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This chapter provides an update on the epidemiology of lung cancer with an emphasis on the rapidly expanding literature exploring host susceptibility to tobacco carcinogenesis. It also reviews chemoprevention and lung screening trials.

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 provides an overview of the evidence on the connections between outdoor and indoor air pollution and lung cancer, as well as other types of malignancy. The evidence on air pollution and lung cancer is now extensive and the review in this chapter is selective, emphasizing the most recent findings, primarily from the epidemiologic literature.

This chapter reviews studies on the link between vitamin A and lung cancer. These include prospective studies, case-control studies, studies of blood vitamin A levels and risk of lung cancer, nested case control studies of blood carotene levels and lung cancer, and randomized trials. The inverse relationship between the intake of fruits and vegetables and the risk of lung cancer, which has been found in many case-control studies and cohort studies using both questionnaire and biochemical measurements of intake, represents one of the best established associations in the field of nutritional epidemiology.

This chapter discusses the smoking and lung cancer within the context of public health in the 1950s. It argues that smoking was the exemplar of what came to be the main style of post-war public health. Such a style emphasized the role of individual behaviour, legitimated through population-based epidemiology, as the dominant focus.

Lung cancer is the most common cancer worldwide, ranking first in men and third in women for new cases and first in both sexes for deaths. Dynamic global patterns in incidence predominantly reflect past and current patterns of cigarette smoking. Incidence rates in most high-income countries have decreased substantially among men but are increasing among women. More than half of all cases occur in economically developing countries where smoking remains common, especially among men. Strong birth cohort patterns dominate temporal trends in high-income countries; these parallel birth cohort patterns in the uptake in cigarette smoking, fifty years earlier. Unlike smoking cessation, which dramatically reduces risk, design changes in cigarettes provide no health benefit. Active cigarette smoking accounts for an estimated 95% of lung cancer cases among smokers and 82% in the general population of the United States; secondhand smoke causes an estimated 7,700 lung cancer deaths among never smokers.

Supportive care is a major component in the management of malignant diseases that affect the respiratory system. It should be included in the overall management plan for the patient from the very outset. Many patients who present with new respiratory or systemic symptoms of lung cancer will need urgent palliation of these problems, even before a definitive histological diagnosis can be made. Indeed, some patients who present late with advanced disease may be too ill for invasive diagnostic investigations, and palliative interventions will be planned on the basis of a working diagnosis of lung cancer, guided on radiological findings and clinical history. This chapter discusses the prevalence of symptoms in cancer, causes and assessment of symptoms in cancer, approaches to symptom management, technical advances in radiotherapy delivery, chemotherapy, comprehensive palliation of symptoms, and management of effusions.

Lung cancer is the most commonly diagnosed cancer among men in most countries, and is the primary cause of cancer death in men and women. Its epidemic increase in incidence began in the first half of the twentieth century, paralleling the uptake of cigarette smoking that occurred 20 years before. A series of landmark studies beginning in 1950 established tobacco as the primary cause of lung cancer. Current smokers have a 10- to 20-fold higher lung cancer risk compared to never smokers. Important for prevention, former smokers substantially reduce this excess risk 5 years after smoking cessation. Exposure to secondhand smoke, a well-established risk factor for lung cancer, has a 20%–25% higher risk for those exposed. There are several occupational exposures associated with lung cancer, including asbestos. Despite the success in defining lung cancer’s etiology, this highly preventable disease remains among the most common and most lethal cancers globally.

Vitamin A has long been recognized to play a central physiologic role in the regulation of cell differentiation. Because loss of differentiation is a basic feature of malignancy, vitamin A may be related to cancer incidence. In numerous animal studies, naturally occurring preformed vitamin A and synthetic analogs have inhibited the occurrence of induced tumors and even reversed metaplastic changes. This chapter describes the unfolding of evidence on vitamin A and lung cancer, both because of the potential importance of the hypothesis and what it has taught us about nutritional epidemiology. Even today, the story is taking another twist with the potential integration of genetic and dietary data on this topic.

This chapter employs the indirect smoking impact ratio method (Peto et al. 1992), which uses absolute lung cancer mortality in a population as a marker for accumulated hazards of smoking, to estimate the global impact of smoking on coronary heart disease (CHD) mortality. In 2000, an estimated 873,000 people died from CHD in the world due to smoking, accounting for 15% of global adult CHD mortality. This figure represents a significant proportion of the more than 4.8 million smoking-attributable deaths in 2000. Of these deaths, 359,000 were in developing countries, marking a transition to an era in which smoking kills a comparable number of people from CHD in developing countries as in industrialized nations.

The Surgeon General's Report of 1964 marks a watershed in the history of public health. Following its publication, both the science and the practice of public health were visibly transformed. This chapter traces the clinical and epidemiological progress in knowledge about smoking and health harm, and the institutional history of the Report. In establishing cigarette smoking as the preeminent public health issue of the second half of the 20th century, the federal government established new responsibilities and authority for science and health in the consumer culture. Surgeons General since have used the authority of their office to shape the policy context of subsequent tobacco regulation.

