SMOKING IS VALEOLOGICALLY DANGEROUS TO HEALTH (9): Cont.: INGREDIENTS IN TOBACCO

[Abbas Bubakar El-ta'alu]

Nicotine: Nicotine (1-methyl-2-[pyridyl] pyrrolidine) is one of the several alkaloids that can be extracted from tobacco leaves. When it was isolated in 1828 by Posselt and Reimann [Feldman, R. S., et al. (1997)], nicotine was found to constitute about 5 per cent of the total weight of the dry plant leaves. However, this relatively minor fraction imbues tobacco with many Physiological and Psychological effects when the leaves are smoked, chewed, or snorted (as snuff) and the nicotine is absorbed into the human bloodstream. Manufacturers have been intensifying the concentration of nicotine in their tobacco and modifying cigarette designs to increase the number of puffs per cigarette. According to a research [NewScientist News. (January, 2007)], the amount of nicotine that smokers typically inhale was increased by 11 per cent between 1998 and 2005, perpetuating a "tobacco pandemic" that makes it harder for smokers to quit. Without nicotine, it is quite likely that tobacco would be regarded as a useless weed.
     Pure nicotine is a colourless liquid that turns brown and smells like tobacco when exposed into the air. It is the major psychoactive ingredient in tobacco. When tobacco smoke is inhaled, nicotine readily passes through the absorbent surface of the lungs whose total area has been estimated to be about equal to the surface of a tennis court. It is absorbed, to a lesser degree, through the membranes of the mouth and nostrils when tobacco is smoked, chewed, or snorted. Once tobacco smoke is inhaled, 25per cent of the nicotine reaches the brain in about 7 seconds
[Feldman, R. S., et al. (1997)], about twice as fast as when the drug is administered intravenously. Thus, for nicotine, tobacco smoke inhalation via the modern cigarette is the fastest and the most efficient method of drug delivery to the brain.
   The current consensus among neuropharmacologists is that nicotine is the psychoactive drug primarily responsible for the addictive nature of tobacco use. It is a stimulant and a sedative drug. Nicotine is highly selective for the so-called "nicotinic receptors" for acetylcholine in the peripheral and central nervous systems, and activation of these receptors is the likely source of the psychoactive effects of the drug. The nicotinic-acetylcholine receptor is a molecularly well-characterized receptor and its activation evidently leads to confirmation changes in its 5 subunits that result in a transient increase in permeability of the neuron membrane to the sodium ion [J. Am. Med. Assoc. (1998)]. The nicotinic-acetylcholine receptor is therefore characterized as a neurotransmitter-gated ion channel. Concentrations of nicotine in blood rise quickly during cigarette smoking and peak at its completion. Nicotine is also deposited in the lungs, spleen, liver, and the brain, where concentrations are typically twice those of measurable blood concentrations.
          Nicotine readily crosses the blood-brain barrier, leading to the release of acetylcholine, norepinephrine, dopamine, serotonin, vasopressin, neurophysin1, cortisol, prolactin, growth hormone, and adrenocorticotrophic hormone, and release of these substances causes various neuropharmacological effects. Concretly, evidence [Funk, et al. (2007)] increasingly suggests that tobacco may act on the mesolimbic dopamine system, a part of the brain that is involved in reward, emotion, memory, and cognition. Brain cells (neurons) that release dopamine – a key chemical involved in addiction – have small docking molecules (receptors) to which nicotine binds. When nicotine receptors are blocked, smokers tend to consume less nicotine [Corrigall, et al. (1994)]. This mechanism of action may explain why tobacco can cause users to crave.
     Nicotine and other constituents in cigarette smoke elevate blood pressure (by 5 to 10 mmHg [Jacqueline Hart. (2004)], because it constricts the blood vessels), causes tachycardia (on average, tobacco increases the heart rate 10 to 20 beats per minute [Jacqueline Hart. (2004)], arrhythmias, and vasoconstriction in the cutaneous tissue and skin, lower body temperature, inhibit diuresis, increase gastrointestinal tonus, antagonize ulcer healing; decrease pain threshold.

Symptoms of Tobacco-Nicotine Poisoning: Excitement, confusion, muscular twitching, weakness, abdominal cramps, colonic convulsions, depression, rapid respirations, palpitations, collapse, coma, central nervous system paralysis (Nicotine stimulates the nervous system and may cause tremors in the inexperienced user, or even convulsions with high doses), respiratory failure [Merck. (1999)]. It was reported [J. Am. Med. Assoc. (1998)] that tobacco industry efforts in the United States, spanned 3 decades to alter the chemical form of nicotine to increase the percentage of freebase nicotine delivered to smokers. Depending on PH nicotine exists as a diprotonated salt, a monoprotonated salt, or an unchanged neutral species. The salt forms, and the neutral species is called the "freebase" form. Nicotine favours the salt form at low values of PH (e.g., PH=3) and the freebase form at high values of PH (e.g. PH=8).Freebase nicotine apparently crosses biological membranes more easily than the charged counterparts, and this affects the physiological response to the drug.

Tolerance and Nicotine Dependence: Most people begin smoking between the ages of 12 and 20. Surprisingly, few people start smoking as adults over 21 (see chapter three). Once smoking has become a habit, whether physical addiction occurs or not, Psychological factors play a significant role in continuing to smoke. A decrease in a person's sensitivity to the effects of a drug is often refered to as tolerance. The phenomenon occurs when a person must consume more of a substance in order to achieve the same rewarding effect. This, in case of tobacco, puts him/her at greater risk for developing dependence.
   Successful smoking cessation programs must treat both the Physical and Psychological aspects of nicotine addiction.