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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction Section II Evidence for the Science Base
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction This page in the original is blank.
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction 9 Nicotine Pharmacology BASIC AND HUMAN PHARMACOLOGY It is some 550 years since the eponymous Jean Nicot sent tobacco and seeds from Portugal to Paris, passing Nicotiana tabacum from the Americas to Northern Europe by way of the Iberian peninsula. Nicotine itself was subsequently extracted and synthesized, culminating in the identification of the spatial orientation of the natural (S) isomer in the late 1970s (Domino, 1999). Up to 10% of the nicotine in tobacco smoke is the (R) isomer, probably arising from racemization during combustion (Benowitz, 1986). Nicotine has gained particular prominence as the addictive constituent of most tobacco based products and, to a lesser extent, as an effective insecticide. Nicotine, 3-(1-methyl-2-pyrrolidinyl) pyridine, has a molecular weight of 162.23 and is a volatile, colorless base (pKa=8.5) that turns brown and acquires the typical odor of tobacco on exposure to light. Roughly 69% of its pyrrolidine nitrogen is ionized (positively charged) at pH 7.4 and 37°C, whereas its pyridine nitrogen is un-ionized. This feature of nicotine renders its absorption and renal excretion highly pH dependent, because uncharged lipophilic bases pass easily over lipoprotein membranes and charged organic bases do not. For example, nicotine is primarily ionized at the pH (5.5) of smoke from the flue-cured tobaccos in most American cigarettes, and buccal absorption is minimal (Gorrod and Wahren, 1993). By contrast, smoke from air-cured tobaccos in pipes, cigars, and many European cigarettes is less acidic and is well absorbed through
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction the mouth (Armitage et al., 1978; Gori et al., 1986). Nicotine constitutes about 95% of the total alkaloid content of commercial cigarette tobacco (Gorrod and Jenner, 1975). The mechanisms by which nicotine exerts its actions at a molecular level are complex. Dale (Dale, 1914) noticed the structural similarity between nicotine and acetylcholine (Ach) and the resemblance of the effects of nicotine in vivo to those of Ach after pretreatment with the muscarinic antagonist atropine. The muscarinic effects of Ach are now recognized to be mediated via one of the five heptahelical muscarinic receptors (M1-M5). Ligation of these receptors may activate downstream signaling pathways via their interaction with diverse G proteins. Nicotinic receptors (nAchRs), by contrast, are ligand gated ion channels (Domino, 1999; Lena and Changeux, 1998). These pentamers are comprised of various combinations of α, β, γ, and δ subunits. Recent studies have demonstrated that specific configurations of these subunits mediate the diverse effects of nicotine. Although this area of research is evolving, the neuronal subunits that appear to be primarily responsible for the effects of nicotine contain α3,4,7 and β2 and 4 subunits. The α4β2 subtype is particularly prevalent in the brain and may be responsible for the self-administration of nicotine. Mice deficient in the β2 subunit do not self-administer nicotine (Cordero-Erausquin et al., 2000), suggesting that this subunit in particular may be important in reinforcing the effects of nicotine. In addition, some preliminary evidence suggests that the α7 subunit may play a significant role in withdrawal and sensory gating functions of schizophrenics (Adler et al., 1998; Nomikos et al., 2000; Panagis et al., 2000). Localization studies have identified nAchRs in the brain, neuromuscular junctions, autonomic ganglia, and adrenal medulla (Gundisch, 2000). Ligation of nAchRs by nicotine opens the channel, and the ionic influx activates signal transduction pathways, culminating in release of a number of different neurotransmitters, which have been related to nicotine’s pharmacodynamic effects. These include dopamine (pleasure and appetite suppression), serotonin (appetite suppression and mood modulation), epinephrine and norepinephrine (arousal and appetite suppression), Ach (arousal and cognitive enhancement), vasopressin (memory improvement), glutamate (improvement in learning), β-endorphin (mood modulation and analgesia), and δ-aminobutyric acid. Nicotine also increases nAchR expression. For example, prenatal nicotine exposure upregulates the pulmonary expression of the α7 receptor subunit and consequently affects fetal lung development in monkeys (Sekhon et al., 1999). Nicotine caused lung hypoplasia and reduced surface complexity of developing alveoli in this model. Collagen surrounding the large airways and vessels was increased, as was the number of type II cells and neuroendocrine cells in neuropepithelial
