Tobacco in Australia Facts & Issues A comprehensive online resource
tobaccoinaustralia.org.au Book excerpt
List of chapters available at tobaccoinaustralia.org.au Introduction Chapter 1 Trends in the prevalence of smoking Chapter 2 Trends in tobacco consumption Chapter 3 The health effects of active smoking Chapter 4 The health effects of secondhand smoke Chapter 5 Factors influencing the uptake and prevention of smoking Chapter 6 Addiction Chapter 7 Smoking cessation Chapter 8 Tobacco use among Aboriginal peoples and Torres Strait Islanders Chapter 9 Smoking and social disadvantage Chapter 10 The obaccot industry in Australian society Chapter 11 Tobacco advertising and promotion Chapter 12 The construction and labelling of Australian cigarettes Chapter 13 The ricingp and taxation of tobacco products in Australia Chapter 14 Social marketing and public education campaigns Chapter 15 Smokefree environments Chapter 16 Tobacco litigation in Australia Chapter 17 The economics of tobacco control Chapter 18 The WHO Framework Convention on Tobacco Control Appendix 1 Useful weblinks to tobacco resources
Tobacco in Australia: Facts and Issues. A comprehensive review of the major issues in smoking and health in Australia, compiled by Cancer Council Victoria. First edition published by ASH (Australia) Limited, Surry Hills, NSW, 1989 Second edition published by the Victorian Smoking and Health Program, Carlton South, Victoria (Quit Victoria), 1995 Third (2008) and fourth (2012) editions, and ongoing updating, published by Cancer Council Victoria in electronic format only. ISBN number: 978-0-947283-76-6 Suggested citation: Scollo, MM and Winstanley, MH. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2016. Available from www.TobaccoInAustralia.org.au OR
Chapter 3 The health effects of active smoking Chapter 3: The health effects of active smoking 1 Chapter 3 The health effects of active smoking
Margaret Winstanley Table of contents
3.0 Introduction Further updates marked per section 3.1 Smoking and heart disease
3.2 Respiratory diseases
3.3 Smoking and cancer
3.4 Lung cancers
3.5 Other cancers
3.6 Reproductive health
3.7 Pregnancy and smoking
3.8 Child health and maternal smoking before and after birth
3.9 Increased susceptibility to infection in smokers
3.10 Eye diseases
3.11 Dental diseases
3.12 Gastro-intestinal diseases
3.13 Musculoskeletal disease
3.14 Skin
3.15 The impact of smoking on treatment of disease
3.16 Smoking and diabetes Tobacco in Australia: 2 Facts and Issues
3.17 Inflammatory conditions and autoimmune disease
3.18 Other conditions with possible links to smoking
3.19 Smoking and accidents
3.20 Tobacco poisoning
3.21 Health effects for younger smokers
3.22 Poorer quality of life and loss of function
3.23 Smoking, dementia and cognitive decline
3.24 Genetic influences on tobacco-caused disease
3.25 Smoking compared with or in combination with other pollutants
3.26 Health effects of brands of tobacco products which claim or imply, delivery of lower levels of tar, nicotine and carbon monoxide
3.27 Health effects of smoking tobacco in other forms
3.28 Health ‘benefits’ of smoking?
3.29 Smoking and body weight
3.30 Deaths attributable to tobacco by disease category
3.31 Morbidity and mortality due to tobacco-caused disease and socio-economic disadvantage
3.32 Health effects of smoking other substances
3.33 Health effects of chewing tobacco, and of other smokeless tobacco products
3.34 Public perceptions of tobacco as a drug, and knowledge and beliefs about the health consequences of smoking
3.35 Health and other benefits of quitting
3.36 The global tobacco pandemic Chapter 3: Health Effects » 3.0 Introduction
3.0 Introduction
Last updated: March 2015 Suggested citation: Winstanley, MH & Greenhalgh, EM. 3.0 Introduction. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/chapter-3-health-effects/3-0-background
Smoking of tobacco as we know it today, in the form of manufactured or 'factory-made' cigarettes, became common in Australia in the late 1800s. Pipe and cigar smoking was already widespread among men, but the convenience and ready availability of the cigarette soon made it a popular alternative.1 Manufactured cigarettes were supplied to Australians and their allies in the trenches of World War I,1 and by the end of World War II, nearly three quarters of Australian men and one quarter of women were smokers, the majority using cigarettes (see also Chapter 1, Section 1.1).
Similar changes in smoking behaviour had occurred in Western Europe and North America, and with them, a marked escalation in lung cancer death rates and the growing suspicion that cigarette use was implicated in this trend. By 1950 several studies had been published in the medical literature2 and the finding that cigarette smoking and lung cancer appeared to be causally linked was reported.3,4
Several series of authoritative, landmark reports have since been published by national and international agencies,i documenting the damaging effects of smoking and calling for action to help halt the smoking epidemic. Of these, the most regular series has been that issued by the Office of the US Surgeon General. Since 1964, comprehensive and rigorous reports on various aspects of tobacco and health have been issued by the US Surgeon General, repeating the conclusion that smoking is "the single greatest cause of avoidable morbidity and mortality in the United States," and never finding reason to reverse any earlier conclusions of causality.5
The 2004 report of the US Surgeon General, The Health Consequences of Smoking, published the following four major conclusions:6 1. Smoking harms nearly every organ of the body, causing many diseases and reducing the health of smokers in general. 2. Quitting smoking has immediate as well as long-term benefits, reducing risks for diseases caused by smoking and improving health in general. 3. Smoking cigarettes with lower machine-measured yields of tar and nicotine provides no clear benefit to health. 4. The list of diseases caused by smoking has been expanded to include abdominal aortic aneurysm, acute myeloid leukaemia, cataract, cervical cancer, kidney cancer, pancreatic cancer, pneumonia, periodontitis and stomach cancer.
In addition, the 2014 report of the US Surgeon General, The Health Consequences of Smoking – 50 Years of Progress, published these major conclusions in regard to the health effects of smoking:7 1. The century-long epidemic of cigarette smoking has caused an enormous avoidable public health tragedy. Since the first Surgeon General’s report in 1964 more than 20 million premature deaths [in the U.S] can be attributed to cigarette smoking. 2. The tobacco epidemic was initiated and has been sustained by the aggressive strategies of the tobacco industry, which has deliberately misled the public on the risks of smoking cigarettes. 3. Even 50 years after the first Surgeon General’s report, research continues to newly identify diseases caused by smoking, including such common diseases as diabetes mellitus, rheumatoid arthritis, and colorectal cancer. 4. In addition to causing multiple diseases, cigarette smoking has many other adverse effects on the body, such as causing inflammation and impairing immune function. 5. The burden of death and disease from tobacco use in the United States is overwhelmingly caused by cigarettes and other combusted tobacco products; rapid elimination of their use will dramatically reduce this burden.
3.0.1 Defining causality
The US Surgeon General's reports have provided a detailed review of definitions of causality of disease, and how measures of causality may be applied. Causality is determined by evaluating the range of available evidence and considering it against well-established criteria. The more that an observed association fulfils the criteria, the more likely it is that a causal relationship can be inferred. These criteria are outlined in the US Surgeon General's Report for 2004:8
Consistency: This refers to the persistence of the finding of an association between exposure and outcome in a number of methodologically valid studies undertaken in a range of settings. This helps ensure that possible confounding effects are eliminated, and also increases the statistical validity of the finding through the accumulation of additional evidence.
Strength of association: Strength refers both to magnitude of the association, and to its statistical strength. The greater the measured association and the more sound its statistical basis, the less likely it is that the findings are influenced by chance, bias, or unmeasured or poorly controlled confounding factors. However the observed association must also have a plausible basis in understood biological processes.
Specificity: Specificity refers to the degree to which exposure to the suspected disease causing agent can predict outcome. Other biological and epidemiological factors may need to be taken into account. For example, not all smokers develop lung cancer, and not all cases of lung cancer are caused by smoking. However, the extremely high relative risk for lung cancer in smokers, and the high percentage of lung cancers attributable to smoking, gives the association between smoking and lung cancer "a high degree of specificity".
Temporality: Exposure to the causative factor must precede the onset of the disease. Considered alone, temporality is a poor predictor of causality, but no association can be considered to fulfil the criteria for causality if temporality is not satisfied.
Coherence, Plausibility and Analogy: Taken together, these three criteria require that the proposed causal relationship must not defy known scientific principles, and that it must be biologically plausible and consistent with experimentally demonstrated biological mechanisms and other relevant patterns.
Biologic Gradient (Dose-Response): This criterion refers to the observation of increased effect (for example incidence of disease) in response to increased dose (heavier and/or longer duration of smoking). Meeting this criterion forms a strong support for causality, except in the unlikely event that there is an unidentified confounder, which happens to be varying in the same manner as the observed dose and which could account for the measured association. Virtually all health outcomes causally linked to smoking have demonstrated a dose-response relationship of some description.
Experiment: This criterion refers to naturally occurring "experiments" that might be considered to imitate the conditions of a properly conducted experiment in a scientific environment, and whose outcomes might have the force of a true experiment. An example of a 'natural experiment' in the smoking arena is assessing the health consequences of quitting smoking. To attribute observed improvements in health outcomes to factors other than smoking cessation would necessitate identifying alternative influences and demonstrating that those who continued smoking had also attained a health benefit where that alternative influence was present. The more closely an association fulfils the above criteria, the stronger its claim to causality. Not all inferences of causality will necessarily satisfy all criteria. For example where biological mechanisms may not be completely understood, causality may still be justified by satisfaction of other criteria, such as consistency and strength of association. Those applying the criteria must weigh the all of the scientific evidence and make a multidisciplinary judgement.8
3.0.2 Tobacco—a leading preventable cause of death and disease
Smoking is one of the leading preventable causes of death and disease in Australia, responsible for about 15 000 deaths annually.ii 9,10 In 2003, tobacco caused more than 1 in every 10 deaths in Australia, and taking into consideration sickness and disability as well as deaths, tobacco caused more disease and injury in Australia than any other single risk factor (Table 3.1).9 Tobacco is also responsible for most (90%) of all drug-caused deaths.iii In 2004-05, smoking caused 14 times as many deaths as alcohol, and 17 times the number of deaths due to illicit drug use.10 (see Table 3.0.1).
Table 3.0.1 Deaths attributable to leading selected risk factors in Australia, 2003
Number of Percentage of total deaths Percentage of total burden of Risk factor deaths from all causes disease and injury High blood 22 504 17.0 7.6 pressure Tobacco 15 511 11.7 7.8 High blood 15 351 11.6 6.2 cholesterol Physical inactivity 13 491 10.2 6.6 High body mass 9525 7.2 7.5 Alcohol* 1084 0.8 2.3 *Net effects, i.e. offsetting beneficial effects against harmful effects. Source: compiled from Begg et al.9
It has been conservatively estimated that smoking kills about one half of all persistent users.2 A more recent study puts this figure at closer to two in three.11 Over the decades, the death toll from tobacco use has been vast. In the 50 years from 1960 to 2010, smoking is estimated to have killed 821,000 Australians.12 Tobacco use is also responsible for a global pandemic of death and disease, causing nearly six million deaths a year. More than five million of those deaths are caused by direct tobacco use, while more than 600 000 are caused by exposure to second-hand smoke13 (see Section 3.36). i For example the reports of the US Surgeon General, most of which are available at http://profiles.nlm.nih.gov /NN/Views/AlphaChron/date/10006/ , the Royal College of Physicians of London, some of which may be viewed at http://www.rcplondon.ac.uk/news/smoking.asp, and the Monographs of the International Agency for Research into Cancer at http://monographs.iarc.fr/ENG/Monographs/index.php . ii The most widely used estimate of deaths in Australia is currently that produced for by Begg et al in The burden of disease and injury in Australia, 20036. The estimate used for detailed calculations in the report by Collins and Lapsley 2004/057 is based on figures for a later year but comes up with a similar result (14 901). iii Figures based on estimated number of deaths taking into account deaths prevented (Collins & Lapsley 2004/05 p.52 & p. 56).
References 1. Walker R. Under fire. A history of tobacco smoking in Australia Melbourne: Melbourne University Press, 1984.
2. Doll R, Peto R, Boreham J and Sutherland I. Mortality in relation to smoking: 50 years' observations on male British doctors. British Medical Journal 2004;328:1519-33. Available from: http://www.bmj.com /cgi/reprint/328/7455/1519
3. Doll R and Hill A. Smoking and carcinoma of the lung. British Medical Journal 1950;2:739-48. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2038856/?tool=pubmed
4. Wynder E and Graham E. Tobacco smoking as a possible etiologic factor in bronchogenic carcinoma. Journal of the American Medical Association 1950;143:329-36. Available from: http://www.tobacco.neu.edu /box/BOEKENBox/Journal%20Articles/1950%20Wynder%20Possible%20Etiolog%20Factor.pdf
5. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/
6. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
7. U.S. Department of Health and Human Services. The Health Consequences of Smoking: 50 Years of Progress. A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014, Printed with corrections, January 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/full-report.pdf
8. US Department of Health and Human Services. The health consequences of smoking. A report of the Surgeon General. Rockville, Maryland: US Department of Health and Human Services, Public Health Service, Office of the Surgeon General, 2004. Available from: http://www.surgeongeneral.gov/library /smokingconsequences/
9. Begg S, Vos T, Barker B, Stevenson C, Stanley L and Lopez A. The burden of disease and injury in Australia 2003. PHE 82. Canberra: Australian Institute for Health and Welfare, 2007. Available from: http://www.aihw.gov.au/publications/index.cfm/title/10317
10. Collins D and Lapsley H. The costs of tobacco, alcohol and illicit drug abuse to Australian society in 2004/05. P3 2625. Canberra: Department of Health and Ageing, 2008. Available from: http://www.nationaldrugstrategy.gov.au/internet/drugstrategy/publishing.nsf/Content/mono64/$File /mono64.pdf
11. Banks E, Joshy G, Weber MF, Liu B, Grenfell R, et al. Tobacco smoking and all-cause mortality in a large Australian cohort study: findings from a mature epidemic with current low smoking prevalence. BMC Medicine, 2015; 13(1):38. Available from: http://www.biomedcentral.com/1741-7015/13/38
12. Peto R, Lopez A, Boreham J and Thun M. Mortality from smoking in developed countries 1950-2000. Australia. Oxford: Clinical Trial Service Unit and Epidemiological Studies Unit, University of Oxford, 2006. Available from: http://www.ctsu.ox.ac.uk/~tobacco/C5020.pdf
13. World Health Organization (WHO). Tobacco: Fact sheet No. 339. 2014. Available from: http://www.who.int/mediacentre/factsheets/fs339/en Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.1 Smoking and heart disease
3.1 Smoking and heart disease
Last updated: March 2015 Suggested citation: Briffa, T, Greenhalgh, EM & Winstanley, MH. 3.1 Smoking and heart disease. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-2-cardiovascular-diseases
Cardiovascular disease (CVD) covers all disease processes of the heart and blood vessels. In 2007, 46 623 Australians died from CVD, accounting for just over a third of all deaths in that year.1 CVD is the second largest contributor to the burden of disease in Australia after cancer—estimated at 18% and 19% respectively in 2003.2
Premature CVD is highly preventable. Tobacco smoking, raised blood pressure, elevated blood cholesterol, insufficient physical activity, overweight and obesity, poor nutrition, drinking at harmful levels and diabetes are major preventable risk factors for CVD. There is also recognition that socio-economic and psychosocial factors, such as low income, unemployment, depression and social isolation influence the development of CVD. Disease trends in Australia show that CVD impacts most heavily on population groups that suffer socio-economic disadvantage, including Australia's Aboriginal people and Torres Strait Islanders.1,2
Cigarette smoking contributes to CVD in a number of ways. Toxic products from cigarette smoke, in particular nicotine and carbon monoxide (CO), circulate in the bloodstream, interfering with the efficient working of the endothelium (the inner cellular layer of the arterial wall), eliciting blood fat abnormalities and impairing glucose regulation. Each effect is implicated in the development of atherosclerotic lesions (collections of cholesterol, fat and other matter) in the arterial walls. These collections narrow the arteries, gradually impairing blood flow, and making the arteries harder, less elastic, and more liable to rupture. The process leading to atherosclerosis—plaque (fatty streaks) deposited within the inner layers of the arteries—is slow and complex, often starting in childhood and progressing with age. Smoking also has a direct effect on platelets (blood cells involved in the clotting process), leading to increased activation and stickiness. This in turn causes an increased risk of thrombosis, or development of blood clots.3
Smoking a cigarette also temporarily increases heart rate and blood pressure and also affects the ability of the heart to contract. These circulatory changes result in increased work for the heart muscles, which in turn raises the body's demand for oxygen. At the same time, the body is deprived of oxygen through the effects of CO on reducing transport oxygen. The resulting imbalance in oxygen supply and demand promotes the complications of atherosclerosis. These include ischaemia (lack of oxygen due to poor blood supply), with resultant angina pectoris (chest pain or tightness) or myocardial dysfunction (poor heart muscle function).3,4
While nicotine and CO in tobacco smoke are strongly implicated in the processes leading to development of CVD, other chemicals may also be involved.3 There is now strong evidence that exposure to secondhand cigarette smoke is also a cause of coronary heart disease in non-smokers (see Chapter 4).
3.1.1 Coronary heart disease
Coronary heart disease (CHD), also known as ischaemic heart disease, is the most common form of CVD, and the most common cause of sudden death in Australia.5 It occurs when the arteries supplying the heart become progressively narrowed by a fatty fibrous plaque or atheroma. This reduces the blood flow, forcing the heart to work harder to compensate, and can lead to symptoms of angina. If the plaque breaks up, a blood clot may form, blocking the artery completely. If not promptly treated, this can lead to death of vital heart muscle due to oxygen starvation (termed acute myocardial infarction or heart attack), or, in the worst case, sudden death.3
Smoking is a cause of CHD,3,6 increasing the risk of disease incidence by between two- and four-fold, the risk increasing with heaviness of smoking.7 Smoking in adolescence and young adulthood is also associated with an increased risk of coronary artery atherosclerosis in adulthood.8 Even light smoking significantly increases the risk of dying from CHD, the steepest increase in risk occurring in smokers of up to four cigarettes a day.9
Smokers who have CHD are more likely to die of the disease than non-smokers with the disease. A 2013 study looking at 50-year trends in smoking-related mortality found that although overall death rates from CHD have declined, these declines were proportionately larger for never smokers than for current smokers. The mortality rate was more than three times higher for current smokers compared with never smokers aged between 55 and 74, with two thirds of the deaths among smokers being attributable to their smoking. There was also a significantly increasing risk of CHD mortality for both men and women with increasing consumption through 40 or more cigarettes per day.10 The heaviest burden of excess death due to tobacco- caused CHD is felt in early middle age. In Australia in 2004–05, 40% of all deaths due to CHD occurring in males between the ages of 35 and 39 were due to smoking. Among women aged 40–44, smoking caused about 34% of all deaths due to CHD. The effects of active smoking compared with no exposure are likely to be underestimated because most CVD studies have not excluded persons who had secondhand smoke exposure from the comparison group.
Lower tar and nicotine cigarettes have not been shown to reduce the incidence of CHD due to smokers increasing the number of cigarettes smoked per day or by taking deeper, faster, more or longer puffs. Thus, such cigarettes do not provide a lower risk alternative for smokers who cannot or do not wish to quit.3
The risks of myocardial infarction and death from CHD are lower among former smokers than among continuing smokers. The 2010 report of the US Surgeon General states that the risk halves within the first year and takes between 10–14 years before it approaches that of a lifetime non-smoker.3 The International Agency for Research on Cancer11 describes the benefits of quitting more conservatively:
'... there is a substantial reduction in risk of CHD compared with that of continuing smokers with the first two to four years of smoking abstinence, followed by a slower decline of risk, with risk approaching that of never smokers in fifteen to twenty years. For methodological reasons, the assessment of risk reduction is problematic within the first two years of cessation.'(p 342)
The International Agency for Research on Cancer also cites a reduced risk of 35% within two to four years for persons already suffering from CHD, and says studies on subjects without diagnosed CHD are 'compatible with this conclusion and point toward similar relative risk reduction.' 11(p 336).
3.1.2 Cerebrovascular disease (stroke)
A stroke occurs when blood flow to the brain is interrupted, leading to injury or death of brain tissue. This occurs most commonly because of arterial blockage caused by atherosclerosis or a blood clot, an event known as an ischaemic stroke. Happening less often, but more likely to be fatal when it does arise, is a haemorrhagic stroke, in which bleeding occurs from a leaking or ruptured arterial wall at a point weakened by atherosclerosis. Sometimes the artery stretches at the site of weakness, causing it to balloon out, forming an aneurysm. The bigger the aneurysm, the more likely it is to rupture, causing haemorrhage and a resultant stroke.
One in five people experiencing their first stroke episode will die within four weeks, and one in three will die within 12 months. Among the people who survive the first month after their first-ever stroke, about half will survive five years.12 Stroke is a major cause of disability in Australia. By the end of the first year following a stroke, about half of stroke survivors still require assistance with daily activities.12
Smoking is an important cause of stroke, with the risk of having a stroke rising with the amount of tobacco smoked.3,13 Smokers are one and a half times more likely to have a stroke than non-smokers.6,3
As with CVD, the impact of stroke caused by tobacco is greatest among the middle aged. In Australia in 2004–05, 40% of all deaths due to stroke in men aged between 35 and 39 were caused by smoking. The greatest impact occurred in women aged 40–44, among whom 35% of all stroke deaths were due to tobacco.12 Research has shown that the risk of having a stroke decreases steadily after quitting smoking, ex-smokers having the same risk as never-smokers after 5–15 years, depending on the study.6,3
3.1.3 Atherosclerotic peripheral vascular disease
Atherosclerotic peripheral arterial disease (PAD) occurs when blockages within the blood vessels prevent proper blood circulation. PAD most commonly occurs in the legs and feet, but it can also develop in the arms and hands. This may result in severe pain (claudication), especially when physically active. PAD can lead to death of part of the limb. Amputation may be necessary for relief of pain, and to prevent the development of gangrene. Given that it's the same atherosclerotic disease process, it is not uncommon for individuals with PAD to die from heart attack or stroke.15
Smoking is a cause of PAD. There is a strong dose–response relationship between the number of cigarettes smoked and the likelihood of developing PAD even after adjustment for other CVD risk factors.3 In Australia in 2004–05, about 37% of all deaths due to PAD in males aged over 35 were attributable to smoking, as were 30% of all PAD deaths in women aged over 35.14
Patients who suffer vascular-related leg pain are less likely to suffer serious obstruction of the arteries in their legs if they quit. Quitting smoking also reduces the risk of re-occlusion after peripheral vascular surgery.16,17
3.1.4 Abdominal aortic aneurysm
Abdominal aortic aneurysm is a weakening of the wall of the aorta (the major artery carrying oxygenated blood from the heart to the body) in the region below the diaphragm. The weakening occurs as a result of atherosclerotic lesions developing in the aortic wall. The wall may eventually stretch and then leak or burst. Abdominal aortic aneurysm is frequently fatal.3
Smoking is a cause of abdominal aortic aneurysm, the risk rising with increased exposure to tobacco smoke.3 Further, active smoking in adolescence and young adulthood can cause early abdominal aortic atherosclerosis in young adults.8 Smoking is one of the few currently modifiable risk factors for this disease. With increasing time after stopping smoking, the risk of developing an abdominal aneurysm appears to slowly decline.3
3.1.5 Sudden cardiac death
Sudden cardiac death describes death occurring due to sudden, unexpected loss of heart function. Most sudden death is due to CVD, in particular CHD accompanied by smoking. Cardiac dysrhythmias (irregular muscular contractions of the heart, also referred to as cardiac arrhythmias) also cause sudden cardiac death. Smokers have a three-fold greater risk of suffering sudden cardiac death than non-smokers.3,6,7,18 Importantly, cigarette smoking may be the only modifiable risk factor for sudden cardiac death in the presence or absence or CHD.3
In Australia it is estimated that smoking causes 30–40% of all deaths due to cardiac dysrhythmias in men aged 35–59, and about one-third of all deaths due to cardiac dysrhythmias in women aged 35–44.14 3.1.6 Congestive heart failure
Congestive heart failure (CHF) occurs when the heart becomes less able to pump blood through the body effectively. The heart may become enlarged or thicken, and fluid may collect in lungs (causing shortness of breath) or in other parts of the body (causing swelling or weight gain). CHF usually occurs in individuals with a history of heart problems such as high blood pressure or coronary heart disease.19 As well as contributing to the disease processes that primarily lead to CHF, smoking is an independent risk factor for CHF.6
CHF sufferers experience high levels of disability and have a reduced life expectancy.6 In Australia, it is estimated that smoking causes 30–40% of all deaths due to CHF in men aged 35–59, and about one-third of all deaths due to CHF in women aged 35–44.14
In conclusion, cigarette smoking and exposure to secondhand cigarette smoke are major causes of CVD. The risk arises from atheroma narrowing the affected blood vessels and with a higher risk of acute thrombosis. The cardiovascular risks attributable to cigarette smoking escalate with smoking just a few cigarettes per day, low level exposure to secondhand cigarette smoke and the duration of smoking. Stopping cigarette smoking and eliminating exposure to secondhand cigarette smoke rapidly and substantially reduces the risks of various CVDs.
References
1. Australian Institute of Health and Welfare. Australia's health 2010. Australia's health series no. 12, cat. no. AUS 122. Canberra: AIHW, 2010. Available from: http://www.aihw.gov.au/publication-detail/?id=6442468376
2. Begg S, Vos T, Barker B, Stevenson C, Stanley L and Lopez A. The burden of disease and injury in Australia 2003. cat. no. PHE 82. Canberra: Australian Institute of Health and Welfare, 2007. Available from: http://www.aihw.gov.au/publications/index.cfm/title/10317
3. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease. A report of the US Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: http://www.surgeongeneral.gov/library/tobaccosmoke/report/index.html
4. Benowitz N. Drug therapy: pharmacologic aspects of cigarette smoking and nicotine addiction. New England Journal of Medicine 1988;319(20):1318–30. Available from: http://content.nejm.org/cgi/content/brief /319/20/1318
5. Australian Institute of Health and Welfare. Cardiovascular disease mortality: trends at different ages. Cardiovascular disease series no. 31, cat. no. 47. Canberra: AIHW, 2010. Available from: http://www.aihw.gov.au/publication-detail/?id=6442468344
6. US Department of Health and Human Services. The health consequences of smoking. A report of the Surgeon General. Rockville, Maryland: US Department of Health and Human Services, Public Health Service, Office of the Surgeon General, 2004. Available from: http://www.surgeongeneral.gov/library /smokingconsequences/
7. US Department of Health and Human Services. The health consequences of smoking: cardiovascular disease. Rockville, Maryland: Public Health Service, Office on Smoking and Health, 1983. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/pre_1994/index.htm
8. US Department of Health and Human Services. Preventing tobacco use among young people: A report of the Surgeon General. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2012. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/2012/
9. Bjartveit K and Tverdal A. Health consequences of smoking 1−4 cigarettes per day: response to G F Cope (E-letter). Tobacco Control, 2006; 15(1):71−2. Available from: http://tc.bmjjournals.com
10. Thun MJ, Carter BD, Feskanich D, Freedman ND, Prentice R, et al. 50-Year trends in smoking-related mortality in the United States. The New England Journal of Medicine, 2013; 368(4):351-364. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3632080/
11. International Agency for Research on Cancer. Reversal of risk after quitting smoking. IARC handbooks of cancer prevention, tobacco control, 11 Vol. 11.Lyon, France: IARC, 2007. Available from: http://apps.who.int /bookorders/anglais/detart1.jsp?sesslan=1&codlan=1&codcol=76&codcch=22
12. Senes S. How we manage stroke in Australia. Cardiovascular disease series no.24, cat. no. CVD 31.Canberra: AIHW, 2006. Available from: http://www.aihw.gov.au/publication-detail/?id=6442467815
13. Doll R, Peto R, Boreham J, and Sutherland I. Mortality in relation to smoking: 50 years' observations on male British doctors. British Medical Journal (Clinical Research Ed.), 2004; 328(7455):1519. Available from: http://www.bmj.com/cgi/content/abstract/328/7455/1519
14. Collins D and Lapsley H. The costs of tobacco, alcohol and illicit drug abuse to Australian society in 2004/05. P3 2625.Canberra: Department of Health and Ageing, 2008. Available from: http://www.nationaldrugstrategy.gov.au/internet/drugstrategy/publishing.nsf/Content/mono64/$File /mono64.pdf
15. Australian Institute of Health and Welfare and National Heart Foundation of Australia. Heart, stroke and vascular diseases—Australian facts 2004. Cardiovascular disease series no. 22, cat. no. CVD 27.Canberra: AIHW and NHFA, 2004. Available from: http://www.aihw.gov.au/publications/cvd/hsvd04/hsvd04.pdf
16. U.S. Department of Health and Human Services. The Health Consequences of Smoking: 50 Years of Progress. A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014, Printed with corrections, January 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/full-report.pdf
17. US Department of Health and Human Services. The health benefits of smoking cessation. A report of the Surgeon General. Atlanta, GA: Centers for Disease Control, Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 1990. Available from: http://profiles.nlm.nih.gov/NN/B/B /C/V/_/nnbbcv.pdf
18. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/
19. National Heart Foundation of Australia. Let's talk about heart failure. Canberra: NHFA, February 2003. Available from: http://www.heartfoundation.org.au/document/NHF/heartfailureinfosheet.pdf
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.2 Respiratory diseases (excluding lung cancer)
3.2 Respiratory diseases (excluding lung cancer)
Last updated: March 2015 Suggested citation: Peters, M, Greenhalgh, EM & Winstanley, MH. 3.2 Respiratory diseases. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-4-respiratory-diseases
The airways and lungs, being the route of tobacco smoke exposure, are exposed to higher concentrations of the toxic constituents of smoke than any other system in the body. The adverse effects of smoking range from impairment of the protective mechanisms in the lungs that reduce the risk of infection to actual lung destruction.1,2
3.2.1 Impairment of pulmonary immune and protective responses
The lungs are continually exposed to gases, particles and micro-organisms in the air. To avoid the ill effects from these potential insults, the respiratory system employs a set of protective mechanisms. Cigarette smoke can impair or overwhelm the lungs' defences, leading to chronic disease.1
Every time we breathe, we inhale particles. Some are harmless dust and others are potentially injurious particles, viruses, or bacteria. Large and very small particles are mostly trapped in the nose and upper airway and cleared without reaching the lung at all. Intermediate sized particles, between 0.001 and 10 microns, penetrate deep into the lungs.1 From here they are cleared by the mucociliary system: particles become trapped in the mucus blanket on the surface of the cells lining the airways, and are swept out of the lung by the synchronised movement of cilia, which are tiny hair-like structures on the surface of airway cells.3
About 60% of the particles from cigarette smoke are deposited in the lung. Exposure to cigarette smoke reduces the clearance rate of particles from the lung.1 This is in part due to shortening, loss or disco- ordination of cilia, but may also be due to changes in the thickness of mucus that reduces the effective propulsion of the mucus by the cilia.3–6 This impairment of the mucociliary system increases the risk of infection.1 Smokers also become increasingly reliant on coughing to clear mucus, rather than the normal clearance process which is more effective and less irritating.7 Long-term smokers retain a substantial amount of particles in their lungs.1 Smoking cessation improves mucocilary clearance in the nose after two weeks, and in the lungs after three months.4,8
Lying under the mucociliary system, the outer layer of lung cells lining the airway form a physical barrier between lung tissue and airspace. Chronic exposure to cigarette smoke damages this protective barrier, increasing its permeability, which leads to inflammation.1,9,10
Smoking compromises the immune system, provoking an inflammatory response and increasing the potential for infection.1,9,11 The ability of the lung's immune system to sense and eliminate viruses and bacteria is impaired.10,12 All smokers have inflammation in their lungs, which may persist for many years after smoking cessation.1,13 3.2.2 The effect of smoking on acute respiratory illnesses
Adults who smoke are more likely to develop acute respiratory illnesses, including bronchitis, bronchiolitis, influenza, legionnaires disease, and pneumonia.12,14 The risk of pneumococcal infection, the most common cause of severe pneumonia, is two- to four-fold in smokers compared to non-smokers, with the risk increasing as daily cigarette consumption increases.14,15 Smokers are more likely to be infected with influenza in an epidemic. Seasonal influenza is more common and severe in non-vaccinated smokers.12,14
Smoking also causes active tuberculosis disease and death from tuberculosis.11 Tuberculosis in not common in Australia, but there are groups vulnerable to TB infection including Aboriginal Australians, migrants from countries where TB is common and people with HIV.17 Smoking cessation and avoiding secondhand smoke reduces the risk of tuberculosis disease.18
In Australia in 2004–5, it is estimated that about 15% of all deaths due to lower respiratory tract infection in men aged over 35, and 12% in women of the same age, were caused by smoking.19
3.2.3 Smoking and respiratory symptoms
Active smoking causes respiratory symptoms in adults, teenagers and children, including coughing, phlegm, wheezing and dyspnea (difficulty breathing and shortness of breath). These symptoms are associated with a number of acute and chronic respiratory illnesses. They may also indicate underlying lung injury and disease. The population prevalence of these symptoms decreases with smoking cessation.12
3.2.4 Smoking and lung function
Active smokers in childhood and adolescence have both reduced lung function and impaired lung growth.20 Smoking causes the early onset of decline in lung function during late adolescence and early adulthood. All adults experience a loss of lung function as they age, but this process occurs earlier and at a greater rate among smokers than non-smokers.12 Among smokers, there appears to be a sliding scale of susceptibility to loss of lung function.21,22 A few smokers may lose lung function almost as slowly as non-smokers, but for a significant minority of smokers, their rapid loss of lung function becomes disabling or fatal.1,9,21 Most smokers will fall between these groups.22 A diagnosis of chronic obstructive lung disease (COPD) can be made after a significant and non-reversible loss of lung function. In the population of smokers without COPD, the age-related rate of lung function decline slows down to that seen in people who have never smoked within five years of smoking cessation. However, they do not regain the lung function they have already lost.13
3.2.5 Major diseases caused by smoking
3.2.5.1 Chronic bronchitis
Bronchitis is defined by symptoms of cough together with frequent and increased production of sputum or phlegm. Chronic bronchitis is diagnosed when these symptoms are present for three months in each of two successive years.1 It occurs in about half of all heavy smokers.13 Chronic bronchitis is associated with inflammation in the large and small bronchial airways, which results in the enlargement of mucus-producing glands and remodelling (thickening) of the airway walls. People with chronic bronchitis have a greater frequency of respiratory infections.1,23 In persons who also have chronic obstructive pulmonary disease (COPD), symptoms of chronic bronchitis increase the risk of death from respiratory infections.24
Chronic bronchitis often co-occurs with COPD, but it does not influence airflow limitation unless the inflammation extends into the small airways.1 Having symptoms of chronic bronchitis is associated with an accelerated decline in lung function as seen in COPD.1,12 It was previously thought that chronic bronchitis was a necessary first step in the development of COPD. However, since then research has shown that airflow limitation can develop without symptoms of chronic bronchitis.1 Also, in people with normal lung function, the presence of chronic bronchitis does not increase their likelihood of developing COPD.1,13
Symptoms of chronic bronchitis decrease by one to two months after smoking cessation, and the population prevalence of cough and phlegm returns to the level of never smokers within five years.13 In people with severe COPD, chronic cough associated with chronic bronchitis is more likely to persist after smoking cessation.23
3.2.5.2 Chronic Obstructive Pulmonary Disease (COPD)
Chronic obstructive pulmonary disease (COPD) is characterised by airflow limitation that is usually progressive and not fully reversible.1 In 2011, COPD was the fifth leading cause of death in Australia, representing 4.4% of all deaths in people aged 55 and over.25 These statistics may underestimate the contribution of highly prevalent, slowly progressive, chronic diseases such as COPD to mortality, as the reported number of deaths is based on the underlying cause of death only. In Australia, only 40% of all deaths with COPD as any cause had COPD recorded as the underlying cause of death for the period 2007–2011.25
Death rates from COPD have declined over time.25 COPD is more prevalent among the elderly, when it has important interactions with many other acute and chronic illnesses.17,26 The evidence also suggests that women may be more susceptible to developing severe COPD at younger ages.11 Beyond the effect on mortality, the chronic nature of COPD means those who develop COPD may live for many years, with various degrees of discomfort and disability.17 Even individuals with mild COPD have reduced quality of life, which worsens as the disease becomes more severe.27
The greatest cause of COPD by far is smoking.25 In 2004–5, it is estimated that of all deaths in Australians aged over 35 caused by COPD, 77% of cases in males and 71% of cases in females were attributable to smoking.19 In 2007-08, among Australians aged 55 years and over who had self-reported COPD, 20% were current smokers, 52% were former smokers, and 28% had never smoked.28 Limited data suggests that, of the current smokers who survive to their mid-70s, around half may develop mild to severe COPD.29
COPD arises from progressive, permanent damage to the airways and airway sacs (alveoli) of the lungs. The main processes thought to be important in the development of COPD are inflammation, oxidative stress, and an imbalance of proteases (enzymes that affect proteins) and antiproteases in the lung. Oxidative stress is the result of highly reactive chemicals in tobacco smoke creating an imbalance between oxidants and antioxidants in the lung. Oxidative stress can directly damage lung cells, promote inflammation, and contribute to the protease-antiprotease imbalance. While all smokers have inflammation of the lungs, not all develop COPD. People who develop COPD are thought to have an enhanced or abnormal inflammatory response to noxious particles or gases.1,13
Different disease processes result in the airflow limitation that characterises COPD. The main diseases are obstructive bronchiolitis and emphysema.1,13 Chronic bronchitis often co-occurs with COPD (as described above). Smokers have different susceptibilities to each disease process and this will influence their symptoms.
Obstructive bronchiolitis
Inflammation in the small airways is seen to some extent in all smokers.12,30 Obstruction of the small airways occurs when abnormally heightened inflammation and remodelling occur in the small bronchi and bronchioles in the lungs. The term 'remodelling' describes a cycle of injury and repair in the presence of inflammation, that results in the thickening of the airway wall and narrowing of the lumen (airway space).1 In addition, excess mucus accumulates in the small airway lumen.9 This process obstructs air flow through the small airways to the lung's air sacs (alveoli) where gas exchange occurs. For as long as smoking continues, the condition progresses. The main symptom is breathlessness, because the gradually altered lung structure cannot allow increases in the flow of air that is needed to exercise comfortably.9 Smoking cessation slows lung function decline.12 In some smokers, airway inflammation persists, possibly for life, after stopping smoking.13
Emphysema
Emphysema is irreversible loss of the walls of the alveoli–the small air sacs where gas exchange occurs. As this framework is lost, the alveoli walls cannot regenerate and air spaces enlarge. The resulting loss of the surface area where gas exchange occurs reduces the capacity of the lungs to transfer oxygen to red blood cells and remove carbon dioxide from the bloodstream–its essential functions.4,26
Smoking causes oxidative stress, which tips the protease–anti-protease balance towards proteases.1 Proteases are enzymes that degrade structural proteins, such as elastin and collagen, in the lungs airways and alveoli.12 The lung becomes less elastic, restricting its capacity to contract and expand. The loss of elastic recoil reduces the force driving the air out the lungs, so it takes longer to breathe out.1,9 In advanced emphysema, the inelastic lungs enlarge leading to a large barrel-shaped chest.
Course of COPD after smoking cessation
Smoking cessation is the only action known to protect from rapid declines in lung function.31 In populations with COPD, there is a small improvement in lung function in the year after smoking cessation. Thereafter, age-related decline in lung function that is less than half of that seen in continuing smokers.13 Reduction in the number of cigarettes smoked does not change the loss of lung function.32 Former smokers have a reduced risk of hospitalisation related to COPD and death from COPD compared with those who continue to smoke.13,33
3.2.6 Other respiratory illnesses related to smoking
3.2.6.1 Asthma
In Australia, one in ten people suffer from asthma.34 Smoking rates in people with asthma are at least as high as those without asthma.28 Active smoking is associated with an increased risk for asthma in adolescents and adults. Smoking exacerbates asthma in adults and research suggests that it may also do so in children and adolescents.11 Smoking increases asthma symptoms and impairs the response to asthma treatment.28,35 People with asthma who smoke are more likely to have accelerated loss of lung function.11,36,37 The risk of severe asthma events, such as hospitalisation, use of emergency services and death, are increased in smokers.11,37,38 Smoking cessation improves asthma control.39,40
3.2.6.2 Interstitial Lung Diseases (ILD)
Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal fibrotic interstitial lung disease. It has the worst prognosis of all idiopathic interstitial diseases of the lung, with a median survival time of three to four years.41 Although its cause is unknown, evidence suggests that both genetic and environmental factors are involved in its development. The latest Surgeon General’s report concluded that cigarette smoking is associated with an increased risk of IPF.16
Respiratory bronchiolitis-interstitial lung disease (RB-ILD) is seen in very heavy smokers, typically those smoking more than 30 cigarettes per day. Unlike typical COPD, it can be seen in young smokers.42,43 RB-ILD is a greatly exaggerated form of bronchiolitis that spreads to create inflammation in the nearby alveoli. RB-ILD impairs lung function and has an abnormal appearance on chest X-rays. Smoking cessation is recommended.42 3.2.6.3 Histiocytosis X (Langerhan's Cell Histiocytosis)
Histiocytosis X is rarer than RB-ILD. It involves the development of inflammatory nodules in the lung along with cystic degeneration of the lungs themselves. It has a distinct appearance on X-rays. Patients are commonly young adults and the vast majority have a history of smoking.42 Smoking cessation is strongly encouraged, because case reports show improvement after quitting, and even restoration of normal or near-normal lung structure.42,40
3.2.7 Other respiratory illnesses related to smoking
3.2.7.1 Sense of smell
Being a smoker is associated with having an impaired sense of smell (hyposmia).45,46 Smoke directly damages the olfactory sensory neurons, located in the nasal airways, which detect different odours.45 Smokers are about twice as likely to have olfactory impairment compared to non-smokers. Following quitting, sense of smell is restored to levels of a never smoker.46,47 (Also see section 3.22.5 )
3.2.7.2 Snoring
Snoring is more common in smokers and former smokers than in never smokers. Frequency of snoring increases with the amount of tobacco smoked, and is independent of obesity, another well-established risk factor for snoring. Snoring is likely to occur in response to the effects of tobacco smoke on the airways, including upper airway inflammation, cough and sputum production.48 (Also see section 3.22.4 )
References
1. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease. A report of the US Surgeon General. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: http://www.surgeongeneral.gov/library/tobaccosmoke/report/index.html
2. Churg A, Cosio M and Wright JL. Mechanisms of cigarette smoke-induced COPD: insights from animal models. American Journal of Physiology and Lung Cell Molecular Physiology 2008;294(4):L612-31. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18223159
3. Leopold P, O'Mahony M, Lian X, Tilley A, Harvey B and Crystal R. Smoking is associated with shortened airway cilia. PLoS One 2009;4(12):e8157. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles /PMC2790614/?tool=pubmed
4. US Department of Health and Human Services. The health consequences of smoking: chronic obstructive lung disease. A report of the Surgeon General. Rockville, Maryland: US Department of Health and Human Services, Public Health Service, Office on Smoking and Health, 1984. Available from: http://www.cdc.gov /tobacco/data_statistics/sgr/pre_1994/index.htm
5. Stanley PJ, Wilson R, Greenstone MA, MacWilliam L and Cole PJ. Effect of cigarette smoking on nasal mucociliary clearance and ciliary beat frequency. Thorax 1986;41(7):519-23. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18223159 6. Kreindler JL, Jackson AD, Kemp PA, Bridges RJ and Danahay H. Inhibition of chloride secretion in human bronchial epithelial cells by cigarette smoke extract. American Journal of Physiolgy and Lung Cell Molecular Physiology 2005;288(5):L894-902. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15626749
7. Houtmeyers E, Gosselink R, Gayan-Ramirez G and Decramer M. Regulation of mucociliary clearance in health and disease. European Respiratory Journal 1999;13(5):1177-88. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10414423
8. Ramos EM, De Toledo AC, Xavier RF, Fosco LC, Vieira RP, Ramos D, et al. Reversibility of impaired nasal mucociliary clearance in smokers following a smoking cessation programme. Respirology 2011;16(5):849-55. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21545372
9. Hogg JC. Pathophysiology of airflow limitation in chronic obstructive pulmonary disease. The Lancet 2004;364(9435):709-21. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15325838
10. Stampfli MR and Anderson GP. How cigarette smoke skews immune responses to promote infection, lung disease and cancer. Nature Reviews. Immunology 2009;9(5):377-84. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19330016
11. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/
12. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
13. International Agency for Research on Cancer, IARC Handbooks of cancer prevention, Tobacco Control, Vol. 11: reversal of risk after quitting smoking. Lyon, France: IARC; 2007.
14. Arcavi L and Benowitz NL. Cigarette smoking and infection. Archives of Internal Medicine, 2004; 164(20):2206−16. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15534156
15. Nuorti JP, Butler JC, Farley MM, Harrison LH, McGeer A, et al. Cigarette smoking and invasive pneumococcal disease. Active Bacterial Core Surveillance Team. New England Journal of Medicine, 2000; 342(10):681−9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10706897
16. U.S. Department of Health and Human Services. The Health Consequences of Smoking: 50 Years of Progress. A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014, Printed with corrections, January 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/full-report.pdf
17. Australian Institute of Health and Welfare. Australia's health 2010. Canberra: AIHW, 2010. Available from: http://www.aihw.gov.au/publications/index.cfm/title/11374
18. Slama K, Chiang CY, Enarson DA, Hassmiller K, Fanning A, et al. Tobacco and tuberculosis: a qualitative systematic review and meta-analysis. Internatioanl Journal Tuberculosis of Lung Disease, 2007; 11(10):1049−61. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17945060
19. Collins D and Lapsley H. The costs of tobacco, alcohol and illicit drug abuse to Australian society in 2004–05. Canberra: Department of Health and Ageing, 2008. Available from: http://www.nationaldrugstrategy.gov.au/internet/drugstrategy/publishing.nsf/Content/mono64/$File /mono64.pdf
20. US Department of Health and Human Services. Preventing tobacco use among young people: A report of the Surgeon General. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2012. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/2012/
21. Fletcher C and Peto R. The natural history of chronic airflow obstruction. British Medical Journal, 1977; 1(6077):1645−8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/871704
22. Rennard S and Vestbo J. COPD: the dangerous underestimate of 15%. The Lancet, 2006; 367:1216−19. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16631861
23. Braman SS. Chronic cough due to chronic bronchitis: ACCP evidence-based clinical practice guidelines. Chest, 2006; 129(1 suppl.):104S−115S. Available from: http://www.ncbi.nlm.nih.gov/pubnmed/16428699
24. Prescott E, Lange P, and Vestbo J. Chronic mucus hypersecretion in COPD and death from pulmonary infection. European Respiratory Journal, 1995; 8(8):1333−8. Available from: http://www.ncbi.nlm.nih.gov /pubmed/7489800
25. Australian Institute of Health and Welfare, Poulos LM, Cooper SJ, Ampon R, Reddel HK, et al. Mortality from asthma and COPD in Australia. Cat. no. ACM 30 Canberra 2014. Available from: http://www.aihw.gov.au/WorkArea/DownloadAsset.aspx?id=60129548230 .
26. Australian Institute of Health and Welfare. Chronic diseases and associated risk factors in Australia, 2001. cat. no. PHE 33.Canberra: AIHW, 2002. Available from: http://www.aihw.gov.au/publication-detail /?id=6442467343
27. Devereux G. The ABC of chronic obstructive pulmonary disease. Definition, epidemiology, and risk factors. British Medical Journal, 2006; 332:1142−4. Available from: http://www.bmj.com/cgi/reprint/332/7550 /1142.pdf
28. Australian Centre for Asthma Monitoring. Asthma in Australia 2011: with a focus chapter on chronic obstructive pulmonary disease. AIHW asthma series no. 4, cat. no. ACM 22.Canberra: Australian Institute for Health and Welfare, 2011. Available from: http://www.aihw.gov.au/publication-detail/?id=10737420159&tab=2
29. Lundback B, Lindberg A, Lindstrom M, Ronmark E, Jonsson AC, et al. Not 15 but 50% of smokers develop COPD?--Report from the Obstructive Lung Disease in Northern Sweden Studies. Respiratory Medicine, 2003; 97(2):115−22. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12587960
30. Hogg JC, Wright JL, Wiggs BR, Coxson HO, Opazo Saez A, et al. Lung structure and function in cigarette smokers. Thorax, 1994; 49(5):473-8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/8016769
31. Barnes PJ. Chronic obstructive pulmonary disease. New England Journal of Medicine, 2000; 343(4):269−80. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10911010
32. Godtfredsen NS, Vestbo J, Osler M, and Prescott E. Risk of hospital admission for COPD following smoking cessation and reduction: a Danish population study. Thorax, 2002; 57(11):967−72. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12403880
33. Godtfredsen N, Lam T, Hansel T, Leon M, Gray N, et al. COPD-related morbidity and mortality after smoking cessation: status of the evidence. The European Respiratory Journal, 2008; 32(4):844–53. Available from: http://erj.ersjournals.com/cgi/content/full/32/4/844
34. Australian Institute of Health and Welfare. Asthma, 2015. Available from: http://www.aihw.gov.au/asthma
35. Chalmers GW, Macleod KJ, Little SA, Thomson LJ, McSharry CP, et al. Influence of cigarette smoking on inhaled corticosteroid treatment in mild asthma. Thorax, 2002; 57(3):226−30. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11867826
36. James AL, Palmer LJ, Kicic E, Maxwell PS, Lagan SE, et al. Decline in lung function in the Busselton Health Study: the effects of asthma and cigarette smoking. American Journal of Respiratory and Critical Care Medicine, 2005; 171(2):109−14. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15486340 37. Thomson NC and Spears M. The role of cigarette smoking on persistent airflow obstruction in asthma. Annals of Respiratory Medicine, 2010; ii(1). Available from: http://www.slm-respiratory.com/uploads/media /The_Role_of_Cigarette_Smoking_on_Persistent_Airflow_Obstruction_in_Asthma.pdf
38. Ulrik CS and Frederiksen J. Mortality and markers of risk of asthma death among 1,075 outpatients with asthma. Chest, 1995; 108(1):10−5. Available from: http://www.ncbi.nlm.nih.gov/pubmed/7606941
39. Chaudhuri R, Livingston E, McMahon AD, Lafferty J, Fraser I, et al. Effects of smoking cessation on lung function and airway inflammation in smokers with asthma. American Journal of Respiratory and Critical Care Medicine, 2006; 174(2):127−33. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16645173
40. Tonnesen P, Pisinger C, Hvidberg S, Wennike P, Bremann L, et al. Effects of smoking cessation and reduction in asthmatics. Nicotine and Tobacco Research, 2005; 7(1):139−48. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15804686
41. Behr J. The diagnosis and treatment of idiopathic pulmonary fibrosis. Deutsches Ärzteblatt International, 2013; 110(51-52):875. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3928534/
42. Caminati A and Harari S. Smoking-related interstitial pneumonias and pulmonary Langerhans cell histiocytosis. Proceedings of the American Thoracic Society, 2006; 3(4):299−306. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16738193
43. Portnoy J, Veraldi KL, Schwarz MI, Cool CD, Curran-Everett D, et al. Respiratory bronchiolitis-interstitial lung disease: long-term outcome. Chest, 2007; 131(3):664−71. Available from: http://www.ncbi.nlm.nih.gov /pubmed/17356078
44. Negrin-Dastis S, Butenda D, Dorzee J, Fastrez J, and d'Odemont JP. Complete disappearance of lung abnormalities on high-resolution computed tomography: a case of histiocytosis X. Canadian Respiratory Journal, 2007; 14(4):235−7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17551600
45. Vent J, Robinson A, Gentry-Nielsen M, Conley D, Hallworth R, et al. Pathology of the olfactory epithelium: smoking and ethanol exposure. Laryngoscope, 2004; 114:1383−8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15280712
46. Murphy C, Schubert C, Cruickshanks K, Klein B, Klein R, et al. Prevalence of olfactory impairment in older adults. The Journal of the American Medical Association, 2002; 288(18):2307−12. Available from: http://jama.ama-assn.org/cgi/reprint/288/18/2307
47. Frye RE, Schwartz BS, and Doty RL. Dose-related effects of cigarette smoking on olfactory function. The Journal of the American Medical Association, 1990; 263(9):1233−6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/2304239
48. Franklin K, Gíslason T, Omenaas E, Jõgi R, Jensen E, et al. The influence of active and passive smoking on habitual snoring. American Journal of Respiratory and Critical Care Medicine, 2004; 170:799−803. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15242843
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.3 Smoking and cancer
3.3 Smoking and cancer
Last updated: March 2015 Suggested citation: Hurley, S, Greenhalgh, EM & Winstanley, MH. 3.3 Smoking and cancer. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/chapter-3-health-effects/3-3-smoking- and-cancer
Two expert bodies, the International Agency for Research on Cancer (IARC) and the US Surgeon General's office, periodically examine the evidence on smoking and cancer and issue comprehensive reports. Reports from both the IARC in 2004 and Surgeon General in 2014 stated that smoking causes cancers of the lung, upper aerodigestive tract (oral cavity, larynx, pharynx and oesophagus), pancreas, bladder, kidney, liver, cervix and stomach, and acute myeloid leukaemia.1, 2 The Surgeon General’s report also concluded that smoking causes colorectal cancer. In 2011 a Canadian expert panel concluded that smoking increases breast cancer risk.3 The Surgeon General’s report also highlighted an association between smoking and breast cancer, but concluded that there is insufficient evidence to infer a causal relationship.2 Details of the links between smoking and these cancers are discussed in Chapter 3, Sections 3.4 (lung cancer) and 3.5 (all other cancers).
In this section the mechanisms by which smoking causes cancer are summarised. Lung cancer is used as an example because it is one of the most thoroughly investigated cancers. Although more than 85% of lung cancers are attributable to smoking, not all smokers develop lung cancer and lung cancer does occur in non-smokers. In fact, lung cancer in non-smokers is believed to be a different disease from lung cancer in smokers.4 A compelling explanation of cancer causation needs to reflect these facts and the summary presented here discusses the issue of susceptibility to cancer.
This section draws heavily on the US Surgeon General's 2010 report How Tobacco Smoke Causes Disease: The Biology and Behavioural Basis for Smoking-Attributable Diseases,5 and unless otherwise referenced the information has been sourced from this report.
The mechanisms by which cigarette smoking causes cancer are extremely complex, but nevertheless can be classified into two categories: genotoxic and non-genotoxic, or epigenetic.6 Genotoxicity means that the constituents of cigarette smoke damage the DNA of genes. This is believed to occur in a multi-step pathway: the carcinogens in cigarette smoke are activated by enzymes (which in turn have been activated, or induced, by cigarette smoke); the activated carcinogens bind to DNA to form compounds known as DNA adducts; DNA adducts disrupt normal DNA repair mechanisms causing gene mutations—inactivating tumour- suppressor genes and activating oncogenes (cancer promoters); and these gene mutations then disrupt normal cell growth control mechanisms, eventually resulting in cancer. The epigenetic pathway affects the last step of this pathway. The constituents of cigarette smoke alter the expression of genes (without affecting the underlying DNA), activating cell receptors, which then disrupt multiple processes involved in cell cycle regulation. These pathways are discussed in more detail below. Cigarette smoke also alters a range of immunologic functions and it is thought that these effects may promote tumours or act as co-carcinogenic stimuli.
Although much is known about smoking-associated carcinogenesis, particularly in relation to lung cancer, and to a lesser extent bladder cancer, there are still many unanswered questions. Further, the available data are unhelpful in terms of cancer prevention. Smoking cessation is the only proven strategy to reduce the pathogenic processes that lead to cancer.
3.3.1 Carcinogens in cigarette smoke
There are thousands of compounds in cigarette smoke, including more than 60 known carcinogens from multiple chemical classes, including polycyclic aromatic hydrocarbons (PAHs), N-nitrosamines, aldehydes, volatile organic hydrocarbons and metals.
The fact that carcinogens in cigarette smoke are absorbed into the bloodstream of smokers has been confirmed by the measurement of these substances or their metabolites (biomarkers) in breath, blood and urine. Measurement of urinary biomarkers is the most convenient method to quantify carcinogen exposure. However, many carcinogens found in cigarette smoke are also found in food and the general environment, so their metabolites are also detected in the urine of non-smokers. For example, PAHs occur in grilled foods and engine exhausts. The phenolic compounds, catechol and caffeic acid, are common dietary constituents. However, the N-nitrosamine, NNK (4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone) is specific to tobacco. Its metabolite, NNAL (4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol) is therefore the most discriminatory biomarker because the only source of its parent carcinogen (NNK) is tobacco products. NNAL is only detected in non-smokers if they have been exposed to secondhand tobacco smoke.
PAHs and NNK are the major carcinogens involved in the development of lung cancer. In rodents, NNK primarily produces the adenocarcinoma sub-type of lung cancer. The concentration of NNK in tobacco smoke increased from 1959 to 1997 as the nitrate concentration in tobacco increased, and the risk of adenocarcinoma also appears to have increased since the 1960s. The latest Surgeon General’s report suggested that ventilated filters and increased levels of tobacco specific nitrosamines in cigarettes since the 1950s might have played a role in this increased risk.7 Other compounds that could also be involved in lung cancer include: 1,3-butadiene, ethylene oxide, ethyl carbamate, aldehydes, benzene and metals.
3.3.2 Activation of carcinogens to form DNA adducts
The next major step in the carcinogenic process is binding of carcinogens to DNA to form the compounds known as DNA adducts. Most cigarette smoke carcinogens have to be converted to a form that can bind to DNA. This process is referred to as 'activation' and generally requires an enzyme, often one of the cytochrome P-450s (P-450s), to catalyse (speed) the process. These enzymes are 'induced' (essentially produced) by cigarette smoke.
Detoxification processes, which excrete carcinogen metabolites in harmless forms, compete with the activation process. The balance between activation and detoxification varies between people. This may be due to the existence of multiple forms (polymorphisms) of the genes that code for the enzymes that metabolise carcinogens. For example, the CYP2A13 gene, which is expressed primarily in the respiratory tract and participates in the activation of NNK, has a variant with one-half to one-third the capacity to activate NNK. In a study of about 700 lung cancer patients and almost 800 control subjects this variant was associated with a reduced risk of lung cancer. Genetic polymorphisms may be part of the explanation for differential susceptibility to cancer, but further research is required.
DNA adducts are central to the carcinogenic process. Measurement of DNA adducts is difficult because the amount of DNA available from routine procedures (such as bronchoscopy of the lung) is usually small, and adduct concentrations are typically low. Nevertheless, adducts of NNK and other carcinogens with deoxyguanosine and other DNA bases have been identified in human lung tissue, and DNA adduct levels are higher in most tissues of smokers than in corresponding tissues of non-smokers.
3.3.3 Conversion of DNA adducts to mutations DNA adducts are not mutations per se, and can be removed by various DNA repair mechanisms that protect human cells. There is variability between people in this DNA repair capacity, and researchers hypothesise that this is also due to gene polymorphism, which leads to further differential susceptibility to tobacco- induced cancer.
When DNA repair is not completed before a normal DNA replication takes place, DNA synthesis can slow or halt. In some instances it continues, a process known as 'translesion DNA synthesis', which can result in the insertion of an incorrect nucleotide (a component of RNA and DNA). In other words, a mutation occurs.
Inactivation of a number of tumour-suppressor genes, and activation of a number of oncogenes that promote cancer, are thought to be part of the development of lung cancer. These inactivations and activations occur as a consequence of mutations. For example, 90% of patients with small-cell lung cancer, and 15% of patients with non-small cell lung cancer, have loss of function of the RB tumour-suppressor gene, and the TP53 tumour-suppressor gene is mutated and inactivated in 70% of patients with small-cell lung cancer and 50% of non-small cell lung cancer patients. Activating mutations of the KRAS oncogene are seen in non-small cell lung cancers, but rarely in lung cancers of non-smokers.
Mutation is a complex process and subject. More than 22 000 mutations have been identified in a small-cell lung cancer cell line, highlighting the impact of the carcinogen cocktail in cigarette smoke.8
3.3.4 Loss of normal cell growth control mechanisms
Gene mutations can lead to a disruption of the normal regulation process for cell proliferation (growth) and apoptosis (death). The latter is a natural process for eliminating injured or unstable cells and it prevents the malignant growth of cancer cells. Deregulation of apoptosis mechanisms is a characteristic of cancer cells.
As mentioned above, in addition to adversely affecting normal cell growth regulation though gene mutations, components of cigarette smoke can disrupt cell control through epigenetic pathways, and this disruption can eventually result in cancer. For example, nicotinic acetylcholine receptors (nAChRs), which are the first line of contact between cells and cigarette smoke, are believed to be activated by NNK and by nicotine. This activation of nAChRs then promotes the processes required for the development of lung cancer, for example by stimulation of kinases that mediate cancer cell survival, by proliferation and resistance to chemotherapy and by promotion of angiogenesis (the growth of new blood vessels and a fundamental step in carcinogenesis).9
Genes can also be inactivated (silenced) and activated by hypermethylation, rather than chromosomal mutation. In lung cancer, more than 50 genes involved in regulating cell growth have been found to be affected by hypermethylation.
References
1. International Agency for Research on Cancer Working Group on the Evaluation of Carcinogenic Risks to Humans. Tobacco smoke and involuntary smoking. IARC monographs on the evaluation of the carcinogenic risk of chemicals to humans. Volume 83. Lyon: International Agency for Research on Cancer, 2004. Available from: http://monographs.iarc.fr/ENG/Monographs/allmonos90.php
2. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm 3. Johnson K, Miller A, Collishaw N, Palmer J, Hammond S, Salmon A, et al. Active smoking and secondhand smoke increase breast cancer risk: the report of the Canadian Expert Panel on Tobacco Smoke and Breast Cancer Risk (2009). Tobacco Control 2011;Jan 20(1):e2. Available from: http://tobaccocontrol.bmj.com/content/early/2010/10/27/tc.2010.035931.full
4. Stewart B, Cotter T and Bishop J. Cancer and tobacco: its effects on individuals and populations. In: Robotin M, Olver I and Girgis A, eds. When cancer crosses disciplines. A physician's handbook, London: Imperial College Press, 2010.
5. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease. A report of the US Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: http://www.surgeongeneral.gov/library/tobaccosmoke/report/index.html
6. Chen RJ, Chang LW, Lin P and Wang YJ. Epigenetic effects and molecular mechanisms of tumorigenesis induced by cigarette smoke: an overview. Journal of Oncology 2011;2011:654931. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21559255
7. U.S. Department of Health and Human Services. The Health Consequences of Smoking: 50 Years of Progress. A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014, Printed with corrections, January 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/full-report.pdf
8. Pleasance E, Stephens P, O'Meara S, McBride D, Meynert A, Jones D, et al. A small-cell lung cancer genome with complex signatures of tobacco exposure. Nature 2010;463(7278):184–90. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2880489/pdf/ukmss-28042.pdf
9. Minna JD. Nicotine exposure and bronchial epithelial cell nicotinic acetylcholine receptor expression in the pathogenesis of lung cancer. The Journal of Clinical Investigation 2003;111(1):31–3. Available from: http://pubmedcentralcanada.ca/picrender.cgi?accid=PMC151841&blobtype=pdf
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.4 Lung cancer
3.4 Lung cancer
Last updated: March 2015 Suggested citation: Hurley, S, Greenhalgh, EM & Winstanley, MH. 3.4 Lung cancer. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/chapter-3-health-effects/3-3-lung-cancer
The two lungs are located on either side of the heart, near the backbone. The function of the lungs is to transport oxygen from the air to the blood, and carbon dioxide from the blood to the atmosphere. These two gases are 'exchanged' in the alveoli (the thin-walled cells containing air) of the lungs.
There are four main types of lung cancer: squamous cell carcinoma, small-cell undifferentiated carcinoma, adenocarcinoma and large-cell carcinoma.
Lung cancer is now the most common type of cancer in the world. In 2008, the number of new cases that occurred was estimated to be 1.1 million with just under 949 000 deaths occurring in the same year.i 1 The number of lung cancer deaths worldwide attributable to smoking has been estimated to be 0.85 million, making lung cancer the third-ranking cause of smoking-attributable deaths, after cardiovascular disease and chronic obstructive pulmonary disease.2
In Australia, lung cancer is the fifth most common cancer diagnosed; there were an estimated 11,280 new cases and 8,410 deaths in 2012.3 Five-year survival in the period 2006 – 2010 was only 13% for males and 17% for females.3 In Australian males, lung cancer is the most common cause of cancer death and is the third leading contributor to burden of disease, accounting for 4.5% of total disability-adjusted life-years (DALYs) lost due to illness or accident.4 In Australian women, lung cancer is the second most common cause of cancer death, after breast cancer.5
3.4.1 Risk associated with smoking
The evidence that tobacco smoking causes lung cancer is unequivocal. Cigarette smoking causes most cases of lung cancer. In fact, in populations with prolonged cigarette use, up to 90% of cases of lung cancer are attributable to smoking.
Lung cancer was one of the first diseases to be causally linked with smoking. The story of the research that established this link, and the controversies the emerging data created, is told in articles by Colin White6 and Michael Thun;7 in the biography of the late Sir Richard Doll, one of the key researchers of the topic;8 and in the commentary9 published in conjunction with the re-publication of a pivotal 1959 review of the smoking and lung cancer relationship by Cornfield and colleagues.10
The following is a brief summary. In the early 1900s, lung cancer was a rare disease. By the 1930s and 1940s an increase in lung cancer incidence was becoming obvious, and at least seven small studies found an association between smoking and lung cancer. However, it was thought that better diagnosis of the disease, or increased life expectancy, might be the explanation for the increase in lung cancer and these early studies were not widely accepted internationally, or perhaps even read. In the late 1940s and early 1950s, it became obvious that the increase in lung cancer and lung cancer deaths was real and important. In 1950, two large case–control studies were published, one by Wynder and Graham in the US, and the other by Doll and Hill in the UK. Both found a large increase in the risk of lung cancer associated with smoking. The British study found that the risk for smokers compared with never smokers was 14-fold higher and the American study found that the risk was seven-fold higher. It is noteworthy that while conducting their research, Doll, Hill and Graham, who were all smokers, were doubtful that smoking was a cause of lung cancer. Their results provoked much controversy and disbelief, but nevertheless large prospective studies were initiated in Britain (by Doll and Hill) and in the US to investigate the possible link in a manner free of the potential bias in retrospective case–control studies. These large studies soon confirmed the relationship between smoking and lung cancer.
Doll and Hill's study warrants special mention. They sent questionnaires about smoking habits to almost 35 000 male British doctors in 1951, and periodically thereafter. Deaths and causes of death were monitored for almost 99% of these doctors over 50 years and results were published in 195411 and 195612 and after 10,13, 14 20,15 4016 and 50 years follow-up.17 As early as 1956, Doll and Hill had concluded, in relation to lung cancer deaths, that smokers had a higher mortality than non-smokers, heavy smokers had a higher mortality than light smokers, cigarette smokers had a higher mortality than pipe smokers and those who continued to smoke had a higher mortality than those who gave up.12
The cohort studies initiated in the US reported similar findings, and expert bodies eventually found the evidence that smoking causes lung cancer compelling. The US Surgeon General, for example, concluded in 1964 that smoking causes lung cancer in men, and in 1968 concluded that smoking causes lung cancer in women.18
The 50-year follow-up of the British doctors study found that lung cancer mortality rates were 16-fold higher (averaged across all ages) for cigarette smokers compared with never smokers.17
3.4.2 How tobacco smoke causes lung cancer
This issue is discussed in Chapter 3, Section 3.3.
3.4.3 Factors affecting risk
3.4.3.1 Intensity and duration
The risk of lung cancer increases with the number of cigarettes smoked and the duration of smoking.1,18 The latter is the strongest determinant. A modelling study of the excess odds ratio for lung cancer per pack-year of smoking found a greater risk for a total exposure delivered for a longer duration than for an equivalent exposure delivered at higher intensity (shorter duration). So the earlier the age a person starts smoking and the longer they continue, the greater the risk.19 For example, the annual excess incidence of lung cancer increases approximately 100-fold for men who have smoked for 45 years compared with men who have smoked for 15 years. In contrast, American Cancer Prevention Study II found that the lung cancer mortality rate for women who had smoked for 21–30 years was about 35% higher in those who reported smoking more than 20 cigarettes per day compared with those who reported smoking 20 cigarettes per day.1
3.4.3.2 Smoking cessation
Stopping smoking decreases the risk of lung cancer. In fact, Julian Peto has pointed out that when a smoker quits, the lung cancer mortality rate stops increasing steeply and remains almost constant.20 The International Agency for Research on Cancer summarised this effect as follows: 'Stopping smoking at any age avoids the further increase in lung cancer incurred by continued smoking. The younger the age at cessation, the greater the benefit.'1 3.4.3.3 Histological type
Smoking increases the risk of all histological types of lung cancer, but the association between adenocarcinoma and smoking has become stronger over time and it is now the most common type of lung cancer in smokers.21,22 For example, in the American Cancer Prevention Study I (initiated in 1959) the relative risk of death from lung adenocarcinoma for male smokers compared with non-smokers was 4.6, whereas in the American Cancer Prevention Study II (initiated in 1982) the comparable risk was 19.23 The 2014 Surgeon General’s report highlights the substantial changes that have taken place since the 1950s in the design and composition of cigarettes. Although these changes are not fully understood, they have resulted in different patterns of smoking (e.g., more intense puffing) and alterations in the chemical composition of cigarette smoke, and have caused the increased risk of lung adenocarcinoma from smoking. There is currently not enough research to specify which changes have caused this increase, but the evidence suggests that ventilated filters and increased levels of tobacco-specific nitrosamines are partially responsible.24
3.4.3.4 Gender differences
Some studies have suggested that women who smoke are at greater risk for developing lung cancer than men who smoke. The weight of evidence now suggests that there is little, if any, difference between women and men in their vulnerability to the carcinogenic effects of cigarette smoke.1,25 For example, a US study that followed almost 300 000 men and almost 200 000 women aged 50–71 years from 1995 to 2003 found no statistically significant difference between sexes in the incidence of lung cancer for those who smoked more than two packs of cigarettes per day.26
However, there is mounting evidence that the biology of lung cancer differs between the sexes.25 The US study mentioned above found a 30% higher incidence of lung cancer in women who had never smoked compared with men who had never smoked, and this difference was almost statistically significant.26 Although adenocarcinoma is currently the most common histological type of lung cancer in both men and women, women have proportionally more adenocarcinoma and less squamous cell carcinoma.22,25 Female hormones and reproductive factors may influence lung carcinogenesis.25, 27 Data from the Nurses' Health Study in the US suggest that early onset of menopause and past oral contraceptive use increase lung cancer risk.28 In this study, postmenopausal hormone use did not affect lung cancer incidence, but a prospective cohort study in the US state of Washington found that oestrogen plus progesterone replacement therapy was associated with increased lung cancer risk.29 Further research will be needed to elucidate the impact of such factors on lung cancer incidence and their interaction, if any, with the influence of smoking.
3.4.3.5 Other factors
The role of alcohol in lung cancer is controversial. Some studies have suggested that alcohol consumption, particularly binge drinking, increases the risk of lung cancer in smokers but not in non-smokers.30, 31 Another study found that moderate red wine consumption decreases lung cancer risk.32 Further studies are needed to clarify this association.
Emphysema (a form of chronic obstructive pulmonary disease), which is itself a smoking-associated condition, may increase the risk of lung cancer.33
There are ethnic differences in susceptibility to lung cancer caused by smoking.1 In the US, the risk of lung cancer has been found to differ between racial/ethnic groups after taking into account the duration and intensity of smoking. Compared to Caucasians, African Americans and native Hawaiian smokers have an increased risk, whereas Latino and Japanese American smokers have a lower risk.31,32 Researchers have hypothesised that ethnic/racial differences in the activity of an enzyme that metabolises nicotine may lead to different smoking behaviour, resulting in different levels of tobacco smoke carcinogens for the same number of cigarettes smoked per day, in turn resulting in elevated lung cancer risk in groups with greater nicotine metabolism, and reduced risk in those with lower metabolism. A study of nicotine metabolism in a multiethnic cohort supports this hypothesis.33
3.4.4 Impact of smoking on prognosis
Smoking not only increases the risk of lung cancer, but appears to adversely impact prognosis once lung cancer is diagnosed. In patients with non-small cell lung cancer, the survival rate has been found to be lower in patients who had smoked for more pack-years.37, 38
In the US, more than 80% of patients continue to smoke after being diagnosed with lung cancer.36 A meta-analysis published in 2010 has provided preliminary evidence that such patients have a worse prognosis than those who quit.39 Most patients in the studies had early stage tumours. For both small cell and non-small cell lung cancer, the risk of death (from any cause) was greater in patients who continued to smoke compared with those who quit.40 Most patients in the studies had early stage tumours. For both small cell and non-small cell lung cancer, the risk of death (from any cause) was greater in patients who continued to smoke compared with those who quit. Models developed by the authors suggested that the quitters’ improved prognosis was due to a reduction in cancer progression, rather than the cardiovascular benefits of quitting. The meta-analysis results were consistent with this suggestion—the risk of recurrence for both types of lung cancer was higher in continuing smokers.40
Women appear to have a better response to therapy for lung cancer, irrespective of stage of disease, histological type and whether they are being treated with surgery, chemotherapy, radiotherapy or a combination of these modalities.25
3.4.5 Temporal trends in lung cancer rates
The impact of tobacco-control efforts and falling smoking rates on smoking-associated illnesses is clearly of interest to researchers, public health program funders and the wider community. In this context, interest has focused on lung cancer, because most lung cancer is caused by smoking, and because reliable national mortality statistics are widely available. Two analyses of data in the US have found links between tobacco- control efforts and lung cancer rates. The first was based on data from California, where an enhanced tobacco-control program, involving increased taxes and comprehensive strategies to change social norms, was initiated in 1988. The analysis found that over the period 1988–1997 per capita cigarette consumption declined more rapidly in California compared with the rest of the US and that the decline in lung cancer incidence rates in men was 1.5 times greater than in other states where tobacco-control measures were less intensive. In women, lung cancer incidence rates fell by 4.8% in California, but increased by 13.2% in other states.41 The second analysis compared data from the 51 US states found that an index reflecting the intensity of tobacco-control efforts in a state was correlated with both lung cancer incidence and mortality in young adults.42
Analyses of data in the UK,43 US44 and Australia45 have found lung cancer incidence and mortality trends in line with smoking patterns and the lag between smoking initiation and disease occurrence. The benefits of smoking cessation in men are now being reflected in national statistics. For example, in Australia, lung cancer incidence in men decreased by 32% between 1982 and 2007, but increased by 72% in women over the same period. However, by 2007 incidence in women was still only about half that in men.46 Similar trends have been seen in lung cancer death rates. In men, mortality fell by 1.9% per year between 1993 and 1998, but increased by 0.3% per annum, on average, in women.5
In the US, the steadily increasing lung cancer death rate began to level off for men in the mid-1970s, peaked in 1991 and had decreased by 20% by 2003. In women, the death rate steadily increased until 1991, after which it began to level off, although still increasing by 9.6% between 1991 and 2003. Thun and Jemal estimated from these data that the reductions in tobacco smoking in the US over the previous half-century had prevented at least 146 000 deaths from lung cancer.44
So, the payoff from tobacco control has only just begun, with lung cancer mortality in men peaking 20–25 years after the peak in smoking rates.45 Researchers anticipate that smoking cessation by women will soon be reflected in disease statistics.47 i See the International Agency Against Cancer's Facts sheet at http://globocan.iarc.fr/factsheets/populations /factsheet.asp?uno=900
References
1. International Agency for Research on Cancer Working Group on the Evaluation of Carcinogenic Risks to Humans. Tobacco smoke and involuntary smoking. IARC monographs on the evaluation of the carcinogenic risk of chemicals to humans. Volume 83. Lyon: International Agency for Research on Cancer, 2004. Available from: http://monographs.iarc.fr/ENG/Monographs/allmonos90.php
2. Ezzati M and Lopez AD. Estimates of global mortality attributable to smoking in 2000. The Lancet 2003;362(9387):847–52. Available from: http://www.ncbi.nlm.nih.gov/pubmed/13678970
3. Australian Institute of Health and Welfare and Australasian Association of Cancer Registries. Cancer in Australia: an overview, 2010. Cancer series no. 60. AIHW cat. no. CAN 56. Canberra: AIHW, 2010. Available from: http://www.aihw.gov.au/publication-detail/?id=6442472459&tab=2
4. Australian Institute of Health and Welfare. Cancer survival and prevalence in Australia: cancers diagnosed from 1982 to 2004. Cancer series no. 42. AIHW cat. no CAN 38. Canberra: AIHW, 2008. Available from: http://www.aihw.gov.au/publication-detail/?id=6442468141&libID=6442468139
5. Australian Institute of Health and Welfare. Cancer survival and prevalence in Australia: cancers diagnosed from 1982 to 2004. Cancer series no. 42. AIHW cat. no CAN 38, Canberra: AIHW, 2008. Available from: http://www.aihw.gov.au/publication-detail/?id=6442468141&libID=6442468139
6. White C. Research on smoking and lung cancer: a landmark in the history of chronic diseases. Yale Journal of Biology and Medicine, 1990; 63(1):29–46. Available from: http://pubmedcentralcanada.ca /picrender.cgi?accid=PMC2589239&blobtype=pdf
7. Thun MJ. When truth is unwelcome: the first reports on smoking and lung cancer. Bulletin of the World Health Organization, 2005; 83(2):144–5.
