Nicotine, combustion and harm: common mistakes

A patient with coronary disease refuses the nicotine patch because "nicotine causes heart attacks" and keeps smoking. A teenager thinks the product they use is harmless because "it's just nicotine". A colleague on call says nicotine is the substance in cigarettes that causes cancer. All three statements start from half-truths, and each leads to a worse decision than the correct information would lead to.

This text organizes the most common misconceptions about nicotine, combustion and harm, in both directions: overestimating and underestimating the role of nicotine. It stays at the level of toxicology and risk perception. It does not cover the choice of treatment, which is in the text on how to choose among the treatment options.

Key points

• Nicotine is the main driver of dependence; smoke from combustion is the main driver of disease.
• The evidence is inadequate to state that nicotine alone causes cancer, but smokeless tobacco is still associated with cancer.
• Nicotine has real cardiovascular effects, which matter more in people who already have heart disease.
• Nicotine replacement did not increase serious cardiovascular events in clinical trials.
• In pregnancy and adolescence, nicotine matters on its own, regardless of smoke.
• Quitting smoking is associated with improvement, not worsening, of anxiety and depression.
• Doctors also get nicotine wrong, and the form of the question changes the answer.

Summary

• Why misconceptions about nicotine matter in the consultation
• Dependence and harm: the role of nicotine and the role of combustion
• "Nicotine causes cancer": what the evidence says
• Nicotine and the heart: what is known and what is uncertain
• Nicotine replacement and the cardiovascular fear
• Pregnancy and adolescence: where nicotine matters on its own
• "Smoking calms you down": nicotine, stress and mental health
• What research shows about the beliefs of doctors and patients
• Frequently asked questions
• Final checklist

Why misconceptions about nicotine matter in the consultation

Beliefs about risk guide choices. Someone who believes nicotine causes most of the harm from cigarettes tends to see nicotine replacement as swapping one poison for another. Someone who believes nicotine is harmless tends to minimize dependence and the effect on the fetus or the developing brain. Both errors appear in patients and in professionals.

The problem is that each misconception has a true core. Nicotine has cardiovascular effects; nicotine is not the main carcinogen; nicotine causes dependence. A short sentence, said with conviction, takes on the force of a complete truth. It is an example of what the text on when heuristics help and when they get in the way discusses: the shortcut works up to the point where it stops working.

Emotion also plays a part. Fear of a heart attack, guilt about smoking during pregnancy or irritation with a patient who "doesn't want to stop" change what is heard and what is said, as the text on why emotion gets in the way of reasoning shows. Separating what is known from what is feared is part of clinical work.

Finally, smoking often disappears from the consultation precisely because the professional does not quite know what to say. The mechanisms that make this happen are described in the text on the biases that make smoking disappear from the consultation. Being clear about the role of nicotine helps to talk about the subject with confidence.

Dependence and harm: the role of nicotine and the role of combustion

The central distinction is simple. Nicotine is what keeps a person smoking; the smoke produced by burning tobacco is what makes them ill. A review on the cardiovascular toxicity of nicotine notes that cigarette smoke contains more than 9000 chemical substances and more than 69 known carcinogens, the vast majority produced by tobacco combustion (Benowitz and Burbank, 2016). Among the components of most concern for the heart are oxidants, carbon monoxide, volatile organic compounds, particles and heavy metals (Benowitz and Burbank, 2016). The first author declares consultancy for pharmaceutical companies that sell cessation medications and work as a paid expert in litigation against tobacco companies.

The 2014 report on 50 years of evidence about smoking concluded that the evidence is sufficient to infer that nicotine activates multiple biological pathways through which smoking increases disease risk (US Department of Health and Human Services, 2014). In other words, nicotine is not inert: it takes part in disease mechanisms, even without being the main cause of the harm.

