Peripheral Neuropathies
Toxic peripheral neuropathies
Jun. 11, 2026
MedLink, LLC
3525 Del Mar Heights Rd, Ste 304
San Diego, CA 92130-2122
Toll Free (U.S. + Canada): 800-452-2400
US Number: +1-619-640-4660
Support: service@medlink.com
Editor: editor@medlink.com
ISSN: 2831-9125
Toll Free (U.S. + Canada): 800-452-2400
US Number: +1-619-640-4660
Support: service@medlink.com
Editor: editor@medlink.com
ISSN: 2831-9125
Worddefinition
At vero eos et accusamus et iusto odio dignissimos ducimus qui blanditiis praesentium voluptatum deleniti atque corrupti quos dolores et quas.
It is believed that tobacco use dates back to around 6000 BC. The plant Nicotiana tabacum, native exclusively to the Americas, was first smoked by Native American populations for medicinal and cultural purposes. After 1492, Spanish explorers observed these practices and brought the habit back to Europe (30).
Although initially condemned by the Holy Inquisition, smoking rapidly gained popularity among Europeans traveling between continents. Portuguese sailors began commercially cultivating tobacco in Brazil, laying the foundation for a profitable transatlantic industry. By the late 16th century, the use of tobacco, whether smoked or snuffed, had become widespread across Europe. At the time, physicians believed tobacco had medicinal benefits and promoted its use for therapeutic purposes (94).
In the 19th century, cigarettes emerged as a popular form of tobacco consumption. Initially sold as hand-rolled Turkish cigarettes, mass production began in 1881 with the invention of the first cigarette-making machine by James Bonsack. This innovation led to the establishment of the American Tobacco Company, which continues today as British American Tobacco (13). Cigarettes gained further popularity during World War I and World War II, when they were included in soldiers’ rations and widely used on the battlefield. By the 1920s, targeted advertising campaigns expanded their appeal to women, opening a new and rapidly growing consumer market (94).
Beyond its pharmacological effects, smoking developed deep sociocultural associations throughout the 20th century. It was portrayed in film and advertising as a symbol of status, sophistication, sexuality, and rebellion, often endorsed by celebrities and public figures (13).
Concerns about the harmful effects of smoking began to surface early on. In the 1760s, British and German physicians warned of a possible link between tobacco use and cancers of the nose and lip. In the United States, the association between smoking and lung cancer was not widely recognized until the 1930s and 1940s, culminating in the landmark studies of Doll and Hill in the 1950s (13).
From the 1970s through the 1990s, tobacco companies faced increasing legal challenges due to mounting evidence of the link between smoking and cancer. They were forced to limit marketing practices, print health warnings on product labels, and contribute to anti-smoking campaigns. By the end of the 20th century, public smoking bans had been implemented in most parts of the world (104).
In more recent decades, the use of electronic cigarettes (e-cigarettes) has grown exponentially. Introduced to the U.S. market around 2006, these devices became especially popular among teenagers, young adults, former tobacco users, and even individuals with no prior history of smoking (65). In 2016, the U.S. Food and Drug Administration (FDA) began regulating e-cigarettes and initiated long-term research through the NIH to better understand their health effects (26).
|
• Tobacco use remains a major global health concern, with 7.7 million deaths attributed to smoking in 2019 and projections estimating at least 9 million annual deaths by 2030. | |
|
• Smoking is an independent risk factor for neurologic diseases, including stroke, cognitive impairment, and multiple sclerosis. | |
|
• Nicotine drives addiction through its action on nicotinic acetylcholine receptors, leading to dopamine release and long-term tolerance and dependence. | |
|
• Vaping poses neurologic risks due to the presence of harmful compounds, such as nicotine, aldehydes, and nitrosamines, on the combusting liquids. | |
|
• Cannabis smoking has also been linked to neurologic effects, including reported associations with cerebral ischemia and increased oxidative stress. |
It is believed that tobacco use dates back to around 6000 BC. The plant Nicotiana tabacum, native exclusively to the Americas, was first smoked by Native American populations for medicinal and cultural purposes. After 1492, Spanish explorers observed these practices and brought the habit back to Europe (30).
