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Steps to carcinogenesis Exposure to smoke MICHAEL MURPHY ET AL. The harmful consequences of smoking are well known. The smoking of tobacco is an efficient method of delivering nicotine to the brain where it elicits rewarding effects. However tobacco smoke also carries more than 50 carcinogens direct to the lungs, including polycyclic aromatic hydrocarbons (PAHs) such as benzo[a]pyrene and several nitrosamine-based compounds that are specific to tobacco. Actual doses of nicotine, carcinogens, and toxins will vary, depending on an individual’s intensity and method of smoking and also on the smoking device. Genetic predisposition to nicotine addiction (discussed previously) will also contribute to risk via modulation of both amount smoked and ability to stop smoking. Activation of procarcinogens Tobacco carcinogens are metabolized by complex enzyme systems and involve both activation and detoxification. Phase 1 enzymes such as those from the cytochrome P450 family are primarily responsible for the activation (via oxidation) of procarcinogens. Many genes encoding CYP enzymes are polymorphic and this inherited variation will influence the activity of specific CYP isozymes, resulting in individual differences in exposure to activated carcinogens. CYP1A1 (on chromosome 2, see gene map earlier in chapter) is the principal enzyme that metabolizes PAHs and possessing polymorphic variant alleles seems to confer elevated risk of lung cancer, in certain ethnic populations (Vineis et al. 1999). Adduct formation Smoking-related DNA adducts (long-lasting aggregates of tobacco carcinogens and genetic material) have been detected by a variety of analytical methods in respiratory tract, bladder, cervix. DNA adducts are found at higher levels in tissues of smokers compared to non-smokers (Perera et al. 1987). Biomarker data provide convincing evidence that carcinogen uptake, activation, and binding to cellular macromolecules (including DNA) are higher in smokers than non-smokers (Randerath and Randerath 1993). Failure of DNA repair DNA repair plays a crucial role in maintenance of genome stability by removing these kinds of lesions, thus diminished DNA repair capacity may increase susceptibility to smoking-related cancers. Reduced DNA repair has been shown in lymphocytes from lung cancer patients in vitro compared to age-matched controls (Wei et al. 2000), although poor repair is thought to be independent of smoking status. Whilst DNA repair is undertaken, cell cycle checkpoints will arrest the growth of the cell, 635
636 GENES, NICOTINE ADDICTION, SMOKING BEHAVIOUR, AND CANCER and if the damage is too severe to repair, apoptosis occurs. A key-player in deciding the cell’s fate is p53, and mutation of this gene is a common event in tumour cells. Thus variation in p53 activity (and that of other proteins involved in these checkpoints) will also have an important role in the long-term effects of adduct formation on the cell. If not repaired, such damage can result in gene mutations and instability, which may in turn result in malignant transformation. Individual variation Many studies have shown a relationship between tobacco smoke exposure, carcinogen- DNA adduct formation, DNA repair capacity, and cancer risk. An individual’s susceptibility is a complex interplay of (a) exposure to tobacco smoke and (b) response to exposure, and inherited variation in key (and possibly overlapping) genes in both cases will modulate both smoking behaviour (exposure) and detoxification and repair (response). The hypothesis under test is that a smoker with low capacity to detoxify carcinogens (or who has enhanced activation), and/or low capacity to repair damaged DNA will be at higher risk of tobacco-related cancers. Detoxification There are a large number of studies examining metabolic susceptibility genes, and the most conspicuous aspect is the lack of a consistent role for this group of enzymes as cancer risk factors. This is perhaps not surprising given the low penetrance of these genes, and their indirect involvement in the complex process of cellular malignant transformation. The Phase II enzyme superfamily of glutathione S-transferases (GSTs) plays an important role in the detoxification of smoke-derived carcinogen metabolites and people who have variant alleles of GSTM1 in particular appear to have increased susceptibility to lung cancer after exposure to tobacco smoke (Vineis et al. 1999). The N-acetyl transferases (NAT1 and NAT2) are responsible for inactivation of various aromatic amines and several allelic variants of both genes have been detected some of which contribute to reduced enzyme function. Several studies have found a significant association between NAT2 slow acetylation and bladder cancer after smoking or occupational exposure. As a susceptibility locus for lung cancer the risk associated with NAT2 variants is inconsistent (Vineis et al. 1999). A recent large study suggested the NAT2 slow acetylator phenotype as a risk factor for lung cancer only in heavy smokers (80 pack-years) (Zhou et al. 2002). The sulfotransferases, which catalyse the sulfation of numerous carcinogenic and mutagenic compounds, have recently also been implicated as risk factors for lung cancer. The variant allele of SULT1A1 (SULT1A1*2), which encodes for low activity, is more commonly found in lung cancer cases, compared to age, sex, and smoking-status matched controls (Wang et al. 2002). Furthermore, this modest increase in risk was significantly higher in current smokers.