From this come the two opposite misconceptions. Saying that "nicotine is what kills in cigarettes" ignores combustion. Saying that "nicotine is harmless" ignores dependence and the biological effects. The umbrella review on e-cigarettes, which gathered 400 publications, found conclusive evidence of poisoning and immediate toxicity by inhalation, including seizures, linked to these products (Banks and colleagues, 2023). It also found substantial evidence that nicotine products can cause dependence in people who never smoked (Banks and colleagues, 2023). Smokeless nicotine is not a synonym for a harmless product. The table summarizes where each statement is right and where it is wrong.

Common statement	What the evidence shows	What remains uncertain	How to explain it to the patient
"Nicotine causes cancer"	Inadequate evidence for causality; most carcinogens come from combustion	Long-term effects of nicotine alone	"What causes the most cancer in cigarettes is the smoke, not the nicotine"
"Nicotine is harmless"	It causes dependence and activates biological pathways of disease	Size of the risk in prolonged smokeless use	"It is not the most dangerous part, but it is not neutral"
"Nicotine replacement is bad for the heart"	No increase in serious cardiovascular events in trials	Very prolonged use in people with heart disease	"Cigarettes harm the heart far more than the treatment"
"Smoking calms you down"	Quitting is associated with less anxiety and depression	Residual confounding in observational studies	"The relief comes from the withdrawal that the cigarette itself creates"
"In pregnancy, less smoking is enough"	Nicotine by itself affects pregnancy and the fetal brain	How much of the harm is due only to nicotine	"The ideal is to stay without nicotine and without smoke; let us see how"

"Nicotine causes cancer": what the evidence says

This is the most widespread misconception among professionals. The 2014 report concluded that the evidence is inadequate to infer the presence or absence of a causal relationship between nicotine exposure and cancer risk (US Department of Health and Human Services, 2014). This is not the same as saying that nicotine is proven safe; it means the data allow neither affirming nor denying causality.

The point that is often lost is that smokeless tobacco is not the same as pure nicotine. A systematic review of 80 observational studies found a higher risk of cancer mortality among smokeless tobacco users, with a relative risk of 1.38 (confidence interval 1.22 to 1.56) (Htay and colleagues, 2025). For cancer incidence, the relative risk was 1.17 (interval 1.08 to 1.27), with associations for head and neck, mouth, esophagus, stomach and pancreas cancer (Htay and colleagues, 2025). The authors report important heterogeneity between studies. Smokeless tobacco contains substances other than nicotine, and the result does not allow attributing cancer to nicotine alone.

In the conversation, the useful sentence is twofold: nicotine is not the main cause of cancer in cigarettes, and smokeless tobacco products still carry cancer risk. Separating the two ideas avoids both panic about nicotine replacement and the illusion that any smokeless product is safe. To read observational studies like these without drawing conclusions beyond the design, it helps to review study designs and their weaknesses.

Nicotine and the heart: what is known and what is uncertain

Nicotine is a sympathetic stimulant: it increases heart rate, blood pressure and contractility, and can constrict vessels. The review on cardiovascular toxicity concludes that pharmacology in animals and some studies in people support the biological plausibility that nicotine contributes to acute cardiovascular events in smokers with cardiovascular disease, in addition to effects that may accelerate atherosclerosis (Benowitz and Burbank, 2016).

The size of that risk, however, is much smaller than that of smoke. Studies with nicotine-based medicines and with smokeless tobacco indicate that the risks of nicotine without the combustion products are low compared with smoking, but they remain a cause for concern in people with cardiovascular disease (Benowitz and Burbank, 2016). The same review notes that prolonged use of smokeless tobacco does not appear to accelerate atherosclerosis, but it may contribute to acute events when cardiovascular disease is already present (Benowitz and Burbank, 2016).

What remains uncertain is the effect of very prolonged use of smokeless nicotine in people who already have heart disease, and the effect of new products used for years. The 2014 report is cautious: it acknowledges that nicotine takes part in disease pathways, without quantifying the cardiovascular risk of nicotine alone (US Department of Health and Human Services, 2014). For the patient, the honest summary is that nicotine is not neutral for the heart, but smoke is much worse.