Although initially condemned by the Holy Inquisition, smoking rapidly gained popularity among Europeans traveling between continents. Portuguese sailors began commercially cultivating tobacco in Brazil, laying the foundation for a profitable transatlantic industry. By the late 16th century, the use of tobacco, whether smoked or snuffed, had become widespread across Europe. At the time, physicians believed tobacco had medicinal benefits and promoted its use for therapeutic purposes (94).
In the 19th century, cigarettes emerged as a popular form of tobacco consumption. Initially sold as hand-rolled Turkish cigarettes, mass production began in 1881 with the invention of the first cigarette-making machine by James Bonsack. This innovation led to the establishment of the American Tobacco Company, which continues today as British American Tobacco (13). Cigarettes gained further popularity during World War I and World War II, when they were included in soldiers’ rations and widely used on the battlefield. By the 1920s, targeted advertising campaigns expanded their appeal to women, opening a new and rapidly growing consumer market (94).
Beyond its pharmacological effects, smoking developed deep sociocultural associations throughout the 20th century. It was portrayed in film and advertising as a symbol of status, sophistication, sexuality, and rebellion, often endorsed by celebrities and public figures (13).
Concerns about the harmful effects of smoking began to surface early. In the 1760s, British and German physicians warned of a possible link between tobacco use and cancers of the nose and lip. In the United States, the association between smoking and lung cancer was not widely recognized until the 1930s and 1940s, culminating in the landmark studies of Doll and Hill in the 1950s (13).
From the 1970s through the 1990s, tobacco companies faced increasing legal challenges due to mounting evidence of the link between smoking and cancer. They were forced to limit marketing practices, print health warnings on product labels, and contribute to anti-smoking campaigns. By the end of the 20th century, public smoking bans had been implemented in most parts of the world (104).
In more recent decades, the use of electronic cigarettes (e-cigarettes) has grown exponentially. Introduced to the U.S. market around 2006, these devices became especially popular among teenagers, young adults, former tobacco users, and even individuals with no prior history of smoking (65). In 2016, the U.S. Food and Drug Administration began regulating e-cigarettes and initiated long-term research through the NIH to better understand their health effects (26).
• Current smokers show a significantly lower risk of developing Parkinson disease, and this effect appears to be dose dependent. | |
• Smoking does not affect motor symptoms but is associated with increased cognitive decline and a higher risk of Parkinson disease–related dementia. |
Unlike most neurologic conditions, tobacco smoking has shown an inverse association with Parkinson disease. A meta-analysis reported that current smokers had a 60% lower risk of developing Parkinson disease (RR: 0.42; 95% CI: 0.31 to 0.47) (55). Similarly, data from the British doctors’ registry revealed that current smokers had a 40% lower risk of Parkinson disease compared to never smokers, with a 34.7% reduction in crude death rates. An inverse dose-response relationship was also noted: those who smoked more on a daily basis had a lower risk of Parkinson disease. Furthermore, individuals who quit smoking 0 to 9 years prior to the onset of the study had a 29% lower risk, whereas those who quit 10 or more years before had a 14% lower risk, compared to never smokers (63).
Although the mechanisms remain unclear, some authors propose that nicotine may exert neuroprotective effects by stimulating dopamine release in the striatal and mesolimbic systems (80). However, transdermal nicotine has not shown therapeutic benefit in clinical studies (99). Other theories include the neutralization of nasal or gut-derived pathogenic proteins via tobacco’s toxic effects on the nasal mucosa (37), or nicotine-induced inhibition of monoamine oxidase, reducing toxin formation (63).
Importantly, in patients with Parkinson disease who are active smokers, smoking does not appear to impact motor symptoms, but it has been associated with worsened cognitive outcomes, including higher incidence and faster progression of Parkinson disease–related dementia (63). Thus, any potential protective effect is likely offset by cognitive harm.
• Smoking doubles the risk of developing Alzheimer disease and accelerates progression from mild cognitive impairment to dementia. |
Cognitive disorders have received substantial attention in tobacco-related research. A prospective study in elderly patients found that regular smokers had a 2-fold increased risk of developing Alzheimer disease (14). Another study comparing non-smokers to individuals who had smoked for 2 years showed accelerated brain atrophy and loss of structural integrity in the latter group (24). Chronic smokers exhibit neurobiological patterns similar to early-stage Alzheimer disease (54), and the risk increases with cumulative cigarette exposure (85). Among patients with subjective memory complaints, smoking was linked to a significantly higher risk of progression to mild cognitive impairment and dementia (HR: 2.04; 95% CI: 1.20–3.50) (04). Additionally, smoking predicts progression from mild cognitive impairment to Alzheimer disease in various cohorts (03). Overall, smoking promotes cognitive decline, and its use should be discouraged.
