SOMOKING IS VALEOLOGICALLY DANGEROUS TO HEALTH (8): Continuation!!!

[Abbas Bubakar El-ta'alu]

Tar: This is the term used to describe the toxic chemical compounds found in manufactured cigarettes. Concentration of tar in a stick of cigarette determines its ratings [Terry Martins. (2003)].
   High–tar cigarettes contain at least 22 mg of tar,
   Medium–tar cigarettes – from 15 to 21 mg,
   Low–tar cigarettes – from 7 mg or less, of tar.

          Filters were first added to cigarettes in the 1950s, when it was reported that the in cigarettes was associated with an increased risk of lung cancer. The idea was that the filter would trap harmful tars and nicotine, but the design never worked as hoped. Toxins still make it through and into the smokers' lungs, exposing them to the risks of smoking-related disease.
          In solid form, tar is the brown, tacky substance that is left behind on the end of cigarette filter. It stains the smoker's teeth and fingers brown and coats everything it touches. In this form, about 70 per cent of uncondensed tar settles in the delicate pink tissue of the smoker's lungs and clogs them up.
   Tar is present in all types of cigarette and tends to increase as the cigarette is burnt down. This may mean that the last puffs on a stick of cigarette may contain as much as twice the amount of tar as the first puffs.
   Tar in cigarette smoke paralyzes the cilia in the lungs, and contributes to lung diseases such as Chronic Emphysema, Chronic Bronchitis and Lung Cancer (see Respiratory System).
      
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.