, Park K, Pan Y, Lejuez CW, Volkow ND, Du C | title = Neurovascular effects of cocaine: relevance to addiction | journal = Frontiers in Pharmacology | volume = 15 | pages = 1357422 | date = 2024 | pmid = 38455961 | pmc = 10917943 | doi = 10.3389/fphar.2024.1357422 | doi-access = free }}</ref>

=== Short-term effects ===
Insufflating (snorting) cocaine commonly causes increased [[mucus]] production due to irritation and inflammation of the nasal passages. This irritation leads to symptoms such as a [[Rhinorrhea|runny nose]], [[nasal congestion]], and excessive or thickened mucus.

Acute exposure to cocaine has many effects on humans, including euphoria, increases in heart rate and blood pressure, and increases in cortisol secretion from the adrenal gland.<ref>{{Cite journal | vauthors = Heesch CM, Negus BH, Keffer JH, Snyder RW, Risser RC, Eichhorn EJ | title = Effects of cocaine on cortisol secretion in humans | journal = The American Journal of the Medical Sciences | volume = 310 | issue = 2 | pages = 61–4 | date = August 1995 | pmid = 7631644 | doi = 10.1097/00000441-199508000-00004 | s2cid = 11042810 }}</ref> In humans with acute exposure followed by continuous exposure to cocaine at a constant blood concentration, the acute tolerance to the [[chronotropic]] cardiac effects of cocaine begins after about 10 minutes, while acute tolerance to the euphoric effects of cocaine begins after about one hour.<ref name=Ambre1988 /><ref>{{Cite journal | vauthors = Pudiak CM, KuoLee R, Bozarth MA | title = Tolerance to cocaine in brain stimulation reward following continuous cocaine infusions | journal = Pharmacology, Biochemistry, and Behavior | volume = 122 | pages = 246–52 | date = July 2014 | pmid = 24768900 | doi = 10.1016/j.pbb.2014.04.006 | s2cid = 207332822 }}</ref><ref>{{Cite journal | vauthors = Gullapalli BT, Natarajan A, Angarita GA, Malison RT, Ganesan D, Rahman T |title=On-body Sensing of Cocaine Craving, Euphoria and Drug-Seeking Behavior Using Cardiac and Respiratory Signals |journal=Proceedings of the ACM on Interactive, Mobile, Wearable and Ubiquitous Technologies |date=21 June 2019 |volume=3 |issue=2 |pages=1–31 |doi=10.1145/3328917|s2cid=195357215 }}</ref><ref>{{Cite journal | vauthors = Calipari ES, Ferris MJ, Jones SR | title = Extended access of cocaine self-administration results in tolerance to the dopamine-elevating and locomotor-stimulating effects of cocaine | journal = Journal of Neurochemistry | volume = 128 | issue = 2 | pages = 224–32 | date = January 2014 | pmid = 24102293 | pmc = 3947316 | doi = 10.1111/jnc.12452 }}</ref> With excessive or prolonged use, the drug can cause [[itch]]ing, [[tachycardia|fast heart rate]], and [[formication|paranoid delusions or sensations of insects crawling on the skin]].<ref name="weizhao2008">{{Cite book |title=Mechanisms Mediating Sex Differences in the Effects of Cocaine | vauthors = Zhao W |year=2008 |isbn=978-0-549-99458-9 |page=3 | publisher = University of Michigan |access-date=25 September 2012 |url=https://books.google.com/books?id=AF8zjRBtSuIC&pg=PA3 |url-status=live |archive-url=https://web.archive.org/web/20140404151302/https://books.google.com/books?id=AF8zjRBtSuIC&pg=PA3 |archive-date=4 April 2014 }}</ref> Intranasal cocaine and crack use are both associated with pharmacological violence. Aggressive behavior may be displayed by both addicts and casual users. Cocaine can induce [[psychosis]] characterized by [[paranoia]], impaired [[reality testing]], [[hallucinations]], irritability, and physical aggression. [[Cocaine intoxication]] can cause hyperawareness, [[hypervigilance]], [[psychomotor agitation]], and [[delirium]]. Consumption of large doses of cocaine can cause violent outbursts, especially by those with preexisting psychosis.<ref>{{Cite journal | vauthors = Boles SM, Miotto K |title=Substance abuse and violence: A review of the literature |journal=Aggression and Violent Behavior |date=March–April 2003 |volume=8 |issue=2 |pages=155–174 |doi=10.1016/S1359-1789(01)00057-X }}</ref> Acute exposure may induce [[arrhythmia]], including [[atrial fibrillation]], [[supraventricular tachycardia]], [[ventricular tachycardia]], and [[ventricular fibrillation]]. Acute exposure may also lead to [[angina]], [[myocardial infarction|heart attack]], and [[congestive heart failure]].<ref>{{Cite journal | vauthors = Pergolizzi JV, Magnusson P, LeQuang JA, Breve F, Varrassi G | title = Cocaine and Cardiotoxicity: A Literature Review | journal = Cureus | volume = 13 | issue = 4 | pages = e14594 | date = April 2021 | pmid = 34036012 | pmc = 8136464 | doi = 10.7759/cureus.14594 | issn=2168-8184  | doi-access = free }}</ref> Cocaine overdose may cause [[seizures]], [[hyperthermia|abnormally high body temperature]] and a marked elevation of blood pressure, which can be life-threatening,<ref name="weizhao2008" /> [[Heart arrhythmia|abnormal heart rhythms]],<ref name="Nav">{{Cite journal | vauthors = O'Leary ME, Hancox JC | title = Role of voltage-gated sodium, potassium and calcium channels in the development of cocaine-associated cardiac arrhythmias | journal = British Journal of Clinical Pharmacology | volume = 69 | issue = 5 | pages = 427–42 | date = May 2010 | pmid = 20573078 | pmc = 2856043 | doi = 10.1111/j.1365-2125.2010.03629.x }}</ref> and death.<ref name="Nav" /> Anxiety, paranoia, and restlessness can also occur, especially during the [[Comedown (drugs)|comedown]]. With excessive dosage, [[tremor]]s, [[convulsion]]s, and [[Hypothermia|increased body temperature]] are observed.<ref name=WHO2004 /> 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.<ref name="Nav" />

