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This chapter discusses the identification of carcinogens and tumour promoters in tobacco smoke, changes in cigarette smoke composition with various design changes, and observations on cigarette smokers. Major modifications in the make-up of the commercial cigarette were introduced between 1950 and 1975, but since that time there have been few substantive changes toward a further reduction of the toxic and carcinogenic potential of cigarette smoke. A variety of changes in cigarette design and filtration have resulted in chemical changes in cigarette smoke, some of which have demonstrated decreased toxicity in animal assays. Changes in the agricultural, curing, and manufacturing processes of cigarettes have increased the amounts of tobacco-specific nitrosamines in cigarette smoke. These changes are considered to have contributed to the increase in adenocarcinoma of the lung observed over the past several decades.

This chapter illustrates the tobacco industry's efforts over the last fifty years to deceive the public against the adverse health effects of smoking and the fact that nicotine was a drug or that it was addictive. It presents in chronological order, the industry commentary, some public, but most secret.

This chapter reviews epidemiological studies on the link between oral cancer and tobacco product use, including cigarette smoking, pipe tobacco and cigar smoking, and smokeless tobacco use (snuff dipping and chewing tobacco). In most studies, ‘oral cancer’ includes cancer of the tongue, mouth, and pharynx, with a few including the larynx. In 1986, an International Agency for Research on Cancer (IARC) Working Party concluded that there was sufficient evidence that tobacco was carcinogenic to humans and that the occurrence of malignant tumours of the upper digestive tract was causally related to the smoking of different forms of tobacco. IARC has also concluded that there is sufficient evidence that oral use of snuff of the types commonly used in North America and western Europe is carcinogenic to humans, and there was sufficient evidence that the habit of chewing betel quid containing tobacco was carcinogenic in humans. More recent epidemiological studies and experimental studies further support these conclusions. There is convincing evidence that a large attributable risk can be ascribed to the joint habits of cigarette smoking and alcohol consumption.

This chapter begins with a review of global trends in women and smoking. It then discusses the health effects of tobacco use, the economic impact of tobacco use on women, smoking cessation among women, and the marketing of tobacco to women. At the beginning of the 20th century few people could have imagined how such a stigmatized behaviour as female smoking would be transformed, through judicious marketing by the tobacco companies, into a socially acceptable and desirable behaviour in high-income countries. The challenge facing us in the 21st century is to how stem the second wave of the tobacco epidemic, particularly in low- and middle-income countries and among disadvantaged women in high-income countries.

This chapter examines the contributions of several large prospective studies conducted over the second half of the 20th century to our understanding of the health hazards of tobacco use. Beginning in the early 1950s, large cohort studies played a major role in helping to identify the multitude of adverse health effects caused by tobacco use, particularly manufactured cigarettes. They demonstrated that the harmful effects applied to women as well as men, that cigarettes with low machine-measure tar and nicotine were no less hazardous with respect to lung cancer than filter-tip ‘regular’ tar cigarettes, and that the burden of disease caused by smoking increased over time as smokers initiated regular cigarette smoking at progressively earlier ages. Large cohort studies will continue to be important for monitoring the course of the epidemic as it evolves in different cultures and for sustaining the political resolve to end it.

This chapter provides an overview and introduction to the now vast data on the adverse health consequences of passive smoking, covering the risks to passive smokers, including the fetus, infants and children, and adults. In about three decades, progression has been made from the first studies on passive smoking and health to definitive evidence that passive smoking causes disease. The evidence derives from not only epidemiological studies, but studies with biomarkers documenting that tobacco smoke inhaled by non-smokers delivers doses of toxic components and metabolites to target organs. There are also animal studies and extensive data on patterns of exposure. The strength of the evidence and its public health implications have been a strong force for motivating tobacco control policy.

It is over forty years since the public health community came to the consensus that smoking tobacco, particularly cigarettes, caused lung cancer. Despite widespread dissemination of the likely health consequences, cigarette smoking is still a prevalent behaviour in all developed countries and is a rapidly increasing behaviour in developing countries. There is an extensive literature on quitting studies indicating that, for many smokers, successful quitting is one of the hardest lifestyle changes to achieve. Given this, many argue that the majority of the emphasis should be on preventing the initiation of smoking in the first place. This chapter focuses on influences encouraging young people to become smokers.

The establishment of the causal link between smoking and lung cancer was an epidemiological triumph won against considerable resistance marshalled by the tobacco industry. This chapter reviews how the evidence that smoking causes lung cancer was accumulated and weighed against criteria adopted to establish the causal significance of epidemiological associations between an exposure and disease. The history of elucidating the association between lung cancer and smoking is now fundamental to modern epidemiological thinking and practice but in the early to mid-20th century the science of epidemiology was new and in the making, and the research on smoking and lung cancer contributed to the development of epidemiology as a discipline. In addition to the evaluation of epidemiological evidence, the case for causality was strengthened by evidence from human pathology and by evidence from experimental studies using animal models.

This chapter reviews studies on the link between smoking and an endometrial cancer risk, and changes in urinary hormone concentrations that may underlie this smoking-cancer association. The available data suggest that cigarette smoking is associated with a reduced risk of endometrial cancer among current-smokers, mainly among postmenopausal women, and that the association weakens with time since quitting. Studies that examined quantitative measures of exposure to cigarette smoke have shown greater reductions in risk among women who were current-smokers and smoked either more intensely or for a longer duration than women who smoked relatively less. The mechanisms by which this association may be driven remain unclear.

The indisputable relationship between the world's most widespread exogenous chemical carcinogen exposure — tobacco smoke — and cancer, provides a framework for a better understanding of cancer mechanisms in general, particularly the interaction between carcinogen exposure and host factors, and for the development of novel preventive and therapeutic strategies. Furthermore, the biomarkers that are developed in this research can be applied in the approaching era of tobacco product regulation. This chapter discusses the mechanisms of tumour induction by tobacco carcinogens and the status of tobacco carcinogen biomarkers.