8. Keating C, Smoking kills. The revolutionary life of Richard Doll. Oxford: Signal Books; 2009.
9. Vandenbroucke J. 'Smoking and lung cancer'--the embryogenesis of modern epidemiology [Commentary]. International Journal of Epidemiology, 2009; 38(5):1193–6. Available from: http://ije.oxfordjournals.org /content/38/5/1193.full.pdf
10. Cornfield J, Haenszel W, Hammond E, Lilienfeld A, Shimkin M, et al. Smoking and lung cancer: recent evidence and a discussion of some questions. International Journal of Epidemiology, 2009; 38(5):1175–91. Available from: http://ije.oxfordjournals.org/content/38/5/1175.full.pdf
11. Doll R and Hill AB. The mortality of doctors in relation to their smoking habits: a preliminary report. British Medical Journal, 1954; 1(4877):1451–5. Available from: http://pubmedcentralcanada.ca /picrender.cgi?accid=PMC2085438&blobtype=pdf
12. Doll R and Hill AB. Lung cancer and other causes of death in relation to smoking. A second report on the mortality of British doctors. British Medical Journal, 1956; 2(5001):1071–81. Available from: http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2035864&blobtype=pdf 13. Doll R and Hill AB. Mortality in relation to smoking: ten years' observations of British doctors. British Medical Journal, 1964; 1(5395):1399-410.
14. Doll R and Hill AB. Mortality in relation to smoking: ten years' observations of British doctors. British Medical Journal, 1964; 1(5396):1460-7 [Concludes].
15. Doll R and Peto R. Mortality in relation to smoking: 20 years' observations on male British doctors. British Medical Journal, 1976; 2(6051):1525-36. Available from: http://www.ncbi.nlm.nih.gov/pubmed/1009386
16. Doll R, Peto R, Wheatly L, Gray R, and Sutherland I. Mortality in relation to smoking: 40 years' observations on male British doctors. British Medical Journal (Clinical Research Ed.), 1994; 309(6959):901–11. Available from: http://www.bmj.com/cgi/content/full/309/6959/901
17. Doll R, Peto R, Boreham J, and Sutherland I. Mortality in relation to smoking: 50 years' observations on male British doctors. British Medical Journal, 2004; 328:1519–1527.
18. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
19. Lubin JH, Caporaso N, Wichmann HE, Schaffrath-Rosario A, and Alavanja MC. Cigarette smoking and lung cancer: modeling effect modification of total exposure and intensity. Epidemiology, 2007; 18(5):639-48. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17700253
20. Peto J. That lung cancer incidence falls in ex-smokers: misconceptions 2. British Journal of Cancer, 2011; 104(3):389. Available from: http://www.nature.com/bjc/journal/v104/n3/full/6606080a.html
21. U.S. Department of Health and Human Services. The Health Consequences of Smoking: 50 Years of Progress. A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014, Printed with corrections, January 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/full-report.pdf
22. Australian Institute of Health and Welfare (AIHW) and Cancer Australia. Lung cancer in Australia: an overview. Cancer series no. 64. Cat. no. CAN 58., Canberra 2011. Available from: http://www.aihw.gov.au /publication-detail/?id=10737420419
23. Thun MJ, Lally CA, Flannery JT, Calle EE, Flanders WD, et al. Cigarette smoking and changes in the histopathology of lung cancer. Journal of the National Cancer Institute, 1997; 89(21):1580–6. Available from: http://jnci.oxfordjournals.org/cgi/content/abstract/89/21/1580
24. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/
25. Patel J. Lung cancer: a biologically different disease in women? Women's Health (London, England), 2009; 5(6):685–91. Available from: http://www.futuremedicine.com/doi/full/10.2217/whe.09.66?cookieSet=1
26. Freedman N, Leitzmann M, Hollenbeck R, Schatzkin A, and Abnet C. Cigarette smoking and subsequent risk of lung cancer in men and women: analysis of a prospective cohort study. The Lancet oncology, 2008; 9(7):649–56. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2601691/pdf/nihms57281.pdf
27. Paulus J, Asomaning K, Kraft P, Johnson B, Lin X, et al. Parity and risk of lung cancer in women. American Journal of Epidemiology, 2010; 171(5):557–63. Available from: http://pubmedcentralcanada.ca /picrender.cgi?accid=PMC2842216&blobtype=pdf
28. Baik C, Strauss G, Speizer F, and Feskanich D. Reproductive factors, hormone use, and risk for lung cancer in postmenopausal women, the Nurses' Health Study. Cancer Epidemiology, Biomarkers & Prevention, 2010; 19(10):2525–33. Available from: http://cebp.aacrjournals.org/content/19/10/2525.long
29. Slatore C, Chien J, Au D, Satia J, and White E. Lung cancer and hormone replacement therapy: association in the Vitamins and Lifestyle Study. Journal of Clinical Oncology, 2010; 28(9):1540–6. Available from: http://pubmedcentralcanada.ca/picrender.cgi?accid=PMC2849773&blobtype=pdf
30. Toriola A, Kurl S, Laukkanen J, and Kauhanen J. Does binge drinking increase the risk of lung cancer: results from the Findrink study. European Journal of Public Health, 2009; 19(4):389–93. Available from: http://eurpub.oxfordjournals.org/content/19/4/389.long
31. Bagnardi V, Rota M, Botteri E, Scotti L, Jenab M, et al. Alcohol consumption and lung cancer risk in never smokers: a meta-analysis. Annals of Oncology, 2011; [Epub ahead of print]. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation& list_uids=21427064
32. Chao C, Slezak J, Caan B, and Quinn V. Alcoholic beverage intake and risk of lung cancer: the California men's health study. Cancer Epidemiology, Biomarkers & Prevention, 2008; 17(10):2692–9. Available from: http://cebp.aacrjournals.org/cgi/content/full/17/10/2692
33. Li Y, Swensen S, Karabekmez L, Marks R, Stoddard S, et al. Effect of emphysema on lung cancer risk in smokers: a computed tomography-based assessment. Cancer Prevention Research, 2011; 4(1):43–50. Available from: http://cancerpreventionresearch.aacrjournals.org/content/4/1/43.long
34. Le Marchand L, Wilkens LR, and Kolonel LN. Ethnic differences in the lung cancer risk associated with smoking. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 1992; 1(2):103-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/1306091
35. Haiman CA, Stram DO, Wilkens LR, Pike MC, Kolonel LN, et al. Ethnic and racial differences in the smoking-related risk of lung cancer. New England Journal of Medicine, 2006; 354(4):333-42. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16436765
36. Derby K, Cuthrell K, Caberto C, Carmella S, Franke A, et al. Nicotine metabolism in three ethnic/racial groups with different risks of lung cancer. Cancer Epidemiology, Biomarkers & Prevention, 2008; 17:3526–35. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2599805/pdf/nihms76008.pdf
37. Bryant A and Cerfolio R. Differences in epidemiology, histology, and survival between cigarette smokers and never-smokers who develop non-small cell lung cancer. Chest, 2007; 132(1):185–92. Available from: http://www.chestjournal.org/cgi/reprint/132/1/185
38. Janjigian Y, McDonnell K, Kris M, Shen R, Sima C, et al. Pack-years of cigarette smoking as a prognostic factor in patients with stage IIIB/IV nonsmall cell lung cancer. Cancer, 2010; 116(3):670–5. Available from: http://www3.interscience.wiley.com/user/accessdenied?ID=123222528&Act=2138&Code=4719&Page=/cgi- bin/fulltext/123222528/HTMLSTART
39. Cataldo JK, Dubey S, and Prochaska JJ. Smoking cessation: an integral part of lung cancer treatment. Oncology, 2010; 78(5-6):289–301. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20699622
40. Parsons A, Daley A, Begh R, and Aveyard P. Influence of smoking cessation after diagnosis of early stage lung cancer on prognosis: systematic review of observational studies with meta-analysis. British Medical Journal, 2010; 340:b5569. Available from: http://pubmedcentralcanada.ca /picrender.cgi?accid=PMC2809841&blobtype=pdf
41. Centers for Disease Control and Prevention. Declines in Lung Cancer Rates—California, 1988-1997. Morbidity and Mortality Weekly Report, 2000; 49(47):1066-9. Available from: http://www.cdc.gov /mmwr/preview/mmwrhtml/mm4947a4.htm
42. Polednak AP. Tobacco control indicators and lung cancer rates in young adults by state in the United States. Tobacco Control, 2008; 17(1):66–9. Available from: http://tobaccocontrol.bmj.com/content /17/1/66.long
43. Peto R, Darby S, Deo H, Silcocks P, Whitley E, et al. Smoking, smoking cessation, and lung cancer in the UK since 1950: combination of statistics with two case-control studies. British Medical Journal (Clinical Research Ed.), 2000; 321(7257):323–9. Available from: http://www.bmj.com/cgi/reprint/321/7257/323
44. Thun MJ and Jemal A. How much of the decrease in cancer death rates in the United States is attributable to reductions in tobacco smoking? Tobacco Control, 2006; 15:345–7.
45. Adair T, Hoy D, Dettrick Z, and Lopez AD. Reconstruction of long-term tobacco consumption trends in Australia and their relationship to lung cancer mortality. Cancer Causes & Control, 2011; 22(7):1047–53. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21617924
46. Australian Institute of Health and Welfare and Australasian Association of Cancer Registries. Cancer in Australia: an overview, 2010. Cancer series no. 60. AIHW cat. no. CAN 56., Canberra: AIHW, 2010. Available from: http://www.aihw.gov.au/publication-detail/?id=6442472459&tab=2
47. Shibuya K, Inoue M, and Lopez AD. Statistical modeling and projections of lung cancer mortality in 4 industrialized countries. Journal international du cancer, 2005; 117(3):476-85. Available from: http://onlinelibrary.wiley.com/store/10.1002/ijc.21078/asset/21078_ftp.pdf?v=1&t=gokpqr43& s=2fedf34080ba36a7dfd925e9c4caa6c5e204ad4ddd
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.5 Other cancers
3.5 Other cancers
Last updated: March 2015 Suggested citation: Hurley, S, Greenhalgh, EM & Winstanley, MH. 3.5 Other cancers. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-5-other-cancers-caused-by-or-associated- with-smo
3.5.1 Upper aerodigestive tract cancers The upper aerodigestive tract comprises the oral cavity (the mouth—including the lip, cheek, gum, tongue and mouth lining), pharynx (throat), larynx (voice box) and oesophagus (the gullet—the muscular tube through which food passes from the throat to the stomach). In epidemiologic studies, cancers of these areas are often grouped together and referred to as upper aerodigestive tract cancer (UADTC). Another grouping is 'head and neck cancer', which comprises cancer of the oral cavity, pharynx and larynx (i.e. the fourth UADTC, oesophageal cancer, is excluded).
In Australia in 2007, there were 1996 new cases of cancer of the lip, tongue or mouth and 328 deaths; 719 new cases of cancer of the pharynx and 280 deaths; 581 new cases and 214 deaths due to cancer of the larynx; and 1264 new cases of oesophageal cancer and 1098 deaths.1 The five-year relative survival rate for cancers of the head and neck was 56.3%.2
3.5.1.1 Risk associated with smoking
Smoking causes all of the UADTCs.3-5 A meta-analysis of 85 studies that included data on more than 50 000 people with UADTC reported an almost four-fold higher risk of these cancers for smokers compared with never smokers and a two-and-a-half-fold higher risk compared with non-smokers.6 Concern about the increasing incidence of UADTC in young people prompted a case–control study in 10 European countries that included people aged under 50 years. Smoking was associated with a five-and-a-half-fold increase in the risk of UADTC.5
The strength of the association between smoking and cancer differs between the sub-types of UADTC. The larynx is directly exposed to tobacco smoke when it is inhaled through the space between the vocal chords, and smoking is particularly strongly associated with cancer of the larynx. Risks for smokers 20-fold higher than for non-smokers have been reported in some studies.3 The meta-analysis of 85 UADTC studies, referred to above, found that the risk of laryngeal cancer was nine times greater for current smokers than never smokers, whereas the risks of oropharyngeal and oesophageal cancer were about three-fold higher in smokers.6
Oesophageal cancer has two histological types: adenocarcinoma (which has further sub-types) and squamous cell carcinoma. An Australian case–control study that included more than 1000 cases found the risk of both squamous cell carcinoma and gastro-oesophageal junction adenocarcinoma was about four-fold higher in smokers compared with never smokers. The risk of oesophageal adenocarcinoma was about two-and-a-half-fold higher in smokers.7 A pooled analysis of data from 10 case–control studies of adenocarcinoma also found that smoking doubled the risk.8 Another pooled analysis of 13 case-control and two cohort studies found a similar (85%) increase in the risk of oesophageal adenocarcinoma associated with smoking.9
3.5.1.2 How tobacco smoke causes UADTC
The 2010 US Surgeon General's report (2010) suggests that the polycyclic aromatic hydrocarbons (PAHs) in the particulate phase of cigarette smoke have a role in the development of cancer of the larynx, and that PAHs and two other constituents of cigarette smoke—NNN (N'-nitrosonornicotine) and NNK (4-(methylnitrosamino)-1(3-pyridyl)-1-butanone)—are the cause of oral cancer.10 Such carcinogens can affect DNA repair, producing chromosomal aberrations, which have been found in increased numbers in the oral mucosa of smokers.11 NNN may also be the key cause of oesophageal cancer; N-nitrosamines are the most potent oesophageal carcinogen known and NNN is the most prevalent N-nitrosamine in cigarette smoke.10
Although the links between smoking and UADTCs are well established, only a small proportion of people exposed to tobacco develop these cancers. Aided by emerging information about the human genome, scientists are therefore studying the impact of gene polymorphisms on differential susceptibility to UADTC (and other cancers) among tobacco users. A 2011 meta-analysis, for example, found that the glutathione S-transferase M1 (GSTM1) null polymorphism (i.e. absence of the gene), was associated with an increased risk of oral cancer in Asians but not Caucasians.12 However, in people with this null polymorphism, the study found that smokers were at lower risk of oral cancer than non-smokers or light smokers. The authors cautioned that the studies they considered had not been designed to investigate this interaction and called for further research.
3.5.1.3 Factors affecting risk
Intensity and duration of smoking
There is a dose–response relationship for smoking and each of the UADTCs. The risk of developing these types of cancer increases with the duration of smoking and the amount smoked.3,4 6 A pooled analysis of 15 case–control studies found that the risk of cancer of the larynx was more strongly associated with greater amounts smoked (cigarettes per day) than the duration of smoking (pack-years).13
Alcohol consumption
Alcohol is also a cause of all UADTC sub-types, and exacerbates the effects of smoking on the risk of UADTC. In other words, the effects of smoking and alcohol are synergistic in relation to UADTC (meaning that the combined effect of tobacco and alcohol exceeds the sum of their individual effects).3,4 In the meta-analysis of 85 studies referred to above, 24 studies investigated the combined effects of alcohol and smoking.6 The risk of UADTC in people who had the highest consumption of alcohol and tobacco was almost five times higher than the risk among heavy smokers who did not drink alcohol, or drank moderately. The synergistic effect of tobacco and alcohol on cancer risk is strongest for cancer of the larynx and weakest for cancer of the oesophagus. A pooled analysis of 17 European and American case–control studies found that 4% of head and neck cancers (oral cavity, pharynx and larynx cancers) were attributable to alcohol alone, 33% were due to tobacco alone and almost 35% were due to tobacco and alcohol combined.14 For cancer of the larynx, these figures were: 3% due to alcohol alone, 52% due to tobacco alone and 33% due to tobacco and alcohol combined.
Smoking cessation
In 2007, the International Agency for Research on Cancer reported that, even after a long period of abstinence, the risk for laryngeal cancer and for carcinoma of the oesophagus does not return to that of never smokers.15 Alternatively, a meta-analysis in 2009 found that risks of all UADTCs decline when people quit smoking relative to continued smoking, and can reach the level of non-smokers about 10 years after smoking cessation.6
3.5.1.4 Impact of smoking on prognosis
Continued smoking after diagnosis of a UADTC increases the risk of a second primary tumour in the region. This is consistent with the concept of 'field cancerisation', which is the concomitant occurrence of carcinogenic alterations in multiple areas of the upper aerodigestive tract.4
Recent studies of patients with head and neck cancer have shown poorer local-regional control,16,17 disease-free survival17 and overall survival16–19 for patients who were smoking at diagnosis or had smoked in the past, compared with never smokers. Patients who continue to smoke while receiving treatment have poorer local-regional control,20 disease-free survival16,20 and overall survival16,19–21 compared with those who quit.
3.5.2 Pancreatic cancer
The pancreas is an abdominal organ that secretes hormones that assist with digestion.
There were 2525 new cases of pancreatic cancer in Australia in 2007 and 2248 deaths.1 Pancreatic cancer has the lowest survival rate of any cancer, and is the seventh most common cause of cancer death in Australia.2,22 Between 1984 and 2004, the 5-year relative survival of patients with pancreatic cancer was only 4.6%, in contrast with 88% for breast cancer.2
3.5.2.1 Risk associated with smoking
Smoking is a well-recognised cause of pancreatic cancer.3,4 A pooled analysis of 12 international prospective cohort studies involving almost 1500 cases found that current smokers had a 77% higher risk of pancreatic cancer than never smokers.23
One of the European cohort studies in the pooled analysis found that exposure to environmental tobacco smoke (ETS) at home or work increased the risk of pancreatic cancer. Exposure to ETS during childhood was also associated with pancreatic cancer, but the increase in risk was not statistically significant.24
3.5.2.2 How tobacco smoke causes pancreatic cancer
NNN and its metabolite NNK, mentioned in Chapter 3, Section 3.5.1.2, are the two known pancreatic carcinogens in tobacco products.10
3.5.2.3 Factors affecting risk
The pooled analysis referred to above found that the risk of pancreatic cancer increases with smoking intensity (cigarettes per day), smoking duration (years smoked) and cumulative smoking dose (pack-years). The risk of pancreatic cancer decreases after quitting, reaching the risk level of non-smokers after about 15 years.23 In Australia, for example, male pancreatic cancer mortality has declined in line with reductions in tobacco consumption approximately 15 years previously.25 However, pancreatic cancer mortality has continued to rise in Australian women. This may be because of the later peak in female tobacco consumption (compared with male tobacco consumption) or because other factors, such as obesity, are also affecting female pancreatic cancer mortality trends.25
3.5.2.4 Impact of smoking on prognosis This issue does not appear to have been studied, presumably because of the short survival time after diagnosis.
3.5.3 Stomach cancer
The stomach is located between the oesophagus and the small intestine and has a role in digestion of food, secreting enzymes and acids.
Gastric (stomach) cancer is categorised according to the site in the stomach where it occurs. Cancers occurring at the gastric cardia, which is near the junction of the oesophagus and stomach, are referred to as gastric cardia cancers. Cancers of the gastric antrum, corpus or fundus are termed non-cardia cancers. The pathogenesis of gastric cancer is thought to differ between cardia and non-cardia gastric cancer.
There were 1897 new cases of stomach cancer in Australia in 2007 and 1129 deaths.1 The 5-year relative survival rate in Australia is 25%, the fifth lowest of cancers.2 Cancer of the stomach was the 10th most common cause of cancer death in Australia in 2007.22
3.5.3.1 Risk associated with smoking
Smoking causes gastric cancer.3,4 A meta-analysis of 46 case–control studies found approximately a 50% increased risk for people who had ever smoked.26 For current smokers compared with never smokers the increase in risk of gastric cancer was about 70%. A meta-analysis of 21 case-control and three cohort studies found that smoking increased the risk of gastric cardia adenocarcinoma by 76%.9
3.5.3.2 How tobacco smoke causes stomach cancer
As yet, there is no well-defined model of stomach cancer genesis. However, it appears that smoking is associated with intestinal metaplasia and dysplasia, which precede cancer,27 and DNA adducts (DNA bonded to a carcinogenic chemical) have been identified in tissue samples from the stomach of smokers.10 Nicotine itself also affects gastric physiology, although it is not clear whether this impacts on carcinogenesis.27
3.5.3.3 Factors affecting risk
The 2004 International Agency for Research on Cancer (IARC) report stated that eight of 16 cohort studies found significant dose–response relationships between intensity of smoking and risk of stomach cancer and five studies found a relationship between duration of smoking and risk. Most of the case–control studies that have examined the dose–response issue have found relationships between both intensity and duration of smoking and gastric cancer risk.4 The IARC concluded that stomach cancer risk increases with duration of smoking and number of cigarettes smoked.
The risk of gastric cancer decreases with increasing duration of quitting.4
The 2004 US Surgeon General's report concluded that: 'The evidence is suggestive but not sufficient to infer a causal relationship between smoking and noncardia gastric cancers'.3 This issue has been difficult to resolve because many studies of the risk of gastric cancer associated with smoking have not distinguished between cancer sub-site types. However, the meta-analysis referred to above identified five studies of non-cardia gastric cancer and four studies of cardia gastric cancer.26 Smoking significantly increased the risk of both types of stomach cancer; the risk of cardia cancer was increased by 47% and the risk of non-cardia cancer by 32%.
A prospective study of approximately 1000 Japanese men who were followed up for 14 years found that smoking and Helicobacter pylori infection had a synergistic effect on the risk of gastric cancer.28 The risk of gastric cancer for men who smoked but did not have H. pylori infection was almost six-fold higher than that of non-smokers without H. pylori infection, whereas the risk for men who both smoked and had H. pylori infection was 11-fold higher. In this population, 7.3% of gastric cancer was estimated to be due to smoking alone, 30.1% was due to H. pylori infection alone and 49.6% was due to cigarette smoking with H. pylori infection.
3.5.4 Kidney and bladder cancers
The urinary system includes the bladder, ureters, urethra and kidneys, which filter the blood and excrete waste (urine), which is transferred to the bladder via the ureters, and exits the body via the urethra. The kidneys also have homeostatic roles in relation to blood pressure, acid-base balance and electrolytes.
In Australia in 2007, there were 2580 new cases of kidney (renal cell) cancer, 2217 new cases of bladder cancer and 399 new cases of cancer of other urinary organs.1 Kidney cancer was the ninth most commonly reported cancer.22 Five-year relative survival rates for cancers diagnosed between 1998 and 2004 were 65.8% for kidney cancer and 60.4% for bladder cancer. Deaths from these cancers numbered 855, 925 and 70, for kidney, bladder and other urinary organ cancers respectively.1
3.5.4.1 Risk associated with smoking
Smoking causes cancer of the kidney,3 bladder and renal pelvis (a portion of the ureter).3, 4
A meta-analysis that included more than 8000 cases of kidney cancer found a 50% higher risk of for men who had smoked cigarettes compared with never smokers.29 The corresponding risk for women was 22%. ETS may increase the risk of kidney cancer. Non-smokers with high combined exposure to home and work ETS have been found in one study to have a two- to four-fold higher risk of renal cell carcinoma compared with non-smokers who were not exposed to tobacco smoke.30
A case–control study and accompanying editorial published in the Journal of the National Cancer Institute in 2009 suggest that the association between bladder cancer and smoking has increased substantially between 1994 and 2004.30,31 The risk of bladder cancer for current smokers relative to never smokers was 2.9 in 1994–1998, 4.2 in 1998–2001 and 5.5 in 2001–2004. The editorial points out that the concentrations of specific carcinogens in tobacco smoke have increased, and hypothesises that this may be the cause of the observed increase in smoking-attributable bladder cancer risk.31
The IARC has estimated that 66% of bladder cancer in men and 30% in women is due to smoking.4
3.5.4.2 How tobacco smoke causes kidney and bladder cancers
Aromatic amines, including 2-naphthylamine and 4-aminobiphenyl (4-ABP), are combustion products of cigarette smoke and are known bladder carcinogens. They are thought to contribute to bladder cancer.4, 10
3.5.4.3 Factors affecting risk
The risk of kidney cancer increases with the amount smoked, and declines after quitting.28
The risks of bladder cancer and cancer of the renal pelvis and the ureter increase with the amount of tobacco consumed and the duration of smoking, although for bladder cancer a levelling off of risk at high daily consumption levels, possibly due to under-reporting of consumption by heavy smokers, has been reported.4
The risk of bladder cancer declines after smoking cessation, rapidly in the first one to four years. However, even after 25 years the risk is not as low as for non-smokers.4
3.5.4.4 Impact of smoking on prognosis A 2002 systematic review found that smoking cessation might favourably alter the course of bladder cancer, but the evidence was insufficient to conclusively recommend to patients that quitting will improve their prognosis.33 A recent study found that smoking status and a higher cumulative smoking exposure are associated with worse prognosis in patients with primary non–muscle-invasive bladder cancer, who had higher rates of disease recurrence and progression, and lower overall survival.34
3.5.5 Cervical cancer
The cervix is the lower portion of the uterus, where it joins the vagina.
There were 739 new cases and 208 deaths from cancer of the cervix in Australia in 2007.1 The 5-year relative survival rate was 71.8%.2
3.5.5.1 Risk associated with smoking
Infection with human papilloma virus (HPV) is the main risk factor for cancer of the cervix, and until recently it had been unclear whether the observed association between smoking and cervical cancer was due to confounding, as women who are HPV-positive have been found to be more likely to be smokers.35 The IARC and US Surgeon General concluded in 2004 that smoking causes cervical cancer,3, 4 and two recent case–control studies36,37 and a review38 confirm that smoking is an independent risk factor for cervical cancer. The review cited articles that suggest smoking increases the risk of squamous cell cervical carcinoma, but not adenocarcinoma, and that risk increases significantly with intensity and duration of smoking.38
Small studies have recently reported associations between smoking and neoplasia of other genital tract tissue.39, 40 Neoplasia is the abnormal proliferation of cells and can progress to cancer.
3.5.5.2 How tobacco smoke causes cervical cancer
Smokers' cervical mucus is mutagenic and contains the carcinogen NNK. Levels of DNA adducts are higher in the cervical tissue of smokers than non-smokers, indicating DNA damage, and it is thought that in combination with HPV these compounds may contribute to the development of cervical cancer in smokers.4,10
3.5.5.3 Factors affecting risk
There is a dose–response relationship between smoking and cervical cancer; the risk of cervical cancer increases with the duration of smoking.3
3.5.5.4 Impact of smoking on prognosis
A study in the US involving approximately 2500 women with cervical cancer, who were followed for up to 5 years, found that smokers were about 20% more likely to die from cervical cancer.41
3.5.6 Acute myeloid leukaemia
Acute myeloid leukaemia (AML) is a type of cancer that affects the blood and bone marrow. Myeloid leukaemias involve overproduction of immature white blood cells called myeloblasts (in contrast to lymphoid leukaemias which arise in immature blood cells called lymphoblasts). This overproduction of myeloblasts prevents the bone marrow from making normal blood cells. AML develops quickly, with anaemia, bleeding and bruising occurring because of inadequate numbers of red cells or platelets. If untreated, AML is rapidly fatal. In contrast, chronic myeloid leukaemia develops more slowly and urgent treatment is usually not necessary.
There were 849 new cases and 721 deaths from AML in Australia in 2007.2 AML is the second most common myeloid cancer,2 and myeloid cancers were the sixth most common cancers reported in 2007.22
3.5.6.1 Risk associated with smoking
Smoking causes AML.3,4 Studies have generally reported an approximate doubling of the risk of AML for current smokers, but the Whitehall study (of almost 20 000 male government employees who were followed up from the 1960s to 2005) found a five-fold increase in risk of myeloid cancers for current smokers.42
3.5.6.2 How tobacco smoke causes acute myeloid leukaemia
Benzene, which is contained in cigarette smoke, is thought to be the likely carcinogen in AML. Polonium-210 and lead-210, both of which emit ionising radiation, are also found in cigarette smoke. Ionising radiation is a recognised cause of leukaemia.3,10
3.5.6.3 Factors affecting risk
The risk of AML increases with the amount smoked and the duration of smoking.3
3.5.6.4 Impact of smoking on prognosis
A small study of 148 patients undergoing stem cell transplantation for treatment of acute leukaemia found that smokers had longer hospitalisation and poorer survival.43
3.5.7 Liver cancer
The liver is an abdominal organ essential for metabolism and detoxification.
In 2007, there were 1169 new cases of liver cancer and 1109 deaths in Australia.1
3.5.7.1 Risk associated with smoking
The IARC concluded in 2004 and the Surgeon General concurred in 2014 that tobacco smoking causes liver cancer.4,44 Researchers from the IARC and the US conducted a meta-analysis of 38 cohort studies and 58 case–control studies to clarify the potential association, and found a ‘moderate’ statistically significant 50% increase in risk for current smokers compared with never-smokers.45 More recently, the US Surgeon General reported a 60-70% increased risk of liver cancer in current smokers compared with never-smokers.46
3.5.7.2 How tobacco smoke causes kidney and bladder cancers
The liver metabolises many circulating carcinogens from tobacco smoke,46 with NNK, other nitrosamines and furan identified as likely liver carcinogens.10 A number of potential mechanisms have been identified in liver carcinogenesis, including long-term exposure to carcinogens in cigarette smoke increasing the risk of cellular damage in the liver and in turn the development of cancer. Smoking also increases the risk of liver fibrosis, primary biliary cirrhosis, and chronic liver disease, which can progress to liver cancer.46
3.5.7.3 Factors affecting risk A meta-analysis found some evidence of an increase in risk with the number of cigarettes smoked per day, but this effect differed between studies.45 There is also limited evidence suggesting that the effect of smoking on risk for liver cancer may be modified by viral hepatitis, but further studies are needed to clarify this relationship.46
3.5.8 Colorectal (bowel) cancer
The colon is the major part of the large intestine and its primary function is absorption of water from digested material. The rectum is the final (straight) portion of the large intestine, where faeces are stored before defecation through the anus.
Bowel cancer was the second most commonly reported cancer (after prostate cancer) and the second most common cause of cancer death (after lung cancer) in Australia in 2007.21 There were 14 234 new cases of bowel cancer and 4047 deaths.1 The 5-year relative survival rate was 61.8%.2
3.5.8.1 Risk associated with smoking
Four meta-analyses47–50 and an analysis of a large US prospective cohort study,51 have concluded that cigarette smoking is associated with colorectal cancer. The increase in risk is about 20%. Similarly, the US Surgeon General concluded in 2014 that smoking causes colorectal adenomatous polyps and colorectal cancer.44
In fact, colorectal cancer is a complex collection of diseases and causation appears likely to differ between molecularly defined subsets. A study in women from Iowa in the US found only a moderately increased risk of colorectal cancer associated with smoking, but much higher risks for sub-types defined by anatomical location, phenotype and BRAF mutation status.52,53
A case–control study found the risk estimates for the association between smoking and colorectal cancer increased when smokers were compared with non-smokers who had not been exposed to ETS, suggesting that ETS may be associated with colorectal cancer.54
The evidence that smoking is associated with colorectal cancer has led to a suggestion that screening guidelines for bowel cancer be amended to recommend that screening for smokers start at age 45 years rather than 50 years.52,55
3.5.8.2 How tobacco smoke causes bowel cancer
The evidence strongly suggests an effect of smoking in increasing the formation of polyps, the precursor of colorectal cancer, and possibly also the development of malignancy.44 The many carcinogens in cigarette smoke can reach the bowel via the bloodstream. Higher concentrations of DNA adducts to metabolites of PAHs have been found in the bowel tissue of smokers than non-smokers.56 The identification of sub-types of colorectal cancer for which the causative link with smoking is stronger has led to suggestions that smoking's impact on colorectal cancer is mediated through interference with normal DNA methylation pathways.52
3.5.8.3 Factors affecting risk
The recent analyses have generally reported increases in risk with amount smoked per day, pack-years of smoking and longer duration of smoking.47,49,51
Two of the meta-analyses analysed risk by sub-site of cancer and found that the risk associated with smoking is higher for rectal cancer than colon cancer.49,50
Former smokers generally have lower risk than current smokers and the large US cohort analysis found a trend for decreased risk of colorectal cancer with longer time since cessation and no association for former smokers who had quit before age 40 years or had been non-smokers for 31 years or more.51
3.5.8.4 Impact of smoking on prognosis
Two of the meta-analyses investigated the link between smoking and death from colorectal cancer and found that mortality rates are higher in smokers.47,49 This could reflect an impact of smoking on prognosis as well as bowel cancer incidence. A small study of people with cancer of the anus found that recurrence rates and cancer-related deaths were higher in patients who continued to smoke.57
3.5.9 Breast cancer
In Australia in 2007, breast cancer was the third most commonly reported cancer22 (and the most commonly diagnosed cancer in women)1 and the fourth most common cause of cancer death.22 There were 12 670 new cases and 2706 deaths.1 The five-year relative survival rate was 87.7%.2
3.5.9.1 Risk associated with smoking
In 2011, a Canadian expert panel reviewed the evidence and concluded that active smoking causes breast cancer and that the association between exposure to ETS and breast cancer in young women who have never smoked is also consistent with causality.58 The results of a US cohort study involving almost 80,000 women were consistent with this conclusion.59 Most recently, the US Surgeon General concluded that there is sufficient evidence to identify mechanisms by which cigarette smoking may cause breast cancer, and both active and passive smoking are associated with an increased risk of breast cancer.44 Although there are at least 20 known or suspected mammary carcinogens in tobacco smoke,58 further data and analyses will be needed before the association between smoking and breast cancer can definitely be regarded as causative.
3.5.9.2 How tobacco smoke causes breast cancer
There are biologically plausible mechanisms, particularly for DNA adduct formation and unrepaired DNA mutations, by which exposure to tobacco smoke could cause breast cancer. These mechanisms are supported by research to date; however, further studies are needed to identify a specific model of these effects.44
3.5.9.3 Factors affecting risk
Having ever smoked relates to an increased relative risk for breast cancer by an average of 10%; smoking for 20 or more years, 20 or more cigarettes per day, or 20 or more pack-years of smoking has been shown to significantly increase this risk by 13-16%, depending on the study.
There is emerging evidence that premenopausal women may be at greater risk for breast cancer from smoking than postmenopausal women, with risks of 17% and 7% respectively.44
3.5.9.4 Impact of smoking on prognosis
The US Surgeon General has highlighted the difficulty in inferring a causal association between smoking and breast cancer mortality; there are many confounding variables relating to treatment and other noncancer, smoking-related comorbidities that can contribute to mortality. There is currently insufficient evidence to conclude that either active or passive smoking influences breast cancer mortality.44
3.5.10 Other cancers 3.5.10.1 Hodgkin lymphoma
Studies of Hodgkin lymphoma and smoking reviewed by the IARC reported weak or no association.4 A study published in 2009 found that people who smoked for 25 years or more were at increased risk of Hodgkin lymphoma, but this association is unconfirmed.60
3.5.10.2 Prostate cancer
Both the IARC in 2004 and the US Surgeon General in 2014 concluded in 2004 that the evidence did not support a causal relationship between prostate cancer and smoking.4,44 A subsequent meta-analysis of cohort studies found no increase in risk of prostate cancer overall in smokers, but did find a slightly increased risk associated with higher daily consumption of cigarettes or greater pack-years of smoking.61 A large prospective US cohort study, involving over a quarter of a million men, found that current and former smokers may be at decreased risk of being diagnosed with prostate cancer,62 and a review of the epidemiologic evidence found that smokers are not at appreciably higher risk of developing prostate cancer.63
The US Surgeon General concluded that the evidence suggests that smokers have a higher mortality rate from prostate cancer than non-smokers, as well as a higher risk of advanced-stage disease, less well-differentiated cancer, and a higher risk of disease progression.44 The elevated risk of death from prostate cancer noted by the US Surgeon General has also been reported in the meta-analysis61 and other studies,62 and the review of epidemiologic evidence concluded that smokers appear to have more advanced disease at diagnosis, a worse prognosis and a greater risk of fatal prostate cancer.63
Smoking is known to alter sex steroid hormone levels, and this effect may be a confounder in studies to date. Further research is needed to clarify the role of smoking in prostate cancer.
References
1. Australian Institute of Health and Welfare and Australasian Association of Cancer Registries. Cancer in Australia: an overview, 2010. Cancer series no. 60. AIHW cat. no. CAN 56. Canberra: AIHW, 2010. Available from: http://www.aihw.gov.au/publication-detail/?id=6442472459&tab=2
2. Australian Institute of Health and Welfare. Cancer survival and prevalence in Australia: cancers diagnosed from 1982 to 2004. Cancer series no. 42. AIHW cat. no CAN 38. Canberra: AIHW, 2008. Available from: http://www.aihw.gov.au/publication-detail/?id=6442468141&libID=6442468139
3. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
4. International Agency for Research on Cancer Working Group on the Evaluation of Carcinogenic Risks to Humans. Tobacco smoke and involuntary smoking. IARC monographs on the evaluation of the carcinogenic risk of chemicals to humans. Volume 83. Lyon: International Agency for Research on Cancer, 2004. Available from: http://monographs.iarc.fr/ENG/Monographs/allmonos90.php
5. Macfarlane T, Macfarlane G, Oliver R, Benhamou S, Bouchardy C, Ahrens W, et al. The aetiology of upper aerodigestive tract cancers among young adults in Europe: the ARCAGE study. Cancer Causes & Control 2010;21(12):2213-21. Available from: http://www.springerlink.com/content/b340005471h2g8m7/fulltext.html 6. Ansary-Moghaddam A, Huxley R, Lam T and Woodward M. The risk of upper aero digestive tract cancer associated with smoking, with and without concurrent alcohol consumption. Mount Sinai Journal of Medicine 2009;76(4):392–403. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve& db=PubMed&dopt=Citation&list_uids=19642154
7. Pandeya N, Williams G, Sadhegi S, Green A, Webb P and Whiteman D. Associations of duration, intensity, and quantity of smoking with adenocarcinoma and squamous cell carcinoma of the esophagus. American Journal of Epidemiology 2008;168(1):105–14. Available from: http://aje.oxfordjournals.org /cgi/content/full/kwn091v1
8. Cook M, Kamangar F, Whiteman D, Freedman N, Gammon M, Bernstein L, et al. Cigarette smoking and adenocarcinomas of the esophagus and esophagogastric junction: a pooled analysis from the international BEACON consortium. Journal of the National Cancer Institute 2010;102(17):1344–53. Available from: http://jnci.oxfordjournals.org/content/102/17/1344.long
9. Tramacere I, La Vecchia C and Negri E. Tobacco smoking and esophageal and gastric cardia adenocarcinoma: a meta-analysis. Epidemiology 2011;[Epub ahead of print]. Available from: http://journals.lww.com/epidem/Abstract/publishahead /Tobacco_Smoking_and_Esophageal_and_Gastric_Cardia.99596.aspx
10. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease. A report of the US Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: http://www.surgeongeneral.gov/library/tobaccosmoke/report/index.html
11. Sabitha K, Reddy M and Jamil K. Smoking related risk involved in individuals carrying genetic variants of CYP1A1 gene in head and neck cancer. Cancer Epidemiology 2010;34(5):587–92. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation& list_uids=20887941
12. Zhang Z, Hao K, Shi R, Zhao G, Jiang G, Song Y, et al. Glutathione S-Transferase M1 (GSTM1) and Glutathione S-Transferase T1 (GSTT1) null polymorphisms, smoking, and their interaction in oral cancer: a HuGE review and meta-analysis. American Journal of Epidemiology 2011;173(8):847–57. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21436184
13. Lubin J, Purdue M, Kelsey K, Zhang Z, Winn D, Wei Q, et al. Total exposure and exposure rate effects for alcohol and smoking and risk of head and neck cancer: a pooled analysis of case-control studies. American Journal of Epidemiology 2009;170(8):937–47. Available from: http://pubmedcentralcanada.ca /picrender.cgi?accid=PMC2800266&blobtype=pdf
14. Hashibe M, Brennan P, Chuang SC, Boccia S, Castellsague X, Chen C, et al. Interaction between tobacco and alcohol use and the risk of head and neck cancer: pooled analysis in the International Head and Neck Cancer Epidemiology Consortium. Cancer Epidemiology, Biomarkers & Prevention 2009;18(2):541–50. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3051410/pdf/nihms270552.pdf
15. International Agency for Research on Cancer, Reversal of risk after quitting smoking. Vol. 11. World Health Organization; 2007.
16. Fortin A, Wang C, and Vigneault E. Influence of smoking and alcohol drinking behaviors on treatment outcomes of patients with squamous cell carcinomas of the head and neck. International Journal of Radiation Oncology, Biology, Physics, 2008; 74(4):1062−9. Available from: http://www.ncbi.nlm.nih.gov/pubmed /19036528
17. Chen A, Chen L, Vaughan A, Farwell D, Luu Q, et al. Head and neck cancer among lifelong never- smokers and ever-smokers: matched-pair analysis of outcomes after radiation therapy. American Journal of Clinical Oncology, 2010; [Epub ahead of print]. Available from: http://journals.lww.com/amjclinicaloncology /Abstract/publishahead/Head_and_Neck_Cancer_Among_Lifelong_Never_Smokers.99768.aspx 18. Duffy S, Ronis D, McLean S, Fowler K, Gruber S, et al. Pretreatment health behaviors predict survival among patients with head and neck squamous cell carcinoma Journal of Clinical Oncology, 2009; 27(12):1969−75. Available from: http://jco.ascopubs.org/cgi/reprint/JCO.2008.18.2188v1
19. Mayne S, Cartmel B, Kirsh V, and Goodwin W, Jr. Alcohol and tobacco use prediagnosis and postdiagnosis, and survival in a cohort of patients with early stage cancers of the oral cavity, pharynx, and larynx. Cancer Epidemiology, Biomarkers & Prevention, 2009; 18(12):3368–74. Available from: http://cebp.aacrjournals.org/content/18/12/3368.long
20. Chen A, Chen L, Vaughan A, Sreeraman R, Farwell D, et al. Tobacco smoking during radiation therapy for head-and-neck cancer is associated with unfavorable outcome. International Journal of Radiation Oncology, Biology, Physics, 2011; 79(2):414–9 Available from: http://www.redjournal.org/article /S0360-3016%2809%2903526-3/pdf
21. Hilgert E, Bergmann C, Fichtner A, Gires O, and Issing W. Tobacco abuse relates to significantly reduced survival of patients with oropharyngeal carcinomas. European Journal of Cancer Prevention, 2009; 18(2):120–6. Available from: http://journals.lww.com/eurjcancerprev/pages/articleviewer.aspx?year=2009& issue=04000&article=00005&type=abstract
22. Australian Institute of Health and Welfare Cancer. Available from: http://www.aihw.gov.au/cancer/
23. Lynch S, Vrieling A, Lubin J, Kraft P, Mendelsohn J, et al. Cigarette smoking and pancreatic cancer: a pooled analysis from the pancreatic cancer cohort consortium. American Journal of Epidemiology, 2009; 170(4):403–13. Available from: http://pubmedcentralcanada.ca/picrender.cgi?accid=PMC2733861& blobtype=pdf
24. Vrieling A, Bueno-de-Mesquita H, Boshuizen H, Michaud D, Severinsen M, et al. Cigarette smoking, environmental tobacco smoke exposure and pancreatic cancer risk in the European prospective investigation into cancer and nutrition. International Journal of Cancer, 2009; 126(10):2394-403. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19790196
25. Adair T, Hoy D, Dettrick Z, and Lopez A. Tobacco consumption and pancreatic cancer mortality: what can we conclude from historical data in Australia? European Journal of Public Health, 2011; [Epub ahead of print]. Available from: http://eurpub.oxfordjournals.org/content/early/2011/05/26/eurpub.ckr048.long
26. La Torre G, Chiaradia G, Gianfagna F, De Lauretis A, Boccia S, et al. Smoking status and gastric cancer risk: an updated meta-analysis of case-control studies published in the past ten years. Tumori, 2009; 95(1):13–22. Available from: http://www.tumorionline.it/allegati/00410_2009_01/fulltext /03-LaTorre%20(13-22).pdf
27. US Department of Health and Human Services. The health benefits of smoking cessation. A report of the Surgeon General. Atlanta, GA: Centers for Disease Control, Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 1990. Available from: http://profiles.nlm.nih.gov/NN/B/B /C/V/_/nnbbcv.pdf
28. Shikata K, Doi Y, Yonemoto K, Arima H, Ninomiya T, et al. Population-based prospective study of the combined influence of cigarette smoking and Helicobacter pylori infection on gastric cancer incidence: the Hisayama study. American Journal of Epidemiology, 2008; 168(12):1409–15. Available from: http://aje.oxfordjournals.org/content/168/12/1409.full.pdf
29. Hunt JD, van der Hel OL, McMillan GP, Boffetta P, and Brennan P. Renal cell carcinoma in relation to cigarette smoking: meta-analysis of 24 studies. Journal international du cancer, 2005; 114(1):101–8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15523697
30. Theis R, Dolwick Grieb S, Burr D, Siddiqui T, and Asal N. Smoking, environmental tobacco smoke and risk of renal cell cancer: a population-based case-control study. BMC Cancer, 2008; 8(1):387. Available from: http://www.biomedcentral.com/content/pdf/1471-2407-8-387.pdf
31. Baris D, Karagas M, Verrill C, Johnson A, Andrew A, et al. A case-control study of smoking and bladder cancer risk: emergent patterns over time. Journal of the National Cancer Institute, 2009; 101(22):1553–61. Available from: http://pubmedcentralcanada.ca/picrender.cgi?accid=PMC2778671&blobtype=pdf
32. Alberg A and Hebert J. Cigarette smoking and bladder cancer: a new twist in an old saga? Journal of the National Cancer Institute, 2009; 101(22):1525–6. Available from: http://pubmedcentralcanada.ca /picrender.cgi?accid=PMC2778672&blobtype=pdf
33. Aveyard P, Adab P, Cheng K, Wallace D, Hey K, et al. Does smoking status influence the prognosis of bladder cancer? A systematic review. BJU international, 2002; 90(3):228-239. Available from: http://www.phc.ox.ac.uk/publications/311349
34. Rink M, Furberg H, Zabor EC, Xylinas E, Babjuk M, et al. Impact of Smoking and Smoking Cessation on Oncologic Outcomes in Primary Non–muscle-invasive Bladder Cancer. European urology, 2013; 63(4):724-732. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3969986/
35. Lindau S, Drum M, Gaumer E, Surawska H, and Jordan J. Prevalence of high-risk human papillomavirus among older women. Obstetrics and Gynecology, 2008; 112(5):979–89. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2698799/pdf/nihms108535.pdf
36. Collins S, Rollason T, Young L, and Woodman C. Cigarette smoking is an independent risk factor for cervical intraepithelial neoplasia in young women: a longitudinal study. European Journal of Cancer, 2009; 46(2):405–11. Available from: http://pubmedcentralcanada.ca/picrender.cgi?accid=PMC2808403& blobtype=pdf
37. Kapeu A, Luostarinen T, Jellum E, Dillner J, Hakama M, et al. Is smoking an independent risk factor for invasive cervical cancer? A nested case-control study within Nordic biobanks. American Journal of Epidemiology, 2009; 169(4):480–8. Available from: http://aje.oxfordjournals.org/cgi/content/full/169/4/480
38. Gadducci A, Barsotti C, Cosio S, Domenici L, and Riccardo Genazzani A. Smoking habit, immune suppression, oral contraceptive use, and hormone replacement therapy use and cervical carcinogenesis: a review of the literature. Gynecological Endocrinology, 2011; [Epub ahead of print]. Available from: http://informahealthcare.com/doi/full/10.3109/09513590.2011.558953
39. Sherman J, Mount S, Evans M, Skelly J, Simmons-Arnold L, et al. Smoking increases the risk of high-grade vaginal intraepithelial neoplasia in women with oncogenic human papillomavirus. Gynecologic Oncology, 2008; 110(3):396−401. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18586314
40. Khan A, Freeman-Wang T, Pisal N, and Singer A. Smoking and multicentric vulval intraepithelial neoplasia. Journal of Obstetrics and Gynaecology, 2009; 29(2):123–5. Available from: http://www.informaworld.com/smpp/content~db=all?content=10.1080/01443610802668938
41. Coker A, Desimone C, Eggleston K, Hopenhayn C, Nee J, et al. Smoking and survival among Kentucky women diagnosed with invasive cervical cancer: 1995–2005 Gynecologic Oncology, 2008; 112(2):365−9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19036421
42. Batty G, Kivimaki M, Gray L, Smith G, Marmot M, et al. Cigarette smoking and site-specific cancer mortality: testing uncertain associations using extended follow-up of the original Whitehall study. Annals of Oncology, 2008; 19(5):996–1002. Available from: http://annonc.oxfordjournals.org/cgi/content/full/19/5/996
43. Ehlers S, Gastineau D, Patten C, Decker P, Rausch S, et al. The impact of smoking on outcomes among patients undergoing hematopoietic SCT for the treatment of acute leukemia. Bone Marrow Transplantation, 2011; 46(2):285−90. Available from: http://www.nature.com/bmt/journal/vaop/ncurrent/full/bmt2010113a.html
44. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/
45. Lee YC, Cohet C, Yang YC, Stayner L, Hashibe M, et al. Meta-analysis of epidemiologic studies on cigarette smoking and liver cancer. International Journal of Epidemiology, 2009; 38(6):1497–511. Available from: http://ije.oxfordjournals.org/cgi/content/full/dyp280v1
46. U.S. Department of Health and Human Services. The Health Consequences of Smoking: 50 Years of Progress. A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library /reports/50-years-of-progress/full-report.pdf
47. Botteri E, Iodice S, Bagnardi V, Raimondi S, Lowenfels A, et al. Smoking and colorectal cancer: a meta-analysis. Journal of the American Medical Association, 2008; 300(23):2765–78. Available from: http://jama.ama-assn.org/cgi/content/full/300/23/2765
48. Huxley R, Ansary-Moghaddam A, Clifton P, Czernichow S, Parr C, et al. The impact of dietary and lifestyle risk factors on risk of colorectal cancer: a quantitative overview of the epidemiological evidence. International Journal of Cancer, 2009; 125(1):171–80. Available from: http://www3.interscience.wiley.com /user/accessdenied?ID=121684303&Act=2138&Code=4719&Page=/cgi-bin/fulltext/121684303/HTMLSTART
49. Liang P, Chen T, and Giovannucci E. Cigarette smoking and colorectal cancer incidence and mortality: systematic review and meta-analysis International Journal of Cancer, 2009; 124(10):2406–15. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19142968
50. Tsoi K, Pau C, Wu W, Chan F, Griffiths S, et al. Cigarette smoking and the risk of colorectal cancer: a meta-analysis of prospective cohort studies. Clinical Gastroenterology and Hepatology, 2009; 7(6):682-8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19245853
51. Hannan L, Jacobs E, and Thun M. The association between cigarette smoking and risk of colorectal cancer in a large prospective cohort from the United States. Cancer Epidemiology, Biomarkers & Prevention, 2009; 18(12):3362–7. Available from: http://cebp.aacrjournals.org/content/18/12/3362.long
52. Limsui D, Vierkant R, Tillmans L, Wang A, Weisenberger D, et al. Cigarette smoking and colorectal cancer risk by molecularly defined subtypes. Journal of the National Cancer Institute, 2010; 102(14):1012–22. Available from: http://jnci.oxfordjournals.org.ezp.lib.unimelb.edu.au/content/102/14 /1012.full.pdf
53. Boland C and Goel A. Clearing the air on smoking and colorectal cancer. Journal of the National Cancer Institute, 2010; 102(14):1012–22. Available from: http://jnci.oxfordjournals.org/cgi/content/full/djq241v1
54. Peppone L, Reid M, Moysich K, Morrow G, Jean-Pierre P, et al. The effect of secondhand smoke exposure on the association between active cigarette smoking and colorectal cancer. Cancer Causes & Control, 2010; 21(8):1247−55. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20376547
55. Acott A, Theus S, Marchant-Miros K, and Mancino A. Association of tobacco and alcohol use with earlier development of colorectal cancer: should we modify screening guidelines? American Journal of Surgery, 2008; 196(6):915–9. Available from: http://www.ajsfulltextonline.com/article/S0002-9610(08)00644-2/pdf
56. Raimondi S, Botteri E, Iodice S, Lowenfels A, and Maisonneuve P. Gene-smoking interaction on colorectal adenoma and cancer risk: review and meta-analysis. Mutation Research, 2009; 670(1−2):6−14. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19589345
57. Ramamoorthy S, Luo L, Luo E, and Carethers J. Tobacco smoking and risk of recurrence for squamous cell cancer of the anus. Cancer Detection and Prevention., 2008; 32(2):116–120. Available from: http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6X28-4T0X2K0-2-5&_cdi=7264&_user=10& _orig=search&_coverDate=12%2F31%2F2008&_sk=999679997&view=c&wchp=dGLbVtz-zSkWA& md5=4d46f0ee9e9e18d2ea47a24805958273&ie=/sdarticle.pdf
58. Johnson K, Miller A, Collishaw N, Palmer J, Hammond S, et al. Active smoking and secondhand smoke increase breast cancer risk: the report of the Canadian Expert Panel on Tobacco Smoke and Breast Cancer Risk (2009). Tobacco Control, 2011; Jan 20(1):e2. Available from: http://tobaccocontrol.bmj.com/content /early/2010/10/27/tc.2010.035931.full 59. Luo J, Margolis K, Wactawski-Wende J, Horn K, Messina C, et al. Association of active and passive smoking with risk of breast cancer among postmenopausal women: a prospective cohort study. British Medical Journal, 2011; 342:d1016. Available from: http://pubmedcentralcanada.ca /picrender.cgi?accid=PMC3047002&blobtype=pdf
60. Karunanayake C, Singh G, Spinelli J, McLaughlin J, Dosman J, et al. Occupational exposures and Hodgkin lymphoma: Canadian case-control study. Journal of Occupational and Environmental Medicine, 2009; 51(12):1447–54. Available from: http://journals.lww.com/joem/pages/articleviewer.aspx?year=2009& issue=12000&article=00014&type=abstract
61. Huncharek M, Haddock S, Reid R, and Kupelnick B. Smoking as a risk factor for prostate cancer: a meta-analysis of 24 prospective cohort studies. American Journal of Public Health, 2010; 100(4):693–701. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19608952
62. Watters J, Park Y, Hollenbeck A, Schatzkin A, and Albanes D. Cigarette smoking and prostate cancer in a prospective US cohort study. Cancer Epidemiology, Biomarkers & Prevention, 2009; 18(9):2427–35. Available from: http://cebp.aacrjournals.org/content/18/9/2427.long
63. Zu K and Giovannucci E. Smoking and aggressive prostate cancer: a review of the epidemiologic evidence. Cancer Causes and Control, 2009; 20(10):1799–810. Available from: http://www.ncbi.nlm.nih.gov /pubmed/19562492
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.6 Reproductive health
3.6 Reproductive health
Last updated: March 2015 Suggested citation: Hurley, S, Greenhalgh, EM & Winstanley, MH. 3.6 Reproductive health. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-6-reproductive-health-and-smoking
3.6.1 Menstrual function, menarche and menopause The 2001 US Surgeon General's report reached suggestive conclusions about the impact of smoking on menstrual cycles and reproductive lifespan: the period from the commencement of menstruation (menarche) to its cessation (menopause).1 The 2010 US Surgeon General's report expanded on these conclusions.2
Women who smoke are, generally, at higher risk of dysmenorrhoea (painful menstruation) and a range of other symptoms such as premenstrual tension and heavy periods.2 In the US Nurses' Health Study, for example, smokers were twice as likely as non-smokers to develop premenstrual syndrome over a two- to four-year period.3 Smokers also tend to have a shorter and more variable menstrual cycle. The former has been attributed to a shortening of the follicular phase. A non-statistically significant higher risk of anovulation in smokers has been found in some studies. These effects are consistent with an increased risk of infertility (see Section 3.6.2) as the timing of ovulation is less predictable in women with variable cycle length and a shortened follicular phase may indicate abnormal formation of follicles and maturation of ova.2
Smoking may also result in an earlier menopause. A meta-analysis found that smokers were between 0.8 to 1.7 years younger than non-smokers at menopause.2 More menopausal symptoms have also been reported, although hot flushes associated with smoking may result from a non-hormonal mechanism.2, 4 It has been suggested that shorter cycles may deplete oocytes earlier leading to an earlier menopause and thus a shorter reproductive life span. An earlier age at menarche has been reported for the daughters of women who smoked heavily during pregnancy.2
3.6.2 Fertility
Measures of fertility include fecundability (the monthly probability of conception), infertility (defined as lack of conception after one year of unprotected intercourse), and sub-fertility (reduced fertility, measured by time to conception or inability to conceive within six months). Smoking reduces fertility in women. Studies have found reduced pregnancy rates, longer time to pregnancy and decreased fecundability in women who smoke.2 A trend of decreased fertility with increasing number of cigarettes smoked has been reported.5 The American Society for Reproductive Medicine estimated that 13% of infertility may be attributable to smoking. Impaired fertility has been attributed to the polycyclic aromatic hydrocarbons in cigarette smoke and diminished oviductal functioning.2
In relation to the impact of male smoking on sperm quality and fertility, the 2004 US Surgeon General's report concluded that although the evidence suggests that smoking may decrease semen volume and sperm number, and increase the number of abnormal forms present, it was insufficient to establish causality.6 The 2010 report found strengthened evidence for decreased semen quality and fertility associated with exposure to tobacco smoke either in utero or in adulthood. The report found consistent evidence linking smoking to chromosome changes or DNA damage in sperm, adversely affecting male fertility and pregnancy viability as well as anomalies in offspring. 2
3.6.3 Assisted reproduction
(See 3.15.5 Treatment of infertility)
3.6.4 Sexual function
The link between smoking and erectile dysfunction (ED; defined as the persistent inability to attain and maintain penile erection adequate for satisfactory sexual performance) has been studied extensively.8 The 2014 US Surgeon General’s report concluded that smoking causes ED.8 Vasospasm induced by the nicotine in cigarette smoke has been suggested as a mechanism for the acute deleterious effects of smoking on erectile function, while the chronic effects are caused by impaired vascular physiology of the erectile tissue. The Surgeon General has recommended promoting non-smoking to prevent ED, and cessation to limit the risk of ED.8
A study of about 130 Italian women found that smokers have decreased blood flow to genital blood vessels, which may impair sexual function.9
3.6.5 Sexually transmitted diseases
(See 3.9.7 Infections of reproductive organs)
References
1. US Department of Health and Human Services. Women and smoking. A report of the US Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2001. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/sgr_2001/index.htm
2. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease. A report of the US Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: http://www.surgeongeneral.gov/library/tobaccosmoke/report/index.html
3. Bertone-Johnson E, Hankinson S, Johnson S and Manson J. Cigarette smoking and the development of premenstrual syndrome. American Journal of Epidemiology 2008;168(8):938–45. Available from: http://pubmedcentralcanada.ca/picrender.cgi?accid=PMC2727205&blobtype=pdf
4. Cochran C, Gallicchio L, Miller S, Zacur H and Flaws J. Cigarette smoking, androgen levels, and hot flushes in midlife women. Obstetrics and Gynecology 2008;112(5):1037–44. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2673540/pdf/nihms-108532.pdf 5. Howe G, Westhoff C, Vessey M and Yeates D. Effects of age, cigarette smoking, and other factors on fertility: findings in a large prospective study. British Medical Journal (Clinical Research Ed.) 1985;290(6483):1697–700. Available from: http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1416131& blobtype=pdf
6. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
7. Tengs T and Osgood N. The link between smoking and impotence: two decades of evidence. Preventive Medicine 2001;32(6):447–452. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11394947
8. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress
9. Battaglia C, Battaglia B, Mancini F, Persico N, Nappi R, Paradisi R, et al. Cigarette smoking decreases the genital vascularization in young healthy, eumenorrheic women. Journal of Sexual Medicine 2011; [Epub ahead of print]. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21477023
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.7 Pregnancy and smoking
3.7 Pregnancy and smoking
Last updated: March 2015 Suggested citation: Ford, C, Greenhalgh, EM & Winstanley, MH. 3.7 Pregnancy and smoking. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-7-pregnancy-and-smoking
Smoking during pregnancy is harmful to the health of both the mother and the unborn child. The 2002 United States Linked Birth/Infant Death Data Set reveals that it remains one of the most prevalent preventable causes of infant death and illness.1
In 2010, 11.7% of Australian women smoked during some or all of their pregnancy. In the period before they knew they were pregnant, 11.7% of pregnant women smoked and 7.7% reported that they smoked after they knew they were pregnant. The likelihood of smoking during pregnancy was higher among teenagers, women in disadvantaged circumstances and Indigenous women.2 See Chapter 1, Section 1.10.
Many of the constituents of cigarette smoke are potentially toxic to the developing foetus, including lead, nicotine, cotinine, cyanide, cadmium, mercury, carbon monoxide and polycyclic aromatic hydrocarbons (PAHs).3,4 Carbon monoxide (CO) reduces the oxygen supply to the baby, leading to hypoxia (insufficient oxygen). CO binds to haemoglobin with an affinity 200 times that of oxygen, and also has an inhibiting effect on the release of oxygen to the cells. Chronic mild hypoxia of foetal tissue can persist for five or six hours after the mother has stopped smoking.4 Cadmium, a carcinogen, which accumulates in the placenta and has been detected in umbilical cord blood, is associated with a reduction in foetal capillary volume.4 Nicotine is found in foetal blood, amniotic fluid and breast milk,3 and has short- and long-term effects likely to be related to several adverse pregnancy outcomes.4 Studies suggest that exposure to PAHs may disrupt hormones, alter enzyme levels or activity, and damage DNA, which, if not repaired, can lead to cell death, cancer or foetal abnormalities.4
There are various mechanisms through which smoking may affect the pregnancy and the development of the foetus. Both smoking and nicotine by itself change hormone patterns, affecting the pregnancy outcome and the endocrine profile of the infant. Smoking and nicotine affect the functioning and structure of the oviduct (fallopian tube) in ways that could impair fertilityi and complicate the pregnancy. Smoking disturbs the development of the placenta, disrupting the implantation process and interfering with the transformation of the uterine spiral arteries. Studies consistently show thickening of the villous membrane of the placenta in smokers, which decreases the ability of nutrients to diffuse through the placenta. Smoking and nicotine impair amino acid transport across the placenta, which the baby needs to make foetal proteins. Nicotine may decrease the pumping of fluid across the placenta, leading to lower oxygen levels in the foetus and acidosis (excessive acid in the blood and tissues). Nicotine can alter embryonic movements that are important in the early development of the organs. Consistent evidence shows that smoking can affect the development of the foetal lung and brain. Smoking a cigarette temporarily increases maternal heart rate and blood pressure and decreases foetal heart rate variability (a measure of the infant's wellbeing).4 Studies show a decrease in foetal movement for at least an hour after smoking one cigarette, consistent with a reduction of oxygen to the foetus.5 Smoking may present further risks to the pregnancy by increasing the mother's risk of infectious disease and altering the inflammatory response of her immune system. Smokers have lower levels of micronutrients that play a vital role in the health of the pregnancy, such as zinc (in cord blood) and vitamin C. Vitamin C is important for immune function and the formation of collagen. Genetic variation in enzymes that metabolise chemicals from tobacco smoke mediate the risk of adverse pregnancy outcomes. Several proposed mechanisms for the effects of smoking on pregnancy are presented in more detail in the US Surgeon General's report of 2010.4
3.7.1 Spontaneous abortion
Smoking during pregnancy is associated with spontaneous abortion or miscarriage (the involuntary termination of a pregnancy prior to 20 weeks of gestation).4,6 Because many miscarriages occur too early to be recognised and confirmed, and miscarriage can be caused by a number of preconditions, exposures or events, spontaneous abortions are difficult to study. However there are multiple ways in which smoking could potentially increase the risk for miscarriage. Proposed mechanisms include placental insufficiency, chronic reduced oxygen to the foetus, and direct toxic effects of constituents of cigarette smoke.4Tobacco or nicotine may also affect the quality of the egg and embryonic development.6
3.7.2 Ectopic pregnancy
Maternal active smoking causes ectopic pregnancy (the implantation of a fertilised egg occurring outside the uterus, usually in the fallopian tubes).6 Nicotine slows down the movement of the fertilised ovum in the fallopian tubes, and impairment of oviduct function can lead to ectopic pregnancy.4 Smokers also have a higher risk of developing pelvic inflammatory disease, which is associated with ectopic pregnancy.3
3.7.3 Complications of pregnancy
Smoking affects the healthy development and function of the umbilical cord and placenta, and causes abnormalities or insufficiencies that can lead to serious complications for the success of the pregnancy and the safe delivery of the baby. Smoking causes premature rupture of the membranes (breaking of the amniotic sac before the onset of labour), placenta previa (when the placenta is attached to the uterine wall close to or over the cervix), and placental abruption (premature separation of the placenta from the wall of the uterus).3,4 These complications increase the risk of preterm delivery, haemorrhaging that requires a blood transfusion, and death of the mother or baby. Research indicates that stopping smoking between pregnancies reduces the risk of placental abruption, suggesting that, for this complication, the effects of smoking do not persist.4
3.7.4 Preterm delivery
Smoking is a cause of preterm delivery (birth at less than 37 completed weeks of gestation) and shortened gestation.3 Preterm delivery is a leading cause of neonatal death and illness.4 Australian data show that in 2003, babies born to mothers who smoked in pregnancy had a 60% higher risk of preterm delivery than babies of non-smoking mothers.7 It is not known how smoking contributes to preterm delivery, but researchers have proposed various mechanisms. Smokers are more susceptible to vaginal infection; for example they have two to three times the risk of bacterial vaginosis, which is a risk factor for preterm delivery. Some research suggests that smokers may be more sensitive to stimuli that lead to contractions. Smoking may affect collagen formation, leading to weakening and rupture of the membranes. Smokers are more likely to develop complications that are risk factors for preterm delivery, such as placental abruption and placenta previa.4
Limited research suggests that women who quit smoking within the first three months of pregnancy reduce their risk of placental complications at birth, premature birth, infant illness and perinatal death.8
i Refer to Section 3.6 for discussion of smoking and reproductive health.
References
1. Dietz P, England L, Shapiro-Mendoza C, Tong V, Farr S and Callaghan W. Infant morbidity and mortality attributable to prenatal smoking in the US. American Journal of Preventive Medicine 2010;39(1):45–52. Available from: http://www.ajpm-online.net/article/PIIS074.937.9710002588/fulltext
2. Laws P, Li Z and Sullivan E. Australia's mothers and babies 2008. Perinatal statistics series no. 24, AIHW cat. no. PER 50. Sydney: Australian Institute of Health and Welfare National Perinatal Statistics Unit, 2010. Available from: http://www.aihw.gov.au/publication-detail/?id=644.247.2399&tab=2
3. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
4. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease. A report of the US Surgeon General, Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: http://www.surgeongeneral.gov/library/tobaccosmoke/report/index.html
5. US Department of Health and Human Services. The health consequences of involuntary exposure to tobacco smoke: a report of the Surgeon General. Atlanta, Georgia: US Dept. of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2006. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/sgr_2006/index.htm
6. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress
7. Laws P, Grayson N and Sullivan E. Smoking and pregnancy. AIHW cat. no. PER 33. Sydney: Australian Institute of Health and Welfare National Perinatal Statistics Unit, 2006. Available from: http://www.npsu.unsw.edu.au/NPSUweb.nsf/resources/AMB_2004_2008/$file /Smoking+and+pregnancy+for+web.pdf
8. British Medical Association Board of Science and Education and Tobacco Control Resource Centre. Smoking and reproductive life. The impact of smoking on sexual, reproductive and child health. London: British Medical Association, 2004. Available from: http://www.bma.org.uk/images/smoking_tcm41-21289.pdf
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.8 Child health and maternal smoking before and after birth
3.8 Child health and maternal smoking before and after birth
Last updated: March 2015 Suggested citation: Ford, C, Greenhalgh, EM & Winstanley, MH. 3.8 Child health and maternal smoking before and after birth. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-8-infant- health-and-smoking
There are several possible routes by which the effects of tobacco smoke may compromise infant health. Before birth, paternal active smoking may alter chromosomes or damage DNA in sperm, and the foetus may be exposed to maternal active smoking or maternal exposure to secondhand smoke during pregnancy.1,2 Following birth, infants may be exposed to parental secondhand smoke in the home,2 to thirdhand smoke in household dust and indoor surfaces,3 and to an increased bacterial load carried by a parent or carer who smokes.4,5,6 Both prenatal and postnatal exposure have been found to contribute to several health conditions in children.1,2 Maternal smoking also has negative effects on the quality and quantity of breast milk.7,8 Delineating the impact of each route of exposure in the causation of disease can sometimes be difficult, particularly for rarer conditions such as birth defects and childhood cancers.
Exposure to secondhand smoke during pregnancy is also a cause of reduced infant birthweight, and is associated with other health problems for the developing foetus.9,10 See Chapter 4, Section 4.11 for further information.
3.8.1 Foetal size and growth
3.8.1.1 Birthweight
Smoking in pregnancy causes restricted growth and low birthweight in the infant. Intrauterine growth retardation is reduced foetal growth during gestation. Babies born with low birthweight have a higher risk of subsequent illness, death and longer-term poor health outcomes through childhood and adult life.9 Low birthweight is associated with heart disease, type 2 diabetes, high blood pressure and being overweight in adulthood.11,12,13
Babies born to smokers weigh, on average, about 150 g to 200 g less than babies born to non-smokers.9 Australian data show that babies of women who smoke during pregnancy are twice as likely to be of low birthweight (defined as weighing less than 2500 g) compared to babies whose mothers are non-smokers. They are also more likely to be admitted to special care nurseries or neonatal intensive care units.14,15 In Australia in 2004–5, it is estimated that about 14% of all deaths due to low birthweight were attributable to tobacco use in pregnancy.16 The effect of maternal smoking on low birthweight is largely due to intrauterine growth retardation and to a lesser extent shortened gestation. Growth retardation is likely to be caused by chronic mild oxygen deprivation in the foetus from exposure to carbon monoxide, with a more minor role played by the effects of smoking on the placenta leading to nutritional deficiency of the foetus.1 The effects of smoking on birthweight appear to be stronger among older mothers and in mothers who have particular genotypes for drug-metabolising enzymes. The risk for low birthweight increases with the number of cigarettes the mother smokes per day.1 However, some research indicates that birthweight declines far more sharply at low levels of exposure, such as that experienced by women exposed to secondhand smoke and possibly by women who smoke a low number of cigarettes per day.17,18,19,20,21 This may help account for the observation that the benefits of cutting down the number of cigarettes smoked per day on birthweight are considerably smaller than for complete smoking cessation.7,22,20
Mothers who stop smoking early in their pregnancy have babies with similar birthweights to babies of non-smokers. Even mothers who stop before their third trimester can avoid much of the effect of smoking on birthweight.9
3.8.1.2 Respiratory health
Maternal smoking during pregnancy causes reduced lung function in infants, and may also cause an increase in the number of lower respiratory tract illnesses, including wheezing, during infancy.23,1 The effects of maternal smoking in utero may also be related to an increased risk of impaired lung function in childhood and adulthood.9 Australian research suggests that infants born to women who have smoked during pregnancy have weakened innate immune defences, and develop their acquired immune system more slowly than infants of non-smoking mothers. This may explain why infants of smokers are more prone to be asthmatic and to develop respiratory infections.24 In Australia in 2004–05, it is estimated that about 13% of all deaths due to lower respiratory tract infections in babies less than one year of age were attributable to exposure to maternal tobacco smoking before and/or after pregnancy.16
Infants living with smokers are also more likely to experience a range of respiratory symptoms and chest illnesses.2 These findings are discussed in greater detail in Chapter 4, Section 4 .9.
3.8.2 Perinatal and infant death
3.8.2.1 Stillbirth
Maternal smoking is associated with an increased risk of stillbirth (foetal death after 28 weeks' gestation) and neonatal mortality (death of an infant within the first 28 days of life).9 Data from the Australian Institute of Health and Welfare's National Perinatal Statistics Unit show that in 2003, babies born to mothers who smoked during pregnancy had a 50% greater risk of perinatal deathi than babies of non-smoking women.14
Proposed mechanisms by which smoking increases perinatal mortality include complications of pregnancy (abruption, placenta previa), preterm delivery, premature and prolonged rupture of the membranes (“water breaking”), and through physiologic responses of the foetus and newborn to stress.25
3.8.2.2 Sudden infant death syndrome
Sudden infant death syndrome (SIDS) is the sudden, unexplained, unexpected death of a child before one year of age.9 Smoking has been established as a cause of SIDS, whether the baby has been exposed to smoking before birth or in the home following birth.9 The biological pathway remains uncertain, but may be due to the effects of chronic oxygen deficiency on the development of the central nervous system and other neurotoxic effects of tobacco smoke on the foetal brain.9 Neurochemical changes to the cardiorespiratory control centres of the brainstem can result in changes in the development of respiratory control. Several studies have linked smoking during pregnancy to alterations in breathing patterns, ventilatory responses, and arousal responses in infants.9,25 Almost one in five deaths from SIDS in Australia (19%) is thought to be caused by maternal tobacco use.16
For information on secondhand smoke and SIDS see Chapter 4, Sub-section 4.9.2.
3.8.3 Birth defects
A large meta-analysis of studies published between 1959 and 2010 found that maternal smoking is associated with an increased risk for limb reduction defects; oral clefts; clubfoot; defects of the eyes; and defects of the gastrointestinal system, especially gastroschisis and abdominal hernia. More modest associations were found for digit anomalies (abnormal number or formation of fingers); cryptorchidism (undescended testes); and defects of the heart and musculoskeletal system, including craniosynostosis (premature fusing of the skull bones).27
The US Surgeon General’s report (2014) concluded that maternal smoking in early pregnancy causes orofacial clefts, and that maternal smoking is associated with other defects such as clubfoot, gastroschisis (the guts protruding through an opening in the abdominal wall), and atrial septal heart defects.25 Proposed mechanisms for oral clefts include the alteration of embryonic movements in early pregnancy that are important to the development of the organ systems, reduced supply of essential nutrients (such as vitamins and folate) for embryonic tissues, oxygen deficiency, and DNA damage. Mothers and babies with certain genotypes may be more susceptible to damage from tobacco smoke. Further work is needed to establish the mechanism. Studies also support an increased risk of oral clefts with paternal smoking, although it is not clear whether this is due to exposure of the mother to secondhand smoke or if it is due to the effects of tobacco smoke on sperm.1
3.8.4 Health complaints in infancy
A few studies have reported an association between maternal smoking, both during and after pregnancy, and infantile colic or excessive crying.28,29 Infantile colic is characterised by the frequent sudden fits of irritability, inconsolable crying and screaming accompanied by clenched fists, drawn-up legs and a red face. It occurs in the first weeks after birth and usually resolves by four months of age.28 One study suggests that maternal smoking may be linked to colic through gastrointestinal tract dysregulation. More research is needed to confirm this theory.28
The evidence is uncertain regarding the effect maternal smoking during pregnancy on risk of allergic sensitisation and atopic disease, including allergic symptoms, eczema, rhinitis and dermatitis. More studies addressing potential genetic determinants of susceptibility are needed.2 While smoking during pregnancy may increase the risk of wheezing illnesses in infants,9 the potential role of prenatal tobacco exposure as an independent cause of asthma is still unclear.2
3.8.5 Long-term development
3.8.5.1 Neurodevelopment
Investigating the impact of maternal smoking on the cognitive and behavioural development in infants and children is difficult as many factors affect the outcomes, including genetic and environmental effects.1 This has produced mixed results in the research. So while various studies have found an association between smoking during pregnancy and poorer outcomes in children, including for impaired learning and memory, lowered IQ, cognitive dysfunction, later childhood conduct problems, substance use, and early adult criminality, their findings are called into question by other studies reporting no association and the problems of inadequate study design.30 Recently, the US Surgeon General concluded that maternal prenatal smoking increases the risk of disruptive behavioural disorders, particularly attention deficit hyperactivity disorder, among children. However, there is insufficient evidence to infer a relationship between maternal prenatal smoking and anxiety, depression, Tourette syndrome, schizophrenia, and intellectual disability among children.25
General assessments of children's cognition and intelligence have been mixed. However, studies of children's general verbal skills and specific language and auditory tests have found a more consistent association between smoking during pregnancy and children's poorer performance on these tests.1
More comprehensively designed studies that take into account the many confounding factors on child development are needed.30
3.8.5.2 Nicotine dependence
Evidence is emerging that suggests that exposure to nicotine in utero predisposes an individual to a greater likelihood of nicotine dependence later in life, independent of socio-economic and other factors that influence uptake of smoking.31 It is possible that this may occur by nicotine having a direct effect on the developing foetal brain, causing permanent abnormalities in neurotransmitter regulation.31, 32 Other research, while confirming that offspring of women who smoked during pregnancy are more likely to become smokers in early adolescence, suggests that environmental influences on smoking uptake such as the mother's current smoking status and peer group behaviour are stronger predictors.33 This is an area requiring further study.
