Epidemiological novelties in lung cancer

Lung cancer is the most common cause of cancer-related mortality throughout the world representing around 18% of the total. There is still a male predominance but this is becoming less pronounced and in the US, lung cancer is now the most common cause of cancer-related mortality in women. In France, it had risen to second place in women in 2005 after having been in 6th place in 1975. Median age at diagnosis differs according to countries and health system and is around 70 years in the US and around 65 years in France. The distribution of histological subtypes has changed considerably during recent decades with an increasing frequency of adenocarcinoma at the expense of squamous cell carcinoma. The main risk factor for lung cancer remains active tobacco smoking but the attributable risk of smoking varies from one country to another and according to gender. In Japan, the great majority of lung cancer in women is not attributable to active tobacco smoking. Environmental tobacco smoke exposure has a less important role than active tobacco smoking although it is not negligible. The specific impact of smoking cannabis is difficult to assess precisely as, in most cases, it is mixed with tobacco. However, despite important differences with tobacco smoke, cannabis exposure doubles the risk of developing lung cancer. Occupational risk factors have for a long time been neglected and thus occupational lung cancers have been under-reported. Finally, lung cancer in never-smokers is driving considerable interest as it represents by itself the 7th largest cause of mortality due to cancer. Risk factors involved might be air pollution (indoors and outdoors) but also hormone replacement therapy in women.     

Epidemiology of pancreatic cancer

Cancer of the pancreas remains one of the deadliest cancer types. Based on the GLOBOCAN 2012 estimates, pancreatic cancer causes more than 331000 deaths per year, ranking as the seventh leading cause of cancer death in both sexes together. Globally, about 338000 people had pancreatic cancer in 2012, making it the 11~(th) most common cancer. The highest incidence and mortality rates of pancreatic cancer are found in developed countries. Trends for pancreatic cancer incidence and mortality varied considerably in the world. A known cause of pancreatic cancer is tobacco smoking. This risk factor is likely to explain some of the international variations and gender differences. The overall five-year survival rate is about 6%(ranges from 2% to 9%), but this vary very small between developed and developing countries. To date, the causes of pancreatic cancer are still insufficiently known, although certain risk factors have been identified, such as smoking, obesity, genetics, diabetes, diet, inactivity. There are no current screening recommendations for pancreatic cancer, so primary prevention is of utmost importance. A better understanding of the etiology and identifying the risk factors is essential for the primary prevention of this disease.     

Lung cancer epidemiology and risk factors in Asia and Africa.

In industrialised countries, lung cancer is the most common form of cancer among males and it is growing among females. For both sexes, rates reflect smoking behaviours. The pattern appears to be different in Asia, particularly in China, where lung cancer rates in men reflect high smoking rates but high rates among non-smoking women appear to be related to other factors. The incidence of lung cancer is low in most African countries, but it is increasing. In addition to tobacco smoking, a number of etiological factors have been identified for lung cancer: indoor exposure to environmental tobacco smoke, cooking oil vapour, coal burning, or radon, outdoor air pollution and occupational exposure to asbestos and other carcinogens. Recent studies have shown that dietary factors may be important, with high consumption of vegetables and fruits being protective while preserved food and fatty food are harmful, and certain infections such as Mycobacterium tuberculosis, human papilloma virus and Microsporum canis are associated with a high risk of lung cancer. Among non-smokers, the probable role of genetic predisposition in lung cancer by increasing the individual's susceptibility to environmental carcinogens is currently being studied actively. As the single most important cause for lung cancer is tobacco smoke and, with increased sales, a major epidemic is predicted for both Asia and Africa, all health care professionals, government health authorities and national and international health organisations must join in a concerted effort against tobacco.     

Smoking and cardiovascular disease

Tobacco, especially cigarette, smoking is a major cause of cardiovascular disease (CVD), responsible for about one third of all CVD deaths in most Western populations. The risk of CVD death increases with increasing exposure to cigarette smoke, as measured by the number of cigarettes smoked daily, the duration of smoking, the degree of inhalation and the age of initiation. The relative risk for CVD is substantially greater in early adult life than in old age, and is associated more strongly with cigarettes than with other types of tobacco. Exposure to environmental tobacco smoke in never-smokers is also associated with 20-30% excess risk of coronary heart disease. There is convincing evidence that stopping smoking works, even after a heart attack, and that the excess risk declines fairly rapidly, with the risk approaching the level of never-smokers within about 10 years of quitting. Although the smoking prevalence has declined dramatically over the last few decades in many Western populations, it is increasing rapidly in most developing countries, with an emerging epidemic of tobacco related death.     