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Tobacco and Public Health: Science
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Tobacco and Public Health: Science
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Preface Tobacco: The public health
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PREFACE vii The cigarette companies
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dramatically. Once more, I am not s
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it impairs quality of life for year
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documents and through litigation by
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PREFACE xv it will not succeed. Now
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Stratton, K., Shetty, P., Wallace,
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Contents Preface v C. Everett Koop
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27 Tobacco and pancreas cancer 479
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Contributors Amanda Amos Reader in
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Stephen S. Hecht University of Minn
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Cecily S. Ray Project Assistant Epi
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Abbreviations AAA Abdominal aortic
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Introduction The publication of thi
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Part 1 Tobacco: History
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Introduction Chapter 1 Evolution of
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RICHARD DOLL 5 However, little atte
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RICHARD DOLL 7 lung’ (Doll and Hi
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Table 1.1 Principal diseases caused
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Table 1.4 Manufactured cigarette co
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in 1995 was approaching the maximum
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References Adler, I. (1912). Primar
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Introduction Chapter 2 The great st
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MICHAEL J. THUN AND JANE HENLEY 19
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it seems likely that some of this v
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steady increase in lung cancer occu
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cigarette smoking in deaths from co
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the effects of smoking and smoking
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Lung cancer death rate (per 100,000
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Lickint, F. (1929). Zeitschrift fur
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Chapter 3 Dealing with health fears
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LYNN T. KOZLOWSKI AND RICHARD J. O
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Table 3.3 Selected cigarette advert
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Part 2 Tobacco: Composition
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Introduction Chapter 4 The changing
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ILSE HOFFMANN AND DIETRICH HOFFMANN
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Table 4.4 (continued) Carcinogens i
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Table 4.5 Standard conditions for m
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Table 4.7 Comparison of experimenta
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the lung in rats treated with NNK (
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serve as the scientific basis in su
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Senkus, M. (ed.) (1976). Leaf compo
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Introduction Chapter 5 Tobacco smok
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STEPHEN S. HECHT 95 Established pul
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STEPHEN S. HECHT 97 magnitude lower
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STEPHEN S. HECHT 99 generally great
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Table 5.1 1-Hydroxypyrene in the ur
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Table 5.2 NNAL and its glucuronides
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STEPHEN S. HECHT 105 Table 5.2 (con
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Table 5.3 Representative DNA adduct
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G No (Wang et al. 2001a) N 2 CHCH 2
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STEPHEN S. HECHT 111 N-Nitrosopyrro
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(Kozack et al. 2000; Seo et al. 200
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the DNA adducts resulting from toba
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Culp, S. J., Gaylor, D. W., Sheldon
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STEPHEN S. HECHT 119 International
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STEPHEN S. HECHT 121 Melchior, W. B
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STEPHEN S. HECHT 123 Rivenso, A., H
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Wang, M., McIntee, E. J., Cheng, G.