Nicotine replacement and the cardiovascular fear

The mistaken belief that nicotine replacement is dangerous for the heart keeps away from treatment exactly those who would benefit most from quitting. A network meta-analysis of clinical trials gathered 63 trials, 21 of them on nicotine replacement, to assess cardiovascular events with cessation medicines (Mills and colleagues, 2014). There was an increase in the combined set of cardiovascular events with replacement, with a relative risk of 2.29 (interval 1.39 to 3.82), driven mainly by less serious events (Mills and colleagues, 2014). For major cardiovascular events, such as cardiovascular death, heart attack and nonfatal stroke, the relative risk was 1.95, with a wide interval, from 0.26 to 4.30, with no clear evidence of harm (Mills and colleagues, 2014).

The authors mention that less serious events, such as tachycardia and nonspecific chest pain, had already appeared in an earlier analysis, and that few trials were done in people with established cardiovascular disease (Mills and colleagues, 2014). The study's conclusion was that cessation treatments do not appear to increase the risk of serious cardiovascular events (Mills and colleagues, 2014). Two authors declare consulting on methods for pharmaceutical companies, among them a manufacturer of a cessation medicine, and one author received research funding from that manufacturer; the article states that there was no funding from these companies for the work.

The review of cardiovascular toxicity reaches a similar conclusion by another route: short-term use of nicotine, as in treatment to stop smoking, appears to carry little cardiovascular risk, even in patients with known cardiovascular disease (Benowitz and Burbank, 2016). The comparison that matters is with continuing to smoke, not with using nothing. Thinking in all-or-nothing terms here is the same trap described in the text about all-or-nothing thinking as a bias.

Pregnancy and adolescence: where nicotine weighs on its own

Here the mistake is the opposite one: underestimating nicotine. The 2014 report concluded that the evidence is sufficient to infer that exposure to nicotine during fetal development, a critical window for brain development, has lasting adverse consequences for that development (US Department of Health and Human Services, 2014). The same report concluded that the evidence is sufficient to infer that nicotine adversely affects maternal and fetal health during pregnancy, contributing to outcomes such as premature birth and stillbirth (US Department of Health and Human Services, 2014).

A review of nicotine and human development brings together human and animal data that support multiple adverse consequences of nicotine exposure during periods of developmental vulnerability, from the fetus to the adolescent, including harm to fetal brain and lung development (England and colleagues, 2015). The authors explain that nicotine crosses the placenta and binds to receptors widely expressed in the fetal nervous system, which regulate brain maturation (England and colleagues, 2015). They also point out that the fraction of the damage attributable to nicotine alone, separate from the rest of the smoke, has not yet been precisely quantified (England and colleagues, 2015).

In adolescence, the strength of the evidence is lower. The 2014 report classified as suggestive, not sufficient, the evidence that nicotine exposure in adolescence, another critical window for brain development, may have lasting adverse consequences (US Department of Health and Human Services, 2014). The umbrella review on e-cigarettes found substantial evidence that nicotine products can cause dependence in non-smokers, and considered the evidence on developmental and mental health effects insufficient or unavailable (Banks and colleagues, 2023).

In practice, this means two things. During pregnancy, the goal is to stay free of nicotine and smoke, and the decision about treatment compares real risks, which belongs to the approach discussed in another text. In adolescence, the strongest argument is dependence, which is well established, not numbers on brain damage, which the evidence does not yet support with precision.

"Smoking calms you down": nicotine, stress and mental health

Many people who smoke say that cigarettes calm them, and many professionals hesitate to propose cessation to those with anxiety or depression. The feeling of relief is real, but much of it corresponds to relief from the withdrawal that cigarettes themselves create between one cigarette and the next. Studies that followed people before and after quitting suggest the opposite of the misconception.