3.8.5.3 Physical development
Studies into the possible effects of smoking during pregnancy on subsequent physical growth of children have been mixed. Where differences have been found between children of smokers and non-smokers, they have generally been small. More research is needed.9,1
3.8.5.4 Cardiovascular disease risk
Several studies have examined the link between smoking during pregnancy and the development of cardiovascular risk factors in the child. Among other risk factors, maternal smoking during pregnancy is associated being overweight or obese in childhood. This effect appears to be independent of the effects of smoking on foetal growth, and is likely to be an effect of smoking in early pregnancy.34–37 Two possible mechanisms are the effects of smoking on hypothalamic function affecting food intake and energy expenditure, or abnormalities in fat cells.35,36 Breastfeeding for more than six months may reduce the risk of child obesity associated with smoking in pregnancy.37
The evidence is unclear as to whether there is an increased risk of higher blood pressure in children born to women who smoked during pregnancy.38 However, limited research indicates that maternal smoking in pregnancy leads to impaired blood pressure regulation in infants39 and adverse lipid (cholesterol) profiles in adult offspring.40–42 Smoking throughout pregnancy is a risk factor for cardiovascular developmental changes, including aortic narrowing, in early childhood and adolescence.43,44 One study found that the foetuses of smoking mothers are more likely to have lesions in the walls of the foetal artery and adjoining vessels, which are the initial stages of atherosclerosis (narrowing of the arteries by fatty deposits).45
3.8.5.5 Other long-term consequences
A few studies suggest that smoking during pregnancy may affect the reproductive development of male offspring, increasing the risk for lower sperm counts and quality, lower fertility, smaller testicles, undescended testes and hypospadias (a penis abnormality).46–50,26,1 Limited research suggests that smoking during pregnancy may also affect reproduction in female offspring. It is associated with a smaller uterus, a reduced number of somatic cells (which are necessary for egg survival), and slightly lower fertility in female offspring.52–53,1 More research is required to confirm these findings.
The link between parental smoking and development of childhood cancers is discussed in Chapter 4, Section 4.9.9.
3.8.6 Breastfeeding and smoking
Breastfeeding has wide-ranging health benefits for both baby and mother. These include well-recognised benefits such as reduced risk of diarrhoeal illness, reduced risk of developing allergies to cow's milk and possible reduced risk of obesity later in childhood. They also include less well-recognised benefits such as improved sight and psycho-motor development, reduced incidence of orthodontic problems resulting from under-development of the jaw and other facial bones, and possibly reduced risk of autoimmune diseases such as diabetes and inflammatory bowel disease.54
Babies who are breastfed gain better levels of immunity to infectious disease, particularly against respiratory and ear infections associated with secondhand smoke exposure.7,55–58 Women who have breastfed have a reduced risk of developing breast cancer and possibly ovarian cancer,59 as well as possible improvements in bone mineralisation.54
There is consistent evidence that women who smoke are less likely to breastfeed their infant and are more likely to wean their child earlier than mothers who do not smoke. This effect persists even after adjusting for other influences on the decision to breastfeed, such as socio-economic factors.7,8
Tobacco smoke appears to have a direct negative effect on milk quality, as well as the quantity produced. It is thought that nicotine may affect the activity of prolactin, a hormone essential for milk production.7,8 Nicotine is found in the breast milk of mothers who smoke. Cotinine, one of the main metabolites of nicotine, is found in the urine of breastfed infants of smokers, as well as in the urine of infants who are exposed to secondhand smoke.60 Nicotine absorbed by infants through breast milk can produce short-term symptoms such as restlessness, insomnia, nausea, vomiting, diarrhea and rapid pulse, and may affect infants' autonomic cardiovascular control and sleeping patterns.60,61 However, as nicotine has a short half-life in milk of about two hours, breastfeeding mothers who cannot quit can minimise the exposure of their baby to nicotine by prolonging the time between their last cigarette and breastfeeding.60 Although smoking and breastfeeding is not ideal, the benefits of breastfeeding outweigh the risks associated with smoking and not breastfeeding.58
i Perinatal death is defined as 'a fetal or neonatal death of at least 20 weeks gestation or at least 400 grams birthweight', Laws et al (2006) (p42).
References
1. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease. A report of the US Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: http://www.surgeongeneral.gov/library/tobaccosmoke/report/index.html
2. US Department of Health and Human Services. The health consequences of involuntary exposure to tobacco smoke: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2006. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/sgr_2006/index.htm
3. Matt GE, Quintana PJ, Hovell MF, Bernert JT, Song S, Novianti N, et al. Households contaminated by environmental tobacco smoke: sources of infant exposures. Tobacco Control 2004;13(1):29-37. Available from: http://www.ncbi.nlm.nih.gov/pubmed/14985592
4. Arcavi L and Benowitz NL. Cigarette smoking and infection. Archives of Internal Medicine 2004;164(20):2206-16. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15534156
5. Brook I and Gober A. Recovery of potential pathogens in the nasopharynx of healthy and otitis media-prone children and their smoking and nonsmoking parents. Annals of Otology, Rhinology, and Laryngology 2008;117(10):727–30. Available from: http://www.annals.com/toc/auto_abstract.php?id=15299
6. Robinson P, Taylor K and Nolan T. Risk-factors for meningococcal disease in Victoria, Australia, in 1997. Epidemiology and Infection 2001;127(2):261-8. Available from: http://www.ncbi.nlm.nih.gov/pubmed /11693503
7. US Department of Health and Human Services. Women and smoking. A report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2001. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/sgr_2001/index.htm
8. British Medical Association Board of Science and Education and Tobacco Control Resource Centre. Smoking and reproductive life. The impact of smoking on sexual, reproductive and child health. London: British Medical Association, 2004. Available from: http://www.bma.org.uk/images/smoking_tcm41-21289.pdf
9. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
10. Office of Environmental Health Hazard Assessment California Air Resources Board. Health effects of exposure to environmental tobacco smoke: Final Report, approved at the Panel's June 24, 2005 meeting. Sacramento: California Environmental Protection Agency Cal/EPA, 2005. Available from: http://www.oehha.ca.gov/air/environmental_tobacco/2005etsfinal.html
11. Lumley J, Chamberlain C, Dowswell T, Oliver S, Oakley L and Watson L. Interventions for promoting smoking cessation during pregnancy. Cochrane Database Systematic Reviews 2009(3):CD001055. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19588322
12. Barker DJ, Eriksson JG, Forsen T and Osmond C. Fetal origins of adult disease: strength of effects and biological basis. International Journal of Epidemiology 2002;31(6):1235-9. Available from: http://ije.oxfordjournals.org/content/31/6/1235.long
13. Barker DJ. In utero programming of chronic disease. Clinical Sciences (London) 1998;95(2):115-28. Available from: http://www.clinsci.org/cs/095/0115/cs0950115.htm
14. Laws P, Grayson N and Sullivan E. Smoking and pregnancy. AIHW cat. no. PER 33. Sydney: Australian Institute of Health and Welfare National Perinatal Statistics Unit, 2006. Available from: http://www.npsu.unsw.edu.au/NPSUweb.nsf/resources/AMB_2004_2008/$file /Smoking+and+pregnancy+for+web.pdf
15. Laws P, Li Z and Sullivan E. Australia's mothers and babies 2008. Perinatal statistics series no. 24, AIHW cat. no. PER 50. Sydney: Australian Institute of Health and Welfare National Perinatal Statistics Unit, 2010. Available from: http://www.aihw.gov.au/publication-detail/?id=6442472399&tab=2
16. Collins D and Lapsley H. The costs of tobacco, alcohol and illicit drug abuse to Australian society in 2004-05. P3 2625. Canberra: Department of Health and Ageing, 2008. Available from: http://www.nationaldrugstrategy.gov.au/internet/drugstrategy/publishing.nsf/Content/mono64/$File /mono64.pdf
17. Ellard GA, Johnstone FD, Prescott RJ, Ji-Xian W and Jian-Hua M. Smoking during pregnancy: the dose dependence of birthweight deficits. British Journal of Obstetrics & Gynaecology 1996;103(8):806-13. Available from: http://www.ncbi.nlm.nih.gov/pubmed/8760712
18. England L, Kendrick J, Gargiullo P, Zahniser S and Hannon W. Measures of maternal tobacco exposure and infant birth weight at term. American Journal of Epidemiology 2001;153(10):954–60. Available from: http://aje.oxfordjournals.org/cgi/content/full/153/10/954
19. England LJ, Kendrick JS, Wilson HG, Merritt RK, Gargiullo PM and Zahniser SC. Effects of smoking reduction during pregnancy on the birth weight of term infants. American Journal of Epidemiology 2001;154(8):694-701. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11590081
20. Secker-Walker RH and Vacek PM. Infant birth weight as a measure of harm reduction during smoking cessation trials in pregnancy. Health Education & Behavior 2002;29(5):557-69. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12238700
21. Gomez C, Berlin I, Marquis P and Delcroix M. Expired air carbon monoxide concentration in mothers and their spouses above 5 ppm is associated with decreased fetal growth. Preventive Medicine 2005;40(1):10-15. Available from: http://www.ncbi.nlm.nih.gov/entrez/pubmed/5530575
22. Pisinger C and Godtfredsen NS. Is there a health benefit of reduced tobacco consumption? A systematic review. Nicotine & Tobacco Research 2007;9(6):631-46. Available from: http://www.ncbi.nlm.nih.gov/pubmed /17558820
23. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General: executive summary. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.surgeongeneral.gov/library /smokingconsequences/
24. Noakes PS, Hale J, Thomas R, Lane C, Devadason SG and Prescott SL. Maternal smoking is associated with impaired neonatal Toll-like receptor (TLR) mediated immune responses. European Respiratory Journal 2006;28(4):721–9. Available from: http://erj.ersjournals.com/cgi/content/abstract /28/4/721
25. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/
26. Sawnani H, Olsen E, and Simakajornboon N. The effect of in utero cigarette smoke exposure on development of respiratory control: a review. Pediatric Allergy, Immunology, and Pulmonology, 2010; 23(3):161–7. Available from: http://www.liebertonline.com/doi/pdfplus/10.1089/ped.2010.0036
27. Hackshaw A, Rodeck C, and Boniface S. Maternal smoking in pregnancy and birth defects: a systematic review based on 173 687 malformed cases and 11.7 million controls. Human Reproduction Update, 2010; 17(5):589−604. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21747128
28. Shenassa ED and Brown MJ. Maternal smoking and infantile gastrointestinal dysregulation: the case of colic. Pediatrics, 2004; 114(4):e497−505. Available from: http://www.ncbi.nlm.nih.gov/entrez/pubmed /15466076
29. Canivet CA, Östergren P-O, Jakobsson IL, Dejin-Karlsson E, and Hagander BM. Infantile colic, maternal smoking and infant feeding at 5 weeks of age. Scandinavian Journal of Public Health, 2008; 36(3):284–91. Available from: http://sjp.sagepub.com/content/36/3/284.full.pdf+html
30. Knopik V. Maternal smoking during pregnancy and child outcomes: real or spurious effect? Developmental Neuropsychology, 2009; 34(1):1–36. Available from: http://www.informaworld.com /smpp/content~content=a907760348~db=all~order=page
31. Buka SL, Shenassa ED, and Niaura R. Elevated risk of tobacco dependence among offspring of mothers who smoked during pregnancy: a 30-year prospective study. American Journal of Psychiatry, 2003; 160(11):1978−84. Available from: http://ajp.psychiatryonline.org/cgi/content/abstract/160/11/1978
32. Al Mamun A, Lawlor D, Alati R, O'Callaghan M, Williams G, et al. Does maternal smoking during pregnancy have a direct effect on future offspring obesity? Evidence from a prospective birth cohort study. American Journal of Epidemiology 2006; 164(4):317−25. Available from: http://aje.oxfordjournals.org /cgi/content/full/164/4/317
33. Cornelius M, Leech S, Goldschmidt L, and Day N. Is prenatal tobacco exposure a risk factor for early adolescent smoking? A follow-up study. Neurotoxicology and Teratology, 2005; 27:667−76. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16014324
34. Oken E, Levitan E, and Gillman M. Maternal smoking during pregnancy and child overweight: systematic review and meta-analysis. International Journal of Obesity, 2008; 32(2):210−10. Available from: http://www.nature.com/ijo/journal/v32/n2/abs/0803760a.html
35. Ino T. A meta-analysis of association between maternal smoking during pregnancy and offspring obesity. Pediatrics International, 2010; 52(1):94–9. Available from: http://onlinelibrary.wiley.com/doi/10.1111 /j.1442-200X.2009.02883.x/full
36. Somm E, Schwitzgebel V, Vauthay D, Aubert M, and Hüppi P. Prenatal nicotine exposure and the programming of metabolic and cardiovascular disorders. Molecular and Cellular Endocrinology, 2009; 304(1–2):69–77. Available from: www.ncbi.nlm.nih.gov/pubmed/19433250
37. Mendez MA, Torrent M, Ferrer C, Ribas-Fitó N, and Sunyer J. Maternal smoking very early in pregnancy is related to child overweight at age 5–7 y. American Journal of Clinical Nutrition, 2008; 87(6):1906–13. Available from: http://www.ajcn.org/cgi/content/full/87/6/1906
38. Brion M, Leary S, Lawlor D, Smith G, and Ness A. Modifiable maternal exposures and offspring blood pressure: a review of epidemiological studies of maternal age, diet and smoking. Pediatric Research, 2008; 63(6):593–8. Available from: http://journals.lww.com/pedresearch/Fulltext/2008/06000 /Modifiable_Maternal_Exposures_and_Offspring_Blood.1.aspx
39. Cohen G, Jeffery H, Lagercrantz H, and Katz-Salamon M. Long-term reprogramming of cardiovascular function in infants of active smokers. Hypertension, 2010; 55(3):722–8. Available from: http://hyper.ahajournals.org/cgi/content/full/55/3/722
40. Jaddoe V, de Ridder M, van den Elzen A, Hofman A, Uiterwaal C, et al. Maternal smoking in pregnancy is associated with cholesterol development in the offspring: a 27-years follow-up study. Atherosclerosis 2008; 196(1):42−8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17336310
41. Wen X, Triche E, Hogan J, Shenassa E, and Buka S. Birth weight and adult hypercholesterolemia: subgroups of small-for-gestational-age based on maternal smoking status during pregnancy. Epidemiology, 2010; 21(6):786–90. Available from: www.ncbi.nlm.nih.gov/pubmed/20798636
42. Ng SP, Conklin D, Bhatnagar A, Bolanowski DD, Lyon J, et al. Prenatal exposure to cigarette smoke induces diet- and sex dependent dyslipidemia and weight gain in adult murine offspring Environmental Health Perspectives, 2009; 117:1042–8. Available from: http://www.ehponline.org/members/2009/0800193 /0800193.pdf
43. Geelhoed J, El Marroun H, Verburg B, van Osch-Gevers L, Hofman A, et al. Maternal smoking during pregnancy, fetal arterial resistance adaptations and cardiovascular function in childhood. British Journal of Obstetrics & Gynacology, 2011; 118(6):755–62. Available from: http://onlinelibrary.wiley.com/doi/10.1111 /j.1471-0528.2011.02900.x/pdf
44. Edstedt Bonamy A-K, Bengtsson J, Nagy Z, De Keyzer H, and Norman M. Preterm birth and maternal smoking in pregnancy are strong risk factors for aortic narrowing in adolescence. Acta Pædiatrica, 2008; 97(8):1080–5. Available from: http://onlinelibrary.wiley.com/doi/10.1111/j.1651-2227.2008.00890.x/full
45. Mecchia D, Lavezzi AM, Mauri M, and Matturri L. Feto-placental atherosclerotic lesions in intrauterine fetal demise: role of parental cigarette smoking. Open Cardiovascular Medicine Journal, 2009; 3:51–6. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=19572018
46. Fowler P, Cassie S, Rhind S, Brewer M, Collinson J, et al. Maternal smoking during pregnancy specifically reduces human fetal desert hedgehog gene expression during testis development The Journal of Clinical Endocrinology & Metabolism, 2008; 93(2):619−26. Available from: http://jcem.endojournals.org /cgi/content/abstract/93/2/619
47. Jensen MS, Mabeck LM, Toft G, Thulstrup AM, and Bonde JP. Lower sperm counts following prenatal tobacco exposure. Human Reproduction, 2005; 20(9):2559−66. Available from: http://humrep.oxfordjournals.org/content/20/9/2559.full.pdf+html
48. Fowler PA, Bhattacharya S, Flannigan S, Drake AJ, and O'Shaughnessy PJ. Maternal cigarette smoking and effects on androgen action in male offspring: unexpected effects on second-trimester anogenital distance. The Journal of Clinical & Endocrinological Metabolism, 2011; 96(9). Available from: http://www.ncbi.nlm.nih.gov/pubmed/21752894
49. Ravnborg TL, Jensen TK, Andersson AM, Toppari J, Skakkebaek NE, et al. Prenatal and adult exposures to smoking are associated with adverse effects on reproductive hormones, semen quality, final height and body mass index. Human Reproduction, 2011; 26(5):1000−11. Available from: http://www.ncbi.nlm.nih.gov /pubmed/21335416
50. Mamsen LS, Lutterodt MC, Andersen EW, Skouby SO, Sorensen KP, et al. Cigarette smoking during early pregnancy reduces the number of embryonic germ and somatic cells. Human Reproduction, 2010; 25(11):2755−61. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20823112
51. Hart R, Sloboda D, Doherty D, Norman R, Atkinson H, et al. Prenatal determinants of uterine volume and ovarian reserve in adolescence. The Journal of Clinical Endocrinology and Metabolism, 2009; 94(12):4931–7. Available from: http://jcem.endojournals.org/cgi/content/full/94/12/4931
52. Lutterodt M, Sorensen K, Larsen K, Skouby S, Andersen C, et al. The number of oogonia and somatic cells in the human female embryo and fetus in relation to whether or not exposed to maternal cigarette smoking. Human Reproduction 2009; 24(10):2558–66. Available from: http://www.ncbi.nlm.nih.gov/pubmed /19553240
53. Ye X, Skjaerven R, Basso O, Baird D, Eggesbo M, et al. In utero exposure to tobacco smoke and subsequent reduced fertility in females. Human Reproduction, 2010; 25(11):2901–6. Available from: http://humrep.oxfordjournals.org/content/25/11/2901.long
54. National Health and Medical Research Council. Dietary guidelines for children and adolescents in Australia incorporating the infant feeding guidelines for healthworkers. Canberra: NHMRC, 2003. Available from: http://www.nhmrc.gov.au/_files_nhmrc/file/publications/synopses/n34.pdf
55. Yilmaz G, Hizli S, Karacan C, Yurdakök K, Coşkun T, et al. Effect of passive smoking on growth and infection rates of breast-fed and non-breast-fed infants. Pediatrics International 2009; 51(3):352–8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19400822
56. Ladomenou F, Kafatos A, and Galanakis E. Environmental tobacco smoke exposure as a risk factor for infections in infancy. Acta Pædiatrica 2009; 98(7):1137–41. Available from: http://onlinelibrary.wiley.com /doi/10.1111/j.1651-2227.2009.01276.x/full
57. Chatzimichael A, Tsalkidis A, Cassimos D, Gardikis S, Tripsianis G, et al. The role of breastfeeding and passive smoking on the development of severe bronchiolitis in infants. Minerva Pediatrica, 2007; 59(3):199–206. Available from: http://direct.bl.uk/bld/PlaceOrder.do?UIN=211194970&ETOC=RN& from=searchengine
58. Dorea JG. Maternal smoking and infant feeding: breastfeeding is better and safer. Maternal and Child Health Journal, 2007; 11(3):287−91. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17226091
59. Allen J and Hector D. Benefits of breastfeeding. NSW Public Health Bulletins, 2005; 16:42–6. Available from: http://www.health.nsw.gov.au/public-health/phb/HTML2005/marchapril05html/article3p42.htm
60. Llaquet H, Pichini S, Joya X, Papaseit E, Vall O, et al. Biological matrices for the evaluation of exposure to environmental tobacco smoke during prenatal life and childhood. Analytical and Bioanalytical Chemistry, 2009; 396(1):379–99. Available from: http://www.springerlink.com/content/4960m70q40652246/fulltext.html
61. Mennella JA, Yourshaw LM, and Morgan LK. Breastfeeding and smoking: short-term effects on infant feeding and sleep. Pediatrics, 2007; 120(3):497−502. Available from: http://www.ncbi.nlm.nih.gov/pubmed /17766521
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.9 Increased susceptibility to infection in smokers
3.9 Increased susceptibility to infection in smokers
Last updated: March 2015 Suggested citation: Bellew, B, Greenhalgh, EM & Winstanley, MH. 3.9 Increased susceptibility to infection in smokers. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au /3-9-increased-susceptibility-to-infection-in-smoke
Inhaling the complex chemical mixture of combustion compounds in tobacco smoke causes adverse health outcomes through mechanisms that include DNA damage, inflammation and oxidative stress.1 Smoking has substantial adverse effects on the immune system, both locally (such as in the respiratory tract and soft tissues in the lungs) and throughout the body. As a result, smokers are at increased risk of a wide range of infections.2, 3 This chapter examines the evidence with respect to acute infections, pneumococcal and meningococcal disease, tuberculosis, complications among persons with existing HIV infection, as well as some other viral and bacterial infections. Evidence regarding periodontitis is covered in Section 3.11.1 and surgical infection is discussed in Section 3.15.1. Chronic respiratory conditions such as chronic obstructive pulmonary disease and asthma are covered in Section 3.2.
3.9.1 Acute respiratory infections
Evidence suggests that there is a causal relationship between smoking and acute respiratory illnesses, as well as all major respiratory symptoms among adults.1 Upper respiratory tract infections (URI or URTI) are the illnesses caused by an acute infection. This involves the upper respiratory tract: nose, sinuses, pharynx or larynx and commonly includes tonsillitis, pharyngitis, laryngitis, sinusitis, otitis media and the common cold.4
Cigarette smoking is a major risk factor for acute respiratory tract infections, with both active and passive smoke exposure increasing the risk of infection.3, 5 Smoking increases the incidence, duration and/or severity of respiratory viral infection.6 The mechanism of this enhanced susceptibility is multifactorial and includes alteration in structural and immune defences—a substantial report of immunologic effects of cigarette smoking was published in 2004; it described the harmful effects on cell counts and distribution in peripheral blood and lung fluids as well as impairment of the functioning of white blood cells, lymphocytes (natural killer cells) and humoral immune system function (production of antibodies).3 Recent studies provide additional detail of the adverse effects on the immune system, such as those on the retinoic acid-inducible gene I (RIG-I),7 inflammatory factors in nasal lavage fluids (NLF IL-6)8, NF-kappaB regulation (regulation of critical defence genes)9, pulmonary T-cell responses10, type II interferon responses (antiviral mechanisms) in airway epithelial cells6, and the functioning of intelectin 1 (an immune defence protein).11 There is also evidence that cigarette smokers have distortions to the normal microbial communities of the upper respiratory tract, which are thought to contribute to the prevalence of respiratory tract complications in this population.12
The patient problems most commonly managed overall by Australian general practitioners are respiratory related (accounting for 22 problems per 100 encounters in 2009–10) and this category also comprises the majority of new problems presented by patients (39% of all problems, managed at a rate of 59 per 100 encounters).13 Cigarette smokers get more colds and worse colds, have much higher rates (several-fold higher) and more severe cases of influenza infection and are at increased risk of bacterial pneumonia compared with non-smokers.3, 5
3.9.2 Chronic respiratory infections
For discussion of chronic respiratory diseases associated with infection such as chronic bronchitis and chronic obstructive pulmonary disease (COPD), see Section 3.2.5.
3.9.3 Pneumococcal and meningococcal disease
Pneumonia is an infection of the lungs, usually caused by bacteria or viruses. Bacteria and viruses living in the nose, sinuses or mouth may spread to the lungs; a person may also breathe some of these germs directly into the lungs. The most common cause of pneumonia in adults is infection with Streptococcus pneumoniae (pneumococcus). Viruses are a common cause of pneumonia, especially in infants and young children. Atypical pneumonia (sometimes called 'walking pneumonia') is caused by bacteria such as Legionella pneumophila, Mycoplasma pneumoniae, or Chlamydophila pneumoniae. Pneumocystis jiroveci pneumonia is sometimes seen in people whose immune system is impaired (due to AIDS or to certain medications that suppress the immune system). Staphylococcus aureus, Moraxella catarrhalis, Streptococcus pyogenes, Neisseria meningitidis, Klebsiella pneumoniae, or Haemophilus influenzae are other bacteria that can cause pneumonia.14
Exposure to tobacco smoke suppresses the activation of the innate immune system response to bacterial infection; this mechanism is considered important in people's susceptibility to pneumonia.15, 16 Evidence from several studies confirms that smoking is significantly associated with the development of bacterial pneumonia.5, 17 There is a dose–response relationship between the current number of cigarettes smoked per day, pack-years of smoking and time since quitting and invasive pneumococcal disease, with approximately 50% of those with invasive pneumococcal disease being cigarette smokers.18
Cigarette smoking is an especially prominent risk factor for pneumococcal pneumonia in patients with chronic obstructive pulmonary disease, but even without COPD, smoking remains a major risk factor. There are reported estimates of increased risk for pneumococcal pneumonia among smokers ranging from an almost two-fold (OR 1.88; 95% CI, 1.11–3.19) to a four-fold increase in risk (OR 4.1; (95% CI, 2.4–7.3) for active smoking. Exposure to secondhand smoke has been found to more than double the risk of this infection (OR 2.5; 95% CI, 1.2–5.1) compared with non-exposed non-smokers.3 A recent review indicates active smoking19 and a recent case–control study indicates secondhand smoke exposure20 as factors that predispose the elderly population to pneumonia. Evidence from several longitudinal studies conducted in large populations confirms significantly increased pneumonia associated mortality in smokers compared with non-smokers (other evidence to date from cross sectional and meta-analytic studies is inconsistent).2 There is also strong evidence that smoking is an independent risk factor for Legionnaires disease, an atypical pneumonia that usually develops two to 14 days after exposure to Legionella pneumophila.17, 21
Meningococcal disease describes infections caused by the bacterium Neisseria meningitidis (also called meningococcus). The meningococcal bacteria (Neisseria meningitidis) are a significant cause of disease in Australia, especially in the very young, teenagers, young adults and those with medical risk factors. The meningococcal bacteria can cause meningitis (inflammation of the meninges, the membrane lining of the brain and spinal cord) and/or septicaemia (blood poisoning). Meningococcal disease is an uncommon but life-threatening infection. There are 13 different types of meningococcal bacteria with the most common in Australia being meningococcal group B and C.22 Notifications of meningococcal disease in Australia for 2006–2007 were at average annual rate of 7.0/100 000 population.23 Neisseria meningitidis remains a major cause of bacterial meningitis and other invasive bacterial infections worldwide with major fluctuations in the incidence of endemic disease and the occurrence of outbreaks and epidemics.24 There is evidence from case–control studies that tobacco smoke exposure independently increases the risk of developing meningococcal disease.2, 25 Children under 18 years of age are at almost four times the risk of infection from maternal smoking (OR 3.8; 95% CI, 1.6–8.9). All age groups have more than a doubling of risk from active smoking (OR 2.4; 95% CI, 0.9–6.6) or from exposure to secondhand smoke (OR 2.5; 95% CI, 0.9–6.9). There is a dose–response relationship between exposure to secondhand smoke and the risk of meningococcal disease in all age groups.25
3.9.4 Tuberculosis
Tuberculosis is an infectious disease caused by various strains of mycobacteria but usually by Mycobacterium tuberculosis. It typically attacks the lungs but can also affect other parts of the body. Approximately one-third of the human population is skin test positive for the infection and is thus thought to harbour the bacterium. The infectious bacilli are inhaled as droplet nuclei that have been exhaled into the atmosphere. These droplets are small enough to remain airborne for several hours. Estimations of the minimum infectious dose range from a single bacterium upwards. In developed countries, tuberculosis is held in check by effective public health systems; in countries where the disease is truly endemic, control remains a huge challenge and one that is exacerbated as highly drug-resistant strains continue to evolve.26 Tuberculosis results in an estimated 1.7 million deaths each year and the worldwide number of new cases (more than nine million) is higher than at any other time in history.27 Overall, Australia has one of the lowest incidence rates of tuberculosis in the world; however it has a relatively high incidence rate among Indigenous people. In 2007 the crude incidence rate was 5.4 cases per 100 000 population but the rate among Indigenous people (6.6/100 000) was more than seven times that in the non-Indigenous Australian-born population (0.9/100 000). The incidence rate for Indigenous people in the Northern Territory was 32.2 per 100 000 population, 13 times that in the non-Indigenous Australian-born population. Looking at tuberculosis rates in countries with a comparable Indigenous population, Australia has a similar rate ratio between the Indigenous and non-Indigenous populations compared with New Zealand and the US and a much lower rate ratio compared with Canada. There are no grounds for complacency given the probability of ongoing transmission of tuberculosis as well as the obvious need to address the ongoing inequalities.28
The US Surgeon General’s report in 2014 was the first in its series to address the evidence regarding smoking and tuberculosis. It concluded that smoking causes both an increased risk of Mycobacterium tuberculosis disease and mortality from tuberculosis, and is associated with higher rates of recurrent tuberculosis. More evidence is needed to determine whether active smoking causes tuberculosis infection, although the report notes that both active and passive smoking are risk factors.29
Other reviews confirm that active smoking is a risk factor for infection and that it increases the risk of progression to tuberculosis disease and death.30,31 Up to one in five deaths from tuberculosis could be avoided if patients were not smokers.32–34 As with active smoking, exposure to secondhand tobacco smoke is also a risk factor for the development of tuberculosis,35 especially for children.30 Quitting smoking and prevention of exposure to secondhand smoke are both important measures in the control of tuberculosis.17 These measures are underscored by the earlier comments about incidence rates among Indigenous people, given that smoking prevalence is markedly higher in this community than in the non-Indigenous population.36
3.9.5 Risks for and complications of HIV
The authors of a recent systematic review suggested that smoking may be an independent risk factor for acquiring HIV infection37 but this finding remains controversial.2 Research into the association between smoking and HIV disease progression has produced inconsistent findings.38 One recent North American study of more than 2000 people living with HIV/AIDS found that current smokers (HR 1.8; 95% CI, 1.3–2.3) and individuals with an increased dose and/or duration of smoking were at greater risk of all-cause mortality compared to never smokers.39 Among people with HIV, smoking may compound the risk of developing COPD, and increase the risk of cervical cancer (in those who also have human papil¬lomavirus; HPV) and liver cancer.29 A review concluded that social class, intravenous drug use and compliance with highly active antiretroviral treatment (HAART) are factors that may interact with smoking behaviour, and the independent role of these factors may be difficult to assess in relation to the outcome of HIV infection.2
3.9.6 Other viral infections
Smoking may also have indirect adverse outcomes such as the increased risk of hepatocellular carcinoma (cancer of the liver) due to the potential smoking-related progression of chronic viral hepatitis.2
3.9.7 Infections of reproductive organs
A small but growing number of research studies deal with the association between cigarette smoking and infections of reproductive organs. Bacterial vaginosis, although often asymptomatic, can cause considerable discomfort and is associated with the development of more serious infections, such as septicaemia and increased risk of poor pregnancy outcome. A recent review found that tobacco smoking is significantly correlated with bacterial vaginosis, typically being in the region of twice as common in smokers as non-smokers, with a greater prevalence noted in young women. Tobacco use was also independently associated with a higher prevalence of specific sexually transmitted bacterial infections—chlamydia and gonorrhoea.17
Persistent infection with oncogenic human papilloma virus (HPV), leading to precancerous lesions and potentially cervical cancer, is a serious health burden.40 Cancer-causing HPV infections can result from interactions of the virus, the host, and many other cofactors; a recent prospective study found that smoking may induce impaired antibody response among HPV-infected young women. Non-smokers were five times more likely to develop HPV antibodies than young (<30 years old) female smokers (OR 0.2; 95% CI, 0.0–0.9). In addition these younger female smokers had a significantly decreased tendency of maintaining constant HPV antibody positive status by the end of the follow-up compared with non-smokers, who were 10 times more likely to do so (OR 0.1; 95% CI, 0.0–0.8).41
3.9.8 Periodontitis
(See Dental 3.11.1.)
3.9.9 Surgical infections
(See 3.15.1.)
3.9.10 Other bacterial infections
There is evidence that smoking may cause an increased risk of peptic ulcer disease owing to an increased rate of Helicobacter pylori infection.2 There is mixed evidence on the relationship between active smoking, bacteraemia (bloodstream infections) and sepsis (a severe illness in which the bloodstream is overwhelmed by bacteria) with about half of studies recently reviewed finding an adverse effect (a positive association).2 References
1. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease. A report of the US Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: http://www.surgeongeneral.gov/library/tobaccosmoke/report/index.html
2. Huttunen R, Heikkinen T and Syrjanen J. Smoking and the outcome of infection. Journal of Internal Medicine 2011;269(3):258-69. Available from: http://onlinelibrary.wiley.com/doi/10.1111 /j.1365-2796.2010.02332.x/pdf
3. Arcavi L and Benowitz N. Cigarette smoking and infection. Archives of Internal Medicine 2004;16:2206-16. Available from: http://archinte.ama-assn.org/cgi/content/full/164/20/2206
4. Eccles MP, Grimshaw JM, Johnston M, Steen N, Pitts NB, Thomas R, et al. Applying psychological theories to evidence-based clinical practice: identifying factors predictive of managing upper respiratory tract infections without antibiotics. Implementation Science 2007;2:26. Available from: http://www.ncbi.nlm.nih.gov /pubmed/17683558
5. Murin S and Bilello KS. Respiratory tract infections: another reason not to smoke. Cleveland Clinic Journal of Medicine 2005;72(10):916-20. Available from: http://www.ccjm.org/content/72/10/916.full.pdf+html
6. Modestou MA, Manzel LJ, El-Mahdy S and Look DC. Inhibition of IFN-gamma-dependent antiviral airway epithelial defense by cigarette smoke. Respiratory Research 2010;11:64. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2890646/pdf/1465-9921-11-64.pdf
7. Wu W, Patel K, Booth J, Zhang W and Metcalf J. Cigarette smoke extract suppresses the RIG-I initiated innate immune response to influenza virus in human lung. American Journal of Physiology - Lung Cellular and Molecular Physiology 2011;[Epub ahead of print]. Available from: http://ajplung.physiology.org/content /early/2011/02/18/ajplung.00267.2010.full.pdf+html
8. Noah T, Zhou H, Monaco J, Horvath K, Herbst M and Jaspers I. Tobacco smoke exposure and altered nasal responses to live attenuated influenza virus. Environmental Health Perspectives 2011;119(1):78-83. Available from: http://ehp03.niehs.nih.gov/article/info:doi/10.1289/ehp.1002258
9. Manzel LJ, Shi L, O'Shaughnessy PT, Thorne PS and Look DC. Inhibition by cigarette smoke of nuclear factor-kappaB-dependent response to bacteria in the airway. American Journal of Respiratory Cell and Molecular Biology 2011;44(2):155-65. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20348206
10. Feng Y, Kong Y, Barnes PF, Huang FF, Klucar P, Wang X, et al. Exposure to cigarette smoke inhibits the pulmonary T-cell response to influenza virus and Mycobacterium tuberculosis. Infection and Immunity 2011;79(1):229-37. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20974820
11. Carolan BJ, Harvey BG, De BP, Vanni H and Crystal RG. Decreased expression of intelectin 1 in the human airway epithelium of smokers compared to nonsmokers. Journal of Immunology 2008;181(8):5760-7. Available from: http://www.jimmunol.org/content/181/8/5760.abstract
12. Charlson ES, Chen J, Custers-Allen R, Bittinger K, Li H, Sinha R, et al. Disordered microbial communities in the upper respiratory tract of cigarette smokers. PLoS One 2010;5(12):e15216. Available from: http://www.plosone.org/article /fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0015216&representation=PDF
13. Britt H, Miller G, Charles J, Henderson J, Bayram C, Pan Y, et al. General practice activity in Australia 2009–10. General practice series no. 27, cat. no. GEP 27. Canberra: Australian Institute of Health and Welfare, 2010. Available from: http://www.aihw.gov.au/WorkArea/DownloadAsset.aspx?id=6442472722& libID=6442472703
14. National Center for Biotechnology Information (NCBI). Pneumonia. Bethseda, Maryland: US National Library of Medicine, 2010 [viewed 31 May 2011]. Available from: http://www.ncbi.nlm.nih.gov/pubmedhealth /PMH0001200/
15. Herr C, Beisswenger C, Hess C, Kandler K, Suttorp N, Welte T, et al. Suppression of pulmonary innate host defence in smokers. Thorax 2009;64(2):144-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed /18852155
16. Baqir M, Chen C, Martin R, Thaikoottathil J, Case S, Minor M, et al. Cigarette smoke decreases MARCO expression in macrophages: implication in Mycoplasma pneumoniae infection. Respiratory Medicine 2008;102(11):1604-10. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18590957
17. Bagaitkar J, Demuth DR and Scott DA. Tobacco use increases susceptibility to bacterial infection. Tobacco Induced Diseases 2008;4(1):12. Available from: http://www.tobaccoinduceddiseases.com/content /pdf/1617-9625-4-12.pdf
18. Nuorti JP, Butler JC, Farley MM, Harrison LH, McGeer A, Kolczak MS, et al. Cigarette smoking and invasive pneumococcal disease. Active Bacterial Core Surveillance Team. The New England Journal of Medicine 2000;342(10):681-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10706897
19. Fung HB and Monteagudo-Chu MO. Community-acquired pneumonia in the elderly. American Journal of Geriatric Pharmacotherapy 2010;8(1):47-62.
20. Loeb M, Neupane B, Walter SD, Hanning R, Carusone SC, Lewis D, et al. Environmental risk factors for community-acquired pneumonia hospitalization in older adults. Journal of the American Geriatric Society 2009;57(6):1036-40. Available from: http://onlinelibrary.wiley.com/doi/10.1111/j.1532-5415.2009.02259.x/pdf
21. Ginevra C, Duclos A, Vanhems P, Campese C, Forey F, Lina G, et al. Host-related risk factors and clinical features of community-acquired legionnaires disease due to the Paris and Lorraine endemic strains, 1998-2007, France. Clinical Infectious Diseases 2009;49(2):184-91. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19508168
22. The Meningitis Centre. Website. [viewed 31 May 2011]. Available from: http://meningitis.com.au
23. Australian Government Department of Health and Ageing. Vaccine preventable diseases in Australia, 2005 to 2007. Communicable Diseases Intelligence. 2010 [viewed 31 May 2011]. Available from: http://www.health.gov.au/internet/main/publishing.nsf/Content/cdi3403-1
24. Harrison LH. Epidemiological profile of meningococcal disease in the United States. Clinical Infectious Diseases 2010;50(suppl. 2 ):ii7-44. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820831 /pdf/nihms151126.pdf
25. Fischer M, Hedberg K, Cardosi P, Plikaytis BD, Hoesly FC, Steingart KR, et al. Tobacco smoke as a risk factor for meningococcal disease. Pediatric Infectious Disease Journal 1997;16(10):979–83. Available from: http://cat.inist.fr/?aModele=afficheN&cpsidt=2044935
26. Russell DG, Barry CE, 3rd and Flynn JL. Tuberculosis: what we don't know can, and does, hurt us. Science 2010;328(5980):852-6. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2872107 /pdf/nihms-200284.pdf
27. Lawn S and Zumla A. Tuberculosis. The Lancet 2011;[Epub ahead of print] . Available from: http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2810%2962173-3/fulltext
28. Robertus LM, Konstantinos A, Hayman NE and Paterson DL. Tuberculosis in the Australian Indigenous population: history, current situation and future challenges. Australian and New Zealand Journal of Public Health 2011;35(1):6-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21299692
29. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/ 30. Lin HH, Ezzati M, and Murray M. Tobacco smoke, indoor air pollution and tuberculosis: a systematic review and meta-analysis. PLoS Medicine, 2007; 4(1):e20. Available from: http://www.ncbi.nlm.nih.gov /pmc/articles/PMC1769410/pdf/pmed.0040020.pdf
31. Bates MN, Khalakdina A, Pai M, Chang L, Lessa F, et al. Risk of tuberculosis from exposure to tobacco smoke: a systematic review and meta-analysis. Archives of Internal Medicine, 2007; 167(4):335-342. Available from: http://archinte.jamanetwork.com/article.aspx?articleid=411801
32. Sitas F, Urban M, Bradshaw D, Kielkowski D, Bah S, et al. Tobacco attributable deaths in South Africa. Tobacco Control, 2004; 13(4):396−9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15564624
33. Leung CC, Li T, Lam TH, Yew WW, Law WS, et al. Smoking and tuberculosis among the elderly in Hong Kong. American Journal of Respiratory and Critical Care Medicine, 2004; 170(9):1027−33. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15282201
34.Gajalakshmi V, Peto R, Kanaka TS, and Jha P. Smoking and mortality from tuberculosis and other diseases in India: retrospective study of 43000 adult male deaths and 35000 controls. Lancet, 2003; 362(9383):507−15. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12932381
35. Leung CC, Lam TH, Ho KS, Yew WW, Tam CM, et al. Passive smoking and tuberculosis. Archives of Internal Medicine, 2010; 170(3):287−92. Available from: http://archinte.ama-assn.org/cgi/reprint/170/3/287
36. Centre for Excellence in Indigenous Tobacco Control. Just the facts: a fact sheet about tobacco use among Indigenous Australians. Parkville, Victoria: CEITC, 2010. Last update: Viewed Available from: http://www.ceitc.org.au/
37. Furber AS, Maheswaran R, Carroll CJ, and Newell JN. Is smoking tobacco an independent risk factor for HIV infection and progression to AIDS? Sexually Transmitted Infection, 2007; 83:41−6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16923740
38. Kabali C, Cheng D, Brooks D, Bridden C, Horsburgh R, Jr, et al. Recent cigarette smoking and HIV disease progression: no evidence of an association. AIDS Care, 2011; [Epub ahead of print]:1–10. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21400309
39. Pines H, Koutsky L, and Buskin S. Cigarette smoking and mortality among HIV-infected individuals in Seattle, Washington (1996−2008). AIDS and Behavior, 2011; 15(1):243–51. Available from: www.ncbi.nlm.nih.gov/pubmed/20390335
40. Huh WK. Human papillomavirus infection: a concise review of natural history. Obstetrics and Gynaecology, 2009; 114(1):139−43. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19546771
41. Simen-Kapeu A, Kataja V, Yliskoski M, Syrjanen K, Dillner J, et al. Smoking impairs human papillomavirus (HPV) type 16 and 18 capsids antibody response following natural HPV infection. Scandinavian Journal of Infectious Diseases, 2008; 7:1–7. Available from: http://www.informaworld.com /smpp/content~db=all?content=10.1080/00365540801995360
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.10 Eye diseases
3.10 Eye diseases
Last updated: March 2015 Suggested citation: Hurley, S, Greenhalgh, EM & Winstanley, MH. 3.10 Eye diseases. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-10-eye-diseases
Cataract and age-related macular degeneration (AMD) are the two leading causes in Australia of vision impairment not correctable by refraction (eye glasses). Cataract is responsible for 37% of such vision loss and AMD is responsible for 26%.1 AMD is responsible for 48% of blindness in Australia and cataract for 12%.1 Smoking increases the risk of both cataract2 and AMD.3, 4 Smoking may also be associated with the rare eye condition Graves' ophthalmopathy, and recent studies suggest a link between smoking and ocular inflammation.
3.10.1 Cataract
The ocular lens, which is behind the pupil, focuses light onto the retina. It is normally a transparent organ but with age tends to develop opaque areas, which impair vision. These opaque areas are called cataracts.
There are three main types of cataract, classified by their location within the lens structure: nuclear, cortical and posterior subcapsular. Nuclear cataract, which occurs in the centre of the lens, is the most common.5 Each type of cataract has its own distinct risk factors.2 Smoking is a cause of nuclear cataract.2 A study of almost 4000 Australians aged 49 years and older who were followed up for 10 years found that people who had smoked at some time (ever smokers) had a 40% higher risk of developing nuclear cataract than people who had never smoked.5 Although the exact mechanism of causation is not known, many trace metals and other chemicals in cigarette smoke are capable of damaging the proteins in the eyes' lens. Quitting smoking may reduce the risk of developing nuclear cataract and of progression of cataract.2
Smoking may also be associated with an increased risk for developing posterior subcapsular cataract (situated under the external membrane, usually behind the lens) but more research is required.2
3.10.2 Age-related macular degeneration
The macula is the central area of the retina. It contains the fovea, which is responsible for high-resolution vision. There are two main types of AMD: neovascular (or exudative) and atrophic. The 2014 US Surgeon General’s report concluded that smoking causes both types of AMD.4 A meta-analysis of large studies from the US, Netherlands, Australia, France and Japan also found that the evidence strongly suggests that smoking causes AMD.3 The pooled analysis found a four-fold increase in risk for neovascular AMD and a two- to three-fold increase in the risk of atrophic AMD associated with smoking. A further meta-analysis of studies published up until 2007 confirmed that smoking increases the risk of AMD (neovascular and atrophic combined).6 There are a number of proposed mechanisms for smoking-related damage to retinal structures, primarily oxidative stress; cigarette smoke is a strong oxidant that causes systemic oxidative stress.4 Smoking may also increase oxidative stress on the macula by removing its defences and reducing macular pigment and plasma levels of antioxidants. Inadequate peripheral blood flow might also contribute to the development of AMD.4
The first meta-analysis also found evidence of reversibility, because ex-smokers had a lower risk of AMD. Furthermore, in patients with neovascular AMD who were treated successfully, there was a higher recurrence rate in those who continued smoking compared with those who quit.3 Quitting smoking appears to reduce the risk of AMD, but several decades after quitting smoking, the risk remains higher for former smokers than for never smokers.4
Australian researchers developed a model predicting the decline in risk of AMD after quitting smoking and used it to assess the cost-effectiveness of smoking cessation in relation to AMD. They found that because of the high cost of treating AMD, smoking cessation interventions are cost-effective in terms of their impact on AMD alone (see Section 17.4.1.3).7
3.10.3 Graves' ophthalmopathy
Graves' ophthalmopathy is a complication of Graves' disease, a fairly rare autoimmune thyroid disease. The eye complications include protrusion of the eyeballs, double vision, inflammation of eye tissue and damage to the optic nerve. A number of studies have observed an increased risk among smokers for developing the ocular complications of Graves' disease. At this time the evidence is not conclusive, and further research is required.2
3.10.4 Ocular inflammatory disease
Ocular inflammatory disease is inflammation of one or more part of the eye and encompasses uveitis (inflammation of the middle layer of the eye), scleritis (inflammation of the white outer coating) and inflammation of the ocular surface.
Two recent studies have suggested that smoking may be associated with ocular inflammation. One study found that smokers were twice as likely to have uveitis as never smokers.8 The second study found that ocular inflammation was more severe in patients who were smokers and recurred more quickly.9 Cigarette smoke has an inflammatory effect and this may be the mechanism of action.8
References
1. Access Economics. Clear insight. The economic impact and cost of vision loss in Australia. Eye Research Australia, 2004. Available from: http://www.cera.org.au/uploads/CERA_clearsight.pdf
2. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
3. Thornton J, Edwards R, Mitchell P, Harrison R, Buchan I and Kelly S. Smoking and age-related macular degeneration: a review of association. Eye 2005;19:935-44. Available from: http://www.ncbi.nlm.nih.gov /pubmed/16151432
4. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress
5. Tan J, Wang J, Younan C, Cumming R, Rochtchina E and Mitchell P. Smoking and the long-term incidence of cataract: the Blue Mountains Eye Study. Ophthalmic Epidemiology 2008;15(3):155–61. Available from: http://www.informaworld.com/smpp/content~db=all?content=10.1080/09286580701840362
6. Chakravarthy U, Wong TY, Fletcher A, Piault E, Evans C, Zlateva G, et al. Clinical risk factors for age-related macular degeneration: a systematic review and meta-analysis. BMC Ophthalmology 2010;10:31. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21144031
7. Hurley S, Matthews J and Guymer R. Cost-effectiveness of smoking cessation to prevent age-related macular degeneration. Cost Effective Resource Allocation 2008;6(1):18. Available from: http://www.resource- allocation.com/content/pdf/1478-7547-6-18.pdf
8. Lin P, Loh A, Margolis T and Acharya N. Cigarette smoking as a risk factor for uveitis. Ophthalmology 2010;117:585–90. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve& db=PubMed&dopt=Citation&list_uids=20036011
9. Galor A, Feuer W, Kempen J, Kacmaz R, Liesegang T, Suhler E, et al. Adverse effects of smoking on patients with ocular inflammation. British Journal of Ophthalmology 2010;94(7):848–53. Available from: http://bjo.bmj.com/content/94/7/848.long
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.11 Dental diseases
3.11 Dental diseases
Last updated: March 2015 Suggested citation: Hurley, S, Greenhalgh, EM & Winstanley, MH. 3.11 Dental diseases. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-11-dental-diseases
The oral cavity is the first part of the anatomy to be exposed to mainstream smoke in smokers and, as described in Chapter 3, Section 3.5.1, smoking causes oral cancers. Smoking also damages the soft and hard tissue structures that support the teeth, known as the periodontium.1 The periodontium includes the gingiva and the ligaments that attach the tooth root to the jaw. The gingiva is the soft tissue covering the gums and overlapping the teeth; it protects the root surfaces of the teeth. Gingivitis is an inflammation of the gingiva, triggered by the build-up of plaque, leading to reddening of the gums, bleeding and swelling. Untreated gingivitis can lead to chronic periodontitis, an inflammation of the gingiva and the adjacent tooth attachment apparatus. Plaque on the teeth spreads below the gum line behind the gingiva, triggering an inflammatory response. A range of symptoms, including bleeding, swelling, gum recession and separation of the gingiva from the surface of the tooth, lead to further infection. This in turn can lead to bone loss, loosening of teeth, development of abscesses in soft tissue and bone, a greater risk of decay of the exposed root surfaces of the tooth (root surface caries) and tooth loss.1
3.11.1 Periodontitis
Smoking causes periodontitis. Increased tobacco use and longer duration of smoking are associated with more severe disease and a higher risk of dental damage. Cessation appears to reduce the risk.1-5
Analysis of the Australian National Survey of Adult Health (2004–2006) suggested that about 32% of moderate to severe periodontitis is due to smoking. This extrapolates to an estimated 700 000 adults affected by periodontitis due to their smoking.6
The precise means by which smoking causes periodontitis have not been determined, but three mechanisms have been suggested. First, smoking may increase the quantity of plaque and the likelihood that bacterial pathogens colonise the plaque. Second, smoking impairs the body's immune response, making the smoker more susceptible to bacterial infection and also impairing the regeneration and repair of periodontal tissues. Third, the vasoconstrictive effect of tobacco smoke and nicotine may reduce gingival blood flow and impair oxygen and nutrient delivery to gingival tissue.1
Smoking also results in poorer bone regeneration after surgical treatment aimed at replacing all missing tissues of the periodontium. A meta-analysis found statistically significant less bone gain in smokers than non-smokers after such treatment.7
3.11.2 Dental caries Dental caries (cavities) is a disease that occurs when acids produced by bacteria dissolve the hard enamel of the tooth surface. It is then possible for bacteria to penetrate the tooth and reach the pulp tissue. Pain, infection and the need for tooth extraction can result.1
The 2014 US Surgeon General’s report found that smokers are more likely to have dental caries, missing teeth due to decay, or fillings, although more research is needed to establish smoking as a cause.8 Data from a US national healthy survey of more than 5,000 women found that smoking is a risk factor for untreated caries and DMFS: decayed, missing (due to disease) and filled permanent tooth surfaces.3
3.11.3 Tooth loss
The main biological causes of tooth loss (edentulism) are periodontal disease and caries. As outlined above, smoking is linked to the risk of both.
A systematic review found significant associations between smoking and tooth loss in each of the six cross- sectional and two cohort studies considered.9 Most studies found a dose-response relationship and a decrease in the risk of tooth loss for former smokers.
The Australian '45 and Up Study' investigated the association between smoking and the chance of being edentulous (having no teeth remaining) in approximately 100 000 residents of New South Wales. Smokers had a 2.5-fold higher risk of being edentulous compared with never smokers. The more and the longer people smoked, the higher their risk. Former smokers had lower risk than current smokers but the chance of being edentulous was still higher than that of never smokers 30 years after quitting.10 A Japanese study also found that smoking was associated with the number of missing teeth.11 The Australian study suggested environmental tobacco smoke might also increase the risk of edentulism.10
3.11.4 Complications and failure of dental procedures
Because of the established adverse effects of smoking on the oral cavity, researchers have investigated the impact of smoking on the outcome of surgical procedures for periodontal disease12 and the success of prosthetic implants for missing teeth.13
A meta-analysis published in 200713 and an evaluation of implants in almost 500 patients published in 201014 found that smoking approximately doubles the risk of implant failure. A review by the Massachusetts Dental Society noted that in a cross-sectional study of 109 patients, the prevalence of implant loss in smokers was 15.3%, compared with 2% in non-smokers.15 The review also cited studies reporting that smoking increases the risk of peri-implantitis and that implants failed earlier in patients who smoked more, and concluded that smoking is a relative contraindication to implant placement.
Root-coverage procedures for people with periodontal disease were less successful in smokers than non-smokers.12 The US Surgeon General concluded that the evidence suggests that smoking compromises the survival of dental implants, but more research is needed to confirm it as a cause of dental implant failure.8
References
1. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
2. Al-Habashneh R, Al-Omari M and Taani D. Smoking and caries experience in subjects with various form of periodontal diseases from a teaching hospital clinic. International Journal of Dental Hygiene 2009;7(1):55–61. Available from: http://onlinelibrary.wiley.com/doi/10.1111/j.1601-5037.2008.00349.x/abstract
3. Iida H, Kumar JV, Kopycka-Kedzierawski DT and Billings RJ. Effect of tobacco smoke on the oral health of US women of childbearing age. Journal of Public Health Dentistry 2009;69(4):231–41. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19453866?ordinalpos=15& itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVBrief
4. Zini A, Sgan-Cohen HD and Marcenes W. Socio-economic position, smoking, and plaque: a pathway to severe chronic periodontitis. Journal of Clinical Periodontology 2010;38(3):229–35. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21198768
5. Vered Y, Livny A, Zini A and Sgan-Cohen H. Periodontal health status and smoking among young adults. Journal of Clinical Periodontology 2008;35(9):768–72. Available from: http://onlinelibrary.wiley.com /doi/10.1111/j.1600-051X.2008.01294.x/abstract
6. Do LG, Slade GD, Roberts-Thomson KF and Sanders AE. Smoking-attributable periodontal disease in the Australian adult population. Journal of Clinical Periodontology 2008;35(5):398-404. Available from: http://dx.doi.org/10.1111/j.1600-051X.2008.01223.x
7. Patel R, Wilson R and Palmer R. The effect of smoking on periodontal bone regeneration: a systematic review and meta-analysis. Journal of Periodontology 2011;[Epub ahead of print] Available from: http://www.ncbi.nlm.nih.gov/pubmed/21627463
8. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress
9. Hanioka T, Ojima M, Tanaka K, Matsuo K, Sato F and Tanaka H. Causal assessment of smoking and tooth loss: a systematic review of observational studies. BMC Public Health 2011;11(1):221. Available from: http://www.biomedcentral.com/content/pdf/1471-2458-11-221.pdf
10. Arora M, Schwarz E, Sivaneswaran S and Banks E. Cigarette smoking and tooth loss in a cohort of older Australians: the 45 and up study. Journal of the American Dental Association 2010;141(10):1242–9. Available from: http://jada.ada.org/cgi/content/full/141/10/1242
11. Yanagisawa T, Marugame T, Ohara S, Inoue M, Tsugane S and Kawaguchi Y. Relationship of smoking and smoking cessation with number of teeth present: JPHC Oral Health Study. Oral Diseases 2009;15(1):69. Available from: http://onlinelibrary.wiley.com/store/10.1111/j.1601-0825.2008.01472.x/asset /j.1601-0825.2008.01472.x.pdf?v=1&t=ghzos013&s=b4b8ac23f7fe9512cdc8dfe6c9b59e989b1b6ee1
12. Chambrone L, Chambrone D, Pustiglioni F, Chambrone L and Lima L. The influence of tobacco smoking on the outcomes achieved by root-coverage procedures: a systematic review. Journal of the American Dental Association 2009;140(3):294–306. Available from: http://jada.ada.org/cgi/reprint/140/3/294.pdf
13. Strietzel F, Reichart P, Kale A, Kulkarni M, Wegner B and Küchler I. Smoking interferes with the prognosis of dental implant treatment: a systematic review and meta-analysis. Journal of Clinical Periodontology 2007;34(6):523–44. Available from: http://www3.interscience.wiley.com/journal/118533327 /abstract
14. Anner R, Grossmann Y, Anner Y and Levin L. Smoking, diabetes mellitus, periodontitis, and supportive periodontal treatment as factors associated with dental implant survival: a long-term retrospective evaluation of patients followed for up to 10 years. Implant Dentistry 2010;19(1):57–64. Available from: http://journals.lww.com/implantdent/pages/articleviewer.aspx?year=2010&issue=02000&article=00009& type=abstract
15. Snider T, Cottrell D and Batal H. Summary of current consensus on the effect of smoking on implant therapy. Journal of the Massachusetts Dental Society 2011;59(4):20–2. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation& list_uids=21446616
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.12 Gastro-intestinal diseases
3.12 Gastro-intestinal diseases
Last updated: March 2015 Suggested citation: Hurley, S, Greenhalgh, EM & Winstanley, MH. 3.12 Gastro-intestinal diseases. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-12-gastrointestinal-diseases
3.12.1 Peptic ulcer disease
Mucus and other secretions line the gastrointestinal tract, protecting it from gastric acid. If this protective mechanism is impaired or if there is an increase in gastric acid or other damaging agents, then ulceration may occur. Peptic ulcer disease involves the formation of ulcers in either the lining of the stomach (gastric ulcers) or the duodenum, the section of the small intestine closest to the stomach (duodenal ulcers).
The presence of the gastric bacterium Helicobacter pylori causes infection and damage to the gastrointestinal wall, greatly increasing the risk of developing peptic ulcers. The Helicobacter pylori organism is present in all people with duodenal ulcers and 70–90% of people with gastric ulcers. The risk of developing peptic ulcers is also increased among people who take non-steroidal anti-inflammatory drugs (NSAIDS).
Peptic ulcers were the eleventh most common cause of hospital admissions in Australia in 2007–2008,1 and almost 3% of Australians report having some sort of peptic ulcer.2
Smoking increases the risk of peptic ulcer disease in people who are infected with Helicobacter pylori.3 In Australia, about 9% of peptic ulcer disease in men and 6% in women has been attributed to smoking.4
Smoking affects the gastrointestinal tract in a number of ways: it reduces the production of gastric mucus and other protective secretions, promotes duodenal reflux and reduces blood flow to the lining of the tract. In this compromised environment, Helicobacter pylori is better able to spread and cause damage.3 Smoking may also be related to an increased risk of developing complications of peptic ulcer disease, such as ulcer perforation or bleeding, but this effect may be confined to people who are not taking NSAIDS.3
The increased risk of peptic ulcer disease consequential to smoking appears to reverse with smoking cessation.3
The higher prevalence of peptic ulcer disease in people with mental disorders has been largely explained by smoking and alcohol dependence in this population.5
3.12.2 Inflammatory bowel disease
Inflammatory bowel disease (IBD) is a group of conditions in which the intestines are inflamed. The two major types of IBD are Crohn's disease and ulcerative colitis. Crohn's disease can involve any part of the gastrointestinal tract, but most commonly affects the small intestine or the colon. Ulcerative colitis is restricted to the colon and the rectum. The presenting symptoms of these two IBDs are often similar (abdominal pain, vomiting, diarrhoea), but the pathophysiology differs. Crohn's disease is thought to be an autoimmune disease (see Section 3.17), but ulcerative colitis is not. Tissue inflammation tends to be deeper with Crohn's disease than with ulcerative colitis. Both conditions are treated with drugs and/or surgery.6, 7
The 2014 US Surgeon General’s report concluded that smoking increases the risk of Crohn’s disease, but more evidence is needed to confirm whether it is a cause.8 A 2006 meta-analysis of the research found that smoking increases the risk of Crohn’s disease by about 76%.9 In Australia, about 36% of Crohn’s disease in men, and about 40% in women, has been attributed to smoking.10
Patients with Crohn's disease who continue to smoke have a worse prognosis. Their symptoms are exacerbated and, after surgery, they are more than twice as likely as non-smokers to have a disease recurrence. Smokers have a 2.5-fold increased risk of repeat surgery within 10 years. Quitting smoking reduces the risk of relapse.11
Smoking affects the immune system in a variety of ways and it is not clear which of its immunologic effects are relevant to Crohn's disease.7
In contrast to its impact on Crohn’s disease, smoking seems to decrease the risk of ulcerative colitis by about 40% and quitting increases the risk,9 although more research is needed to confirm that smoking causes this effect.8 Ex-smokers have an almost 80% higher risk of ulcerative colitis compared with never smokers.9 The reason or reasons for the contradictory effect of smoking on the two main IBDs is unknown.7
3.12.3 Disorders of the liver and gallbladder
Smoking adversely affects the hepatobiliary system.
The 'Million Women Study' in the UK found that smoking increases the risk of liver cirrhosis two- to three-fold and the risk of gallbladder disease (symptomatic gallstones or cholecystitis) by about 10–30%.12 Ex-smokers were found to have elevated risks for these conditions compared with never smokers, but lower risks than current smokers.
Smoking appears to increase the severity of non-alcoholic fatty liver disease,13 and large case–control studies in the UK and US have found that smoking increases the risk of primary biliary cirrhosis (an autoimmune disease that results in the destruction of hepatic bile ducts) by about 50–60%.14, 15 A 2011 meta-analysis of five published studies, that together included almost 2 000 cases of primary biliary cirrhosis, confirmed the association and found that smoking increases risk by almost 70%.16 See Section 3.17 for a discussion of autoimmune disease.
3.12.4 Disorders of the pancreas
Pancreatitis is inflammation of the pancreas. It can be acute or chronic. The most common symptom is severe abdominal pain. Gallstones cause acute pancreatitis and high alcohol intake is a risk factor for chronic pancreatitis. Smoking increases the risk of gallstones and smoking is also strongly associated with drinking alcohol. It has therefore been difficult to determine whether smoking per se increases the risk of pancreatitis.
A cohort study of over 18 000 residents of Copenhagen found that smoking does increase the risk of pancreatitis, independently of its effect on gallstones and its association with alcohol consumption. In fact about 46% of cases of pancreatitis in this group of people were attributed by the researchers to smoking.17
Note that pancreatitis may increase the risk of pancreatic cancer, which is one of the malignancies caused by smoking (see Section 3.5.2).3 3.12.5 Other gastrointestinal disorders
Data from an Australian twin study suggest that smoking increases the risk of appendicitis by about 65%, but that this risk decreases by 15% every year after quitting.18 A retrospective survey of more than 6 000 male British construction workers who underwent appendicectomy over a 33-year period found that smoking increased the risk of perforated appendix and also increased the risk of post-operative complications in non-perforated appendicitis (see Section 3.15).19
For information about anal fistula, see Section 3.17.2.
References
1. Australian Institute of Health and Welfare. Australia's health 2010. Australia's health series no. 12. AIHW cat. no. AUS 122. Canberra: AIHW, 2010.
2. Australian Institute of Health and Welfare. Australia's health 2004. Australia's health series no. 9. AIHW cat. no. AUS 44. Canberra: AIHW, 2004.
3. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
4. Ridolfo B and Stevenson C. Quantification of drug-caused mortality and morbidity in Australia, 1998. Drug statistics series no. 7. AIHW cat. no. PHE 29. Canberra: Australian Institute of Health and Welfare, 2001. Available from: http://www.aihw.gov.au/publications/phe/qdcmma98/
5. Goodwin R, Keyes K, Stein M and Talley N. Peptic ulcer and mental disorders among adults in the community: the role of nicotine and alcohol use disorders. Psychosomatic Medicine 2009;71(4):463–8. Available from: http://www.psychosomaticmedicine.org/cgi/content/full/71/4/463
6. Langholz E. Current trends in inflammatory bowel disease: the natural history. Therapeutic Advances in Gastroenterology 2010;3(2):77–86. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21180592
7. El-Tawil A. Smoking and inflammatory bowel diseases: what in smoking alters the course? International Journal of Colorectal Disease 2010;25(6):671–80. Available from: https://commerce.metapress.com/content /g2604t35xu673395/resource-secured/?target=fulltext.pdf&sid=l2ro41f42zla4cynsxo4sw45&sh=http: //www.springerlink.com
8. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress
9. Mahid SS, Minor KS, Soto RE, Hornung CA and Galandiuk S. Smoking and inflammatory bowel disease: a meta-analysis. Mayo Clinic Proceedings 2006;81(11):1462–71. Available from: http://www.mayoclinicproceedings.com/content/81/11/1462.full.pdf
10. English DR, Holman CD, Milne E, Winter MG, Hilse GK, Codde JP, et al. The quantification of drug caused morbidity and mortality in Australia 1995: Part 1. Canberra: Commonwealth Department of Human Services and Health, 1995. 11. Reese G, Nanidis T, Borysiewicz C, Yamamoto T, Orchard T and Tekkis P. The effect of smoking after surgery for Crohn's disease: a meta-analysis of observational studies. International Journal of Colorectal Disease 2008;23:1213–21. Available from: https://commerce.metapress.com/content/x360n4584k3306t7 /resource-secured/?target=fulltext.html&sid=valmbbarwdmcid453lxmtezv&sh=http://www.springerlink.com
12. Liu B, Balkwill A, Roddam A, Brown A and Beral V. Separate and joint effects of alcohol and smoking on the risks of cirrhosis and gallbladder disease in middle-aged women. American Journal of Epidemiology 2008;169(2):153–60. Available from: http://aje.oxfordjournals.org/cgi/content/full/kwn280v2
13. Zein C, Unalp A, Colvin R, Liu Y and McCullough A. Smoking and severity of hepatic fibrosis in nonalcoholic fatty liver disease. Journal of Hepatology 2010;54(4):753–9. Available from: http://www.ncbi.nlm.nih.gov/PubMed/21126792
14. Prince M, Ducker S and James O. Case-control studies of risk factors for primary biliary cirrhosis in two United Kingdom populations. Gut 2010;59(4):508–12. Available from: http://gut.bmj.com/content /59/4/508.long
15. Gershwin ME, Selmi C, Worman HJ, Gold EB, Watnik M, Utts J, et al. Risk factors and comorbidities in primary biliary cirrhosis: a controlled interview-based study of 1032 patients. Hepatology 2005;42(5):1194–202. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16250040
16. Liang Y, Yang Z and Zhong R. Smoking, family history and urinary tract infection are associated with primary biliary cirrhosis: a meta-analysis. Hepatology Research 2011;41(6):572–8. Available from: http://onlinelibrary.wiley.com/doi/10.1111/j.1872-034X.2011.00806.x/full
17. Tolstrup J, Kristiansen L, Becker U and Grønbaek M. Smoking and risk of acute and chronic pancreatitis among women and men. Archives of Internal Medicine 2009;169(6):603–9. Available from: http://archinte.ama-assn.org/cgi/content/full/169/6/603
18. Oldmeadow C, Wood I, Mengersen K, Visscher P, Martin N and Duffy D. Investigation of the relationship between smoking and appendicitis in Australian twins. Annals of Epidemiology 2008;18(8):631–6. Available from: http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6T44-4T1Y003-9-1&_cdi=4964& _user=10&_orig=search&_coverDate=08%2F31%2F2008&_sk=999819991&view=c&wchp=dGLbVzb- zSkWz&md5=f9d22a460f86d293be2f83b0387d602c&ie=/sdarticle.pdf
19. Lindström D, Sadr Azodi O, Adami J, Bellocco R, Linder S and Wladis A. Impact of body mass index and tobacco smoking on outcome after open appendicectomy. British Journal of Surgery 2008;95(6):751–7. Available from: http://www3.interscience.wiley.com/cgi-bin/fulltext/118639075/PDFSTART
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.13 Musculoskeletal diseases
3.13 Musculoskeletal diseases
Last updated: 2011 Suggested citation: Hurley, S & Winstanley, MH. 3.13 Musculoskeletal diseases. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-13-bone-density-and-risk-of-fractures
3.13.1 Bone density, osteoporosis and the risk of fractures
Osteoporosis is a skeletal disease characterised by low bone mass density (BMD) and deterioration of bone, with a consequential increase in bone fragility and risk of fractures. The diagnosis of osteoporosis is based on low BMD. The most common osteoporotic fractures are of the hip, lumbar spine and wrist. Hip fractures are the most severe.1
Osteoporosis is common and is associated with older age and female gender. Women aged 50 have almost a 50% lifetime risk of an osteoporotic fracture.1 In Australia, there were more than 16 000 osteoporotic hip fractures in 2006–2007; about three-quarters were in women whose average age was 83 years.2
Smoking decreases BMD in the middle and later years of life. The 2004 US Surgeon General's report concluded that smoking causes low BMD in postmenopausal women.3 BMD decreases by about an additional 2% per year in smokers compared with non-smokers, leading to a difference of about 6% by age 80.4
Although the Surgeon General concluded only that smoking 'may' cause low BMD in older men,3 a meta-analysis of the effect of smoking on BMD that included data from more than 40 000 subjects found that smoking has a more deleterious effect on bone mass for men than women.5 This meta-analysis also found that the effect of smoking on BMD is dose dependent. The more that people smoked—reflected in higher pack-years, cigarettes per day or number of years smoked—the lower their bone mass.
Both the meta-analysis and the Surgeon General's report found insufficient evidence that smoking lowers BMD in younger women and younger men.3, 5 The meta-analysis suggested that this is because the total exposure to smoking in young adults is insufficient to produce discernible decrements in BMD, and cited several studies that demonstrate a significant negative impact of smoking on BMD in young adults who are heavy smokers.5
Smoking cessation may slow or even partially reverse bone mass loss, but more research is needed to evaluate this issue.5
Because smoking lowers BMD and increases the risk of osteoporosis, it would be expected to increase the risk of bone fractures. Projections from the meta-analysis of the effect of cigarette smoking on BMD suggest that smoking will increase the lifetime risk of a vertebral fracture by 13% in women and 32% in men. For hip fractures, smoking-attributable increases in risk were projected to be 31% in women and 40% in men.5 The Surgeon General3 and two meta-analyses of studies investigating fracture risk in smokers have confirmed this effect.4, 6 The 2004 Surgeon General's report concluded that smoking increases the risk of hip fractures, but found that there was inadequate evidence at that time to reach the same conclusion about smoking and fractures of other bones.3 The first meta-analysis of fracture risk, published in 1997, found that female smokers had a 41% increase in hip fractures at age 70 years.4 The most recent fracture meta-analysis, published in 2005, included data for almost 60 000 people and reported a 25% increase in risk of any fracture, and an 84% increase in the risk of hip fracture, associated with smoking.6
A number of mechanisms may contribute to the loss of BMD in later life consequential to smoking. Nicotine and cadmium in cigarette smoke may have a direct effect on bone cells, and smokers' bone density could also be impaired through lower absorption of calcium and vitamin D, and altered metabolism of some other hormones. Smoking also affects oestrogen levels and the effectiveness of hormonal replacement therapy. Smokers tend to have a lower body weight and be less physically active than non-smokers. Both of these factors adversely affect BMD. Smokers also reach menopause earlier, on average, thereby extending the postmenopausal period of accelerated bone mineral loss.3
Data from the 2005 meta-analysis of smoking and fracture risk suggest that smoking may also increase the risk of fractures independently of its effect on BMD.6 In this meta-analysis, there was still a 12% increase in the risk of any fracture associated with smoking, after adjustment for age, BMD and body mass index, and this increase was just statistically significant. The authors suggested that this effect could be due to the poorer balance and poorer physical function that has been reported in smokers (see Chapter 3, Section 3.13.4).7
3.13.2 Delayed bone union
There is increasing evidence from both observational and experimental studies that smoking delays bone healing (union) after fracture or surgery.8-11 After elective foot surgery, for example, a 42% increase in the time to bone healing has been reported.12 Smoking has been found to increase the chance of non-union after spinal fusion surgery13 and to worsen outcomes.14
3.13.3 Back pain
There have been suggestions in the medical and health economic literature that smoking causes low back pain and increases the incidence of sick leave due to back pain.15, 16 A meta-analysis of all studies published until February 2009 has confirmed an increase in low back pain in current and former smokers.17 The association was stronger in adolescents than adults and was more pronounced for chronic back pain and severe back pain. The authors of the meta-analysis speculated that the effect could be due to reduced perfusion of intervertebral discs.
An analysis of the link between smoking and low back pain in more than 70 000 Canadians was published in 2010.18 Smoking increased the likelihood that survey participants of all ages would have lower back pain, after adjustment for body mass index, level of activity and other factors that could have explained the association. The risk of having lower back pain was about 80% higher in daily smokers aged 20 to 29 years. The excess risk decreased with age but was still statistically significant at all ages.
3.13.4 Other musculoskeletal problems
Smoking might increase joint cartilage loss,19 and has been reported to increase the risk of tears of the rotator cuff (the muscles and tendons that stabilise the shoulder),20 but further research is needed before these adverse effects could be regarded as confirmed.
A study of almost 10 000 women aged 65 years and over in the US found that smokers had poorer physical function than non-smokers, as measured by tests of muscle strength, agility, co-ordination, gait and balance, and self-reported physical status.7 The researchers likened the poorer physical function to a hastening of ageing by about five years, and suggested that the effect may be due to the poorer vascular function consequential to smoking.
A 2011 meta-analysis of 48 studies, including more than 500 000 participants, investigated the association between smoking and osteoarthritis.21 The analysis found that the protective effect of smoking observed in some studies, but not others, is likely to be false and may be caused by selection bias. The effect was seen in hospital-based case-control studies (where the control subjects are more likely to have smoking-related conditions), but not in community-based case-control studies, cohort studies or cross-sectional studies.