The introduction to discrete irreversible processes in Chapter 13 noted that there are two important examples of groups of diseases that follow this pattern: immune sensitization and carcinogenesis. Unfortunately, much less is known about the intermediate steps in sensitization, and few examples of biologically based models have been applied to studies of immune diseases in humans, as was noted. This chapter discusses carcinogenesis, which has been more extensively studied.

This chapter discusses the effects of smoking cessation on lung cancer mortality and on all-cause mortality in Europe and North America, under-estimation of eventual hazards of smoking and benefits of stopping in many studies of other populations, contrasting national trends in tobacco-attributed mortality at ages 35-69, and worldwide trends in smoking.

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 provides an overview of causal inference, focusing on the interpretation of epidemiologic data on cancer risk. It begins with an introduction to the centuries-old discussion on cause and causation and next considers the epidemiologic concept of causation, setting the discussion in the context of current understanding of carcinogenesis as a multistep process. The criteria for causation, often attributed to the British medical statistician Sir Austin Bradford Hill (Hill, 1965) or to the 1964 Report of the U.S. Surgeon General on tobacco (US Department of Health Education and Welfare—DHEW, 1964), have provided a framework for evaluating evidence to judge the causality of associations. These criteria are addressed in depth, and their application is illustrated with the example of smoking, both active and passive, and lung cancer. The chapter concludes with a consideration of emerging issues concerned with causation, including the interpretation of data coming from the new technologies of contemporary “molecular epidemiology” and new approaches to evaluating causation.

This chapter examines the ways in which public health information is communicated to the public and evaluates public health educational initiatives. It argues that the information concerning the relationship between smoking and lung cancer can convey the wrong messages. It discusses health promotion in relation to smoking and highlights the difficulties and dilemmas of health messages even where epidemiological evidence is strong. It contends that health education should be judged by the success with which it leads to people holding accurate beliefs.

This chapter focuses on lung cancer or the carcinoma of the bronchial tree, which is often associated with smoking and mesothelioma, or the malignancy arising from the pleural or peritoneal surfaces due to exposure to asbestos. The first section focuses on lung cancer, with discussions on its pathology and natural history, its prognosis, its common symptoms, and its symptom management. The second section of the chapter describes mesothelioma and discusses its history, clinical features, symptoms, and symptom management. A case history and practice points are provided at the end of the chapter.

It has become fashionable to start discussions of disease related to fibrous inorganic materials by referring to Pliny the Younger (A.D. 61-114), who commented in a letter on the sickness of slaves who worked with asbestos. His observation was forgotten, as evidenced by the fact that during the Middle Ages, Paracelsus (1493–1541) as well as Agricola (1494–1556) wrote extensively on “miner’s disease” without mentioning asbestos. Later, Zenker (1867) coined the word pneumo(no)coniosis to describe the diseases endemic to coal and iron miners. Differential diagnosis of the pulmonary disorders, tuberculosis, silicosis, pneumonia, and other lung disease was attempted thereafter, although the varieties were often confused even by experienced physicians. The industry that provided asbestos to modern society started at about this same time (in the 1870s). The first indication of pulmonary disorder in an asbestos worker came in an autopsy report of fibrosis by Dr. Montague- Murray at Charing Cross Hospital, London, in 1899–1900 (Peters and Peters, 1980). By 1902 asbestos was included in the list of dusts considered injurious by the Lady Inspector of Factories, Adelaide Anderson (Oliver, 1902). Auribault (1906) appears to have been the first to note high mortality in workers in an asbestos mill and weaving establishment, but he attributed their illness to calcium carbonate dust rather than asbestos. Scarpa (1908) believed the pulmonary disease of 30 asbestos workers was caused by tuberculosis, and Fahr (1914), who published the case of a female asbestos worker who died of “pleuro-pneumonia . . . with a large number of crystals in pulmonary tissue of a peculiar nature,” was clearly somewhat mystified at the presence of nonbiological materials. It was Cooke (1924, 1927, 1929) who first defined asbestos as a specific etiologic agent in pulmonary fibrosis. He described extensive fibrosis with thickened pleura and adhesions to the chest wall and pericardium in asbestos workers and noted the presence of abundant mineral matter (“curious bodies”), but also tubercular lesions. The term asbestosis was used in the 1927 publication. Pancoast and Pendergrass (1925) argued that the fibrosis seen in asbestos workers was a result of ad-mixed silica and an expression of “asbestosilicosis,” signifying uncertain etiology of the observed symptoms, a view that survivied into the 1930s (Lynch and Smith, 1935).

This chapter considers the magnitudes of risk for the development of asbestosis, malignant mesothelioma (MM), and lung cancer (LC) resulting from exposure to different airborne concentrations of asbestos. Information on risk is obtained from epidemiological studies. The risk analysis requires three components: (i) the level of exposure, (ii) cases that have occurred, and (iii) factors that might confound or modify the exposure-response relationship.