Acute nicotine toxicity in children is on the rise due to the increase in “vaping” with electronic cigarettes by adults. E-cigarettes utilize nicotine and flavoring dissolved in a solution of propylene glycol, polyethylene glycol, and/or vegetable glycerin. When a small quantity of this liquid is passed over an interior heating element, a dense vapor is produced that simulates the smoke of burning tobacco. Although some e-cigarettes are disposable when empty, most have an intact, self-contained cartridge (cartomizer) with a refillable reservoir, holding 0.3 to 1.6 mL of nicotine liquid. The nicotine concentration typically ranges from 0 to 36 mg/mL, but as high as 72 mg/mL. Liquid nicotine refill bottles typically range in size from 10 to 100 mL, and contain potentially fatal amounts of nicotine if ingested.
Other sources of nicotine include traditional tobacco products; smoking cessation aids in the form of gum, lozenges, transdermal patches, metered dose inhalers, nasal sprays, and spittoons of expectorated saliva from smokeless tobacco users. Blue cohosh, an herbal product used as an abortifacient, contains methylcysteine, a nicotine-like alkaloid.
Ganglionic stimulation then paralysis: Nicotine is systemically absorbed by all routes. Toxicity is dose-related and occurs in 2phases: initial acetylcholine receptor stimulation followed by receptor inhibition and failure. Initial stimulation of ganglion-type nicotinic acetylcholine receptors occurs in the CNS and parasympathetic and sympathetic autonomic ganglia, including epinephrine release from the adrenal gland. Muscle-type nicotinic receptors are not as readily affected. Peripheral symptoms can be various combinations of sympathetic and parasympathetic activations, such as salivation and vomiting plus tachycardia and hypotension or vagal – mediated bradycardia. Adrenergic influences dominate the cardiovascular system early in toxicity and also with lower doses. Secondary acetylcholine receptor fatigue and inhibition follows continued presence of high concentration of nicotine at the receptors, so that ganglia do not transmit signals from the brain to the vasculature and other innervated tissues. At very high nicotine doses, neuromuscular transmission may fail causing weakness and respiratory compromise. Death results from the paralysis of respiratory muscle and/or central respiratory failure.
Symptoms of Acute Nicotine Toxicity:
Gastrointestinal: Sharp burning in the mouth and throat on contact, gagging, nausea, vomiting, profuse salivation, cramping abdominal pain, occasionally diarrhea.
Central Nervous System: Headache, dizziness, lethargy, agitation, confusion, incoordination, delirium, seizures and coma.
Cardiovascular: Transient vasospasm-induced hypertension and tachycardia, followed in high doses by hypotension and bradycardia. Hypotension has a prominent orthostatic component if sympathetic ganglia fail. Transient cardiac standstill due to intense vagal stimulation; arrhythmias, and coronary ischemia.
Neuromuscular: Muscles fasciculation, poor reflexes, hypotonia, muscle weakness, and respiratory failure.
One cigarette contains 12 to 20 mg of nicotine/gram tobacco.
Approximately 10% of the available nicotine is delivered by smoking and about 1.5 to 4 mg remains in the cigarette butt after smoking. One cigar contains 15 to 40 mg nicotine/gram tobacco.
About 2-3mg nicotine/kg may cause significant signs and symptoms of toxicity; 2 to 3 cigarettes or 6 to 8 butts or 1 to 2 mL of 18 mg/mL nicotine liquid for electronic cigarettes are potentially toxic ingestions in children. Two to 5 mg of nicotine can rapidly cause nausea and vomiting, which unloads the stomach of much of the ingested tobacco and its nicotine content. However, vomiting may do little to reduce the rapidly absorbed dose from nicotine liquid.
In general, more than 1 mg/kg is expected to cause nausea, vomiting, and other mild symptoms in children and naïve adults; 7 to 10 mg/kg is potentially life threatening.
Management of nicotine exposure:
– Wash hands and any contaminated skin, if necessary.
– Avoid activated charcoal due to the expected rapid vomiting and potential for seizures if toxicity is severe.
– Observe for vomiting within 20 minutes as an early sign of a potentially significant ingestion, especially when the amount of tobacco or nicotine liquid involved is uncertain.
– Give symptomatic and supportive care with attention to blood pressure, oxygenation, and respiratory effort.
There is no specific antidote for nicotine. EKG is not routinely required. Fluids and vasopressors for hypotension; atropine for bradycardia and excessive secretions; benzodiazepines for seizures; ventilator support for patients with muscle weakness or respiratory failure.
The half-life of nicotine is an hour or less. Mild toxicity rapidly resolves in 1 to 4 hours, but severe toxicity may last 18 to 24 hours.
Nicotine levels are not clinically useful. Urinary cotinine, a metabolite, can confirm a suspected exposure.
Things to remember:
E-cigarette liquid contains very concentrated nicotine and is more readily bioavailable than the nicotine in tobacco. Nicotine is rapidly absorbed if ingested; the onset of symptoms can be within minutes. Dermal absorption is possible. There is no antidote; treatment of more severe symptoms is symptomatic and supportive.
Assistance with nicotine is just a phone call away!
For consultation with a specially trained Certified Specialist in Poison Information or our Medical Toxicologist; please contact the Missouri Poison Center at 1-800-222-1222. Healthcare providers can also call 1-888-268-4195.