=== Chronic ===
[[File:Side effects of chronic use of Cocaine.png|class=skin-invert-image|thumb|upright=1.4|Side effects of chronic cocaine use]]

Because cocaine is highly addictive and has poor bioavailability when taken orally, individuals often engage in repeated use by either insufflating it intranasally or converting it to [[crack cocaine]] for vaporization. Cocaine’s effects last longest when insufflated (60–90 minutes),<ref name="Zimmerman2012" /> but cocaine has a shorter [[half-life]] than most drugs, which further encourages frequent redosing over extended periods. This cycle of repeated use can lead to "[[#Cocaine nose|cocaine nose]]," referring to severe nasal tissue damage from intranasal use, and "[[#Crack lung|crack lung]]," which describes respiratory complications from vaporizing cocaine. Both cocaine nose and crack lung can also affect the throat, leading to additional complications.

Cocaine use leads to an increased risk of hemorrhagic and ischemic [[stroke]]s.<ref name="Sordo2014" /> Cocaine use also increases the risk of having a [[myocardial infarction|heart attack]].<ref name="Havakuk2017">{{Cite journal | vauthors = Havakuk O, Rezkalla SH, Kloner RA | title = The Cardiovascular Effects of Cocaine | journal = Journal of the American College of Cardiology | volume = 70 | issue = 1 | pages = 101–113 | date = July 2017 | pmid = 28662796 | doi = 10.1016/j.jacc.2017.05.014 | type = Review | doi-access = free }}</ref>

Cocaine use also promotes the [[thrombosis|formation of blood clots]].<ref name="Zimmerman2012" /> This increase in blood clot formation is attributed to cocaine-associated increases in the activity of [[Plasminogen activator inhibitor-1|plasminogen activator inhibitor]], and an increase in the number, activation, and aggregation of [[platelet]]s.<ref name="Zimmerman2012" />

Cocaine [[Vasoconstriction|constricts blood vessels]], [[Mydriasis|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 their [[appetite]] and experience severe [[malnutrition]], leading to being [[underweight]].