References
1. Johnell O and Kanis J. Epidemiology of osteoporotic fractures. Osteoporosis International 2005;16 (suppl. 2):S3–S7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15365697
2. Australian Institute of Health and Welfare. The problem of osteoporotic hip fracture in Australia. AIHW bulletin no. 76. Cat. no. AUS 121. Canberra: AIHW, 2010. Available from: http://www.aihw.gov.au /publications/index.cfm/title/10695
3. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
4. Law MR and Hackshaw AK. A meta-analysis of cigarette smoking, bone mineral density and risk of hip fracture: recognition of a major effect. British Medical Journal 1997;315(7112):841–6. Available from: http://pubmedcentralcanada.ca/picrender.cgi?artid=607368&blobtype=pdf
5. Ward KD and Klesges RC. A meta-analysis of the effects of cigarette smoking on bone mineral density. Calcified Tissue International 2001;68(5):259–70. Available from: http://www.ncbi.nlm.nih.gov/pubmed /11683532
6. Kanis JA, Johnell O, Oden A, Johansson H, De Laet C, Eisman JA, et al. Smoking and fracture risk: a meta-analysis. Osteoporosis International 2005;16(2):155–62. Available from: http://www.ncbi.nlm.nih.gov /pubmed/15175845
7. Nelson H, Nevitt M, Scott J, Stone K, Cummings S et al. Smoking, alcohol, and neuromuscular and physical function of older women. Study of Osteoporotic Fractures Research Group. Journal of the American Medical Association 1994;272:1825-31. Available from: http://jama.ama-assn.org/content/272/23/1825.short
8. Adams C, Keating J and Court-Brown C. Cigarette smoking and open tibial fractures. Injury: International Journal of the Care of the Injured 2001;32(1):61–5. Available from: http://www.sciencedirect.com /science?_ob=MImg&_imagekey=B6T78-426XWS4-F-1&_cdi=5052&_user=559483&_orig=search& _coverDate=01%2F31%2F2001&_sk=999679998&view=c&wchp=dGLzVlz-zSkzS& md5=aca882f55aa98c3089be60973580d6db&ie=/sdarticle.pdf
9. Al-Mukhtar SA. The effect of cigarette smoking on bone healing in elderly individuals with Colle's fracture. Tobacco Use Insights 2010;3:17–22. Available from: http://www.la-press.com/the-effect-of-cigarette-smoking- on-bone-healing-in-elderly-individuals-article-a2225
10. Schmitz MA, Finnegan M, Natarajan R and Champine J. Effect of smoking on tibial shaft fracture healing. Clinical Orthopaedics and Related Research 1999;365(0):184–200. Available from: http://c- orthopaedicpractice.com/pt/re /cop/ abstract.00003086-199908000-00024.htm;jsessionid=LRLpGVMGVtQZltYTCh9ytZqFMyFbjyycdnxDWlGFkd2zX
Qy7Kt42!383905 11. Sloan A, Hussain I, Maqsood M, Eremin O and El-Sheemy M. The effects of smoking on fracture healing. Surgeon 2010;8(2):111–6. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve& db=PubMed&dopt=Citation&list_uids=20303894
12. Krannitz K, Fong H, Fallat L and Kish J. The effect of cigarette smoking on radiographic bone healing after elective foot surgery. Journal of Foot and Ankle Surgery 2009;48(5):525–7. Available from: http://www.jfas.org/article/S1067-2516%2809%2900193-8/abstract
13. Andersen T, Christensen FB, Laursen M, Hoy K, Hansen ES and Bunger C. Smoking as a predictor of negative outcome in lumbar spinal fusion. Spine 2001;26(23):2623–8. Available from: http://www.spinejournal.com/pt/re/spine /abstract.00007632-200112010-00018.htm;jsessionid=LHnXqKMVqBDB159Kz1XGhm88nJsNSJb4WPy68Jh65qShJsLnb3l1!1629792
14. Luca A, Mannion A and Grob D. Should smoking habit dictate the fusion technique? European Spine Journal 2010;20(4):629–34. Available from: http://www.springerlink.com/content/42nx4p40390121t8 /fulltext.html
15. Alkherayf F and Agbi C. Cigarette smoking and chronic low back pain in the adult population. Clinical and Investigative Medicine 2009;32(5):e360–7. Available from: http://cimonline.ca/index.php/cim/article/view/6924
16. Skillgate E, Vingard E, Josephson M, Holm L and Alfredsson L. Is smoking and alcohol consumption associated with long-term sick leave due to unspecific back or neck pain among employees in the public sector? Results of a three-year follow-up cohort study. Journal of Rehabilitation Medicine 2009;41(7):550–6. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation& list_uids=19543666
17. Shiri R, Karppinen J, Leino-Arjas P, Solovieva S and Viikari-Juntura E. The association between smoking and low back pain: a meta-analysis. American Journal of Medicine 2010;123(1):87 e7–35 Available from: http://aje.oxfordjournals.org/cgi/content/full/171/2/135
18. Alkherayf F, Wai EK, Tsai EC and Agbi C. Daily smoking and lower back pain in adult Canadians: the Canadian Community Health Survey. Journal of Pain Research 2010;3:155–60. Available from: http://pubmedcentralcanada.ca/picrender.cgi?artid=1768844&blobtype=pdf
19. Davies-Tuck M, Wluka A, Forbes A, Wang Y, English D, Giles G, et al. Smoking is associated with increased cartilage loss and persistence of bone marrow lesions over 2 years in community-based individuals. Rheumatology (Oxford) 2009;48(10):1227–31. Available from: http://www.ncbi.nlm.nih.gov/entrez /query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=19696062
20. Baumgarten KM, Gerlach D, Galatz LM, Teefey SA, Middleton WD, Ditsios K and, Yamaquchi K. Cigarette smoking increases the risk for rotator cuff tears. Clinical Orthopaedics and Related Research 2010;468(6):1534–41. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19283436
21. Hui M, Doherty M and Zhang W. Does smoking protect against osteoarthritis? Meta-analysis of observational studies. Annals of the Rheumatic Diseases 2011;[Epub ahead of print] Available from: http://www.ncbi.nlm.nih.gov/pubmed/21474488
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.14 Skin
3.14 Skin
Last updated: March 2015 Suggested citation: Hurley, S, Greenhalgh, EM & Winstanley, MH. 3.14 Skin. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-14-effects-of-smoking-on-the-skin
Smoking adversely affects the skin. Delayed wound healing is discussed in Chapter 3, Section 3.15.1.2 and other smoking-associated skin conditions are detailed in this section.
3.14.1 Facial appearance and premature skin ageing
Smoking affects facial appearance in men and women, independent of sun exposure and age. Increased wrinkling1-5 and altered complexion colour1 have been attributed to smoking, as have elastosis (loss of elasticity in the skin resulting from degeneration of connective tissue) and, in men, telangiectasia (dilatation of fine blood vessels in the skin visible as fine red lines).6 One recent study found that smokers appear up to 4.7 years older than non-smokers, and in the majority of cases smokers and non-smokers could be correctly distinguished by examining photographs of the face and temple region.7 Two studies of twins have confirmed that smokers tend to look older.8, 9
Visible wrinkling is most evident in older smokers, but even smokers aged in their 20s and 30s may show evidence of microscopic superficial wrinkling.4 Combined exposure to both sunlight and tobacco smoke causes a greater degree of damage than exposure to one agent alone,10 possibly through the phototoxic effects of tobacco smoke condensate, which increase the skin's vulnerability to UV radiation.11 Even non-facial, non-sun-exposed skin may be more wrinkled in smokers than non-smokers.12
A possible mechanism for premature wrinkling is that smoke affects the function of human skin fibroblasts (cells present in connective tissue that form collagen and elastin), thereby accelerating the appearance of ageing.3 Recent research has suggested a connection between wrinkling in smokers and the development of chronic obstructive pulmonary disease (COPD). Smokers with severe facial wrinkling may also have a higher susceptibility to developing COPD; possible mechanisms being damage to collagen and elastin, which are important to both skin and lung function.13
3.14.2 Acne and other sebaceous conditions
A review of smoking-associated skin conditions published in 2010 noted that the evidence linking acne to smoking is conflicting. Only two of the five studies reviewed reported an association.14 Another study, published after the review, found a higher prevalence of comedonal postadolescent acne in women who were smokers compared with non-smokers.15
The evidence linking some other sebaceous conditions with smoking is stronger. Smoking appears to cause hidradenitis suppurativa (clusters of chronic abscesses or cysts in areas of sweat or sebaceous glands); up to 98% of patients with this condition are smokers.14, 16, 17 A case–control study found smoking was a risk factor for epidermal inclusion cysts in men, but not in women.18
3.14.3 Dermatitis
The 2010 review of smoking and the skin concluded that the evidence linking smoking to dermatitis and eczema remains controversial.14 A small case–control study published after the review found that smoking increased the risk of adult-onset atopic dermatitis in smokers and members of their family who were exposed to environmental tobacco smoke.19 Cigarettes themselves can cause allergic contact dermatitis in both occupational and non-occupational settings.14, 20
3.14.4 Psoriasis
Smoking is a well-established risk factor for psoriasis, a chronic autoimmune disease, the most common type being plaque psoriasis, which is characterised by scaly patches on the top layer of the skin.14, 21 Higher intensity smoking is associated with clinically severe disease,14, 22, 23 and psoriasis is less responsive to treatment in smokers.14, 24 The risk of developing psoriasis decreases progressively with increased time since smoking cessation.24
Multiple mechanisms are thought to explain the association between smoking and psoriasis. Smoking enhances the expression of genes known to confer an increased risk of psoriasis. It increases oxidative damage—the free radicals in cigarette smoke, for example, trigger a cascade of systemic reactions. Smoking also promotes inflammatory changes by suppressing immune cell processes and nicotine depletes calcium stores in T lymphocytes, probably impairing their function.24
The form of psoriasis known as palmoplantar pustulosis (which is confined to the hands and soles and is also known as 'pustular psoriasis of the extremities') is strikingly correlated with smoking; up to 95% of patients are smokers when the disease is diagnosed.14, 25
3.14.5 Lupus erythematosus
Lupus erythematosus is an autoimmune condition that can manifest as a systemic disease, involving many different organs, or as a cutaneous disease, involving only the skin. The systemic form is referred to as systemic lupus erythematosus (SLE). It often involves a rash, and sometimes involves scaly patches or ulcers.
A meta-analysis of seven case–control studies and two cohort studies has confirmed that smoking is associated with SLE. Current smokers have around a 50% increased risk of SLE compared with never smokers.26 The risk is not elevated for ex-smokers. Smokers also have increased SLE disease activity,27 and poorer health-related quality of life has been reported.28 In 2014, the US Surgeon General’s report found that there is mixed and therefore inadequate evidence that smoking causes SLE, or affects its severity or treatment.29
Smoking also increases the risk of developing some of the cutaneous forms of lupus14, 30 and has been reported to decrease the effectiveness of the antimalarial drugs that are sometimes prescribed for cutaneous lupus.31 The 2014 US Surgeon General’s report concluded that smoking is a risk factor for cutaneous lupus, but the evidence is too limited to determine if it is a cause.29
3.14.6 Other skin conditions
Smoking is a risk factor for the development of alopecia (hair loss, usually from the scalp) and may increase the likelihood of premature grey hair.14
A retrospective survey of more than 58 000 women in Denmark found an increased risk of genital warts in smokers, which the authors concluded could be due to immunosuppressive effects or uncontrolled confounding.32
For information about anal fistula, see Section 3.17.2.
References
1. Model D. Smoker's face: an underrated clinical sign? British Medical Journal 1985;291:1760-2. Available from: http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1419177&blobtype=pdf
2. Ernster V, Grady D, Miike R, Black D, Selby J and Kerlikowske K. Facial wrinkling in men and women, by smoking status. American Journal of Public Health 1995;85:78-82. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=7832266
3. Yin L, Morita A and Tsuji T. Skin ageing induced by ultraviolet exposure and tobacco smoking: evidence from epidemiological and molecular studies. Photodermatology Photoimmunology Photomedicine 2001;17:178-83. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11499540
4. Koh JS, Kang H, Choi SW and Kim HO. Cigarette smoking associated with premature facial wrinkling: image analysis of facial skin replicas. International Journal of Dermatology 2002;41(1):21–7. Available from: http://www3.interscience.wiley.com/journal/118906869/abstract?CRETRY=1&SRETRY=0
5. Leung W and Harvey I. Is skin ageing in the elderly caused by sun exposure or smoking? British Journal of Dermatology 2002;147:1187-91. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12452869
6. Kennedy C, Bastiaens M, Bajdik C, Willemze R, Westerndorp R, Bouwes Bavinck J, et al. Effect of smoking and sun on the aging skin. Journal of Investigative Dermatology 2003;120:548-54. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12648216
7. Raitio A, Kontinen J, Rasi M, Bloigu R, Röning J and Oikarinen A. Comparison of clinical and computerised image analyses in the assessment of skin ageing in smokers and non-smokers. Acta Dermato Venereologica 2004;84:422-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15844630
8. Guyuron B, Rowe D, Weinfeld A, Eshraghi Y, Fathi A and Iamphongsai S. Factors contributing to the facial aging of identical twins. Plastic and Reconstructive Surgery 2009;123(4):1321–31. Available from: http://journals.lww.com/plasreconsurg/pages/articleviewer.aspx?year=2009&issue=04000&article=00019& type=abstract
9. Martires K, Fu P, Polster A, Cooper K and Baron E. Factors that affect skin aging: a cohort-based survey on twins. Archives of Dermatology 2009;145(12):1375–9. Available from: http://archderm.ama-assn.org /cgi/content/full/145/12/1375
10. Kadunce D, Burr R, Gress R, Kanner R, Lyon J and Zone J. Cigarette smoking: risk factor for premature facial wrinkling. Annals of Internal Medicine 1991;114:840-4. Available from: http://www.annals.org/content /114/10/840.extract
11. Placzek M, Kerkmann U, Bell S, Koepke P and Przybilla B. Tobacco smoke is phototoxic. British Journal of Dermatology 2004;150:991-3. Avilable from: http://www.ncbi.nlm.nih.gov/pubmed/15149514
12. Helfrich Y, Yu L, Ofori A, Hamilton T, Lambert J, King A, et al. Effect of smoking on ageing of photoprotected skin. Archives of Dermatology 2007;143:397-402. Available from: http://archderm.ama- assn.org/cgi/content/full/143/3/397
13. Freiman A, Bird G, Metelitsa A, Barankin B and Lauzon G. Cutaneous effects of smoking. Journal of Cutaneous Medical Surgery 2004;8(6):415–23. Available from: http://www.springerlink.com/content /p172v6547r1p3231/
14. Metelitsa A and Lauzon G. Tobacco and the skin. Clinics in Dermatology 2010;28(4):384–90. Available from: http://www.cidjournal.com/article/PIIS0738081X10000453/fulltext
15. Capitanio B, Sinagra J, Bordignon V, Fei P, Picardo M and Zouboulis C. Underestimated clinical features of postadolescent acne. Journal of the American Academy of Dermatology 2010;63(5):782–8. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation& list_uids=20619486
16. Simonart T. Hidradenitis suppurativa and smoking. Journal of the American Academy of Dermatology 2010;62(1):149–50. Available from: http://www.eblue.org/article/S0190-9622%2809%2900239-4/fulltext
17. Canoui-Poitrine F, Revuz J, Wolkenstein P, Viallette C, Gabison G, Pouget F, et al. Clinical characteristics of a series of 302 French patients with hidradenitis suppurativa, with an analysis of factors associated with disease severity. Journal of the American Academy of Dermatology 2009;61(1):51–7. Available from: http://www.eblue.org/article/PIIS0190962209002394/fulltext
18. Lin S, Yang Y, Chen W and Wu W. Facial epidermal inclusion cysts are associated with smoking in men: a hospital-based case-control study. Dermatologic Surgery 2010;36(6):894–8. Available from: http://www3.interscience.wiley.com/user/accessdenied?ID=123429583&Act=2138&Code=4719&Page=/cgi- bin/fulltext/123429583/HTMLSTART
19. Lee C, Chuang H, Hong C, Huang S, Chang Y, Ko Y, et al. Lifetime exposure to cigarette smoking and the development of adult-onset atopic dermatitis. British Journal of Dermatology 2010;164(3):483–9. Available from: http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2133.2010.10116.x/pdf
20. Glick ZR, Saedi N and Ehrlich A. Allergic contact dermatitis from cigarettes. Dermatitis 2009;20(1):6–13. Available from: http://www.bcdecker.com/pubMedLinkOut.aspx?pub=AJCDO&vol=20&iss=1&page=6
21. Wolk K, Mallbris L, Larsson P, Rosenblad A, Vingard E and Stahle M. Excessive body weight and smoking associates with a high risk of onset of plaque psoriasis. Acta Dermato-Venereologica 2009;89(5):492–7. Available from: http://adv.medicaljournals.se/article/pdf/10.2340/00015555-0711
22. Attwa E and Swelam E. Relationship between smoking-induced oxidative stress and the clinical severity of psoriasis. Journal of the European Academy of Dermatology and Venereology 2010;[Epub ahead of print] Available from: http://onlinelibrary.wiley.com/doi/10.1111/j.1468-3083.2010.03860.x/full
23. Gerdes S, Zahl V, Weichenthal M and Mrowietz U. Smoking and alcohol intake in severely affected patients with psoriasis in Germany. Dermatology 2010;220(1):38–43. Available from: http://content.karger.com/produktedb/produkte.asp?typ=fulltext&file=000265557
24. Armstrong A, Armstrong E, Fuller E, Sockolov M and Voyles S. Smoking and pathogenesis of psoriasis: a review of oxidative, inflammatory, and genetic mechanisms. The British Journal of Dermatology 2011;[Epub ahead of print] Available from: http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2133.2011.10526.x/pdf
25. Miot H, Miot L, Lopes P, Haddad G and Marques S. Association between palmoplantar pustulosis and cigarette smoking in Brazil: a case-control study. Journal of the European Academy of Dermatology and Venereology 2009;23(10):1173–7. Available from: http://www3.interscience.wiley.com /user/accessdenied?ID=122372044&Act=2138&Code=4719&Page=/cgi-bin/fulltext/122372044/HTMLSTART
26. Costenbader KH, Kim DJ, Peerzada J, Lockman S, Nobles-Knight D, Petri M, et al. Cigarette smoking and the risk of systemic lupus erythematosus: a meta-analysis. Arthritis and Rheumatism 2004;50(3):849–57. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15022327 27. Ghaussy NO, Sibbitt W, Jr., Bankhurst AD and Qualls CR. Cigarette smoking and disease activity in systemic lupus erythematosus. Journal of Rheumatology 2003;30(6):1215–21. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12784392
28. Barta Z, Harrison M, Wangrangsimakul T, Shelmerdine J, Teh L, Pattrick M, et al. Health-related quality of life, smoking and carotid atherosclerosis in white British women with systemic lupus erythematosus. Lupus 2010;19(3):231-8. Available from: http://lup.sagepub.com/cgi/rapidpdf/0961203309351032v1
29. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress
30. Boeckler P, Cosnes A, Frances C, Hedelin G and Lipsker D. Association of cigarette smoking but not alcohol consumption with cutaneous lupus erythematosus. Archives of Dermatology 2009;145(9):1012–6. Available from: http://archderm.ama-assn.org/cgi/content/full/145/9/1012
31. Rahman P, Gladman DD and Urowitz MB. Smoking interferes with efficacy of antimalarial therapy in cutaneous lupus. Journal of Rheumatology 1998;25(9):1716–9. Available from: http://www.ncbi.nlm.nih.gov /pubmed/9733451
32. Hansen B, Hagerup-Jenssen M, Kjaer S, Munk C, Tryggvadottir L, Sparen P, et al. Association between smoking and genital warts: longitudinal analysis. Sexually Transmitted Infections 2010;86(4):258–62. Available from: http://sti.bmj.com/content/86/4/258.long
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.15 The impact of smoking on treatment of disease
3.15 The impact of smoking on treatment of disease
Last updated: March 2015 Suggested citation: Hurley, S, Greenhalgh, EM & Winstanley, MH. 3.15 The impact of smoking on treatment of disease. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-15- smoking-and-complications-in-medical-treatmen
3.15.1 Surgery Smoking increases the risk of postoperative complications. Smokers' higher prevalence of chronic diseases, impaired pulmonary reserve, altered immune responses and impaired wound healing are thought to cause such complications. Poorer surgical outcomes result.1
3.15.1.1 Anaesthesia
The effectiveness of a number of commonly used anaesthetic drugs is reduced in smokers. Higher doses are therefore required. These drugs include opioids,2 neuromuscular blocking agents and some of the volatile agents that are administered by inhalation (via a mask or tracheal tube). The polycyclic aromatic hydrocarbons in cigarette smoke induce the liver enzymes that metabolise anaesthetics, at least partly accounting for these effects.3 Smoking does however decrease postoperative nausea and vomiting, possibly because of the increased metabolism of volatile anaesthetics.3
Smoking increases the risk of intraoperative and postoperative respiratory complications, including bronchospasm, aspiration, hypoventilation and hypoxaemia.4-6 An increased risk for smokers of admission to intensive care after general or orthopaedic surgery has been reported,4 and was attributed to smokers' higher perioperative pulmonary complication rate.
The Australian and New Zealand College of Anaesthetists recommends that patients who smoke be encouraged to quit at any time before surgery.7 The optimal timing of smoking cessation has been a source of controversy, though there is agreement that longer quitting is best.7 Research suggests that recent quitters are no worse off than continuing smokers in terms of pulmonary complications. (see Section 3.15.1.3).8, 9
3.15.1.2 Postoperative complications
Smoking delays wound healing after surgery. Complications such as infection,10 dehiscence (bursting of sutures)11 and erosions (destruction of tissue surfaces) are increased.12, 13
Such smoking-associated complications are particularly problematic after plastic and reconstructive surgery, orthopaedic surgery (see Section 3.13.2), bowel surgery, dental surgery (see Section 3.11.4), microsurgery and organ transplantation.14–15
For example, after breast reconstruction, smoking has been associated with a doubling of the risk of complications (such as mastectomy flap necrosis or infection) and a five-fold increase in the risk of implant failure.17 Such poor surgical outcomes have led to a call for caution when undertaking breast reconstruction in smokers.18 Similarly, impaired wound healing and wound infection in smokers undergoing breast reduction surgery19, 20 have led to a suggestion that perioperative smoking cessation be an essential eligibility criterion for this surgery.20
Specific post-surgical complications linked with smoking include: a higher failure rate for oral mucosa graft urethroplasty;21 worse hearing and the need for repeat operations after ear surgery;22 increased complications post appendicectomy;23 increased mortality after liver transplantation;15 increased kidney transplant rejection;24 and poorer survival after heart transplantation if either the donor was, or the recipient is, a smoker.16, 25 The poorer organ transplantation outcomes in smokers, combined with the high demand for donated organs, have led to suggestions that smokers be given lower priority for organ transplants and debate about the ethics of such a policy.26-28
Smoking has also been implicated (in a report of four cases) as a risk factor for late-onset infection and other complications after facial injection of a filler substance for cosmetic purposes.29
The magnitude of the impact of smoking on perioperative outcomes was studied in a retrospective review of data from more than 500 000 patients in the US who had non-cardiac surgery.30, 31 Information on the 30-day period following surgery was compared for 82 304 current smokers and 82 304 control patients. Current smokers were 40% more likely to die than never smokers. Their risk of major morbidity also increased: the risk of pneumonia doubled, the risk of unplanned intubation almost doubled, and the odds of postoperative ventilation increased by 50%, cardiac arrest by 60%, myocardial infarction by 80%, and stroke by 70%. The risk of superficial and deep infections increased by 30% and 40%, respectively, and sepsis, organ space infections and septic shock were 30% to 50% more likely. The increased perioperative mortality and morbidity were confined to patients who had smoked more than 11 pack-years.
3.15.1.3 Impact of smoking cessation
A meta-analysis published in 2011 reviewed data from randomised trials and observational studies that had compared postoperative complications in smokers and people who quit smoking before surgery. The analysis found that smoking cessation decreases postoperative complications. In the randomised trials, complications were reduced by about 40%. The review found that the longer the period of preoperative smoking cessation, the greater the reduction in complications.32
Another meta-analysis, also published in 2011, investigated the possibility that smoking cessation just before surgery may be harmful (see Section 3.15.1.1).9 Data from nine studies that had studied the impact of quitting within eight weeks of surgery were combined. The analysis found no increase (or decrease) in overall postoperative complications in recent quitters compared with smokers. Although the study authors suggested that concern about possible adverse effects associated with stopping smoking just before surgery might therefore be unfounded, an accompanying 'Invited Commentary' pointed out that there was significant heterogeneity in the results of the studies that were combined, which was not surprising because some included patients who had quit two to three days before surgery whereas others included patients who had quit eight weeks prior to surgery.8 The commentators affirmed the wisdom of encouraging patients to quit smoking several months prior to surgery, but queried whether clinicians should be reassured that the timing of smoking cessation in anticipation of surgery is immaterial.
A systematic review published in 2012 explored the relationship between short-term preoperative smoking cessation and postoperative complications, and concluded that at least four weeks of abstinence from smoking reduces respiratory complications, and abstinence of at least three to four weeks reduces wound- healing complications. Short-term (less than four weeks) smoking cessation did not appear to increase or reduce the risk of postoperative respiratory complications.33 The Australian and New Zealand College of Anaesthetists recommend that, based on the current available evidence, anaesthetists and surgeons should not be dissuaded from advising patients to quit at any time before surgery.8
3.15.2 Drug interactions
Smoking alters the effects of a number of medications (see also Section 3.15.1.1 on interactions with anaesthetics). Doctors and other healthcare workers need to be aware of these interactions when medications are prescribed and also when patients quit smoking, as drug dosages may need to be adjusted.34
Drug interactions fall into two categories: (i) pharmacokinetic interactions, which occur when cigarette smoke alters a drug's metabolism; or (ii) pharmacodynamic interactions, which occur when the physiological effects of cigarette smoke modify the physiological effects of the drug.35, 36
Pharmacokinetic interactions include increased metabolism of caffeine, heparin, warfarin, theophylline, a number of antipsychotic drugs and a number of benzodiazepines. A meta-analysis of the interaction between smoking and warfarin, for example, found that smoking increased warfarin dosage requirements by about 12%.37 Although it is difficult to know which of the estimated 4800 compounds in cigarette smoke cause these interactions, the polycyclic aromatic hydrocarbons are suspected. These hydrocarbons induce liver enzymes (see Chapter 13, Section 13.15.1.1) and thereby hasten the clearance of any drug (or substance) whose metabolism requires the enzymes.35, 36
Pharmacodynamic interactions include: reduced response to corticosteroids in smokers who are asthmatic,39, 40 decreased sedation with benzodiazepines (possibly due to the stimulant effects of nicotine), slowed absorption of sub-cutaneous insulin (possibly due to reduced blood flow to the skin, mediated by nicotine), and an increased risk of cardiovascular adverse effects in women taking oral contraceptives.35, 36
In the above examples, smoking modifies the effects of particular drugs. It has also been hypothesised that bronchodilator drugs (mainly beta-2-agonists), prescribed for people with chronic obstructive pulmonary disease (COPD), may worsen the effects of cigarette smoke. The theory is that bronchodilation improves smoke inhalation, and may increase the deposition of cigarette smoke on the lungs, thereby increasing cardiovascular disease morbidity and mortality. This hypothesis is yet to be tested.41
3.15.3 Cardiovascular disease
As detailed in Section 3.1, smoking causes cardiovascular disease, and generally, if a person continues to smoke after developing cardiovascular disease their prognosis is worse than if they had quit.
For example, a study of more than 18 000 patients with coronary disease who were receiving a statin drug for coronary disease found that over a five-year period those who continued to smoke had about a 50% higher chance of a major cardiovascular event (death, myocardial infarction, stroke or cardiac arrest) than patients who quit.42 Similarly, poorer treatment outcomes have been reported for people who continue to smoke after coronary artery bypass grafting (CABG)43 or a diagnosis of heart failure,44 compared with people who quit.
3.15.4 Cancer
As detailed in Section 3.5, smoking causes numerous cancers. A review has concluded that overall survival is poorer in smokers with cancer. Studies of lung cancer, prostate cancer, cervical cancer, and head and neck cancer were cited.45 All these studies involved radiotherapy, leading to suggestions that radiotherapy is less effective in smokers. Higher irradiation complication rates for smokers in the studies covered by the review, and other studies,46, 47 support this suggestion. The review also found that the risk of secondary primary tumours is increased in smokers, for malignancies that are related to cancer and also for those that are not.45 The review found little information about the impact of smoking on chemotherapy for cancer, but suggested that treatment outcomes are likely to be worse because of the effects of cigarette smoke on immune function, appetite and basal metabolic rate.45
More severe pain has been associated with smoking in patients with cancer,48 and specifically for lung cancer49 and head and neck cancer.50 This may be because of the decreased effectiveness of opioids (due to induction of liver enzymes by components of cigarette smoke) described in Chapter 13, Section 13.15.1.1 , and failure to increase the dose in response.
The 2014 Surgeon General’s report was the first in its series to review the associations between cigarette smoking and health outcomes in cancer patients and survivors. It concluded that smoking causes adverse health outcomes in people with cancer, while cessation improves their prognosis. Smoking increases all-cause mortality and cancer-specific mortality in cancer patients and survivors, and increases the risk for second primary cancers that are caused by cigarette smoking, such as lung cancer. Smoking is also associated with an increased risk of recurrence, poorer response to treatment, and increased treatment- related toxicity.51
A review of smoking cessation interventions in patients with cancer found that interventions increase quit rates but the difference was not statistically significant. Given the benefits of quitting on cancer outcomes, the authors called for research to identify more effective interventions for cancer patients.48
3.15.5 Treatment of infertility including assisted reproduction
As detailed in Section 3.2, women who smoke have reduced fertility and there is emerging evidence that fertility may also be reduced in male smokers. Smoking also has a negative impact on the outcomes of infertility treatment.53 In women participating in assisted reproduction programmes, a meta-analysis found that smoking is associated with lower pregnancy rates, higher chances of miscarriage and of ectopic pregnancy, and a lower probability of a live birth.54
One study found that for couples who smoked (either female, male or both), the risk of not achieving a pregnancy was about twice as high as for non-smokers.55 Female smoking during the period of infertility treatment has been associated with a decreased number of retrieved ova56 and a higher risk of repeated tubal ectopic pregnancies;57 male smoking has been associated with decreased live birth rates.56 Researchers have estimated that women who smoke need up to twice the number of in vitro fertilisation (IVF) cycles to conceive and suggest there is a correlation between the number of smoking years and the risk of not conceiving through IVF.53 Smoking cessation for both women and men is recommended for couples aiming to become pregnant58 and it has been suggested that access to fertility treatment should be conditional on quitting smoking.53
3.15.6 Contraception
As detailed in Section 3.2, smoking causes coronary heart disease, increasing the risk two- to four-fold.1 The 'combined' oral contraceptive pill (which contains the hormone oestrogen) also increases the risk of myocardial infarction two-fold.59 Women who both take the oral contraceptive pill and smoke have a 20-fold increase in the risk of coronary heart disease, compared with non-smokers who are not taking 'the pill'.60 The impact of smoking and the contraceptive pill is therefore 'synergistic', meaning that the risk of disease is multiplicative rather than additive. Heavier smokers have an even higher risk of coronary heart disease.61
Although the newer 'lower dose' versions of the pill may be associated with a lesser risk of developing coronary heart disease, risk is still elevated in smokers. There is insufficient evidence to evaluate the risk profile of the 'third-generation' pills (containing 30 μg or less of ethynyl estradiol and either gestodene or desogestrel) combined with smoking, but clinicians are advised to be wary when prescribing oral contraceptives to smokers aged in their mid-30s and to exercise extreme caution or avoid using them altogether in smokers aged over 40 years.61 In past decades the risk of stroke, particularly subarachnoid haemorrhage, has been significantly higher among smokers using the contraceptive pill. However research published since the 1990s following up women using lower dose pills is conflicting; some studies show increased risk, other studies have shown no significant effect.61
There is some evidence to suggest that the combined contraceptive pill has a higher failure rate in smokers than in non-smokers.60
3.15.7 Other conditions
A meta-analysis published in 2011 found that in patients receiving long-term haemodialysis or peritoneal dialysis, smoking increased the death rate (all-cause mortality) by 65%.62
References
1. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
2. Woodside JJ. Female smokers have increased postoperative narcotic requirements. Journal of Addictive Diseases 2000;19(4):1–10. Available from: http://www.haworthpress.com/store/E-Text/View_EText.asp?a=4& fn=J069v19n04_01&i=4&s=J069&v=19
3. Sweeney B and Grayling M. Smoking and anaesthesia: the pharmacological implications. Anaesthesia 2009;64(2):179–86. Available from: http://www3.interscience.wiley.com/journal/121575043/abstract
4. Moller AM, Maaloe R and Pedersen T. Postoperative intensive care admittance: the role of tobacco smoking. Acta Anaesthesiologica Scandinavica 2001;45(3):345–8. Available from: http://www3.interscience.wiley.com/journal/118965538/abstract
5. Schwilk B, Bothner U, Schraag S and Georgieff M. Perioperative respiratory events in smokers and nonsmokers undergoing general anaesthesia. Acta Anaesthesiologica Scandinavica 1997;41(3):348–55. Available from: http://www.ncbi.nlm.nih.gov/pubmed/9113178
6. Al-Sarraf N, Thalib L, Hughes A, Tolan M, Young V and McGovern E. Effect of smoking on short-term outcome of patients undergoing coronary artery bypass surgery. Annals of Thoracic Surgery 2008;86(2):517–23. Available from: http://www.sciencedirect.com/science?_ob=MImg& _imagekey=B6T11-4T14Y6K-16-1&_cdi=4877&_user=10&_orig=search&_coverDate=08%2F31%2F2008& _sk=999139997&view=c&wchp=dGLbVlW-zSkWW&md5=2599b7362e9bd6f024ef9edd3feab3f8& ie=/sdarticle.pdf
7. Australian and New Zealand College of Anaesthetists. Statement on smoking as related to the perioperative period. Review PS12 (2007). Melbourne: Australian and New Zealand College of Anaesthetists, 2007. Available from: http://www.anzca.edu.au/resources/professional-documents/documents /professional-standards/professional-standards-12.html
8. Chow CK and Devereaux PJ. The Optimal Timing of Smoking Cessation Before Surgery: Comment on "Smoking Cessation Shortly Before Surgery and Postoperative Complications". Archives of Internal Medicine 2011;171(11):989–90. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21403012 9. Myers K, Hajek P, Hinds C and McRobbie H. Stopping smoking shortly before surgery and postoperative complications: a systematic review and meta-analysis. Archives of Internal Medicine 2011;[Epub ahead of print] Available from: http://archinte.ama-assn.org/cgi/content/full/archinternmed.2011.97v1
10. Araco A, Gravante G, Sorge R, Araco F, Delogu D and Cervelli V. Wound infections in aesthetic abdominoplasties: the role of smoking. Plastic and Reconstructive Surgery 2008;121(5):e305–310. Available from: http://www.plasreconsurg.com/pt/re /prs/abstract.00006534-200805000-00045.htm;jsessionid=LX1cvKLdqrlv69R8HlLPKKjXJJRQvmJGznxJLQJYYGvzQFvbZy1W!932896
11. Abbas SM and Hill AG. Smoking is a major risk factor for wound dehiscence after midline abdominal incision; case-control study. Australian and New Zealand Journal of Surgery 2009;79(4):247–50. Available from: http://www3.interscience.wiley.com/user/accessdenied?ID=122364626&Act=2138&Code=4719& Page=/cgi-bin/fulltext/122364626/HTMLSTART
12. Araco F, Gravante G, Sorge R, Overton J, De Vita D, Primicerio M, et al. The influence of BMI, smoking, and age on vaginal erosions after synthetic mesh repair of pelvic organ prolapses. A multicenter study. Acta Obstetricia et Gynecologica Scandinavica 2009;88(7):772-80. Available from: http://www.ncbi.nlm.nih.gov /pubmed/19452293
13. Cundiff G, Varner E, Visco A, Zyczynski H, Nager C, Norton P, et al. Risk factors for mesh/suture erosion following sacral colpopexy. American Journal of Obstetrics and Gynecology 2008;199(6):688 e1–5. Available from: http://linkinghub.elsevier.com/retrieve/pii/S0002-9378(08)00810-7
14. Australian and New Zealand College of Anaesthetists. Statement on smoking as related to the perioperative period. Review PS12 (2007). Melbourne: Australian and New Zealand College of Anaesthetists, 2007. Available from: http://www.anzca.edu.au/resources/professional-documents/documents /professional-standards/professional-standards-12.html
15. Leithead J, Ferguson J and Hayes P. Smoking-related morbidity and mortality following liver transplantation. Liver Transplantation 2008;14(8):1159–64. Available from: http://www3.interscience.wiley.com/cgi-bin/fulltext/121358287/PDFSTART
16. Arora S, Aukrust P, Andreassen A, Simonsen S, Gude E, Grov I, et al. The prognostic importance of modifiable risk factors after heart transplantation. American Heart Journal 2009;158(3):431–6. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation& list_uids=19699867
17. McCarthy C, Mehrara B, Riedel E, Davidge K, Hinson A, Disa J, et al. Predicting complications following expander/implant breast reconstruction: an outcomes analysis based on preoperative clinical risk. Plastic & Reconstructive Surgery 2008;121(6):1886–92. Available from: http://www.plasreconsurg.com/pt/re /prs/abstract.00006534-200806000-00002.htm;jsessionid=LVLGDPrp2BnPy2Mmj4GQLXggJRl2pPDFcLRVFbh2JMn43x1vTY27!9820
18. Padubidri A, Yetman R, Browne E, Lucas A, Papay F, Larive B, et al. Complications of postmastectomy breast reconstructions in smokers, ex-smokers, and nonsmokers. Plastic & Reconstructive Surgery 2001;107(2):342–9. Available from: http://lib.bioinfo.pl/pmid:11214048
19. Bartsch R, Weiss G, Kästenbauer T, Patocka K, Deutinger M, Krapohl B, et al. Crucial aspects of smoking in wound healing after breast reduction surgery. Journal of Plastic, Reconstructive & Aesthetic Surgery 2007;60(9):1045–9. Available from: http://www.sciencedirect.com/science?_ob=ArticleURL& _udi=B7XNJ-4N74JF2-8&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221& _version=1&_urlVersion=0&_userid=10&md5=a7fa0121f8317e38ffca36d80b1d2ae7
20. Bikhchandani J, Varma S and Henderson H. Is it justified to refuse breast reduction to smokers? Journal of Plastic, Reconstructive & Aesthetic Surgery 2007;60(9):1050–4. Available from: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B7XNJ-4NSPW85-1&_user=10&_rdoc=1& _fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10& md5=8ae7d4d8802e2027d266e6dab42a8a0e
21. Sinha R, Singh V and Sankhwar S. Does tobacco consumption influence outcome of oral mucosa graft urethroplasty? Urology Journal 2010;7(1):45–50. Available from: http://www.urologyjournal.org/index.php /uj/article/view/574/430
22. Kaylie D, Bennett M, Davis B and Jackson C. Effects of smoking on otologic surgery outcomes. Laryngoscope 2009;119(7):1384-90. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19418530
23. Lindström D, Sadr Azodi O, Adami J, Bellocco R, Linder S and Wladis A. Impact of body mass index and tobacco smoking on outcome after open appendicectomy. British Journal of Surgery 2008;95(6):751–7. Available from: http://www3.interscience.wiley.com/cgi-bin/fulltext/118639075/PDFSTART
24. Nogueira J, Haririan A, Jacobs S, Cooper M and Weir M. Cigarette smoking, kidney function, and mortality after live donor kidney transplant. American Journal of Kidney Diseases 2010;55(5):907-15. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20176427
25. Tsao C, Chen R, Chou N, Ko W, Chi N, Yu H, et al. The influence of donor characteristics on survival after heart transplantation. Transplantation Proceedings 2008;40(8):2636–7. Available from: http://linkinghub.elsevier.com/retrieve/pii/S0041-1345(08)01076-2
26. Bright R. Denial of hepatic transplantation on the basis of smoking: is it ethical? Current Opinion in Organ Transplantation 2010;15(2):49-53. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20154621
27. Ehlers S. Ethical analysis and consideration of health behaviors in organ allocation: focus on tobacco use. Transplantation Reviews 2008;22(3):171–7. Available from: http://www.sciencedirect.com /science?_ob=MImg&_imagekey=B75B4-4SBRTJV-2-3&_cdi=12972&_user=10&_orig=browse& _coverDate=07%2F31%2F2008&_sk=999779996&view=c&wchp=dGLbVtz-zSkzV& md5=4e4b3ce5b52ef1f96c0d94f1f8b44ce4&ie=/sdarticle.pdf
28. Sharkey K and Gillam L. Should patients with self-inflicted illness receive lower priority in access to healthcare resources? Mapping out the debate. Journal of Medical Ethics 2010;36(11):661-5. Available from: http://jme.bmj.com/content/early/2010/09/03/jme.2009.032102.long
29. Goldan O, Garbov-Nardini G, Regev E, Orenstein A and Winkler E. Late-onset infections and granuloma formation after facial polylactic acid (New-Fill) injections in women who are heavy smokers. Plastic & Reconstructive Surgery 2008;121(5):e336–8. Available from: http://www.plasreconsurg.com/pt/re /prs/abstract.00006534-200805000-00082.htm;jsessionid=LX1JQZT7pbk10S2NC3pTHHDRQd2L1dFTMMrSQTgZbV1czpKJK1QH!98
30. Turan A, Mascha E, Roberman D, Turner P, You J, Kurz A, et al. Smoking and perioperative outcomes. Anesthesiology 2011;[Epub ahead of print[Available from: http://journals.lww.com/anesthesiology/Abstract /publishahead/Smoking_and_Perioperative_Outcomes.99256.aspx
31. Katznelson R and Beattie W. Perioperative smoking risk. Anesthesiology 2011;[Epub ahead of print] Available from: http://journals.lww.com/anesthesiology/Citation/publishahead /Perioperative_Smoking_Risk.99257.aspx
32. Mills E, Eyawo O, Lockhart I, Kelly S, Wu P and Ebbert JO. Smoking Cessation Reduces Postoperative Complications: A Systematic Review and Meta-analysis. American Journal of Medicine 2011;124(2):144–54 e8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21295194
33. Wong J, Lam DP, Abrishami A, Chan MT, and Chung F. Short-term preoperative smoking cessation and postoperative complications: a systematic review and meta-analysis. Canadian Journal of Anesthesia/Journal canadien d'anesthésie, 2012; 59(3):268-279. Available from: http://link.springer.com /article/10.1007/s12630-011-9652-x#page-1
34. Schaffer SD, Yoon S and Zadezensky I. A review of smoking cessation: potentially risky effects on prescribed medications. Journal of Clinical Nursing 2009;18(11):1533–40. Available from: http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2702.2008.02724.x/abstract
35. Benowitz N. Drug therapy: pharmacologic aspects of cigarette smoking and nicotine addiction. New England Journal of Medicine 1988;319(20):1318–30. Available from: http://content.nejm.org/cgi/content/brief /319/20/1318 36. Kroon LA. Drug interactions with smoking. Am J Health Syst Pharm 2007;64(18):1917–21. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17823102
37. Nathisuwan S, Dilokthornsakul P, Chaiyakunapruk N, Morarai T, Yodting T and Piriyachananusorn N. Assessing evidence of interaction between smoking and warfarin: a systematic review and meta-analysis. Chest 2011;139(5):1130–9. Available from: http://chestjournal.chestpubs.org/content/139/5/1130.long
38. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease. A report of the US Surgeon General, Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: http://www.surgeongeneral.gov/library/tobaccosmoke/report/index.html
39. Ahmad T, Barnes PJ and Adcock IM. Overcoming steroid insensitivity in smoking asthmatics. Current Opinion in Investigational Drugs 2008;9(5):470–7. Available from: http://www.biomedcentral.com/1472-4472 /9/470
40. Braganza G, Chaudhuri R and Thomson N. Treating patients with respiratory disease who smoke. Therapeutic Advances in Respiratory Disease 2008;2(2):95–107. Available from: http://tar.sagepub.com /cgi/reprint/2/2/95
41. van Dijk W, Heijdra Y, Scheepers P, Lenders J, van Weel C and Schermer T. Interaction in COPD experiment (ICE): a hazardous combination of cigarette smoking and bronchodilation in chronic obstructive pulmonary disease. Medical Hypotheses 2010;74(2):277–80. Available from: http://www.ncbi.nlm.nih.gov /19800175
42. Frey P, Waters D, Demicco D, Breazna A, Samuels L, Pipe A, et al. Impact of smoking on cardiovascular events in patients with coronary disease receiving contemporary medical therapy (from the Treating to New Targets [TNT] and the Incremental Decrease in End Points Through Aggressive Lipid Lowering [IDEAL] trials). American Journal of Cardiology 2011;107(2):145–50. Available from: http://www.ncbi.nlm.nih.gov /pubmed/21129718
43. Lindsay GM, Tolmie EP, Martin WM, Hutton IM and Belcher PR. Smoking after coronary artery bypass: high three-year mortality. Thoracic and Cardiovascular Surgeon 2009;57(3):135–40. Available from: http://www.thieme-connect.com/ejournals/html/thoracic/doi/10.1055/s-2008-1039271
44. Conard M, Haddock C, Poston W and Spertus J. The impact of smoking status on the health status of heart failure patients. Congestive Heart Failure 2009;15(2):82–6. Available from: http://www3.interscience.wiley.com/user/accessdenied?ID=122324641&Act=2138&Code=4719&Page=/cgi- bin/fulltext/122324641/HTMLSTART
45. Gritz ER, Dresler C and Sarna L. Smoking, the missing drug interaction in clinical trials: ignoring the obvious. Cancer Epidemiology Biomarkers & Prevention 2005;14:2287–93. Available from: http://cebp.aacrjournals.org/content/14/10/2287.full.pdf
46. Sauter E, Westgate S and Templemire J. Skin necrosis in cigarette smokers receiving partial breast irradiation: two case reports. Cases Journal 2008;1(1):230. Available from: http://www.casesjournal.com /content/pdf/1757-1626-1-230.pdf
47. Zevallos J, Mallen M, Lam C, Karam-Hage M, Blalock J, Wetter D, et al. Complications of radiotherapy in laryngopharyngeal cancer: effects of a prospective smoking cessation program. Cancer 2009;115(19):4636-44. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19569250
48. Bastian L. Pain and smoking among cancer patients: the relationship is complex but the clinical implication is clear. Pain 2011;152(1):10–1. Available from: http://www.painjournalonline.com/article /PIIS0304395910006500/fulltext
49. Daniel M, Keefe F, Lyna P, Peterson B, Garst J, Kelley M, et al. Persistent smoking after a diagnosis of lung cancer is associated with higher reported pain levels. Journal of Pain 2009;10(3):323–8. Available from: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WKH-4VR3PHJ-4&_user=10&_rdoc=1& _fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10& md5=023816b4442c522df6d19faa5fc0671b
50. Logan H, Fillingim R, Bartoshuk L, Sandow P, Tomar S, Werning J, et al. Smoking status and pain level among head and neck cancer patients. The Journal of Pain 2010;11(6):528-34. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20015696
51. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/
52. Cox LS, Africano NL, Tercyak KP and Taylor KL. Nicotine dependence treatment for patients with cancer. Cancer 2003;98(3):632–44. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12879483
53. Dondorp W, de Wert G, Pennings G, Shenfield F, Devroey P, Tarlatzis B, et al. Lifestyle-related factors and access to medically assisted reproduction. Human Reproduction 2010;25(3):578–83. Available from: http://humrep.oxfordjournals.org/content/25/3/578.full.pdf
54. Waylen A, Metwally M, Jones G, Wilkinson A and Ledger W. Effects of cigarette smoking upon clinical outcomes of assisted reproduction: a meta-analysis. Human Reproduction Update 2009;15(1):31–44. Available from: http://humupd.oxfordjournals.org/content/15/1/31.long
55. Klonoff-Cohen H, Natarajan L, Marrs R and Yee B. Effects of female and male smoking on success rates of IVF and gamete intra-Fallopian transfer. Human Reproduction 2001;16(7):1382–90. Available from: http://humrep.oxfordjournals.org/cgi/content/full/16/7/1382
56. Fuentes A, Munoz A, Barnhart K, Midwife B, Diaz M and Pommer R. Recent cigarette smoking and assisted reproductive technologies outcome. Fertility and Sterility 2010;93:189-95. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18973890
57. Weigert M, Gruber D, Pernicka E, Bauer P and Feichtinger W. Previous tubal ectopic pregnancy raises the incidence of repeated ectopic pregnancies in in vitro fertilization-embryo transfer patients. Journal of Assisted Reproduction and Genetics 2009;26(1):13-17. Available from: http://www.ncbi.nlm.nih.gov/pubmed /19020971
58. Barbieri RL. The initial fertility consultation: recommendations concerning cigarette smoking, body mass index, and alcohol and caffeine consumption. American Journal of Obstetrics and Gynecology 2001;185(5):1168–73. Available from: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6W9P- 45SR5B8-40&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_version=1&_urlVersion=0& _userid=10&md5=3513a812898f93109316929b2526c6fc
59. Keeling D. Combined oral contraceptives and the risk of myocardial infarction. Annals of Medicine 2003;35:413-18. Available from: http://www.ncbi.nlm.nih.gov/pubmed/14572165
60. British Medical Association Board of Science and Education & Tobacco Control Resource Centre. Smoking and reproductive life. The impact of smoking on sexual, reproductive and child health. London: British Medical Association, 2004. Available from: http://www.bma.org.uk/ap.nsf/Content /SmokingReproductiveLife
61. US Department of Health and Human Services. Women and smoking. A report of the US Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2001. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/sgr_2001/index.htm
62. Liebman S, Lamontagne S, Huang L, Messing S and Bushinsky D. Smoking in dialysis patients: a systematic review and meta-analysis of mortality and cardiovascular morbidity. American Journal of Kidney Diseases 2011;58(2):257–65. Available from: http://www.ajkd.org/article/S0272-6386%2811%2900810-9 /fulltext
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.16 Smoking and diabetes
3.16 Smoking and diabetes
Last updated: March 2015 Suggested citation: Bellew, B, Greenhalgh, EM & Winstanley, MH. 3.16 Smoking and diabetes. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-16-smoking-and-diabetes
Diabetes mellitus (diabetes) is an umbrella term for a number of metabolic diseases which affect the body's ability to control blood glucose levels; it is a disease marked by high blood glucose levels resulting from defective insulin production, insulin action or both. The hormone insulin is produced in the pancreas, and helps the body use glucose for energy. If insulin production or the effectiveness of an individual's insulin is impaired, then diabetes may result.1
There are three major types of diabetes: type 1 (sometimes referred to as 'insulin dependent diabetes'), type 2 (sometimes referred to as 'non-insulin dependent' or 'adult onset' diabetes); and gestational diabetes. Type 1 diabetes most often occurs in childhood or young adulthood (though it can occur at any age), and is the result of low levels of or the inability to produce insulin. People with type 1 diabetes need insulin replacement for survival.1 Based on data from the 2007–08 National Health Survey, 10% of people with diabetes reported that they had type 1, while the majority (88%) of people with diabetes reported type 2. Another 2% of people reported diabetes, but did not know which type.2 These figures correspond to an estimated 818 200 persons (4% of the population) in 2007–08 with diabetes mellitus who had been medically diagnosed (excluding those with gestational diabetes).2
As noted, type 2 is the most common form of diabetes; it occurs mostly in people aged 40 years and over and is marked by reduced or less effective insulin. Although uncommon in childhood, it is becoming increasingly recognised in that younger age group.1 Gestational diabetes, the onset of diabetes in pregnancy, occurs in a small proportion of otherwise unaffected women and is usually transient, although women who develop gestational diabetes have a higher risk of developing type 2 diabetes later in life. The Australasian Diabetes in Pregnancy Society estimates that about 5% of pregnant women are affected by gestational diabetes.3
Some population groups are at much higher risk for diabetes, notably Indigenous Australians, people born overseas, and those subject to the poorest socio-economic circumstances. Aboriginal and Torres Strait Islander peoples are three times as likely as non-Indigenous people to have diabetes and have much greater hospitalisation and death rates than other Australians. Rates of diabetes, hospitalisations and/or mortality are more common among overseas-born people from the South Pacific Islands, Southern Europe, Middle East, North Africa and Southern Asia. Diabetes prevalence and death rates for the worst-off fifth of the population are nearly twice as high as for the best-off fifth of the population.1
Many factors contribute to the onset and development of diabetes. Type 1 diabetes is believed to be caused by particular biological interactions and exposure to environmental agents among people genetically predisposed to diabetes. Obesity, physical inactivity and unhealthy diet play a role in the onset of type 2 diabetes, as well as genetic predisposition such as family history, ethnic background and age. There is some evidence that depression can increase the risk of developing type 2 diabetes and diabetes complications. It is thought that the increased risk of type 2 may be due to elevated stress levels and weight gain. Poor foetal nutrition leading to low birthweight for gestational age may predispose some individuals to type 2 diabetes. If these individuals are exposed to other risk factors (such as obesity and physical inactivity) the likelihood of developing type 2 diabetes becomes greater.1
The risk factors for gestational diabetes are similar to those for type 2 diabetes: women are at higher risk if they are of relatively advanced age or obese when pregnant. There are also a number of additional risk factors for diabetes complications, including high blood pressure, high blood cholesterol and tobacco smoking. The 'metabolic syndrome'—the clustering of a number of risk factors including abdominal obesity, impaired fasting blood glucose, raised blood pressure, raised blood triglycerides and reduced blood HDL-cholesterol—substantially increases the risk of type 2 diabetes.1
As well as being life threatening in its own right, diabetes can lead to a range of other serious health problems, including coronary heart disease, stroke, peripheral vascular disease, kidney disease, eye disease, and complications in pregnancy and childbirth.4 Smoking greatly increases the risk of pancreatic cancer in patients with diabetes mellitus and there is evidence that a combined risk of family history of pancreatic cancer, current smoking and current diabetes mellitus confers a 10-fold increase in risk of being diagnosed with this cancer.5, 6 Among male cancer survivors there is evidence that a history of smoking before diagnosis, obesity and insulin resistance increase the risk for several second primary cancers, indicating the need for screening for second primary cancers among cancer survivors with these risk factors.7 Smoking is related to low bone mass and increased risk of fracture risk in postmenopausal women in the general population, but recent evidence suggests that women with diabetes who are current smokers have more than a three-fold increase in risk (3.47; 95% CI, 1.82–6.62) of non-vertebral fractures than diabetic women who were never smokers.8
Among the lifestyle-related factors, smoking makes the largest contribution to the absolute risk of macrovascular complications for people with diabetes. The added risk from smoking is greater than in people without diabetes.9 Smokers with type 1 and type 2 diabetes are at increased risk of illness and premature death, mostly through development of cardiovascular disease, but other disease processes associated with diabetes may also be made worse by smoking. Smokers with type 1 diabetes in particular may have a higher risk of developing kidney disease, and possibly eye and nerve damage as well, whereas smokers with type 2 diabetes are more likely to increase their risk of coronary heart disease, stroke and peripheral vascular disease. Studies of individuals with diabetes consistently demonstrate that smokers have a heightened risk of cardiovascular disease, premature death and increased rate of microvascular complications of diabetes.4
The 2014 US Surgeon General’s report concluded that smoking causes type 2 diabetes, with the risk of developing diabetes 30–40% higher for active smokers than nonsmokers. Further, there is a positive dose-response relationship between the number of cigarettes smoked and the risk of developing diabetes. The report highlights that reducing tobacco use should be promoted as a key public health strategy to prevent and control the increasing worldwide epidemic of diabetes.10
Plausible biological mechanisms for this association include include increased central obesity in smokers, increased inflammation and oxidative stress,10 increased insulin resistance, altered insulin secretion and other impairments to pancreatic function noted in smokers.11 Further corroboration for the Surgeon General’s finding that smokers are more likely to develop type 2 diabetes than non-smokers has been provided in a 2007 systematic review11 and recent studies conducted in Japan,12 Korea,13,14 Taiwan,15 China16 and the US.11
There is also evidence that exposure to secondhand smoke is positively and independently associated with the risk of type 2 diabetes, from several observational studies recently conducted in the US,17,18 Germany19 and Japan.20 Some recent evidence suggests that smoking cessation among people with diabetes can lead to short-term increased risk of diabetes (probably because of weight gain) and that this may deter smokers with diabetes from attempting to quit.21,22 The research indicates that any temporary increase in risk may occur in the first three years after quitting, thereafter gradually decreasing to zero.21 Other studies also report that the risk of type 2 diabetes in former smokers returns to that of non-smokers after a number of years.10 A 2015 retrospective cohort study of more than 10,000 adults found that smoking cessation is associated with deterioration in glycaemic control in smokers with type 2 diabetes, which lasts for 3 years and is unrelated to weight gain.23 This evidence underscores the need for smoking cessation to be accompanied by other strategies for diabetes prevention and early detection, as recommended in current clinical guidelines in the US and in Australia.4,9
In conclusion, cigarette smoking produces insulin resistance and chronic inflammation, which can accelerate macrovascular and microvascular complications, including nephropathy. Many clinical and experimental studies have found significant associations between cigarette smoking and development of diabetes, impaired glycaemic control, and diabetic complications (microvascular and macrovascular). A different lifestyle of smokers, in contrast to that maintained by non-smokers, may also contribute to these effects. The development of type 2 diabetes is yet another harmful consequence of cigarette smoking, and one that adds to the heightened risks of CVD; smoking cessation is crucial to facilitating glycaemic control and limiting development of complications.24
References
1. Australian Institute of Health and Welfare. Diabetes: Australian facts 2008. AIHW cat. no. CVD 40. Canberra: AIHW, 2008. Available from: http://www.aihw.gov.au/publication-detail/?id=6442468075
2. Australian Bureau of Statistics (ABS). 4364.0 National Health Survey: Summary of Results, 2007-2008 (Reissue) Released 25/08/2009. 2009. Available from: http://www.abs.gov.au/AUSSTATS/[email protected] /Latestproducts/4364.0Main%20Features12007-2008%20(Reissue)?opendocument&tabname=Summary& prodno=4364.0&issue=2007-2008%20(Reissue)&num=&view=
3. Australasian Diabetes in Pregnancy Society. Corporate website. Sydney, New South Wales: ADPS, 2011 [viewed 24 May 2011] . Available from: http://adips.org
4. American Diabetes Association. Standards of medical care in diabetes-2011. Diabetes Care 2011;34(suppl. 1):S11-S61. Available from: http://care.diabetesjournals.org/content/34/Supplement_1 /S11.long
5. Dite P, Trna J, Belobradkova J, Novotny I, Hermanova M, Vlckova P, et al. Pancreatic cancer--association with diabetes mellitus and smoking. Vnitrni lekarstvi 2011;57(2):159-62. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21416856
6. Matsubayashi H, Maeda A, Kanemoto H, Uesaka K, Yamazaki K, Hironaka S, et al. Risk factors of familial pancreatic cancer in Japan: current smoking and recent onset of diabetes. Pancreas 2011;40(6):974-8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21487321
7. Park SM, Lim MK, Jung KW, Shin SA, Yoo KY, Yun YH, et al. Prediagnosis smoking, obesity, insulin resistance, and second primary cancer risk in male cancer survivors: National Health Insurance Corporation Study. Journal of clinical oncology 2007;25(30):4835-43. Available from: http://jco.ascopubs.org/content /25/30/4835.full.pdf+html
8. Jorgensen L, Joakimsen R, Ahmed L, Stormer J and Jacobsen BK. Smoking is a strong risk factor for non-vertebral fractures in women with diabetes: the Tromso Study. Osteoporosis International 2011;22(4):1247-53. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20607217
9. Diabetes Australia and Royal Australian College of General Practitioners. Diabetes management in general practice: guidelines for Type 2 diabetes, 15th edn. South Melbourne, Victoria: RACGP, 2009. Available from: https://www.racgp.org.au/Content/NavigationMenu/ClinicalResources/RACGPGuidelines /Diabetesmanagement/200910diabetesmanagementingeneralpractice.pdf 10. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress
11. Willi C, Bodenmann P, Ghali W, Faris P and Cornuz J. Active smoking and the risk of type 2 diabetes. A systematic review and meta-analysis. Journal of the American Medical Association 2007;298(22):2654-64. Available from: http://jama.ama-assn.org/content/298/22/2654.full.pdf+html
12. Kawada T, Otsuka T, Inagaki H, Wakayama Y, Li Q, Ji Li Y, et al. Association of smoking status, insulin resistance, body mass index, and metabolic syndrome in workers: a 1-year follow-up study. Obesity Research & Clinical Practice 2010;4(3):e163–9. Available from: http://www.sciencedirect.com/science/journal /1871403X
13. Jee SH, Foong AW, Hur NW and Samet JM. Smoking and risk for diabetes incidence and mortality in Korean men and women. Diabetes Care 2010;33(12):2567-72. Available from: http://www.ncbi.nlm.nih.gov /pubmed/20823342
14. Cho N, Chan J, Jang H, Lim S, Kim H and Choi S. Cigarette smoking is an independent risk factor for type 2 diabetes: a four-year community-based prospective study. Clinical Endocrinology 2009;71(5):679-85. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19508609
15. Hsu CC, Hwang SJ, Tai TY, Chen T, Huang MC, Shin SJ, et al. Cigarette smoking and proteinuria in Taiwanese men with type 2 diabetes mellitus. Diabetic Medicine 2010;27(3):295-302. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20536492
16. Xie X, Liu Q, Wu J and Wakui M. Impact of cigarette smoking in type 2 diabetes development. Acta Pharmacologica Sinica 2009;30(6):784–7. Available from: http://www.nature.com/aps/journal/v30/n6 /full/aps200949a.html
17. Zhang L, Curhan G, Hu F, Rimm E and Forman J. Association between passive and active smoking and incident type 2 diabetes in women. Diabetes Care 2011;34(4):892–7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21355099
18. Houston TK, Person SD, Pletcher MJ, Liu K, Iribarren C and Kiefe CI. Active and passive smoking and development of glucose intolerance among young adults in a prospective cohort: CARDIA study. British Medical Journal 2006;332:1064-9. Available from: http://www.bmj.com/content/332/7549/1064.full.pdf+html
19. Kowall B, Rathmann W, Strassburger K, Heier M, Holle R, Thorand B, et al. Association of passive and active smoking with incident type 2 diabetes mellitus in the elderly population: the KORA S4/F4 cohort study. European Journal of Epidemiology 2010;25(6):393-402. Available from: http://www.njgasp.org /Association_of_passive_and_active_smoking_diabetes_04_2010_study.pdf
20. Hayashino Y, Fukuhara S, Okamura T, Yamato H, Tanaka H, Tanaka T, et al. A prospective study of passive smoking and risk of diabetes in a cohort of workers: the High-Risk and Population Strategy for Occupational Health Promotion (HIPOP-OHP) study. Diabetes Care 2008;31(4):732-4. Available from: http://care.diabetesjournals.org/content/31/4/732.full.pdf
21. Yeh H, Duncan B, Schmidt M, Wang N and Brancati F. Smoking, smoking cessation, and risk for type 2 diabetes mellitus: a cohort study. Annals of Internal Medicine 2010;152(1):10–7. Available from: http://www.acponline.org/acp_news/misc/smoking.pdf
22. Tonstad S. Cigarette smoking, smoking cessation, and diabetes. Diabetes Research and Clinical Practice 2009;85(1):4-13. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19427049
23. Lycett D, Nichols L, Ryan R, Farley A, Roalfe A, et al. The association between smoking cessation and glycaemic control in patients with type 2 diabetes: a THIN database cohort study. The Lancet Diabetes & Endocrinology. Available from: http://dx.doi.org/10.1016/S2213-8587(15)00082-0
24. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease. A report of the US Surgeon General. Rockville, Maryland: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: http://www.surgeongeneral.gov/library/tobaccosmoke/report/index.html
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.17 Inflammatory conditions and autoimmune disease
3.17 Inflammatory conditions and autoimmune disease
Last updated: March 2015 Suggested citation: Hurley, S, Greenhalgh, EM & Winstanley, MH. 3.17 Inflammatory conditions and autoimmune disease. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-17- inflammatory-conditions-and-autoimmune-disease
The role of smoking in cancer, lung diseases and cardiovascular diseases is now widely recognised. The fact that smoking also affects the immune system is less well known. In fact, smoking has wide ranging and severe impacts on the immune system: it increases the risk of a number of allergic conditions, increases the incidence of autoimmune diseases, decreases innate and acquired immunity and increases infection rates.1 The 2014 US Surgeon General’s report concluded that components of cigarette smoke have both immune activating and immune-suppressive effects. Smoking compromises the immune system and immune homeostasis, which relates to a heightened risk for pulmonary infections and several disorders with an underlying immune predisposition.2
Cigarette smoke triggers a systemic inflammatory response, through the release and inhibition of pro-inflammatory and anti-inflammatory molecules. These molecules are often referred to as cytokines or mediators or immunomodulating agents. For example, cigarette smoke induces the release of inflammatory cytokines such as TNF-α, interleukin (IL)-1, IL-6, IL-8 and granulocyte-macrophage colony-stimulating factor (GM-CSF). It increases production of endotoxin, one of the most potent inflammatory agents. It increases polymorphonuclear neutrophils (PMNs) with consequential adverse effects on the respiratory passage.1 A review of evidence about possible molecular pathways for smoking's impact on inflammation concluded that activation of the nuclear factor kappa B (NF-kB) family is the main mechanism.2
3.17.1 Rheumatoid arthritis
Rheumatoid arthritis is a systemic autoimmune disease characterised by disabling and painful destruction of the joints, and sometimes inflammation of the lungs and other organs. The incidence is about three-fold higher in women than men. A large proportion of patients (but not all) have the rheumatoid factor (RF) antibody.
Smoking causes rheumatoid arthritis.2 The risk is most markedly elevated in men who are RF-positive (RF is a type of antibody).4 There have been suggestions that smoking only increases susceptibility to rheumatoid arthritis in individuals who have specific genetic profiles.5
A number of studies have reported a poorer response to drug treatments in patients with rheumatoid arthritis who continue to smoke.6 Smoking reduces the effectiveness of tumour necrosis factor-alpha (TNF-a) inhibitors, a type of immunomodulatory drug that is currently used to treat rheumatoid arthritis.2 Rheumatoid arthritis sufferers have a higher mortality rate than the general population. Recent cohort studies have found this excess mortality confined to patients who are RF-positive.7,8 It has therefore been suggested that this excess mortality could be due to smoking.8
3.17.2 Anal abscess and fistula
Anal abscess is an inflammatory, fistulising cutaneous disease. A small case-control study in the US of 74 patients with anal abscess/fistula found that smoking within the previous year doubled the risk of this condition.9
3.17.3 Graves' opthamology
(See Eye 3.10.3)
3.17.4 Psoriasis
(See Skin 3.14.4)
3.17.5 Lupus erythematosus
(See Skin 3.14.5)
References
1. Arnson Y, Shoenfeld Y and Amital H. Effects of tobacco smoke on immunity, inflammation and autoimmunity. Journal of Autoimmunity 2010;34(3):j258-65. Available from: http://www.ncbi.nlm.nih.gov /entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=20042314
2. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress
3. Goncalves R, Coletta R, Silverio K, Benevides L, Casati M, da Silva J, et al. Impact of smoking on inflammation: overview of molecular mechanisms. Inflammation Research 2011;[Epub ahead of print] Available from: http://www.ncbi.nlm.nih.gov/pubmed/21298317
4. Sugiyama D, Nishimura K, Tamaki K, Tsuji G, Nakazawa T, Morinobu A, et al. Impact of smoking as a risk factor for developing rheumatoid arthritis: a meta-analysis of observational studies Annals of the Rheumatic Diseases 2010;69(1):70–81. Available from: http://ard.bmj.com/cgi/rapidpdf/ard.2008.096487v2
5. Bang S, Lee K, Cho S, Lee H, Lee K and Bae S. Smoking increases rheumatoid arthritis susceptibility in individuals carrying the HLA-DRB1 shared epitope, regardless of rheumatoid factor or anti-cyclic citrullinated peptide antibody status. Arthritis & Rheumatism 2010;62(2):369–77. Available from: http://www3.interscience.wiley.com/user/accessdenied?ID=123235521&Act=2138&Code=4719&Page=/cgi- bin/fulltext/123235521/HTMLSTART 6. Saevarsdottir S, Wedren S, Seddighzadeh M, Bengtsson C, Wesley A, Lindblad S, et al. Patients with early rheumatoid arthritis who smoke are less likely to respond to treatment with methotrexate and TNF inhibitors. Observations from the EIRA cohort and the Swedish Rheumatology Register. Arthritis & Rheumatism 2010; 63(1):26-36. Available from: http://onlinelibrary.wiley.com/doi/10.1002/art.27758/pdf
7. Gonzalez A, Icen M, Kremers HM, Crowson CS, Davis JM, 3rd, Therneau TM, et al. Mortality trends in rheumatoid arthritis: the role of rheumatoid factor. Journal of Rheumatology 2008;35(6):1009–14. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18412312
8. Goodson NJ, Farragher TM and Symmons DPM. Rheumatoid factor, smoking, and disease severity: associations with mortality in rheumatoid arthritis. Journal of Rheumatology 2008;35(6):945–9. Available from: http://www.jrheum.com/subscribers/08/06/945.html
9. Devaraj B, Khabassi S and Cosman B. Recent smoking is a risk factor for anal abscess and fistula. Diseases of the Colon and Rectum 2011;54(6):681–5. Available from: http://www.ncbi.nlm.nih.gov/pubmed /21552051
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.18 Other conditions with possible links to smoking
3.18 Other conditions with possible links to smoking
Last updated: March 2015 Suggested citation: Hurley, S, Greenhalgh, EM & Winstanley, MH. 3.18 Other conditions with possible links to smoking. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-18-other- conditions-with-possible-links-to-smoking
This section provides information about the many other conditions (in addition to those discussed in Sections 3.1 to 3.17) that have been linked to smoking. The list of conditions discussed in this section is comprehensive but not exhaustive; because cigarette smoke can adversely affect most, if not all, organs of the body, the list of diseases that may be caused by tobacco is still growing.
Generally, causality between smoking and the conditions discussed in this section has not been definitively established. Before a causal link is confirmed by expert bodies such as the US Surgeon General's office, a plausible biological mechanism and multiple studies reporting the association (with large numbers of subjects, unbiased design and confounding controlled) are needed.
3.18.1 Mental illnesses
People with mood disorders or mental illness have a higher prevalence of smoking than the general population, and account for a large proportion of smokers.1 More than 32% of current smokers report some sort of mental health problem in the last 12 months, compared to about 18% of ex-smokers and 16% of people who have never smoked.2
Smokers often report that smoking allays anxiety and has an antidepressant effect, but many studies suggest the reverse association, i.e. that smoking leads to anxiety,3 bruxism (teeth clenching and grinding),4 panic attacks,5, 6 depression,3, 7 suicide attempts,3, 8 and schizophrenia.9 The difficulties involved in establishing the causal direction of the association between mental disorders and smoking have been well summarised (specifically for depression) by Munafò and Araya,10 who comment:
Depression may cause people to smoke (perhaps to self-medicate their symptoms), or smoking may cause increased risk of depression (via alterations to neurotransmitter pathways following chronic exposure). The relationship may even be bidirectional (acute or infrequent tobacco use may reduce negative affect, but chronic use may exacerbate it), or be caused by shared risk factors (possibly genetic) so that the relationship is not causal at all.