The mechanisms are multifactorial. Smoking exacerbates amyloid pathology in animal models (67) and contributes to oxidative stress, neuroinflammation, and neuronal loss (32; 82). It enhances production of reactive oxygen species (ROS), activates pro-inflammatory transcription, and stimulates cytokine release, particularly of tumor necrosis alpha (TNF-alpha) (56; 107; 77; 09). TNF-alpha promotes beta-secretase activity and impairs amyloid-beta clearance, leading to greater amyloid-beta burden (56; 107). A case-control study that investigated the association of cigarette smoking with biomarkers of neurodegeneration, oxidation, and neuroinflammation revealed that smokers have increased CSF levels of at-risk biomarkers, such as amyloid-beta 42 and TNF-alpha. In contrast, non-smokers had lower CSF levels of TNF-alpha and increased CSF levels of superoxide dismutase and nitric oxide synthase, enzymes in charge of accelerating reactions that reduce oxidation and damage (59).
• Smoking is a potential risk factor for amyotrophic lateral sclerosis. Women appear to be more susceptible to smoking-related amyotrophic lateral sclerosis risk and have higher related amyotrophic lateral sclerosis mortality. |
Research in this field has been scarcer and at times inconsistent, but overall, heavy smoking has been identified as a risk factor for amyotrophic lateral sclerosis. A longitudinal study involving five cohorts and 832 patients with amyotrophic lateral sclerosis found that earlier smoking onset correlated with greater amyotrophic lateral sclerosis risk (100). However, no clear dose-response relationship was observed. Other case-control studies have shown a doubled amyotrophic lateral sclerosis risk in ever-smokers compared to never smokers (50; 71), with similar findings from European groups (93). Notably, a UK study failed to find a significant association, but stratification by sex revealed increased amyotrophic lateral sclerosis risk and mortality in women who smoked (RR: 1.53; 95% CI: 1.04–2.23) (05).
Proposed mechanisms include the direct neurotoxic effect of smoking on motor neurons and oxidative stress. Nitric oxide and pesticides used in tobacco cultivation have been proposed as offending factors (22). Formaldehyde, a by-product of the combustion process, increases risk of amyotrophic lateral sclerosis as well (102). Regarding the differences in gender, women may be more sensitive to the deleterious effects of smoking through differences in the metabolism of its compounds (05).
• Smoking is associated with increased disability, higher relapse rate, greater MRI lesion load, and faster progression to secondary progressive multiple sclerosis. | |
• Smoking cessation improves prognosis and lowers disease risk to baseline; nicotine alone may have immunosuppressive and anti-inflammatory effects. |
Multiple sclerosis is a multifactorial disease with genetic and environmental factors playing a role in its presentation. Smoking is a key modifiable risk factor that is associated with increased disability (95), higher relapse frequency, greater MRI lesion load (38), and progression from relapsing-remitting multiple sclerosis (RRMS) to secondary progressive multiple sclerosis (SPMS) (84; 81). Smoking also raises multiple sclerosis–related mortality risk (HR: 2.9; 95% CI: 1.09–2.74) (62).
Additionally, smoking is thought to trigger the onset of symptoms and to increase the risk of hepatotoxicity with certain disease-modifying therapies, such as teriflunomide, due to shared CYP1A2 metabolism (97; 43). Smokers also exhibit higher rates of neutralizing antibodies against natalizumab (OR: 2.4; 95% CI: 1.2–4.4) and interferon-beta 1a (OR: 1.9; 95% CI: 1.3–2.8), potentially reducing treatment efficacy (33; 35).
Smoking worsens cognitive function (73), fatigue, depression (46), and quality of life. The number of cigarettes and duration of exposure correlate with faster disease progression. Encouragingly, smoking cessation slows progression, reduces disability, and improves prognosis (81).
Smoking increases multiple sclerosis risk by 50% in active and passive users (34), but cessation lowers the risk to that of never smokers (36). Individuals with other risk factors, such as family history of multiple sclerosis, comorbid autoimmunity, or Epstein-Barr virus infection, are particularly vulnerable (34).