Although it has been commonly asserted, the available evidence does not show that chronic use of cocaine is associated with broad [[cognitive impairment]].<ref>{{Cite journal | vauthors = Frazer KM, Richards Q, Keith DR | title = The long-term effects of cocaine use on cognitive functioning: A systematic critical review | journal = Behavioural Brain Research | volume = 348 | pages = 241–262 | date = August 2018 | pmid = 29673580 | doi = 10.1016/j.bbr.2018.04.005 | s2cid = 4992738 }}</ref> Research is inconclusive on age-related loss of [[striatum|striatal]] [[dopamine transporter]] (DAT) sites, suggesting cocaine has [[neuroprotective]] or [[Neurodegenerative disease|neurodegenerative]] properties for dopamine neurons.<ref>{{Cite book|title=Biological Psychiatry | veditors = D'haenen H, den Boer JA, Willner P | publisher = Wiley | volume = 2 | edition = 2 | isbn=978-0-471-49198-9|year=2002 |page=528}}</ref><ref>{{Cite journal | vauthors = Wang GJ, Volkow ND, Fowler JS, Fischman M, Foltin R, Abumrad NN, Logan J, Pappas NR |author6-link=Naji Abumrad | title = Cocaine abusers do not show loss of dopamine transporters with age | journal = Life Sciences | volume = 61 | issue = 11 | pages = 1059–65 | date = 8 August 1997 | pmid = 9307051 | doi = 10.1016/s0024-3205(97)00614-0 | doi-access = free }}</ref><ref>{{Cite journal | vauthors = Little KY, Ramssen E, Welchko R, Volberg V, Roland CJ, Cassin B | title = Decreased brain dopamine cell numbers in human cocaine users | journal = Psychiatry Research | volume = 168 | issue = 3 | pages = 173–80 | date = August 2009 | pmid = 19233481 | doi = 10.1016/j.psychres.2008.10.034 | s2cid = 27618292 }}</ref> Exposure to cocaine may lead to the breakdown of the [[blood–brain barrier]].<ref>{{Cite journal | vauthors = Sharma HS, Muresanu D, Sharma A, Patnaik R | title = Cocaine-induced breakdown of the blood–brain barrier and neurotoxicity | journal = International Review of Neurobiology | volume = 88 | pages = 297–334 | year = 2009 | pmid = 19897082 | doi = 10.1016/S0074-7742(09)88011-2 | isbn = 978-0-12-374504-0 }}</ref><ref>{{Cite book| vauthors = Karch SB |title=Karch's pathology of drug abuse|date=2009|publisher=CRC Press|location=Boca Raton|isbn=978-0-8493-7881-2|page=70|edition=4|url=https://books.google.com/books?id=G9E7gfJq0KkC&pg=PA70|url-status=live|archive-url=https://web.archive.org/web/20170910234911/https://books.google.com/books?id=G9E7gfJq0KkC&pg=PA70|archive-date=10 September 2017}}</ref>

Chronic cocaine use, but not cocaine itself, can contribute to [[tooth wear]] and the development of [[tooth decay]] through indirect mechanisms. Cocaine use is frequently associated with involuntary tooth grinding, known as [[bruxism]], which can cause [[dental attrition]] and [[gingivitis]].<ref>{{cite journal | vauthors = Shekarchizadeh H, Khami MR, Mohebbi SZ, Ekhtiari H, Virtanen JI | title = Oral Health of Drug Abusers: A Review of Health Effects and Care | journal = Iranian Journal of Public Health | volume = 42 | issue = 9 | pages = 929–940 | date = September 2013 | pmid = 26060654 | pmc = 4453891 }}</ref><ref>{{Cite journal | vauthors = Baigent M | title = Physical complications of substance abuse: what the psychiatrist needs to know | journal = Curr Opin Psychiatry | volume = 16 | issue = 3 | pages = 291–296 | year = 2003 | doi = 10.1097/00001504-200305000-00004 }}</ref> Additionally, stimulants like cocaine, methamphetamine, and even caffeine cause dehydration and [[Xerostomia|dry mouth]]. Since saliva is an important mechanism in maintaining one's oral [[PH|pH]] level, people who use cocaine over a long period of time who do not hydrate sufficiently may experience [[Demineralization (physiology)|demineralization]] of their teeth due to the pH of the tooth surface dropping too low (below 5.5). Poor [[oral hygiene]], which is common among individuals with substance use disorders, may contribute significantly to [[tooth decay]] in cocaine users.

