Health effects of nicotine
Nicotine is an alkaloid found primarily in plants of the nightshade family, notably in tobacco; it is also synthesized.[1] Nicotine is used recreationally for its stimulant and anxiolytic effects.
In humans, nicotine acts primarily as a stimulant by binding to and activating nicotinic acetylcholine receptors (nAChRs) in the central nervous system and peripheral tissues. This results in the release of neurotransmitters such as dopamine, acetylcholine, and norepinephrine, producing effects including increased alertness, reduced anxiety, and mild euphoria.[2] Nicotine is typically consumed through tobacco smoking, vaping, or other nicotine delivery systems.
Effects on brain development
Exposure to nicotine, from conventional or electronic cigarettes during adolescence can impair the developing human brain.[3] E-cigarette use is recognized as a substantial threat to adolescent behavioral health.[4] Furthermore, youth and young adults are more vulnerable than adults to the long-term consequences of nicotine exposure, including susceptibility to nicotine addiction and potentially reduced impulse control, deficits in attention and cognition, and mood disorders.[4]
The use of tobacco products, no matter what type, is almost always started and established during adolescence when the developing brain is most vulnerable to nicotine addiction.[notes 1] Young people's brains build synapses faster than adult brains.[6] Because addiction is a form of learning, adolescents can get addicted more easily than adults.[6] The nicotine in e-cigarettes can also prime the adolescent brain for addiction to other drugs such as cocaine.[6]
Addiction to nicotine
Nicotine is addictive, and nicotine dependence is characterized by tolerance, physical dependence, psychological dependence, and nicotine withdrawal symptoms such as irritability, anxiety, and difficulty concentrating.[7][8]
According to studies by Henningfield and Benowitz, nicotine is more addictive than cannabis, caffeine, alcohol, cocaine, and heroin when considering both somatic and psychological dependence. However, due to the stronger withdrawal effects of alcohol, cocaine and heroin, nicotine may have a lower potential for somatic dependence than these substances.[9][10]
Although nicotine does play a role in acute episodes of some diseases (including stroke, impotence, and heart disease) by its stimulation of adrenaline release, which raises blood pressure,[11] heart and respiration rate, and free fatty acids, the most serious longer- term effects are more the result of the products of tobacco smoking. This has led to the development of various nicotine delivery systems, such as the nicotine patch or nicotine gum, that can satisfy the addictive craving by delivering nicotine without the harmful combustion by-products. This can help the heavily dependent smoker to quit gradually while discontinuing further damage to health.[12]
Nicotine in tobacco products
The health effects of nicotine also depend on its delivery methods, nicotine concentration on the product and accompanying compounds.
Smoking
When tobacco is smoked, most of the nicotine is pyrolyzed; a dose sufficient to cause mild somatic dependency and mild to strong psychological dependency remains. The amount of nicotine absorbed by the body from smoking depends on many factors, including the type of tobacco, whether the smoke is inhaled, and whether a filter is used. There is also a formation of harmane (a MAO inhibitor) from the acetaldehyde in cigarette smoke, which seems to play an important role in nicotine addiction[13] probably by facilitating dopamine release in the nucleus accumbens in response to nicotine stimuli.