Large longitudinal studies of smoking and mental health in Norway,3 New Zealand,11 Copenhagen7 and Finland8 have enabled researchers to account for previous mental illness in their analyses. These studies support the claim that smoking increases the risk of anxiety, depression and suicidality, especially in nicotine- dependent (i.e. heavy) smokers. Munafò and Araya point out that this creates a paradox, namely, that smoking may cause depression, but smokers say they smoke to alleviate depression.10 Munafò and Araya suggest that because of nicotine's short half-life, and the consequential speed with which withdrawal symptoms appear in heavy smokers who stop smoking, acute abstinence is associated with anxiety. Smoking alleviates this anxiety. There is evidence that after a few weeks of smoking cessation the withdrawal syndrome ends and mood elevates above that reached when the individual was smoking.10
The association between smoking and schizophrenia is different from the link between smoking and mood disorders. A meta-analysis of studies from 20 countries found consistent evidence that schizophrenia patients have a biological predisposition to smoke; genetic factors increase the risk of both becoming a smoker and developing schizophrenia. Schizophrenia is also associated with greater frequencies of heavy smoking and high nicotine dependence.9
3.18.2 Neurological diseases
Smoking may be a precipitating factor for migraine12, 13 and smokers may be at increased risk of developing cranial autonomic symptoms (for example, facial sweating) during an attack.14
An association between smoking and hearing loss has been suggested. A case–control study in the US, which included more than 3 000 cases, found only a very small, marginally statistically significant increase in risk associated with smoking.15
An analysis of the Nurses Health Study II in the US reported an increased risk of seizures associated with smoking.16
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative condition; it is a type of motor neurone disease. A 2010 meta-analysis of 15 case–control and five cohort studies found that smoking increases the risk of ALS in women, but not in men.17 However a 2011 pooled analysis of data from more than half a million men and more than half a million women enrolled in five prospective cohort studies in the US found that smoking increases the risk of ALS by about 40% for both men and women.18 This large study therefore strongly supports the existence of a link between smoking and ALS. The risk in smokers increased with decreasing age at smoking initiation. Smoking has also been reported to decrease survival rates in female smokers.19
Multiple sclerosis (MS) is a disease in which the myelin sheaths surrounding nerves in the brain and spinal cord become damaged and are eventually destroyed through an autoimmune process. A 2011 meta-analysis investigating the possible link between smoking and MS pooled data on more than 3 000 cases from 14 studies.20 The study found that smoking increases the risk of MS by about 50%. Smoking has also been reported to accelerate the clinical progression of MS, and the progression of the typical disease lesions visible on magnetic resonance images.21-24 However, a review article in 2011 looking at smoking and the onset and progression of MS found that while most of the studies on onset supported a positive association, the evidence on progression was more limited and mixed.25 The meta-analysis also analysed four studies that addressed this issue. Smoking did appear to increase the risk of progression from relapsing-remitting MS to secondary progressive disease, but the magnitude of the effect varied between studies and the pooled result was not statistically significant.20 Evidence on a potential mechanism is also limited.25
3.18.3 Kidney disease
Smoking has physiological effects on the kidney. It has been reported to increase the glomerular filtration rate,26, 27 possibly by relaxing renal arteries.26 There is evidence that smoking increases the risk of developing chronic kidney disease. For example, a 10-year follow-up study of more than 100 000 Japanese people found that smoking increased the risk of developing proteinuria and renal dysfunction.28 A case–control study in Syria found that smokers had a higher risk of hypertensive nephropathy and diabetic nephropathy, but the risk of kidney disease with other aetiologies was not increased by smoking.29 3.18.4 Other conditions
Recent studies have suggested that smoking may worsen quality of life for patients with hepatitis C30 and increase the risk of moderate to severe hepatic lesions, which in turn hastens progression to cirrhosis.31 Impaired liver metabolism of nicotine and smoking-induced hypoxia are possible mechanisms.31
Cystic fibrosis (CF) is a heritable disorder that severely affects the lungs and digestive system. Studies have shown that smoking worsens CF, and predisposes people with CF to infection. Children with CF exposed to secondhand smoke experience higher rates of hospital admissions and increased use of antibiotics. The mechanism underlying these associations is likely the suppression of antimicrobial host defenses, which is compromised already in people with CF.32
References
1. Leonard S, Alder L, Benhammou K, Berger R, Breese C, Drebing C, et al. Smoking and mental illness. Pharmacology, Biochemistry and Behavior 2001;70(4):561–70. Available from: http://www.sciencedirect.com /science?_ob=ArticleURL&_udi=B6T0N-44W8G76-D&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d& view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10& md5=7c178ac568c5182744dcceb7089a2dec
2. Australian Bureau of Statistics. 4326.0 Mental health and well-being: profile of adults: summary of results 2007 Canberra, 2008. Available from: http://www.abs.gov.au/AUSSTATS/[email protected]/allprimarymainfeatures /3F8A5DFCBECAD9C0CA2568A900139380?opendocument
3. Pedersen W and von Soest T. Smoking, nicotine dependence and mental health among young adults: a 13-year population-based longitudinal study Addiction 2008;104(1):129–37. Available from: http://www3.interscience.wiley.com/cgi-bin/fulltext/121567015/HTMLSTART
4. Rintakoski K, Ahlberg J, Hublin C, Broms U, Madden P, Kononen M, et al. Bruxism is associated with nicotine dependence: a nationwide Finnish Twin Cohort study. Nicotine & Tobacco Research 2010;12(12):1254-60. Available from: http://ntr.oxfordjournals.org/content/early/2010/11/01/ntr.ntq190.full
5. Cosci F, Knuts I, Abrams K, Griez E and Schruers K. Cigarette smoking and panic: a critical review of the literature. Journal of Clinical Psychiatry 2010;71(5):606-15. Available from: http://article.psychiatrist.com /dao_1-login.asp?ID=10006601&RSID=73120138221212
6. Abrams K, Zvolensky MJ, Dorflinger L, Galatis A, Blank M and Eissenberg T. Fear reactivity to bodily sensations among heavy smokers and nonsmokers. Experimental and Clinical Psychopharmacology 2008;16(3):230–9. Available from: http://psycnet.apa.org/index.cfm?fa=buy.optionToBuy&id=2008-06716-006
7. Flensborg-Madsen T, Bay von Scholten M, Flachs E, Mortensen E, Prescott E and Tolstrup J. Tobacco smoking as a risk factor for depression: a 26-year population-based follow-up study. Journal of Psychiatric Research 2010;45(2):143–9. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve& db=PubMed&dopt=Citation&list_uids=20630542
8. Riala K, Taanila A, Hakko H and Räsänen P. Longitudinal smoking habits as risk factors for early-onset and repetitive suicide attempts: the Northern Finland 1966 Birth Cohort Study. Annals of Epidemiology 2009;19(5):329-35. Available from: http://www.sciencedirect.com/science/journal/10472797
9. de Leon J and Diaz FJ. A meta-analysis of worldwide studies demonstrates an association between schizophrenia and tobacco smoking behaviors. Schizophrenia Research 2005;76(2-3):135–57. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15949648 10. Munafo M and Araya R. Cigarette smoking and depression: a question of causation. British Journal of Psychiatry 2010;196(6):425–6. Available from: http://bjp.rcpsych.org/cgi/content/full/196/6/425
11. Boden J, Fergusson D and Horwood L. Cigarette smoking and depression: tests of causal linkages using a longitudinal birth cohort. British Journal of Psychiatry 2010;196(6):440–6. Available from: http://bjp.rcpsych.org/cgi/content/full/196/6/440
12. Lopez-Mesonero L, Marquez S, Parra P, Gamez-Leyva G, Munoz P and Pascual J. Smoking as a precipitating factor for migraine: a survey in medical students. Journal of Headache and Pain 2009;10(2):101-3. Available from: http://www.springerlink.com/content/m7321n0664672p45/
13. Straube A, Pfaffenrath V, Ladwig K, Meisinger C, Hoffmann W, Fendrich K, et al. Prevalence of chronic migraine and medication overuse headache in Germany-the German DMKG headache study. Cephalalgia 2010;30(2):207-13. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve& db=PubMed&dopt=Citation&list_uids=19489879
14. Hershey A and Lipton R. Lifestyles of the young and migrainous. Neurology 2010;75(8):680–1. Available from: http://www.neurology.org/cgi/content/full/75/8/680
15. Shargorodsky J, Curhan S, Eavey R and Curhan G. A prospective study of cardiovascular risk factors and incident hearing loss in men. Laryngoscope 2010;120(9):1887–91. Available from: http://onlinelibrary.wiley.com/doi/10.1002/lary.21039/pdf
16. Dworetzky B, Bromfield E, Townsend M and Kang J. A prospective study of smoking, caffeine, and alcohol as risk factors for seizures or epilepsy in young adult women: data from the Nurses' Health Study II. Epilepsia 2010;51(2):198-220. Available from: http://www3.interscience.wiley.com/cgi-bin/fulltext/122563552 /HTMLSTART
17. Alonso A, Logroscino G and Hernan M. Smoking and the risk of amyotrophic lateral sclerosis: a systematic review and meta-analysis. Journal of Neurology, Neurosurgery & Psychiatry 2010;81(11):1249–5. Available from: http://jnnp.bmj.com.ezp.lib.unimelb.edu.au/content/81/11/1249.full.pdf
18. Wang H, O'Reilly E, Weisskopf M, Logroscino G, McCullough M, Thun M, et al. Smoking and risk of amyotrophic lateral sclerosis: a pooled analysis of 5 prospective cohorts. Archives of Neurology 2011;68(2):207–13. Available from: http://archneur.ama-assn.org/cgi/content/full/68/2/207
19. Alonso A, Logroscino G, Jick S and Hernan M. Association of smoking with amyotrophic lateral sclerosis risk and survival in men and women: a prospective study. BMC Neurology 2010;10(1):6. Available from: http://www.biomedcentral.com/content/pdf/1471-2377-10-6.pdf
20. Handel AE, Williamson AJ, Disanto G, Dobson R, Giovannoni G and Ramagopalan SV. Smoking and multiple sclerosis: an updated meta-analysis. PLoS One 2011;6(1):e16149. Available from: http://pubmedcentralcanada.ca/picrender.cgi?accid=PMC3020969&blobtype=pdf
21. Di Pauli F, Reindl M, Ehling R, Schautzer F, Gneiss C, Lutterotti A, et al. Smoking is a risk factor for early conversion to clinically definite multiple sclerosis. Multiple Sclerosis 2008;14(8):1026-30. Available from: http://msj.sagepub.com/cgi/rapidpdf/1352458508093679v1
22. Healy BC, Ali EN, Guttmann CR, Chitnis T, Glanz BI, Buckle G, et al. Smoking and disease progression in multiple sclerosis. Archives of Neurology 2009;66(7):858–64. Available from: http://archneur.ama-assn.org /cgi/content/full/66/7/858?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=& fulltext=Smoking+and+disease+progression+in+multiple+sclerosis&searchid=1&FIRSTINDEX=0& resourcetype=HWCIT
23. Pittas F, Ponsonby A, van der Mei I, Taylor B, Blizzard L, Groom P, et al. Smoking is associated with progressive disease course and increased progression in clinical disability in a prospective cohort of people with multiple sclerosis. Journal of Neurology 2009;256(4):577-85. Available from: https://commerce.metapress.com/content/7364256wg80p1770/resource-secured/?target=fulltext.pdf& sid=we5okf45o1fnvw55lwpg3bnc&sh=http://www.springerlink.com 24. Zivadinov R, Weinstock-Guttman B, Hashmi K, Abdelrahman N, Stosic M, Dwyer M, et al. Smoking is associated with increased lesion volumes and brain atrophy in multiple sclerosis. Neurology 2009;73(7):504–10. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve& db=PubMed&dopt=Citation&list_uids=19687451
25. Jafari N and Hintzen RQ. The association between cigarette smoking and multiple sclerosis. Journal of the neurological sciences, 2011; 311(1):78-85. Available from: http://www.jns-journal.com/article /S0022-510X(11)00553-3/abstract
26. Halmai R, Andras Szijarto I, Feher E, Fesus G, Molnar G, Brasnyo P, et al. Cigarette smoke elicits relaxation of renal arteries. European Journal of Clinical Investigation 2010;41(2):195–202. Available from: http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2362.2010.02386.x/full
27. Yoon H, Park M, Yoon H, Son K, Cho B and Kim S. The differential effect of cigarette smoking on glomerular filtration rate and proteinuria in an apparently healthy population. Hypertension Research 2009;32(3):214–9. Available from: http://www.nature.com/hr/journal/v32/n3/full/hr200837a.html
28. Yamagata K, Ishida K, Sairenchi T, Takahashi H, Ohba S, Shiigai T, et al. Risk factors for chronic kidney disease in a community-based population: a 10-year follow-up study. Kidney International 2007;71(2):159–66. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17136030
29. Yacoub R, Habib H, Lahdo A, Al Ali R, Varjabedian L, Atalla G, et al. Association between smoking and chronic kidney disease: a case control study. BMC Public Health 2010;10(1):731. Available from: http://www.biomedcentral.com/content/pdf/1471-2458-10-731.pdf
30. Yamini D, Basseri B, Chee GM, Arakelyan A, Enayati P, Tran TT, et al. Tobacco and other factors have a negative impact on quality of life in hepatitis C patients. Journal of Viral Hepatitis 2010. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20723039
31. De Luca L, De Angelis C, Fagoonee S, Di Bella S, Rizzetto M and Pellicano R. Is smoking a prognostic factor in patients with chronic hepatitis C? Minerva Gastroenterologica e Dietologica 2009;55(2):139–43. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19305373
32. U.S. Department of Health and Human Services. The Health Consequences of Smoking: 50 Years of Progress. A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library /reports/50-years-of-progress/full-report.pdf
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.19 Smoking and accidents
3.19 Smoking and accidents
Last updated: 2011 Suggested citation: Bellew, B & Winstanley, MH. 3.19 Smoking and accidents. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2011. Available from http://www.tobaccoinaustralia.org.au/3-18-smoking-motor-vehicle-crashes- and-other-injur
This section covers two sorts of accidents: accidents caused by the distraction of smoking while engaged in driving or other activities, and burns caused by cigarettes or sustained in fires caused by discarded cigarettes. For further information about measures to reduce cigarette-caused fires, see Chapter 12, Attachment A12.2 concerning reduced fire risk cigarettes.
3.19.1 Smoking, motor vehicle crashes and other injuries
Driver distraction is an important cause of motor vehicle crashes.1 Loss of concentration (thinking about other things or daydreaming), adjusting controls for accessories in the car, and being distracted by passengers or people or events outside the car are common causes of driver distraction.2 In research from New South Wales and Western Australia examining driver distraction and road safety, 10% of drivers reported that they had smoked during their most recent driving trip of five minutes or more duration, ahead of 9% who had used mobile telephones and 6% who had eaten while driving.2 A study using video analysis of people driving while smoking suggests an average of measured driving distraction time to be about 12 seconds, or enough to cover a distance of 160 m at a speed of 50 km/h. The authors suggest that distraction of drivers through smoking may be greater in the case of mobile phone use and that it constitutes a remarkable risk for road safety.3 A small study conducted among Italian adolescents compared those who had not experienced any motor vehicle accidents with those having one or more crash; it reported that the latter were more likely to be tobacco users and the adjusted analyses found that tobacco use was independently predictive of a motor vehicle accident (OR 3.2, p< 0.0001).4 Similarly, North American research among teenagers and young adults found that being a current smoker was associated with having been in a crash,5 while Canadian researchers found that smokers are more likely to have a car crash than non-smokers, whether or not they are actually smoking at the time of the incident.6 The Canadian study speculates that as well as the distraction factor, smokers may suffer physiological impairment due to smoking, or that there may be underlying behavioural differences between smokers and non-smokers that contribute to the difference in crash data.6 Whatever the explanation, Australian reviews have concluded that smoking while driving increases the risk of having a motor vehicle crash.1, 7 This is consistent with findings from an earlier review by North American researchers that smokers are 1.5 times more likely than non-smokers to have a motor vehicle crash.8 Being a waterpipe and/or cigarette smoker was found to predict the number of traffic crashes in an adjusted analysis within a recent study of drivers in Iran.9 Other Italian research has estimated that about 7% of car injuries in that country may involve a subject who smokes while driving,10 while analysis of US motor vehicle crash data concluded that distraction caused by smoking may be responsible for almost 1% of car crashes over the five-year period 1995–1999, or about 12 780 crashes.11 Smokers are also more likely to be die from injury in motor vehicle crashes and other types of accidents, including those involving falls, fires and other unintentional injuries.12-14 Possible reasons for this include the effects of smoking on physical performance (such as strength, agility, balance and speed) and recovery from physical trauma (such as post-operative complications and wound healing).14 A meta-analysis of randomised, controlled trials was conducted to examine whether cigarette smoking causes, and smoking cessation prevents, excessive injury burden. Intervention (cessation) was associated with pooled estimated injury risk reduction of 35% within the trials (RR 0.65; 95% CI, 0.36–1.19) and of 32% (RR 0.68; 95% CI, 0.43–1.09) with additional follow-up in two of the three studies; it should be noted that these associations were only of borderline statistical significance.15
3.19.2 Burns and fires caused by tobacco use
Cigarettes and cigarette lighters have been shown to be a major cause of burn injury; globally they are responsible for one million fires per year.16 In the US, fires and burns are among the top 10 leading causes of unintentional death, with thousands of deaths occurring annually; the majority of these deaths and injuries occur in residential fires, and smoking has been identified as the leading cause of home fire deaths in the US.17, 18 Some data suggest that the rate of injuries is higher for fires that were started by smoking, heating equipment, or children playing with fire (relative risk, 2.6).19 There is evidence that reductions in smoking and increases in cigarette prices are associated with fewer fires.18 Smokers engage in behaviours such as smoking in bed and leaving lit cigarettes unattended that may place them at an increased risk of cigarette- caused fires; in a Canadian study 1 in 4 smokers admitted to leaving lit cigarettes unattended in the previous month, while 15% admitted to smoking while in bed.20 It is a sad irony that smoking also compromises the prognosis of patients with severe burn injury.21
Smoking is conservatively estimated to be the direct cause of at least 4574 fires in Australia each year, the real number probably being much higher.22 It is estimated that in 2004–05, 24 people died in Australia due to fires caused by cigarettes, and that nearly a quarter (23%) of all deaths caused by fire are due to cigarette use.23 The National Coroners' Information System has reported that between the financial years 2000–01 and 2005–06, 67 deaths were caused in Australia by cigarette-related fires.24 The authors of this report emphasise that this is highly likely to be an under-representation of the true number of deaths, particularly for the more recent years reported, since cases not concluded or as yet uncoded in their national database are not accounted for in the data. In a recent New Zealand study (conducted among callers to the national smoking cessation service) 6.8% reported one or more fires caused by cigarettes, 60% described at least one cigarette-caused burn and 5.2% reported burns which required medical attention.25 Studies have emphasised the particular fire risk associated with smoking in long-term care settings such as nursing homes,26, 27 and in relation to the usage of certain highly flammable products such as liquid petroleum gas (LPG),28 automatic air-fresheners,29 or equipment used for home oxygen therapy.30, 31 In-car cigarette lighters have also been reported as a cause of burn injuries.32
The role of smoking-related materials in causing fires has led to demands for tobacco manufacturers to introduce 'reduced ignition propensity' (RIP) cigarettes, which only burn while being actively inhaled upon, as opposed to when they are left idling between puffs, or after they have been discarded.22 Research into the ignition propensity of cigarettes has grown, notably during the past decade.22, 33-45 Among the research results are the important findings that RIP cigarettes do not adversely impact public perceptions about the need for safety,33 appear to reduce consumption although resulting in small increases in smoker exposure to the compound phenanthrene,35 may have little change in the carcinogenic aspects of particulate matter44 and tend to reduce risk behaviours such as leaving a cigarette burning unattended and smoking in bed.36 Recently a systematic review of the public health, scientific, technological, trade literatures and internal industry information has been made available following the Master Settlement Agreement between US states and tobacco companies. It reveals that the industry has made advancements in understanding the key parameters involved in cigarette smouldering combustion and ignition of substrates, developing new cigarette and paper wrapper designs to reduce ignition propensity, including banded and non-banded cigarette paper approaches, assessing toxicology, and measuring performance. It is possible that this technical knowledge, now in the public domain, will in the future allow further improvements in the fire safety aspects of cigarettes.38 For further discussion about regulation of tobacco products, see Chapter 12.
References
1. Young K, Regan M and Hammer M. Driver distraction: a review of the literature. Report 206. Clayton, Victoria: Monash University Accident Research Centre, 2003. Available from: http://www.monash.edu.au /muarc/reports/muarc206.pdf
2. McEvoy S, Stevenson M and Woodward M. The impact of driver distraction on road safety: results from a representative survey in two Australian states. Injury Prevention.2006. 12(4):242-7 Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2586781/pdf/242.pdf
3. Mangiaracina G and Palumbo L. Smoking while driving and its consequences on road safety. Annali di Igiene 2007;19(3):253-67. Available from: http://www.seu-roma.it/annali_igiene/apps/autos.php?id=414
4. Pizza F, Contardi S, Antognini AB, Zagoraiou M, Borrotti M, Mostacci B, et al. Sleep quality and motor vehicle crashes in adolescents. Journal of Clinical Sleep Medicine 2010;6(1):41-5. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20191936
5. Hutchens L, Senserrick TM, Jamieson PE, Romer D and Winston FK. Teen driver crash risk and associations with smoking and drowsy driving. Accident Analysis & Prevention 2008;40(3):869–76. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18460353
6. Brison R. Risk of automobile accidents in cigarette smokers. Canadian Journal of Public Health 1990;81(2):102-6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/2331646
7. Collins D and Lapsley H. Economic aspects of drug taking and road safety. In Inquiry into the effects of drugs (other than alcohol) on road safety in Victoria. First report incorporating collected papers Melbourne: Road Safety Committee, Parliament of Victoria, 1995. Available from: http://www.parliament.vic.gov.au /rsc/drugs/drugcola.htm
8. Sacks JJ and Nelson DE. Smoking and injuries: an overview. Preventive Medicine 1994;23(4):515-20. Available from: http://www.sciencedirect.com/science/article/pii/S009174358471070X
9. Saadat S and Karbakhsh M. Association of waterpipe smoking and road traffic crashes. BMC Public Health 2010;10:639. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20969795
10. Iacobelli N, Gallus S, Petridou E, Zuccaro P, Colombo P, Pacifici R, et al. Smoking behaviors and perceived risk of injuries in Italy, 2007. Preventive Medicine 2008;47(1):123–6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18501413
11. Stutts J, Reinfurt D, Staplin L and Rodgman E. The role of driver distraction in crashes. Report for the AAA Foundation for Traffic Safety 2001 Available from: http://www.aaafoundation.org/pdf/distraction.pdf
12. Leistikow BN, Martin DC and Samuels SJ. Injury death excesses in smokers: a 1990-1995 United States national cohort study. Injury Prevention 2000;6:277-80. Available from: http://injuryprevention.bmj.com /cgi/reprint/6/4/277
13. Wen CP, Tsai SP, Cheng TY, Chan HT, Chung WSI and Chen CJ. Excess injury mortality among smokers: a neglected tobacco hazard. Tobacco Control 2005;14(suppl. 1):i28–32. Available from: http://tobaccocontrol.bmj.com/content/14/suppl_1/i28.full.pdf
14. Leistikow BN, Martin D, Jacobs J and Rocke D. Smoking as a risk factor for injury death: a meta-analysis of cohort studies. Preventive Medicine 1998;27(6):871-8. Available from: http://www.ncbi.nlm.nih.gov /pubmed/9922070
15. Leistikow BN and Shipley MJ. Might stopping smoking reduce injury death risks? A meta-analysis of randomized, controlled trials. Preventive Medicine 1999;28(3):255-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10072743
16. Leistikow BN, Martin DC and Milano CE. Fire injuries, disasters, and costs from cigarettes and cigarette lights: a global overview. Preventive Medicine 2000;31(2 Pt 1):91-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10938207
17. United States Fire Administration. Facts about smoking and home fires. Emmitsburg, Maryland: USFA. 2007.
18. Markowitz S. Where there's smoking, there's fire: the effects of smoking policies on the incidence of fires in the United States. NBER working paper no.1665. Cambridge, Massachusetts: National Bureau of Economic Research 2010. Available from: http://papers.nber.org/papers/w16625
19. Istre GR, McCoy MA, Osborn L, Barnard JJ and Bolton A. Deaths and injuries from house fires. New England Journal of Medicine 2001;344(25):1911-6. Available from: http://www.nejm.org/doi/pdf/10.1056 /NEJM200106213442506
20. O'Connor RJ, Bauer JE, Giovino GA, Hammond D, Hyland A, Fong GT, et al. Prevalence of behaviors related to cigarette-caused fires: a survey of Ontario smokers. Injury Prevention 2007;13(4):237-42. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17686933
21. Brusselaers N, Monstrey S, Vogelaers D, Hoste E and Blot S. Severe burn injury in Europe: a systematic review of the incidence, etiology, morbidity, and mortality. Critical Care 2010;14(5):R188. Available from: http://ccforum.com/content/pdf/cc9300.pdf
22. Chapman S and Balmain A. Time to legislate for fire-safe cigarettes in Australia [Editorial]. Medical Journal of Australia 2004;181(6):292-3. Available from: http://www.mja.com.au/public/issues/181_06_200904 /cha10373_fm.html
23. Collins D and Lapsley H. The costs of tobacco, alcohol and illicit drug abuse to Australian society in 2004/05. P3 2625. Canberra: Department of Health and Ageing, 2008. Available from: http://www.nationaldrugstrategy.gov.au/internet/drugstrategy/publishing.nsf/Content/mono64/$File /mono64.pdf
24. Hoy M and Morton S. NCIS Database Search. Deaths associated with fires caused by cigarettes between 1 June 2000 and 30 June 2006. Report produced for NSW Fire Brigades. Southbank, Victoria: National Coroners Information System, Victorian Institute of Forensic Medicine, 2006. Available from: http://www.fire.nsw.gov.au/gallery/files/pdf/research/CigDeathsReport_NCIS_3Oct_2006.pdf
25. Smith J, Bullen C, Laugesen M and Glover MP. Cigarette fires and burns in a population of New Zealand smokers. Tobacco Control 2009;18(1):29-33 Available from: http://tobaccocontrol.bmj.com/content /18/1/29.full
26. Weber M. Must nursing home residents who smoke be supervised? Fire in the nursing home. Pflege Zeitschrift 2011;64(2):112-4. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21384611
27. Lester PE and Kohen I. Smoking in the nursing home: a case report and literature review. Journal of the American Medical Directors Association 2008;9(3):201-3. Available from: http://www.ncbi.nlm.nih.gov /pubmed/18294605
28. Knobloch K, Ipaktchi R, Rennekampff H and Vogt P. Hand and facial burns related to liquefied petroleum gas (LPG) refuelling and cigarette smoking. An underestimated risk? Burns 2010;36(7):e140–2. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20728999
29. Hawkins S, Hunter J and Drew P. Domestic automated air fresheners: a significant burns risk to smokers. Burns 2009;35(7):1036–7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18947928
30. Wendling T and Pelletier A. Fatal fires associated with smoking during long-term oxygen therapy--Maine, Massachusetts, New Hampshire, and Oklahoma, 2000-2007. Morbidity and Mortality Weekly Report 2008;57(31):852–4. Available from: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5731a3.htm
31. Edelman DA, Maleyko-Jacobs S, White MT, Lucas CE and Ledgerwood AM. Smoking and home oxygen therapy--a preventable public health hazard. Journal of Burn Care Research 2008;29(1):119-22. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18182908
32. Rughani MG, Furniss D and Ghosh SJ. Burn injuries from in-car cigarette lighters. Burns 2010;36(3):e21-3. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19427128
33. Seidenberg AB, Rees VW, Alpert HR, O'Connor RJ, Giovino GA, Hyland A, et al. Smokers' self-reported responses to the introduction of reduced ignition propensity (RIP) cigarettes. Tobacco Control 2011;Epub ahead of publication. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21752794
34. Seidenberg AB, Rees VW, Alpert HR, O'Connor RJ and Connolly GN. Ignition strength of 25 international cigarette brands. Tobacco Control 2011;20(1):77-80. Available from: http://www.ncbi.nlm.nih.gov/pubmed /20974622
35. O'Connor RJ, Rees VW, Norton KJ, Cummings KM, Connolly GN, Alpert HR, et al. Does switching to reduced ignition propensity cigarettes alter smoking behavior or exposure to tobacco smoke constituents? Nicotine &Tobacco Research 2010;12(10):1011-8. Available from: http://www.ncbi.nlm.nih.gov/pubmed /20805292
36. O'Connor RJ, Fix BV, Hammond D, Giovino GA, Hyland A, Fong GT, et al. The impact of reduced ignition propensity cigarette regulation on smoking behaviour in a cohort of Ontario smokers. Injury Prevention 2010;16(6):420-2. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20643872
37. Cote F, Letourneau C, Mullard G and Voisine R. Estimation of nicotine and tar yields from human- smoked cigarettes before and after the implementation of the cigarette ignition propensity regulations in Canada. Regulatory Toxicology and Pharmacology 2010;Epub ahead of publication. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20303374
38. Alpert HR, O'Connor RJ, Spalletta R and Connolly GN. Recent advances in cigarette ignition propensity research and development. Fire Technology 2010;46(2):275-89. Available from: http://www.ncbi.nlm.nih.gov /pmc/articles/PMC2873202/pdf/nihms122218.pdf
39. O'Connor RJ, Giovino GA, Fix BV, Hyland A, Hammond D, Fong GT, et al. Smokers' reactions to reduced ignition propensity cigarettes. Tobacco Control 2006;15(1):45-9. Available from: http://www.ncbi.nlm.nih.gov /pubmed/16436405
40. Connolly GN, Alpert HR, Rees V, Carpenter C, Wayne GF, Vallone D, et al. Effect of the New York State cigarette fire safety standard on ignition propensity, smoke constituents, and the consumer market. Tobacco Control 2005;14(5):321-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16183983
41. Laugesen M, Duncanson M, Fraser T, McClellan V, Linehan B and Shirley R. Hand rolling cigarette papers as the reference point for regulating cigarette fire safety. Tobacco Control 2003;12(4):406-10. Available from: http://www.ncbi.nlm.nih.gov/pubmed/14660777
42. Barillo DJ, Brigham PA, Kayden DA, Heck RT and McManus AT. The fire-safe cigarette: a burn prevention tool. Journal of Burn Care and Rehabilitation 2000;21(2):162-4; discussion 164-70. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10752750
43. Brigham P and McGuire A. Progress towards a fire-safe cigarette. Journal of Public Health Policy 1995;16(4):433-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/8907764
44. Brunnemann KD, Hoffmann D, Gairola CG and Lee BC. Low ignition propensity cigarettes: smoke analysis for carcinogens and testing for mutagenic activity of the smoke particulate matter. Food and Chemical Toxicology 1994;32(10):917-22. Available from: http://www.ncbi.nlm.nih.gov/pubmed/7959447
45. Botkin JR. The fire-safe cigarette. Journal of the American Medical Association 1988;260(2):226-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/3290519
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.20 Tobacco poisoning
3.20 Tobacco poisoning
Last updated: March 2015 Suggested citation: Bellew, B, Greenhalgh, EM & Winstanley, MH. 3.20 Tobacco poisoning. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-20-tobacco-poisoning
Smokers subject their bodies to continued exposures to low amounts of nicotine, leading to tolerance. However dizziness, nausea and vomiting may occur in response to tobacco use before tolerance is established.1 These symptoms also accompany cases of acute nicotine poisoning, which may occur through ingestion of tobacco or other products containing nicotine (such as pesticides or nicotine-replacement medications) or through absorption of nicotine through the skin, either from exposure to pesticides, unprocessed tobacco leaves (see 'green tobacco sickness' below), or nicotine replacement medications.1
Symptoms of mild nicotine poisoning may include nausea and vomiting, progressing with increased exposure to cholinergic syndrome, which includes diarrhoea, increased salivation, increased respira¬tory secretions, and bradycardia (slow heart rate). Severe poisonings can lead to seizures and respiratory depression.2 Death may occur through respiratory failure.1 Although highly toxic, death due to ingested tobacco is extremely rare due to the unpleasant flavour of tobacco, the vomit response and early metabolism of the nicotine.1
3.20.1 Ingestion
A study of cigarette or cigarette butt ingestion by children as reported to a state Poison Control Centre in the United States has shown that vomiting is the most common response, and that significant toxicity is rare.3 Cases have also been reported in which children have ingested or had transdermal exposure to nicotine replacement therapy patches, causing symptoms of nicotine poisoning and, in more severe cases, requiring hospitalisation.4 Reports of ingestion of novel smokeless nicotine products have also increased since the availability of these on the market in the US.5
Solutions containing nicotine from cigarettes have also been reported in suicide attempts.6,7,8
Nicotine is a scheduled poison in Australia, its distribution being controlled by state and territory drugs and poisons legislation, all of which refer to a nationally-accepted Standard for Uniform Scheduling of Drugs and Poisons devised by the Therapeutic Goods Administration of the Australian Government.9 In an exemption considered by many public health interests to be anomalous, tobacco prepared and packed for smoking is excluded from the standard. See Chapter 12 for further information.
3.20.1 Green tobacco sickness
Green tobacco sickness (GTS) affects individuals involved in tobacco farming, especially during the harvesting season.10, 11 GTS occurs when nicotine is absorbed through the skin from direct contact with tobacco leaves and enters the bloodstream. Sufferers commonly experience dizziness, nausea, headache and vomiting; less frequent symptoms include abdominal pain, shortness of breath, diarrhoea, altered heart rate and blood pressure, sweating and increased salivation.10, 11 Non-smokers are more likely to be affected by GTS than smokers,12 which has in some cases lead to tobacco growers encouraging workers to take up smoking.11 GTS is treated with rest and rehydration, and treatment of additional symptoms if required. The incidence of GTS is reduced by provision of appropriate protective clothing and other workplace safety measures.10 11
GTS is common, a recent international review reporting that 8–89% of tobacco harvesters may be affected in the course of a season, this wide variation probably being due to differences between study methodologies as well as a range of working conditions.11 There are an estimated 33 million tobacco farm workers in the world, a substantial proportion living in developing countries. Long-term health outcomes for individuals exposed to nicotine transdermally for extended periods of time are not known.11
References
1. US Department of Health and Human Services. The health consequences of smoking. Nicotine addiction. A report of the Surgeon General. Rockville, Maryland: Center for Health Promotion and Education, Office on Smoking and Health, DHHS Publication No (CDC) 88-8406, 1988. Available from: http://profiles.nlm.nih.gov /NN/B/B/Z/D/segments.html
2. US Department of Health and Human Services, The health consequences of smoking - 50 years of progress, 2014, US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health: Atlanta, GA.
3. McGee D, Brabson T, McCarthy J and Picciotti M. Four-year review of cigarette ingestions in children. Pediatric Emergency Care 1995;11:13-16. Available from: http://www.ncbi.nlm.nih.gov/pubmed/7739954
4. Woolf A, Burkhart K, Caraccio T and Litovitz T. Childhood poisoning involving transdermal nicotine patches. Pediatrics 1997;99:e4. Available from: http://pediatrics.aappublications.org/cgi/content/abstract /99/5/e4
5. Connolly G, Richter P, Aleguas A, Jr, Pechacek T, Stanfill S and Alpert H. Unintentional child poisonings through ingestion of conventional and novel tobacco products. Pediatrics 2010;125(5):896–9. Available from: http://pediatrics.aappublications.org/content/125/5/896.long
6. Corkery J, Button J, Vento A and Schifano F. Two UK suicides using nicotine extracted from tobacco employing instructions available on the Internet. Forensic Science International 2010;199((1–3)):e9–13. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20202767
7. Schneider S, Diederich N, Appenzeller B, Schartz A, Lorang C and Wennig R. Internet suicide guidelines: report of a life-threatening poisoning using tobacco extract. Journal of Emergency Medicine 2010;38(5):610–3. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19272738
8. Solarino B, Rosenbaum F, Riesselmann B, Buschmann C and Tsokos M. Death due to ingestion of nicotine-containing solution: case report and review of the literature. Forensic Science International 2010;195((1–3)):e19–22. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19954906
9. Therapeutic Goods Administration. Standard for the uniform scheduling of drugs and poisons (SUSDP). Canberra, Australia: Department of Health and Ageing, 2007. Available from: http://www.tga.gov.au/ndpsc /susdp.htm
10. McBride JS, Altman DG, Klein M and White W. Green tobacco sickness. Tobacco Control 1998;7:294-8. Available from: http://tobaccocontrol.bmj.com/cgi/reprint/7/3/294
11. Schmitt N, Schmitt J, Kouimintzis D and Kirch W. Health risks in tobacco farm workers - a review of the literature. Journal of Public Health 2007;15:255-64. Available from: http://www.springerlink.com/content /rq0351564h1v60jp/
12. Arcury TA, Quandt SA and Preisser JS. Predictors of incidence and prevalence of green tobacco sickness among Latino farmworkers in North Carolina, USA. Journal of Epidemiology and Community Health 2001;55:818-24. Available from: http://jech.bmj.com/cgi/reprint/55/11/818
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.21 Health effects for younger smokers
3.21 Health effects for younger smokers
Last updated: April 2015 Suggested citation: Letcher, T, Greenhalgh, EM & Winstanley, MH. 3.21 Health effects for younger smokers. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-21-health-effects- for-younger-smokers
Most of the risk of dying prematurely due to smoking is reversed if people quit smoking before the age of 30.1 However smoking during childhood and adolescence also causes a range of immediate health problems, as well as laying the foundation for the development of serious disease in adulthood.2
3.21.1 Early signs of addiction
There is contention around how best to characterise nicotine dependence in young people, with increasing recognition that it may be inappropriate to extend adult criteria to adolescent smokers. Recent research has also highlighted qualitative differences between adolescents and adults in their experiences of withdrawal; craving tends to be the predominant symptom that is experienced by young people during abstinence, while withdrawal symptoms are minimal.2 Nonetheless, evidence shows that nicotine addiction can be developed rapidly by young people, with adolescent smokers reporting some symptoms of dependence at even low levels of cigarette consumption.3 The majority of people who begin to use tobacco products regularly have great trouble breaking this addiction.3 Factors influencing smoking behaviour in young people are discussed in Chapter 5. Research in Victoria tracking the smoking career of a large cohort of teenagers over a 10-year period has found a greater likelihood of substance abuse (especially cannabis dependence) and psychiatric illness in continuing smokers.4
3.21.2 Respiratory infections and exacerbation of asthma
Active smoking is associated with an increased risk for developing asthma and for exacerbating existing asthma in adolescents.5 Smoking also causes wheezing severe enough to be diagnosed as asthma in children and adolescents.2 Surveys among adolescent smokers (12–14 year olds) have found active smoking to be associated with asthma/wheezing and rhinitis,6,7 particularly in girls,7 and with asthma-related wheezing symptoms in 15–16 year old adolescents.8
Active smoking causes respiratory symptoms including shortness of breath, coughing, phlegm production and wheezing in children and adolescents.19 Even occasional smoking (on at least 5 days in the prior 30 days) has been found to be associated with shortness of breath/fatigue following regular activity in 18–24 year old college students,9 while regular smokers among this group were more likely than non-smokers to report having any cough or sore throat in the past 30 days.9 The prevalence of self-reported bronchitis symptoms (chronic cough and sputum production) among a cohort of 18–21 year old Finnish males was significantly higher among daily smokers than occasional smokers, and symptoms were significantly associated with smoking history.10
3.21.3 General health of young smokers
Young smokers are more likely to report suffering an overall diminished level of health compared with non-smokers.11 Recurrent headache has been associated with current smoking (daily and occasional) in Norwegian students aged 13–18 years,12 while among US students (grades 6 to 10), adolescent daily and experimental smokers were more likely than never smokers to report recurrent subjective health complaints such as headache and backache.13 Among a cohort of young US Navy recruits (average age 19.7 years at baseline), cigarette smoking was a prospective predictor of hospitalisation: data for more than 5000 young healthy female recruits from entry into the Navy for up to 7–8 years of service indicated that daily smokers had higher rates of hospitalisation for any reason and for musculoskeletal conditions.14 Daily smokers were also hospitalised for a significantly greater mean number of days compared with never smokers and other smokers (including experimental, occasional and former smokers), following adjustment for differences in time in service and socio-demographic variables.14
Evidence suggests other health effects among young people associated with current smoking; these include significantly reduced taste sensitivity and atrophic papillary structures compared with non-smokers (all male participants, mean age 24.9 years),15 as well as an association between an increase in some sleep disorders and current smoking in adolescents.16 For example, a study among about 29 000 Chinese adolescents aged 12–18 years found current smoking to be associated with increased snoring, difficulty breathing during sleep and difficulty maintaining sleep compared with never smokers.16
3.21.4 Fitness and lung function in young smokers
Young smokers tend to be less physically fit than their non-smoking peers, fitness declining with increasing levels of tobacco consumption.11 The cumulative effects of smoking from a young age on physical performance in midlife was assessed in a large British cohort study with data on smoking history from age 20 (median age at smoking initiation 16 years).17 Researchers found that at age 53, ever-smokers had significantly poorer overall physical performance, balance and chair rising than never smokers, with performance decreasing significantly for every 10 pack-years smoked.17
A study among a cohort of 18–21 year old Finnish males found levels of aerobic fitness to be significantly lower in regular smokers compared with non-smokers (after controlling for physical activity, education and body mass index) and fitness was associated with smoking history.10 A small study among a group of healthy young smokers (mean age 21.4 years) found that smoking was associated with resting and exercise tachycardia, demonstrating significant and acute negative effects on cardiac autonomic function due to smoking both at rest and during exercise. Results suggested that pre-exercise smoking of a single cigarette impaired physiological response to both peak and sub-maximal exercise; this may greatly increase vulnerability to myocardial electrical instability and therefore predispose to higher risk of cardiovascular events.18
3.21.5 Early signs of lung disease
Lung development is also altered by early tobacco use. Active smoking causes impaired lung growth during childhood and adolescence, and the early onset of lung function decline during late adolescence and early adulthood.19 Young smokers’ lungs stop growing earlier, they attain lower maximal lung function, they have a briefer plateau phase, and their lung function declines earlier. This reduced lung growth can increase the risk of chronic obstructive pulmonary disease later in life. Early quitting may therefore be particularly beneficial, to potentially avoid these effects on growing lungs.2 3.21.6 Early signs of cardiovascular disease
Cigarette smoking during adolescence and young adulthood begins the damaging processes that lead to cardiovascular disease.2 Damage to the circulatory system becomes evident in young smokers, and may become clinically significant in early adulthood.11 There is robust evidence demonstrating that smoking during adolescence and young adulthood increases the development of atherosclerosis. By early middle age, the more rapid progression of atherosclerosis and the rapid decline of lung function mentioned above lead to higher rates of coronary heart disease, stroke, and COPD. These diseases play a major role in the premature mortality of middle-aged and elderly smokers.2 While premenopausal women are typically relatively protected from heart disease compared with men and develop coronary heart disease 10 years later, smoking increases cardiovascular risk in young women and removes the protective effect of the premenopausal state; this is possibly caused by smoking disrupting the normal ovarian pattern of sympathetic nervous system activity.20
A study assessing the influence of smoking on blood biochemistry in male Taiwanese university students (mean age 19.4 years) found young smokers had significantly increased risk of several conditions associated with cardiovascular and haematological disorders, including hypertriglyceridaemia, neutrophilia and hyperchromia, compared with non-smokers.21 There is also evidence suggesting that even occasional smoking on a regular basis (<1 pack per week for at least 1 year) is associated with both acute and chronic impairment of arterial function (related to the development of atherosclerosis and future cardiovascular complications) in otherwise healthy young people (20–26 year olds).22 Similarly, a study on the effect of chronic smoking on arterial stiffness among young smokers (mean age 24.3 years) compared with non-smokers (mean age 20.2 years) found significantly higher arterial stiffness among smokers, suggesting that the negative effect of cigarette smoking on the vascular system may be apparent even in young smokers who have been smoking for fewer than 10 years.23 Arterial stiffness is an important factor in the development of a range of pathophysiological processes including atherosclerosis, left ventricular hypertrophy and aneurysm.23
Tobacco use among young men, particularly cigarette smoking, is strongly associated with thromboangiitis obliterans (Buerger's disease), a recurrent inflammatory, non-atherosclerotic vasoocclusive disease.24 Caused by vasculitis (inflammation of the blood vessels), Buerger's disease mostly affects males aged 20–40 (average age of symptom onset about 35 years) with a current or recent history of heavy smoking or chewing tobacco.25 Typically it involves progressive inflammation and thrombosis (clotting) of blood vessels of the hands and feet, and the development of ulcers and gangrene of extremities as a result of vascular ischaemia.26 Commonly necessitating amputation, major amputations (of limbs rather than fingers/toes) are almost twice as likely in patients who continue to smoke. Buerger's disease has also been documented to involve scrotal and penile necrosis resulting in partial penectomy and scrotal debridement.24 The only apparent therapeutic measure to slow or prevent disease progression is smoking cessation.27
Smoking has been identified as one of the major risk factors for hospital admission for acute coronary syndrome and more severe acute myocardial infarction (AMI) among Middle Eastern28 and Swedish29 populations, particularly among younger patients (≤40 years old,28; 25–<65 years old,29). A prospective study to evaluate the impact of smoking habits on long-term outcome in individuals who sustained AMI at the age of ≤35 years found that the most common risk factor at initial presentation was smoking.30 During follow-up (for up to 10 years) most patients (55.6%) reported continuing to smoke. One-third (32.6%) presented cardiac events during the follow-up period, including readmission for acute coronary syndrome, cardiac death or coronary revascularisation because of clinical deterioration. Continuation of smoking was the most significant predictor of cardiac events during follow-up.30
Smoking has also been found to be a determinant of isolated systolic hypertension among younger US adults (18–39 year olds); this is of concern because even small increases in systolic blood pressure in early adulthood increase risk of further cardiovascular disease (CVD) morbidity in later life.31 Studies of hypertension in young adults have found associations with structural changes in the heart including increases in left ventricular wall thickness, left ventricular mass and higher prevalence of left ventricular hypertrophy.31 Particular populations of young smokers may be at greater risk of experiencing tobacco-related adverse health effects, such as youth with chronic conditions because their health is already compromised.32 For example, people with diabetes mellitus are at increased risk of developing health problems such as CVD: a large US study among young people (10–22 years old) with diabetes mellitus found that current and past smokers were significantly more likely than non-smokers with the same condition to display cardiometabolic risk factors such as high triglyceride levels and to be physically inactive.32
Evidence suggests there is a strong dose–response relationship between cigarette smoking and ischemic stroke risk in younger women.33,34 For example, a population-based case–control study of risk factors in more than 1000 US women aged 15–49 years found that the OR for ischemic stroke risk comparing current smokers to never smokers was 2.6 (p<0.0001), after multivariable adjustment (including for age, race, education, hypertension, diabetes, body mass index, coronary heart disease, oral contraceptive use and elevated total cholesterol); the adjusted OR increased with increasing number of cigarettes smoked per day.33 No difference in stroke risk was observed between former smokers (those who had smoked more than 100 cigarettes in their lifetime, but had not smoked in the 30 days before their stroke) and never smokers.33 A prospective cohort study among more than 45 000 Swedish women aged 30–50 years (mean age 40 years) at time of enrolment found that, after an average of 11 years of follow-up, current smoking significantly increased the risk of stroke, particularly for ischemic stroke. There was a dose–response effect of current smoking on all strokes, with those smoking ≥10 cigarettes/day having a three-fold excess risk compared with never smokers. Similar risk patterns were observed using cumulative pack-years as an indicator of smoking exposure. Former smokers had a 60% increased risk for all strokes, which was of borderline statistical significance.34 The use of the oral contraceptive pill is a risk factor for stroke, and research among teenage girls (15–17 year olds) who have suffered stroke suggests its use has a negative synergistic effect with smoking, risk increasing with the number of cigarettes smoked.35
3.21.7 Dental health problems in young people
Smoking is also a major risk factor for poor periodontal health and oral cavity diseases36; about half of the periodontitis seen in those aged under 30 is thought to be linked to smoking.37 Daily smoking and infrequent tooth brushing (less than twice a day) among 14–18 year old Finnish adolescents have been found to be strongly associated.38 There is also evidence to suggest that among young males (20–25 years old), even moderate smoking of 10 cigarettes per day induces variations of salivary lipid pattern.36 The regulation of salivary lipid levels is important in the maintenance of oral cavity health: elevated lipid levels are associated with an increase of caries incidence, plaque development, calculus formation and periodontal disease.36
3.21.8 Muscular skeletal problems in young people
While considerable evidence associates tobacco use with low bone mass and increased fracture risk in older people,39,40 research has emerged more recently linking smoking at a young age with unfavourable bone geometry and density, reduction in peak bone mass and increased fracture prevalence.41,42 A cross- sectional population-based study among 677 healthy male Belgian siblings at the age of peak bone mass (aged 25–45 years, mean age 33.4–35.7 years) found that those who took up smoking at an early age (16 years old or younger) had lower areal bone mineral density (aBMD), lower cortical bone area at the tibia and lower trabecular and cortical bone density at the radius compared with current and never smokers.41 There were significant negative associations between number of pack-years smoked and lumbar spine, hip and total body aBMD, as well as total body bone mineral content. In addition, self-reported fractures were significantly more prevalent in early and current smokers, after adjustment for age, weight, education and alcohol use, and exclusion of childhood fractures.41 It has been suggested this may be caused by smoking disrupting the acquisition of peak bone mass during puberty, possibly due to an interaction with sex steroid action.41
Similarly, in a large population-based study of more than 1000 young Swedish men (mean age 18.9 years), significantly lower aBMD of the total body, lumbar spine, femoral neck, and trochanter was found among current smokers (at least one cigarette per day) compared with non-smokers.42 The magnitude of observed differences was considerable, including a mean difference of 3.3% in the spine and 5% in the trochanter after adjusting for age, height, weight, calcium intake and physical activity. Volumetric BMD (vBMD) and bone size were also measured: smokers had lower cortical thickness than non-smokers of both the radius and tibia. The authors suggest that the effects of smoking on bone mass may occur quite rapidly, because the mean duration of smoking in this study was 4.1 years.42
References
1. Doll R, Peto R, Boreham J and Sutherland I. Mortality in relation to smoking: 50 years' observations on male British doctors. British Medical Journal (Clinical Research Ed.) 2004;328(7455):1519. Available from: http://www.bmj.com/cgi/content/abstract/328/7455/1519
2. US Department of Health and Human Services. Preventing tobacco use among young people. A report of the Surgeon General, 1994. Atlanta, Georgia: Public Health Service, Centers for Disease Control and Prevention, Office on Smoking and Health, 1994. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/sgr_1994/index.htm
3. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease. A report of the US Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: http://www.surgeongeneral.gov/library/tobaccosmoke/report/index.html
4. Patton G, Coffey C, Carlin J, Sawyer S and Wakefield M. Teen smokers reach their mid twenties. Journal of Adolescents Health 2006;39:214-20. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16857533
5. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
6. Burr M, Anderson H, Austin J, Harkins L, Kaur B, Strachan D, et al. Respiratory symptoms and home environment in children: a national survey. Thorax 1999;54:27-32. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1745333/pdf/v054p00027.pdf
7. Gomez M, Vollmer WM, Caceres ME, Jossen R and Baena-Cagnani CE. Adolescent smokers are at greater risk for current asthma and rhinitis. International Journal of Tuberculosis and Lung Disease 2009;13(8):1023–8. Available from: http://www.ingentaconnect.com/content/iuatld/ijtld/2009/00000013 /00000008/art00016
8. Yoo S, Kim H, Lee S, Kim B, Kim J, Yu J, et al. Effect of active smoking on asthma symptoms, pulmonary function, and BHR in adolescents. Pediatric Pulmonology 2009;44(10):954–61. Available from: http://www3.interscience.wiley.com/user/accessdenied?ID=122588335&Act=2138&Code=4719&Page=/cgi- bin/fulltext/122588335/PDFSTART http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation& list_uids=19657196
10. Hamari A, Toljamo T, Nieminen P and Kinnula V. High frequency of chronic cough and sputum production with lowered exercise capacity in young smokers. Annals of Medicine 2010;42(7):512–20. Available from: http://informahealthcare.com/doi/full/10.3109/07853890.2010.505933 http://www.cdc.gov/tobacco/data_statistics/sgr/sgr_1994/index.htm http://www.neurology.org/cgi/content/full/75/8/712
13. Botello-Harbaum M, Haynie D, Murray K and Iannotti R. Cigarette smoking status and recurrent subjective health complaints among US school-aged adolescents. Child: Care, Health and Development 2010; [Epub ahead of print]. Available from: http://onlinelibrary.wiley.com/doi/10.1111 /j.1365-2214.2010.01147.x/full
14. Woodruff S, Conway T, Shillington A, Clapp J, Lemus H and Reed M. Cigarette smoking and subsequent hospitalization in a cohort of young U.S. Navy female recruits. Nicotine & Tobacco Research 2010;12(4):365-73. Available from: http://ntr.oxfordjournals.org/cgi/content/full/ntq007v1
15. Pavlos P, Vasilios N, Antonia A, Dimitrios K, Georgios K and Georgios A. Evaluation of young smokers and non-smokers with electrogustometry and contact endoscopy. BMC Ear, Nose and Throat Disorders 2009;9(9):1-7. Available from: http://www.biomedcentral.com/content/pdf/1472-6815-9-9.pdf
16. Mak K, Ho S, Thomas G, Lo W, Cheuk D, Lai Y, et al. Smoking and sleep disorders in Chinese adolescents. Sleep Medicine 2010;11(3):268–73. Available from: http://www.sleep-journal.com/article /PIIS1389945710000560/fulltext
17. Strand B, Mishra G, Kuh D, Guralnik J and Patel K. Smoking history and physical performance in midlife: results from the British 1946 birth cohort. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 2011;66(1):142–9. Available from: http://biomedgerontology.oxfordjournals.org/content /66A/1/142.long
18. Mendonca G, Pereira F and Fernhall B. Effects of cigarette smoking on cardiac autonomic function during dynamic exercise. Journal of Sports Sciences 2011; [Epub ahead of print]:1–8. Available from: http://www.informaworld.com/smpp/content~db=all?content=10.1080/02640414.2011.572991 http://www.cdc.gov/tobacco/data_statistics/sgr/index.htm http://www.ncbi.nlm.nih.gov/pubmed/19525371
21. Kung C-M, Wang H-L and Tseng Z-L. Cigarette smoking exacerbates health problems in young men. Clinical and Investigative Medicine 2008;31(3):E138–49. Available from: http://www.mediatropes.com /index.php/cim/article/view/3471/0
22. Stoner L, Sabatier M, Black C and McCully K. Occasional cigarette smoking chronically affects arterial function. Ultrasound in Medicine and Biology 2008;34(12):1885–92. Available from: http://www.umbjournal.org/article/PIIS0301562908002457/fulltext
23. Binder S, Navratil K and Halek J. Chronic smoking and its effect on arterial stiffness. Biomedical Papers of the Medical Faculty of the University Palack√Ω, Olomouc, Czechoslovakia 2008;152(2):299–302. Available from: http://publib.upol.cz/~obd/fulltext/Biomed/2008/2/299.pdf
24. Aktoz T, Kaplan M, Yalcin O, Atakan I and Inci O. Penile and scrotal involvement in Buerger's disease. Andrologia 2008;40(6):401–3. Available from: http://www3.interscience.wiley.com /user/accessdenied?ID=121537834&Act=2138&Code=4719&Page=/cgi-bin/fulltext/121537834/HTMLSTART
25. Olin J. Other peripheral arterial diseases. In Goldman, L and Ausiello, D, eds. Cecil Medicine. Philadelphia: Saunders Elsevier, 2007.
26. Hoeft D, Kroger K, Grabbe S and Dissemond J. Thromboangiitis obliterans: an overview. Journal der Deutschen Dermatologischen Gesellschaft 2004;2(10):827-32. Available from: http://www.ncbi.nlm.nih.gov /pubmed/16281585
27. Paraskevas K, Liapis C, Briana D and Mikhailidis D. Thromboangiitis obliterans (Buerger's disease): searching for a therapeutic strategy. Angiology 2007;58(1):75–84. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17351161
28. Alanbaei M, Zubaid M, Al-Mallah M, Rashed W, Shehab A, Al-Lawati J, et al. Impact of diabetes and smoking epidemic in the Middle East on the presentation with acute coronary syndrome in very young patients. Angiology 2011; [Epub ahead of print]. Available from: http://ang.sagepub.com/content/early /2011/04/25/0003319711406255.long
29. Björck L, Rosengren A, Wallentin L and Stenestrand U. Smoking in relation to ST-segment elevation acute myocardial infarction: findings from the Register of Information and Knowledge about Swedish Heart Intensive Care Admissions. Heart 2009;95(12):1006–11. Available from: http://heart.bmj.com/cgi/content /full/95/12/1006
30. Rallidis L, Lekakis J, Panagiotakos D, Fountoulaki K, Komporozos C, Apostolou T, et al. Long-term prognostic factors of young patients (
31. Grebla RC, Rodriguez CJ, Borrell LN and Pickering TG. Prevalence and determinants of isolated systolic hypertension among young adults: the 1999-2004 US National Health and Nutrition Examination Survey. Journal of Hypertension 2010;28(1):15-23. Available from: http://journals.lww.com/jhypertension/Abstract /publishahead/Prevalence_and_determinants_of_isolated_systolic.99789.aspx
32. Reynolds K, Liese A, Anderson A, Dabelea D, Standiford D, Daniels S, et al. Prevalence of tobacco use and association between cardiometabolic risk factors and cigarette smoking in youth with type 1 or type 2 diabetes mellitus. The Journal of Pediatrics 2011;158(4):594–601. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21129757
33. Bhat V, Cole J, Sorkin J, Wozniak M, Malarcher A, Giles W, et al. Dose-response relationship between cigarette smoking and risk of ischemic stroke in young women. Stroke 2008;39(9):2439–43. Available from: http://stroke.ahajournals.org/cgi/content/full/39/9/2439
34. Lu M, Ye W, Adami H and Weiderpass E. Stroke incidence in women under 60 years of age related to alcohol intake and smoking habit. Cerebrovascular Diseases (Basel, Switzerland) 2008;25(6):517–25. Available from: http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowFulltext& ArtikelNr=000131669&Ausgabe=237384&ProduktNr=224153
35. Christerson S and Stromberg B. Childhood stroke in Sweden I: incidence, symptoms, risk factors and short-term outcome. Acta Paediatrica 2010;99(11):1641–9. Available from: http://onlinelibrary.wiley.com /doi/10.1111/j.1651-2227.2010.01925.x/full
36. Palmerini C, Saccardi C, Ferracci F and Arienti S. Lipid patterns in the saliva of smoking young adults. Human & Experimental Toxicology 2011; [Epub ahead of print]. Available from: http://het.sagepub.com /content/early/2011/02/04/0960327111398672.long
37. Page R and Beck J. Risk assessment for periodontal diseases. International Dental Journal 1997;47(2):61-87. Available from: http://www.ncbi.nlm.nih.gov/pubmed/9448791
38. Honkala S, Honkala E, Newton T and Rimpela A. Toothbrushing and smoking among adolescents- aggregation of health damaging behaviours. Journal of Clinical Periodontology 2011;38(5):442–8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21480940
39. Kanis J, Johnell O, Oden A, Johansson H, De Laet C, Eisman J, et al. Smoking and fracture risk: a meta-analysis. Osteoporosis International 2005;16(2):155-62. Available from: http://www.ncbi.nlm.nih.gov /pubmed/15175845
40. Law M and Hackshaw A. A meta-analysis of cigarette smoking, bone mineral density and risk of hip fracture: recognition of a major effect. British Medical Journal 1997;315(7112):841-6. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2127590/pdf/9353503.pdf 41. Taes Y, Lapauw B, Vanbillemont G, Bogaert V, De Bacquer D, Goemaere S, et al. Early smoking is associated with peak bone mass and prevalent fractures in young healthy men. Journal of Bone and Mineral Research 2010;25(2):379–87. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19653814
42. Lorentzon M, Mellström D, Haug E and Ohlsson C. Smoking is associated with lower bone mineral density and reduced cortical thickness in young men. Journal of Clinical Endocrinology and Metabolism 2007;92(2):497-503. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17077132
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.22 Poorer quality of life and loss of function
3.22 Poorer quality of life and loss of function
Last updated: April 2015 Suggested citation: Bellew, B, Greenhalgh, EM & Winstanley, MH. 3.22 Poorer quality of life and loss of function. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-17-poorer-levels- of-general-health
This section is about impacts on health-related quality of life (HRQOL), activities of daily living (ADL) and general health caused by smoking. The discussion here goes beyond the burden of morbidity and mortality from specific diseases that are comprehensively described in other sections. The evidence presented here confirms that exposure to tobacco smoke should be considered an important contributing factor to wide-ranging non-specific morbidity and a diminished quality of life.
3.22.1 Poorer health-related quality of life
The concept of health-related quality of life (HRQOL) and its determinants have evolved since the 1980s to encompass those aspects of overall quality of life that can be clearly shown to affect health–either physical or mental. Several instruments have been used to assess HRQOL and related concepts of functional status. Among them are the Medical Outcomes Study Short Forms (SF-12 and SF-36), the Sickness Impact Profile, and the Quality of Well-Being Scale.1 The SF-36 is the measure most commonly used in the HRQOL studies cited in this chapter.
There is compelling evidence linking active smokingi and poor HRQOL; this has been demonstrated in large longitudinal studies conducted in North America,3,4 Spain5 and Finland6; in cross-sectional studies conducted in Croatia,7 Finland8 and North America9; in a large study of Medicare beneficiaries in North America10 and in a British study conducted among female patients with atherosclerosis.11
3.22.2 Impaired activities of daily living (ADL) and instrumental ADL
'Activities of daily living' (ADL) are those skills needed in typical daily self-care, while 'Instrumental activities of daily living' (IADL) refer to skills beyond basic self-care that evaluate how individuals function within their homes, workplaces and social environments. IADL may include typical domestic tasks such as driving, cleaning, cooking and shopping, as well as other less physically demanding tasks such as operating electronic appliances and handling budgets.12 Researchers use various tools to measure these capacities, such as the Katz or Barthel scales for ADL13 and the Lawton IADL scale.14
A longitudinal study conducted in Japan examined the relationship between smoking in middle age and long-term risk of impaired activities of daily living (ADL) in more than 2000 men and women. The researchers reported more than double the risk of impaired ADL among current smokers compared with non-smokers (OR 2.11; 95% CI, 1.09–4.06). Risk of impaired ADL was higher as the number of cigarettes increased. The study concluded that smoking in middle age increases future risks of impaired ADL and that smoking cessation may be important to prevent future impairment of ADL.15 Another, similar longitudinal study was conducted in North America involving more than 10 000 middle-aged people; the study found that smoking was significantly associated with deterioration in ADL status.16 Impairment in instrumental activities of daily living (IADL) was associated with smoking in a Japanese longitudinal study involving more than 1200 elderly people 17 and a North American cross-sectional study involving more than 9500 subjects.18 There is also evidence that women with COPD are more than twice as likely to have impaired ADL (OR 2.63; 95% CI, 1.15–5.99), and more than four times as likely to have impaired IADL (OR 4.23; 95% CI, 1.92–9.29).19
3.22.3 Smoking, low bone density and hip fracture
A causal relationship exists between smoking, low bone density and hip fractures.20 The causal relationship with low bone density was previously established for older women only; however there is now systematic review evidence that smoking is a risk factor for low bone mineral density/bone loss among men over 50 years of age as well.21 These findings linking smoking to the risk of low bone density and hip fracture are important; it is well established that there is a pronounced and long-term reduction in HRQOL as a result of hip fracture22, 23 and independence in many of the normal activities of daily living is compromised.24 (See Chapter 3, Section 3.13 for more detailed discussion of musculoskeletal disease.)
3.22.4 Diminished general health, accelerated ageing, disturbed sleep
There is established scientific evidence of a causal relationship between smoking and diminished health status, and this evidence is consistent across studies and indicators. Smokers of different ages, genders, and locations experience poorer physical and mental health compared with people who have never smoked. Manifestations of this diminished overall health include smokers’ increased absenteeism at work, self-reported poorer health, and higher health care costs and utilisation, and these relationships remain after controlling for a broad range of potential confounders25 This more general decrement in health may be the result of altered inflammatory/immune processes, oxidative stress and sub-clinical organ injury. However, there are many direct and indirect mechanisms that link smoking to poorer health.20
Smoking modifies leukocyte telomere length (TL – or DNA sequencing), which is thought to accelerate biological ageing as well as development of smoking-induced chronic diseases.26 A range of recent studies support the contention that smoking is associated with accelerated biological ageing.27-31 There is evidence that tobacco smoking is a contributing factor in a wide range of skin diseases,32, 33 and that it is a cause of premature skin ageing34, 35 with estimates of almost four times the amount of facial wrinkling in 'heavy' smokers (>40 packs per year) compared with non-smokers.36 (This issue is discussed in more detail in Chapter 3, Section 3.14.1.)
A large cross-sectional study conducted in North America found that tobacco use and exposure to secondhand smoke were associated with increased odds of earlier age at menopause.37
Cigarette smoking is associated with sleep disorders in the general population; smokers are also more likely to experience sleep disturbances, including taking longer to fall asleep, being less likely to stay asleep, and having less total sleep time than non-smokers.38-40 There is also emerging evidence of an association with obstructive sleep apnoea.41 Recent evidence from a very large cross-sectional study conducted in North America indicates an association between smokeless tobacco use, secondhand smoke exposure and insufficient rest/sleep. Current users of smokeless tobacco were more than 70% (OR 1.74; 95% CI, 1.37–2.22) more likely to report insufficient rest/sleep compared to never smokeless tobacco users. For those who were both current smokers and current smokeless tobacco users there was more than a doubling of this risk (OR 2.21; 95% CI, 1.66–2.94). Those with secondhand smoke exposure had an estimated 29% increased risk for insufficient rest/sleep than those without (OR 1.29; 95% CI, 1.02–1.63).42 3.22.5 Other impairments
In the elderly, smoking is associated with accelerated declines in physical function, and increased levels of clinical illness and physical and cognitive impairment.20, 43 (See Chapter 3, Section 3.23).
Recent research into the association between back pain and other types of chronic pain and smoking has indicated the possibility of a causal link; this finding is supported by recent prospective studies.44 Smokers are also more likely to report pain during health examinations.45
Other studies show that smoking is associated with hearing impairment,46-51 (also see Chapter 3, Section 3.25) and poorer sense of taste52-55 and smell.56, 57 Smoking increases the risk of both cataract and age-related macular degeneration (AMD), responsible for a large burden of vision impairment and blindness (also see Chapter 3, Section 3.10), which impose substantial costs on the Australian community.58
Many other impacts associated with exposure to tobacco smoke have clear implications for HRQOL even if specific confirmatory research to quantify the impairment with precision may not yet be available. For example, dental diseases59 are described in Chapter 3, Section 3.11, Gastro-intestinal diseases in Section 3.12, and the impact of smoking on treatment of disease60, 61 in Section 3.15.
3.22.6 Smoking and absence from work due to illness
Smoking is associated with the amount and duration of sick leave and degree of productivity loss at work.62-64 Smokers are more likely to miss work due to ill-health, have longer duration of absence from work, and access all levels of medical care more frequently.65, 20 Level of consumption also plays a role, with heavier smokers having more absences than lighter smokers.25 Work absences are reportedly higher in smokers resulting from a broad range of symptoms, including problems with the digestive tract, neck, back and upper limbs.65 These effects are evident in younger smokers, before the effects of major tobacco-caused disease become apparent during middle age and later years.20 There is also evidence that smokers are more likely to suffer injury in the workplace than non-smokers.20
Australian data show that men who smoke are 66% more likely to be absent from work than male never smokers, and that female smokers are 23% more likely to miss work than female never smokers.66 This in turn has a major quantifiable economic impact on the nation's productivity.67 (Also see Chapter 17, Section 17.2.2.2.) i A recent cross-sectional study of 2500 never smokers in Switzerland found that exposure to secondhand smoke was also associated with reduced HRQOL, more significantly so in women. Exposure to secondhand smoke at home and high levels of exposure were associated with lower SF-36 scores, suggesting a dose–response relationship.