Tobacco smoke is linked to neuroinflammation more than neurodegeneration in multiple sclerosis, but it certainly participates in both processes. Nicotine alone does not seem to drive multiple sclerosis progression. In fact, it may dampen autoimmune responses, as seen in experimental autoimmune encephalomyelitis models, by reducing CNS immune cell infiltration (88). It suppresses migration of CD4+, CD8+, CD19+, CD11c+, CD11b+, and CD45+ cells, reducing antigen presentation and inflammation (76).
• Smoking increases the risk of stroke, attack recurrence, post-stroke depression, and poor functional outcomes. |
Smoking has long been known to be a vascular risk factor. For the combined outcome of stroke, myocardial infarction, and all-cause mortality, current smokers are at a higher risk when compared to never smokers (HR: 1.56; 95% CI: 1.16–2.09) (06). They also face a higher risk of stroke recurrence (106; 17; 108; 06), which is dose-dependent and mitigated by cessation (17). Functional outcomes are typically poorer (OR: 1.25; 95% CI: 1.08–1.45) (64), and post-stroke depression is more common (adjusted OR: 2.34; 95% CI: 1.50–3.66) (89).
In aneurysmal disease, smoking increases the risk of both aneurysm growth and rupture (OR: 2.2; 95% CI: 1.89–2.59), though quitting significantly reduces this risk (45; 11; 16).
Mechanistically, tobacco smoke promotes endothelial dysfunction, platelet activation, and pro-inflammatory cascades (42). Even at low concentrations, it induces monocyte-to-macrophage differentiation and induces vascular pro-inflammatory responses by upregulating pro-inflammatory genes and cytokines, such as IL-1beta, TNF-alpha, and metalloproteinase-2 and -9 (MMP-2 and MMP-9) (40; 69). This ultimately compromises the blood-brain barrier (83) and facilitates cerebrovascular pathology. Tobacco smoke also enhances angiogenesis and atherosclerosis via ApoE gene upregulation, raising cholesterol levels (91). Both tobacco smoke and vaping exposure induce oxidative stress, impair blood-brain barrier function, and worsen stroke outcomes (48).
• Smoking may enhance CNS vulnerability to infections through oxidative stress and blood-brain barrier dysfunction. |
Smokers may be more susceptible to bacterial and viral invasion of the CNS. This is attributed to increased oxidative stress, systemic inflammation, and compromised blood-brain barrier integrity. They also express an increased number of receptors that promote viral invasion into the brain parenchyma. For example, smoking upregulates the expression of ACE2 receptor, which binds the S protein of SARS-CoV, coronavirus NL63, and SARS-CoV-2 (12).
• Smoking overwhelms the body’s antioxidant defenses, leading to endothelial dysfunction, reactive oxygen species accumulation, and tissue damage. This mechanism is also observed with e-cigarette and marijuana smoke. | |
• Smoking elevates cytokines like IL-6, CRP, and TNF-alpha; activates microglia; and impairs mitochondrial function, promoting a neurotoxic inflammatory environment. | |
• Smoking and vaping reduce tight junction protein expression, increase paracellular leakiness, impair glucose and ion transport, and contribute to vasogenic edema and reduced cerebral metabolism. | |
• Nicotine metabolism via CYP450 enzymes may alter the pharmacokinetics of CNS medications by competing for blood-brain barrier transporters. |
Tobacco smoke exerts multiple downstream effects through both acute and chronic mechanisms. Acutely, nicotine exposure increases dopamine levels in the nucleus accumbens and activates the thalamus, prefrontal cortex, and visual cortex, leading to enhanced attention, improved reaction times, and temporarily heightened cognitive performance. Chronically, tobacco smoke reduces MAO-A and MAO-B activity in the basal ganglia and decreases the availability of nicotinic acetylcholine receptors in the same region (15).