This chapter reviews studies on the link between smoking and colorectal adenoma and cancer. The overall body of evidence indicates that colorectal cancer is a smoking-related malignancy. Two factors probably have contributed to the fact that this has not been appreciated until relatively recently. First, there appears to be a relatively long time lag between the onset of smoking and the period of risk, and second, colorectal cancers are common even in non-smokers so the population attributable risk has been moderate compared to other malignancies.

The tobacco industry has been spectacularly successful in marketing its products over a long period of time. Advertising campaigns for cigarette brands such as Marlboro, Benson & Hedges, Winston, Camel, and Lucky Strike have garnered positions in the top 100 list of all advertising campaigns. A distinguishing feature of tobacco industry marketing is that, rather than relying on traditional avenues such as television, radio, and print media, a full range of advertising and promotional opportunities has been used. This chapter first examines the gradual move by tobacco companies from measured media towards other marketing communications. It then focuses on two tobacco marketing communications of prime importance: point-of-sale marketing and tobacco packaging. The final section considers corporate social responsibility programmes and youth smoking prevention programmes, which have emerged as traditional avenues for advertising have been closed, or have threatened to be limited by tobacco control legislation or legal agreements.

This chapter discusses the issue of tobacco harm reduction. Tobacco harm reduction can be considered as one approach to reduce tobacco-caused mortality and morbidity, but should not be considered as the primary approach. To date the only known method for reducing population harm is to eliminate the use of tobacco products through prevention or cessation. Yet, in order to assess the potential public health impact of novel products being introduced onto the market, it is essential to continue to monitor and study the evolving characteristics of tobacco products. Some new products are advertised with either explicit or implicit claims of reduced exposure or health risks which are not evidence-based and which may mislead consumers into thinking they are using ‘safer’ or ‘safe’ products. In addition, some of these novel products are advertised to be used in situations where smokers cannot smoke which may contribute to sustained dependence and continued use of tobacco products. However, some of these products may lead to reduced health risks if smokers were able to switch completely to using these products and may lead to eventual cessation of all tobacco products.

This chapter assesses the role of tobacco smoking as a cause of premature mortality in Europe, and its contribution to the health gap between the EU10 and EU15 countries, using several complementary approaches. It reviews the history of tobacco smoking in the EU10 countries and analyses the patterns of tobacco smoking. Since lung cancer is the cause of death most strongly associated with tobacco smoking, the chapter also analyses temporal trends in lung cancer mortality in Europe. Finally, it estimates the mortality attributable to tobacco smoking in the EU countries.

This chapter reviews studies on the link between smoking and cervical cancer. Epidemiologic evidence strongly links smoking with squamous cell cervical cancer and high-grade cervical intraepithelial neoplasia (CIN). However, some controversy still exists as to whether the link is causal or in some way reflects residual confounding with unmeasured aspects of sexual behaviour, although the case for causality has strengthened considerably in the past few years. Attempts to adjust for sexual behaviour through variables such as age at first intercourse and number of sexual partners have generally reduced the strength of the relationship with smoking, but it has not disappeared: it remains at or above two-fold for current-smokers and shows a dose-response relationship in many studies.

This chapter reviews studies on the link between smoking and cardiovascular disease. The smoking of tobacco is a major independent risk factor for life-threatening diseases in all four principal arterial territories. The totality of the evidence indicates that this relationship goes beyond statistical association to one of cause-and-effect. Most importantly, compared with other factors such as hypertension, hypercholesterolaemia, and lack of physical activity, cessation of smoking requires a once-only change on the part of the individual, and a change to non-smoking is followed by a rapid and complete disappearance of the excess risk of ischaemic heart disease and stroke, the two most common fatal manifestations of arterial disease.

This chapter begins with a discussion of the development of tobacco smoking and the factors leading to the shift to the fashion for cigarettes. It then discusses the impact of tobacco on health, the spread of the smoking epidemic, and future expectations for countries with increased cigarette consumption.

This chapter reviews studies on the link between smoking and chronic obstructive pulmonary disease (COPD). Cigarette smoking is the dominant cause of chronic obstructive pulmonary disease for both men and women. Changes in the lungs of smokers can be demonstrated within a few years of beginning to smoke. By the age 25–34 years, evidence of functional loss is evident in populations of heavy-smokers. The risks of developing ventilatory impairment and of dying of COPD increase with increasing number of cigarettes smoked per day and increased duration of smoking. Cessation of smoking alters the rate of lung function decline and risk of dying from COPD, but the benefits of cessation are greatest when cessation can be achieved early before substantial lung injury has occurred.

This chapter presents an overview of the effects of smoking on other disorders, using published reviews and the results of published meta-analyses where available. Smoking is a risk factor for many chronic and non-fatal disorders other than cancer, respiratory, and cardiovascular diseases. It is associated with significant morbidity, which significantly impairs quality of life. Disorders associated with smoking include peptic ulcer, Crohn's disease, psoriasis, hip fracture, and type 2 diabetes.

Tobacco control policy has evolved over time and will continue to do so. To every action by the tobacco industry there has been a reaction by public health authorities and vice versa. As a result there has been a continuing struggle between those committed to market expansion (the industry) and those committed to market shrinkage (public health authorities). This chapter considers the following issues: prevention of smoking initiation; management of addiction; regulation of the cigarette, the way it is sold, its nicotine content and its emissions; protection of non-smokers from second-hand smoke; public education and control of labelling and trademarks; disincentives to purchase (tax) and restrictions on sales to minors. The chapter will summarize what is, in effect, modern comprehensive policy.