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction bodies. Many animal studies have also demonstrated that nicotine administration upregulates expression of nAchRs in the brain. Similarly, ligand-binding studies have demonstrated an increase in binding sites for nicotine analogues in the cerebral cortex and hippocampus of smokers compared to nonsmokers (Perry et al., 1999), although the extent to which this may contribute to the differential central effects of nicotine observed in smokers is unknown. Dopamine is believed to be the dominant neurotransmitter in the maintenance of drug-taking behavior (DiChiara, 1999; Koob, 1992). The area of the brain that is responsible for the reinforcing effects of all drugs of abuse is the mesolimbic pathway, which contains the ventral tegmental area (VTA), nucleus accumbens, amygdala, cingulate gyrus, and frontal lobe and is rich in dopamine. The VTA and nucleus accumbens seem particularly important in nicotine’s reinforcing effects. Activation of nAchRs in the VTA and other parts of the midbrain, modulates the ascending mesolimbic dopamine system, including the nucleus accumbens (George et al., 2000; Yu et al., 2000). Nicotine self-administration behavior is diminished by either surgical or chemical ablation of dopaminergic pathways or by treatment with dopamine antagonists (Kameda et al., 2000). Nicotine evokes an increase in dopamine levels in brain microdialysis studies (Fu et al., 2000). In addition, monoamine oxidase A and B, responsible for the metabolism of dopamine, are reduced by a compound in tobacco smoke that also results in higher levels of neurotransmitters (Quattrocki et al., 2000). The release or inhibition of other transmitters may also play a role in nicotine addiction. They may be responsible for mood modulation, the modest enhancement of performance, and the weight-reducing effects of nicotine (Benowitz, 1999; Chiodera et al., 1990; Chowdhury et al., 1989; U.S. DHHS, 1988). Mood modulation by nicotine has been a controversial topic, since laboratory studies do not validate the smoking-induced enhancement of mood self-reported by smokers. Furthermore, individuals experience greater positive affect when smoking after a period of abstinence. The relief of negative affect by tobacco use may be more a function of abating withdrawal symptoms (Cinciripini et al., 1997; RCP, 2000). Finally, in addition to its traditional pre- and postsynaptic actions at synapses and at chemoreceptors in the carotid and aortic bodies, nicotine also evokes the release of epinephrine from the adrenal medulla and may act directly to activate ion channels distinct from nAchRs. For example, nicotine has been shown to block directly inward rectifier potassium channels, an effect of potential relevance to cardiac arrhythmogenesis (Wang et al., 2000b).
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction PHARMACOKINETICS Absorption Although buccal absorption is influenced by the pH of tobacco or tobacco smoke, tobacco smoke from all sources is rapidly absorbed from the large surface area of the small airways and the alveoli, following dissolution in the pulmonary fluid at pH 7.4 (Zevin et al., 1998). Nicotine is also readily absorbed from the skin; this property has been exploited in the use of patch delivery in nicotine replacement therapy (NRT) for cigarette smokers (Figure 9–1). Nicotine is well tolerated as a dermal application, even in individuals who suffer from irritant skin disorders (Benowitz, 1995). FIGURE 9–1 Time curves of plasma nicotine concentrations. NOTE: Time curves of plasma nicotine concentration after application of four different transdermal nicotine delivery systems. The Ciba-Geigy Habitrol, the Alza (SmithKline Beecham) Nicoderm, and the Elan Prostep patches were worn for 24 hours, while the Kabi-Cygnus (Pharmacia) Nicotrol patch was worn for 16 hours. SOURCE: Benowitz, 1993. Reprinted from Drugs 1993; 45(2):157–170 with permission. © Adis International, Inc.
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction Following ingestion, as with chewing tobacco, the pH dependence of nicotine ionization favors its absorption by the small intestine, rather than the stomach, although a timed-release preparation, which permits colonic absorption (Green et al., 1999), has also been developed for use in ulcerative colitis as discussed below. Although the peak levels of nicotine attained after chewing tobacco may approximate those after smoking, the shape of the curve of plasma concentration versus time is quite different (Figure 9–2). Thus, after smoking a cigarette, plasma levels of nicotine rise rapidly to a peak, which is maintained transiently after the cigarette is inhaled, rather than the more gradual and sustained elevation after oral FIGURE 9–2 Blood nicotine concentrations. NOTE: Blood nicotine concentrations during and after cigarette smoking for nine minutes, oral snuff (2.5 grams), chewing tobacco (average 7.9 grams), and nicotine gum (two 2 mg pieces). Data represent average values for 10 subjects (±SEM). Horizontal bars above time axis indicate period of tobacco or nicotine gum exposure. SOURCE: Benowitz et al., 1988. Reprinted with permission from Mosby, Inc.