It has been hypothesized that vaping is less harmful than regular tobacco smoking; however, recent evidence suggests otherwise. This public perception has attracted adolescents and young adults to the use of e-cigarettes, yet it has rarely encouraged conventional tobacco smokers to abandon the habit (27). The concentration of nicotine delivered through vaping is variable, and some devices may allow for the inhalation of higher doses than traditional cigarettes, thereby increasing their addictive potential. Chemicals, such as formaldehyde, acrolein, diacetyl, and propylene glycol, may contribute to the neurologic damage associated with e-cigarettes, and in vitro studies have confirmed e-cigarette–induced endothelial dysfunction (79; 44). It is worth noting that human exposure to e-cigarettes has been significantly shorter than to conventional tobacco, and despite this, clear deleterious consequences have already been identified. This may suggest that the effects of vaping are even more severe, given the same duration of use (10).
Smoking-related research has demonstrated that injury to the nervous system occurs through multiple interrelated mechanisms.
Increased oxidative stress. Oxidative stress is a key contributor to endothelial dysfunction and operates in a dose-dependent manner. In addition to disrupting tight junctions, oxidative stress activates pro-inflammatory pathways (78) and causes local tissue injury (02). Chronic exposure to tobacco products often overwhelms the body’s endogenous antioxidant defenses (77; 47), which include enzymes, such as superoxide dismutase, catalase, and glutathione peroxidase; vitamins like ascorbic acid and alpha-tocopherol; and regulatory proteins, such as nuclear factor erythroid 2–related factor 2 (Nrf2) (18; 39). These protective elements trigger downstream pathways that increase the production of antioxidants, anti-inflammatory molecules, free-radical scavengers, and drug-metabolizing enzymes (77).
Epidemiological studies have also linked exposure to heavy metals, common in tobacco smoke, to increased oxidative stress (58). Oxidative damage is not exclusive to tobacco smoke. Other studies suggest that e-cigarette vapor and marijuana smoke also generate reactive oxygen species and promote oxidative stress (07). Although there are some reports of potential antioxidant effects of cannabinoids, this remains controversial (52).
In summary, combustion appears to be the primary driver of oxidative damage. Just as the toxic effects of tobacco smoke outweigh those of nicotine alone, the harmful byproducts of marijuana combustion seem to pose a greater oxidative threat than cannabinoids themselves (70).
Neuroinflammation. Smokers exhibit elevated levels of pro-inflammatory cytokines, such as interleukin-6, C-reactive protein, and TNF-alpha. These cytokines activate microglia and amplify the production of additional inflammatory mediators, which are neurotoxic and promote tissue injury (23; 66).
Cigarette smoking impairs mitochondrial respiratory chain function in both central and peripheral glial cells, further contributing to the inflammatory and oxidative environment (25). Similarly, studies have shown that tetrahydrocannabinol (the main psychoactive compound in cannabis) can inhibit complexes I, II, and III of the mitochondrial electron transport chain, leading to excess generation of reactive oxygen species, such as hydrogen peroxide and superoxide (105). This contributes to mitochondrial stress and neuronal vulnerability, reinforcing a common pathway of oxidative and inflammatory injury across smoked substances.
Procoagulability. Smoking has been linked to increased circulating levels of von Willebrand factor, a glycoprotein essential for platelet adhesion and factor VIII transport (57). It also suppresses thrombomodulin, an anticoagulant that normally binds thrombin and inhibits the prothrombinase complex via factor V degradation. As a result, smoking is considered a procoagulant factor that increases the risk of ischemic stroke and cerebral venous thrombosis (48; 77).
Blood-brain barrier disruption. Nicotine alters blood-brain barrier integrity by downregulating tight junction proteins, particularly claudin-5, thereby increasing paracellular permeability between endothelial cells and allowing for the leaking of fluids. Exposure to tobacco and e-cigarette vapor reduces transendothelial electrical resistance, further compromising barrier function and increasing permeability.
Additionally, nicotine affects ion transporter expression, which can lead to vasogenic cerebral edema through altered extracellular potassium concentrations (01). Glucose transport is also impaired, with decreased expression of glucose transporters across the blood-brain barrier (87). In animal models, e-cigarettes reduce cerebral glucose utilization (90).
Different studies have aimed to distinguish the effects of cigarette smoke and e-cigarette vapor condensate on the brain. Both nicotine-free cigarette smoke and nicotine-free vapor condensate cause cellular damage to the blood-brain barrier and pulmonary lining, whereas unheated vapor liquid causes significantly less damage. This reinforces the concept that combustion is a central factor in the pathogenesis of smoking-related injury (70; 86).