Ingesting a compound by smoking is one of the most rapid and efficient methods of introducing it into the bloodstream, second only to injection, which allows for the rapid feedback which supports the smokers' ability to titrate their dosage. On average, it takes about ten seconds for the substance to reach the brain. As a result of the efficiency of this delivery system, many smokers feel as though they are unable to cease. Those who achieve one year of continuous abstinence are highly likely to remain so, with the vast majority of relapses occurring within the first eight days after attempting cessation.[14]
An average cigarette yields about 2 mg of absorbed nicotine, a dose sufficient to produce reinforcement and dependence while remaining far below toxic levels.[16]
Smokeless tobacco
Smokeless tobacco are tobacco products that is used by means other than smoking, for example by chewing, sniffing, or placing the product between gum and the cheek or lip.[17]
Smokeless tobacco differs depending on the type of product, the types of tobacco used, and the amount of each tobacco type used within a product. Each variable results in a different level of nicotine. Furthermore, nicotine is absorbed by the body to different degrees depending on the pH level of the product, which is known as the free nicotine or unionized nicotine level.[18]
The amounts of nicotine in saliva from using smokeless tobacco could be at amounts that can be toxic to cells in the oral cavity.[19]
Smokeless tobacco (including products where tobacco is chewed) is a cause of oral cancer, oesophagus cancer, and pancreas cancer.[20] Increased risk of oral cancer caused by smokeless tobacco is present in countries such as the United States but particularly prevalent in Southeast Asian countries where the use of smokeless tobacco is common.[21][22]
Nicotine replacement therapy
Nicotine replacement therapy (NRT) products, including gums, patches, and lozenges, deliver the compound in slower, lower doses that are less addictive and are used medically to help people quit smoking.[23][24]
Synthetic derivatives of nicotine, such as varenicline, act as partial agonists at nicotinic receptors and are also used as smoking cessation aids.[25]
See also
- Health effects of tobacco smoking
- Health effects of electronic cigarettes
- Health effects of smokeless tobacco
Notes
- ^ A 2018 review found "Nicotine is the third most commonly used substance by adolescents and use of electronic cigarettes has become twice as popular as traditional tobacco products. Concomitantly, e-cigarettes have been found to increase the risk for transitioning to more traditional tobacco cigarettes. Although acute administration of nicotine may enhance cognition in teens and young adults, especially memory and attention, chronic use has been linked with attention and working memory deficits in teens. Acute withdrawal from nicotine in adolescent users has also been associated with abnormal reward processing, working memory, and verbal memory fMRI tasks, highlighting the necessity to measure last use of nicotine prior to neurocognitive assessment."[5]
References
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- ^ Sajja RK, Rahman S, Cucullo L (March 2016). "Drugs of abuse and blood-brain barrier endothelial dysfunction: A focus on the role of oxidative stress". Journal of Cerebral Blood Flow and Metabolism. 36 (3): 539–554. doi:10.1177/0271678X15616978. PMC 4794105. PMID 26661236.
- ^ England LJ, Bunnell RE, Pechacek TF, Tong VT, McAfee TA (August 2015). "Nicotine and the Developing Human: A Neglected Element in the Electronic Cigarette Debate". American Journal of Preventive Medicine. 49 (2): 286–293. doi:10.1016/j.amepre.2015.01.015. PMC 4594223. PMID 25794473.
- ^ a b Stratton, Kathleen; Kwan, Leslie Y.; Eaton, David L. (January 2018). Stratton, Kathleen; Kwan, Leslie Y.; Eaton, David L. (eds.). Public Health Consequences of E-Cigarettes (PDF). National Academies of Sciences, Engineering, and Medicine (National Academies Press). pp. 1–774. Bibcode:2018nap..book24952N. doi:10.17226/24952. ISBN 978-0-309-46834-3. PMID 29894118.
- ^ Lisdahl, Krista M.; Sher, Kenneth J.; Conway, Kevin P.; Gonzalez, Raul; Feldstein Ewing, Sarah W.; Nixon, Sara Jo; Tapert, Susan; Bartsch, Hauke; Goldstein, Rita Z.; Heitzeg, Mary (2018). "Adolescent brain cognitive development (ABCD) study: Overview of substance use assessment methods". Developmental Cognitive Neuroscience. 32: 80–96. doi:10.1016/j.dcn.2018.02.007. ISSN 1878-9293. PMC 6375310. PMID 29559216.
- ^ a b c "Know The Risks: E-Cigarettes & Young People – Addiction". Surgeon General of the United States. 2016. This article incorporates text from this source, which is in the public domain.
- ^ CDC (2025-01-31). "Health Effects of Vaping". Smoking and Tobacco Use. Retrieved 2026-01-03.
- ^ Perkins KA, Karelitz JL (August 2013). "Reinforcement enhancing effects of nicotine via smoking". Psychopharmacology. 228 (3): 479–486. doi:10.1007/s00213-013-3054-4. PMC 3707934. PMID 23494236.
- ^ Hilts PJ (1994-08-02). "Relative Addictiveness of Drugs". The New York Times. Retrieved 2012-05-06.