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction ingestion. The evoked liking, systemic response, and addiction potential of the former pattern of nicotine delivery exceed those of the latter (Benowitz et al., 1988). It takes roughly 10–15 seconds for nicotine, inhaled by puffing a cigarette, to reach the brain, and puffing is associated with a marked arterial-venous gradient of nicotine (Benowitz, 1995; Benowitz et al., 1988; Guthrie et al., 1999). This rapid central nervous system (CNS) delivery permits the smoker to adjust the nicotine dosage to a desired effect, reinforcing self-administration and facilitating the development of addiction (Benowitz, 1995). This contrasts with the slower increase and lesser increment in brain nicotine attained after transdermal delivery, which facilitates the development of tolerance (see below). The average cigarette contains 10–15 mg of nicotine and delivers, on average, roughly 1–2 mg of nicotine systemically to the smoker. However, smoking habit— puff intensity, duration, and so forth—can markedly alter nicotine bioavailability. By comparison, the systemic doses of nicotine from other delivery systems are roughly 1 mg from a 2 mg gum; 5–22 mg per day from transdermal patches; 0.5 mg per dose from one spray per nostril; 3.6 mg from 2.5 grams of snuff, held in the mouth for 30 minutes and 4.5 mg from 7.9 grams of chewing tobacco chewed for 30 minutes (Benowitz and Jacob, 1999). Following its absorption, nicotine circulates with roughly 60% in the ionized form. It is poorly (around 5%) protein bound (Benowitz et al., 1982) and widely distributed, at least in rats and rabbits, particularly in liver, lungs, and brain (Benowitz et al., 1990). Distribution and Metabolism The presence of both aromatic and aliphatic carbon and nitrogen atoms in nicotine affords multiple sites for metabolic oxidation and subsequent conjugation reactions (Figure 9–3). The disposition of nicotine has been reviewed in depth elsewhere (Benowitz and Jacob, 1999; Gorrod and Schepers, 1999). Briefly, roughly 80% of the metabolic inactivation of nicotine involves oxygenation of the 5'-carbon to yield cotinine. This appears to involve an intermediate cytochrome P-450 (CYP)- derived 1',5'-imminium ion, which is further metabolized by aldehyde oxidase to yield cotinine (Brandange and Lindblom, 1979; Gorrod and Hibberd, 1982; Murphy, 1973). This iminium ion is an alkylating agent and has been speculated to have relevance to the carcinogenicity of tobacco, although this is not established (Hibberd and Gorrod, 1983). Oxidation of this radical may also yield nornicotine or 4-(3-pyridyl)-4-oxo-N-methylbutylamine. CYP2A6 and, to a lesser extent, 2B6 appear to play the predominant roles in nicotine carbon oxidation in humans (Benowitz and Jacob, 1999; Nakajima et al., 2001; Nakajima et al., 2000; Yamazaki et al., 1999). Although roughly
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction FIGURE 9–3 Nicotine metabolic pathways. SOURCE: Benowitz and Jacob, 1999. Copyright (1999) Wiley-Liss, Inc. Reprinted with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons. Translated by permission of John Wiley & Sons, Inc. All rights reserved.
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction 15% of a nicotine dose is excreted in human urine unchanged, all of the primary metabolites, including cotinine, are subject to further oxidation reactions. Oxidation appears to involve only the alicyclic pyrrolidine nitrogen in biological systems (Gorrod and Schepers, 1999). Nicotine-1'-N-oxide may be reduced to nicotine in man by gut bacteria (Dajani et al., 1975). Phase two metabolites can be formed by methylation, glucuronidation, sulfation, or glutathione conjugation reactions with primary oxidation metabolites. Formation of such polar, water soluble molecules facilitates excretion. Although great interindividual variation is noticeable, glucuronides may account for roughly 40% of the urinary nicotine metabolites in humans. This variability may also be apparent among ethnic groups. Thus, the most abundant phase 2 metabolite in the urine of North Americans is the N-glucuronide of cotinine, whereas in Europeans the O-glucuronide of trans-3'-hydroxycotinine predominates (Gorrod and Schepers, 1999). Similarly, the metabolism of nicotine is slower in African Americans than in Caucasians, due to both slower oxidative metabolism of nicotine to cotinine and slower N-glucuronidation (Benowitz et al., 1999; Caraballo et al., 1998; Perez-Stable et al., 1998). Asian Americans also metabolize both nicotine and cotinine more slowly than do Caucasians. Nicotine clearance declines with age (Molander et al., 2001). Although there is some evidence for differences between men and women in the pharmacodynamic response to nicotine (Pomerleau et al., 1991), this does not appear to reflect systematic differences in nicotine pharmacokinetics. Nicotine readily crosses the placental barrier, although there is no apparent conversion of nicotine to cotinine by placental tissues or microsomal fractions (Pastrakuljic et al., 1998). Although the potential for fetal toxicity must be considered in women undergoing NRT (as discussed below), this consideration usually occurs in the context of relativity. Thus, the hazard to the fetus of maternal cigarette smoking is well established (Oncken et al., 1998; Robinson et al., 2000), whereas the theoretically much smaller risk of NRT remains entirely notional. Clearance of nicotine falls with hepatic blood flow during sleep (Gries et al, 1996) and a circadian pattern in both circulating nicotine and cotinine is evident (Figure 9–4). Although the half-life of nicotine is about 2–3 hours when based on plasma levels, it approximates 11 hours when based on urinary excretion (Benowitz and Jacob, 1994, 1999), so circulating levels tend to accumulate during the day. The afternoon levels of nicotine in the plasma of smokers generally range from 10 to 50 ng/ml, whereas steady-state levels with patches range from 10 to 20 ng/ml and with the nasal spray from 5 to 15 ng/ml (Benowitz and Jacob, 1999). Sophisticated approaches to analysis not just of nicotine and cotinine, but of minor oxidative metabolites and many phase 2 metabolites, have
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction FIGURE 9–4 Circadian blood concentrations of nicotine and cotinine during unrestricted smoking. NOTE: Data are mean±SE for eight subjects. SOURCE: Benowitz et al., 1983. Reprinted with permission from Mosby, Inc.
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