References
1. US Centers for Disease Control and Prevention. Health-Related Quality of Life (HRQOL). Atlanta, Georgia: USA Government, 2011 [viewed 31 May 2011] . Available from: http://www.cdc.gov/hrqol /concept.htm#5
2. Bridevaux PO, Cornuz J, Gaspoz JM, Burnand B, Ackermann-Liebrich U, Schindler C, et al. Secondhand smoke and health-related quality of life in never smokers: results from the SAPALDIA cohort study 2. Archives of Internal Medicine 2007;167(22):2516-23. Available from: http://www.ncbi.nlm.nih.gov/pubmed /18071176
3. McClave A, Dube S, Strine T and Mokdad A. Associations between health-related quality of life and smoking status among a large sample of US adults. Preventive Medicine 2009;48(2):173–9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19103219
4. Sarna L, Bialous SA, Cooley ME, Jun H-J and Feskanich D. Impact of smoking and smoking cessation on health-related quality of life in women in the Nurses' Health Study. Quality of Life Research 2008;17(10 ):1217–27. Available from: www.ncbi.nlm.nih.gov/pubmed/18931942
5. Guiterrez-Bedmar M, Segui-Gomez M, Gomez-Gracia E, Bes-Rastrollo M and Martinez-Gonzalez MA. Smoking status, changes in smoking status and health-related quality of life: findings from the SUN ("Seguimiento Universidad de Navarra") cohort. International Journal of Environmental Research and Public Health 2009;6(1):310-20. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19440285
6. Strandberg A, Strandberg T, Pitkälä K, Salomaa V, Tilvis R and Miettinen T. The effect of smoking in midlife on health-related quality of life in old age: a 26-year prospective study Archives of Internal Medicine 2008;168(18):1968–74. Available from: http://archinte.ama-assn.org/cgi/content/full/168/18/1968
7. Samardzic S and Marvinac GV. Health related quality of life of smokers in Croatia. Collegium Antropologicum 2009;33(suppl. 1):i107-14. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19563155
8. Heikkinen H, Jallinoja P, Saarni SI and Patja K. The impact of smoking on health-related and overall quality of life: a general population survey in Finland. Nicotine & Tobacco Research 2008;10(7):1199–207. Available from: http://www.informaworld.com/smpp/content~content=a794991807~db=all~order=page
9. Strine TW, Okoro CA, Chapman DP, Balluz LS, Ford ES, Ajani UA, et al. Health-related quality of life and health risk behaviors among smokers. American Journal of Preventive Medicine 2005;28(2):182-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15710274
10. Hays RD, Smith AW, Reeve BB, Spritzer KL, Marcus SE and Clauser SB. Cigarette smoking and health- related quality of life in Medicare beneficiaries. Health Care Financing Review 2008;29(4):57-67. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18773614
11. Barta Z, Harrison MJ, Wangrangsimakul T, Shelmerdine J, Teh LS, Pattrick M, et al. Health-related quality of life, smoking and carotid atherosclerosis in white British women with systemic lupus erythematosus. Lupus 2010;19(3):231-8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20007814
12. Encyclopedia of Nursing & Allied Health. Activities of Daily Living Evaluation: eNotes. Encyclopedia of Nursing & Allied Health. 2006 [viewed 31 May 2011] . Available from: http://www.enotes.com/nursing- encyclopedia/activities-daily-living-evaluation
13. Hartigan I. A comparative review of the Katz ADL and the Barthel Index in assessing the activities of daily living of older people. International Journal of Older People Nursing 2007;2(3):204-12. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20925877
14. Graf C. The Lawton Instrumental Activities of Daily Living (IADL) Scale. Medsurg Nursing 2009;18(5):315-6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19927971
15. Takashima N, Miura K, Hozawa A, Okamura T, Hayakawa T, Okuda N, et al. Cigarette smoking in middle age and a long-term risk of impaired activities of daily living: NIPPON DATA80. Nicotine & Tobacco Research 2010;12(9):944–9. Available from: http://ntr.oxfordjournals.org/content/12/9/944.long
16. Jung SH, Ostbye T and Park KO. A longitudinal study of the relationship between health behavior risk factors and dependence in activities of daily living. Journal of Preventive Medicine and Public Health 2006;39(3):221-8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16764496
17. Hayakawa T, Okamura T, Okayama A, Kanda H, Watanabe M, Kita Y, et al. Relationship between 5-year decline in instrumental activity of daily living and accumulation of cardiovascular risk factors: NIPPON DATA90. Journal of Atherosclerosis and Thrombosis 2010;17(1):64-72. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20081323
18. Hardy SE, McGurl DJ, Studenski SA and Degenholtz HB. Biopsychosocial characteristics of community- dwelling older adults with limited ability to walk one-quarter of a mile. Journal of the American Geriatrics Society 2010;58(3):539-44. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20210817
19. Kanervisto M, Saarelainen S, Vasankari T, Jousilahti P, Heistaro S, Heliovaara M, et al. COPD, chronic bronchitis and capacity for day-to-day activities: negative impact of illness on the health-related quality of life. Chronic Respiratory Disease 2010;7(4):207-15. Available from: http://www.ncbi.nlm.nih.gov/pubmed /21084545
20. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
21. Papaioannou A, Kennedy CC, Cranney A, Hawker G, Brown JP, Kaiser SM, et al. Risk factors for low BMD in healthy men age 50 years or older: a systematic review. Osteoporosis International 2009;20(4):507-18. Available from: http://www.springerlink.com/content/73h490888m320p77/fulltext.pdf
22. Hallberg I, Bachrach-Lindstrom M, Hammerby S, Toss G and Ek AC. Health-related quality of life after vertebral or hip fracture: a seven-year follow-up study. BMC musculoskeletal disorders 2009;10:135. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19886998
23. Salaffi F, Cimmino MA, Malavolta N, Carotti M, Di Matteo L, Scendoni P, et al. The burden of prevalent fractures on health-related quality of life in postmenopausal women with osteoporosis: the IMOF study. Journal of Rheumatology 2007;34(7):1551-60. Available from: http://www.ncbi.nlm.nih.gov/pubmed /17516618
24. Alarcon T, Gonzalez-Montalvo JI, Gotor P, Madero R and Otero A. Activities of daily living after hip fracture: profile and rate of recovery during 2 years of follow-up. Osteoporosis International 2011;22(5):1609-13. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20521027
26. Babizhayev MA and Yegorov YE. Smoking and health: association between telomere length and factors impacting on human disease, quality of life and life span in a large population-based cohort under the effect of smoking duration. Fundamental & Clinical Pharmacology 2010;25(4):425-42. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20698892
27. Syndrome of accelerated aging induced by carcinogenic environmental factors. Rossiĭskii fiziologicheskiĭ zhurnal imeni I.M. Sechenova 2010;96(8):817-33. Available from: http://www.ncbi.nlm.nih.gov/pubmed /20968066
28. Nyunoya T, Monick MM, Klingelhutz AL, Glaser H, Cagley JR, Brown CO, et al. Cigarette smoke induces cellular senescence via Werner's syndrome protein down-regulation. American Journal of Respiratory and Critical Care Medicine 2009;179(4):279-87. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19011155
29. Csiszar A, Podlutsky A, Wolin MS, Losonczy G, Pacher P and Ungvari Z. Oxidative stress and accelerated vascular aging: implications for cigarette smoking. Frontiers in Bioscience 2009;14:3128-44. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19273262
30. Nicita Mauro V, Basile G, Maltese G, Nicita Mauro C, Gangemi S and Caruso C. Smoking, health and aging. Immunity and Ageing 2008;5(1):10. Available from: http://www.immunityageing.com/content /pdf/1742-4933-5-10.pdf
31. Bernhard D, Moser C, Backovic A and Wick G. Cigarette smoke-an aging accelerator? Experimental Gerontology 2007;42(3):160-5. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17084574
32. Thomsen SF and Sorensen LT. Smoking and skin disease. Skin therapy letter 2010;15(6):4-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20532469
33. Metelitsa AI and Lauzon GJ. Tobacco and the skin. Clinics in Dermatology 2010;28(4):384-90. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20620754
34. Morita A, Torii K, Maeda A and Yamaguchi Y. Molecular basis of tobacco smoke-induced premature skin aging. Journal of Investigative Dermatology 2009;14(1):53-5. Available from: http://www.ncbi.nlm.nih.gov /pubmed/19675554
35. Morita A. Tobacco smoke causes premature skin aging. Journal of Dermatological Science 2007;48(3):169-75. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17951030
36. Raduan AP, Luiz RR and Manela-Azulay M. Association between smoking and cutaneous ageing in a Brazilian population. Journal of the European Academy of Dermatology and Venereology 2008;22(11):1312-8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18624854
37. Fleming LE, Levis S, LeBlanc WG, Dietz NA, Arheart KL, Wilkinson JD, et al. Earlier age at menopause, work, and tobacco smoke exposure. Menopause 2008;15(6):1103-8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18626414
38. Conway S, Roizenblatt S, Palombini L, Castro L, Bittencourt L, Silva R, et al. Effect of smoking habits on sleep. Brazilian Journal of Medical and Biological Research 2008;41(8):722–7. Available from: http://www.scielo.br/pdf/bjmbr/v41n8/7109.pdf
39. Zhang L, Samet J, Caffo B and Punjabi N. Cigarette smoking and nocturnal sleep architecture. American Journal of Epidemiology 2006;164:529-37. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16829553
40. Phillips B and Danner F. Cigarette smoking and sleep disturbance. Archives of Internal Medicine 1995;155:734-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/7695462
41. Aksu K, Firat GS, Aksu F, Ciftci B, Ulukavak CT, Aksaray S, et al. Obstructive sleep apnoea, cigarette smoking and plasma orexin-a in a sleep clinic cohort. The Journal of International Medical Research 2009;37(2):331–40. Available from: http://www.jimronline.net/content/full/2009/90/1132.pdf
42. Sabanayagam C and Shankar A. The association between active smoking, smokeless tobacco, second-hand smoke exposure and insufficient sleep. Sleep Medicine 2011;12(1):7–11. Available from: http://www.sleep-journal.com/article/S1389-9457%2810%2900361-8/pdf
43. Plassman BL, Williams JW, Jr., Burke JR, Holsinger T and Benjamin S. Systematic review: factors associated with risk for and possible prevention of cognitive decline in later life. Annals of Internal Medicine 2010;153(3):182-93. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20547887
44. Pisinger C, Aadahl M, Toft U, Birke H, Zytphen-Adeler J and Jorgensen T. The association between active and passive smoking and frequent pain in a general population. European Journal of Pain 2011;15(1):77–83. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20627783
45. John U, Hanke M, Meyer C, Volzke H, Baumeister S and Alte D. Tobacco smoking in relation to pain in a national general population survey. Preventive Medicine 2006;43:477-81. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16949655
46. Mohammadi S, Mazhari MM, Mehrparvar AH and Attarchi MS. Effect of simultaneous exposure to occupational noise and cigarette smoke on binaural hearing impairment. Noise Health 2010;12(48):187-90. Available from: http://www.noiseandhealth.org/article.asp?issn=1463-1741;year=2010;volume=12;issue=48; spage=187;epage=190;aulast=Mohammadi
47. Gopinath B, Flood V, McMahon C, Burlutsky G, Smith W and Mitchell P. The effects of smoking and alcohol consumption on age-related hearing loss: the Blue Mountains Hearing study. Ear and Hearing 2010;31(2):277–82. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20054277
48. de Oliveira D and de Lima M. Low and high frequency tonal threshold audiometry: comparing hearing thresholds between smokers and non-smokers. Brazilian Journal of Otorhinolaryngology 2009;75(5):738–44. Available from: http://www.ncbi.nlm.nih.pubmed/19893945
49. Fransen E, Topsakal V, Hendrickx J, Van Laer L, Huyghe J, Van Eyken E, et al. Occupational noise, smoking, and a high body mass index are risk factors for age-related hearing impairment and moderate alcohol consumption is protective: a European population-based multicenter study. Journal of the Association for Research in Otolaryngology 2008;9(3):264–76. Available from: http://www.springerlink.com/content /571104t223m0174h/fulltext.pdf
50. Pouryaghoub G, Mehrdad R and Mohammadi S. Interaction of smoking and occupational noise exposure on hearing loss: a cross-sectional study. BMC Public Health 2007;7:137. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1925081/?tool=pubmed
51. Nakanishi N, Okamoto M, Nakamura K, Suzuki K and Tatara K. Cigarette smoking and risk for hearing impairment. A longitudinal study in Japanese male office workers. Journal of Occupational and Environmental Medicine 2000;42(11):1045–9. Available from: http://www.joem.org/pt/re /joem/abstract.00043764-200011000-00001.htm;jsessionid=L1KKx1gy812jQQQnR2QVy7VYq1S8rjvkYTzXcNqLjtfCJHG2pnQy!353761
52. Said Yekta S, Luckhoff A, Ristic D, Lampert F and Ellrich J. Impaired somatosensation in tongue mucosa of smokers. Clinical Oral Investigations 2010;Epub ahead of print Available from: http://www.springerlink.com /content/10646v0t17628372/
53. Konstantinidis I, Chatziavramidis A, Printza A, Metaxas S and Constantinidis J. Effects of smoking on taste: assessment with contact endoscopy and taste strips. Laryngoscope 2010;120(10):1958–63. Available from: http://onlinelibrary.wiley.com/doi/10.1002/lary.21098/full
54. Pavlidis P, Nikolaidis V, Anogeianaki A, Koutsonikolas D, Kekes G and Anogiannakis G. Evaluation of young smokers and non-smokers with electrogustometry and contact endoscopy. BMC Ear, Nose, and Throat Disorders 2009;9(1):9. Available from: http://www.biomedcentral.com/content/pdf/1472-6815-9-9.pdf
55. Parker L and Docet K. The effects of nicotine and nicotine withdrawal on taste reactivity. Pharmacology, Biochemistry, and Behavior 1995;52(1):125–9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/7501654
56. Vennemann M, Hummel T and Berger K. The association between smoking and smell and taste impairment in the general population. Journal of Neurology 2008;255(8):1121–6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18677645
57. Frye R, Schwartz B and Doty R. Dose-related effects of cigarette smoking on olfactory function. Journal of the American Medical Association 1990;263(9):1233–6. Available from: http://jama.ama-assn.org /cgi/content/abstract/263/9/1233
58. Access Economics. Clear insight. The economic impact and cost of vision loss in Australia in 2009. Melbourne: Eye Research Australia, 2010. Available from: http://www.vision2020australia.org.au/assets /content/3650/v2020aus_report_clear_focus_overview_jun10.pdf
59. Zhou X, Wang Z, Song Y, Zhang J and Wang C. Periodontal health and quality of life in patients with chronic obstructive pulmonary disease. Respiratory Medicine 2011;105(1):67-73. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20630736
60. Balduyck B, Sardari Nia P, Cogen A, Dockx Y, Lauwers P, Hendriks J, et al. The effect of smoking cessation on quality of life after lung cancer surgery. European Journal of Cardio-thoracic Surgery 2011;Epub ahead of publication Available from: http://www.ncbi.nlm.nih.gov/pubmed/21498082
61. Sanden B, Forsth P and Michaelsson K. Smokers show less improvement than nonsmokers two years after surgery for lumbar spinal stenosis: a study of 4555 patients from the Swedish spine register. Spine 2011;36(13):1059-64. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21224770
62. Robroek SJ, van den Berg TI, Plat JF and Burdorf A. The role of obesity and lifestyle behaviours in a productive workforce. Occupational and environmental medicine 2011;68(2):134-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20876556 63. Alavinia SM, van den Berg TI, van Duivenbooden C, Elders LA and Burdorf A. Impact of work-related factors, lifestyle, and work ability on sickness absence among Dutch construction workers. Scandinavian Journal of Work and Environmental Health 2009;35(5):325-33. Available from: http://www.ncbi.nlm.nih.gov /pubmed/19554244
64. Lundborg P. Does smoking increase sick leave? Evidence using register data on Swedish workers. Tobacco Control 2007;16(2):114-8. Available from: http://tobaccocontrol.bmj.com/content/16/2/114.abstract
65. Skillgate E, Vingard E, Josephson M, Holm LW and Alfredsson L. Is smoking and alcohol consumption associated with long-term sick leave due to unspecific back or neck pain among employees in the public sector? Results of a three-year follow-up cohort study. Journal of Rehabilitation Medicine 2009;41(7):550-6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19543666
66. Bush R and Wooden M. Smoking and absence from work: Australian evidence. Social Science & Medicine 1995;41:437-46. Available from: http://www.ncbi.nlm.nih.gov/pubmed/7481938
67. Collins D and Lapsley H. The costs of tobacco, alcohol and illicit drug abuse to Australian society in 2004-05. P3 2625. Canberra: Department of Health and Ageing, 2008. Available from: http://www.nationaldrugstrategy.gov.au/internet/drugstrategy/publishing.nsf/Content/mono64/$File /mono64.pdf
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.23 Smoking, dementia and cognitive decline
3.23 Smoking, dementia and cognitive decline
Last updated: April 2015 Suggested citation: Letcher, T, Greenhalgh, EM & Winstanley, MH. 3.23 Smoking, dementia and cognitive decline. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-23- smoking-dementia-and-cognitive-decline
Several systematic reviews have concluded that there is a likely association between current smoking and an increased risk of incident dementia, especially Alzheimer's disease, and that smoking may be a risk factor for cognitive decline.1,2,3
A review of comparable research published up to June 2005 concluded that older smokers may have a greater risk of developing dementia (including Alzheimer's disease and vascular dementia) and cognitive decline than non-smokers.1 This meta-analysis focused on those over the age of 65 years, and included only longitudinal studies. It showed that current smokers had a 40–80% increased likelihood of experiencing dementia and cognitive decline compared with never smokers. The authors of this review observed that individual lifestyle and physiological factors may also influence the association between smoking, dementia and cognitive decline, and that further research is needed.1
A similar systematic review based on longitudinal studies published between 1995 and 2007 examined the relationship between smoking, dementia and cognitive decline in an elderly population (aged 65 years and over).2 Meta-analyses found current smokers compared with never or non-smokers had a significantly increased risk of Alzheimer's disease and a higher but not significantly increased risk of cognitive decline, vascular and unspecified dementia.2 Contrary to the findings of a number of early studies suggesting that smoking may be protective against Alzheimer's disease,4-9 a systematic review of all research published up to 2007 concluded that current or ever smoking is in fact a significant risk factor for Alzheimer's disease.3 The review controlled for study design, quality, secular trend and tobacco industry affiliation of study authors. One-quarter of the 43 studies reviewed had tobacco-affiliated authors. Based on average quality cohort studies with no tobacco industry affiliation published in 2007, the average risk of Alzheimer's disease associated with smoking was estimated to be 1.72 +/– 0.19 (p<0.0005).3
A review of the peer-reviewed literature on the neurocognitive and neurobiological implications of chronic smoking (not defined specifically) concluded there is increasing evidence that chronic cigarette smoking is associated with demonstrable abnormalities in brain neurobiology and neurocognition across the lifespan, and is related to abnormal rates of loss of brain volume in the elderly.10 Focusing on smoking among cohorts and population-based samples not seeking treatment for substance use or psychiatric disorders, the authors found a likely association between chronic smoking and diminished executive functions, cognitive flexibility, general intellectual abilities, learning and/or memory processing speed, and working memory.10
Several prospective cohort studies not included in the above reviews have also examined the effect of smoking in middle age on cognitive decline and dementia.11,12,13 This is partly to address the selection bias caused by differential mortality among smokers when examining the effects of smoking among the elderly:13 middle-aged smokers are more likely to be lost to follow-up by death or through non-participation in cognitive tests.14 These studies provide further evidence of associations between smoking and dementia,11,12 Alzheimer's disease,12 vascular dementia, loss of cognitive flexibility and global cognitive function.13
Most recently, Alzheimer’s Disease International conducted a large-scale review of the association between lifestyles and dementia risk, and reported robust evidence for a relationship between current smoking (vs. never smoking) and the incidence of Alzheimer’s disease. Evidence also suggested (though the relationship was non-statistically significant) a similar association with vascular dementia, and a smaller association with any dementia. Conversely, ex-smokers were at a similar risk to those who have never smoked for all types of incident dementia. These findings are important for prevention and cessation efforts, as the increased risk of dementia might be avoided by quitting smoking.15
References
1. Anstey K, von Sanden C, Salim A and O'Kearney R. Smoking as a risk factor for dementia and cognitive decline: a meta-analysis of prospective studies. American Journal of Epidemiology 2007;166(4):367–78. Available from: http://aje.oxfordjournals.org/cgi/reprint/166/4/367
2. Peters R, Poulter R, Warner J, Beckett N, Burch L and Bulpitt C. Smoking, dementia and cognitive decline in the elderly, a systematic review. BMC Geriatrics 2008;8(1):36. Available from: http://www.biomedcentral.com/content/pdf/1471-2318-8-36.pdf
3. Cataldo J, Prochaska J and Glantz S. Cigarette smoking is a risk factor for Alzheimer's disease: an analysis controlling for tobacco industry affiliation. Journal of Alzheimer's Disease 2010;19(2):465–80. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20110594
4. Fratiglioni L and Wang H. Smoking and Parkinson's and Alzheimer's disease: review of the epidemiological studies. Behavioral Brain Research 2000;113(1-2):117-20. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10942038
5. Graves A, van Duijn C, Chandra V, Fratiglioni L, Heyman A, Jorm A, et al. Alcohol and tobacco consumption as risk factors for Alzheimer's disease: a collaborative re-analysis of case-control studies. EURODEM Risk Factors Research Group. International Journal of Epidemiology 1991;20(suppl. 2):S48-S57. Available from: http://www.ncbi.nlm.nih.gov/pubmed/1833354
6. Lee P. Smoking and Alzheimer's disease: a review of the epidemiological evidence. Neuroepidemiology 1994;13(4):133-44. Available from: http://www.ncbi.nlm.nih.gov/pubmed/8090255
7. Smith C and Giacobini E. Nicotine, Parkinson's and Alzheimer's disease. Reviews in the Neurosciences 1991;3(1):25-43. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21561277
8. van Duijn C, Clayton D, Chandra V, Fratiglioni L, Graves A, Heyman A, et al. Interaction between genetic and environmental risk factors for Alzheimer's disease: a reanalysis of case-control studies. EURODEM Risk Factors Research Group. Genetic Epidemiology 1994;11(6):539-51. Available from: http://www.ncbi.nlm.nih.gov/pubmed/7713394
9. Chen G, Payne T, Lou X, Ma J, Zhu J and Li M. Association of amyloid precursor protein-binding protein, family B, member 1 with nicotine dependence in African and European American smokers. Human Genetics 2008;124(4):393-8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18777128
10. Durazzo TC, Meyerhoff DJ and Nixon SJ. Chronic cigarette smoking: implications for neurocognition and brain neurobiology. International Journal of Environmental Research and Public Health 2010;7(10):3760–91. Available from: http://www.mdpi.com/1660-4601/7/10/3760/pdf
11. Alonso A, Mosley T Jr, Gottesman R, Catellier D, Sharrett A and Coresh J. Risk of dementia hospitalisation associated with cardiovascular risk factors in midlife and older age: the Atherosclerosis Risk in Communities (ARIC) study. Journal of Neurology, Neurosurgery & Psychiatry 2009;80(11):1194-201. Available from: http://jnnp.bmj.com/content/80/11.toc
12. Rusanen M, Kivipelto M, Quesenberry C, Jr, Zhou J and Whitmer R. Heavy smoking in midlife and long-term risk of Alzheimer disease and vascular dementia. Archives of Internal Medicine 2011;171(4):333–9. Available from: http://archinte.ama-assn.org/cgi/content/full/171/4/333
13. Nooyens AC, van Gelder BM and Verschuren WM. Smoking and cognitive decline among middle-aged men and women: the Doetinchem cohort study American Journal of Public Health 2008;98(12):2244-50. Available from: http://www.ajph.org/cgi/reprint/AJPH.2007.130294v1
14. Sabia S, Marmot M, Dufouil C and Singh-Manoux A. Smoking history and cognitive function in middle age from the Whitehall II Study Archives of Internal Medicine 2008;168(11):1165–73. Available from: http://archinte.ama-assn.org/cgi/content/full/168/11/1165
15. Alzheimer's Disease International. World Alzheimer Report 2014. London, UK 2014. Available from: http://www.alz.co.uk/research/WorldAlzheimerReport2014.pdf
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.24 Genetic influences on tobacco-caused disease
3.24 Genetic influences on tobacco-caused disease
Last updated: 2011 Suggested citation: Winstanley, MH. 3.24 Genetic influences on tobacco-caused disease. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2011. Available from http://www.tobaccoinaustralia.org.au/3-22-genetic-influences-on-tobacco-caused- disease
There is evidence that the development of tobacco-caused disease may be mediated by the influence of an individual's genetic make-up.1–4 If confirmed, this means that someone with a genetic susceptibility to heart disease (or lung cancer or any of the other many diseases caused by smoking) could be at higher risk of developing these diseases if they smoke, and conversely, that some individuals may theoretically be at less risk of developing certain diseases. These findings have given rise to some debate about whether genetic screening might usefully contribute to the prevention of tobacco-caused disease,5–7 but the concept of genetic screening to ascertain individual risk of developing tobacco-related disease is considered to be impractical for the following three reasons:
Firstly, it is likely that many different genes, each contributing only a small portion of the overall risk, influence a smoker's individual risk of developing a particular disease which is caused by smoking. As discussed throughout this chapter, it is already well understood that smokers have a much higher risk than non-smokers of developing many conditions. Given this, it may be that being able to assess an individual smoker's personal risk of developing disease is in fact not much more informative than predicting risk simply on the basis of being a smoker.6
Secondly, smoking is the cause of many different diseases. Even to test smokers for susceptibility to the most commonly-caused diseases such as cardiovascular disease, lung cancer and chronic obstructive pulmonary disease, would mean screening for a large number of polymorphisms (common, naturally occurring variations in a gene, DNA sequence or chromosome).6
Finally, even if all these processes are eventually elucidated and genetic pathways identified for each kind of disease, it is probable that virtually everybody will have at least one susceptibility gene for one or more smoking-related disease.5,8
Screening for susceptibility to tobacco-caused diseases therefore cannot be regarded as a viable tool for smoking prevention, and from a public health perspective, the only workable message is that smoking is not safe for anyone.8,5 References
1. Talmud P, Stephens J, Hawe E, Demissie S, Cupples L, Hurel S, et al. The significant increase in cardiovascular disease risk in APOE ε4 carriers is evident only in men who smoke: potential relationship between reduced antioxidant status and ApoE4. Annals of Human Genetics 2005;69:613-22. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16266401
2. Devereux TR, Taylor JA and Barrett JC. Molecular mechanisms of lung cancer. Interaction of environmental and genetic factors. Giles F. Filley Lecture. Chest 1996;109(3):14S-19. Available from: http://www.chestjournal.org/cgi/reprint/109/3/14S
3. Amos C, Xu W and Spitz M. Is there a genetic basis for lung cancer susceptibility? Recent Results Cancer Research 1999;151:3-12. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10337715
4. Kaprio J. Genetic epidemiology of smoking behavior and nicotine dependence. Chronic Obstructive Pulmonary Disease 2009;6(4):304-6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19811391
5. Hall W, Madden P and Lynskey M. The genetics of tobacco use: methods, findings and policy implications. Tobacco Control 2002;11:119-24. Available from: http://tobaccocontrol.bmj.com/cgi/reprint/11/2/119.pdf
6. Hall W. A research agenda for assessing the potential contribution of genomic medicine to tobacco control. Tobacco Control 2007;16:53-8. Available from: http://tobaccocontrol.bmj.com/cgi/reprint/16/1/53.pdf
7. Hall W, Mathews R and Morley K. Being more realistic about the public health impact of genomic medicine. PLoS Medicine 2010;7(10):pii: e1000347. Available from: http://www.ncbi.nlm.nih.gov/pubmed /20967240
8. Wang X and Mahaney M. Genotype-specific effects of smoking on risk of CHD [Editorial]. The Lancet 2001;358:87-8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11463406
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.25 Smoking compared with or in combination with other pollutants
3.25 Smoking compared with or in combination with other pollutants
Last updated: 2011 Suggested citation:Bellew, B & Winstanley, MH. 3.25 Smoking compared with or in combination with other pollutants. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2011. Available from http://www.tobaccoinaustralia.org.au/3-25- air-pollution-cigarette-smoking-and-ill-healt
A preliminary note of caution about tobacco industry interference is appropriate before embarking on a discussion of other pollutants and health. Tobacco companies have historically sought to distract the public from the issue of secondhand smoke by emphasising the dangers of other pollutants, including carpet glue fumes and car exhaust. A broader discussion of indoor air quality, ventilation and 'sick building syndrome' has served, in some cases, to drown out concerns about the harms of secondhand smoke. According to a Philip Morris publication developed for Europe, the range of pollutants found in offices which cause sick building syndrome include fumes and gases emitted from carpets, computer screens, photocopiers, etc., with the problem often augmented by bacteria, moulds and dusts from ventilation equipment. It has even been argued that tobacco smoke can be a useful visual marker of bad ventilation inside buildings. Tobacco companies have invested heavily in research on air quality issues. Substantial funds have been channelled to outside investigators through scientific organisations and companies focusing on indoor air research that were meant to appear independent and objective, but in fact were run by tobacco industry consultants.1-3 The tobacco industry and its interference tactics are discussed more fully in Chapter 10, Section 10.12.
Particulate matter (PM), also known as particle pollution, is the term commonly used in discussion of outdoor air pollution. PM is a complex mixture of extremely small particles and liquid droplets suspended in air. It is made up of a number of components, including acids (such as nitrates and sulphates), organic chemicals, metals, and soil or dust particles and allergens (such as fragments of pollen or mould spores). The size of particles is directly linked to their potential for causing health problems; it is now generally accepted that the very small particles emitted into the surrounding air by combustion and abrasion have a large effect on annual death rates. The evidence points to PM2.5 as the most satisfactory index of particulate air pollution for quantitative assessments of the effects of policy interventions.4 Fine particle pollution or PM2.5 describes particulate matter that is 2.5 micrometres in diameter and smaller (about 1/30th the diameter of a human hair).5 A 2008 systematic review of the relation between long-term exposure to ambient air pollution and chronic diseases was conducted by Chen and colleagues.6 The analysis showed that long-term exposure to PM2.5 increases the risk of non-accidental mortality by 6% per 10 microg/m3 increase, independent of age, gender and geographic region. Exposure to PM2.5 was found to be associated with an increased risk of mortality from lung cancer (range: 15% to 21% per 10 microg/ m3 increase) and total cardiovascular mortality (range: 12% to 14% per 10 microg/ m3 increase). Living close to busy traffic is associated with elevated risks of these three outcomes. Evidence suggested that exposure to PM2.5 is positively associated with mortality from coronary heart diseases and that exposure to sulphur dioxide (SO2) increases mortality from lung cancer. For other pollutants and health outcomes, there are insufficient data to make solid conclusions.6 Studies examined in the systematic review are available as an online appendix.7 Virtually all studies covering non-accidental mortality and exposure to PM2.5 have adjusted for the effects of active smoking; in other words, researchers used statistical techniques that attempted to allow for the adverse health effects of this exposure when estimating the risk from air pollution. One of these studies adjusted for exposure to secondhand smoke; McDonnell et al provided a risk estimate of 1.09 (95% CI, 0.98–1.21) for men, which is only on the cusp of statistical significance while there was a non-significant finding for women. Lung cancer mortality was also examined in this secondhand smoke adjusted study whereby a (non-significant) risk estimate of 1.39 (95% CI, 0.79–2.46) was obtained.8
A number of studies provide insights into road traffic-specific component of outdoor air pollution. As noted earlier, a systematic review has concluded that living close to busy traffic is associated with elevated risks of the adverse outcomes associated with exposure to PM2.5.6 Other recent studies have found that long-term exposure to traffic-related air pollution may contribute to the development of chronic obstructive pulmonary disease with possibly enhanced susceptibility in people with diabetes and asthma;9 that medium-term exposure to traffic-related air pollution may induce an increased inflammatory/endothelial response, especially among diabetics and those not using statins;10 and that traffic intensity near the home is associated with natural-cause mortality (highest relative risks for respiratory mortality).11
The National Pollutant Inventory holds data for all sources of particulate matter emissions in Australia.12 Overall, air quality in Australia is relatively good, but for some places, such as large cities and mining areas, air quality can be an issue. The 'headline indicator' for atmosphere in Measures of Australia's Progress has generally regressed compared with 10 years ago.13 In recognition of the effects of these pollutants on health and climate, a range of standards has been introduced across Australia over recent decades. The National Environment Protection Measures describe standards for six main pollutants, including PM10 (particulate matter, or inhalable particles, more than 10 microns in diameter). The maximum PM10 concentration allowed under the standard is 50 microg /m3 and for a maximum of five days a year. (In 2003 the National Environment Protection Measures was varied to add an advisory reporting standard for PM2.5; the advisory standard for PM2.5 is a maximum concentration of 25 microg /m3 in one day and 8 microg /m3 per year.) All capital cities except Hobart had PM10 concentrations above the standard between 1991 and 2001. In Melbourne the levels of PM10 remained above the standard from 2001 to 2006, with concentration peaks seen in 2003 and 2006. New South Wales also recorded PM10 levels above the standard from 2001 to 2006, with a peak in 2003. The peaks can be attributed to severe bushfires and dust storms in those years. Most capital cities have shown a fairly steady rate of sulphur dioxide emissions and met the National Environment Protection Measures standards for highest daily average and highest daily maximum between 1991 and 2001. This trend was maintained in Sydney and Melbourne from 2002 to 2006. Until 1996, Adelaide exceeded the standards but since then the levels have been below the standard.14
Outdoor air pollution is a significant cause of sickness and death in Australia. It is estimated that in 2003, about 2000 deaths in Australia were attributable to long-term exposure to urban air pollution, and a further 1000 deaths were caused by short-term exposure through exacerbation of pre-existing illness.15 Most deaths were due to ischaemic heart disease, followed by stroke, lung cancer and chronic obstructive pulmonary disease. In total, urban air pollution caused 2.3% of all deaths in Australia in 2003. Tobacco caused almost five times that amount.15
Tobacco smoke is, of course, also a source of environmental particulate matter. A study comparing the output of particulate matter from three single cigarettes burning consecutively over 30 minutes showed that the total delivery of particulate matter was up to 10 times greater than emissions of particulate matter from the exhaust of a modern turbo diesel motor car with the engine left idling for the same amount of time.16 Tobacco smoke is also a major source of indoor carbon monoxide pollution17–see following section.
Policy action to reduce levels of air pollutants is important and it is reasonable to assume that a reduction in air pollution will lead to considerable health benefits.18 However, since the adverse effects of outdoor air pollution may also be used by the tobacco industry to distract attention from policy measures for secondhand smoke, it is worth noting the recent report by the World Health Organization, which provides risk estimates for exposure to secondhand smoke across a wide range of adverse health outcomes for both children and adults.19 These well quantified risks from secondhand smoke exposure,19 the relative ease and low cost of policy measures to reduce or eliminate the risks, and the immediacy of their impact20 are all powerful arguments that should help ensure a clearer focus in the attention of policy-makers and members of the public alike.
3.25.2 Indoor pollution
3.25.2.1 Indoor pollution: generic
With Australians spending up to 90% of their time indoors,21 indoor air quality, whether it be domestic or workplace, is an important health consideration. Sources of indoor pollution in Australia include asbestos products, radon gas, secondhand tobacco smoke, house dust mite allergens, formaldehyde (used in production of pressed wood products such as particleboard, or insulation products), nitrogen dioxide emissions from unflued gas appliances, and pesticides applied under buildings.22 Moulds, dust, animal fur or dander (tiny flakes from fur, skin or feathers), and chemicals arising from paint, glues or other household solvents are also a cause of irritation. 'Off-gassing', the emission of toxic fumes from furniture, carpets, paints, glues and sealants in newer buildings and houses may remain at high levels for several months.21 Of course, outdoor pollutants may also infiltrate the indoor environment. Exposures to these agents may cause a variety of responses, from mild irritation through to asthma and disease.
Of all these pollutants, the three most significant in Australia are asbestos fibres, radon gas and secondhand tobacco smoke.22 As already noted, asbestos fibres are a cause of lung cancer and other respiratory disease, and although it is no longer mined and its use in building products has been phased out, asbestos remains present in many structures. Radon gas is also a known human carcinogen that occurs naturally in soil and rocks, collecting in buildings from the soil beneath. Radon levels in Australian buildings are, for the most part, well below internationally recommended indoor levels, and significantly lower than for buildings in the US and the UK, probably due to different soils, building practices and the coastal proximity for much housing.22 Secondhand tobacco smoke causes lung cancer, as well as a range of other respiratory symptoms and illnesses among non-smoking adults and children.23 In past decades, exposure to secondhand smoke has been ubiquitous. Restrictions on smoking in the workplace and in many public places have reduced exposure to secondhand smoke for many Australians over the past 20 years, although exposure in recreational facilities and establishments such as hotels and nightclubs has remained high. A significant number of adults and children also remain exposed in the home (see Chapter 4, Section 4.14). For further information on secondhand smoke refer to Chapter 4. Smokefree environments are discussed in Chapter 15.
3.25.2.2 Indoor pollution: workplace exposure
Workplace exposures to a range of substances can cause illness. For example, environments containing fine particulate matter from grains, flours, plants, coal dust, asbestos, silica, wood, feathers, insects and fungi, drugs and enzymes, chlorofluorocarbons, alcohols, metals and their salts and welding fumes can cause asthma, progressive lung damage and other serious respiratory disease.24, 25 Combining smoking with these exposures may greatly increase disease risk.25
A well-documented example is the interaction between workplace exposure to asbestos and cigarette smoking. Among the population not exposed to asbestos, smoking increases the lung cancer rate approximately 10-fold. In non-smoking asbestos workers, the lung cancer rate is increased five-fold; but among asbestos workers who smoke, the lung cancer rate is increased 50-fold. In other words, for those workers who both smoke and are exposed to asbestos, the risk of developing and dying from lung cancer is 50 times greater than the risk for individuals who neither smoke nor are exposed to asbestos at work. The risk is also dose-responsive, varying with exposure to both contributing factors. Heavy smokers heavily exposed to asbestos will have a higher than 50-fold increase.25 In Australia, most exposure to asbestos now occurs through the removal of asbestos from buildings, but the long lag-time for development of asbestos- caused disease means that death rates will continue to rise for the next two decades.26 There is also ample evidence suggesting that exposures to petrochemicals, aromatic amines, ionising radiation and pesticides interact with tobacco smoke.25 Evidence on occupational exposures and health effects has further expanded in recent years. Researchers have reported on occupational exposures and lung cancer; 4.9% (95% CI, 2.0 - 7.8) of lung cancers in men were attributable to occupation in known higher risk professions; past exposure to occupational carcinogens is judged an important determinant of lung cancer incidence 27, 28. A follow up study of 15 million people in Denmark, Finland, Iceland, Norway and Sweden showed that male waiters and tobacco workers had the highest risk of lung cancer, probably attributable to active and passive smoking. Miners and quarry workers also had a high risk, which might be related to their exposure to silica dust and radon daughters. Among women, tobacco workers and engine operators had a more than four-fold risk as compared with the lung cancer risk among farmers, gardeners and teachers. Waiters had the highest risk of bladder cancer among men; tobacco workers had the highest risk among women; the low-risk categories were the same ones as for lung cancer. The researchers stated that all of this could be accounted for by smoking.29 A systematic review found consistent evidence that exposure to benzene at work increases the risk of leukaemia with a dose–response pattern.30 Studies have also demonstrated negative consequences from inhaling fumes during welding,31 and the impact of silica exposure on the risk of developing rheumatoid arthritis32 and lung cancer,33 with greatly increased risk for these diseases among smokers. Current or previous occupational exposure to organic solvents has been found to double the smoking-related risk of chronic bronchitis.34 Cigarette smoking accompanied by exposure to workplace noise has also been associated with a five-fold increase in risk of noise induced hearing loss among smokers compared with non-smokers.35, 36 The risk of infertility and spontaneous abortion has been found to be 30% higher among female hairdressers than among women in other occupations, thought to be due to their occupational chemical exposure and found primarily among never smokers.37 Being a current smoker is a risk factor for sensitisation to workplace allergens. Smokers are more than twice as likely as non-smokers to have positive tests of allergic reactions (OR 2.39; 95% CI, 1.01–5.65).38
Inhalation exposure to particulates such as cigarette smoke and coal dust is known to contribute to the development of chronic lung disease and several studies of the health and wellbeing of coal miners have been reported.39-42 These studies provide evidence that: (i) elemental carbon levels in the lungs and pack-years of cigarette smoking correlate significantly, as do elemental carbon levels and the severity of small airway disease;39 (ii) cumulative exposure to coal dust is a significant risk factor for the development of emphysema and has an additive effect to smoking;40, 41 (iii) exposure to coal mine dust leads to increased mortality, even in the absence of smoking42; (iv) increased exposure to coal dust is associated with increased risk of death from chronic obstructive pulmonary disease;40 and (v) that in newly employed coal miners, bronchitis symptoms are associated with a rapid decline in lung function within two years after starting work.40 Other studies of exposure to dust or fumes have reported associations with the incidence of chronic obstructive pulmonary disease,44 and asthma45; chronic bronchitis occurs more frequently among individuals exposed to mineral dust, and smoking doubles this risk.45
The US Surgeon General has concluded that 'for the majority of American workers who smoke, cigarette smoke represents a greater cause of death and disability than their workplace environment'.25 The Australian Burden of Disease Study confirms this. It is estimated that in 2003, occupational exposures and hazards accounted for 2% of the total disease and injury burdeni and 1.3% of all deaths, while tobacco use accounted for 7.8% of the total disease and injury burden and 11.7% of all deaths.15
The accumulation of evidence about workplace health hazards over previous decades has led to the introduction of industrial health and safety standards, which have greatly reduced exposures to carcinogenic and other toxic substances in developed countries. However the relocation of hazardous industry to less developed countries, where occupational safety may be less regulated (and where, incidentally, there is more likely to be a higher prevalence of smoking), is a major cause for concern.26
3.25.2.3 Sick building syndrome
Over the past 15 to 20 years awareness has risen about 'sick building syndrome'.22 The term sick building syndrome is used to refer to a heterogeneous group of work-related symptoms, including irritation of the skin and mucous membranes of the eyes, nose and throat; headache; fatigue; and difficulty concentrating. These are considered illnesses because of the occurrence of symptoms, even though affected workers do not have objective clinical or laboratory abnormalities and causative agents cannot be found. The clinical symptoms of sick building syndrome, although not life-threatening, are disruptive: they reduce productivity and increase absenteeism from work.46 It is likely that the cause of sick building syndrome is multifactorial, involving ventilation, airborne particulates from a wide range of sources (including chemicals, micro-organisms and non-organic matter) and other vectors in the indoor environment. A recent update review concluded that sick building syndrome is related to both personal and environmental risk factors and, in the office environment, may have important economic implications.47 United States Environmental Protection Agency studies have identified four distinct groups of symptoms, representing 'tiredness', 'mucosal irritation', 'neuropsychological' and 'lower respiratory' conditions. Rather than a dichotomy of healthy versus unhealthy ('sick') buildings the Environmental Protection Agency found that the prevalence of health problems related to buildings spans a continuum; the distribution of work-related symptoms and identification of symptom groups can help in identification of problems.48
A recent review of the literature on ventilation rates and health found biological plausibility for an association of health outcomes with ventilation rates, but a lack of clear evidence on particular agent(s) for the effects.49 Higher ventilation rates in offices, up to about 25 litres per person, are associated with reduced prevalence of sick building syndrome symptoms.
The limited available data suggest that inflammation, respiratory infections, asthma symptoms and short-term sick leave increase with lower ventilation rates. Home ventilation rates above 0.5 air changes per hour (h(–1)) have been associated with a reduced risk of allergic manifestations among children in a Nordic climate.49 Improved ventilation practices and reduction of pollutants are key factors in alleviating sick building syndrome, along with adherence to building and maintenance standards and improved controls over temperature, humidity and lighting.22 During the 1980s the tobacco industry took a particular interest in sick building syndrome, using it as a means of deflecting attention away from newly emerging evidence about the health consequences of exposure to environmental tobacco smoke.1 This is discussed further in Chapter 15, Section 15.3.1. i The measure used to express total burden of disease and injury is the 'disability-adjusted life year' (DALY). The DALY 'describes the amount of time lost due to both fatal and non-fatal events; that is, years of life lost due to premature death coupled with years of 'healthy' life lost due to disability'.(p2) (ref is Begg, S et al - AIHW 2007).
References
1. Drope J, Bialous SA and Glantz SA. Tobacco industry efforts to present ventilation as an alternative to smoke-free environments in North America. Tobacco Control 2004;13(suppl. 1):i41-7. Available from: http://tobaccocontrol.bmj.com/cgi/reprint/13/suppl_1/i41.pdf
2. Pan American Health Organization/ World Health Organization. Second-hand smoke and the tobacco industry - factsheet. Washington DC: World Health Organization, 2001, viewed 1 September 2011. Available from: www.paho.org/english/ad/sde/ra/wntd-factsheet3.doc
3. Lee C and Glantz S. The tobacco industry's successful efforts to control tobacco policy making in Switzerland. San Francisco: School of Medicine University of California, San Francisco, 2001, [viewed 1 September 2011]. Available from: http://www.who.int/tobacco/media/en/InquirySwiss.pdf
4. Committee on the Medical Effects of Air Pollutants. Long-term exposure to air pollution: effect on mortality. Whitehall, London: Department of Health, 2009, [viewed 1 September 2011]. Available from: http://www.advisorybodies.doh.gov.uk/comeap/pdfs/finallongtermeffectsmort2009report.pdf
5. US Environmental Protection Agency (EPA). EPA Website - Particulate matter. 2011 Available from: http://www.epa.gov/air/particlepollution/index.html
6. Chen H, Goldberg MS and Villeneuve PJ. A systematic review of the relation between long-term exposure to ambient air pollution and chronic diseases. Reviews on Environmental Health 2008;23(4):243-97. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19235364
7. Chen H, Goldberg MS and Villeneuve PJ. A systematic review of the relation between long-term exposure to ambient air pollution and chronic diseases: On-line Appendix. Reviews on Environmental Health 2008 Available from: http://www.med.mcgill.ca/epidemiology/goldberg /Review%20of%20Outdoor%20Air%20Pollution.pdf
8. McDonnell WF, Nishino-Ishikawa N, Petersen FF, Chen LH and Abbey DE. Relationships of mortality with the fine and coarse fractions of long-term ambient PM10 concentrations in nonsmokers. Journal of Exposure Analysis and Environmental Epidemiology 2000;10(5):427-36. Available from: http://www.ncbi.nlm.nih.gov /pubmed/11051533
9. Andersen Z, Hvidberg M, Jensen S, Ketzel M, Loft S, Sorensen M, et al. Chronic obstructive pulmonary disease and long-term exposure to traffic-related air pollution: a cohort study. American Journal of Respiratory and Critical Care Medicine 2011;183(4):455–61. Available from: http://ajrccm.atsjournals.org /cgi/content/full/183/4/455
10. Alexeeff SE, Coull BA, Gryparis A, Suh H, Sparrow D, Vokonas PS, et al. Medium-term exposure to traffic-related air pollution and markers of inflammation and endothelial function. Environmental Health Perspectives 2011;119(4):481-6. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3080929 /pdf/ehp-119-481.pdf
11. Brunekreef B, Beelen R, Hoek G, Schouten L, Bausch-Goldbohm S, Fischer P, et al. Effects of long-term exposure to traffic-related air pollution on respiratory and cardiovascular mortality in The Netherlands: the NLCS-AIR study. Research Report (Health Effects Institute) 2009(139):5-71; discussion 73-89. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19554969
12. Australian Government Department of Sustainability E, Water, Population and Communities,. National Pollutant Inventory - Particulate matter (PM10 and PM2.5): . Available from: http://www.npi.gov.au /substances/particulate-matter/index.html
13. Australian Bureau of Statistics. 1370.0 Measures of Australia's progress. Atmosphere and progress. Canberra: ABS, 2010. Available from: http://www.abs.gov.au/ausstats/[email protected]/mf/1370.0
14. Australian Institute of Health and Welfare. Australia's health 2010. Australia's health series no. 12, cat. no. AUS 122. Canberra: AIHW, 2010. Available from: http://www.aihw.gov.au/WorkArea /DownloadAsset.aspx?id=6442452962&libID=6442452962
15. Begg S, Vos T, Barker B, Stevenson C, Stanley L and Lopez A. The burden of disease and injury in Australia 2003. AIHW cat. no. PHE 82. Canberra: Australian Institute of Health and Welfare, 2007. Available from: http://www.aihw.gov.au/publications/index.cfm/title/10317
16. Invernizzi G, Ruprecht A, Mazza R, Rossetti E, Sasco A, Nardini S, et al. Particulate matter from tobacco versus diesel car exhaust: an educational perspective. Tobacco Control 2004;13(3):219–21. Available from: http://tc.bmjjournals.com/cgi/content/abstract/13/3/219
17. Department of the Environment and Heritage. Carbon monoxide. Air quality fact sheet. Canberra: Department of the Environment and Heritage, 2005. Available from: http://www.environment.gov.au /atmosphere/airquality/publications/carbonmonoxide.html
18. World Health Organization - Regional Office for Europe. Health Aspects of Air Pollution: results from the WHO project "Systematic Review of Health Aspects of Air Pollution in Europe". 2004. Available from: http://www.euro.who.int/__data/assets/pdf_file/0003/74730/E83080.pdf 19. Öberg M, Jaakkola MS, Prüss-Üústün A, Schweizer C and Woodward A. Second-hand smoke: assessing the environmental burden of disease at national and local levels. WHO Environmental Burden of Disease Series, no.18. Geneva, : World Health Organization, 2010. Available from: http://www.who.int /quantifying_ehimpacts/publications/SHS.pdf
20. Hopkins DP, Razi S, Leeks KD, Priya Kalra G, Chattopadhyay SK and Soler RE. Smokefree policies to reduce tobacco use. A systematic review. American Journal of Preventive Medicine 2010;38(suppl. 2):S275-89. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20117612
21. Australian Bureau of Statistics. 1301.0 Australia now. Environment. Air Pollution Canberra: ABS, 2004. Available from: http://www.abs.gov.au/ausstats/[email protected] /0/8f1a0bea81c1d6eeca256dea00053a5e?OpenDocument
22. Brown S. Indoor air quality, Australia: State of the Environment Technical Paper Series (Atmosphere). Canberra: Department of the Environment, Sport and Territories, 1997. Available from: http://www.deh.gov.au /soe/techpapers/series1/pubs/12indora.pdf
23. US Department of Health and Human Services. The health consequences of involuntary exposure to tobacco smoke: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2006. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/sgr_2006/index.htm
24. Driscoll T, Steenland K, Imel Nelson D and Leigh J. Occupational airborne particulates. Assessing the environmental burden of disease at national and local levels. Environmental burden of disease series, no. 7. Geneva: World Health Organisation, 2004. Available from: http://www.who.int/quantifying_ehimpacts /publications/en/ebd7.pdf
25. US Department of Health and Human Services. The health consequences of smoking: cancer and chronic lung disease in the workplace. A report of the Surgeon General. Rockville, Maryland: US Department of Health and Human Services, Public Health Service, Office on Smoking and Health, 1985. Available from: http://profiles.nlm.nih.gov/NN/B/C/B/N/segments.html
26. Stewart B, Kleihues P and Editors. IARC World Cancer Report. Lyon, France: International Agency for Research on Cancer, 2003.
27. Consonni D, De Matteis S, Lubin J, Wacholder S, Tucker M, Pesatori A, et al. Lung cancer and occupation in a population-based case-control study. American Journal of Epidemiology 2010;171(3):323–33. Available from: http://aje.oxfordjournals.org/cgi/content/full/171/3/323
28. Paris C, Clement-Duchene C, Vignaud J, Gislard A, Stoufflet A, Bertrand O, et al. Relationships between lung adenocarcinoma and gender, age, smoking and occupational risk factors: a case-case study. Lung Cancer 2010;68(2):146–53. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19586681
29. Pukkala E, Martinsen JI, Lynge E, Gunnarsdottir HK, Sparen P, Tryggvadottir L, et al. Occupation and cancer - follow-up of 15 million people in five Nordic countries. Acta Oncologica 2009;48(5):646-790. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19925375
30. Khalade A, Jaakkola MS, Pukkala E and Jaakkola JJ. Exposure to benzene at work and the risk of leukemia: a systematic review and meta-analysis. Environmental Health 2010;9:31. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20584305
31. Gube M, Ebel J, Brand P, Goen T, Holzinger K, Reisgen U, et al. Biological effect markers in exhaled breath condensate and biomonitoring in welders: impact of smoking and protection equipment. International Archives of Occupational and Environmental Health 2010;83(7):803–11. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20130903
32. Stolt P, Yahya A, Bengtsson C, Kallberg H, Ronnelid J, Lundberg I, et al. Silica exposure among male current smokers is associated with a high risk of developing ACPA positive rheumatoid arthritis. Annals of the Rheumatic Diseases 2010;69(6):1072–6. Available from: http://ard.bmj.com/content/69/6/1072.long
33. Vida S, Pintos J, Parent M, Lavoue J and Siemiatycki J. Occupational exposure to silica and lung cancer: pooled analysis of two case-control studies in Montreal, Canada. Cancer Epidemiology, Biomarkers & Prevention 2010;Epub ahead of print Available from: http://cebp.aacrjournals.org/content/early/2010/05 /21/1055-9965.EPI-10-0015.full.pdf+html
34. Ebbehoj NE, Hein HO, Suadicani P and Gyntelberg F. Occupational organic solvent exposure, smoking, and prevalence of chronic bronchitis-An epidemiological study of 3387 men. Journal of Occupational & Environmental Medicine 2008;50(7):730 – 5. Available from: http://www.joem.org/pt/re /joem/abstract.00043764-200807000-00002.htm;jsessionid=LLwQJLvnJThFbhJQv1mpvDhmtJpMB0pt2TzCRN7YysQ1Xxh29l4H!5238
35. Mohammadi S, Mazhari MM, Mehrparvar AH and Attarchi MS. Effect of simultaneous exposure to occupational noise and cigarette smoke on binaural hearing impairment. Noise Health 2010;12(48):187-90. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20603575
36. Mohammadi S, Mazhari MM, Mehrparvar AH and Attarchi MS. Cigarette smoking and occupational noise-induced hearing loss. European Journal of Public Health 2010;20(4):452-5. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19887518
37. Baste V, Moen B, Riise T, Hollund B and Oyen N. Infertility and spontaneous abortion among female hairdressers: the Hordaland Health Study. Journal of Occupational and Environmental Medicine 2008;50(12):1371–7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19092492
38. Adisesh A, Gruszka L, Robinson E and Evans G. Smoking status and immunoglobulin E seropositivity to workplace allergens. Occupational Medicine 2011;61(1):62–4. Available from: http://occmed.oxfordjournals.org/content/61/1/62.full
39. Saxena R, McClure M, Hays M, Green F, McPhee L, Vallyathan V, et al. Quantitative assessment of elemental carbon in the lungs of never smokers, cigarette smokers, and coal miners. Journal of Toxicology and Environmental Health 2011;74(11):706–15. Available from: http://www.ncbi.nlm.nih.gov/pubmed /21480045
40. Santo Tomas LH. Emphysema and chronic obstructive pulmonary disease in coal miners. Current Opinion in Pulmonary Medicine 2011;17(2):123-5. Available from: http://www.ncbi.nlm.nih.gov/pubmed /21178627
41. Kuempel ED, Wheeler MW, Smith RJ, Vallyathan V and Green FH. Contributions of dust exposure and cigarette smoking to emphysema severity in coal miners in the United States. American Journal of Respiratory and Critical Care Medicine 2009;180(3):257-64. Available from: http://ajrccm.atsjournals.org /cgi/reprint/180/3/257.pdf
42. Attfield MD and Kuempel ED. Mortality among US underground coal miners: a 23-year follow-up. American Journal of Industrial Medicine 2008;51(4):231-45. Available from: http://www.ncbi.nlm.nih.gov /pubmed/18247381
43. Blanc PD, Menezes AM, Plana E, Mannino DM, Hallal PC, Toren K, et al. Occupational exposures and COPD: an ecological analysis of international data. European Respiratory Journal 2009;33(2):298-304. Available from: http://erj.ersjournals.com/content/33/2/298.full.pdf
44. Sunyer J, Zock JP, Kromhout H, Garcia-Esteban R, Radon K, Jarvis D, et al. Lung function decline, chronic bronchitis, and occupational exposures in young adults. American Journal of Respiratory and Critical Care Medicine 2005;172(9):1139-45. Available from: http://ajrccm.atsjournals.org/cgi/reprint/172/9/1139
45. de Meer G, Kerkhof M, Kromhout H, Schouten JP and Heederik D. Interaction of atopy and smoking on respiratory effects of occupational dust exposure: a general population-based study. Environmental Health 2004;3(1):6. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC443511/pdf/1476-069X-3-6.pdf
46. Epstein Y. Sick building syndrome. Harefuah 2008;147(7):607-8, 662. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18814520 47. Norback D. An update on sick building syndrome. Current Opinion in Allergy and Clinical Immunology 2009;9(1):55-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19532093
48. Brightman HS, Milton DK, Wypij D, Burge HA and Spengler JD. Evaluating building-related symptoms using the US EPA BASE study results. Indoor Air 2008;18(4):335-45. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18717984
49. Sundell J, Levin H, Nazaroff WW, Cain WS, Fisk WJ, Grimsrud DT, et al. Ventilation rates and health: multidisciplinary review of the scientific literature. Indoor Air 2011;21(3):191-204. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21204989
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.26 Health effects of brands of tobacco which claim or imply delivery of lower levels of tar, nicotine and carbon monoxide
3.26 Health effects of brands of tobacco products which claim or imply, delivery of lower levels of tar, nicotine and carbon monoxide
Last updated: March 2015 Suggested citation:Bellew, B, Greenhalgh, EM & Winstanley, MH. 3.26 Health effects of brands of tobacco products which claim or imply, delivery of lower levels of tar, nicotine and carbon monoxide. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-26-health-effects-of-smoking- brands-that-claim-t
With reports published during the 1950s linking cigarette smoking with disease, tobacco companies experimented with various modifications to their products. Firstly, filters were added, and later ventilation holes in the form of tiny perforations were added around the mouthpiece, with the apparent intention of diluting the delivery of tar, nicotine, carbon monoxide (CO) and other compounds to the smoker. Tobacco leaf itself has also undergone various treatments to alter toxic delivery. While it was initially hoped by health interests that lower delivery cigarettes would prove to be a less harmful form of tobacco use, bringing about reductions in death and disease, this has proved not to be the case.1,2
Low delivery cigarettes do not offer a health advantage. Two major, recent reports have reviewed the evidence regarding the impact on health of smoking cigarettes with lower levels of toxicity. The US Surgeon General’s report for 2010 concluded that “changing cigarette designs over the last five decades, including filtered, low-tar, and “light” variations, have not reduced overall disease risk among smokers and may have hindered prevention and cessation efforts.” p. 253 The National Cancer Institute, part of the US National Institutes of Health, stated in its 2001 report that “epidemiological and other scientific evidence, including patterns of mortality from smoking- caused diseases, does not indicate a benefit to public health from changes in cigarette design and manufacturing over the last fifty years,” and that “widespread adoption of lower yield cigarettes in the United States has not prevented the sustained increase in lung cancer among older smokers.” p. 101
The reasons why 'lower delivery' cigarettes have not benefited health lie in the way a smoker typically smokes a cigarette, as opposed to how a machine designed to measure smoke output 'smokes' a cigarette under laboratory conditions. Because addicted smokers need to maintain their level of intake of nicotine, they tend to compensate for the delivery of lower levels of nicotine by adjusting puff frequency, rapidity or depth of inhalation, by increasing the numbers of cigarettes smoked daily, or by blocking with their fingers the ventilation holes around the filter intended to dilute the smoke. Because exposure to tar compared to nicotine appears to be similar among smokers of conventional cigarettes, this results in very little change in the actual intake of tar and other compounds. In contrast, of course, a machine simply "puffs" according to its calibration.1,4,5
Wider public health interests were first alerted2 to the discrepancy between laboratory-measured and smokers' actual exposure by the release of the US Surgeon General's Report of 1981,4 but for the following decade it was generally held that smokers choosing low delivery brands were reducing their intake to at least some degree.2 The tobacco industry operated under no such illusions. It is now known that the industry had long been aware of compensatory smoking and the limitations of machine measurements, and from the 1970s onwards, was using this knowledge to manipulate consumers and subvert the official laboratory testing systems.1 Tobacco companies engineered their products so that smokers could obtain as much nicotine as they needed by altering their smoking behaviour, but also ensured that when tested by standard smoking machine protocols, the same brand of cigarettes would return acceptably low yields.1,2 The tobacco industry also experimented with the composition of cigarettes and filters in order to minimise machine- measured noxious outputs, but took no steps to create a cigarette which truly delivered lower toxins to the smoker under normal conditions.1
Beyond the phenomenon of compensation, the 2014 US Surgeon General’s report explored whether the changes in the design and composition of cigarettes since the 1950s that paralleled the reduction in machine-measured tar yields may have changed smokers’ risk of lung cancer. The report concluded that the increased risk of adenocarcinoma of the lung has been caused by these changes in the design and composition of cigarettes. There is currently insufficient evidence to identify which changes have caused this increase, but ventilated filters and increased levels of tobacco-specific nitrosamines may be partially responsible.6
The production and vigorous marketing of 'light' and 'mild' brands allowed the tobacco industry, over several decades, to reassure smokers that there were less harmful ways of smoking.1, 2 Two major tobacco companies in Australia have agreed to discontinue the use of misleading descriptors and information on tar, nicotine and CO levels on tobacco packages since they have been judged by the Australian Competition Consumer Commission to be misleading.i For detailed discussion about the changes made to manufactured cigarettes in Australia, along with regulatory aspects, refer to Chapter 12, Section 12.4. i See the ACCC website: http://www.accc.gov.au/content/index.phtml/itemId/683533
References
1. Burns D and Benowitz NL. Public health implications of changes in cigarette design and marketing. Tobacco Control Research. Smoking and Tobacco Control Monographs. Monograph 13: Risks associated with smoking cigarettes with low tar machine-measured yields of tar and nicotine. Bethesda, MD: National Cancer Institute, US National Institutes of Health, 2001;Available from: http://www.cancercontrol.cancer.gov /tcrb/monographs/13/m13_1.pdf
2. King W, Carter SM, Borland R, Chapman S and Gray N. The Australian tar derby: the origins and fate of a low tar harm reduction programme. Tob Control 2003;12(suppl. 3):iii61-70. Available from: http://tobaccocontrol.bmj.com/cgi/content/full/12/suppl_3/iii61
3. US Department of Health and Human Services. The health consequences of smoking. A report of the Surgeon General. Rockville, MD: US Department of Health and Human Services, Public Health Service, Office of the Surgeon General, 2004. Available from: http://www.surgeongeneral.gov/library /smokingconsequences/
4. US Department of Health and Human Services. The health consequences of smoking. The changing cigarette. A report of the Surgeon General. Washington DC: US Department of Health and Human Services, Public Health Service, Office of Smoking and Health, 1981. Available from: http://profiles.nlm.nih.gov/NN/B/B /S/N/segments.html 5. McNeill A. Harm reduction. British Medical Journal 2004;328:885-7. Available from: http://www.bmj.com /cgi/reprint/328/7444/885
6. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.27 Health effects of smoking tobacco in other forms
3.27 Health effects of smoking tobacco in other forms
Last updated: March 2015 Suggested citation:Bellew, B, Greenhalgh, EM & Winstanley, MH. 3.27 Health effects of smoking tobacco in other forms. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-27- health-effects-of-smoking-tobacco-in-other-fo
Data from the 2013 National Drug Strategy Household Survey show that while the vast majority of Australian smokers (89%) use manufactured cigarettes, a variety of other tobacco products are also used either regularly or occasionally, either in conjunction with use of cigarettes or exclusively. About one-third (33%) of smokers report any use of roll-your-own, and about ten percent (10.4%) report use of cigarillos or cigars. Fewer than 2% report use of pipe tobacco.1 Unbranded tobacco (also known as chop-chop) is roughly processed loose tobacco that has been grown, distributed and sold without government intervention or taxation.2 In 2013, of smokers aged 14 years or older about one-third had seen or heard of unbranded loose tobacco. The proportion of smokers who had ever smoked and smoked unbranded loose tobacco at the time of the survey declined between 2010 and 2013 (from 24.0% down to 16.5%, and from 4.9% down to 3.6%, respectively). The overall proportion of smokers using it regularly remained low at 0.8%.1
Smoking tobacco by means of a waterpipe (using a system by which smoke passes through water prior to inhalation) is widespread in other parts of the world3-5 and is also practised in Australia. One study reporting prevalence of 11% among Arab-speaking adults).6 Data from the National Drug Strategy Household Survey indicates that 2.4% of all Australians aged over 14 years, and 6.7% of current smokers, had used a waterpipe in the year prior to the survey. Usage was much higher among young adults (18-24 years) who were also current smokers, at 17%.7 For more information on the extent to which tobacco products other than manufactured cigarettes are used in Australia, see Chapter 1, Section 1.11.
3.27.1 Manufactured loose tobacco
Manufactured loose tobacco, hand-rolled into cigarette paper and smoked with or without a filter, causes the same range of diseases as smoking manufactured cigarettes. Variations in quantity of tobacco used per cigarette and filtration make measurements of individual exposure more difficult to assess, but the directly comparable exposure to harmful constituents and method of consumption means that smokers of these products have at least an equivalent risk of developing disease as do smokers of conventional cigarettes. Several decades of research on the health effects of tobacco use have enabled comparisons between products with and without filters, and with high and low nicotine and tar yields. Overall, neither has the incidence of lung cancer varied with tobacco product used, nor have other health benefits become apparent.8
3.27.2 Unbranded loose tobacco ('chop-chop') Chop-chop is used by some as an alternative to other manufactured tobaccos due to its comparative affordability, and common misapprehensions that it is less harmful to health since it is apparently more 'natural' and 'unadulterated,' not having been processed in the usual way.9-11 Research has shown that some batches of chop-chop contain bulking agents such as twigs, raw cotton and grass clippings. Fungal (mould) spores have also been detected. Fungal spores are of particular health concern since they give rise to mycotoxins, including aflotoxin, a known carcinogen. Inhalation of and contact with fungi and their mycotoxins can cause a range of adverse responses in the liver, kidneys and skin, and cause illnesses including allergic reactions, chronic bronchitis, asthma and lung diseases.12 Australian chop-chop users report significantly worse health than smokers of licit tobacco. In a recent study in which a comparison with licit-only tobacco smokers was undertaken, current users of chop-chop had significantly greater odds of reporting below-average social functioning (OR 1.61; 95% CI, 1.06–2.44), measurable disability (OR 1.95; 95% CI, 1.08–3.51), below-average mental health (OR 1.61; 95% CI, 1.22–2.13) and above-average bodily pain (OR 1.40; 95% CI, 1.06–1.85).13
3.27.3 Cigar smoking
Cigar smoke is at least as toxic and carcinogenic as cigarette smoke and possibly more so. Cigars contain more tobacco per stick than cigarettes, take longer to smoke, and produce higher concentrations of a number of noxious compounds including carbon monoxide, nitrogen oxides, carcinogenic N-nitrosamines and ammonia.14 A recent systematic review found that cigar smoking carries many of the same health risks as cigarette smoking. Mortality risks from cigar smoking vary by number of cigars per day and inhalation level, but can be as high as or exceed those of cigarette smoking. Specifically, primary cigar smoking (current, exclusive cigar smoking with no history of previous cigarette or pipe smoking) was associated with all cause-mortality, oral cancer, esophageal cancer, pancreatic cancer, laryngeal cancer, lung cancer, coronary heart disease (CHD), and aortic aneurysm. Strong dose- response relationships were observed between the number of cigars smoked per day and inhalation level, and oral, esophageal, laryngeal, and lung cancers. Among primary cigar smokers who reported that they did not inhale, relative mortality risk was still highly elevated for oral, esophageal, and laryngeal cancers..15 A 2010 European longitudinal study involving more than 100,000 men found that, compared to never smokers, the risk of cancers of the lung, upper aerodigestive tract and bladder combined was more than doubled (HR 2.2; 95% CI, 1.3–3.8) for exclusive cigar smokers. Effects were stronger in current than in ex-smokers and in inhalers than in non-inhalers. For ever-smokers of both cigarettes and cigars there was more than a five-fold increase in the risk of these cancers (HR 5.7; 95% CI, 4.4–7.3) making the risk elevation as high as that among exclusive cigarette smokers.16 A case–control study focusing only on lung cancer found a five-fold increase in risk for smoking cigars only compared to never smokers (OR 5.6; 95% CI, 2.9–10.6)17 consistent with estimates from earlier research.18 Other research has shown that cigar-only smokers had a 60% increased risk of pancreatic cancer compared with those who had never used tobacco (OR 1.6; 95% CI, 1.2– 2.3), the risk with increasing according to the amount of cigar smoked per day (OR 1.82 for ≥10 grams of tobacco),19 which is broadly consistent with risk estimates from a 2008 meta-analytic review.20
Smoke drifting from the burning tip of a lit cigar contains most of the same toxic and carcinogenic compounds as cigarette smoke, and because they are larger, cigars generate smoke for a longer period of time–as long as 90 minutes for a single large cigar. This is a health concern for those constantly exposed to an indoor environment affected by cigar smoke;14 some researchers have concluded that high passive exposure to smoke from cigars and pipes may be associated with lung cancer risk.17 Cigar use has increased in popularity in the US, prompting concern among some tobacco control organisations21; in Australia the proportion of smokers using cigars and pipes alone rose from an estimated 1.2% in 2004 to 1.6% in 2010.22, 23 See Chapter 1, Section 1.11 and Chapter 10, Section 10.6 for further discussion.
3.27.4 Pipe smoking
Longitudinal research conducted in Norway has reported that pipe smoking is not safer than cigarette smoking. The study followed a cohort of more than 16 000 men for up to 13 years. Between pipe and cigarette smokers, no or only minor differences were found in mortality from any cause and the specified smoking-related diseases.24 Pipe smoking is associated with decreased lung function and increased odds of airflow obstruction, even in participants who had never smoked cigarettes;25 it is associated with a significantly higher risk of dying from COPD, cerebrovascular disease and cardiovascular disease. Compared to never smokers, exclusive pipe smokers are estimated to have a three-fold increase in risk (HR 3.0; 95% CI, 2.1–4.5) for cancers of lung, upper aerodigestive tract and bladder combined, 16 and an eight-fold in the risk (OR 8.7; 95% CI, 4.0–18.9) of all upper digestive tract cancers (including a 12-fold risk for oral and seven-fold risk for pharyngeal cancer). Pipe smokers who are also heavy alcohol drinkers have a massive 38-fold increased risk of these cancers (OR 38.8; 95% CI, 13.6–110.9) as compared to never smokers and light drinkers, strongly suggesting that pipe smoking and heavy alcohol drinking may interact in a way that greatly increases the risks.26
As with cigarette smoking, the risk of developing tobacco-caused disease varies in a dose–response relationship, disease risk increasing with the amount smoked, the depth to which it is inhaled and the duration of smoking. For most disease entities, the relative risk of developing tobacco-related disease declines with quitting, increased length of time of cessation and younger age at quitting.27
Disease patterns differ from those observed in cigarette smokers because pipe smokers tend to inhale the smoke less deeply, taking up nicotine through the mucous membranes lining of the mouth instead of predominantly via the lungs. Some earlier studies suggested the possibility of some harm reduction benefits in switching from cigarette to pipe smoking.16 It was suggested that the magnitude of the extra risk was smaller if people had switched to cigars or pipes only (i.e. quit cigarettes) and had not compensated with greater smoking intensity. However it should be noted that recent research has found that men who switched from cigarettes only to pipe only had a risk that was not significantly different from the risk in sustained smokers of cigarettes only,24 so that the overall main conclusion about pipe smoking is that it is very hazardous and is certainly not a safe alternative to cigarette smoking.
3.27.5 Waterpipe smoking
Using a waterpipe to smoke tobacco is not a safe alternative to cigarette smoking.28 Secondhand smoke from waterpipe tobacco use produces a similar level of air pollutants as cigarettes, and poses a serious health risk to those exposed.5,28,29 Names for waterpipe vary and include 'narghile', 'arghile', 'shisha', 'goza', 'hubble bubble' and 'hookah'.30 Waterpipe smoking use spread through the Middle East and Asia, and waterpipes were widely used in Turkey during the Ottoman Empire (15th century), Iran, Lebanon, Syria, Jordan, Greece, India, Pakistan, Palestine, Egypt and Saudi Arabia. As people immigrated to Europe from India, Pakistan, Northern Africa and the Middle East, hookahs and hookah cafes began appearing in European cities. Today, hookah bars and cafés are popular in many parts of Britain, France, Spain, Russia, India, Asia and throughout the Middle East and are growing in popularity in the US,3 with some estimates that about one billion people worldwide are waterpipe users.31
Waterpipe apparatus varies widely in design, but the method of use requires the heating with burning charcoal of moist tobacco (usually sweetened and flavoured) to produce smoke, which is passed through water before being inhaled via a mouthpiece on the end of a hose.4,5 Electronically heated systems have also been developed in recent years, but the effects of these on smokers and the environment have not been well-studied.32 Waterpipe smoking usually occurs in a social setting with a number of participants seated around the waterpipe, taking it in turns to inhale. The availability of pre-moistened, shaped and flavoured tobacco made especially for waterpipe use (‘Maassel’) since the 1990s is likely to have contributed to a resurgence in waterpipe smoking in the Eastern Mediterranean Region, and its increased popularity.5,33 At least in some cultures, women and girls are more likely to use a waterpipe than to use other forms of tobacco, and it is popular among younger smokers. Because the smoke passes through a reservoir of water, waterpipe smoking may erroneously34 be perceived as being less lethal than other methods of tobacco use.5,30,35 Although the moist smoke produced by waterpipe smoking may be more palatable than cigarette smoke,4 many of the harmful gases and chemicals found in cigarette smoke are present in equal or even greater amounts in waterpipe smoke, including carbon monoxide, nicotine and heavy metals.5 Waterpipe smokers are typically exposed to smoke over a longer period than cigarette smokers, a session lasting somewhere between 45 minutes to an hour, but some sessions may continue for many hours.4 Although waterpipe smokers do not usually smoke as frequently as do cigarette smokers,35.36 it has been estimated that during a typical session, a waterpipe smoker inhales more than 100 times the volume of smoke produced by smoking a single cigarette.28
A systematic review was conducted by Akl and colleagues to examine the effects of waterpipe tobacco smoking on health outcomes. While the quality of available studies was poor, the researchers found that waterpipe smoking of tobacco was significantly associated with a doubling, respectively, in the risks of lung cancer (OR 2.12; 95% CI, 1.32– 3.42), respiratory illness (OR 2.3; 95% CI, 1.1– 5.1), low birthweight (OR 2.12; 95% CI, 1.08– 4.18), and at least a trebling in the risk of periodontal disease (OR = 3–5).37
Another recent systematic review and meta-analysis of six cross-sectional studies was conducted to examine the effects of waterpipe tobacco smoking on lung function compared with no smoking.
Despite methodological limitations in the reviewed studies, the authors were able to conclude that waterpipe smoking of tobacco negatively affects lung function, may be as harmful as cigarette smoking and is likely to be a cause of COPD.6 Research into the acute effects of waterpipe smoking on the cardiorespiratory system has been reported. Forty-five similarly sized volunteers (including 30 men) were studied after a single 30-minute domestic open-air group-smoking session of waterpipe smoking. Carboxyhaemoglobin levels were significantly raised post-waterpipe smoking, especially in women. Three of 45 subjects demonstrated carboxyhaemoglobin concentrations varying between 20% and 26%, high enough levels for consideration of inpatient treatment in susceptible individuals. Blood pressure, heart rate, and respiratory rate were all significantly increased post-waterpipe smoking. The authors concluded that one session of waterpipe smoking causes acute biologic changes that might result in marked health problems.38
Accumulating evidence of the health effects associated with waterpipe smoking now makes a compelling case that there are serious risks for those exposed, that is in no way a safe alternative to cigarette smoking and that its spread among young people represents a global problem.39 Associations with lung cancer, respiratory illness, low birthweight, periodontal disease,37 impaired lung function,6 and acute cardiorespiratory effects40 have been noted. There is evidence that waterpipe smoke contains many of the same toxicants as cigarette smoke, including those that cause cardiovascular disease (e.g. carbon monoxide), lung disease (e.g. volatile aldehydes), cancer (e.g. polycyclic aromatic hydrocarbons) and dependence (i.e. nicotine).41 Waterpipe smoking is an efficient means of delivering toxicants to the smoker; for example, recent research reveals that, relative to a single cigarette, a single waterpipe session exposes the smoker to 3–9 times the carbon monoxide and 1.7 times the nicotine.42 WPS is associated with features of dependence, such as drug-seeking behaviour, inability to quit despite repeated attempts, and abstinence- induced withdrawal that is suppressed by subsequent waterpipe use.43 Sharing the waterpipe, a popular practice among youth worldwide, can be associated with infectious disease risks, such as tuberculosis.44,45 Waterpipe smoking-related emissions can harm non-smokers; for example, studies have shown that waterpipe smoking generates high levels of toxicants/carcinogens (e.g. volatile organic compounds, polycyclic aromatic hydrocarbons, metals, carbon monoxide and particulate matter) in the surrounding air, putting non-smokers at risk.46,47 Finally, evidence suggests that waterpipe smoking can undermine tobacco control, because it can be used as a replacement for cigarettes among quitters or serves as a gateway to cigarette initiation.44
3.27.6 Kreteks
Kreteks are cigarettes that contain a combination of cloves and clove oil, tobacco and other additives. Originating in Indonesia, where they account for about 90% of the market,27 a small number of brands are currently imported into Australia.
Although kreteks are smaller than typical cigarettes, they can deliver similar levels of nicotine and carbon monoxide to smokers.28 Gas chromatographic analysis of kreteks has revealed high levels of eugenol, anethole and coumarin compounds. The authors of one such study noted that compounds such as eugenol are known to be hazardous to humans when inhaled in high concentrations, and pose significant health concerns. The researchers concluded that usage of such compounds in smoking products, particularly at high levels, should be discouraged pending the availability of detailed toxicity information.29 Another analysis found that the levels of these compounds found in kreteks are significantly higher than those typically found in commercial cigarette brands.30 Long-term research on the health effects of smoking kreteks is scant, but it can be reasonably assumed that they pose at least the same dangers to health as conventional cigarettes. Popular use of these cigarettes in the US commenced in about 1980; by the mid-1980s warnings had begun to appear in the literature, notably so when 13 cases of severe illness with clove cigarette smoking were reported to the Centers for Disease Control and the California Department of Health Services; the clinical characteristics of these cases included haemorrhagic pulmonary oedema, pneumonia, bronchitis and hemoptysis (spitting up or coughing up of blood).31
Research from Indonesia has shown that regular kretek smokers have 13‒20 times the risk of abnormal lung function than non-smokers.32 Kretek use is associated with a higher risk of acute lung injury, particularly in susceptible individuals such as those with asthma or respiratory infections.33 There is also evidence that clove cigarettes are linked with greatly increased risk of dental disease. In a longitudinal study of more than 1000 male bus drivers in Jakarta, 27% of those who had smoked for 10 years or less had dental caries. This proportion increased to 79.6% among those smoking for 11–15 years and rose to 89.3% among those smoking for more than 15 years. People who smoked 7–12 cigarettes a day were more than twice as likely (RR 2.66, p<0.0001) to develop dental caries compared to those smoking 0–6 cigarettes a day. Those categorised as smoking either 13–18 cigarettes a day (RR 3.19, p<0.0001]) or more than 18 cigarettes a day (RR 2.96, p<0.0001) were three times more likely to do so.34
As previously noted, cloves contain a substance called eugenol, which when inhaled has the characteristics of a local anaesthetic. In the past this attribute has lent kreteks a reputation as soothing for sore throats and asthma,27 but in fact it can reduce the gag reflex, leading to pulmonary aspiration (when substances such as food or drink enter the lungs).33 The American Medical Association reviewed the medical evidence concerning clove cigarettes in 1988 and reached the following conclusions: (i) clove cigarettes are tobacco products; therefore they possess all the harms associated with smoking tobacco cigarettes; and (ii) inhaling clove cigarette smoke has been associated with severe lung injury in a few susceptible persons. People with asthma or with a throat or lung infection in its early stages may have an increased risk of harm from inhaling clove cigarette smoke.33
Kreteks are used by 2.4% of high school and 1.2% of middle school students in the US.35 Consumption patterns in Australia are not known.
3.27.7 Bidis (beedis, beedies, biris)
For information about bidis, see section 3.32.3
References
1. Australian Institute of Health and Welfare. 2010 National Drug Strategy Household Survey: survey report. Drug statistics series no. 25, AIHW cat. no. PHE 145. Canberra: AIHW, 2011. Available from: http://www.aihw.gov.au/publication-detail/?id=32212254712&libID=32212254712&tab=2
2. Auditor-General. Administration of tobacco excise. Audit report no. 55, 2001-02 Performance Audit. Canberra: Australian National Audit Office, Commonwealth of Australia, 2002. Available from: http://www.anao.gov.au/uploads/documents/2001-02_Audit_Report_55.pdf
3. American Lung Association. Tobacco Policy Trend Alert. An emerging deadly trend: waterpipe tobacco use. Washington DC: ALA, 2007. Available from: http://www.lungusa2.org/embargo/slati /Trendalert_Waterpipes.pdf
4. Knishkowy B and Amitai Y. Water-pipe (narghile) smoking: an emerging health risk behaviour. Pediatrics 2005;116(1):113-19. Available from: http://pediatrics.aappublications.org/cgi/reprint/116/1/e113.pdf
5. Maziak W, Ward KD, Afifi Soweid RA and Eissenberg T. Tobacco smoking using a waterpipe: a re-emerging strain in a global epidemic. Tobacco Control 2004;13(4):327–33. Available from: http://tc.bmjjournals.com/cgi/content/abstract/13/4/327
6. Raad D, Gaddam S, Schunemann H, Irani J, Abou Jaoude P, Honeine R, et al. Effects of waterpipe tobacco smoking on lung function: a systematic review and meta-analysis. Chest 2011;139(4):764–74. Available from: http://chestjournal.chestpubs.org/content/139/4/764.long
7. Australian Institute of Health and Welfare. National Drug Strategy Household Survey, 2013 [computer file], 2015, Australian Data Archive, The Australian National University: Canberra.
8. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
9. Aitken C, Fry TR, Grahlmann L and Masters T. Health perceptions of home-grown tobacco (chop-chop) smokers. Nicotine & Tobacco Research 2008;10(3):413-6. Available from: http://www.ncbi.nlm.nih.gov /pubmed/18324558
10. Bittoun R. 'Chop chop' tobacco smoking [Letter]. Medical Journal of Australia 2002;177(2):686-7. Available from: http://www.mja.com.au/public/issues/177_11_021202/bittoun_021202.pdf
11. Lindorff K. Tobacco–time for action. National Aboriginal and Torres Strait Islander Tobacco Control Project. Final report. Canberra: National Aboriginal Community Controlled Health Organisation, 2002. Available from: http://www.weftweb.net/naccho/Files/NACCHO_Tobacco_report.pdf
12. Bittoun R. The medical consequences of smoking 'chop chop' tobacco. Report prepared for the Commonwealth Department of Health and Ageing. Canberra: Department of Health and Ageing, 2004. Available from: http://www.health.gov.au/internet/wcms/publishing.nsf/Content/phd-pub-tobacco-chopchop- cnt.htm/$FILE/chopchop.pdf
13. Aitken C, Fry T, Farrell L and Pellegrini B. Smokers of illicit tobacco report significantly worse health than other smokers. Nicotine & Tobacco Research 2009;11(8):996–1001. Available from: http://ntr.oxfordjournals.org/content/11/8/996.full
14. National Cancer Institute. Cigars: Health effects and trends. Smoking and Tobacco Control Monographs, no. 9. Rockville, MD: National Cancer Institute, US National Institutes of Health, 1998. Available from: http://cancercontrol.cancer.gov/tcrb/monographs/9/index.html
15. Chang CM, Corey CG, Rostron BL, and Apelberg BJ. Systematic review of cigar smoking and all cause and smoking related mortality. BMC Public Health, 2015; 15(1):390. Available from: http://www.biomedcentral.com/1471-2458/15/390
16. McCormack V, Agudo A, Dahm C, Overvad K, Olsen A, Tjonneland A, et al. Cigar and pipe smoking and cancer risk in the European prospective investigation into cancer and nutrition. International Journal of Cancer 2010;127(10):2402–11. Available from: http://onlinelibrary.wiley.com/doi/10.1002/ijc.25252/pdf
17. Boffetta P, Nyberg F, Agudo A, Benhamou E, Jockel K, Kreuzer M, et al. Risk of lung cancer from exposure to environmental tobacco smoke from cigars, cigarillos and pipes. International Journal of Cancer 1999;83(6):805-6. Available from: http://onlinelibrary.wiley.com/doi/10.1002 /(SICI)1097-0215(19991210)83:6%3C805::AID-IJC18%3E3.0.CO;2-I/pdf
18. Higgins IT, Mahan CM and Wynder EL. Lung cancer among cigar and pipe smokers. Preventive Medicine 1988;17(1):116-28. Available from: http://www.ncbi.nlm.nih.gov/pubmed/3362797
19. Bertuccio P, La Vecchia C, Silverman D, Petersen G, Bracci P, Negri E, et al. Cigar and pipe smoking, smokeless tobacco use and pancreatic cancer: an analysis from the International Pancreatic Cancer Case-Control Consortium (PanC4). Annals of Oncology 2011;22(6):1420-6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21245160
20. Iodice S, Gandini S, Maisonneuve P and Lowenfels AB. Tobacco and the risk of pancreatic cancer: a review and meta-analysis. Langenbecks Arch Surg 2008;393(4):535-45. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18193270
21. Campaign for Tobacco-Free Kids. The rise of cigars and cigar-smoking harms. Factsheet. Washington, DC: CTFK, 2011. Available from: http://www.tobaccofreekids.org/research/factsheets/pdf/0333.pdf
22. Australian Institute of Health and Welfare. National Drug Strategy Household Survey, 2004, computer file, Editor. Canberra: Australian Social Science Data Archive, The Australian National University, 2005.