- ^ "The Henningfield-Benowitz substance comparison charts". Archived from the original on 2012-06-19. Retrieved 2012-05-06.
- ^ Narkiewicz K, Kjeldsen SE, Hedner T (2005). "Is smoking a causative factor of hypertension?". Blood Pressure. 14 (2): 69–71. doi:10.1080/08037050510034202. PMID 16036482. S2CID 40476025.
- ^ Hartmann-Boyce, J.; Chepkin, S. C.; Ye, W.; Bullen, C.; Lancaster, T. (2018). "Nicotine replacement therapy versus control for smoking cessation". Cochrane Database of Systematic Reviews (5) CD000146. doi:10.1002/14651858.CD000146.pub5. PMC 6353171. PMID 29852054.
- ^ Talhout R, Opperhuizen A, van Amsterdam JG (October 2007). "Role of acetaldehyde in tobacco smoke addiction". European Neuropsychopharmacology. 17 (10): 627–36. doi:10.1016/j.euroneuro.2007.02.013. PMID 17382522. S2CID 25866206.
- ^ Hughes, J. R.; Keely, J.; Naud, S. (2004). "Shape of the relapse curve and long-term abstinence among untreated smokers". Addiction. 99 (1): 29–38. doi:10.1111/j.1360-0443.2004.00540.x. PMID 14678060.
- ^ "Smokeless Tobacco: Health Effects". Centers for Disease Control and Prevention. 1 December 2016. This article incorporates text from this source, which is in the public domain.
- ^ Mayer B (January 2014). "How much nicotine kills a human? Tracing back the generally accepted lethal dose to dubious self-experiments in the nineteenth century". Archives of Toxicology. 88 (1): 5–7. Bibcode:2014ArTox..88....5M. doi:10.1007/s00204-013-1127-0. PMC 3880486. PMID 24091634.
- ^ "Smokeless Tobacco Products, Including Dip, Snuff, Snus, and Chewing Tobacco". United States Food and Drug Administration. 7 May 2018. Archived from the original on May 24, 2016. This article incorporates text from this source, which is in the public domain.
- ^ "The pH of Smokeless Tobacco Determines Nicotine Buccal Absorption: Results of a Randomized Crossover Trial" (PDF). Retrieved 2025-12-10.
- ^ Holliday, Richard S; Campbell, James; Preshaw, Philip M. (2019). "Effect of nicotine on human gingival, periodontal ligament and oral epithelial cells. A systematic review of the literature". Journal of Dentistry. 86: 81–88. doi:10.1016/j.jdent.2019.05.030. ISSN 0300-5712. PMID 31136818. S2CID 169035502.
- ^ Vidyasagaran, A. L.; Siddiqi, K.; Kanaan, M. (2016). "Use of smokeless tobacco and risk of cardiovascular disease: A systematic review and meta-analysis" (PDF). European Journal of Preventive Cardiology. 23 (18): 1970–1981. doi:10.1177/2047487316654026. ISSN 2047-4873. PMID 27256827. S2CID 206820997.
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- ^ Wyss AB, Hashibe M, Lee YA, Chuang SC, Muscat J, Chen C, et al. (November 2016). "Smokeless Tobacco Use and the Risk of Head and Neck Cancer: Pooled Analysis of US Studies in the INHANCE Consortium". American Journal of Epidemiology. 184 (10): 703–716. doi:10.1093/aje/kww075. PMC 5141945. PMID 27744388.
- ^ "Nicotine: Clinical data". IUPHAR/BPS Guide to Pharmacology. International Union of Basic and Clinical Pharmacology.
Used as an aid to smoking cessation and for the relief of nicotine withdrawal symptoms.
- ^ Etter JF (July 2007). "Addiction to the nicotine gum in never smokers". BMC Public Health. 7 159. doi:10.1186/1471-2458-7-159. PMC 1939993. PMID 17640334.
- ^ Coe JW, et al. (May 2005). "Varenicline: an alpha4beta2 nicotinic receptor partial agonist for smoking cessation". Journal of Medicinal Chemistry. 48 (10): 3474–3477. Bibcode:2005JMedC..48.3474C. doi:10.1021/jm050069n. PMID 15887955.