==== Addiction ====
{{For|harm caused by the freebase form|Crack cocaine#Addiction}}
{{See also|Cocaine Anonymous|Epigenetics of cocaine addiction}}

In humans, cocaine abuse may cause [[addiction-related structural neuroplasticity]], though it is unclear to what extent these changes are permanent.<ref name=Hamp2019>{{cite journal | vauthors = Hampton WH, Hanik I, Olson IR | title = [Substance Abuse and White Matter: Findings, Limitations, and Future of Diffusion Tensor Imaging Research] | journal = Drug and Alcohol Dependence | volume = 197 | issue = 4 | pages = 288–298 | year = 2019 | pmid = 30875650 | pmc = 6440853 | doi = 10.1016/j.drugalcdep.2019.02.005}}</ref>

Relatives of persons with cocaine addiction have an increased risk of cocaine addiction.<ref>{{Cite journal | vauthors = Fernàndez-Castillo N, Cabana-Domínguez J, Corominas R, Cormand B | title = Molecular genetics of cocaine use disorders in humans | journal = Molecular Psychiatry | volume = 27 | issue = 1 | pages = 624–639 | date = January 2022 | pmid = 34453125 | doi = 10.1038/s41380-021-01256-1 | pmc = 8960411 }}</ref> [[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.<ref name="pmid9668659">{{Cite journal | vauthors = Hope BT | title = Cocaine and the AP-1 transcription factor complex | journal = Annals of the New York Academy of Sciences | volume = 844 | issue = 1 | pages = 1–6 | date = May 1998 | pmid = 9668659 | doi = 10.1111/j.1749-6632.1998.tb08216.x | s2cid = 11683570 | bibcode = 1998NYASA.844....1H | url = https://zenodo.org/record/1230756 | access-date = 30 June 2019 | archive-date = 28 July 2020 | archive-url = https://web.archive.org/web/20200728160757/https://zenodo.org/record/1230756 | url-status = live }}</ref> 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 [[dendrite|dendritic]] branches and [[dendritic spine|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.