Cytochrome P450 interactions. Nicotine is primarily metabolized to cotinine via the cytochrome P450 enzyme system. This metabolic pathway may influence the pharmacokinetics of other CNS drugs by competing for shared blood-brain barrier transporters, potentially altering drug efficacy and toxicity profiles (61).
The role of smoking in autoimmunity. It is not uncommon for autoimmune diseases to manifest neurologically. Therefore, one must consider how smoking can favor their development when studying the long-term effects of tobacco and combustion products.
Epidemiological studies have consistently demonstrated a strong association between smoking and the development of autoimmune diseases. Smoking is a well-established risk factor for rheumatoid arthritis, particularly in individuals who are positive for anti-cyclic citrullinated peptide (anti-CCP) antibody (21). Current smokers have a significantly higher risk of developing rheumatoid arthritis compared to never smokers, with a dose-response relationship observed between the number of pack-years and the risk of rheumatoid arthritis (51; 41; 20; 19; 92; 49).
In systemic lupus erythematosus, the relationship between smoking and disease risk is less clear. Although some studies suggest that smoking may increase the risk of systemic lupus erythematosus, others have reported a potential protective effect, possibly due to the immunosuppressive properties of nicotine (101; 96). However, the consensus is that smoking exacerbates disease severity and increases the risk of complications in diagnosed patients with systemic lupus erythematosus (31; 19).
Immunomodulatory effects of smoking. The exact mechanisms behind smoking’s association with the development and progression of autoimmune diseases are unclear. However, the pathophysiology is thought to be complex and multifactorial, as smoking has significant impacts on multiple aspects of the immune system, including activation of the innate and adaptive immune responses, production of pro-inflammatory cytokines, and generation of autoantibodies (75).
One of the key mechanisms by which smoking promotes autoimmunity is through the induction of citrullination, a post-translational modification of proteins that generates neoepitopes recognized by the immune system. In rheumatoid arthritis, smoking increases the expression of peptidyl arginine deiminase (PAD) enzymes, particularly PAD2, in the bronchial mucosa and alveolar compartments (60). This process leads to the generation of anti-CCP antibodies, which are highly specific to rheumatoid arthritis and play a central role in the pathogenesis of the disease.
Effects of smoking on the microbiome. Emerging evidence suggests that smoking may influence the composition and function of the microbiome, which plays a critical role in immune regulation and the development of autoimmune diseases (75). Smoking alters the gut and lung microbiota, leading to dysbiosis and the disruption of immune homeostasis. In rheumatoid arthritis, smoking has been associated with changes in the oral and gut microbiota, including an increase in the abundance of Prevotella species, which have been implicated in the pathogenesis of the disease.
Similarly, in systemic lupus erythematosus, smoking alters the gut microbiota, leading to an increase in the abundance of pro-inflammatory bacteria and a decrease in the abundance of anti-inflammatory bacteria. These changes in the microbiome can lead to the activation of autoreactive T cells and the production of autoantibodies, contributing to the development and progression of systemic lupus erythematosus (28).
Genetic and epigenetic modifications. Smoking induces genetic and epigenetic modifications that can contribute to the development of autoimmune diseases. Smoking has been associated with an increased risk of mutations in key immune regulatory genes, such as the human leukocyte antigen (HLA) genes, which play a critical role in the presentation of antigens to T cells. In rheumatoid arthritis, smoking interacts with specific HLA-DRB1 alleles, known as the shared epitope, to increase the risk of developing ACPA-positive rheumatoid arthritis (74; 53).
In addition to genetic modifications, smoking induces epigenetic changes, including DNA methylation and histone modifications, which can alter gene expression and contribute to the development of autoimmunity. For example, smoking induces hypermethylation of the FOXP3 gene, which encodes a key regulatory protein in T regulatory cells (Tregs). This epigenetic modification reduces Treg function and increases autoreactive T cell responses, contributing to the development of autoimmune diseases.
|
• Although exclusive cigarette smoking in U.S. adults declined from 2017 to 2023, exclusive e-cigarette smoking increased, maintaining overall tobacco product use unchanged. |
In addition to the epidemiological data previously presented in this article, findings from the National Health Interview Survey conducted by the Centers for Disease Control and Prevention (CDC) between 2017 and 2023 revealed a decrease in the prevalence of adults who exclusively smoke cigarettes, from 10.8% to 7.9%, representing an estimated 6.8 million individuals. In contrast, the prevalence of adults who exclusively use e-cigarettes increased from 1.2% to 4.1%, approximately 7.2 million people.