A systematic review with meta-analysis of 26 longitudinal studies compared the mental health of those who quit smoking with that of those who continued (Taylor and colleagues, 2014). Anxiety, depression and stress decreased more in those who quit, with standardized mean differences of minus 0.37 for anxiety, minus 0.25 for depression and minus 0.27 for stress (Taylor and colleagues, 2014). The effect appeared as large in people with psychiatric disorders as in the others (Taylor and colleagues, 2014). Some authors declare fees from manufacturers of cessation products, outside this work.

The later Cochrane review expanded the analysis to 102 studies with more than 169500 participants (Taylor and colleagues, 2021). Quitting smoking was associated with improvement in anxiety symptoms, with a difference of minus 0.28 in 15 studies and 3141 participants, and in depression, with a difference of minus 0.30 in 34 studies and 7156 participants (Taylor and colleagues, 2021). Certainty was low for anxiety and very low for depression, due to possible confounding over time, and the authors concluded that mental health does not worsen when quitting smoking (Taylor and colleagues, 2021).

In the consultation, hesitation to talk about cigarettes with someone in psychological distress usually comes more from fear of making the situation worse than from the data. A stance attentive to what the person feels, as discussed in the text on why empathy enters the reasoning, allows one to acknowledge the relief they report and, at the same time, explain where it comes from.

What research shows about the beliefs of doctors and patients

Misconceptions are not only among patients. In an experiment with 926 physicians from various specialties, two wordings of the same question were randomly assigned, "nicotine" or "nicotine alone" (Bover Manderski and colleagues, 2021). With the first wording, more than eight in ten strongly agreed that nicotine contributes directly to cancer; with the second, about seven in ten (Bover Manderski and colleagues, 2021). The wording changed the answer, but the misconception remained common even with the more precise question (Bover Manderski and colleagues, 2021).

In another survey, at a large hospital group, 279 of 2035 invited physicians and pharmacists responded (Christen and colleagues, 2025). There, 204 of the 279 disagreed that nicotine alone causes cancer, and 44 agreed (Christen and colleagues, 2025). The authors interpreted that the respondents had a relatively correct understanding of most of the direct effects of nicotine, with greater uncertainty about the new products (Christen and colleagues, 2025). The low response rate limits generalization.

Among adults who smoke, overestimation is also frequent. In a population sample of 5507 adults who used cigarettes or cigarillos, about six in ten of those who used cigarillos considered nicotine very or extremely harmful, with no significant difference compared with those who only used cigarettes (Fidalgo and colleagues, 2026). The authors are employees of a tobacco product regulatory agency, which should be considered when reading the results.

These data show that the professional's belief matters as much as the patient's. A physician who thinks nicotine causes cancer conveys that, even unintentionally. Misestimating a risk is a calibration error similar to what the text on why we misjudge the estimate describes for tests. Residency and licensing exams also test this distinction, often hidden in the vignette, as the text on how vignettes hide the clue about substances shows.

The way of speaking also matters. Labels and stock phrases carry judgments that enter the reasoning, as the text on from label to bias discusses. Open questions and phrases that do not close the conversation, described in the text on communication in harm reduction, help to find out what the person believes before correcting it.

Frequently asked questions

Does nicotine cause cancer?

The evidence is inadequate to affirm or deny a causal relationship (US Department of Health and Human Services, 2014). Most of the carcinogens in cigarettes come from combustion. Even so, smokeless tobacco is associated with cancer, because it contains other substances.

Is nicotine bad for the heart?

It has real cardiovascular effects and can contribute to acute events in people who already have heart disease, but the risk is low compared with smoking (Benowitz and Burbank, 2016).

Is nicotine replacement dangerous for people with heart disease?

In the clinical trials gathered in a network meta-analysis, replacement did not clearly increase serious cardiovascular events, although it did increase less serious events (Mills and colleagues, 2014). The relevant comparison is with continuing to smoke.

Does smoking help control anxiety?

Studies suggest the opposite: quitting smoking is associated with less anxiety and depression, including in people with psychiatric disorders (Taylor and colleagues, 2021).