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Part 3 Nicotine and addiction
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Chapter 6 Pharmacology of nicotine
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JACK E. HENNINGFIELD AND NEAL L. BE
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Pickworth et al. 1995; Shiffman et
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American Caucasians and Hispanics (
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(US DHHS 2001). At doses delivered
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References JACK E. HENNINGFIELD AND
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Introduction Chapter 7 Behavioral p
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BRIDGETTE E. GARRETT ET AL. 151 How
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(Fischman and Foltin 1991). Another
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following repeated, infrequent and
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BRIDGETTE E. GARRETT ET AL. 157 oth
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BRIDGETTE E. GARRETT ET AL. 159 cli
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to tobacco product ingredients and
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BRIDGETTE E. GARRETT ET AL. 163 Gom
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BRIDGETTE E. GARRETT ET AL. 165 Ris
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Introduction Chapter 8 Cigarette sc
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JEFF FOWLES AND DENNIS SHUSTERMAN 1
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◆ The pressure drop of the filter
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Nitrosamines Nitrosamines are biolo
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Physical design features of cigaret
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Introduction Chapter 9 Nicotine dos
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world tobacco burden (World Health
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Table 9.2 The ranges of nicotine, n
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MIRJANA V. DJORDJEVIC 187 turing a
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Poland 19 1.4 n.a. n.a. 68−347 36
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MIRJANA V. DJORDJEVIC 191 cigarette
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MIRJANA V. DJORDJEVIC 193 Table 9.5
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MIRJANA V. DJORDJEVIC 195 MS wherea
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MIRJANA V. DJORDJEVIC 197 In recent
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MIRJANA V. DJORDJEVIC 199 Table 9.8
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MIRJANA V. DJORDJEVIC 201 Burns, D.
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International Agency for Research o
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Part 4 Tobacco use: Prevalence, tre
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Chapter 10 Tobacco in Great Britain
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Adult smoking PATTI WHITE 209 Since
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oys who were regular smokers report
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PATTI WHITE 213 cancer, and bringin
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Introduction Chapter 11 The epidemi
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since the late 1980s. In 2001, Phil
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YANG HONGHUAN 219 ◆ Among males,
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Table 11.1 Smoking among adolescent
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(57%) was higher than in males (45%
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20 cigarettes a day had double the
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Chapter 12 Patterns of smoking in R
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DAVID ZARIDZE 229 Ignatova et al. (
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DAVID ZARIDZE 231 Tyumen, respectiv
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References DAVID ZARIDZE 233 Alexee
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Chapter 13 Tobacco smoking in centr
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WITOLD ZATOŃSKI 237 The developmen
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especially post-Soviet countries, w
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No. of Cigarettes 3000 2500 2000 15
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WITOLD ZATOŃSKI 243 young men and
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DEATHS / 100,000 DEATHS / 100,000 7
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WITOLD ZATOŃSKI 247 According to d
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Unfortunately, available data on th
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Kaczmarczyk-Chalas, K., Gdulewicz,
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Chapter 14 The epidemic in India Pr
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aniseed, and musk, also available a
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PRAKASH C. GUPTA AND CECILY S. RAY
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Prevalence among youth PRAKASH C. G
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treatment and premature death were
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Although tobacco control legislatio
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PRAKASH C. GUPTA AND CECILY S. RAY
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Chapter 15 Tobacco in Africa: More
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In assessing tobacco use in Africa
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YUSSUF SALOOJEE 271 plug the gap th
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Table 15.2 Cigarette taxes as perce
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YUSSUF SALOOJEE 275 In recent years
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World Bank (2001). Economics of Tob
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Part 5 Tobacco and health. Global b
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Chapter 16 The future worldwide hea
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RICHARD PETO AND ALAN D LOPEZ 283 a
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UK male death rate at ages 35-69 ha
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Overview Chapter 17 Passive smoking
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evidence have proved to be effectiv
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JONATHAN M. SAMET 291 a thousand de
