What’s the tobacco industry to do, since cigarette and smokeless tobacco use are declining? Surge alternative delivery systems for nicotine, that’s what! Appeal to a demographic that is easily manipulated by social media, that’s what! Following the successful footsteps of electronic cigarettes, nicotine pouches have emerged as the next significant public health concern for teens and young adults. Data indicate a sharp increase in use among them, with some reports showing prevalence nearly quadrupling between 2022 and 2025.
Poison centers across the country have detected this uptick in real-time. Exposure calls about nicotine pouches to the nation’s poison centers rose over seven-fold from 2020 to 2023 and are still climbing. Critically, most of these exposures involve children under age six, who are drawn to brightly colored packaging, appealing flavors, and candy-sized pieces.
PRODUCTS
Nicotine pouches are small cellulose-microfiber packets, about the size of a short stick of gum, which are held in the mouth in the vestibule between the lip and the gums. There is no tobacco leaf involved – the nicotine is powdered and combined with food-grade fillers, sweeteners, alkalinity boosters, and various flavorings, such as mint, citrus, or berry, or vaguely-described flavors such as “chill.” The packet is wet by saliva, which solubilizes and releases the contents for buccal absorption. The nicotine is either purified from tobacco or is a synthesized nicotine salt. Popular brands like on!, ZYN, and VELO offer a range of strengths, usually between 2 mg and 8 mg per pouch, though high-potency versions offering 15 to nearly 50 mg are available online. Products from ex-US sources have been reported to contain up to 130 mg each of nicotine. The typical cost is $5-6 for a container of 20 pouches.
Because they are tobacco-free, “spitless,” and discreet, they are often perceived as a “cleaner” alternative to traditional smokeless tobacco. Especially when compared to conventional cigarettes with their myriad toxic chemicals, nicotine pouches do offer a significant “harm reduction” opportunity for current smokers. However, the pouches still contain a highly addictive drug with potential for acute toxicity as well as long-term cardiovascular effects.
DO POUCHES DELIVER THE NICOTINE KICK?
The prevailing theory is that the effect a nicotine user experiences depends on the peak blood level and how rapidly the peak is reached. The gold standard is smoking tobacco. A puff from a cigarette offers a tiny nicotine load to the brain faster than IV administration. The blood level successively rises as each mini dose is launched from the pulmonary bed. The peak occurs at the last puff when the 1 mg or so total of nicotine has been absorbed from the cigarette. The level begins to decrease immediately.
Like chewing tobacco and oral snuff, the nicotine in pouches takes longer to solubilize and be absorbed across the oral mucosa, so the satisfying jolt of the rapid rise provided by smoking is blunted. Absorption continues as long as the pouch is retained until it is spent, generally in an hour or less. The final nicotine blood level attained depends on the nicotine content of the pouch and the other ingredients. Blood levels of the moderate-strength pouches can easily match or exceed the nicotine levels from cigarettes.
The packet can be opened and the contents accessed directly, but the absorption characteristics have not been formally characterized.
PHARMACOLOGY AND MECHANISM OF TOXICITY
Nicotine pharmacology is well-characterized, but its effects are complex and can be unpredictable. Opposing autonomic systems are affected at the same time, and there are a number of indirectly activated functions, such as central dopamine release, which promotes dependence. Nicotine also activates a number of sensory receptors, causing, for example, the immediate burning taste of nicotine and tobacco when introduced into the mouth, accompanied by salivation, nausea, and vomiting due to stimulation of vagal afferents into the emetic center of the brain. Finally, and importantly, the individual’s state of tolerance or naïveté to nicotine can alter the effects.
Nicotine’s core action is agonism of nicotinic cholinergic receptors in the autonomic ganglia, the CNS, and the skeletal muscles. Effects are dose-dependent and classically occur in two phases:
- Initial Stimulatory Phase: Activation of ganglionic nicotinic receptors increases activity of both the sympathetic and parasympathetic systems, resulting in mixed autonomic effects such as salivation, vomiting, tachycardia, and hypertension.
