On page 19 (Number 5) of ECITA's new report at
http://www.ecita.org.uk/ecita quarterly update.pdf
it states "For a child, nicotine is toxic at a level of 10mg in total." and
"For an adult non-smoker/non-nicotine addict, nicotine is toxic at a level of 30-60mg (0.5-1mg/kg)."
But the cited reference for those purported toxicity levels was published more than 20 years ago at
Nicotine (PIM)
which states:
7.2.1.1 Adults
The mean lethal dose
has been estimated to be 30
to 60 mg (0.5-1.0 mg/kg) (Gosselin, 1988).
7.2.1.2 Children
The lethal dose
is considered to be about 10 mg
of nicotine (Arena, 1974).
7.2.2 Relevant animal data
Dog: oral LD50: 9.2 mg/kg
mouse: oral LD50: 3.3 mg/kg (RTECS, 1985-86)
rat: oral LD50: 50 mg/kg
I'm not aware of any actual scientific or even empirical evidence on nicotine toxicity levels (via ingestion or inhalation) for either adults or children because that type of research is unethical, inhumane and criminal. Besides, smoking a half dozen cigarettes over two hours exposes a smoker to more than 100 mg of nicotine, but that's never killed any smoker.
I'm also not aware of any reported case (worldwide) of any person dying from ingesting nicotine (nor via transdermal absorption), although I suspect there may be a case or two (e.g. someone accidentally ingesting nicotine pesticide, or perhaps a suicide using nicotine pesticide). Even the INCHEM document at
Nicotine (PIM)
didn't cite any cases of nicotine toxicity in humans (i.e. death), and instead stipulated that toxicity level "
has been estimated to be about" and "
is considered to be", and cite as references
Gosselin RE (1988). Clinical toxicology of Commercial Products.
VI.ed Baltimore, Williams & Wilkins: 311-313.
and (Arena, 1974). Poisoning IV Ed. New York Charles Thomas Ed.
If anyone has (or can locate) either of those two references (both of which appear to be books, not studies), please post that info (as I suspect that INCHEM has misrepresented those estimates, and I suspect that Gosselin and Arena simply made guesses based solely on animal toxicity studies).
Also notice the huge discrepency (in INCHEM's document) between the toxic levels of nicotine ingestion for animals compared to what the authors claim has been estimated for adults and for children.
In sum, I think a toxic nicotine dose for children (via ingestion) is significantly higher than 10mg, and that a toxic dose for adults is significanty higher than 60mg.
Please note that that same INCHEM document also makes the following claims that greatly exaggerate the risks of nicotine, and that demonize all nicotine use.
2.1 Main risks and target organs
Nicotine is one of the most toxic of all poisons and has a
rapid onset of action. Apart from local caustic actions, the
target organs are the peripheral and central nervous systems.
Nicotine is also a powerfully addictive drug.
2.2 Summary of clinical effects
Burning sensation in the mouth and throat, salivation,
nausea, abdominal pain, vomiting and diarrhoea.
Gastrointestinal reactions are less severe but can occur even
after cutaneous and respiratory exposure.
4.2 High risk circumstance of poisoning
Nicotine is most frequently encountered in
tobacco products
for smoking, chewing, sniffing and
tobacco "without smoking".
As an insecticide (now rare), and as an adjunct to smoking
cessation programmes (gums, patches). It is a substance of
abuse.
5.1 Oral
Poisoning occurs in children who ingest cigarettes or
cigars or 2nicotine gum.
9.2 Chronic poisoning
9.2.1 Ingestion
Chronic poisoning by nicotine is possible by chewing
tobacco or nicotine gums.
Chronic effects
Nicotine could contribute both to the atherosclerotic
process and to acute coronary events by several
mechanisms. Nicotine could promote atherosclerotic
disease by its actions on lipid metabolism and
coagulation by hemodynamic effects and/or by causing
endothelial injury.