23. Australian Institute of Health and Welfare. 2010 National Drug Strategy Household Survey: survey report. Drug statistics series no. 25, AIHW cat. no. PHE 145.Canberra: AIHW, 2011. Available from: http://www.aihw.gov.au/publication-detail/?id=32212254712&libID=32212254712&tab=2
24. Tverdal A and Bjartveit K. Health consequences of pipe versus cigarette smoking. Tobacco Control 2011;20(2):123-30. Available from: http://tobaccocontrol.bmj.com/content/20/2/123.abstract
25. Rodriguez J, Jiang R, Johnson W, MacKenzie B, Smith L and Barr R. The association of pipe and cigar use with cotinine levels, lung function, and airflow obstruction: a cross-sectional study. Annals of Internal Medicine 2010;152(4):201–10. Available from: http://www.annals.org/content/152/4/201.long
26. Randi G, Scotti L, Bosetti C, Talamini R, Negri E, Levi F, et al. Pipe smoking and cancers of the upper digestive tract. International Journal of Cancer 2007;121(9):2049–51. Available from: http://www3.interscience.wiley.com/journal/114292030/abstract
27. Henley S, Thun M, Chao A and Calle E. Association between exclusive pipe smoking and mortality from cancer and other diseases. Journal of the National Cancer Institute 2004;96(11):853-61. Available from: http://jnci.oxfordjournals.org/cgi/reprint/96/11/853
28. World Health Organization Study Group on Tobacco Product Regulation. Advisory note. Waterpipe tobacco smoking: health effects, research needs and recommended actions by regulators. Geneva: WHO, 2005. Available from: http://www.who.int/tobacco/global_interaction/tobreg /Waterpipe%20recommendation_Final.pdf
29. Maziak W, Rastam S, Ibrahim I, Ward KD and Eissenberg T. Waterpipe-associated particulate matter emissions. Nicotine & Tobacco Research 2008;10(3):519-23. Available from: http://www.ncbi.nlm.nih.gov /pubmed/18324571
30. Maziak W, Ward KD and Eissenberg T. Interventions for waterpipe smoking cessation. Cochrane Database of Systematic Reviews 2007(4) Available from: http://www.mrw.interscience.wiley.com/cochrane /clsysrev/articles/CD005549/frame.html
31. Wolfram R, Chehne F, Oguogho A and Sinzinger H. Narghile (water pipe) smoking influences platelet function and (iso-)eicosanoids. Life Science 2003;74:47-53. Available from: http://www.ncbi.nlm.nih.gov /pubmed/14575812
32. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/
33. Rastam S, Ward K, Eissenberg T and Maziak W. Estimating the beginning of the waterpipe epidemic in Syria. BMC Public Health 2004;4(32):doi:10.1186/1471-2458-4-32. Available from: http://www.biomedcentral.com/content/pdf/1471-2458-4-32.pdf
34. Chan A and Murin S. Up in smoke: the fallacy of the harmless hookah. Chest 2011;139(4):737–8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21467052
35. Asfar T, Ward K, Eissenberg T and Maziak W. Comparison of patterns of use, beliefs, and attitudes related to waterpipe between beginning and established smokers. BMC Public Health 2005;5(19):doi:10.1186/1471-2458-5-19. Available from: http://www.biomedcentral.com/1471-2458/5/19
36. World Health Organization Regional Office for the Eastern Mediterranean. Tobacco use in shisha: studies on waterpipe smoking in Egypt. Cairo: WHO Regional Office for the Eastern Mediterranean, Egyptian Smoking Prevention Research Institute, 2006. Available from: http://www.emro.who.int/TFI/PDF/shisha.pdf
37. Akl E, Gaddam S, Gunukula S, Honeine R, Jaoude P and Irani J. The effects of waterpipe tobacco smoking on health outcomes: a systematic review. International Journal of Epidemiology 2010;39(3):834–57. Available from: http://ije.oxfordjournals.org/cgi/content/full/39/3/834?view=long&pmid=20207606
38. Hakim F, Hellou E, Goldbart A, Katz R, Bentur Y and Bentur L. The acute effects of water pipe smoking on the cardio- respiratory system. Chest 2010;139(4):775–81. Available from: http://chestjournal.chestpubs.org/content/139/4/775.long
39. Maziak W. The waterpipe--a global epidemic or a passing fad [Commentary] International Journal of Epidemiology 2010;39(3):857-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20348109
40. Hakim F, Hellou E, Goldbart A, Katz R, Bentur Y and Bentur L. The acute effects of water-pipe smoking on the cardiorespiratory system. Chest 2011;139(4):775-81. Available from: http://www.ncbi.nlm.nih.gov /pubmed/21030492
41. Shihadeh A and Saleh R. Polycyclic aromatic hydrocarbons, carbon monoxide, 'tar', and nicotine in the mainstream smoke aerosol of the narghile water pipe. Food and Chemistry Toxicology 2005;43(5):655-61. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15778004
42. Eissenberg T and Shihadeh A. Waterpipe tobacco and cigarette smoking: direct comparison of toxicant exposure. American Journal of Preventive Medicine 2009;37(6):518–23. Available from: http://www.ajpm- online.net/article/PIIS0749379709005832/fulltext
43. Maziak W, Rastam S, Ibrahim I, Ward KD, Shihadeh A and Eissenberg T. CO exposure, puff topography, and subjective effects in waterpipe tobacco smokers. Nicotine & Tobacco Research 2009;11(7):806-11. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19420278
44. Steentoft J, Wittendorf J and Andersen JR. Tuberculosis and water pipes as source of infection. Ugeskrift for Laeger 2006;168(9):904-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16513054
45. Munckhof W, Konstantinos A, Wamsley M, Mortlock M and Gilpin C. A cluster of tuberculosis associated with use of a marijuana water pipe. International Journal of Tuberculosis and Lung Disease 2003;7(9):860-5. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12971670
46. Fromme H, Dietrich S, Heitmann D, Dressel H, Diemer J, Schulz T, et al. Indoor air contamination during a waterpipe (narghile) smoking session. Food and Chemistry Toxicology 2009;47(7):1636-41. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19394392
47. Saade G, Seidenberg AB, Rees VW, Otrock Z and Connolly GN. Indoor secondhand tobacco smoke emission levels in six Lebanese cities. Tobacco Control 2010;19(2):138-42. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20378588
48. Maziak W. The waterpipe: time for action. Addiction 2008;103(11):1763-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18778388
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.28 Health 'benefits' of smoking?
3.28 Health 'benefits' of smoking?
Last updated: March 2015 Suggested citation:Bellew, B, Greenhalgh, EM & Winstanley, MH. 3.28 Health 'benefits' of smoking? In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-28-health-benefits- of-smoking-
Important note: smoking may offer a limited degree of protection in some individuals against the development of a small number of diseases, outlined below. However this information is of little relevance to public health, given that the amount of disease that tobacco may be said to prevent is insignificant in comparison with the far greater incidence of disease caused by smoking. Smoking kills one in two of its users.1
Tobacco use confers a small degree of protection against several diseases and conditions, described in the sections below. It is estimated that in 2004–05, tobacco use prevented about 148 deaths in Australia, a very low number compared to the 15 050 deaths caused by smoking in that same year.i 2 On the basis of these figures, tobacco might be said to save about one life for every 100 deaths it causes. Moreover, there is nothing to suggest that possible protection conferred against one disease will stop a given smoker from developing another tobacco-caused disease. So, for example, an individual who may have avoided Parkinson's disease due to his or her smoking still runs a significant risk of dying from heart disease, lung cancer, or any of the multiplicity of other tobacco-caused diseases. Equally, smoking does not prevent Parkinson's disease in all smokers.
While tobacco use cannot in any way be recommended as a prophylactic for these diseases and conditions, research on the mechanisms by which smoking appears to confer a protective effect against development of certain disease processes may lead to therapeutic benefits.3
3.28.1 Ulcerative colitis
Ulcerative colitis is a serious bowel disease in which the inner lining of the colon and rectum becomes inflamed and permanently damaged.[4] Current smokers have a lower risk of developing ulcerative colitis, compared to non-smokers and ex-smokers,5 and according to the US Surgeon General, the evidence suggests that this protective relationship may be causal. A dose-response relationship has also been found, such that greater pack-years or numbers of cigarettes smoked per day were associated with a decreased risk of ulcerative colitis.6 Nicotine in tobacco smoke is thought to be the component that is most likely to affect the course of the disease.7 However, smokers have a greater risk of developing Crohn’s disease, another inflammatory disease of the bowel (see Section 3.12.2). Due to the devastating effects of tobacco use, smoking is not recommended as treatment for ulcerative colitis, even though one research study has canvassed this as an extreme possibility for ex-smokers with steroid-dependent and resistant ulcerative colitis.8 Various forms of nicotine therapy are undergoing research to evaluate any possible benefits for individuals with this bowel disease.7 3.28.2 Parkinson's disease
An association between smoking and a lower incidence of Parkinson's disease has been observed in a number of studies.9, 10 An analysis of longitudinal studies found a protective effect against Parkinson's disease for current and former smokers compared with those who had never smoked; the risk of Parkinson's disease was reduced by about half among ever smokers (RR 0.51; 95% CI, 0.43–0.61) and this protective effect was more pronounced among current smokers, where the risk was about one-third that of never smokers (RR 0.35; 95% CI, 0.26–0.47).10 Similar findings of a protective effect for Parkinson's disease were also reported from a case–control study conducted in Japan.9 Nicotine is thought to be the chemical in tobacco smoke mostly likely to be implicated in this finding, but there may be other chemicals or compounds involved.11-13 Based on data from 2004–05 we can derive theoretical estimates that about 97 deaths from Parkinson's disease are prevented by smoking in Australia annually.2 Finally, recent research also suggests that nicotine can improve compromised semantic processing in Parkinson's disease, and also influence semantic processing in healthy older individuals;14 however, the 2014 US Surgeon General’s report found that controlled trials of the effects of nicotine on cognitive function in patients with Parkin¬son’s disease are limited, with inconsistent findings.6
3.28.3 Endometrial cancer and uterine fibroids
Epidemiological studies have consistently reported that active cigarette smoking is inversely associated with developing cancer of the endometrium (the membrane lining of the uterus) in women who have reached menopause.15-16 A recent meta-analysis found that cigarette smoking was significantly associated with a reduced risk, especially so among postmenopausal women, where a 29% reduction in risk was found (RR 0.71; 95% CI, 0.65–0.78).17 Very similar results have been reported from recent studies conducted in Poland15,16 although the researchers are at pains to point out their important finding that in postmenopausal women, obesity is an important modifier of the association between cigarette smoking and the risk of endometrial cancer. The Polish researchers found that obese women showed the greatest risk reduction for current smoking (OR 0.47; 95% CI, 0.27–0.81), a finding that further underscores the need for caution in interpreting these 'favourable effects' of cigarette smoking, considering the toxic and carcinogenic effects of tobacco.16
Women who smoke may also have a decreased risk for uterine fibroids and endometriosis, but the evidence for this is not conclusive.19 Development of endometrial cancer is predominantly influenced by exposure to the hormone oestrogen, and the protection conferred by smoking is likely to be due to the 'anti-oestrogenic' effect of chemicals in tobacco smoke. This same interaction works to increase the risk among smokers of developing osteoporosis, and reaching menopause earlier than non-smokers (see Sections 3.13 and 3.6.1).19
Based on data from 2004–05 we can derive theoretical estimates that smoking may prevent the loss of about 52 lives from endometrial cancer in Australia.2 However the numbers of lives saved that can be statistically attributed to the prevention of endometrial cancer among smokers pales into insignificance compared with the numbers of deaths due to other diseases caused by tobacco use, particularly in the light of the evidence that has established that smoking causes cancer of the uterine cervix.20
3.28.4 Pre-eclampsia (hypertension in pregnancy)
Pre-eclampsia is a potentially serious condition in pregnancy in which the mother develops high blood pressure, fluid retention and abnormal kidney function. Smokers are less likely to develop pre-eclampsia than non-smokers; recent research points to the impact of smoking on the ratio of soluble fms-like tyrosine kinase-1 (sFlt-1) to placental growth factor (PlGF) as one possible pathway20, however the mechanism by which the observed protective effects occur remains poorly understood.19 A study using Swedish birth registry data on more than 600 000 births examined the effects of snuff and cigarette smoking on pre-eclampsia risk and whether changes in tobacco habits during pregnancy affected the risk of developing term pre-eclampsia. Compared with non-tobacco users, light smokers experienced a one-third reduction in risk (OR 0.66; 95% CI, 0.61–0.71) and heavy smokers a halving of risk (OR 0.51; 95% CI, 0.44–0.58) with ORs lower for term than preterm pre-eclampsia. The study found that tobacco combustion products rather than nicotine are the probable protective ingredients against pre-eclampsia in cigarette smoke and further concluded that it is smoking behaviour in the middle or late rather than in the beginning of pregnancy that seems to have the greatest effect on the risk of pre-eclampsia.21 A potential mediator of these associations might be carbon monoxide (CO), as it has vasoprotective properties, and CO and CO-releasing molecules lower soluble fms-like tyrosine kinase-1 (sFlt-1; a protein that is higher in women who develop preeclampsia) and soluble endoglobin in in vitro cultures.6
The US Surgeon General has concluded that 'the decreased risk of pre-eclampsia among smokers compared with non-smokers does not outweigh the adverse outcomes that can result from prenatal smoking' (p576).20 These conclusions are underscored by findings from a recent case–control study conducted in Canada where notwithstanding a (non-significant) reduction in the risk of pre-eclampsia, persistent smoking was also associated with a 10-fold increase in the risk of low birthweight (OR 10.2; 95% CI, 2.49–41.8) and a four-fold increase in the risk of preterm birth (OR 3.59; 95% CI, 1.06–12.1).22
3.28.5 Cognitive performance?
A meta-analysis of research into the effects of nicotine and smoking on human performance found positive effects of nicotine or smoking on six domains: (i) fine motor, (ii) alerting attention-accuracy, (iii) response time (RT), (iv) orienting attention-RT, (v) short-term episodic memory-accuracy, and (vi) working memory-RT (effect size range = 0.16 to 0.44).23 There is evidence that nicotine may stimulate immediate and sustained improvements in working memory,24 that nicotine replacement in smokers avoids cognitive impairment through direct pharmacological effects on brain neuronal activity,25 and that nicotine may improve prospective memory (the retrieval and implementation of a previously encoded intention).26 Note however that smoking in the longer term has been associated with cognitive decline–see Section 3.23.
3.28.6 Psychiatric symptoms?
The prevalence of smoking is higher among people with psychiatric conditions.27-29 The reasons for this are complex and are discussed in greater detail elsewhere (Chapter 1, Section 1.10.2 and Chapter 9, Section 9.6.4, but one motivating factor for smoking is that tobacco may be regarded by some individuals as a way of relieving unpleasant symptoms of certain types of mental illness, and could therefore be seen as helpful.28
There is evidence that the action of nicotine in enhancing mood and concentration is more pronounced in some individuals with depression and cognitive problems (issues relating to mental awareness and judgement), and also that nicotine can help relieve unwelcome side effects from medication, particularly among patients being treated with antipsychotic drugs.28 These effects may occur because of different actions of nicotine on the brain chemistry reward system, which have been observed in individuals with particular psychiatric conditions.28
It has been suggested that nicotine transiently enhances sustained attention in schizophrenia patients, and that these research findings might provide insights for the development of new treatment strategies for attention deficit and sensory disruption which occur in schizophrenia.30,31 However, in a 2012 Cochrane Review update, the authors reviewed all randomised controlled trials examining nicotine as a treatment for people with schizophrenia, and found no studies that met their inclusion criteria. Hence, there is a need for high quality research that investigates the effects of nicotine for schizophrenia.32 Limited research also suggests that nicotine might help alleviate some of the symptoms of ADHD, such as impulsiveness and memory deficits, which may explain the higher prevalence of smoking in this group.6
Higher smoking rates among the mentally ill mean that they bear a disproportionate burden of morbidity and mortality from tobacco.33 Clinical and epidemiological data indicate that cigarette smoking increases the risk for the development and maintenance of panic disorder and that cessation may be one of the relevant steps in treatment,34 while a recent case–control study suggests that smoking may be a risk factor for late-onset major depression.35 Smokers with severe mental health illnesses have been identified in the Australian National Tobacco Strategy36 as requiring specialised strategies to assist in cessation. See also Chapter 7, Section 7.19.
3.28.7 Thyroid cancer?
Some studies have suggested that smoking may be associated with a reduced risk of developing thyroid cancer,37,38 particularly for women;19 however this protective effect has not been found in all studies39 and more research is required before a definitive statement can be made.
3.28.8 Skin cancer?
Early epidemiological studies suggested a protective effect of smoking for melanoma.40-42 More recent analyses from two large prospective cohort studies provides limited evidence to suggest that smoking may reduce melanoma risk; analyses by smoking status provided inconsistent data and no clear dose–response pattern was found. This weakens the argument for a cause–effect relationship between smoking and a protective effect for melanoma.43
3.28.9 Other possible health 'benefits'
There is some evidence that smokers44 and users of smokeless tobacco45 are less likely to develop aphthous stomatitis (common mouth ulcers). One recent study found that the possible protective effect of smoking was only present when there was heavy cigarette smoking or smoking for long periods of time (>5 years) and no significant associations were found between intensity or duration of smoking and clinical severity of aphthous stomatitis lesions.46 Transient increased incidence of mouth ulcers is commonly reported by individuals on quitting smoking.47
References
1. Doll R, Peto R, Boreham J and Sutherland I. Mortality in relation to smoking: 50 years' observations on male British doctors. British Medical Journal (Clinical Research Ed.) 2004;328(7455):1519. Available from: http://www.bmj.com/cgi/content/abstract/328/7455/1519
2. Collins D and Lapsley H. The costs of tobacco, alcohol and illicit drug abuse to Australian society in 2004/05. P3 2625. Canberra: Department of Health and Ageing, 2008. Available from: http://www.nationaldrugstrategy.gov.au/internet/drugstrategy/publishing.nsf/Content/mono64/$File /mono64.pdf
3. Baron J. Beneficial effects of nicotine and cigarette smoking: the real, the possible and the spurious. British Medical Bulletin 1996;52:58-73. Available from: http://bmb.oxfordjournals.org/cgi/reprint/52/1/58
4. US National Library of Medicine. Ulcerative colitis. Bethseda, Maryland: National Center for Biotechnology Information, PubMed Health, 2010, [viewed 31 May 2011]. Available from: http://www.ncbi.nlm.nih.gov /pubmedhealth/PMH0001296/
5. De Saussure P, Clerson P, Prost P, Truong Tan N, Bouhnik Y and Rch G. Appendectomy, smoking habits and the risk of developing ulcerative colitis: a case control study in private practice setting. Gastroenterologie Clinique et Biologique.2007. 31(5):493–7 Available from: http://www.em-consulte.com//article/130201
6. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/
7. Birrenbach T and Bocker U. Inflammatory bowel disease and smoking: a review of epidemiology, pathophysiology and therapeutic implications. Inflammatory Bowel Diseases 2004;10(6):848-59. Available from: http://www.ncbi.nlm.nih.gov/pubmed/156269037. Cottone M, Georgios A and Sinagra E. Smoking therapy may be an extreme cure in exsmokers with steroid-dependent and resistant ulcerative colitis. Inflammatory Bowel Diseases.2011. [Epub ahead of print] Available from: http://onlinelibrary.wiley.com /doi/10.1002/ibd.21658/full
8. Cottone M, Georgios A and Sinagra E. Smoking therapy may be an extreme cure in exsmokers with steroid-dependent and resistant ulcerative colitis. Inflammatory Bowel Diseases.2011. [Epub ahead of print] Available from: http://onlinelibrary.wiley.com/doi/10.1002/ibd.21658/full
9. Tanaka K, Miyake Y, Fukushima W, Sasaki S, Kiyohara C, Tsuboi Y, et al. Active and passive smoking and risk of Parkinson's disease. Acta Neurologica Scandinavica 2010;122(6):377–82. Available from: http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0404.2010.01327.x/pdf
10. Allam MF, Campbell M, Hofman A, Del Castillo A and Fern√°ndez-Crehuet NR. Smoking and Parkinsons disease: systematic review of prospective studies. Movement Disorders 2004;19(6):614-21. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15197698
11. Quik M, Huang L, Parameswaran N, Bordia T, Campos C and Perez X. Multiple roles for nicotine in Parkinson's disease. Biochemical Pharmacology 2009;78(7):677–85. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19433069
12. Quik M, O'Leary K and Tanner C. Nicotine and Parkinson's disease: implications for therapy. Movement Disorders 2008;23(12):1641–52. Available from: http://onlinelibrary.wiley.com/doi/10.1002/mds.21900/pdf
13. Quik M. Smoking, nicotine and Parkinson's disease. Trends in Neurosciences 2004;27:561-8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15331239
14. Holmes A, Copland D, Silburn P and Chenery H. Nicotine effects on general semantic priming in Parkinson's disease. Experimental and Clinical Psychopharmacology 2011;[Epub ahead of print] Available from: http://www.ncbi.nlm.nih.gov/pubmed/21480732
15. Yang HP, Brinton LA, Platz EA, Lissowska J, Lacey JV, Jr., Sherman ME, et al. Active and passive cigarette smoking and the risk of endometrial cancer in Poland. European Journal of Cancer 2010;46(4):690-6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20036529
16. Polesel J, Serraino D, Zucchetto A, Lucenteforte E, Dal Maso L, Levi F, et al. Cigarette smoking and endometrial cancer risk: the modifying effect of obesity. European Journal of Cancer Prevention 2009;[Epub ahead of print] Available from: http://www.ncbi.nlm.nih.gov/pubmed/19609212
17. Zhou B, Yang L, Sun Q, Cong R, Gu H, Tang N, et al. Cigarette smoking and the risk of endometrial cancer: a meta-analysis. The American Journal of Medicine 2008;121(6):501–8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18501231
18. Al-Zoughool M, Dossus L, Kaaks R, Clavel-Chapelon F, Tjønneland A, Olsen A, et al. Risk of endometrial cancer in relationship to cigarette smoking: results from the EPIC study. International Journal of Cancer 2007;121(12):2741–7. Available from: http://www3.interscience.wiley.com/journal/114297277 /abstract?CRETRY=1&SRETRY=0
19. US Department of Health and Human Services. Women and smoking. A report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health. Atlanta, Georgia, 2001. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/sgr_2001 /index.htm
20. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
21. Jeyabalan A, Powers R, Durica A, Harger G, Roberts J and Ness R. Cigarette smoke exposure and angiogenic factors in pregnancy and preeclampsia. American Journal of Hypertension 2008;21(8):943–7. Available from: http://www.nature.com/ajh/journal/v21/n8/full/ajh2008219a.html
22. Wikstrom A, Stephansson O and Cnattingius S. Tobacco use during pregnancy and preeclampsia risk. Effects of cigarette smoking and snuff. Hypertension 2010;55(5):1254–9. Available from: http://hyper.ahajournals.org/cgi/content/full/55/5/1254
23. Xiong X, Zhang J and Fraser W. Quitting smoking during early versus late pregnancy: the risk of preeclampsia and adverse birth outcomes. Journal of Obstetrics and Gynaecology Canada 2009;31(8):702–7. Available from: http://www.sogc.org/jogc/abstracts/full/200908_Obstetrics_1.pdf
24. Heishman S, Kleykamp B and Singleton E. Meta-analysis of the acute effects of nicotine and smoking on human performance. Psychopharmacology 2010;210(4):453–69. Available from: http://www.ncbi.nlm.nih.gov /pubmed/20414766
25. Castner S, Smagin G, Piser T, Wang Y, Smith J, Christian E, et al. Immediate and sustained improvements in working memory after selective stimulation of alpha7 nicotinic acetylcholine receptors. Biological Psychiatry 2011;69(1):12–18. Available from: http://www.biologicalpsychiatryjournal.com/article /PIIS0006322310008231/fulltext
26. Beaver JD, Long CJ, Cole DM, Durcan MJ, Bannon LC, Mishra RG, et al. The effects of nicotine replacement on cognitive brain activity during smoking withdrawal studied with simultaneous fMRI/EEG. Neuropsychopharmacology 2011;[Epub ahead of print] Available from: http://www.ncbi.nlm.nih.gov/pubmed /21544072
27. Rusted J, Sawyer R, Jones C, Trawley S and Marchant N. Positive effects of nicotine on cognition: the deployment of attention for prospective memory. Psychopharmacology 2009;202((1–3)):93–102. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18815772
28. Lasser K, Boyd L, Woolhandler S, Himmelstein S, McCormick D and Bor D. Smoking and mental illness: a population-based prevalence study. Journal of the American Medical Association 2000;284(2):2606–10. Available from: http://jama.ama-assn.org/cgi/content/full/284/20/2606
29. McNeill A. Smoking and mental health: a review of the literature. London: Smokefree London Programme, 2001. Available from: http://www.ash.org.uk/html/policy/menlitrev.pdf
30. Jablensky A, McGrath J, Herrman H, Castle D, Gureje O, Morgan V, et al. People living with psychotic illness: an Australian study 1997-98. Canberra: Mental Health Branch, Commonwealth Department of Health and Aged Care, 1999.
31. Hong L, Schroeder M, Ross T, Buchholz B, Salmeron B, Wonodi I, et al. Nicotine enhances but does not normalize visual sustained attention and the associated brain network in schizophrenia. Schizophrenia Bulletin 2011;37(2):416–25. Available from: http://schizophreniabulletin.oxfordjournals.org/content /37/2/416.long
32. Conway J. Exogenous nicotine normalises sensory gating in schizophrenia; therapeutic implications. Medical Hypotheses 2009;73(2):259–62. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19328631
33. Lawrence D, Holman C and Jablensky A. Duty to care. Preventable physical illness in people with mental illness. Perth: The University of Western Australia, 2001. 34. Knuts I, Cosci F, Esquivel G, Goossens L, van Duinen M, Bareman M, et al. Cigarette smoking and 35% CO(2) induced panic in panic disorder patients. Journal of Affective Disorders 2010;124(1–2):215–8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19896718
35. Dalby R, Chakravarty M, Ahdidan J, Sorensen L, Frandsen J, Jonsdottir K, et al. Localization of white- matter lesions and effect of vascular risk factors in late-onset major depression. Psychological Medicine 2010;40(8):1389–99. Available from: http://journals.cambridge.org/action/displayAbstract?fromPage=online& aid=7826354
36. Ministerial Council on Drug Strategy. Australian National Tobacco Strategy 2004-2009. Canberra: Department of Health and Ageing, 2005. Available from: http://www.health.gov.au/internet /main/publishing.nsf/Content/tobacco-strat
37. Czarnywojtek A, Kurdybacha P, Florek E, Warmuz-Stangierska I, Zdanowska J, Zgorzlewicz M, et al. Smoking and thyroid diseases-what is new?. Przeglad Lekarski 2010;67(10):1056-60. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21355496
38. Kreiger N and Parkes R. Cigarette smoking and the risk of thyroid cancer. European Journal of Cancer 2000;36(15):1969-73. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11000579
39. Bandurska-Stankiewicz E, Aksamit-Bialoszewska E, Rutkowska J, Stankiewicz A and Shafie D. The effect of nutritional habits and addictions on the incidence of thyroid carcinoma in the Olsztyn province of Poland. Endokrynologia Polska 2011;62(2):145-50. Available from: http://www.ncbi.nlm.nih.gov/pubmed /21528477
40. Grant WB. Skin aging from ultraviolet irradiance and smoking reduces risk of melanoma: epidemiological evidence. Anticancer Research 2008;28(6B):4003–8. Available from: http://www.iiar-anticancer.org /main.php?pid=6951&id=2&ch=52&gch=&volume=28&issue=6B&show=details&page
41. Zanetti R, Loria D and Rosso S. Melanoma, Parkinson's disease and levodopa: causal or spurious link? A review of the literature. Melanoma Research 2006;16(3):201-6. Available from: http://www.ncbi.nlm.nih.gov /pubmed/16718266
42. Freedman DM, Sigurdson A, Doody MM, Rao RS and Linet MS. Risk of melanoma in relation to smoking, alcohol intake, and other factors in a large occupational cohort. Cancer Causes & Control 2003;14(9):847-57. Available from: http://www.ncbi.nlm.nih.gov/pubmed/14682442
43. Delancey JO, Hannan LM, Gapstur SM and Thun MJ. Cigarette smoking and the risk of incident and fatal melanoma in a large prospective cohort study. Cancer Causes & Control 2011;22(6):937-42. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21544529
44. Rivera-Hidalgo F, Shulman J and Beach M. The association of tobacco and other factors with recurrent aphthous stomatitis in a US adult population. Oral Diseases 2004;10(6):335-45. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15533208
45. Grady D, Ernster V, Stillman L and Greenspan J. Smokeless tobacco use prevents aphthous stomatitis. Oral Surgery, Oral Medicine, and Oral Pathology 1992;74:463-5. Available from: http://www.ncbi.nlm.nih.gov /pubmed/1408021
46. Sawair FA. Does smoking really protect from recurrent aphthous stomatitis? Therapeutic Clinical Risk Management 2010;6:573-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21151626
47. Ussher M, West R, Steptoe A and McEwen A. Increase in common cold symptoms and mouth ulcers following smoking cessation. Tobacco Control 2003;12:86-8. Available from: http://tc.bmjjournals.com /cgi/content/abstract/12/1/86 Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.29 Smoking and body weight
3.29 Smoking and body weight
Last updated: March 2015 Suggested citation:Letcher, T, Greenhalgh, EM & Winstanley, MH. 3.29 Smoking and body weight. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-29-smoking-and-body-weight
The relationship between smoking and reduced body weight is widely recognised by smokers, and generally overestimated.
3.29.1 Does smoking cause smokers to weigh less than non-smokers?
While it is true that smokers weigh, on average, less than people who have quit smoking and those who have never smoked, the effect is modest and accrues over decades of smoking.1 For example, some studies have found only a small effect for daily smoking on body weight among some groups of young smokers.2 A US longitudinal study examining the relationship between trajectories of cigarette smoking from early adolescence to young adulthood and obesity in the mid-30s has found that heavy/continuous smokers and those who started smoking in late adolescence had a significantly lower likelihood of obesity compared with nonsmokers,3 however starting smoking does not appear to be associated with short-term weight loss.1
The relationship between smoking and body weight is likely to be due to a range of effects of nicotine on the metabolism.4
It has been suggested that the typically lower body mass index (BMI) of smokers is due to higher total energy expenditure compared with never smokers.5 However, evidence regarding the relative roles of energy intake and expenditure is scant.5 Some research suggests the involvement of plasma leptin, which plays a key role in energy intake and expenditure regulation.6
There is also evidence to suggest that increased cigarette consumption among smokers can be associated with higher BMI.7 For example, a case–control study of over 1000 18–65 year olds found that for those of normal weight, smoking prevalence decreased as BMI increased.8 This trend was reversed among overweight, obese or morbidly obese individuals: smoking prevalence was significantly higher among the morbidly obese compared with those who were overweight or obese. Morbidly obese individuals were twice as likely to smoke as those of normal weight.8
It has been suggested that such findings are due to the contribution of other risk behaviours such as physical inactivity, poor nutrition and higher alcohol consumption among overweight individuals;8 for example, there is some evidence of a positive association between physical activity and smoking, significantly mediating the relationship between smoking and BMI.7
Recent research has found that while smokers tend to have a lower BMI than non-smokers, their fat distribution is more likely to be in the abdominal region (central adiposity or 'male pattern' fat distribution).1, 9 Individuals with the pattern of central fat accumulation are at greater risk of developing a range of cardiovascular1 and metabolic problems related to obesity9 including coronary artery disease.10
The association between smoking and abdominal adiposity may be dose dependent: a large cross-sectional population-based survey among Swiss people aged 35–75 years found that smokers' mean waist circumference and percentage body fat increased with cigarettes smoked per day.11 In addition, there is some evidence that adolescent smoking is associated with abdominal obesity in adulthood: Finnish research found that smoking at least 10 cigarettes daily when aged 16 to 18 years is a risk factor for adult abdominal obesity among both genders and for overweight in females.12
3.29.2 Smoking cessation and weight gain
Sustained cessation is associated with a mean weight gain of about 5–6 kg in the first year of abstinence,4, 13 an issue of concern to some smokers. However the relationship between smoking and body weight is not clear cut. A prospective study of the association between smoking and weight gain among an adult Spanish cohort found that active smokers as well as those who stopped smoking during follow-up (median period 4.2 years) experienced significantly greater weight gains than never smokers.14 For further discussion on implications for cessation, see Chapter 7, Section 7.1.2.
3.29.3 Relative contribution of smoking and obesity to morbidity
Over the last decade, obesity has come to have an equal or even greater contribution to the burden of disease than smoking, and is associated with a greater negative impact on quality of life.15 This is based on US estimates of quality-adjusted life-years (QALYs) lost due to obesity and smoking between 1993 and 2008 and is related to a population obesity increase of 85% and a smoking prevalence decrease of 18.5% among US adults over this time.15 Overall, obesity had a greater effect on morbidity than mortality, while smoking has a negative impact on mortality; this has been demonstrated among US and Western European populations.15,16 Western European data also indicate that people in higher BMI categories spend more years living with disability, whereas life expectancy with disability may not be related to smoking status.16 In Australasia, a report published in 2014 cited dietary risks (accounting for 11% of the total burden), high body mass index (9%) and smoking (8%) as the leading risk factors for disease.17
Childhood and adolescent behaviours and cardiovascular (CVD) risk factor profiles are important determinants of CVD risk factor prevalence later in life. A Finnish study following a cohort of 1809 people aged 3–18 years found the six-year progression of carotid atherosclerosis increased significantly with the number of childhood cardiovascular risk factors, including lipid levels, high blood pressure, obesity, diabetes, smoking and physical inactivity.18 A large prospective cohort study following people aged 18–26 years between 1995 and 1996 and 2001 and 2002 found that overweight and obese adolescents were more likely than those of normal weight to report a diagnosis of high blood pressure and cholesterol by the time they were young adults, regardless of BMI in young adulthood.19 Adolescent smoking and physical activity levels did not independently predict these CVD risk factors.
There is some evidence of a dose–response relationship between pregnancy smoking exposure and overweight and obesity in children. A UK cross-sectional survey of 3038 children aged 5–11 years found that overweight and obesity prevalence estimates were higher for those with mothers who smoked heavily (10+ cigarettes daily) during pregnancy.20 See Section 3.8.5 for further discussion on the long-term effects of smoking during pregnancy.
3.29.4 Smoking compared to and in combination with obesity: contribution to mortality
Since being overweight is strongly associated with many disease entities, it has also given rise to the question of whether it is better to be a leaner smoker or a heavier non-smoker. A large international study has investigated the connection between smoking, body weight and mortality from coronary heart disease.21 The study concludes that although smokers have on average a lower BMI than non-smokers, it is of nowhere near sufficient magnitude to offset the risk of dying from CVD as a result of smoking. The authors conclude that 'it is unquestionably better to quit smoking and gain weight than to continue to smoke'.(p. 834)21 Similarly, smoking appears to offset the CVD risk factor benefits associated with parental longevity such as trends towards lower BMI, weight and waist circumference observed among women in Swiss population-based research.22
Studies covering tens of thousands of deaths provide reliable evidence on mortality from persistent smoking and from adult obesity.23,24 An increase of 10% in the prevalence of smoking and of 2 BMI points in overweight populations reduce the life span in men comparably, each by about one year.23 An increase in life expectancy of about 10 years can be gained through smoking cessation, much greater than a smoker could expect to gain from weight control.23
While smoking and adiposity are independent predictors of mortality, the combination of current or recent smoking with a BMI ≥35 or a large waist circumference is related to an especially high mortality risk (5 to 8 times that of never smokers within normal weight range).25 US all-cause mortality data from 51–72 year olds indicates an increase in mortality rates with greater BMI or waist circumference, and an increase from never to former to current smoking.25 Obese smokers have a 14-year reduction in life expectancy at age 40 compared with lean non-smokers, as well as an increased risk of developing type 2 diabetes and cancer.26
The evidence regarding how smoking and obesity might interact to reduce life expectancy and the degree of interaction is not clear.26 For example, overweight or obesity in late adolescence has been found to increase the risk of all-cause adult mortality regardless of smoking status: obesity and overweight in late adolescence were as hazardous as heavy (>10 cigarettes/day) and light (1–10/day) smoking, respectively, with no interaction between BMI and smoking status.27 US research comparing the burden of mortality due to smoking, education levels and obesity in those aged 55+ years found smoking and low education decreased population life expectancy more than did obesity, with highest life expectancy at age 55 found in highly educated non-smokers, slightly higher than normal BMI.28
Among modifiable dietary, lifestyle and metabolic risk factors, smoking and high blood pressure were responsible for the largest number of deaths in the US in 2005, accounting for about 1 in 5 or 6 adult deaths.29 In comparison, overweight/obesity caused about 9% of deaths, physical inactivity and high blood glucose about 8%, and high LDL cholesterol almost 5%.29
Estimates based on Swedish national data forecast a continued decline in premature deaths among males due to reductions in smoking over the last four decades, despite large increases in overweight and obesity over this time. However, one-third of the survival benefit from reduced smoking was estimated to be offset by the parallel increase in obesity.27
Australian longitudinal research has identified central obesity and smoking as key independent risk factors predicting mortality from coronary heart disease and cardiovascular disease, with no added influence of measured lipids or blood pressure.30 When combined with cigarette smoking, waist-to-hip ratio was as effective as the Framingham risk score (incorporating the contribution of blood pressure, total cholesterol, high density lipoprotein cholesterol and diabetes) in predicting coronary heart disease and cardiovascular disease deaths.30 Similarly, US longitudinal research examining modifiable risk factors for cardiovascular disease found a low-risk profile (not smoking, moderate or high cardiorespiratory fitness, and healthy waist circumference) among men to be associated with a reduced risk of coronary heart disease, cardiovascular disease mortality and all-cause death31 while among women five lifestyle factors independently and significantly predicted mortality: 55% of deaths during follow-up were attributed to the combination of smoking, overweight, physical inactivity and poor diet; 28% of deaths were attributed to smoking.32
Some evidence suggests that natural killer (NK) cells may be a mechanism by which obesity and smoking are associated with an increased risk of malignancy and mortality.26 Crucial in mediating anti-tumour immunity, there is a marked reduction in the numbers and function of NK cells in obese individuals, and increased susceptibility of the cells to the harmful effects of cigarette smoke.26
There is a lack of agreement about how to adjust for potential confounders including smoking status in the association between body mass index (BMI) and mortality.33 Research using 50 cohort data sets from about 30 international studies to examine the relationship between BMI and mortality and any interaction with smoking status found that excluding smokers' data or disregarding smoking status did not affect the association between BMI and mortality.33 Worldwide, mean adult BMI increased between 1980 and 2008, although trends differed significantly between countries.34 In Australia, the prevalence of overweight and obesity in adults had increased to 62.8% in 2011-12, from 61.2% in 2007-08 and 56.3% in 1995.35 Obesity and smoking are significantly more common in the most disadvantaged areas. In 2007-08 almost one-fifth of people who were overweight or obese were also current smokers.
Overweight or obese smokers were twice as likely to have heart disease as people who were within the normal weight range and who had never smoked, 2.2 times as likely to have Type 2 diabetes, and 2.8 times as likely to have bronchitis.36
References
1. US Department of Health and Human Services. Women and smoking. A report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health. Atlanta, Georgia, 2001. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/sgr_2001 /index.htm
2. Sherrill-Mittleman D, Klesges R, Massey V, Vander Weg M and DeBon M. Relationship between smoking status and body weight in a military population of young adults. Addictive Behaviors 2009;34(4):400–2. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19095360
3. Brook D, Zhang C, Brook J and Finch S. Trajectories of cigarette smoking from adolescence to young adulthood as predictors of obesity in the mid-30s. Nicotine & Tobacco Research 2010;12(3):263-70. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20083648
4. Filozof C, Fernandez Pinilla MC and Fernandez-Cruz A. Smoking cessation and weight gain. Obesity Reviews 2004;5(2):95-103. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15086863
5. Bradley D, Johnson L, Zhang Z, Subar A, Troiano R, Schatzkin A, et al. Effect of smoking status on total energy expenditure. Nutrition & Metabolism 2010;7:81. Available from: http://www.nutritionandmetabolism.com/content/7/1/81
6. Koc B, Bulucu F, Karadurmus N and Sahin M. Lower leptin levels in young non-obese male smokers than non-smokers. Upsala Journal of Medical Sciences 2009;114(3):165–9. Available from: http://informahealthcare.com/doi/full/10.1080/03009730902761631?cookieSet=1
7. Dvorak R, Del Gaizo A, Engdahl R and Eliason C. Tobacco use and body mass index: mediated effects through physical inactivity. Journal of Health Psychology 2009;14(7):919–23. Available from: http://hpq.sagepub.com/cgi/reprint/14/7/919
8. Chatkin R, Mottin C and Chatkin J. Smoking among morbidly obese patients. BMC Pulmonary Medicine 2010;10(1):61. Available from: http://www.biomedcentral.com/content/pdf/1471-2466-10-61.pdf
9. Canoy D, Wareham N, Luben R, Welch A, Bingham S, Day N, et al. Cigarette smoking and fat distribution in 21 828 British men and women: a population-based study. Obesity Research 2005;13(8):1466-75. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16129730
10. Chouraki V, Wagner A, Ferrières J, Kee F, Bingham A, Haas B, et al. Smoking habits, waist circumference and coronary artery disease risk relationship: the PRIME study. European Journal of Cardiovascular Prevention and Rehabilitation 2008;15(6):625-30. Available from: http://lib.bioinfo.pl /pmid:18813130
11. Clair C, Chiolero A, Faeh D, Cornuz J, Marques-Vidal P, Paccaud F, et al. Dose-dependent positive association between cigarette smoking, abdominal obesity and body fat: cross-sectional data from a population-based survey. BMC Public Health 2011;11(1):23. Available from: http://www.biomedcentral.com /1471-2458/11/23
12. Saarni S, Pietiläinen K, Kantonen S, Rissanen A and Kaprio J. Association of smoking in adolescence with abdominal obesity in adulthood: a follow-up study of 5 birth cohorts of Finnish twins. American Journal of Public Health 2008;99(2):348-54. Available from: http://www.ajph.org/cgi/reprint/AJPH.2007.123851v1
13. Froom P, Melamed S and Benbassat J. Smoking cessation and weight gain. The Journal of Family Practice 1998;46(6):460-4. Available from: http://www.ncbi.nlm.nih.gov/pubmed/9638109
14. Basterra-Gortari F, Forga L, Bes-Rastrollo M, Toledo E, Martinez J and Martinez-Gonzalez M. Effect of smoking on body weight: longitudinal analysis of the SUN cohort. Revista Espa√±ola de Cardiologia 2010;63(1):20–7. Available from: http://www.revespcardiol.org/cardio_eng/ctl_servlet?_f=40& ident=13146849
15. Jia H and Lubetkin EI. Trends in quality-adjusted life-years lost contributed by smoking and obesity. American Journal of Preventive Medicine 2010;38(2):138–44. Available from: http://www.ajpm-online.net /article/PIIS0749379709007636/fulltext
16. Majer I, Nusselder W, Mackenbach J and Kunst A. Life expectancy and life expectancy with disability of normal weight, overweight, and obese smokers and nonsmokers in Europe. Obesity 2011;Epub ahead of print Available from: http://www.ncbi.nlm.nih.gov/pubmed/21415846
17. Australian Institute of Health and Welfare, Australia’s health 2014. Australia’s health series no. 14. Cat. no. AUS 178.2014, Canberra: AIHW.
18. Juonala M, Viikari J, Kahonen M, Taittonen L, Laitinen T, Hutri-Kahonen N, et al. Life-time risk factors and progression of carotid atherosclerosis in young adults: the Cardiovascular Risk in Young Finns study. European Heart Journal 2010;31(14):1745–51. Available from: http://eurheartj.oxfordjournals.org/content /31/14/1745.long
19. Ford CA, Nonnemaker JM and Wirth KE. The influence of adolescent body mass index, physical activity, and tobacco use on blood pressure and cholesterol in young adulthood. Journal of Adolescent Health 2008;43(6):576–83. Available from: http://linkinghub.elsevier.com/retrieve/pii/S1054-139X(08)00263-2
20. Koshy G, Delpisheh A and Brabin B. Dose response association of pregnancy cigarette smoke exposure, childhood stature, overweight and obesity. European Journal of Public Health 2010;Epub ahead of print Available from: http://eurpub.oxfordjournals.org/content/early/2010/12/01/eurpub.ckq173.long
21. The Diverse Populations Collaboration. Smoking, body weight, and CHD mortality in diverse populations. Preventive Medicine 2004;38(6):834-40. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15193906
22. Jaunin J, Bochud M, Marques-Vidal P, Vollenweider P, Waeber G, Mooser V, et al. Smoking offsets the metabolic benefits of parental longevity in women: the CoLaus study. Preventive Medicine 2008;48(3):224-31. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19138704
23. Peto R, Whitlock G and Jha P. Effects of obesity and smoking on US life expectancy. New England Journal of Medicine 2010;362(9):855–6; author reply 856–7. Available from: http://content.nejm.org /cgi/content/full/362/9/855
24. Prospective Studies Collaboration, Whitlock G, Lewington S, Sherliker P, Clarke R, Emberson J, et al. Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies. The Lancet 2009;373(9669):1083-96. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19299006
25. Koster A, Leitzmann M, Schatzkin A, Adams K, van Eijk J, Hollenbeck A, et al. The combined relations of adiposity and smoking on mortality. American Journal of Clinical Nutrition 2008;88(5):1206–12. Available from: http://www.ajcn.org/cgi/content/full/88/5/1206
26. O'Shea D, Cawood T, O'Farrelly C and Lynch L. Natural killer cells in obesity: impaired function and increased susceptibility to the effects of cigarette smoke. PLoS One 2010;5(1):e8660. Available from: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0008660
27. Neovius K, Rasmussen F, Sundstrom J and Neovius M. Forecast of future premature mortality as a result of trends in obesity and smoking: nationwide cohort simulation study. European Journal of Epidemiology 2010;25(10):703-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20602251
28. Reuser M, Bonneux L and Willekens F. The burden of mortality of obesity at middle and old age is small. A life table analysis of the US Health and Retirement Survey. European Journal of Epidemiology 2008;Epub ahead of print Available from: http://www.springerlink.com/content/h635k22060x47881/
29. Danaei G, Finucane M, Lin J, Singh G, Paciorek C, Cowan M, et al. National, regional, and global trends in systolic blood pressure since 1980: systematic analysis of health examination surveys and epidemiological studies with 786 country-years and 5.4 million participants. The Lancet 2011;377(9765):568–77. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21295844
30. Dhaliwal SS and Welborn TA. Central obesity and cigarette smoking are key determinants of cardiovascular disease deaths in Australia: a public health perspective. Preventive Medicine 2009;Epub ahead of print. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19660494
31. Lee C, Sui X and Blair S. Combined effects of cardiorespiratory fitness, not smoking, and normal waist girth on morbidity and mortality in men. Archives of Internal Medicine 2009;169(22):2096–101. Available from: http://archinte.ama-assn.org/cgi/content/full/169/22/2096
32. van Dam R, Li T, Spiegelman D, Franco O and Hu F. Combined impact of lifestyle factors on mortality: prospective cohort study in US women. British Medical Journal 2008;337(a1440):1–8 Available from: http://www.bmj.com/cgi/content/full/337/sep16_2/a1440
33. Durazo-Arvizu R and Cooper R. Issues related to modeling the body mass index-mortality association: the shape of the association and the effects of smoking status. International Journal of Obesity (2005) 2008;32(suppl. 3):S52–S55. Available from: http://www.nature.com/ijo/journal/v32/n3s/full/ijo200886a.html
34. Finucane M, Stevens G, Cowan M, Danaei G, Lin J, Paciorek C, et al. National, regional, and global trends in body-mass index since 1980: systematic analysis of health examination surveys and epidemiological studies with 960 country-years and 9.1 million participants. The Lancet 2011;377(9765):557–67. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21295846
35. Australian Bureau of Statistics, Overweight and obesity, in 4364.0.55.003 - Australian Health Survey: Updated Results, 2011-2012 2013.
36. Australian Bureau of Statistics, Smoking, risky drinking, and obesity, in 4102.0 - Australian Social Trends, Dec 20092009.
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.30 Deaths attributable to tobacco by disease category
3.30 Deaths attributable to tobacco by disease category
Last updated: 2011 Suggested citation: Winstanley, MH. 3.30 Deaths attributable to tobacco by disease category. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2011. Available from http://www.tobaccoinaustralia.org.au/3-30-deaths-attributable-to-tobacco- by-disease-cat
Three studies conducted in the mid-2000s have estimated the numbers of deaths caused by tobacco use in Australia;1-3.i Some of the key findings are presented in this section.
3.30.1 Estimated mortality from tobacco use in Australia in 2004–05—the Department of Health and Ageing, 2007
The most recent estimates of deaths caused by tobacco use show that almost 15 000 people died due to tobacco use in the financial year 2004–05.1 These calculations are the most recent in a series,2, 4, 5 the first of which was published in 1990.6 The methodology used in these reports has calculated 'attributable fractions' for the proportion of deaths due to specific diseases which can be said to have been caused by tobacco, based on extensive literature reviews and developed progressively since the first publication.
By this methodology, it has been estimated that in 2004–05, tobacco use caused a total of 14 901 deaths.1 Of these deaths, 14 790 were attributable to active smoking (including 56 deaths in infants subjected to maternal smoking) and 113 occurred in adults due to exposure to secondhand smoke (Table 3.30.1).1 As discussed in Section 3.28, smoking also confers a protective effect against a small number of diseases. It is estimated that in 2004–05, smoking prevented death from these specific diseases in 148ii smokers. However it should be noted that prevention of one kind of disease in a certain individual does not confer immunity against other diseases caused by smoking in the same individual; smokers do still die from these specific diseases; and there is no sound medical basis for taking up or continuing smoking in order to prevent or ameliorate the process of any disease.
Table 3.30.1 Estimated deaths caused or prevented by active smoking and secondhand smoke in Australia in 2004–05 according to condition (DoHA* calculations)
Male Female All Condition deaths deaths deaths Active smoking Oropharyngeal cancer 214 81 295 Male Female All Condition deaths deaths deaths Oesophageal cancer 360 152 512 Stomach cancer 39 15 54 Pancreatic cancer 208 198 406 Laryngeal cancer 125 19 144 Lung cancer 4164 1892 6057 Cervical cancer 0 30 30 Endometrial cancer 0 -52 -52 Bladder cancer 214 108 321 Kidney cancer 237 169 407 Ischaemic heart disease 1282 361 1643 Chronic obstructive pulmonary disease 2226 1644 3870 Tobacco abuse 51 40 91 Parkinson's disease -91 -6 -97 Pulmonary circulation disease 72 97 169 Cardiac dysrhythmias 38 21 59 Heart failure 81 43 124 Stroke 338 215 554 Peripheral vascular disease 38 21 59 Lower respiratory tract infection 58 30 89 Crohn's disease 1 1 2 Ulcerative colitis 0 1 1 Antepartum haemorrhage 3 2 5 Low birthweight 8 4 12 SIDS 8 3 11 Fire injuries 12 12 24 Asthma (under 15 years) 0 0 0 Macular degeneration 0 0 0 Otitis media 0 0 0 Total deaths from active smoking 9686 5101 14790 Secondhand smoke (deaths in adults only) Lung cancer 2 9 12 Ischaemic heart disease 33 68 101 Total adult deaths from SHS 35 77 113 Total all deaths from active smoking and exposure in adulthood to 9723 5178 14901 secondhand smoke
^Columns do not add up to totals due to rounding *Department of Health and Ageing Source: Unpublished data from research undertaken for Collins and Lapsley1
The same study also quantified deaths caused by other drug use in Australia. Table 3.30.2 shows that most drug-caused deaths in tobacco are caused by tobacco. Almost 90% of deaths due to drugs in 2004–05 were caused by smoking compared with 6% from alcohol and 5% from illicit drug use.1 Table 3.30.2 Deaths due to drugs in Australia, 2004–05
Drug Males Females Total % of Total Numbers of deaths* Tobacco 9723 5178 14 901 89 Alcohol 1206 -149^ 1057 6 Illicit drugs 583 289 872 5 Total 11 512 5318 16 830 100 *Deaths are net of protective effect conferred for some disease entities ^Alcohol was estimated to have caused 913 deaths in females, but to have prevented 1061 deaths. Source: Collins and Lapsley1
3.30.2 Estimated mortality from tobacco use, 2003–the Australian Institute of Health and Welfare (2007)
The Burden of Disease and Injury in Australia 2003,2 (discussed in Section 3.29.2 above) also quantified deaths due to tobacco use, estimating that smoking caused a total of 15 511 deaths in 2003, or more than 1 in every 10 deaths (11.7%) (Table 3.30.3). The methodology used in this study is similar to that used in the AIHW/DoHA studies described in Section 3.29.1.
Lung cancer was the leading cause of deaths due to smoking, followed by chronic obstructive pulmonary disease, coronary heart disease and stroke (Table 3.30.3). This study did not report separately on fatalities due to tobacco by age or gender. The calculations includes deaths attributable to secondhand smoke, but separate estimates for the numbers of deaths caused by active smoking and exposure to secondhand smoke are not provided.2
Table 3.30.3 Deaths attributable to tobacco by specific cause, Australia, 2003 (Burden of Disease calculations)
Specific cause Number of deaths Percentage of all tobacco-caused deaths (rounded)* Lung cancer 6309 41 COPD 4175 27 CHD 1962 13 Stroke 577 4 Oesophageal cancer 572 4 Other 1916 12 Total 15 511 *Column does not add up to 100% due to rounding. Source: Derived from Begg et al2
3.30.3 Estimated mortality from tobacco use, 2000–Peto et al methodology
Estimates of deaths caused by smoking in Australia have been calculated by Peto et al for 2000,3 using a methodology first described in 1992.7 Extrapolating from WHO mortality for lung cancer and other diseases, and using UN population data, Peto et al estimate that a total of 19 184 deaths were caused by active tobacco use in Australia in 2000 (Table 3.30.4).3 These estimates are likely to be conservative, because they do not include any deaths in individuals aged under 35 (including infants). Just under one third (about 6,000) of all deaths due to smoking occur in individuals aged between 35 and 69, who lose, on average, about 23 years of life.3
Table 3.30.4 Deaths attributable to smoking in Australia by sex, 2000, Peto et al methodology
Cause Males Females Total % of all deaths % of all deaths Number of Number of Number of % of all deaths from this from this deaths deaths deaths from tobacco disease disease caused by caused by caused by attributable to attributable to attributable to smoking smoking smoking this disease smoking smoking Lung cancer 4029 88 1720 74 5749 30 Upper aero-digestive 683 50 225 43 908 5 ca Other cancers 1393 10 307 2 1700 9 COPD 2384 67 1553 63 3937 21 Other 251 10 173 7 424 2 respiratory Vascular 2657 11 1851 7 4508 23 disease Other medical 1086 10 872 7 1958 10 All causes 12 483 19 6701 11 19 184 100
Source: Peto et al3
The robustness and wide applicability of this methodology has enabled Peto et al to expand their calculations to worldwide estimates of mortality due to tobacco.8 (See Section 3.36).
Figure 3.30.1 presents the final column from Peto et al's data shown in the table above. This pie chart shows that of all deaths due to tobacco, 44% are cancer deaths, 23% are due to heart and circulatory diseases, and a further 23% are caused by lung and other respiratory disease.
Figure 3.30.1 Deaths attributable to smoking in Australia by disease entity, as a proportion of all tobacco-caused deaths, 2000 Source: Peto et al, 20063 i This section will be updated when estimates covering more recent years are published. ii From Table 13, Collins and Lapsley.1
References
1. Collins D and Lapsley H. The costs of tobacco, alcohol and illicit drug abuse to Australian society in 2004-05. P3 2625. Canberra: Australian Government Department of Health and Ageing, 2008. Available from: http://www.nationaldrugstrategy.gov.au/internet/drugstrategy/publishing.nsf/Content/mono64/$File /mono64.pdf
2. Begg S, Vos T, Barker B, Stevenson C, Stanley L and Lopez A. The burden of disease and injury in Australia 2003. AIHW cat. no. PHE 82. Canberra: Australian Institute of Health and Welfare, 2007. Available from: http://www.aihw.gov.au/publications/index.cfm/title/10317
3. Peto R, Lopez A, Boreham J and Thun M. Mortality from smoking in developed countries 1950-2000. Australia. Oxford: Clinical Trial Service Unit and Epidemiological Studies Unit, University of Oxford, 2006. Available from: http://www.ctsu.ox.ac.uk/~tobacco/C5020.pdf
4. English D, Holman C, Milne E, Winter M, Hulse G, Codde J, et al. The quantification of drug caused morbidity and mortality in Australia, 1992. Canberra: Commonwealth Department of Human Services and Health, 1995.
5. Ridolfo B and Stevenson C. Quantification of drug-caused mortality and morbidity in Australia, 1998. Drug statistics series no. 7, AIHW cat. no. PHE-29. Canberra, Australia: Australian Institute of Health and Welfare (2001. Available from: http://www.aihw.gov.au/publications/phe/qdcmma98/
6. Holman C, Armstrong B, Arias L, Martin CA, Hatton WM, Hayward LD, et al. The quantification of drug caused morbidity and mortality in Australia 1988, Parts 1 and 2. Canberra: Commonwealth Department of Health, Housing, Local Government and Community Services, 1990.
7. Peto R, Lopez AD, Boreham J, Thun M and Heath CJ. Mortality from tobacco in developed countries: indirect estimation from national vital statistics. The Lancet 1992;339(8804):1268–78. Available from: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T1B-49K5B71-35G&_user=559483& _rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000028178&_version=1&_urlVersion=0& _userid=559483&md5=fb759ffdab48100b2337fb626258540e
8. Ezzati M and Lopez AD. Regional, disease specific patterns of smoking-attributable mortality in 2000. Tobacco Control 2004;13(4):388–95. Available from: http://tc.bmjjournals.com/cgi/content/abstract/13/4/388
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.31 Morbidity and mortality due to tobacco-caused disease and socio-economic disadvantage
3.31 Morbidity and mortality due to tobacco- caused disease and socio-economic disadvantage
Last updated: 2011 Suggested citation: Winstanley, MH. MH. 3.31 Morbidity and mortality due to tobacco-caused disease and socio-economic disadvantage. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2011. Available from http://www.tobaccoinaustralia.org.au/3-31-morbidity-and-mortality-due-to-tobacco-caused
As is the case elsewhere in the world, ill-health and rates of premature death in Australia show a clear gradient across socio-economic status (SES) groups.1–3
People who are poorer or disadvantaged in other ways generally suffer more illness and reduced quality of life and die earlier than people who are better off. The social gradient holds regardless of how socio- economic disadvantage is measured.1
People who are disadvantaged are more likely to live with multiple risks to their health. Lower socio- economic status is associated with higher rates of obesity, lack of adequate physical activity and diabetes– especially so among Indigenous communities.1,2,4
However, with or without such additional risk factors, current smokers are much less likely than non-smokers to be in good health and the incidence of numerous diseases is significantly higher among smokers and recent ex-smokers than among long-time ex-smokers and never smokers.5,6
Social differentials in smoking during pregnancy, smoking prevalence, cigarette consumption, duration of smoking and exposure to environmental tobacco smoke must contribute substantially to socio-economic differentials in health status and mortality.
This section outlines data on relative rates of poor health, disease, mortality and life expectancy across SES groups, and also presents estimates of the contribution of smoking to these health disparities.
3.31.1 Socio-economic position, reported health status and smoking
People who live in disadvantaged areas are much less likely to assess their own health as excellent or good.1, 2
Data from Australian national surveys commonly report higher rates of arthritis, chronic respiratory disease, cardiovascular disease and depression in least advantaged groups in comparison to more advantaged groups in the population.2,7–9 The rates of profound disability and type 2 diabetes in low socio-economic areas are double that of those in the highest socio-economic areas.2 In 2010, only 41% of smokers participating in the National Drug Strategy Household Survey reported their overall health as 'very good' or 'excellent', compared to 50% of ex-smokers and almost 60% of non-smokers. Ex-smokers were more likely to report diagnoses or treatment for heart disease and cancer than smokers and non-smokers. Smokers were more likely to report asthma, and twice as likely as non-smokers to have been diagnosed with, or treated for, mental illness.10
3.31.2 Socio-economic position and illnesses known to be caused by smoking
Hospitalisations for cardiovascular disease show a clear socio-economic gradient. In 2003–04 rates of hospitalisations for males in the most disadvantaged socio-economic group were 1.3 times those of males of least socio-economic disadvantage. The hospitalisation rate for the most disadvantaged females was higher again, with rates 1.4 times that of females in the least disadvantaged socio-economic group. A socio- economic gradient is evident for other chronic diseases for which smoking is a risk factor, with hospitalisations for coronary heart disease and stroke among males and females increasing as socio- economic status decreases.11
The Australian Institute of Health and Welfare has estimatedi that lung cancer was the fourth leading cause of disease among males and the seventh leading cause of disease among females in 2011. Lung cancer incidence is disproportionately high in those of lower socio-economic status in Australia, with increasing incidence of lung cancer associated with decreasing socio-economic status, across the five years 2003–2007. In the year 2008–09, the rate of hospitalisations for lung cancer was higher for those living in the lowest socio-economic areas of Australia. Those living in the lowest socio-economic areas were hospitalised for lung cancer at 1.5 times the rate of those living in areas of highest socio-economic advantage.12
Chronic kidney disease has increasingly been shown to be connected with smoking and cardiovascular disease.13, 14 It is more common in low socio-economic groups and particularly so among Indigenous Australians.2, 14
Between 2000–01 and 2007–08, hospitalisations for chronic kidney disease were highest for Australians living in the most disadvantaged areas. Hospitalisations for kidney dialysis among the lowest socio-economic group were 1.6 times the rate of those in the most advantaged group. After removing the rates for regular dialysis from all chronic kidney disease-related hospitalisations, the rates of hospitalisations among the lowest socio-economic group remained almost twice that of the most advantaged group.15
The worsening of asthma symptoms is known to be associated with active smoking and/or exposure to secondhand smoke. Smoking and asthma are both more common in those living in low socio-economic areas. The Australian Centre for Asthma Monitoring (a collaborating unit of the Australian Institute of Health and Welfare) reported that in 2007–08, not only was asthma much more common among those living in the most deprived socio-economic areas in Australia, but that rates of smoking among asthmatics in low socio- economic areas were far higher than for asthmatic smokers living in areas of higher socio-economic status (37.8% and 12.9% respectively). The disparity between the lowest and highest socio-economic group in asthma prevalence was found to have widened between survey years 2004–05 and 2007–08.16
3.31.3 Socio-economic disparities in death rates from diseases known to be caused by smoking
Australians from lower socio-economic groups have a greater proportion of chronic disease mortality burden than those living in more advantaged areas.17 This sub-section presents information on socio-economic disparities in mortality rates from diseases associated with smoking, however it is important to note the influence and interplay of other health risk factors and social and economic deprivation across a life-course, in the contribution to disease and premature mortality among the disadvantaged. Section 3.31.5 provides a detailed discussion on quantifying the contribution of smoking to socio-economic differentials in heath status; associations between childhood circumstances and health outcomes, smoking and intergenerational poverty are discussed further in Section 3.31.
The potential years of life lost (PYLL)ii due to cancer deaths in 2007 was greater among Australians living in the most disadvantaged areas (55%) compared with those living in the least disadvantaged areas (42%). A gradient across socio-economic groups was evident for cardiovascular disease, chronic respiratory disease, digestive diseases and diabetes, whereby the proportion of PYLL due to premature mortality from these diseases were represented more highly in those living in lower socio-economic areas.17
According to data compiled by the Public Health Information Development Unit in South Australia, a strong economic gradient was evident for premature mortality associated with lung cancer, with more avoidable lung cancer deaths in the most disadvantaged areas (25.9 per 100 000) compared with those in the least disadvantaged areas (15.2 per 100 000) between 2003 and 2007.18
Similar trends of a disproportionate level of mortality burden being borne among those of less socio- economic advantage have been observed in international studies.
A 24-year study of British men and women examined the relationship between socio-economic status and mortality, and the influence smoking, alcohol consumption, diet and physical activity have on mortality. In terms of all-cause mortality, those of lowest socio-economic position had 1.6 times the risk of death in comparison with those of higher socio-economic position. There was also a graded association for cardiovascular disease mortality and socio-economic position. Health risk behaviours, including smoking, were connected with mortality.19
Studies of cancer mortality in the US show disparities related to socio-economic position and also to ethnicity.20,21
3.31.4 Socio-economic disparities in health-adjusted life expectancy
As part of research on preventable causes of disease conducted for the Australian Government, researchers at the University of Queensland examined differentials in the burden of disease across socio-economic groups.6
At birth, those in the lowest socio-economic quintile could expect to die at least three years earlier than those in the highest economic quintile (79.6 compared with 82.7 years). Adjusting for ill-health, those in the lowest quintile could expect to live four years less than those in the highest quintile. By the age of 60, those in the lowest quintile could expect 15% fewer years of health-adjusted life than those in the highest quintile (Table 3.31.1).
Table 3.31.1 Life expectancy, Australia, 2003, by socio-economic quintile Health-adjusted life Health-adjusted life Life expectancy at Life expectancy expectancy at birth expectancy at age birth lost due to at birth (years) (years) 60 (years) disability (%) Socioeconomic quintile 79.6 Low 71.2 17.9 10.6 (79.4–79.7) 80.0 Moderately low 72.0 18.2 10.1 (79.9–80.2) 80.2 Average 72.2 18.4 9.9 (80.0–80.3) 81.2 Moderately high 73.6 19.3 9.4 (81.1–81.4) 82.7 High 75.5 20.6 8.7 (82.5–82.8) Difference between lowest –3.9 –6.0 –15.1 17.9 and highest (%) Source: Begg et al 20076
Researchers estimated that, for the year 2003, a total of 2 632 800 disability-adjusted life years (DALYS) were lost in Australia. DALYs were calculated for each of the five socio-economic quintiles (Table 13.3.2).
Table 3.31.2 Disability-adjusted life years lost, Australia, 2003, by socio-economic quintile, Australia, 2003
DALYs ('000) % of total
Socioeconomic quintile Low 562.5 21.4 Moderately low 564.2 21.4 Average 523.6 19.9 Moderately high 507.7 19.3 High 474.8 18.0 Total 2 632.8 100.0
Source: Begg et al 20076 DALY = disability-adjusted life year
After adjusting for age, loss rates were 31.7% higher in the lowest SES quintile than in the highest.6 Rates of burden were higher for most causes, but particularly for mental disorders and cardiovascular disease. Per head of population, rates of burden were 26.5% higher in remote areas than in major cities.3, 6
Life expectancy among Indigenous Australians is discussed in Chapter 8.
In the US, researchers examined the effects of a number of health risk factors, including smoking, on life expectancy and disparities in life expectancy in eight sub-groups of the population. Individually, smoking and high blood pressure had the most profound effect on life expectancy disparities. They found that variation of life expectancies in the eight sub-groups would decline by 18% in men and 21% in women if the health risks (smoking, blood pressure, elevated blood glucose, and adiposity or obesity) had been reduced to optimal levels.22
The Whitehall study followed more than 18 000 English males over a period of 38 years to examine life expectancy in relation to cardiovascular risk factors, which were recorded at middle age. The study reported that the presence of all three risk factors (smoking, high blood pressure and high cholesterol) at baseline (middle-age) predicted a three-fold rate of vascular mortality and about a 10-year reduced life expectancy from age 50 years, when compared with men who had none of the risk factors present at the commencement of the study.23
3.31.5 Quantifying the contribution of smoking to socio-economic differentials in health status
Estimates of the contribution of smoking to social inequality vary, likely due to differences in study methodology and datasets. Estimates may also be affected by declines in smoking prevalence in developed countries, changing social demographics, latency of disease and death associated with smoking, and the emergence of other risk factors and their contribution to disease and mortality. This section presents research across time and using differing methods to quantify the contribution of smoking to health inequalities. Section 3.31.6 explores whether the inequalities in health outcomes and life expectancy are widening.
In the UK, Jarvis and Wardle used an 'indirect method' to estimate that tobacco caused about two-thirds of the difference in risk of death across social class in men age 35–69 years.24 Prabhat Jha and colleagues reported in a four-country study (England, Wales, Poland and North America) that most social inequalities in adult male mortality during the 1990s were due to smoking.25
Bobak and colleagues reported similar results for Canada, Poland and the US, and contended that eliminating smoking would halve the social gradient in mortality among men.26 Professor Sir Michael Marmot, a public health epidemiologist and expert in health inequality, has been critical of these sorts of estimates, because some estimates have been derived by using lung cancer mortality as a proxy measure for smoking exposure, rather than using crude estimates to determine the contribution of smoking to socio- economic differences in mortality; hence they are likely to overestimate the importance of smoking.27 Authors of these studies have generally acknowledged the limits of indirect estimation.
Blakely and Wilson and colleagues used direct methods to estimate the contribution of smoking to socio- economic and ethnic inequalities in mortality in New Zealand. Between 1996 and 1999, smoking contributed 21% to the gap between men aged 45–74 years with post-school qualifications and those with none. The corresponding figure for women was 11%.28 But other work suggested that only 5–10% of the larger inequality in mortality between Māori and non-Māori individuals was due to smoking, despite large differences in smoking prevalence.29 This estimate contrasted with a much greater estimated contribution by the Ministry of Health using Jha and colleagues' indirect method.30
A study by Siahpush, English and Powles31 estimated that in Australia, smoking could account for just over one-third of the excess deaths in the 1990s that would otherwise be attributed to lower levels of education. Data on deaths among men aged 40–69 years taking part in a prospective cohort study in Melbourne between 1990 and 1994 showed that the association between education and mortality was greatly weakened after adjustment for smoking and the aetiologic fraction for low level of education was reduced from 16.5% to 10.6%.
Vallejo and colleagues used data from the National Health Survey for England to estimate the contribution of lifestyle factors–obesity and smoking–to health inequalities across social classes (classified by level of income). Their findings, released in 2010, show income as a significant contributor to health inequalities, and that obesity and smoking contribute significantly, but less profoundly, to income-related inequalities in health. Obesity and smoking were estimated to contribute 1.2% and 3.2% to inequality respectively. Despite the prevalence of smoking declining over time, its effects on inequalities have slightly increased because of its over-representation among the lowest socio-economic groups and its effects on health.32
It is likely that indirect estimates of the contribution of tobacco smoking overestimate the importance of smoking by failing to take account of higher-than-average prevalence of behavioural and other risk factors in low-SES populations. Direct methods, however, may underestimate the importance of smoking because they do not take into account the long-term impact of smoking during pregnancy and the impact of smoking and exposure to tobacco smoke on diseases other than the ones for which epidemiological data are readily available. They also may not take account of the effects of spending on tobacco products on financial security and intergenerational poverty, which may help to perpetuate continuing high smoking rates in the children of smokers. These issues are explored further in Sections 9.4 to 9.8.
Thun also discusses the difficulties in directly quantifying the contribution of smoking to disparities across social classes in a review of a study by Menvielle and colleagues,33 whose work estimated the degree to which smoking contributes to social class differences (classified by education level) in lung cancer incidences across a cohort of individuals from 10 European countries. Menvielle and colleagues concluded that smoking could account for about 50% of the inequalities in lung cancer risk due social group disparities in education. They noted these findings were unusual, and suggest residual confounding by smoking. They noted that in future studies, other risk factors in relation to smoking should be considered. Thun expressed the complexity in quantifying a direct relationship in this study because of changing demographics in Europe–the relationship between social class, smoking and lung cancer incidences have evolved and changed over time–noting, 'it is extremely difficult for Menvielle et al. to disentangle the historical and birth cohort effects of lifetime smoking on lung cancer risk from any other factors that may have contributed to risk'.34
3.31.6 Are tobacco-related differentials in health status widening?
In the US the socio-economic gap in life expectancy appears to be worsening. In people who had more than 12 years of education, life expectancy in the 1990s was about a year and a half greater than it was in the 1980s. In less educated people, life expectancy increased by only half a year. Much of the growing mortality gap can be attributed to the higher levels of decline in smoking-related diseases such as lung cancer and chronic obstructive pulmonary disease in more advantaged groups.35 Study authors attribute this to the larger declines in smoking prevalence in more advantaged compared with less advantaged groups that have been evident for some time in the US. Irvin and colleagues reported in 2009 that great disparities among socio-economic groups as well as racial groups exist for tobacco-related cancer incidences and mortality in the US. Disparities also 'exist in access to, and quality of, cancer treatment'.36
The situation for Australia is much less clear-cut.
A study published by the Australian Institute of Health and Welfare in 2006 indicated that death rates for cardiovascular disease reduced in all socio-economic groups between 1999 and 2003. There was a decrease in the size of the gap between the rates of death between upper and lower socio-economic groups for coronary heart disease and cardiovascular disease as a whole but an increase in the relative effect of disadvantage (the proportion by which the lowest socio-economic group was higher than the highest socio- economic group) for coronary heart disease, stroke and cardiovascular disease as a whole.11
In 2011, the Australian Institute of Health and Welfare reported death rates from cardiovascular disease have continued falling (based on AIHW mortality data from 2007). However, those of lower socio-economic status, the Indigenous and those living in remote areas of Australia still had the highest rates of hospitalisations and death from cardiovascular disease.37
Between 1982 and 2007, the age standardised mortality rates for lung cancer among Australian males decreased significantly, whereas mortality rates among females increased across this period. This trend is indicative of past smoking patterns. Lung cancer mortality rates for males peaked in the early 1980s, and since this time, have declined substantially; a reflection of declining smoking rates in males in the second half of the 20th century. In the case of women, females took up smoking later in the 20th century (increasing since the mid-1940s and reaching prevalence of about 33% in the mid–1970s), yet they smoked less than males. This pattern is reflected in female lung cancer mortality rates. These have been increasing over time, but more recently in the 1990s and 2000s, the increase has slowed compared with decades prior. Mortality rates from lung cancer show a clear social gradient. For the period 2003–2007, the highest mortality rates for all persons were among those living in the most disadvantaged areas in Australia. The mortality rate for males living in the least advantaged areas was 1.5 times the rate of mortality for males living in the most advantaged areas. Among females, the gap was slightly less, with 1.3 times the mortality rate in females living in the least advantaged areas compared with females living in the most advantaged areas.12 No data could be located on whether or not disparities in lung cancer mortality have widened.
Between 1979 and 2006, mortality rates between low-SES groups and high-SES groups have narrowed in absolute terms among females for ischaemic heart disease (27 to 23 per 100 000). However, absolute differences for ischaemic heart disease widened in males across this period (52 to 63 per 100 000). Absolute differences for stroke between low and high-SES groups declined in males and females (16 to 13 per 100 000 among males and 13 to 7 per 100 000 among females).