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Table 17.2 Occupational ETS exposur
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Table 17.3 Nicotine concentrations
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portable piezobalance to sample aer
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JONATHAN M. SAMET 299 Fetal effects
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JONATHAN M. SAMET 301 Investigation
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Table 17.4 Summary of pooled random
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JONATHAN M. SAMET 305 also reported
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and involuntary exposure to tobacco
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Glantz, S. A. and Parmley, W. W. (1
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JONATHAN M. SAMET 311 O’Connor, G
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JONATHAN M. SAMET 313 US Department
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Introduction Chapter 18 Adolescent
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JOHN P. PIERCE ET AL. 317 would be
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JOHN P. PIERCE ET AL. 319 Indeed, t
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JOHN P. PIERCE ET AL. 321 reached i
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subsequent consumption. Most studie
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Burns, D., Garfinkel, L., and Samet
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JOHN P. PIERCE ET AL. 327 US Depart
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The epidemic Chapter 19 Tobacco and
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AMANDA AMOS AND JUDITH MACKAY 331 w
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AMANDA AMOS AND JUDITH MACKAY 333 T
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AMANDA AMOS AND JUDITH MACKAY 335 w
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AMANDA AMOS AND JUDITH MACKAY 337 p
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AMANDA AMOS AND JUDITH MACKAY 339 T
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AMANDA AMOS AND JUDITH MACKAY 341 o
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AMANDA AMOS AND JUDITH MACKAY 343 M
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such as Jewel and Madonna, who woul
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AMANDA AMOS AND JUDITH MACKAY 347 t
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particularly in developing countrie
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AMANDA AMOS AND JUDITH MACKAY 351 L
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Part 6 Tobacco and cancer
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Chapter 20 Cancer of the prostate F
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Table 20.1 Summary of results of ca
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Andersson et al. 1996 Sweden 256 ca
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Table 20.2 Summary of results of co
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cancer in younger or elderly men, w
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FABIO LEVI AND CARLO LA VECCHIA 365
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Summary Chapter 21 Laryngeal cancer
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12-year follow-up of the American C
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Hedberg et al. USA, 235, 81% P, 547
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cigarettes as compared to blond-tob
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of 3.78 and 11.47. An interpretatio
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Effect on survival In two studies f
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Cattaruzza, M. S., Maisonneuve, P.,
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USDHEW (1964). Laryngeal cancer. In
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Chapter 22 Smoking and cancer of th
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Table 22.1 Results from selected ca
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Asia Gao et al. 1994— Population
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EVA NEGRI 389 Ille-et-Vilaine, Fran
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Odds Ratio 2.5 2 1.5 1 0.5 0 0.30 2
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Garidou et al. 1996— Hospital ≤
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De Stefani, E., Barrios, E., and Fi
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Wynder, E. L. and Bross, I. J. (196
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Introduction Chapter 23 Tobacco use
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Table 23.1 Tobacco use and risk of
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Franceschi et al. Oral cavity, Oral
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Muscat et al. Oral cavity OR = 2.1
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Population-based case-control studi
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Lewin et al. Oral cavity, RR = 6.5
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TONGZHANG ZHENG ET AL. 411 the cont
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TONGZHANG ZHENG ET AL. 413 For smok
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TONGZHANG ZHENG ET AL. 415 per day
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TONGZHANG ZHENG ET AL. 417 than tha
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TONGZHANG ZHENG ET AL. 419 For exam
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TONGZHANG ZHENG ET AL. 421 decline
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Studies in India: Oral cancer is th
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carcinoma compared with other combi
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studies have demonstrated a positiv
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TONGZHANG ZHENG ET AL. 429 Garrote,
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TONGZHANG ZHENG ET AL. 431 Notani,
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Chapter 24 Smoking and stomach canc
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DAVID ZARIDZE 435 such as sex, age,
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DAVID ZARIDZE 437 (Kato et al. 1990
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DAVID ZARIDZE 439 respectively. The
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Gajalakshmi, C. K. and Shanta, V. (
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Pisani, P., Parkin, D. M., Bray, F.