Why is nicotine a concern in pregnancy and adolescence?

Because the developing brain is sensitive to nicotine. The evidence is sufficient for adverse effects in pregnancy and on the fetal brain, and suggestive for adolescence (US Department of Health and Human Services, 2014).

Does this text guide treatment?

No. It deals with toxicology and risk perception and does not replace individual clinical assessment. The choice of treatment is discussed in the text on smoking cessation at each visit.

Final checklist

• Separate dependence, caused mainly by nicotine, from harm, caused mainly by combustion.
• Do not say that nicotine causes cancer; say that the evidence is inadequate and that smoke is the main source of carcinogens.
• Do not say that a smokeless product is safe; smokeless tobacco is still associated with cancer.
• Recognize the cardiovascular effects of nicotine without confusing them with the risk of smoke.
• Compare nicotine replacement with continuing to smoke, not with using nothing.
• In pregnancy and adolescence, treat nicotine as a risk factor in itself.
• Explain that the relief from smoking is largely relief from withdrawal.
• Ask what the person believes about nicotine before correcting it.

References

1. Banks E, Yazidjoglou A, Brown S, et al. Electronic cigarettes and health outcomes: umbrella and systematic review of the global evidence. Med J Aust. 2023. PMID 36939271. DOI 10.5694/mja2.51890.
2. Benowitz NL, Burbank AD. Cardiovascular toxicity of nicotine: implications for electronic cigarette use. Trends Cardiovasc Med. 2016. PMID 27079891. DOI 10.1016/j.tcm.2016.03.001.
3. Bover Manderski MT, Steinberg MB, Wackowski OA, et al. Persistent misperceptions about nicotine among US physicians: results from a randomized survey experiment. Int J Environ Res Public Health. 2021. PMID 34300168. DOI 10.3390/ijerph18147713.
4. Christen SE, Scanniello E, Hammann F, et al. Knowledge and perceptions of nicotine, smoking cessation and electronic nicotine delivery systems among physicians and pharmacists in a Swiss hospital group. Tob Induc Dis. 2025. PMID 40709317. DOI 10.18332/tid/204839.
5. England LJ, Bunnell RE, Pechacek TF, Tong VT, McAfee TA. Nicotine and the developing human: a neglected element in the electronic cigarette debate. Am J Prev Med. 2015. PMID 25794473. DOI 10.1016/j.amepre.2015.01.015.
6. Fidalgo A, Halenar MJ, Merson B, Rajan-Sharma AO. Perceptions of nicotine harm among adults who use little cigars and cigarillos: a cross-sectional analysis of wave 7 of the PATH Study 2022-2023. Tob Induc Dis. 2026. PMID 41551946. DOI 10.18332/tid/214722.
7. Htay ZW, Bhandari AKC, Parvin R, Abe SK. Effects of smokeless tobacco on cancer incidence and mortality: a global systematic review and meta-analysis. Cancer Causes Control. 2025. PMID 39718727. DOI 10.1007/s10552-024-01933-w.
8. Mills EJ, Thorlund K, Eapen S, Wu P, Prochaska JJ. Cardiovascular events associated with smoking cessation pharmacotherapies: a network meta-analysis. Circulation. 2014. PMID 24323793. DOI 10.1161/CIRCULATIONAHA.113.003961.
9. Taylor G, McNeill A, Girling A, et al. Change in mental health after smoking cessation: systematic review and meta-analysis. BMJ. 2014. PMID 24524926. DOI 10.1136/bmj.g1151.
10. Taylor GM, Lindson N, Farley A, et al. Smoking cessation for improving mental health. Cochrane Database Syst Rev. 2021. PMID 33687070. DOI 10.1002/14651858.CD013522.pub2.
11. US Department of Health and Human Services. The Health Consequences of Smoking: 50 Years of Progress. A Report of the Surgeon General. 2014. PMID 24455788.