[[Genetically modified mouse|Genetically modified mice]] exhibiting inducible expression of ΔFosB primarily in the nucleus accumbens and [[dorsal striatum]] exhibit [[drug sensitization|sensitized]] behavioural responses to cocaine.<ref name="pmid10499584">{{Cite journal |author-link13=D. James Surmeier | vauthors = Kelz MB, Chen J, Carlezon WA, Whisler K, Gilden L, Beckmann AM, Steffen C, Zhang YJ, Marotti L, Self DW, Tkatch T, Baranauskas G, Surmeier DJ, Neve RL, Duman RS, Picciotto MR, Nestler EJ | title = Expression of the transcription factor deltaFosB in the brain controls sensitivity to cocaine | journal = Nature | volume = 401 | issue = 6750 | pages = 272–6 | date = September 1999 | pmid = 10499584 | doi = 10.1038/45790 | bibcode = 1999Natur.401..272K | s2cid = 4390717 }}</ref> They self-administer cocaine at lower doses than control,<ref name="pmid12657709">{{Cite journal | vauthors = Colby CR, Whisler K, Steffen C, Nestler EJ, Self DW | title = Striatal cell type-specific overexpression of DeltaFosB enhances incentive for cocaine | journal = The Journal of Neuroscience | volume = 23 | issue = 6 | pages = 2488–93 | date = March 2003 | pmid = 12657709 | doi =  10.1523/JNEUROSCI.23-06-02488.2003| pmc = 6742034 }}</ref> but have a greater likelihood of [[relapse]] when the drug is withheld.<ref name="pmid12657709" /><ref name="pmid11572966">{{Cite journal | vauthors = Nestler EJ, Barrot M, Self DW | title = DeltaFosB: a sustained molecular switch for addiction | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 98 | issue = 20 | pages = 11042–6 | date = September 2001 | pmid = 11572966 | pmc = 58680 | doi = 10.1073/pnas.191352698 | quote = <!-- Although the ΔFosB signal is relatively long-lived, it is not permanent. ΔFosB degrades gradually and can no longer be detected in brain after 1–2 months of drug withdrawal&nbsp;... Indeed, ΔFosB is the longest-lived adaptation known to occur in adult brain, not only in response to drugs of abuse, but to any other perturbation (that doesn't involve lesions) as well. --> | bibcode = 2001PNAS...9811042N | doi-access = free }}</ref> ΔFosB increases the expression of [[AMPA receptor]] subunit GluR2<ref name="pmid10499584" /> and also decreases expression of [[dynorphin]], thereby enhancing sensitivity to reward.<ref name="pmid11572966" />

[[DNA damage (naturally occurring)|DNA damage]] is increased in the brain of rodents by administration of cocaine.<ref name="pmid24552452">{{Cite journal | vauthors = de Souza MF, Gonçales TA, Steinmetz A, Moura DJ, Saffi J, Gomez R, Barros HM | title = Cocaine induces DNA damage in distinct brain areas of female rats under different hormonal conditions | journal = Clinical and Experimental Pharmacology & Physiology | volume = 41 | issue = 4 | pages = 265–9 | date = April 2014 | pmid = 24552452 | doi = 10.1111/1440-1681.12218 | s2cid = 20849951 }}</ref><ref name="pmid19878142">{{Cite journal | vauthors = Alvarenga TA, Andersen ML, Ribeiro DA, Araujo P, Hirotsu C, Costa JL, Battisti MC, Tufik S | title = Single exposure to cocaine or ecstasy induces DNA damage in brain and other organs of mice | journal = Addiction Biology | volume = 15 | issue = 1 | pages = 96–9 | date = January 2010 | pmid = 19878142 | doi = 10.1111/j.1369-1600.2009.00179.x | s2cid = 21347765 }}</ref> During [[DNA repair]] of such damages, persistent [[chromatin]] alterations may occur such as [[DNA methylation|methylation of DNA]] or the acetylation or [[histone methylation|methylation of histones]] at the sites of repair.<ref name="pmid27259203">{{Cite journal | vauthors = Dabin J, Fortuny A, Polo SE | title = Epigenome Maintenance in Response to DNA Damage | journal = Molecular Cell | volume = 62 | issue = 5 | pages = 712–27 | date = June 2016 | pmid = 27259203 | pmc = 5476208 | doi = 10.1016/j.molcel.2016.04.006 }}</ref>  These alterations can be [[epigenetics|epigenetic]] {{Clarify|date=March 2025|reason= epigenetics article doesn't mention 'scars'|text= scars}} in the chromatin that contribute to the persistent [[Epigenetics of cocaine addiction|epigenetic changes found in cocaine addiction]].

==== Dependence and withdrawal ====
[[Cocaine dependence]] develops after even brief periods of regular cocaine use<ref>{{Cite journal | vauthors = Gawin FH, Ellinwood EH | title = Cocaine dependence | journal = Annual Review of Medicine | volume = 40 | pages = 149–61 | date = 1989 | pmid = 2658744 | doi = 10.1146/annurev.me.40.020189.001053 }}</ref> and produces a [[drug withdrawal|withdrawal]] state with emotional-motivational deficits upon cessation of cocaine use.

