What is nicotine poisoning?
Nicotine poisoning occurs when there is too much nicotine in the body. It is either sniffed, chewed or inhaled. Although smoking rates have declined in recent decades, use of electronic nicotine delivery systems (ENDS) (also known as e-cigarettes (ECs)) has substantially gained popularity, especially among teenagers and young adults.1 Nicotine products are promoted by various social media platforms without clear warning labels, and overdose or prolonged use of nicotine causes addiction, permanent damage to the heart and lungs, and causes mouth cancer.
What is the lethal dose of nicotine?
The toxic dose for nicotine is predicted to be 50-60 mg for adults by the CDC.
How do I know if I have poisoning?
Symptoms can take from 15 minutes to 4 hours to appear. Vomiting is the most common symptom.
How long does it last?
The effect of poisoning can last between 18 and 24 hours after exposure and can lead to death as well.
The image shows a hand holding e-cigarette.
Sources of nicotine poisoning
Smoking cigarettes, nicotine gums, patches, pipe, chewing tobacco, vaping (e-liquids), accidental exposure, or exposure to insecticides and plants containing tobacco.1
The image depicts a person smoking a cigarette.
Symptoms of nicotine toxicity
- Mild poisoning - acute exposure causes:
- nausea
- vomiting
- diarrhoea
- dizziness
- salivation
- weakness
- Severe poisoning - lethargy, paralysis, and coma
- Chronic exposure over months or years causes long-term side effects on various organs of the body
The effects of nicotine on the body are mainly categorised as the motor, sensory, and central nervous system responses.2
Motor
- Nicotine acts on the heart, blood vessels, bladder, and gastrointestinal tract by stimulating the sympathetic ganglia in the brain
- Conversely, high-dose nicotine treatment can cause these effects to disappear 2
- Nicotine causes twitching in muscles by acting on the motor endplates
Sensory
- Effects on the sensory system are associated with chemoreceptors. Low doses of nicotine increase breathing rate, heart rate, and blood pressure by stimulating chemoreceptors in the carotid artery and aorta
Effect on organs
| Heart and blood vessels of the heart | Increased heart rateIncreased blood pressureIncreased blood clot formationSudden heart attack and death |
| Brain and nervous system | DizzinessHeadacheSleep problemsDepression |
| Gastrointestinal region | DiarrhoeaUlcers in the stomachIndigestionDry mouth |
| Lungs and respiratory system | Shortness of breathSpasm in the lungs Diseases like chronic obstructive pulmonary disease |
| Muscle system | TremorsTwitchingJoint pain |
Impact on the nervous system - a double-edged sword
Dysregulation of neurotransmitters
Cholinergic receptors are present in the brain, muscles and heart. Nicotine activates cholinergic receptors (nAChRs) in the central nervous system (CNS) and peripheral nervous system (PNS) of the brain, releasing neurotransmitters such as noradrenaline, dopamine, and serotonin, which alter brain activity. Stimulation of these receptors affects breathing and heart rate, causing attentiveness and alertness. The high affinity of nicotine to bind with nAChR receptors causes long-term inactivation of the receptors in smokers, due to increased desensitisation in the receptors.3
Nicotine enhances the release of dopamine from nAChR receptors. It also activates opioid receptors, and GABA neurons in the brain, all of which are responsible for addiction, drug-reward behaviour and drive to consume more and more nicotine-containing products.3
Studies have also shown that the nicotine binding receptors increase in the brain of a tobacco consumer. This can cause withdrawal symptoms and an increased risk of overdosing.3
Cognitive decline and mental health
Nicotine influences a wide variety of cognitive functions, such as attention, memory and learning. Studies have shown mixed effects of nicotine on memory loss and cognitive decline.
Positive action
It has been found to improve cognitive impairment in many brain diseases and conditions, such as: Alzheimer's disease, Parkinson's disease, schizophrenia, stroke, and autism spectrum disorder.4 This action of enhancing cognitive behaviour causes difficulty in quitting smoking, especially in people with psychiatric problems.4
Negative action
Chronic use of nicotine increases phosphodiesterase-5 (PDE-5) enzyme levels in the brain, downstreaming signalling and the blocking of oestrogen hormone production, leading to cognitive decline, reduced attention span, enhanced impulsivity, depression and memory loss. Estrogen stimulates a wide range of neurotransmitters. Low estrogen production in the brain and elevated PDE-5 levels affect cognitive function in healthy individuals.5
Chronic vaping can affect mental health.
Neurotoxicity and neuronal death
Positive action
Studies have shown that nicotine protects against neurotoxicity induced by glutamate, nAChRs being responsible for this protective function. Glutamate is a neurotransmitter responsible for nerve signalling across synapses. Excess glutamate, as seen in Alzheimer’s and Parkinson’s disease, causes nerve damage and degeneration, increasing calcium in the cells, which has toxic effects. The mechanisms involved in the protective functions of nicotine remain unclear.6 Hence, nicotine may help in treating age-related diseases and Attention deficit disorders.
