In the 19th Century, Nicotine was the poison of choice by assassins as it was, then, undetectable.
7.2.1 Human data
The mean lethal dose has been estimated to be 30
to 60 mg (0.5-1.0 mg/kg) (Gosselin, 1988).
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)
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.
Smoking causes coronary and peripheral vascular disease,
cancer, chronic obstructive lung disease, peptic ulcer
and reproductive disturbances, including prematurity.
Nicotine may contribute to tobacco related disease, but
direct causation has not been determined because
nicotine is taken up simultaneously with a multitude of
other potentially harmful substances that occur in
tobacco smoke and smokeless tobacco
The overall effect on the cardiovascular system leads to
tachycardia, peripheral vasoconstriction and elevations
of blood pressure with an attendant increase in the work
of the heart. Nicotine may induce vasospasm and cardiac
arrythmias. Tolerance does not develop to the
catecholamine-releasing effects of nicotine.
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
Nicotine may act by releasing free fatty acids,
enhancing the conversion of VLDL (very low density
lipoproteins) to LDL (low density lipoproteins),
impairing the clearance of LDL and/or by accelerating
the metabolism of HDL (Brischetto, 1983; Gluette Brown,
1986; Grasso, 1986; Hojnacki, 1986.)
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.
--http://www.inchem.org/documents/pims/ch ... nTitle:2.1 Main risks and target organs
Why? Are you infering the Ajahn lied?Ajahn Mun smoked 4 cigarettes a day. The often heard response is: "Oh, well they didn't know about the health risks back then."
My response to this is that surely, such an excellent man as Ajahn Mun would have known the health effects of smoking cigarettes.
It might be a good read, but not one that it is based on evidence.Manapa's link is worth a good read.
You have a nice day too.