==== Cocaine nose ====
[[File:Cocaine nose.jpg|thumb|200px|[[Nasal septum perforation]] caused by cocaine use (pictured)-sometimes referred to as a "cocaine nose hole"-can progress to [[cocaine-induced midline destructive lesions]].]]

"Cocaine nose" or "coke nose" are informal terms that refer to nasal problems resulting from cocaine use.

Problems associated with cocaine nose include:
* [[Cocaine-induced midline destructive lesions]] (CIMDL)<ref name="distribution" />
* [[Nasal septum perforation]]<ref name="pmid34360121" /> ("cocaine nose hole") can progress to CIMDL
* [[Saddle nose]]<ref name="Schreiber2014">{{cite journal | vauthors = Schreiber BE, Twigg S, Marais J, Keat AC | title = Saddle-nose deformities in the rheumatology clinic | journal = Ear, Nose, & Throat Journal | volume = 93 | issue = 4–5 | pages = E45–E47 | date = April–May 2014 | pmid = 24817241 | type = Review }}</ref>

=====Cocaine-induced midline destructive lesions=====
{{main|Cocaine-induced midline destructive lesions}}

[[Cocaine-induced midline destructive lesions]] (CIMDL), colloquially known as "coke nose",<ref name="distribution">{{cite journal | vauthors = Nitro L, Pipolo C, Fadda GL, Allevi F, Borgione M, Cavallo G, Felisati G, Saibene AM | title = Distribution of cocaine-induced midline destructive lesions: systematic review and classification | journal = European Archives of Oto-Rhino-Laryngology | volume = 279 | issue = 7 | pages = 3257–3267 | date = July 2022 | pmid = 35138441 | pmc = 9130192 | doi = 10.1007/s00405-022-07290-1 }}</ref> is the progressive destruction of nasal architecture with the erosion of the [[palate]], [[Nasal Concha|nasal conchae]], and [[ethmoid sinus]]es associated with prolonged [[Insufflation (medicine)|insufflation]], colloquially 'snorting', of cocaine.<ref name="pmid34360121">{{cite journal | vauthors = Di Cosola M, Ambrosino M, Limongelli L, Favia G, Santarelli A, Cortelazzi R, Lo Muzio L | title = Cocaine-Induced Midline Destructive Lesions (CIMDL): A Real Challenge in Diagnosis | journal = International Journal of Environmental Research and Public Health | volume = 18 | issue = 15 | pages = 7831 | date = July 2021 | pmid = 34360121 | pmc = 8345435 | doi = 10.3390/ijerph18157831 | doi-access = free }}</ref>

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]].<ref name="pagliaros">{{Cite book| vauthors = Pagliaro L, Pagliaro AM |title=Pagliaros' Comprehensive Guide to Drugs and Substances of Abuse|publisher=[[American Pharmacists Association]]|location=Washington, D.C.|year=2004|isbn=978-1-58212-066-9|url=https://archive.org/details/pagliaroscompreh0000pagl}}</ref>

=== Mortality ===
Persons with regular or problematic use of cocaine have a significantly higher [[mortality rate]], and are specifically at higher risk of traumatic deaths and deaths attributable to infectious disease.<ref>{{Cite journal | vauthors = Peacock A, Tran LT, Larney S, Stockings E, Santo T, Jones H, Santomauro D, Degenhardt L | title = All-cause and cause-specific mortality among people with regular or problematic cocaine use: a systematic review and meta-analysis | journal = Addiction | volume = 116 | issue = 4 | pages = 725–742 | date = April 2021 | pmid = 32857457 | pmc = 7914269 | doi = 10.1111/add.15239 }}</ref> In 2025, the Liberty House Clinic in the [[United Kingdom]] noted that chronic cocaine usage in fact had a higher risk of death than [[alcoholism]].<ref>{{cite web|url=https://www.libertyhouseclinic.co.uk/blog/substance-abuse/cocaine-or-alcohol-whats-worse/|title=Cocaine or alcohol, what's worse?|publisher=Liberty House Clinic|date=17 February 2025|accessdate=19 April 2025}}</ref>