Negative action
Animal studies have shown that smokeless tobacco treatment causes oxidative stress in the nerves, leading to changes in cell shape, cytotoxicity, production of reactive oxygen species and thus, causing imbalance in neural signalling networks.7
Autonomic nervous system dysregulation
Studies on rats have shown that tobacco smoke extract disrupts the function of cholinergic neurons, specifically the ones that release the neurotransmitter acetylcholine (ACh) to transmit nerve impulses. Also, there is a decrease in the number of nicotinic acetylcholine receptors (nAChRs). Nicotine, being a major constituent along with benzo(a)pyrene, plays a major role in disrupting acetylcholine and serotonin receptors, causing dysregulation in the brain.8
Impact on the heart and blood vessels
Heart diseases remain the leading cause of death around the world, and tobacco acts as a significant risk factor in causing heart problems. Nicotine is responsible for 1.8 million deaths globally each year, due to heart attacks.9
Effects of cigarette smoking
The adverse effects of cigarette smoking on the heart include:
- Structural and functional heart damage
- Arrhythmias and heart rhythm disorders: sudden death and atrial fibrillation
- Myocardial diseases: hypertension (high blood pressure), heart disease, and heart failure
- Vascular diseases: atherosclerosis and damage to blood vessels causing stroke, coronary spasm and thrombosis
Mechanism behind heart diseases
Cholinergic receptors
Nicotine acts on nAChR receptors in the brain, releasing neurotransmitters. These receptors are also present in skin cells, inflammatory cells and cells of the blood vessels. In the presence of nicotine, nAChRs become inactive and cannot be reactivated by nicotine.3
Nicotine through the nAChRs ( from blood vessels and brain) also activates the sympathetic nervous system, causing the release of epinephrine.10
Effects of epinephrine
- Increase in heart rate, blood pressure and muscle contraction
- Constriction of blood vessels, especially the coronary arteries and relaxation of skeletal blood vessels
Nicotine can decrease coronary blood flow by constricting coronary arteries or can increase blood flow by increasing overall output of the heart, called flow-mediated dilation (FMD), depending on the exposure. Thus, balancing the net effect in acute cases.10
In healthy people, smoking a cigarette increases coronary blood flow by up to 40%, but in smokers with heart disease, the effect is reversed and can lead to coronary spasms and angina.10
Tissue remodeling
Activation of the sympathetic nervous system by nicotine leads to tissue remodelling in the heart, which increases the risk of heart failure through fibrosis and changes in the structure of the heart.10
Arrhythmia and nicotine
Release of neurotransmitters and remodelling due to nicotine causes a fatal increase in the heart rate, fibrillations and increased risk of heart attack.
Platelet activation
Mixed data is available on epinephrine-mediated platelet activation. Some studies say it activates platelets acutely in some animals, but long-term studies in rodents showed that it reduced platelet activation and aggregation.11 Hence, the direct role of nicotine in causing clots in the heart is unclear.
Endothelial cell dysfunction
Endothelial dysfunction is seen in both active smokers and in people with indirect smoke exposure.11 The main mechanism behind this is oxidative stress and inflammation.11 Nicotine, infused locally or through a nasal spray in people, has been shown to block endothelial function.10
Chronic inflammation and nicotine
Inflammation plays a key role in causing atherosclerosis. In general, activation of the sympathetic system has an anti-inflammatory effect. Nicotine has both pro- and anti-inflammatory actions
In animal models with chronic inflammatory conditions like sepsis, administration of nicotine suppressed inflammation.10 However, in mouse models, an acute heart attack activates the sympathetic nervous system via beta-3 receptors to induce inflammation and increase atherosclerosis.12 It appears that nicotine is not a major contributor to chronic inflammation during smoking, although smoking cessation reduces inflammation.10
Dyslipidemia and nicotine
Nicotine induces lipolysis resulting in enhanced synthesis of Low density lipoprotein (LDL) and reducing high density lipoprotein synthesis, thus increasing the risk of atherosclerosis. Nicotine cessation improves dyslipidemia and reverses the ill effects of low-density lipoprotein.
Hypertension and nicotine
Smoking a cigarette can acutely shoot up blood pressure. In chronic smokers with hypertension, worsening of the condition is seen.13 The aggravating effect is due to constriction of vessels and progressive injury to the vessels. Nicotine does play a role in worsening blood pressure.
New blood vessel formation and nicotine
Nicotine, through nAChRs, acutely enhances new blood vessel formation, endothelial cell multiplication and movement and also increases response to inflammation and atherosclerosis. However, chronic nicotine exposure found the opposite effect through downregulation of nAChRs present in blood vessels. Thus, the role of nicotine in new blood vessel formation is questionable.