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Introduction Chapter 25 Cigarette s
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attenuated in every study after con
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EDWARD GIOVANNUCCI 449 with a gener
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(Baron et al. 1994) of 352 colon ca
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(U.S. Dept. of Health Education and
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References EDWARD GIOVANNUCCI 455 A
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EDWARD GIOVANNUCCI 457 Kono, S., Ik
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Chapter 26 Smoking and cervical neo
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Tokuhata 1967* Williams 1977* Wigle
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Clarke 1985* Hellberg 1986* La Vecc
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ANNE SZAREWSKI AND JACK CUZICK 465
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case-control study nested in a scre
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five-fold risk of cervical cancer f
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(typically around two-fold), but be
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Introduction Chapter 27 Tobacco and
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Cigar, pipe, and chewing tobacco Wh
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Conclusion Overall, tobacco smoking
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Summary Chapter 28 Smoking and lung
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GRAHAM G. GILES AND PETER BOYLE 487
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quit for 20 years or more (Rogot an
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cancer and others where there is st
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Peto, R. (1986) Influence of dose a
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Chapter 29 Tobacco smoking and canc
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He further noted that case-control
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coefficients from the data in Table
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DIMITRIOS TRICHOPOULOS AND ARETI LA
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Epidemiology Chapter 30 Smoking and
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CRYSTAL N. HOLICK AND HARVEY A. RIS
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and at least the enteric variety of
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Chapter 31 Endometrial cancer Paul
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Table 31.1 Epidemiological studies
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studies (Terry et al. 1999, 2002a),
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Newcomer Population 740/2372 40-79
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PAUL D. TERRY ET AL. 531 levels, an
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Relative body weight Obesity is an
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Key et al. 1991 147 pre- and postme
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lood levels among current smokers,
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Table 31.7 Studies of cigarette smo
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of the association between cigarett
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Jensen, J., Christiansen, C., and R
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PAUL D. TERRY ET AL. 545 Weiderpass
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Part 7 Tobacco and heart disease
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Introduction Chapter 32 Tobacco and
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citations of some of the best-known
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KONRAD JAMROZIK 553 because the dat
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KONRAD JAMROZIK 555 Fig. 32.2 Trend
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Table 32.3 Case-control studies of
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Table 32.5 Cohort studies of active
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Table 32.6 Effect of exclusion of p
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eadily addressed by cohort studies
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Specificity The entries in Table 32
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Table 32.8 Application of Bradford
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KONRAD JAMROZIK 569 arterial CVD re
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elationship goes beyond statistical
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Garland, C., Barrett-Connor, E., Su
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National Health and Medical Researc
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Part 8 Tobacco and respiratory dise
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Introduction Chapter 33 Chronic obs
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Many of the constituents in both th
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DAVID M. BURNS rate of growth in lu
Page 618 and 619: Death rates from COPD in smokers an
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Page 622 and 623: DAVID M. BURNS Higgins, M. W., Enri
Page 624 and 625: Part 9 Tobacco and other diseases
Page 626 and 627: Introduction Chapter 34 Smoking and
Page 628 and 629: ALLAN HACKSHAW 595 several mechanis
Page 630 and 631: Table 34.4 Studies that reported re
Page 632 and 633: Table 34.5 Cohort studies that repo
Page 634 and 635: than non-smokers; they have about h
Page 636 and 637: Table 34.8 Cohort studies that repo
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Page 642 and 643: Table 34.12 Cohort studies that rep
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Page 646 and 647: Table 34.16 Summary of disorders in
Page 648 and 649: References ALLAN HACKSHAW 615 Allar
Page 650 and 651: Johnsen, R., Forde, O. H., Straume,
Page 652 and 653: Seddon, J. M., Willett, W. C., Spei
Page 654 and 655: Part 10 Genetics, nicotine addictio
Page 656 and 657: Chapter 35 Genes, nicotine addictio
Page 658 and 659: Cotinine (ng/ml) 750 500 250 OXCHEC
Page 660 and 661: MICHAEL MURPHY ET AL. 627 of those
Page 662 and 663: MICHAEL MURPHY ET AL. risk associat
Page 664 and 665: Table 35.2 (continued) Gene map Chr
Page 666 and 667: MICHAEL MURPHY ET AL. pre-clinical
Page 670 and 671: DNA repair As previously alluded to
Page 672 and 673: MICHAEL MURPHY ET AL. Lichtenstein,
Page 674 and 675: Part 11 Tobacco and alcohol
Page 676 and 677: Introduction Chapter 36 Tobacco and
Page 678 and 679: Table 36.1 Comparison of alcohol an
Page 680 and 681: Although gene therapy has rarely be
Page 682 and 683: 20+ TABAC 5.1 10-19 0-9 3.4 12.3 0-
Page 684 and 685: Heavy drinking is known to cause ga
Page 686 and 687: Treatment issues and co-dependence
Page 688 and 689: ALBERT B. LOWENFELS AND PATRICK MAI
Page 690 and 691: Part 12 Tobacco control: Successes
Page 692 and 693: Introduction Chapter 37 Global toba
Page 694 and 695: NIGEL GRAY (sometimes at state leve
Page 696 and 697: NIGEL GRAY The first attempt to red
Page 698 and 699: per litre of smoke. Reduction of th
Page 700 and 701: Borland, R., Cappiello, M. and Owen
Page 702 and 703: Chapter 38 Lessons in tobacco contr
Page 704 and 705: entangling relationships with negot
Page 706 and 707: successful country advocates deeply
Page 708 and 709: Thus, when the opportunity arose, t
Page 710 and 711: Chapter 39 A brief history of legis
Page 712 and 713: Committee, mentioned above, little
Page 714 and 715: 4. Tobacco and its related processi
Page 716 and 717: RUTH ROEMER 683 advertising and adv
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or shows, and distribution of free
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RUTH ROEMER 687 threat to the peopl
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RUTH ROEMER 689 The case was settle
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Another study by Harvard researcher
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At the end of 2003, 83 countries ha
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Chapter 40 Roles of tobacco litigat
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NGOs obtained sanctions against tob
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RICHARD A. DAYNARD 699 In a 1980s c
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RICHARD A. DAYNARD 701 Fourth, the
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even impossible. Such a statute pre
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RICHARD A. DAYNARD 705 Daynard, R.