Within the 18- to 24-year-old age group, the prevalence of e-cigarette use increased sharply from 2.7% to 10.3% (at least 2.3 million individuals), and among those aged 25 to 44 years, it rose from 1.5% to 6.1% (around 4 million people).
As a result, the declining number of adults who smoke traditional cigarettes has been counterbalanced by the rising number of exclusive e-cigarette users. Overall, there has been virtually no change in the total prevalence of tobacco product use (08).
Regarding marijuana use, the National Survey for Drug Use and Health (NSDUH) reported that among individuals aged 12 and older, 77% of those who used marijuana smoked it, whereas 38.3% vaped it. Smoking remained the most common method of marijuana consumption across age groups, with the highest prevalence observed in the 18- to 25-year-old group (84.4%) (72). Based on combined 2023 and 2024 information obtained from the national self-reported annual Consumption Habits Survey, 15% of Americans report that they smoke marijuana, more than double the number of people who reported doing so in 2013 (7%) (29).
|
• The World Health Organization recommends focusing on the prevention of smoking initiation, particularly in adolescents. | |
|
• Behavioral interventions and pharmacologic therapies support long-term abstinence. |
It is estimated that approximately half of individuals who attempt to quit smoking relapse within the first year (98). The WHO Framework Convention on Tobacco Control recommends that governments prioritize prevention of smoking initiation, particularly among youth. Policy measures, such as imposing taxes on tobacco products, aim to disincentivize use while generating revenue for cessation strategies. In parallel, advertising by the tobacco industry, especially campaigns targeting younger populations, must be closely regulated.
Graphic warning labels have also been introduced on cigarette packaging, though their efficacy remains limited. A study conducted in India reported that only 20% of non-smokers were persuaded by graphic health warnings to avoid starting the habit and that such images had little to no effect on current smokers (68). Similarly, a study from Pittsburgh found that graphic imagery primarily discouraged individuals with lower levels of nicotine dependence and had little impact on those already dependent.
Although policy measures are essential for reducing overall smoking rates, support at the individual level is often necessary to achieve sustained abstinence. Behavioral interventions can be individualized or population-based and include counseling, educational programs, and mass or social media campaigns. Pharmacologic approaches may also be employed, including nicotine replacement therapies (eg, patches, lozenges, gum) and medications aimed at reducing cravings and withdrawal symptoms, such as bupropion, cytisine, and varenicline (103).
These strategies are particularly relevant in neurologically vulnerable populations, where smoking has been shown to increase disease risk, worsen clinical progression, and reduce treatment efficacy.
All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.
Alejandra Duque Ramirez MD
Dr. Ramirez of the University of Chicago has no relevant financial relationships to disclose.
See ProfileDaming Shao MD
Dr. Shao of Division of Rheumatology of University of Chicago Medical Center has no relevant financial relationships to disclose.
See Profile
Anthony T Reder MD
Dr. Reder of the University of Chicago received honorariums from Genentech, Genzyme, and TG Therapeutics for service on advisory boards and as a consultant and stock options from NKMax America for advisory work and an unrestricted lab research grant from BMS.
See ProfileNearly 3,000 illustrations, including video clips of neurologic disorders.
Every article is reviewed by our esteemed Editorial Board for accuracy and currency.
Full spectrum of neurology in 1,200 comprehensive articles.
Listen to MedLink on the go with Audio versions of each article.
MedLink, LLC
3525 Del Mar Heights Rd, Ste 304
San Diego, CA 92130-2122
Toll Free (U.S. + Canada): 800-452-2400
US Number: +1-619-640-4660
Support: service@medlink.com
Editor: editor@medlink.com
ISSN: 2831-9125
Peripheral Neuropathies
Jun. 11, 2026
Peripheral Neuropathies
Jun. 11, 2026
Neuropharmacology & Neurotherapeutics
Mar. 11, 2026
Peripheral Neuropathies
Mar. 02, 2026
Peripheral Neuropathies
Mar. 02, 2026
Headache & Pain
Jan. 24, 2026
Headache & Pain
Jan. 15, 2026
Peripheral Neuropathies
Dec. 26, 2025