FAQs
What do I do if I have symptoms of nicotine poisoning?
If you think you have symptoms of nicotine poisoning, get medical help immediately. Call 111 for the NHS or 999 for emergencies.
Does nicotine affect everyone in the same way?
No, the effects of nicotine can vary from person to person depending on dose and duration of exposure.
How does nicotine affect the cardiovascular system immediately?
Nicotine causes an increase in heart rate and blood pressure.
Can nicotine damage nerves?
Yes, nicotine overdose can affect nerve signalling, causing mental health problems and cognitive decline.
Summary
Nicotine is a highly addictive and toxic substance. Although most nicotine exposures result in minimal symptoms, nicotine poisoning may present with life-threatening conditions like arrhythmias, paralysis, shock, breathing complications and death, requiring immediate action. Vital organs like the heart and brain can be seriously damaged, although they may have positive effects in the beginning. It is important to understand that there is no antidote to nicotine poisoning, and the treatment is based on symptoms. Hence, focus should be on prevention and intervention.
References
- Cleveland Clinic. ‘Nicotine Poisoning: Symptoms, Causes, Treatments & Prevention’. [Internet]. [updated 2021 October 25; cited: 2025 September 9]. Available from: https://my.clevelandclinic.org/health/diseases/21582-nicotine-poisoning
- Cao, Yun, et al. ‘The Double-Edged Nature of Nicotine: Toxicities and Therapeutic Potentials’. Frontiers in Pharmacology, vol. 15, Aug. 2024, p. 1427314. DOI.org (Crossref), https://doi.org/10.3389/fphar.2024.1427314.
- Tiwari, Raj Kumar, et al. ‘Nicotine Addiction: Neurobiology and Mechanism’. Journal of Pharmacopuncture, vol. 23, no. 1, Mar. 2020, pp. 1–7. DOI.org (Crossref), https://doi.org/10.3831/KPI.2020.23.001.
- Wang, Qian, et al. ‘Nicotine’s Effect on Cognition, a Friend or Foe?’ Progress in Neuro-Psychopharmacology and Biological Psychiatry, vol. 124, June 2023, p. 110723. DOI.org (Crossref), https://doi.org/10.1016/j.pnpbp.2023.110723.
- Singh, Nihaal, et al. ‘Effects of Nicotine on the Central Nervous System and Sleep Quality in Relation to Other Stimulants: A Narrative Review’. Cureus, Nov. 2023. DOI.org (Crossref), https://doi.org/10.7759/cureus.49162.
- Sun X, Liu Y, Hu G, Wang H. Protective effects of nicotine against glutamate-induced neurotoxicity in PC12 cells. Cell Mol Biol Lett. 2004;9(3):409-22. PMID: 15332118
- Biswas, Sushobhan, et al. ‘Smokeless Tobacco Induces Toxicity and Apoptosis in Neuronal Cells: A Mechanistic Evaluation’. Free Radical Research, vol. 54, no. 7, July 2020, pp. 477–96. DOI.org (Crossref), https://doi.org/10.1080/10715762.2020.1805446.
- Slotkin, Theodore A., et al. ‘The Developmental Neurotoxicity of Tobacco Smoke Can Be Mimicked by a Combination of Nicotine and Benzo[a]Pyrene: Effects on Cholinergic and Serotonergic Systems’. Toxicological Sciences, vol. 167, no. 1, Jan. 2019, pp. 293–304. DOI.org (Crossref), https://doi.org/10.1093/toxsci/kfy241.
- Dorotheo, E. Ulysses, et al. ‘Nicotine and Cardiovascular Health: When Poison Is Addictive – a WHF Policy Brief’. Global Heart, vol. 19, no. 1, Jan. 2024, p. 14. DOI.org (Crossref), https://doi.org/10.5334/gh.1292.
- Benowitz, Neal L., and Andrea D. Burbank. ‘Cardiovascular Toxicity of Nicotine: Implications for Electronic Cigarette Use’. Trends in Cardiovascular Medicine, vol. 26, no. 6, Aug. 2016, pp. 515–23. DOI.org (Crossref), https://doi.org/10.1016/j.tcm.2016.03.001.
- Girdhar, G., et al. ‘Reduced-Nicotine Cigarettes Increase Platelet Activation in Smokers in Vivo: A Dilemma in Harm Reduction’. Nicotine & Tobacco Research, vol. 10, no. 12, Dec. 2008, pp. 1737–44. DOI.org (Crossref), https://doi.org/10.1080/14622200802443528.
- Dutta, Partha, et al. ‘Myocardial Infarction Accelerates Atherosclerosis’. Nature, vol. 487, no. 7407, July 2012, pp. 325–29. DOI.org (Crossref), https://doi.org/10.1038/nature11260.