Lung cancer: epidemiology, etiology, and prevention

Lung cancer is the leading cause of cancer death in the United States and around the world. A vast majority of lung cancer deaths are attributable to cigarette smoking, and curbing the rates of cigarette smoking is imperative. Understanding the epidemiology and causal factors of lung cancer can provide additional foundation for disease prevention. This article focuses on modifiable risk factors, including tobacco smoking, occupational carcinogens, diet, and ionizing radiation. It also discusses briefly the molecular and genetic aspects of lung carcinogenesis.     

Risk from tobacco and potentials for health gain.

Evidence that smoking tobacco harms health has accumulated over 200 years, but was largely ignored before 1950, when five case-control studies associated smoking with the development of lung cancer. The idea that it might cause the disease was greeted with scepticism, and it was nearly 10 years before it became generally accepted. By then there had been additional evidence from cohort studies, and known carcinogens had been identified in tobacco tars. Cigarette smoking has now been positively associated with some 40 causes of death and negatively associated with eight or nine. A few of the associations are due to confounding, but the great majority reflect causality. In several instances cigarette smoking increases the risk of death ten-fold, and altogether it doubles the annual risk of death at all ages combined, in both sexes. Tobacco smoke in the environment also has a small effect on the health of non-smokers, particularly in infancy and childhood, but also to some extent later in life. Nearly a quarter of all deaths in men and a tenth in women in industrialised countries in 1990 were attributed to smoking, giving a total of 1.8 million a year. In 20-30 years' time the total is estimated to rise to 10 million a year, with 7 million in low income countries, if smoking habits persist unchanged.     

Chronic obstructive pulmonary disease and lung cancer: common pathogenesis, shared clinical challenges

Environmental inhaled noxious particles have been known to play a role in several lung diseases, including chronic obstructive pulmonary disease (COPD) and lung cancer, the deadliest malignancy in the world in both sexes. Of the known noxious agents, tobacco smoking is the leading preventable cause of death worldwide and is a recognized risk for the development of both diseases. The association between COPD and lung cancer has been demonstrated in population-based studies, lung cancer screening programs, epidemiological surveys, and case control and biological mechanistic studies. There is evidence that cumulative smoking history is associated with the risk of developing lung cancer and COPD; however, the majority of smokers do not develop clinical COPD or lung cancer. This suggests the presence of one or several factors that modulate the responses to the offending agents and define the final risk for disease development. The 54th Aspen Lung Conference was convened to provide a forum for a systematic dissection of the potential mechanisms by which persons exposed to the causative agents are able to handle and control the process or, in the case of dysfunctional response, the mechanisms that take off in different directions and result in injury and disease. This summary reviews the themes presented and attempts to integrate them for those clinicians and researchers interested in these topics. The challenges and future directions emanating from the discussions may help frame future conferences and hopefully inspire the interest of young researchers.     

Exposing a deadly alliance: Novel insights into the biological links between COPD and lung cancer

Chronic obstructive pulmonary disease (COPD) affects more than 200 million people worldwide and is expected to become the third leading cause of death in 2020. COPD is characterized by progressive airflow limitation, due to a combination of chronic inflammation and remodeling of the small airways (bronchiolitis) and loss of elastic recoil caused by destruction of the alveolar walls (emphysema). Lung cancer is the most important cause of cancer-related death in the world. (Cigarette) smoking is the principal culprit causing both COPD and lung cancer; in addition, exposure to environmental tobacco smoke, biomass fuel smoke, coal smoke and outdoor air pollution have also been associated with an increased incidence of both diseases. Importantly, smokers with COPD – defined as either not fully reversible airflow limitation or emphysema – have a two- to four-fold increased risk to develop lung cancer. In this review, we highlight several of the genetic, epigenetic and inflammatory mechanisms, which link COPD and carcinogenesis in the lungs. Elucidating the biological pathways and networks, which underlie the increased susceptibility of lung cancer in patients with COPD, has important implications for screening, prevention, diagnosis and treatment of these two devastating pulmonary diseases.     