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Introduction Chapter 41 Impact of s
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in this chapter, is evidence that s
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RON BORLAND AND CLAIRE DAVEY 711 Wh
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RON BORLAND AND CLAIRE DAVEY 713 On
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RON BORLAND AND CLAIRE DAVEY 715 ro
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you are subject, but this does not
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RON BORLAND AND CLAIRE DAVEY 719 to
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RON BORLAND AND CLAIRE DAVEY 721 fo
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RON BORLAND AND CLAIRE DAVEY 723 (E
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RON BORLAND AND CLAIRE DAVEY 725 th
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advanced. Although in countries lik
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RON BORLAND AND CLAIRE DAVEY 729 Da
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RON BORLAND AND CLAIRE DAVEY 731 Pr
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Introduction Chapter 42 Effective i
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PRABHAT JHA ET AL. 735 India (Gupta
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Average price or tax per pack (US$)
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PRABHAT JHA ET AL. 739 Bans on adve
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PRABHAT JHA ET AL. 741 Table 42.2 T
Page 776 and 777:
PRABHAT JHA ET AL. 743 antismugglin
Page 778 and 779:
Farrelly, M. C., Pechacek, T. F., a
Page 780 and 781:
PRABHAT JHA ET AL. 747 Raw, M., Mc
Page 782 and 783:
Part 13 Treatment of dependence
Page 784 and 785:
Introduction Chapter 43 Treatment o
Page 786 and 787:
Nocturnal sleep-disturbing nicotine
Page 788 and 789:
MICHAEL KUNZE AND E. GROMAN 755 tob
Page 790 and 791:
Fifteen different products were ide
Page 792 and 793:
In summary, tobacco dependence amon
Page 794 and 795:
medications for OTC sale in 1996, t
Page 796 and 797:
MICHAEL KUNZE AND E. GROMAN 763 US
Page 798 and 799:
Chapter 44 Regulation of the cigare
Page 800 and 801:
as these correlate quite well with
Page 802 and 803:
NIGEL GRAY 769 within three major g
Page 804 and 805:
of carcinogens and toxins in its wa
Page 806 and 807:
Index abdominal aortic aneurysm see
Page 808 and 809:
aromatic amines 58, 60, 98 DNA addu
Page 810 and 811:
central and eastern Europe (CEE) (C
Page 812 and 813:
coronary thrombosis 5 see also myoc
Page 814 and 815:
epinephrine 169 epoxide hydrolase g
Page 816 and 817:
health professionals advice on smok
Page 818 and 819:
laryngeal cancer (Continued) animal
Page 820 and 821:
Morris, Philip 207 see also Philip
Page 822 and 823:
nursing home residents 718 nutritio
Page 824 and 825:
Polish Central Statistical Office (
Page 826 and 827:
smoke, tobacco (including cigarette
Page 828 and 829:
Sweden female smoking rates 330-1 l
Page 830 and 831:
United Nations agencies 680-1 Unite
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Tobacco and Public Health - TCSC Indonesia

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