Early cardiovascular effects are primarily adrenergic because the sympathetic system has a stronger influence on the CV system than the parasympathetic. Furthermore, epinephrine is released from the adrenal gland, adding additional receptor activation in the sympathetic system. However, in later stages, after withdrawal of sympathetic influence, vagally mediated bradycardia can occur.CNS stimulation is characterized by tremors, confusion, and headache, and in extreme cases, seizures and coma.Fasciculations and twitching due to skeletal muscle stimulation often go unnoticed due to rapidly developing receptor desensitization and motor inactivation. - Secondary Inhibitory Phase: Sustained activation of nicotinic receptors from high nicotine concentrations leads to receptor desensitization and paralysis, ganglionic blockade, neuromuscular failure, and profound CNS dysfunction. The result is potentially fatal respiratory depression due to combined central nervous system depression and respiratory muscle paralysis, seizures, and coma.
RANGE OF TOXICITY OF INGESTED NICOTINE
- 1–2 mg/kg: Nausea, vomiting, and mild symptoms in children or nicotine-naïve adults.
- >2–3 mg/kg: Significant toxicity.
- >7–10 mg/kg: Potentially life-threatening.
CLINICAL PRESENTATION
| SYSTEM | MINOR TO MODERATE | MAJOR / SEVERE |
| Gastrointestinal | Local burning in mouth/throat, salivation, nausea, vomiting. | Profuse, prolonged vomiting and hypersalivation. |
| Neurological | Dizziness, headache, irritability. | Seizures, agitation, confusion, lethargy, or coma. |
| Cardiovascular | Initial tachycardia and hypertension. | Subsequent bradycardia and hypotension; risk of arrhythmias. |
| Respiratory | Tachypnea/dyspnea, excessive secretions. | Respiratory depression, apnea, or failure. |
| Neuromuscular | Fasciculations or tremors. | Hypotonia and paralysis. |
| Other | Diaphoresis. |
CLINICAL EXPERIENCE
To date, there is only one published case report of a non-smoking young adult who overconsumed 15 nicotine pouches (10.9 mg each) over 12 hours to help study. He became nauseated, agitated, confused, talking nonsense, and eventually slid off his chair to the floor. The patient presented to the ED with BP 184/99, HR 99, tremors, mydriasis, and sweating. He was treated with IV hydration and small doses of benzodiazepine and recovered fully in 24 hours.
Although there are no detailed published case reports in children, data from the National Poison Data System that captures exposure cases from U.S. poison centers suggest that oral nicotine pouches are twice as likely as other nicotine products to be admitted to the hospital, and 1.5 times more likely to result in a serious medical outcome.
MANAGEMENT OF NICOTINE POUCH EXPOSURE
Treatment is symptomatic and supportive; there is no specific antidote for nicotine toxicity. Focus on airway management, oxygenation, and hemodynamic stability. Avoid antacids for two hours post-ingestion, as higher gastric pH can enhance nicotine absorption. Swallowed pouches are not an obstruction risk.
Nicotine levels lack clinical utility due to rapid metabolism; however, urine cotinine can confirm a suspected exposure. In severe cases, monitor CPK, electrolytes, and renal function to assess for rhabdomyolysis. Obtain an ECG if cardiovascular instability is present.
Benzodiazepines are the first-line treatment for seizures. Use levetiracetam or phenobarbital as second-line treatment; escalate to general anesthesia if necessary. Administer atropine to manage excessive parasympathetic activity (e.g., severe bradycardia or bronchorrhea) and treat hypotension with IV fluid boluses and vasopressors as indicated.
The Missouri Poison Center is available around the clock to assist in the expert management of exposures to nicotine. Our specially trained nurses, pharmacists, and physician toxicologist can provide consultation regarding exposures and treatment. For patient-specific guidance, please contact the poison center’s dedicated line for healthcare professionals at 1-888-268-4195.