Smoking and lung cancer

Nowadays, around one-third of adults are known to be smokers, and smoking rates are increasing among the female population. It is estimated that deaths attributable to tobacco use will rise to 10 million by 2025, and one-third of all adult deaths are expected to be related to cigarette smoking. The association between cigarettes and lung cancer has been proven by large cohort studies. Tobacco use has been reported to be the main cause of 90% of male and 79% of female lung cancers. 90% of deaths from lung cancer are estimated to be due to smoking. The risk of lung cancer development is 20-40 times higher in lifelong smokers compared to non-smokers. Environmental cigarette smoke exposure and different types of smoking have been shown to cause pulmonary carcinoma. DNA adducts, the metabolites of smoke carcinogens bound covalently with DNA, are regarded as an indicator of cancer risk in smokers. In recent decades, there has been a shift from squamous and small cell lung cancer types to adenocarcinoma, due to increasing rates of smoking among female population and rising light cigarette usage. After smoking cessation, the cumulative death risk from lung cancer decreases. Patients who continue smoking experience greater difficulties during cancer treatment. Stopping smoking may prolong survival in cancer patients, and also decreases the risk of recurrent pulmonary carcinoma. In order to save lives and prevent smoking related hazards, physicians should advise both healthy individuals and those with cancer of the benefits of stopping smoking.     

Genetic susceptibility to lung cancer

Lung cancer is the most common cause of cancer death in the world. Environmental factors, particularly cigarette smoking, are of paramount importance in determining lung cancer risk. Lung cancer and chronic obstructive lung disease are likely to share some common susceptibility genes, but these have not yet been identified. Evidence from various sources, including twin studies, segregation analyses, and case-control studies, support a heritable component to lung cancer risk in humans. As with many common diseases, susceptibility genes for lung cancer appear to be of low penetrance. Family studies of lung cancer susceptibility using linkage analysis and positional cloning have not been reported; however, a consortium is currently carrying out such studies, and results may soon be available. Association studies support lung cancer risk being partly determined by genes that control the metabolism of carcinogens found in tobacco smoke, with the heritable effects being most prominent in smokers with shorter smoking histories. Of these, the CYP1A1 and GSTM1 polymorphisms have been most consistently implicated. In the mouse, an oligonucleotide repeat polymorphism within an intron of the Ki-ras oncogene is the major lung cancer susceptibility locus; however this locus is not clearly involved in susceptibility to lung cancer in the human. Further understanding of the genetic basis of lung cancer susceptibility has many important implications, ranging from targeting prevention and screening efforts to the most highly susceptible population to developing novel chemopreventive therapies.     

Tobacco use disorder and the lungs

This narrative review provides a summary of the impact of tobacco smoking on the respiratory system and the benefits of smoking cessation. Tobacco smoking is one of the leading preventable causes of death world-wide and a major risk factor for lung cancer and chronic obstructive pulmonary disease. Smoking is also associated with an increased risk of respiratory infections and appears to be related to poorer outcomes among those with COVID-19. Non-smokers with second-hand smoke exposure also experience significant adverse respiratory effects. Smoking imposes enormous health- and non-health-related costs to societies. The benefits of smoking cessation, in both prevention and management of respiratory disease, have been known for decades and, to this day, cessation support remains one of the most important cost-effective interventions that health professionals can provide to people who smoke. Cessation at any age confers substantial health benefits, even in smokers with established morbidities. As other treatments for chronic respiratory disease advance and survival rates increase, smoking cessation treatment will become even more relevant. While smoking cessation interventions are available, the offer of these by clinicians and uptake by patients remain limited.     