Nicotine could affect platelets by increasing the
release of epinephrine, which is known to enhance
platelet reactivity by inhibiting prostacyclin, an
antiaggregatory hormone secreted by endothelial cells,
or perhaps directly (Sonnenfeld, 1980). Alternatively,
by increasing heart rate and cardiac output and thereby
increasing blood turbulence or by a direct action,
nicotine may promote endothelial injury. Cigarette
smoking, most likely mediated by nicotine, facilitates
AV nodal conduction which could result in an increased
ventricular response during atrial fibrillation (Peters,
1987). Nicotine could aggravate peripheral vascular
disease by constricting small collateral arteries and/or
by inducing local thrombosis. Patients with coronary or
peripheral vascular disease are likely to suffer some
increase in risk when taken nicotine. Nicotine could
contribute to the progression of chronic hypertension by
aggravating vasoconstriction either in sympathetic activation
or inhibition of prostaglandin synthesis.
Based on its pharmacological actions, it is likely that
nicotine plays a role in causing or aggravating acute
coronary events. Myocardial infarction can be due to one
or more of these precipitating factors: excessive demand
for oxygen and substrates; thrombosis; and coronary
spasm. Nicotine increases heart rate and blood pressure and,
therefore, myocardial oxygen consumption.
In addition to creating an imbalance between myocardial
oxygen supply and demand, nicotine may promote
thrombosis. Nicotine may also induce coronary spasm by
sympathetic activation or inhibition of prostacyclin.
Coronary spasm has been observed during cigarette
smoking (Maouad, 1984).
Sudden cardiac death in smokers might result from
ischaemia, combined with the arrhythmogenic effects of
increased amounts of circulating catecholamines released
by nicotine.
9.4.2 Respiratory
Acute effects
Initial tachypnoea, but later dyspnoea, decreased
respiratory rate, and cyanosis may be seen. Respiratory
arrest may occur within minutes, and resultant death
within 1 hour.
Chronic effects
Nicotine may directly or indirectly influence the
development of emphysema in smokers, but further
research is needed to define the magnitude of the
contribution of nicotine to the pathogenesis of smoking
including chronic lung disease. Nicotine can also worsen
pulmonary function in smokers who already have lung
disease. Acute exposure to nicotine induces constriction
of both central and peripheral airways (Yamatake, 1978).
The increase in airways resistance by nicotine involves
vagal reflexes and stimulation or parasympathetic
ganglia in the bronchial wall (Nakamme, 1986). The
magnitude of bronchoconstriction
observed in experimental animals and humans following
acute inhalation of cigarette smoke is correlated with
the level of nicotine in the smoke (Beck, 1986)
suggesting that nicotine may be an important factor in
the increased airways resistance of smokers.
9.4.15 Special risks
Pregnancy
Nicotine in any form may be harmful to the fetus.
Exposure to nicotine during the last trimester has been
associated with a decrease in breathing movements.
These effects may be the result of decreased placental
perfusion caused by nicotine. One miscarriage during
nicotine therapy has been reported. Studies of pregnant
rhesus monkeys have shown that maternal nicotine
administration produced acidosis, hypoxia and hypercarbia
in the fetus. Nicotine has been shown to be teratogenic in
mice treated cutaneously with 25 mg/kg, which is
approximately 300 times the human oral dose. Studies in
rats and monkeys have not demonstrated a teratogenic effect
of nicotine in newborn which occur during cigarette smoking.
Cigarette smoking is associated with impaired fetal growth
and development.
11.1 Case reports from literature
Malizia (1983) described four children who ingested two
cigarettes each and developed salivation, vomiting,
diarrhoea, tachypnoea, tachycardia, and hypotension within 30
minutes and depressed respiration and cardiac arrhythmias within
40 minutes. Convulsions occurred within 60 minutes of
ingestion. All recovered after gastric lavage, activated
charcoal, intermittent positive pressure ventilation, and 5
mg diazepam intravenously for convulsions.
A 23 year old woman who had smoked two packs per day for
several years chewed a single piece of nicotine gum (2 mg
nicotine) after which she developed nausea, tremor, flushing,
palpitations, paresthesias, pruritus, vomiting, diarrhoea,
confusion and abdominal pain. She recovered after treatment
and with prochlorperazine, morphine and atropine (Mensch,
1984).