Pharmacologic Agents for Tobacco Dependence Treatment: 2011 Update

Tobacco use remains the most important worldwide cause of preventable death due mainly to cancer, cardiovascular disease, and chronic lung disease. If the current tobacco pandemic continues for another 20 years, the annual global tobacco-attributable mortality will exceed 8 million. In the US and many European countries, public health and tobacco control efforts combined with effective tobacco dependence treatment using combined behavioral treatment and pharmacotherapy have contributed significantly to steadily declining rates of tobacco use. Subsequent declines in cardiovascular disease and lung cancer death rates are directly attributable to these lower rates of tobacco use. Despite smoking bans, health warnings and effective pharmacotherapy, one in five Americans continue to smoke. Continued research in tobacco dependence treatment has resulted in newer and more effective pharmacotherapy. In this review, we provide a current update of pharmacologic agents for tobacco dependence treatment and a discussion of recent controversy regarding adverse effects of some these medications.     

Environmental tobacco smoke and cardiovascular disease. A position paper from the Council on Cardiopulmonary and Critical Care, American Heart Association.

Although the number of cardiovascular deaths associated with environmental tobacco smoke cannot be predicted with absolute certainty, the available evidence indicates that environmental tobacco smoke increases the risk of heart disease. The effects of environmental tobacco smoke on cardiovascular function, platelet function, neutrophil function, and plaque formation are the probable mechanisms leading to heart disease. The risk of death due to heart disease is increased by about 30% among those exposed to environmental tobacco smoke at home and could be much higher in those exposed at the workplace, where higher levels of environmental tobacco smoke may be present. Even though considerable uncertainty is a part of any analysis on the health affects of environmental tobacco smoke because of the difficulty of conducting long-term studies and selecting sample populations, an estimated 35,000-40,000 cardiovascular disease-related deaths and 3,000-5,000 lung cancer deaths due to environmental tobacco smoke exposure have been predicted to occur each year. The AHA's Council on Cardiopulmonary and Critical Care has concluded that environmental tobacco smoke is a major preventable cause of cardiovascular disease and death. The council strongly supports efforts to eliminate all exposure of nonsmokers to environmental tobacco smoke. This requires that environmental tobacco smoke be treated as an environmental toxin, and ways to protect workers and the public from this health hazard should be developed. According to a 1989 Gallup survey commissioned by the American Lung Association, 86% of nonsmokers think that environmental tobacco smoke is harmful and 77% believe that smokers should abstain in the presence of nonsmokers.(ABSTRACT TRUNCATED AT 250 WORDS)     

Passivrauchen als Gesundheitsrisiko

Environmental tobacco smoke (ETS) is the third leading but preventable cause of death worldwide. It is associated with increased risks of obstructive airway diseases, lung cancer, and cardiovascular disease. Dose-response relationships are mostly linear in airway diseases, while they are mainly non-linear in cardiovascular morbidity and mortality. Public smoking bans have been shown to reduce ETS-associated morbidity and mortality.     

Chronic obstructive pulmonary disease in women: exploring gender differences

PURPOSE OF REVIEW: Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality throughout the world. This major public health threat is ranked twelfth as a worldwide burden of disease and is projected to rank fifth by the year 2020 as a cause of lost quantity and quality of life. The impact of this disease in women is significantly understudied but the evidence that does exist reveals potentially substantial gender differences in the susceptibility to, severity of, and response to management of COPD. RECENT FINDINGS: The best known risk factor for the development of COPD is tobacco smoking. While smoking rates in women have largely stabilized in developed countries, the rates are continuing to climb in developing countries. While it is not clear whether women are more susceptible to the toxic effects of cigarette smoke than men, it is known that the incidence and prevalence of COPD will continue to climb as more women smoke. Other known risk factors for the development of COPD include air pollution, infections, occupational exposures, and genetic factors. Air pollution, particularly fine particulate indoor air pollution from biomass fuels disproportionately affects women. Infections such as human immunodeficiency virus (HIV) and tuberculosis (TB) disproportionately affect vulnerable populations such as poor women and occupational exposures to various dusts and toxins are often gender specific. Genetic factors are still being explored but there seems a preponderance of women who are affected by early-onset and non-smoking related COPD. Women with COPD also seem to be underdiagnosed by physicians and may have different responses to medical treatment, smoking cessation interventions, and pulmonary rehabilitation programs. SUMMARY: Chronic obstructive pulmonary disease in women is an understudied subject but is gaining attention as a significant public health threat. In developed countries, efforts at preventing the initiation of tobacco smoking and targeting smoking cessation programs in women are needed. In developing countries, efforts to promote cleaner fuels, improved stoves, better home ventilation, reduce toxic dust and fume exposures, combat infectious diseases such as TB and HIV, and improve nutrition are all ways in which the lung health of women can be improved.     

Chronic obstructive pulmonary disease and lung cancer: new molecular insights

Both chronic obstructive pulmonary disease (COPD) and lung cancer are major causes of death worldwide. In most cases this reflects cigarette smoke exposure which is able to induce an inflammatory response in the airways of smokers. Indeed, COPD is characterized by lower airway inflammation, and importantly, the presence of COPD is by far the greatest risk factor for lung cancer amongst smokers. Cigarette smoke induces the release of many inflammatory mediators and growth factors including TGF-β, EGFR, IL-1, IL-8 and G-CSF through oxidative stress pathways and this inflammation may persist for decades after smoking cessation. Mucus production is also increased by these inflammatory mediators, further linking airway inflammation to an important mechanism of lung cancer. A greater understanding of the molecular and cellular pathobiology that distinguishes smokers with lung cancer from smokers with and without COPD is needed to unravel the complex molecular interactions between COPD and lung cancer. By understanding the common signalling pathways involved in COPD and lung cancer the hope is that treatments will be developed that not only treat the underlying disease process in COPD, but also reduce the currently high risk of developing lung cancer in these patients.     

Recomendações de 2019 para a redução do consumo de tabaco nos países de língua portuguesa

After several decades of initiatives at international and national level inspired by the World Health Organization, tobacco consumption is still the second leading cause of death in the world and the leading cause of premature death and disability, as a result of various types of cancer and pulmonary, cerebrovascular and cardiovascular disease.Tobacco consumption is also an important public health issue in Portuguese‐speaking countries, which fully justifies the launch and implementation of these 2019 recommendations for reducing tobacco consumption in Portuguese‐speaking countries by the Federation of Portuguese Language Cardiology Societies.This position statement reviews recent changes in and the present epidemiology of tobacco consumption in the Portuguese‐speaking countries, discusses the negative health impact of new forms of tobacco consumption, and addresses available prevention and drug treatment strategies.Eliminating smoking requires a coordinated effort between various national and international bodies, with a policy approach in each country focusing on laws, education campaigns for primary prevention aimed at to the general public, particularly to encourage young people not to start smoking, and a health system approach to help smokers quit smoking permanently by a combination of drug treatment and cognitive behavioral therapy. The aim is to control the only cardiovascular risk factor that can be completely eliminated.This position statement aims to alert health professionals to the need to approach the subject of smoking cessation with patients and their families during hospitalizations and outpatient consultations, and to provide them with up‐to‐date knowledge on how to quit smoking and maintain control of this risk factor in the long term.     

Tobacco smoking and new developments in public health and clinical interventions

The public policy environment regarding tobacco use in the United States has experienced a dramatic change during the past year. Along with calls for regulatory review of cigarettes, important new scientific information has become available regarding the health effects of environmental tobacco smoke and the efficacy of nicotine replacement therapy, which is used to support smoking cessation efforts. Specifically, recent studies have suggested that environmental tobacco smoke exposure increases risk for coronary heart disease in nonsmoking adults in addition to causing lung cancer and other respiratory diseases. Children are exposed to environmental tobacco smoke at home and in public, resulting in increased risk of bronchitis, pneumonia, bronchial hyperresponsivity, and sudden infant death syndrome. In a climate of increasing concern about the direct and indirect effects of tobacco smoke, three independent meta-analyses concluded that nicotine replacement therapy increased smoking cessation efficacy two- to threefold. In addition, research is beginning to identify factors associated with successful and unsuccessful cessation attempts using nicotine replacement therapy, resulting in the possibility of individualized treatments and clinical interventions designed for maximum efficacy.     

Environmental tobacco smoke and lung cancer incidence.

Tobacco smoking has been irrefutably linked to lung cancer risk. Exposure to environmental tobacco smoke and lung cancer risk has been more controversial. Various sources have claimed confounding factors such as diet and classification bias could account for the reported link. We review the available evidence and some recent papers on this topic and conclude that the evidence linking environmental tobacco smoke and lung cancer is unequivocal and cannot be explained by confounding factors.