However relative declines were greater in high socio-economic groups compared with low socio-economic groups for both ischaemic heart disease (28% average five yearly decline in high socio-economic status males compared with 21% in low-SES males, and 30% and 21% for females respectively). For stroke, there was a 25% average five yearly decline in high-SES males compared with 21% in low-SES status males; 26% and 23% for females respectively).38 i Estimate projected from a 2003 baseline, derived from AIHW Burden of Disease database, see table 7.1. (p.70)12 ii Potential years of life lost (PYLL): 'an indicator of premature death. PYLL are determined by age at death and takes in to account only deaths that occur before a particular age'.17
References
1. Turrell G, and Mathers C. Socio-economic status and health in Australia. Medical Journal of Australia. 2000;172(9):434–8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10870537
2. Australian Institute of Health and Welfare. Australia's health 2010. Australia's health series no 12, AIHW cat. no. AUS 122. Canberra: AIHW, 2010. Available from: http://www.aihw.gov.au/publication-detail /?id=6442468376&tab=2
3. Begg S, Vos T, Barker DC, Stanley L, and Lopez A. Burden of disease and injury in Australia in the new millenium: measuring health loss from diseases, injuries and risk factors. Medical Journal of Australia. 2007;188(1):36-40. Available from: http://www.mja.com.au/public/issues/188_01_070108/beg10596_fm.html
4. Australian Institute of Health and Welfare. Health determinants, the key to preventing chronic disease. AIHW cat no PHE 157. Canberra: AIHW, 2011. Available from: http://www.aihw.gov.au/publication-detail /?id=10737421466&tab=2
5. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
6. Begg S, Vos T, Barker B, Stevenson C, Stanley L, and Lopez A. The burden of disease and injury in Australia 2003. AIHW cat. no. PHE 82. Canberra: Australian Institute of Health and Welfare, 2007. Available from: http://www.aihw.gov.au/publications/index.cfm/title/10317
7. Australian Bureau of Statistics. 4364.0 National Health Survey 2001: summary of results. Canberra: ABS, 2002. Available from: http://www.abs.gov.au/AUSSTATS/[email protected]/DetailsPage/4364.02001
8. Australian Bureau of Statistics. 4364.0 National Health Survey 2004-05: summary of results. Canberra: ABS, 2006. Available from: http://www.abs.gov.au/AUSSTATS/[email protected]/DetailsPage/4364.02004-05
9. Australian Bureau of Statistics. 4364.0 National Health Survey: summary of results (re-issue), 2007-08. Canberra: ABS, 2009. Available from: http://www.abs.gov.au/ausstats/[email protected]/mf/4364.0
10. Australian Institute of Health and Welfare. 2010 National Drug Strategy Household Survey: survey report. Drug statistics series no 25, AIHW cat. no. PHE 145. Canberra: AIHW, 2011. Available from: http://www.aihw.gov.au/publication-detail/?id=32212254712
11. Moon L, and Waters A. Socioeconomic inequalities in cardiovascular disease in Australia. AIHW Bulletin no. 37. Canberra: Australian Institute of Health and Welfare, 2006. Available from: http://www.aihw.gov.au /publications/index.cfm/title/10307
12. Australian Institute of Health and Welfare, and Cancer Australia. Lung cancer in Australia: an overview. Cancer series no 64, AIHW cat. no. CAN 58. Canberra: AIHW, 2011. Available from: http://www.aihw.gov.au /publication-detail/?id=10737420419&tab=2
13. Orth SR, and Hallan SI. Smoking: a risk factor for progression of chronic kidney disease and for cardiovascular morbidity and mortality in renal patients-absence of evidence or evidence of absence? Clinical Journal of the American Society of Nephrology. 2008;3(1):226-36. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18003763 14. Australian Institute of Health and Welfare. Chronic kidney disease in Australia 2005. AIHW cat. no. 65. Canberra: AIHW, 2005. Available from: http://www.aihw.gov.au/publications/index.cfm/title/10137
15. Australian Institute of Health and Welfare. Chronic kidney disease hospitalisations in Australia 2000-01 to 2007-08. AIHW cat. no. PHE 127. Canberra: AIHW, 2010. Available from: http://www.aihw.gov.au /ckd-publications/
16. Australian Centre for Asthma Monitoring. Asthma in Australia 2011. Asthma series no.4. AIHW cat. no. ACM 22. Canberra: AIHW, 2011. Available from: http://www.aihw.gov.au/publication-detail /?id=10737420159&libID
17. Australian Institute of Health and Welfare. Premature mortality from chronic disease. AIHW bulletin no 84, Cat. no. AUS 133. Canberra: AIHW, 2010. Available from: http://www.aihw.gov.au/publication-detail /?id=6442472466&tab=2
18. Public Health Information Development Unit. Monitoring Inequality in Australia, 2010. South Australia, Australia: The University of Adelaide, 2010. [viewed 7 May 2012] . Available from: http://www.publichealth.gov.au/inequality-graphs/monitoring-inequality-in-australia-australia-2010.html
19. Stringhini S, Sabia S, Shipley M, Brunner E, Nabi H, Kivimaki M, et al. Association of socioeconomic position with health behaviors and mortality. Journal of the American Medical Association. 2010;303(12):1159–66. Available from: http://jama.ama-assn.org/cgi/content/full/303/12/1159
20. Ou S, Ziogas A, and Zell J. Prognostic factors for survival in extensive stage small cell lung cancer (ED-SCLC): the importance of smoking history, socioeconomic and marital statuses, and ethnicity. Journal of Thoracic Oncology. 2009;4(1):37–43. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19096304
21. Soneji S, Iyer SS, Armstrong K, and Asch DA. Racial disparities in stage-specific colorectal cancer mortality: 1960-2005. American Journal of Public Health. 2010;100(10):1912-6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20724684
22. Danaei G, Rimm EB, Oza S, Kulkarni SC, Murray CJ, and Ezzati M. The promise of prevention: the effects of four preventable risk factors on national life expectancy and life expectancy disparities by race and county in the United States. PLoS Medicine. 2010;7(3):e1000248. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20351772
23. Clarke R, Emberson J, Fletcher A, Breeze E, Marmot M, and Shipley M. Life expectancy in relation to cardiovascular risk factors: 38 year follow-up of 19 000 men in the Whitehall study. British Medical Journal. 2009;339:b3513. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19762417
24. Jarvis MJ, and Wardle J. Social patterning of individual health behaviours: the case of cigarette smoking. In: Marmot M, and Wilkinson RG, eds. Social Determinants of Health. Oxford, UK: Oxford University Press, 1999: Available from: http://www.oxfordscholarship.com/view/10.1093/acprof:oso/9780198565895.001.0001 /acprof-9780198565895
25. Jha P, Peto R, Zatonski W, Boreham J, Jarvis M, and Lopez A. Social inequalities in male mortality, and in male mortality from smoking: indirect estimation from national death rates in England and Wales, Poland, and North America. The Lancet 2006;368(9533):367–70. Available from: http://www.thelancet.com/journals /lancet/article/PIIS0140673606689757/abstract
26. Bobak M, Jha P, Nguyen S, and Jarvis M. Poverty and smoking. In: Jha P, and Chaloupka F, eds. Tobacco control in developing countries. Oxford: Oxford University Press, 2000: Available from: http://www.ingentaconnect.com/content/els/art00112
27. Marmot M. Smoking and inequalities. The Lancet. 2006;368(9533):341–2. Available from: http://www.thelancet.com/journals/lancet/article/PIIS0140673606689769/abstract
28. Blakely T, and Wilson N. The contribution of smoking to inequalities in mortality by education varies over time and by sex: two national cohort studies, 1981–84 and 1996–99. International Journal of Epidemiology. 2005;34(5):1054–62. Available from: http://cat.inist.fr/?aModele=afficheN&cpsidt=17204007 29. Blakely T, Fawcett J, Hunt D, and Wilson N. What is the contribution of smoking and socioeconomic position to ethnic inequalities in mortality in New Zealand? The Lancet. 2006;368(9529):44–52. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16815379
30. Hunt D, Blakely T, Woodward A, and Wilson N. The smoking-mortality association varies over time and by ethnicity in New Zealand. International Journal of Epidemiology. 2005;34(5):1020–8. Available from: http://ije.oxfordjournals.org/cgi/content/full/34/5/1020
31. Siahpush M, English D, and Powles J. The contribution of smoking to socio-economic differentials in mortality: results from the Melbourne Collaborative Cohort Study, Australia. Journal of Epidemiology and Community Health. 2006;60(12):1077–9. Available from: http://jech.bmj.com/cgi/content/full/60/12/1077
32. Vallejo-Torres L, and Morris S. The contribution of smoking and obesity to income-related inequalities in health in England. Social Science & Medicine. 2010;71(6):1189-98. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20630642
33. Menvielle G, Boshuizen H, Kunst A, Dalton S, Vineis P, Bergmann M, et al. The role of smoking and diet in explaining educational inequalities in lung cancer incidence. Journal of the National Cancer Institute. 2009;101(5):321–30. Available from: http://jnci.oxfordjournals.org/content/101/5/321.long
34. Thun M. The evolving relationship of social class to tobacco smoking and lung cancer. Journal of the National Cancer Institute. 2009;101(5):285–7. Available from: http://jnci.oxfordjournals.org/cgi/reprint /101/5/285
35. Meara E, Richards S, and Cutler D. The gap gets bigger: changes in mortality and life expectancy by education, 1981-2000. Health Affairs. 2008;27(2):350–60. Available from: http://content.healthaffairs.org /cgi/content/abstract/27/2/350
36. Irvin Vidrine J, Reitzel L, and Wetter D. The role of tobacco in cancer health disparities. Current oncology reports. 2009;11(6):475–81. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19840525
37. Australian Institute of Health and Welfare. Cardiovascular disease: Australian facts 2011. Cardiovascular disease series, no. 35. AIHW cat. no. CVD 53. Canberra: AIHW, 2011. Available from: http://www.aihw.gov.au/publication-detail/?id=10737418510
38. Page A, Lane A, Taylor R, and Dobson A. Trends in socioeconomic inequalities in mortality from ischaemic heart disease and stroke in Australia,1979-2006. European journal of cardiovascular prevention and rehabilitation : official journal of the European Society of Cardiology, Working Groups on Epidemiology & Prevention and Cardiac Rehabilit. 2011;[Epub ahead of print] Available from: http://www.ncbi.nlm.nih.gov /pubmed/22007040
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.32 Health effects of smoking other substances
3.32 Health effects of smoking other substances
Last updated: March 2015 Suggested citation: Bellew, B, Greenhalgh, EM & Winstanley, MH. 3.32 Health effects of smoking other substances. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-32- health-effects-of-smoking-other-substances
This section is not intended to provide a comprehensive overview of drug use other than tobacco, but to demonstrate that the deliberate inhalation of smoke from the combustion of any matter is injurious to the health. The health effects of smoking any substance will depend on various factors, including the age at which smoking commences, the duration for which the body is exposed to the smoke, and the concentration and nature of constituents of the material smoked.
The scientific literature describing the health effects of smoking tobacco is comprehensive but the same cannot generally be said of other smoked substances, particularly where use is illegal. For example, in the case of marijuana, its illegality has militated against broad-based population studies, although data gathering has improved with its growing public acceptance (see Chapter 1, Section 1.10). Lack of adequate funding for medical and epidemiological research is a factor in some countries where smoking of substances other than tobacco may be more widespread. Another reason that these other forms of smoking have been under- researched is that the relatively small numbers of users and the scattered pattern of their geographical distribution make systematic study more challenging. Despite these issues the evidence base is sufficient to allow important conclusions on the adverse health effects of smoking these other substances on their own or in various combinations with tobacco. Here we cover the findings with regard to the smoking of herbal and other non-tobacco cigarettes, cannabis, kreteks and bidis.
3.32.1 Herbal and other non-tobacco cigarettes
Herbal and other non-tobacco cigarettes may erroneously be considered as a safer alternative to smoking, or an aid to quitting smoking, and are actively promoted as such by some manufacturers.1 However, even cigarettes that do not contain tobacco or nicotine may still produce toxic substances including carcinogens. Recent research has examined DNA damage response arising from exposure of human lung cells to smoke from tobacco- and nicotine-free cigarettes (made from lettuce and herbal extracts). This exposure led to formation of double-strand DNA breaks that are potentially carcinogenic; there was a dose–response relationship between exposure to the smoke and the severity of ensuing DNA damage response. The study concluded that smoking tobacco and nicotine-free cigarettes is at least as hazardous as smoking cigarettes containing tobacco and nicotine.2
A 2009 study conducted in China tested the claim by the tobacco industry in that country that herbal cigarettes are less harmful than regular cigarettes. Four discriminating biomarkers were analysed from urine samples provided by 135 herbal cigarette smokers and 143 regular smokers. Importantly, the researchers found a concern about their health to be one of the main reasons that smokers switched from regular to herbal cigarettes and they reported increased consumption after doing so. The researchers found no significant difference in the levels of the four biomarkers between smokers of herbal cigarettes and smokers of regular cigarettes, concluding that herbal cigarettes did not deliver less carcinogens than regular cigarettes and that the Chinese tobacco industry should avoid misleading the public by promoting herbal cigarettes as safer products.3 An analysis of 'vegetable-based cigarettes' manufactured in France and sold in Austria were found to yield levels of carbon monoxide at least as high as those produced by conventional cigarettes. Analysis of other constituents of the smoke was not made, although initial studies had shown that combustion may have produced carcinogens and other noxious chemicals.4 Investigations of a different brand of 'non-nicotine, non-tar' herbal cigarettes popular in the Philippines has also shown significant yields of tar and carbon monoxide.5 Smokers attempting to use herbal cigarettes as an adjunct to quitting are therefore exposing themselves to dangerous tar and carbon monoxide levels, without actually increasing their chance of quitting.
Cigarettes combining herbs and tobacco have been produced in China since 1959, and they are now manufactured in South Korea, Taiwan and Thailand.6 These cigarettes are commonly promoted with messages implying that they are aids in quitting, are less harmful than conventional cigarettes, or with claims for active health benefits such as raising immunity or protecting the kidneys. There is no reliable published literature to support any health claims for herbal-tobacco cigarettes,6 and at least one report (from the tobacco industry) has indicated that the tar and nicotine level of Chinese herbal-tobacco cigarettes is very high.7
3.32.2 Cannabis (marijuana, hash, ganja)
The main forms of cannabis are marijuana, hashish and hashish oil. Marijuana comprises the dried leaves, flowering tops and stems of the hemp plant Cannabis sativa. The more concentrated resin from the flowers is called hashish. Cannabis is usually smoked as a cigarette (joint) or in a pipe (bong).8 The substance in cannabis that causes the user to experience a 'high' is THC (tetrahydrocannabinol), which binds to receptors in the brain. Recent studies have reported the emergence of synthetic cannabinoids; these compounds are more potent than traditional cannabis and have been widely used to deliver products with psychoactive properties while circumventing drug legislation. As a result, authorities around the world are now beginning to exert control by either naming individual compounds or using generic legislation.9 Some early research indicates that synthetic forms of cannabis may be more likely to provoke psychosis in vulnerable individuals.10
Cannabis is the most frequently used illegal drug in Australia, with data published by the Australian Institute of Health and Welfare in 2011 indicating that about 1.9 million people had used the drug in a 12-month period. Between 2007 and 2010 the proportion of people in Australia who had used cannabis in the previous 12 months increased from 9.1% to 10.3%; among cannabis users, 20.9% said they used it once a week or more. More than half of people in Australia aged 30–39 years had used cannabis at some time in their lives, a proportion that was higher than in any other age group and was similar for both males and females. The highest proportion of males who had used cannabis in the last 12 months was for those aged 20–29 years (25%), and for females for those aged 18–19 years (19.3%). Fewer than 1 in 10 (8.8%) teenagers aged 12–17 years had used cannabis in the previous 12 months, but this proportion more than doubled to 1 in 5 (21.3%) among those aged 18–29 years.11 Continued use may lead to both physical and behavioural addiction, especially among regular, heavy users, and those who start using the substance at an earlier age.12
A comprehensive review of the adverse effects of cannabis use was recently undertaken.13 The authors of the review concluded that the effects of cannabis are dose dependent; adverse effects most frequently reported in the literature are mental slowness, impaired reaction times, and accentuation of anxiety. Users can feel dependent on cannabis, but this dependence is usually psychological. Withdrawal symptoms tend to occur within 48 hours following cessation of regular cannabis use, and include increased irritability, anxiety, nervousness, restlessness, sleep difficulties and aggression. Symptoms subside within two to 12 weeks. Serious psychological disorders have been reported with high levels of intoxication. The relationship between poor school performance and early, regular and frequent cannabis use seems to be a vicious circle, in which each sustains the other. Many research studies have examined the possible long-term effects of cannabis on memory, but results to date are inconclusive. Longitudinal studies of the influence of cannabis on depressive thoughts or suicidal ideation have yielded conflicting results and are also inconclusive. Several longitudinal studies have shown a statistical association between psychotic illness and self-reported cannabis use, but methodological problems (particularly the unknown reliability of self-reported data) make it difficult to draw definitive conclusions about causation. Therefore the question as to whether cannabis use causes psychosis cannot yet be answered conclusively because of the limitations in the current evidence.13 This latter finding is supported by another robust review of cohort studies into cannabis and psychosis, conducted by McLaren and colleagues.14 Consistent with these study findings, a 2009 systematic review by Le Bec and colleagues noted that cannabis use may be an independent risk factor for the development of psychotic disorders, with the level of risk increasing by an estimated factor of 1.2–2.8.15 Hall and Degenhardt's review, published in The Lancet in 2009, is also consistent with the studies cited above; with a focus on adverse health effects of greatest potential public health impact (those most likely to occur and to affect a large number of cannabis users) these researchers concluded that the most probable adverse effects were: (i) a dependence syndrome, (ii) increased risk of motor vehicle crashes, (iii) impaired respiratory function, (iv) cardiovascular disease, and (v) adverse effects of regular use on adolescent psychosocial development and mental health.16 Studies have concluded that the provision of advice to vulnerable individuals that cannabis may cause acute psychotic effects (especially at high doses) is appropriate.13, 15 There is evidence supporting an association between cannabis use and the development of major depression, anxiety and panic disorders.12 Cannabis use is linked to a 50% increased risk of a later depression spell (age ≥17 years) from early-onset use of cannabis (age <17 years).17 Recent Australian Institute of Health and Welfare population surveillance data provide corroborative support for these findings, noting the apparent relationship between a person's cannabis use and his or her mental health. For people in Australia aged 18 years or older, those who had reported using cannabis in the previous 12 months (18.7%) or in the previous month (20.5%) were more likely to have been diagnosed or treated for a mental illness than people who had not used it in the previous 12 month (11.3%); those who had used cannabis in the previous month (19.1%) or previous 12 months (16.3%) were more likely to report high or very high levels of psychological distress compared with those who had not recently used cannabis (9.1%).11
A systematic review conducted to assess risk of cannabis-related mortality examined the scientific literature published between 1990 and 2008; it found that evidence published to date is insufficient to assess whether the all-cause mortality rate is elevated among cannabis users in the general population. Nonetheless, case–control study evidence does suggest that some adverse health outcomes may be elevated among heavy cannabis users, namely, fatal motor vehicle accidents, and possibly respiratory and brain cancers. The evidence as to whether regular cannabis use increases the risk of suicide is unclear.18 There is evidence that babies born to women who have smoked marijuana during pregnancy have a greater probability of experiencing developmental problems, evident from early schooling through to adolescence12 and that prenatal exposure may have long-term effects, specifically on attentional skills.19
Mixing tobacco with cannabis elevates the amount of THC administered while smoking; a recent study found that tobacco increases the amount of THC inhaled per gram of cannabis from 32.70 +/– 2.29 mg/g for a 100% cannabis cigarette to 58.90 +/– 2.30 mg/g for a 25% cannabis cigarette. This indicates that tobacco increases the vaporisation efficiency of THC by as much as 45%.20 Recent laboratory studies have compared mainstream and sidestream cannabis and tobacco smoke condensates for their genotoxicity (level of damage or mutation caused to DNA). The cannabis condensates were all found to be more toxic to cells and more mutagenic than the matched tobacco condensates. For tobacco, the resulting genetic damage appeared to be dose dependent, whereas for marijuana it did not.21 Cannabis smoke contains a higher concentration of carcinogens than tobacco smoke, and because of a user's tendency to inhale deeply and hold the smoke in for longer, exposure of the lung and airways to toxic chemicals may be far greater per joint of cannabis than per typical tobacco cigarette.8, 22. Long-term, heavy users of cannabis show a higher frequency of inflammatory and pre-cancerous changes to the bronchial tubes than non-users. A recent review of the evidence concludes that there are good grounds for believing that chronic smoking of cannabis carries a significant risk of cancer.12 There is some evidence of a possible link between cannabis use and testicular cancer; in a hospital-based case–control study, patients with nonseminoma (testicular germ cell cancer) were three times more likely than controls to be frequent cannabis users (OR 3.1; 95% CI, 1.2–8.2).23 Recent research examining the possible link between cannabis use and head and neck cancers did not rule out completely the possibility of moderately increased risk; however large increases in risk levels for these specific cancers have not as yet been detected.24
Cannabis use has been linked to the development of cardiovascular symptoms, particularly in the predisposed.12 Smoking cannabis has a significant impact on lung structure and function; it causes airflow obstruction, impaired large airways function and hyperinflation (overexpansion of the lungs due to reduced elasticity), the effects worsening as the amount smoked increases. Research has shown one joint of cannabis to be equivalent to between 2.5 and 5 tobacco cigarettes in terms of airflow obstruction, probably for the most part due to differences in the way cannabis is smoked (deeper and longer inhalations), as well as the fact that a joint is generally smoked without a filter and down to a smaller butt length, and that the smoke is generated at a higher temperature.22 Cannabis smokers also experience respiratory symptoms including wheezing, coughing, phlegm production and chest tightness.22 Over the longer term, using both cannabis and tobacco has an additive effect on respiratory symptoms and lung function. This means that in users of both substances, respiratory symptoms are increased and lung function is worsened to a greater extent than if just one of the two drugs is used.25 A recent study found that concurrent use of cannabis and tobacco was associated with a two-fold risk of respiratory symptoms (OR 2.39; 95% CI, 1.58–3.62) and an almost three-fold risk of chronic obstructive pulmonary disease (OR 2.90; 95% CI, 1.53–5.51) if the lifetime dose exceeded 50 cannabis cigarettes. The research concluded that these increased risks of respiratory symptoms and of chronic obstructive pulmonary disease were related to a synergistic interaction between cannabis and tobacco.26
3.32.3 Bidis (beedis, beedies, biris)
Bidis are small, thin, hand-rolled cigarettes consisting of sun-dried and cured tobacco flakes rolled up in a piece of dried tendu or temburni leaf (from plants native to Asia). They may be flavoured with a variety of sweet or fruit essences (e.g. chocolate, cherry and mango) or unflavoured, and are secured at either end with colourful threads.36 Bidi use is most prevalent in India, Bangladesh, Nepal, Sri Lanka, Pakistan and the Maldives.37, 38 Up to 56% of men in South Asian countries smoke bidis.39 Smoke from a bidi contains 3–5 times the amount of nicotine as a regular cigarette and places users at risk for nicotine addiction.40 The compounds added to provide flavouring (such as clove, cinnamon, vanilla, cardamom, strawberry, mango, grape, lemon-lime and chocolate) are also present in high levels and may contribute to long-term damage to health, particularly in the case of cloves.41 Bidi smoking increases the risk of oral cancer,42-44 lung cancer,45-47 stomach cancer, and oesophageal cancer;39,48 is associated with a more than three-fold increased risk for coronary heart disease and acute myocardial infarction (heart attack);39, 49 is associated with a nearly four-fold increased risk for chronic bronchitis;39 and is also associated with emphysema.50 Bidi use in pregnancy is associated with perinatal mortality.51 Tobacco factory employees who hand-roll bidis are chronically exposed to potentially toxic levels of tobacco via inhalation of dust and flakes, and through the skin.39
Bidis are smoked by 2.4% of high school and 1.6% of middle school students in the US.35 Consumption patterns in Australia are not known.
References
1. Honeyrose Products. Corporate website. Ipswich, UK: Honeyrose Products, 2007 viewed 20 June 2007. Available from: http://www.honeyrose.co.uk/index.html
2. Jorgensen ED, Zhao H, Traganos F, Albino AP and Darzynkiewicz Z. DNA damage response induced by exposure of human lung adenocarcinoma cells to smoke from tobacco- and nicotine-free cigarettes. Cell Cycle 2010;9(11):2170-6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20404482
3. Gan Q, Yang J, Yang G, Goniewicz M, Benowitz N and Glantz S. Chinese 'herbal' cigarettes are as carcinogenic and addictive as regular cigarettes. Cancer Epidemiology, Biomarkers & Prevention 2009;18(12):3497–501. Available from: http://cebp.aacrjournals.org/content/18/12/3497.long
4. Groman E, Bernhard G, Blauensteiner D and Kunze U. A harmful aid to stopping smoking Letter. The Lancet 1999;353:466-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/9989723
5. Calafat AM, Polzin GM, Saylor J, Richter P, Ashley DL and Watson CH. Determination of tar, nicotine, and carbon monoxide yields in the mainstream smoke of selected international cigarettes. Tobacco Control 2004;13:45-51. Available from: http://tc.bmj.com/cgi/content/abstract/13/1/45
6. Chen A, Glantz SA and Tong E. Asian herbal-tobacco cigarettes: 'not medicine but less harmful'? Tobacco Control 2007;16:e3. Available from: http://tobaccocontrol.bmj.com/cgi/reprint/16/2/e3.pdf
7. Zimmerman C. Herbal cigarettes: blending ancient Chinese medicine. Tobacco Reporter 1991;March:29.
8. National Institute on Drug Abuse. NIDA Infofacts. Marijuana. Rockville, Maryland: US Department of Health and Human Services, 2006. Available from: http://www.drugabuse.gov/infofacts/marijuana.html
9. Hudson S and Ramsey J. The emergence and analysis of synthetic cannabinoids. Drug Testing and Analysis 2011;3(7-8):466-78. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21337724
10. Every-Palmer S. Synthetic cannabinoid JWH-018 and psychosis: an explorative study. Drug and Alcohol Dependence 2011;Epub ahead of print. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21316162
11. Australian Institute of Health and Welfare. 2010 National Drug Strategy Household Survey report. Drug statistics series no. 25, cat. no. PHE 145. Canberra: AIHW, 2011. Available from: http://www.aihw.gov.au /WorkArea/DownloadAsset.aspx?id=10737419578&libID=10737419577
12. Kalant H. Adverse effects of cannabis on health: an update of the literature since 1996. Progress in Neuro-psychopharmacology & Biological Psychiatry 2004;28(5):849–63. Available from: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TBR-4CY0JSM-2&_user=10&_rdoc=1& _fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10& md5=95a842fef02272cc8b862ad11cc89cb8
13. Adverse effects of cannabis; inform psychologically vulnerable patients of the risk of serious, dose-dependent disorders. Prescrire International 2011;20(112):18-23. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21462790
14. McLaren JA, Silins E, Hutchinson D, Mattick RP and Hall W. Assessing evidence for a causal link between cannabis and psychosis: a review of cohort studies. International Journal on Drug Policy 2010;21(1):10-19. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19783132
15. Le Bec PY, Fatseas M, Denis C, Lavie E and Auriacombe M. Cannabis and psychosis: search of a causal link through a critical and systematic review. L'Encephale 2009;35(4):377-85. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19748375
16. Hall W and Degenhardt L. Adverse health effects of non-medical cannabis use. The Lancet 2009;374(9698):1383-91. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19837255
17. de Graaf R, Radovanovic M, van Laar M, Fairman B, Degenhardt L, Aguilar-Gaxiola S, et al. Early cannabis use and estimated risk of later onset of depression spells: epidemiologic evidence from the population-based World Health Organization World Mental Health Survey Initiative. American Journal of Epidemiology 2010;172(2):149-59. Available from: http://aje.oxfordjournals.org/content/172/2/149.long
18. Calabria B, Degenhardt L, Hall W and Lynskey M. Does cannabis use increase the risk of death? Systematic review of epidemiological evidence on adverse effects of cannabis use. Drug and Alcohol Review 2010;29(3):318-30. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20565525 19. Williams JH and Ross L. Consequences of prenatal toxin exposure for mental health in children and adolescents: a systematic review. European Child & Adolescent Psychiatry 2007;16(4):243-53. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17200791
20. Van der Kooy F, Pomahacova B and Verpoorte R. Cannabis smoke condensate II: influence of tobacco on tetrahydrocannabinol levels. Inhalation Toxicology 2009;21(2):87–90. Available from: http://informahealthcare.com/doi/full/10.1080/08958370802187296
21. Maertens RM, White PA, Rickert W, Levasseur G, Douglas GR, Bellier PV, et al. The genotoxicity of mainstream and sidestream marijuana and tobacco smoke condensates. Chemical Research in Toxicology 2009;22(8):1406–14. Available from: http://pubs.acs.org/doi/abs/10.1021/tx9000286
22. Aldington S, Williams M, Nowitz M, Weatherall M, Pritchard A, McNaughton A, et al. The effects of cannabis on pulmonary structure, function and symptoms. Thorax 2007;62:1058-63. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17666437
23. Trabert B, Sigurdson AJ, Sweeney AM, Strom SS and McGlynn KA. Marijuana use and testicular germ cell tumors. Cancer 2011;117(4):848-53. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20925043
24. Berthiller J, Lee Y, Boffetta P, Wei Q, Sturgis E, Greenland S, et al. Marijuana smoking and the risk of head and neck cancer: pooled analysis in the INHANCE Consortium. Cancer Epidemiology, Biomarkers & Prevention 2009;18(5):1544–51. Available from: http://cebp.aacrjournals.org/cgi/content/full/18/5/1544
25. Taylor D and Hall W. Respiratory health effects of cannabis: position statement of the Thoracic Society of Australia and New Zealand. International Medical Journal 2003;33:310-13. Available from: http://www.thoracic.org.au/cannabispositionpaper.pdf
26. Tan W, Lo C, Jong A, Xing L, Fitzgerald M, Vollmer W, et al. Marijuana and chronic obstructive lung disease: a population-based study. Canadian Medical Association Journal 2009;180(8):814–20. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2665947/?tool=pubmed
27. Lawrence S and Collin J. Competing with kreteks: transnational tobacco companies, globalisation, and Indonesia. Tobacco Control 2004;13(suppl. 2):ii96-ii103. Available from: http://tobaccocontrol.bmj.com /cgi/reprint/13/suppl_2/ii96
28. Malson J, Lee E, Murty R, Moolchan E and Pickworth W. Clove cigarette smoking: biochemical, physiological, and subjective effects. Pharmacology, Biochemistry and Behavior 2003;74:739-45 Available from: http://www.ncbi.nlm.nih.gov/pubmed/12543240
29. Stanfill SB, Brown CR, Yan XJ, Watson CH and Ashley DL. Quantification of flavor-related compounds in the unburned contents of bidi and clove cigarettes. Journal of Agriculture and Food Chemistry 2006;54(22):8580-8. Available from: http://pubs.acs.org/doi/abs/10.1021/jf060733o
30. Polzin GM, Stanfill SB, Brown CR, Ashley DL and Watson CH. Determination of eugenol, anethole, and coumarin in the mainstream cigarette smoke of Indonesian clove cigarettes. Food and Chemistry Toxicology 2007;45(10):1948-53. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17583404
31. Guidotti TL, Laing L and Prakash UB. Clove cigarettes. The basis for concern regarding health effects. Western Journal of Medicine 1989;151(2):220-8. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles /PMC1026937/pdf/westjmed00120-0106.pdf
32. Mangunnegoro H and Sutoyo D. Environmental and occupational lung diseases in Indonesia. Respirology 1996;1:85-93. Available from: http://www.ncbi.nlm.nih.gov/pubmed/9434323
33. American Medical Association Council on Scientific Affairs. Council report: evaluation of the health hazard of clove cigarettes. Journal of the American Medical Association 1988;260:3641-4. Available from: http://www.ncbi.nlm.nih.gov/pubmed/3057254
34. Soetiarto F. The relationship between habitual clove cigarette smoking and a specific pattern of dental decay in male bus drivers in Jakarta, Indonesia. Caries Research 1999;33(3):248-50. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10207202
35. Centers for Disease Control and Prevention. Tobacco Use Among Middle and High School Students– United States, 2000–2009. Morbidity and Mortality Weekly Report 2010;59(33):1063-8. Available from: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5933a2.htm
36. Centers for Disease Control and Prevention. Bidis and kreteks. Factsheet. Atlanta, Georgia: Office on Smoking and Health, CDCP, 2011 viewed 29 July 2011. Available from: http://www.cdc.gov/tobacco /data_statistics/fact_sheets/tobacco_industry/bidis_kreteks/index.htm
37. Shafey O, Dolwick S and Guindon G. Tobacco control country profiles. Atlanta, Georgia: American Cancer Society, World Health Organization, International Union Against Cancer, 2003. Available from: http://www.cancer.org/docroot/PRO/content/PRO_1_1_Tobacco_Control_Country_Profiles.asp
38. Rahman M, Nurullah Awal AS, Fukui T and Sakamoto J. Prevalence of cigarette and bidi smoking among rickshaw pullers in Dhaka city. Preventive Medicine 2007;44(3):218-22. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17173963
39. Rahman M and Fukui T. Bidi smoking and health. Public Health 2000;114:123-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10800151
40. Delnevo CD, Pevzner ES, Hrywna M and Lewis MJ. Bidi cigarette use among young adults in 15 states. Preventive Medicine 2004;39(1):207-11. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15208004
41. Stanfill S, Calafat A, Brown C, Polzin G, Chiang J, Watson C, et al. Concentrations of nine alkenylbenzenes, coumarin, piperonal and pulegone in Indian bidi cigarette tobacco. Food and Chemical Toxicology 2003;41:303-17. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12480305
42. Pednekar MS, Gupta PC, Yeole BB and Hebert JR. Association of tobacco habits, including bidi smoking, with overall and site-specific cancer incidence: results from the Mumbai cohort study. Cancer Causes & Control 2011;22(6):859-68. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21431915
43. Jayalekshmi PA, Gangadharan P, Akiba S, Koriyama C and Nair RR. Oral cavity cancer risk in relation to tobacco chewing and bidi smoking among men in Karunagappally, Kerala, India: Karunagappally cohort study. Cancer Science 2011;102(2):460-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21129124
44. Rahman M, Sakamoto J and Fukui T. Calculation of population attributable risk for bidi smoking and oral cancer in south Asia. Preventive Medicine 2005;40(5):510-4. Available from: http://www.ncbi.nlm.nih.gov /pubmed/15749132
45. Prasad R, Ahuja RC, Singhal S, Srivastava AN, James P, Kesarwani V, et al. A case-control study of bidi smoking and bronchogenic carcinoma. Annals of Thoracic Medicine 2010;5(4):238-41. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20981185
46. Prasad R, Singhal S and Garg R. Bidi smoking and lung cancer. Bioscience Trends 2009;3(2):41–3. Available from: http://www.biosciencetrends.com/action/downloaddoc.php?docid=198
47. Jayalekshmy PA, Akiba S, Nair MK, Gangadharan P, Rajan B, Nair RK, et al. Bidi smoking and lung cancer incidence among males in Karunagappally cohort in Kerala, India. International Journal of Cancer 2008;123(6):1390-7. Available from: http://onlinelibrary.wiley.com/doi/10.1002/ijc.23618/pdf
48. Sankaranarayanan R, Duffy SW, Padmakumary G, Nair SM, Day NE and Padmanabhan TK. Risk factors for cancer of the oesophagus in Kerala, India. International Journal of Cancer 1991;49(4):485-9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/1917146
49.. Pais P, Pogue J, Gerstein H, Zachariah E, Savitha D, Jayprakash S, et al. Risk factors for acute myocardial infarction in Indians: a case-control study. The Lancet 1996;348(9024):358-63. Available from: http://www.ncbi.nlm.nih.gov/pubmed/8709733
50. Gupta PC and Asma S. Bidi smoking and public health. New Delhi: Ministry of Health and Family Services, Government of India, 2008. Available from: http://mohfw.nic.in/WriteReadData/l892s /file16-29724885.pdf
51. Centers for Disease Control and Prevention. Bidi use among urban youth-Massachusetts, March-April 1999. Morbidity and Mortality Weekly Reports 1999;48:796-9. Available from: http://www.cdc.gov /mmwr/preview/mmwrhtml/mm4836a2.htm
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.33 Health effects of chewing tobacco, and of other smokeless tobacco products
3.33 Health effects of chewing tobacco, and of other smokeless tobacco products
See Chapter 12, Section 12A.3.
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.34 Public perceptions of tobacco as a drug, and knowledge and beliefs about the health consequences of smoking
3.34 Public perceptions of tobacco as a drug, and knowledge and beliefs about the health consequences of smoking
Last updated: March 2015 Suggested citation: Purcell, K, Greenhalgh, EM & Winstanley, MH. 3.34 Public perceptions of tobacco as a drug, and knowledge and beliefs about the health consequences of smoking. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-28-health-benefits-of-smoking-
3.34.1 Australian attitudes to tobacco as a drug
Findings from the National Drug Strategy Household Survey in 2013 show that as smoking rates continue to decline, fewer people think that tobacco is the drug that causes the most deaths (decreasing from 36% in 2010 to 32% in 2013). The drug perceived to be associated with the most deaths was alcohol (34.0%), followed by tobacco (32.0%) and heroin (14.1%)—see Table 3.34.1.1
Table 3.34.1 Drugs thought either to directly or indirectly cause the most deaths in Australia, population aged 14 and over, Australia 2010 and 2013
Drug 2010 2013 Tobacco 36 32 Alcohol 30 33.6 Heroin 16 14.1 Ecstasy/designer drugs 4 4.6 Cocaine 5 3.7 Meth/amphetamine 4.7 8.7 Other illicit drugs 9 0.5
Source: NDSHS 20131
Tobacco does not rank highly as 'the drug thought to be of most serious concern for the community,' presumably reflecting the greater social disruption caused by alcohol and illegal drugs (Table 3.34.2). In 2013, among people aged 14 years or older, 42.5% thought that excessive alcohol drinking was the most concerning form of drug use for the general community. This was followed by meth/amphetamines, identified by 16.1% of people.1 Tobacco smoking ranked third, at 14.5%. Males and females had similar perceptions about which drugs they thought were the most concerning for the community, but males were more concerned about smoking (16% compared with 13%), and females were more concerned about excessive alcohol use (44% compared with 41 %).
Different age groups were concerned about different drugs, with older people more concerned with excessive alcohol use (45% for those aged 50–59 years compared with 39% for those aged 20-29 years), and younger people more concerned with tobacco use (18% for those aged 14–19 compared with about 13% for those aged 50-59).
Table 3.34.2 Form of drug use thought to be of most serious concern for the general community, population aged 14 and over, Australia 2013
Drug Tobacco 14.5 Alcohol 42.5 Heroin 10.7 Ecstasy 5.2 Meth/amphetamines 16.1 Cannabis 3.8 Cocaine 3.6 Other
Source: Derived from NDSHS 20131
Again presumably reflecting the social disruption caused by other drug use, tobacco is not a drug most likely to be associated with a 'drug problem' by most people (Table 3.34.3).1
Table 3.34.3 Drugs most likely to be associated with a 'drug problem', population aged 14 and over, Australia, 2013
% (rounded) Drug Males Females Tobacco 3 2 Alcohol 8 7 Heroin 25 26 Ecstasy 4 3 Methamphetamine 23 21 Cannabis 23 23 Cocaine 10 12
Source: Derived from NDSHS 20131
Of all drugs used in Australia, alcohol has the greatest degree of personal approval, followed by pharmaceuticals (used for non-medical purposes) and tobacco (Table 3.34.4). Not surprisingly, individuals who have used a particular drug recently are more likely to approve of its regular usage than those who have not used the drug in the preceding year.
In 2013, people aged 14 years and over in the lowest socioeconomic group approved of regular tobacco use by adults more often than those in the highest socioeconomic group (19% compared with 11%, respectively), but were less likely to approve of regular adult alcohol use than those in the highest socioeconomic group (38% compared with 51 %). People in remote or very remote areas (16%), Indigenous Australians (24%), and those who identify as homosexual or bisexual (24%) approved of regular tobacco use more than people in major cities (14%), non-Indigenous Australians (15%), and people who identify as heterosexual (14%).
Table 3.34.4 Personal approval of the regular use by an adult of selected drugs, population aged 14 and over, Australia 2013
% (rounded) Drug Males Females Tobacco 17 12 Alcohol 52 39 Cannabis 13 7 Prescription pain killers 13 13 Over the counter pain killers 13 12 Ecstasy 3 2
Source: NDSHS 20131
3.34.2 Awareness among smokers and recent quitters of damage to health caused by smoking
Most Australian smokers agree that smoking causes disease. As part of the International Tobacco Control Four Country Survey (ITC-4) in 20022, a representative sample of Australian smokers was asked whether smoking causes lung cancer, heart disease, stroke and impotence. Awareness of the first three conditions was high across groups with vary levels of education and income (Table 3.34.5).
Table 3.34.5 Knowledge of health effects of smoking, Australia smokers aged 18+, by education and income, 2002
Percentage* agreeing that smoking is a cause of:
Lung cancer Heart disease Stroke Impotence Education level Low 94 88 80 34 Medium 96 90 81 35 High 96 89 83 43 Income level Low 92 86 78 36 Medium 94 89 81 35 High 97 91 84 37 TOTAL 94 89 81 36 *Percentages rounded Source: Siahpush et al.2
In 2004, 94% of Australian smokers surveyed as part of the same study agreed that smoking caused lung cancer, 89% agreed it caused heart disease, 81% agreed it caused stroke, 36% agreed it caused impotence and 69% agreed smoking caused lung cancer in non smokers.3
Overall, of the four diseases mentioned, smokers had the highest awareness of lung cancer, followed by heart disease, stroke and impotence. Smokers with higher education and income levels tended to have a greater degree of knowledge than other smokers. Although it is widely accepted that smoking causes lung cancer, it is of concern that around 20% of smokers do not believe tobacco use causes stroke, and 10% do not think that smoking causes heart disease. Canadian smokers demonstrated the overall highest awareness of the health risks of smoking, ahead of smokers in Australia, the United Kingdom and the United States of America.2,3
As part of ongoing evaluation of the National Tobacco Campaign staged between June 1997 and December 2000, a series of national annual surveys of public awareness about the health consequences of smoking have been undertaken.4 Because the target group for the campaign was smokers aged between 18 and 40 years, the survey group studied falls within this age-range. The findings reported in the tables below do not, therefore, represent the whole population. However there is strong evidence that the advertising and promotion associated National Tobacco Campaign has had an impact on people aged under 18,5 and it is highly probable that population groups aged over 40 were also educated and influenced by the Campaign to some extent.i
Survey respondents in each year were asked whether, in their opinion, there were any illnesses caused by smoking (Table 3.34.6). If they thought that smoking did cause illness, they were asked to name the diseases. In every survey year, about 95% of respondents believed that smoking caused illness or damage to health. Highest awareness was of lung damage (especially lung cancer) and arterial illness or damage. Four out of five smokers or recent quitters spontaneously nominated smoking as a cause of lung illness or damage, and between a quarter and a third of smokers stated that smoking was a cause of arterial illness or damage. Nomination of particular disease entities varied for some of the years, probably due to timing of various campaign initiatives.4
Table 3.34.6 Unprompted awareness of illness and damage caused by smoking among smokers and people who have quit in the last year, aged 18–40, Australia 1997 to 2000
Follow-up Follow-up Follow-up Follow-up Bench-mark Smokers and recent quitters 1 2 3 4 May 1997 (percentage) Nov 1997 Nov 1998 Nov 1999 Nov 2000 (n=1192) (n=2981) (n=1647) (n=1612) (n=1675) Believe there are illnesses or damage 95 93 95 95 94 caused by smoking Specific illness mentioned Blocked blood arteries 9 13 12 12 9 Blocked blood vessels 3 6 6 6 6 Circulatory disease 4 7 5 8 5 Circulatory problems 8 11 10 12 10 Blood pressure 6 7 6 7 6 Any artery illness/damage 26 32 30 32 26 Emphysema 37 34 36 35 34 Lung damage 13 12 15 11 13 Lung cancer 64 62 61 62 66 Any lung illness/damage 80 79 79 80 80 Genetic/DNA damage 1 2 2 2 1 Heart disease 37 30 34 32 39 Cancer (unspecified) 34 34 32 37 32 Throat cancer 16 17 16 17 20 Clots in the brain - - 4 2 1 Brain damage 1 1 1 1 2 Stroke/vascular disease 3 2 8 6 5 Any brain disease 4 3 12 8 8 Eyesight damage - - - 1 2
Source: Wakefield et al4
Respondents were also asked whether or not they agreed or disagreed with particular statements made about smoking (Table 3.34.7). Compared to the previous table, which shows unprompted awareness, not surprisingly prompted awareness was much higher. About 90% of smokers and recent quitters agreed that smoking causes lung cancer, and almost as many smokers were aware that smoking causes emphysema. Agreement with statements regarding heart disease and environmental tobacco smoke increased significantly over the survey period. Statements were also offered for smokers and recent quitters to express disagreement with. Over the time period surveyed, smokers and recent quitters became significantly less likely to disagree with the notion that the health dangers of smoking have been exaggerated.4 Respondents were also more likely to resist key myths about smoking over the years surveyed. Increasing numbers of smokers and recent quitters expressed disagreement with the statements that 'smoking can't be all that bad because many people smoke all their lives and live to a ripe old age,' and 'smoking the occasional cigarette does not cause any damage to your health.'4
Table 3.34.7 Level of agreement with opinion statements about smoking and health (prompted awareness) among smokers and people who have quit in the last year, aged 18–40, Australia 1997 to 2000
Follow-up Follow-up Follow-up Follow-up Bench-mark 1 2 3 4 Smokers and recent quitters May 1997 Nov 1997 Nov 1998 Nov 1999 Nov 2000 (n=1192) (n=2981) (n=1646) (n=1611) (n=1675) Agree with opinion statements(%) 'Smoking causes lung cancer' 88 87 89 90 *na 'Smoking causes heart disease' 83 84 85 88 na 'Your smoking can harm others' 82 83 80 85 88 'Smoking causes emphysema' 86 86 86 88 na 'It would improve my health if I quit 93 93 94 95 na smoking' Disagree with opinion statements (%) 'The dangers of smoking have been 59 64 61 64 68 exaggerated' 'Smoking can't be all that bad because many people smoke all their lives and 59 61 60 62 66 live to a ripe old age' 'Smoking the occasional cigarette doesn't cause any damage to your 50 57 55 57 60 health' * statements involving specific diseases that were almost universally agreed to be caused by smoking in earlier years were not repeated in the 2000 survey. Source: Wakefield et al4
Smokers were also asked whether or not they thought they were likely to become ill from smoking if they continue to smoke. Both smokers and recent quitters were asked whether they thought they had already sustained some harm from smoking. Over the survey period, smokers became significantly more likely to agree that smoking would make them ill, and more than half of smokers and recent quitters felt that their health had already been damaged by smoking (Table 3.34.8).4 Table 3.34.8 Beliefs about personal risk of experiencing illness or harm from smoking among smokers and people who have quit in the last year, aged 18–40, 1997 to 2000 Follow-up Follow-up Follow-up Follow-up Bench-mark 1 2 3 4 Smokers and recent quitters May 1997 Nov 1997 Nov 1998 Nov 1999 Nov 2000 (n=1192) (n=2981) (n=1646) (n=1611) (n=1675) Likelihood of personally becoming ill from smoking: % of smokers agreeing 45 52 50 50 53 that it is likely Has smoking already done any harm to your body? % of smokers and recent 51 57 57 53 57 quitters agreeing that it probably has
Source Wakefield et al4
A realistic appreciation of the health risk posed by smoking to the individual helps to shape attitudes to quitting. Smokers who have an unrealistic optimism about their personal risk of avoiding illness from smoking are less likely to quit smoking.6 Attitudes to smoking are further explored in Chapter 6 and Chapter 7. i As seen by the downward trend in smoking prevalence reported in older age groups between May 1997 and November 2000, the years during which the National Tobacco Campaign ran. (See Siahpush M, Borland R. Trends in socioeconomic variations in smoking prevalence, 1997-2000. In: Research and Evaluation Committee, editor. Australia's National Tobacco Campaign. Evaluation Report Volume 3. Every cigarette is doing you damage. Canberra: Commonwealth of Australia; 2004. p. 149-59)
References
1. Australian Institute of Health and Welfare. National Drug Strategy Household Survey detailed report: 2013. Cat. no. PHE 183 Canberra: AIHW, 2014. Available from: http://www.aihw.gov.au/publication-detail /?id=60129549469&tab=3 .
2. Siahpush M, McNeill A, Hammond D and Fong GT. Socioeconomic and country variations in knowledge of health risks of tobacco smoking and toxic constituents of smoke: results from the 2002 International Tobacco Control (ITC) Four Country Survey. Tobacco Control 2006;15(suppl. 3):iii65-70. Available from: http://tobaccocontrol.bmj.com/cgi/reprint/15/suppl_3/iii65
3. Hammond D, Fong GT, McNeill A, Borland R and Cummings KM. Effectiveness of cigarette warning labels in informing smokers about the risks of smoking: findings from the International Tobacco Control (ITC) Four Country Survey. Tobacco Control 2006;15(suppl. 3):iii19–25. Available from: http://tc.bmjjournals.com /cgi/content/abstract/15/suppl_3/iii19
4. Wakefield M, Freeman J and Inglis G. Changes associated with the national tobacco campaign: results of the third and fourth follow-up surveys, 1997-2000. In Hassard, K, ed. Australia's National Tobacco Campaign: evaluation report vol. 3. Every cigarette is doing you damage. Canberra: Commonwealth Department of Health and Ageing, 2004;Available from: http://www.health.gov.au/internet/wcms/Publishing.nsf/Content/88ED1349FD03EB05CA257331000C3A17 /$File/tobccamp3.pdf
5. White V, Tan N, Wakefield M and Hill D. Do adult focused anti-smoking campaigns have an impact on adolescents? The case of the Australian National Tobacco Campaign. Tobacco Control 2003;12(suppl. 2):ii23-9. Available from: http://tc.bmjjournals.com/cgi/content/abstract/12/suppl_2/ii23
6. Dillard A, McCaul K and Klein W. Unrealistic optimism in smokers: implications for smoking myth endorsement and self-protective motivation. Journal of Health Communication 2006;11:93-102. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16641076 Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.35 Health and other benefits of quitting
3.35 Health and other benefits of quitting
Last updated: 2011 Suggested citation: Ford, C & Winstanley, MH. 3.35 Health and other benefits of quitting. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2011. Available from http://www.tobaccoinaustralia.org.au/3-35-health-benefits-of-cessation
This content is also featured in Chapter 7, Section 7.1.
A substantial body of research has established that quitting smoking has immediate as well as long-term health benefits for men and women of all ages, reducing risks for diseases caused by smoking and improving health in general.1–4
The strongest evidence for this comes from a landmark 50-year follow-up of 34 000 British male doctors first studied in 1951.5–7 Many participants quit as the evidence on smoking and health accumulated from the 1950s onwards, providing a natural experiment demonstrating the impact of number of years smoking on health and eventual mortality. The study showed just how hazardous tobacco is and estimated that almost two-thirds of persistent smokers were killed by their smoking. Among those who quit, the greatest benefit was seen in those who quit earliest in life.7 Quitting at age 50 halved the risk of smoking-related death, but cessation by age 30 avoided almost all of the excess risk. Stopping at age 60, 50, 40 or 30 resulted in gains, respectively, of about 3, 6, 9 or 10 years of life expectancy.7,8
Changes in disease risk following cessation can be measured in different ways.
A common measure is relative risk, where the likelihood of developing or dying of disease in a population of former smokers is compared to either current or never smokers. At a population level, relative risk represents the fraction of disease attributable to smoking. However this measure is influenced by the rates of disease in the reference population, which should be taken into account when examining the influence of cessation on disease risk.
Another measure is absolute risk, where the actual rates of disease in former smokers are compared to those of current or never smokers. Rates can be directly compared, or the excess rate of disease caused by smoking in smokers can be calculated as can the excess disease rate in former smokers. Another measure is cumulative risk of disease, which enables the cumulative risk for those who quit at different ages to be compared to that of continuing smokers.
A more complete discussion of changes in risk following cessation can be found in a handbook published in 2007 by the International Agency for Research in Cancer.3 i In general, the risk of disease is lower in former smokers than in otherwise similar current smokers. Smoking results in both acute and chronic changes to the body and progression towards disease. Cessation results in reversal of acute changes and slowing of disease progression and provides the potential for damage reversal.3
Many harmful effects of smoking are arrested or begin to decline as soon as a person stops smoking.1,2 Many disease risks in former smokers continue to decrease with prolonged abstinence, compared to continued smoking. The risk for some health effects decreases more rapidly than for others, and improvement may continue for years after quitting. Some disease risks return to the level of never smokers after a long period of abstinence, but others do not, even after 20 years of abstinence.3
The extent of damage to health and risk for smoking-related disease is related to how much the person has smoked and for how long.3 For some health effects, for example inflammation of the lung, the reversal process is not yet well understood.3
However, while some damage may be irreversible or less reversible, there are substantial benefits to be gained from quitting at any age, regardless of smoking history.1,2 Benefits accrue to persons both with and without smoking-related disease.1
3.35.1 Health problems that may be temporarily exacerbated by quitting
While there is no question of the overall long-term benefits of cessation, quitting is associated with a number of bothersome short-term problems such as mouth ulcers and cold symptoms, weight gain and constipation.9
Mouth ulcers and colds
There is evidence that smokers and users of smokeless tobacco are less likely to develop aphthous stomatitis (common mouth ulcers). Individuals commonly report a short-term increase in mouth ulcers and cold symptoms on quitting smoking.10
Depression
Many smokers appear to have an increase in depressed mood and associated negative affect as part of nicotine withdrawal, but for the majority of people who quit this is temporary.11,12 Smokers with a history of depression tend to report higher levels of nicotine dependence and experience more severe and prolonged withdrawal episodes, including greater negative mood.13–16 Among smokers with a history of depression, around 30% who stop smoking will develop a new episode of major depression. The risk remains high for at least six months.17,18
3.35.2 Quitting and weight gain
While smoking cessation usually results in some level of weight gain, there is disagreement about the extent and how long it lasts.
Smokers' average weight is about 3 to 4 kg less than that of non-smokers.12,19 Smoking appears to attenuate weight gain over time, in part due to increasing metabolic rate.19,20 The difference in weight between smokers and non-smokers is more marked in older long-term smokers while the average weight of younger smokers is similar.20–23 The weight difference, however, is further complicated by the finding that despite their lower weight and body mass index (BMI), smokers have a greater waist-to-hip ratio than non-smokers. Increased waist circumference is a stronger predictor of cardiovascular disease than BMI.24
When smokers quit, the majority experience some weight gain.1 Estimates of weight gain associated with cessation vary depending on the sample, study design and follow-up period.25 Most excess weight gain occurs in the first year after cessation, after which the rate of weight gain slows.19,21,26–30 One study found that increase in body weight may continue for longer.31 Estimates of the mean weight gain in people continuously abstinent for a year are about 5 to 6 kg.27–30 Individual experience of weight change after quitting is quite broad, ranging from weight loss to a minority gaining over 10 kg.21,28,30–35Increase in waist circumference per kilogram gained is smaller in people who quit than in continuing smokers, indicating that recent ex-smokers gain less visceral fat.33,36
Limited research suggests that some of the weight gained during the first few years after quitting may be lost with continued abstinence,37,38 however more research is needed to resolve this issue.39 Large cross- sectional studies show that long-term former smokers have a mean waist-to-hip ratio and a mean BMI similar to or approaching that of people who have never smoked.24,32,35,40
Reasons for the association between smoking cessation and weight gain are not fully understood. Predictors of weight gain include younger age, lower socio-economic status and heavier smoking, with some influence of underlying genetic factors.26 Weight gain after smoking cessation is related to a transient increase in food intake41 and to changes in metabolic rate.42 There is some evidence that smoking and obesity are independently associated with specific food cravings and mood states.43
The health benefits of smoking cessation far outweigh the health risk from extra body weight, unless the weight gain is extraordinarily large.1 Despite this, fear of weight gain is a significant factor in discouraging quitting and provoking relapse in smokers. 26,44-52
(See Chapter 3, Section 3.29 for further information on the health effects of smoking in conjunction with and compared with those associated with obesity, and Section 7.8.3 for further information on managing weight gain.)
3.35.3 Immediate improvements in wellbeing and functioning
Upon cessation, the nicotine and carbon monoxide levels in the body decline rapidly. Nicotine levels drop to very low levels within a few hours, and the main metabolites of nicotine are largely eliminated within a week.1,3,53 After 24 hours the level of carbon monoxide in the blood has decreased substantially.1 After a year blood pressure returns to normal levels (this means it generally stabilises at whatever the person's new blood pressure is) and small airway function improves, with further improvements after six months.54 After two months, improvements can be seen in blood viscosity, blood flow to the limbs and blood levels of high-density cholesterol.1,55 Within six months the immune system improves greatly. Within a few months the cilia in the lungs and airways improve at sweeping mucus and debris from the lungs (as long as irreversible damage has not taken place).56 Lung function improves and the presence and severity of respiratory symptoms reduces.9 Symptoms of chronic bronchitis, such as chronic cough, mucus production and wheeze, decrease rapidly, and lung function in asthmatic patients improves within a few months after stopping smoking.3,57,58 Rates of respiratory infections such as bronchitis and pneumonia also decrease, compared to continued smoking.1
3.35.4 Short to medium-term reductions in health risks following quitting
3.35.4.1 Problems during pregnancy
It is extremely dangerous for a woman to smoke during pregnancy. (Refer to Chapter 3, Section 3.7 for a more detailed discussion of health effects, and Section 7.11 for a more detailed discussion of interventions aimed at pregnant women and their partners.) The US Surgeon General has stated that 'smoking is probably the most important modifiable cause of poor pregnancy outcome among women in the United States'.1 Stopping smoking before or during pregnancy is important and has benefits for both the baby and the mother.59 Encouraging women to quit before they become pregnant or early in pregnancy is important because the critical period may be quite early.20 Although the effect of cutting down on the numerous health risks to the foetus is not well studied,59 there is no solid evidence that cutting down significantly reduces the risks to the foetus.3,60
Women who stop smoking either before becoming pregnant or in the first three to four months of pregnancy have infants with a similar birthweight to those infants born to women who have never smoked.1,61 Women who stop smoking any time up to the 30th week of pregnancy have infants with higher birthweights than those who smoke throughout pregnancy. Reducing the number of cigarettes smoked, instead of quitting completely, does not appear to benefit the birthweight of the foetus.1 Low birthweight infants have a higher risk of illness, death and developing diseases in childhood and adulthood.1,2 Women who quit smoking before or during pregnancy reduce their risk of pregnancy complications, including preterm premature rupture of membranes and preterm delivery (birth at less than 37 weeks gestation).1,20 Smoking cessation reduces the risk of infant death.62
3.35.4.2 Diseases for which the risk quickly declines
Heart disease
Smoking cessation reduces the risk of cardiovascular disease and death for male and female smokers of all ages with or without heart disease.4 There are immediate and long-term benefits.63 After one year the increased risk halves and after 15 years the rate is similar to that of a non-smoker.1 Quitting helps to improve peripheral vascular tone64 and to prevent atherosclerosis (the narrowing and hardening of the arteries due to build-up of plaque on the artery walls) advancing to heart disease and stroke.2,3,65 Smoking is a known risk factor for sudden cardiac death (SCD),2 and quitting smoking results in a significant reduction in SCD risk.66
Stroke
There is a marked reduction in risk within two to five years of quitting.3 After 15 years the risk of stroke is the same as a non-smoker.1
Oral health
Stopping smoking can reduce the risk of oral diseases associated with smoking including cancer, and improve the health of the mouth, gums and teeth.2,67–69 Stopping smoking reduces the risk of leukoplakia, and after one to five years about half of leukoplakia disappears.70 Cessation reduces the risk of developing periodontitis, slows down the progress of existing disease, and quite quickly improves wound healing.2,67,71–73 Following cessation, gum colour gradually returns to normal68 and so-called 'smoker's palate' can disappear.67,68 Stopping smoking improves the success rate of dental implants.69 Smoking cessation may be associated with relatively rapid improvement in periodontal health in young adults.73
3.35.5 Medium to long-term health benefits of quitting
Successful cessation appears to stop the progressive increase in the use of health services associated with continued smoking within a few years.74
Specific long-term health benefits include: Lung cancer. Quitting is beneficial for lung cancer risk.75 Quitting at age 30 reduces the risk of lung cancer by several times compared to a lifetime smoker. Even quitting at 50 more than halves the risk over the next 25 years compared to continued smoking.76 The absolute annual risk of developing or dying from lung cancer does not decrease, but by stopping smoking the much greater increase in risk that would result from continuing to smoke is avoided.3 Chronic obstructive pulmonary disease (COPD). Smoking cessation remains the only proven strategy for reducing the disease-causing processes leading to COPD.4 Cessation reduces decline in lung function.77 In smokers without COPD, stopping smoking improves lung function by about 5% within a few months of cessation. The accelerated decline in lung function in smokers stops within five years of smoking cessation, returning to the far slower rates of decline that naturally occur with ageing.1,3 Existing emphysematous damage to lung tissue caused by smoking is permanent1 however cessation slows the progression of COPD.9 Symptoms of COPD will be less likely in the short and long term.1 In people diagnosed with COPD, stopping smoking reduces the rate of lung function decline, and decreases the risk of hospitalisation for COPD.3,56,78 Other cancers. Smoking cessation is the only proven strategy for reducing the disease-causing processes leading to cancer.4 The risks of cancers of the mouth, throat, larynx, oesophagus, stomach, bladder, kidneys, pancreas and cervix are reduced after quitting compared to continued smoking, and continue to decrease over time.1,3 The risk of pancreatic, oral and cervical cancers quite quickly become similar to people who have never smoked, but the risks for the other cancers remain higher than never-smokers even after 15 to 20 years.1,3 Peripheral vascular disease. Quitting slows down the build-up of plaque on artery walls, so that the risk of the disease is substantially reduced. For those who already have the disease, amputations are less likely.1,79 Blindness. Cataract development and macular degeneration risks and progression are reduced.2,53 Male erectile dysfunction is reduced when smokers quit.2,53 Female fertility. Missed and painful periods are reduced after quitting, as is the risk of delayed conception and early menopause.20,80 The higher risk of heart disease and stroke among women smokers who use the contraceptive pill is reduced.81
Overall health and quality of life improve, with some evidence that heavier smokers report greater improvement in quality of life after quitting and report being happier now than when they were smoking.1,2,82–85
3.35.6 Cutting down: are there health benefits?
Cutting down the number of cigarettes smoked each day is a common strategy used by smokers to reduce harm, to move towards quitting, or to save money.86–89 However, research shows no noticeable improvement in health outcomes or lifespan among smokers who are able to cut down on a long-term basis.4,90–92,This is largely because smokers primarily seek a consistent level of nicotine. Those who cut down therefore tend to smoke the remaining cigarettes harder by taking more and larger puffs, and holding each puff longer. Thus they do not reduce their intake of toxins as much as the reduction in the number of cigarettes suggests.87,93
3.35.7 Other benefits of quitting
There are other benefits of quitting smoking. Financial savings for a pack-a-day smoker are about $5000 per year (2012 prices).94 Smokers who quit reduce their likelihood of financial stress and are likely to enhance their material wellbeing.95 As more public and private places become smokefree, ex-smokers avoid the inconvenience of having to find somewhere to smoke. Quitting avoids further smoking-related damage to skin, and slows the development of wrinkles.96 Life insurance is often cheaper,97 the risk of smoking-related fires is reduced98,99 and people who quit have fewer sick days.2
3.35.8 Population beliefs about the benefits of quitting
There are limited data on population beliefs of the benefits of smoking cessation. There is a strong belief among smokers that stopping smoking will improve their health.100,101 Evidence from Victorian surveys show that smokers mention saving money (57%), feeling healthier (55%) and breathing and fitness (31%) as particular advantages of quitting.102 Quitting protects the health of pets and smokers do perceive this as a benefit of quitting.103 i See IARC (2007). IARC Handbooks of Cancer Prevention, Tobacco Control, Vol. 11: Reversal of Risk after Quitting Smoking. Lyon, France. References
1. US Department of Health and Human Services. The health benefits of smoking cessation: a report of the Surgeon General. Atlanta, Georgia: Centers for Disease Control, Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 1990. Available from: http://www.cdc.gov/tobacco /data_statistics/sgr/pre_1994/index.htm
2. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
3. International Agency for Research on Cancer. Reversal of risk after quitting smoking. IARC handbooks of cancer prevention, tobacco control, Vol. 11. Lyon, France: IARC, 2007. Available from: http://apps.who.int /bookorders/anglais/detart1.jsp?sesslan=1&codlan=1&codcol=76&codcch=22
4. US Department of Health and Human Services. How smoking causes diseases: a report of the Surgeon General: . Atlanta, Georgia: US Dept. of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: www.surgeongeneral.gov/library /tobaccosmoke/Cached
5. Doll R and Hill AB. The mortality of doctors in relation to their smoking habits: a preliminary report. British Medical Journal 1954;1(4877):1451–5. Available from: http://www.pubmedcentral.nih.gov /picrender.fcgi?artid=2085438&blobtype=pdf
6. Doll R, Peto R, Wheatly L, Gray R and Sutherland I. Mortality in relation to smoking: 40 years' observations on male British doctors. BMJ (Clinical Research Ed.) 1994;309(6959):901–11. Available from: http://www.bmj.com/cgi/content/full/309/6959/901
7. Doll R, Peto R, Boreham J and Sutherland I. Mortality in relation to smoking: 50 years' observations on male British doctors. BMJ (Clinical Research Ed.) 2004;328(7455):1519. Available from: http://www.bmj.com /cgi/content/abstract/328/7455/1519
8. Taylor DH, Hasselblad V, Henley SJ, Thun MJ and Sloan FA. Benefits of smoking cessation for longevity. American Journal of Public Health 2002;92(6):990–6. Available from: http://www.ajph.org/cgi/content/full/92 /6/990
9. Gratziou C. Respiratory, cardiovascular and other physiological consequences of smoking cessation. Current Medical Research and Opinion 2009;25(2):535–45. Available from: http://www.informapharmascience.com/doi/abs/10.1185/03007990802707642
10. Ussher M, West R, Steptoe A and McEwen A. Increase in common cold symptoms and mouth ulcers following smoking cessation. Tobacco Control 2003;12:86-8. Available from: http://tc.bmjjournals.com /cgi/content/abstract/12/1/86
11. Hughes J. Effects of abstinence from tobacco: valid symptoms and time course. Nicotine & Tobacco Research 2007;9(3):315–27. Available from: http://www.informaworld.com /smpp/content~db=all?content=10.1080/14622200701188919
12. Royal College of Physicians of London. Nicotine addiction in Britain. A report of the Tobacco Advisory Group of the Royal College of Physicians. London: Royal College of Physicians of London, 2000. Available from: http://bookshop.rcplondon.ac.uk/details.aspx?e=131
13. Breslau N, Kilbey MM and Andreski P. DSM-III-R nicotine dependence in young adults: prevalence, correlates and associated psychiatric disorders. Addiction 1994;89(6):743-54. Available from: http://www.ncbi.nlm.nih.gov/pubmed/8069175 14. Breslau N. Psychiatric comorbidity of smoking and nicotine dependence. Behavioural Genetics 1995;25(2):95-101. Available from: http://www.ncbi.nlm.nih.gov/pubmed/7733862
15. Kahler CW, Brown RA, Strong DR, Lloyd-Richardson EE and Niaura R. History of major depressive disorder among smokers in cessation treatment: associations with dysfunctional attitudes and coping. Addictive Behaviors 2003;28(6):1033-47. Available from: http://www.ncbi.nlm.nih.gov/12834649
16. Wilhelm K, Richmond R and Wodak A. Clinical aspects of nicotine dependence and depression. Medicine Today 2004;3:40–6.
17. Glassman AH, Covey LS, Stetner F and Rivelli S. Smoking cessation and the course of major depression: a follow-up study. Lancet 2001;357(9272):1929-32. Available from: http://www.ncbi.nlm.nih.gov /pubmed/11425414
18. Killen JD, Fortmann SP, Schatzberg A, Hayward C and Varady A. Onset of major depression during treatment for nicotine dependence. Addictive Behaviors 2003;28(3):461-70. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12628619
19. Perkins K. Weight gain following smoking cessation. Journal of Consulting and Clinical Psychology 1993;61(5):768–77.
20. US Department of Health and Human Services. Women and smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2001. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/index.htm
21. Klesges RC, Ward KD, Ray JW, Cutter G, Jacobs DR, Jr. and Wagenknecht LE. The prospective relationships between smoking and weight in a young, biracial cohort: the Coronary Artery Risk Development in Young Adults Study. Journal of Consulting Clinical Psychology 1998;66(6):987-93. Available from: http://www.ncbi.nlm.nih.gov/pubmed/9874912
22. Akbartabartoori M, Lean ME and Hankey CR. Relationships between cigarette smoking, body size and body shape. International Journal of Obesity 2005;29(2):236-43. Available from: http://www.ncbi.nlm.nih.gov /pubmed/15505632
23. O'Loughlin J, Karp I, Henderson M and Gray-Donald K. Does cigarette use influence adiposity or height in adolescence? Annals of Epidemiology 2008;18(5):395-402. Available from: http://www.ncbi.nlm.nih.gov /pubmed/18346909
24. Canoy D, Wareham N, Luben R, Welch A, Bingham S, Day N, et al. Cigarette smoking and fat distribution in 21 828 British men and women: a population-based study. Obesity Research 2005;13(8):1466-75. Available from: http://www.ncbi.nlm.nih.gov/16129730
25. Eisenberg D and Quinn B. Estimating the effect of smoking cessation on weight gain: an instrumental variable approach. Health Services Research 2006;41(6):2255–66. Available from: http://www3.interscience.wiley.com/journal/118580318/abstract
26. Filozof C, Fernandez Pinilla MC and Fernandez-Cruz A. Smoking cessation and weight gain. Obesity Reviews 2004;5(2):95-103. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15086863
27. Nides M, Rand C, Dolce J, Murray R, O'Hara P, Voelker H, et al. Weight gain as a function of smoking cessation and 2-mg nicotine gum use among middle-aged smokers with mild lung impairment in the first 2 years of the Lung Health Study. Health Psychology 1994;13(4):354-61. Available from: http://www.ncbi.nlm.nih.gov/pubmed/7957014
28. O'Hara P, Connett JE, Lee WW, Nides M, Murray R and Wise R. Early and late weight gain following smoking cessation in the Lung Health Study. American Journal of Epidemiology 1998;148(9):821-30. Available from: http://www.ncbi.nlm.nih.gov/pubmed/9801011
29. Pirie PL, McBride CM, Hellerstedt W, Jeffery RW, Hatsukami D, Allen S, et al. Smoking cessation in women concerned about weight. American Journal of Public Health 1992;82(9):1238-43. Available from: http://www.ncbi.nlm.nih.gov/pubmed/1503165
30. Klesges RC, Winders SE, Meyers AW, Eck LH, Ward KD, Hultquist CM, et al. How much weight gain occurs following smoking cessation? A comparison of weight gain using both continuous and point prevalence abstinence. Journal of Consulting and Clinical Psychology 1997;65(2):286–91. Available from: http://psycnet.apa.org/index.cfm?fa=main.landing
31. Suwazono Y, Dochi M, Oishi M, Tanaka K, Morimoto H and Sakata K. Longitudinal effect of smoking cessation on physical and laboratory findings. American Journal of Preventive Medicine 2010;38(2):192–200. Available from: http://www.ajpm-online.net/article/PIIS0749379709007594/fulltext
32. Flegal KM, Troiano RP, Pamuk ER, Kuczmarski RJ and Campbell SM. The influence of smoking cessation on the prevalence of overweight in the United States. New England Journal of Medicine 1995;333(18):1165-70. Available from: http://www.ncbi.nlm.nih.gov/pubmed/7565970
33. Pisinger C and Jorgensen T. Waist circumference and weight following smoking cessation in a general population: the Inter99 study. Preventive Medicine 2007;44(4):290-5. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17222450
34. Swan GE and Carmelli D. Characteristics associated with excessive weight gain after smoking cessation in men. American Journal of Public Health 1995;85(1):73-7. Available from: http://www.ncbi.nlm.nih.gov /pubmed/7832265
35. Williamson D, Madans J, Anda R, Kleinman J, Giovini G and Byers T. Smoking cessation and severity of weight gain in a national cohort. New England Journal of Medicine 1991;14(11):739–45. Available from: http://content.nejm.org/cgi/content/abstract/324/11/739
36. Lissner L, Bengtsson C, Lapidus L and Bjorkelund C. Smoking initiation and cessation in relation to body fat distribution based on data from a study of Swedish women. American Journal of Public Health 1992;82(2):273-5. Available from: http://www.ncbi.nlm.nih.gov/pubmed/1739163
37. Chen Y, Horne SL and Dosman JA. The influence of smoking cessation on body weight may be temporary. American Journal of Public Health 1993;83(9):1330-2. Available from: http://www.ncbi.nlm.nih.gov /pubmed/8363012
38. Kadowaki T, Watanabe M, Okayama A, Hishida K, Okamura T, Miyamatsu N, et al. Continuation of smoking cessation and following weight change after intervention in a healthy population with high smoking prevalence. J Occup Health 2006;48(5):402-6. Available from: http://www.ncbi.nlm.nih.gov/pubmed /17053308
39. Froom P, Melamed S and Benbassat J. Smoking cessation and weight gain. The Journal of Family Practice 1998;46(6):460-4. Available from: http://www.ncbi.nlm.nih.gov/pubmed/9638109
40. Munafò M, Tilling K and Ben-Shlomo Y. Smoking status and body mass index: a longitudinal study. Nicotine & Tobacco Research 2009;11(6):765–71. Available from: http://ntr.oxfordjournals.org/cgi/content /full/11/6/765
41. Hudmon KS, Gritz ER, Clayton S and Nisenbaum R. Eating orientation, postcessation weight gain, and continued abstinence among female smokers receiveing an usolicited smoking cessation intervention. Health Psychology 1999;18(1):29–36. Available from: http://psycnet.apa.org/index.cfm?fa=main.landing
42. Kadota K, Takeshima F, Inoue K, Takamori K, Yoshioka S, Nakayama S, et al. Effects of smoking cessation on gastric emptying in smokers. Journal of Clinical Gastroenterology 2010;44(4):e71–5. Available from: http://journals.lww.com/jcge/pages/articleviewer.aspx?year=2010&issue=04000&article=00001& type=abstract
43. Pepino MY, Finkbeiner S and Mennella JA. Similarities in food cravings and mood states between obese women and women who smoke tobacco. Obesity (Silver Spring) 2009;17(6):1158-63. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19247281 44. Shraim M, Parsons A, Aveyard P and Hajek P. Interventions for preventing weight gain after smoking cessation. (Protocol) 2006. [viewed 16 September 2008] ; Available from: http://www.mrw.interscience.wiley.com/cochrane/clsysrev/articles/CD006219/frame.html
45. Pomerleau CS and Saules K. Body image, body satisfaction, and eating patterns in normal-weight and overweight/obese women current smokers and never-smokers. Addictive Behaviors 2007;32(10):2329-34. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17320305
46. Pomerleau CS, Zucker AN and Stewart AJ. Characterizing concerns about post-cessation weight gain: results from a national survey of women smokers. Nicotine Tob Res 2001;3(1):51-60. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11260811
47. Brouwer RJ and Pomerleau CS. "Prequit attrition" among weight-concerned women smokers. Eat Behav 2000;1(2):145-51. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15001057
48. Copeland AL, Martin PD, Geiselman PJ, Rash CJ and Kendzor DE. Predictors of pretreatment attrition from smoking cessation among pre- and postmenopausal, weight-concerned women. Eat Behav 2006;7(3):243-51. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16843227
49. Alberg AJ, Carter CL and Carpenter MJ. Weight gain as an impediment to cigarette smoking cessation: a lingering problem in need of solutions. Preventive Medicine 2007;44(4):296-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17316778
50. White MA, McKee SA and O'Malley S S. Smoke and mirrors: magnified beliefs that cigarette smoking suppresses weight. Addictive Behaviours 2007;32(10):2200-10. Available from: http://www.ncbi.nlm.nih.gov /pubmed/17428615
51. Fiore M, Bailey W, Cohen S and Dorfman S. Smoking cessation clinical practice guideline no. 18. Rockville, Maryland: Agency for Health Care Policy and Research, US Department of Health and Human Services, Public Health Service, 1996.
52. Fiore M, Bailey W and Cohen S, et al. Treating Tobacco Use and Dependence. Clinical Practice Guideline. Rockville, Maryland: US Department of Health and Human Services. Public Health Service, 2000. Available from: http://www.surgeongeneral.gov/tobacco/
53. US Department of Health and Human Services. The health consequences of smoking: nicotine addiction. A report of the Surgeon General. Rockville, Maryland: US Department of Health and Human Services, Public Health Service, Centers for Disease Control, Center for Health Promotion and Education, Office on Smoking and Health, 1988. Available from: http://profiles.nlm.nih.gov/NN/B/B/Z/D/_/nnbbzd.pdf
54. Rodrigo C. The effects of cigarette smoking on anesthesia. Anesthesia Progress 2000;47(4):143-50. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11432181
55. US Department of Health and Human Services. The health consequences of smoking: cardiovascular disease. A report of the Surgeon General. Rockville, Maryland: Public Health Service, Office on Smoking and Health, 1983. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/previous_sgr.htm
56. US Department of Health and Human Services. The health consequences of smoking: chronic obstructive lung disease. A report of the Surgeon General. Rockville, Maryland: US Department of Health and Human Services, Public Health Service, Office on Smoking and Health, 1984. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/previous_sgr.htm
57. Jang A, Park S, Kim D, Uh S, Kim Y, Whang H, et al. Effects of smoking cessation on airflow obstruction and quality of life in asthmatic smokers. Allergy, Asthma & Immunology Research 2010;2(4):254–9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20885910
58. Tonnesen P, Pisinger C, Hvidberg S, Wennike P, Bremann L, Westin A, et al. Effects of smoking cessation and reduction in asthmatics. Nicotine & Tobacco Research 2005;7(1):139–48. Available from: http://www.informaworld.com/smpp/content~db=all?content=10.1080/14622200412331328411 59. Lumley J, Chamberlain C, Dowswell T, Oliver S, Oakley L and Watson L. Interventions for promoting smoking cessation during pregnancy. Cochrane Database Systematic Review 2009(3):CD001055. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19588322
60. Shea AK and Steiner M. Cigarette smoking during pregnancy. Nicotine &Tobacco Research 2008;10(2):267-78. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18236291
61. Lightwood J, Phibbs C and Glantz S. Short term health and economic benefits of smoking cessation: low birthweight. Pediatrics 1999;104(6):1312–20. Available from: http://pediatrics.aappublications.org/cgi/content /full/104/6/1312
62. Johansson A, Dickman P, Kramer M and Cnattingius S. Maternal smoking and infant mortality: does quitting smoking reduce the risk of infant death? Epidemiology 2009;20(4):590–7. Available from: http://journals.lww.com/epidem/pages/articleviewer.aspx?year=2009&issue=07000&article=00019& type=abstract
63. Kawachi I, Colditz G, Stampfer M, Willett W, Mason J, Rosner B, et al. Smoking cessation and time course of decreased risks of coronary heart disease in middle aged-women. Archives of Internal Medicine 1994;154(2):169–75. Available from: http://www.ncbi.nlm.nih.gov/pubmed/8285812
64. Roux A, Motreff P, Perriot J, Pereira B, Lusson J, Duale C, et al. Early improvement in peripheral vascular tone following smoking cessation using nicotine replacement therapy: aortic wave reflection analysis. Cardiology 2010;117(1):37–43. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20881393
65. US Department of Health and Education and Welfare. Smoking and health: a report of the Surgeon General. DHEW Publication no (PHS) 79-50066. Atlanta: US Department of Health, Education and Welfare, Public Health Service, Office of the Assistant Secretary for Health, Office on Smoking and Health, 1979. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/previous_sgr.htm
66. Goldenberg I, Jonas M, Tenenbaum A, Boyko V, Matetzky S, Shotan A, et al. Current smoking, smoking cessation, and the risk of sudden cardiac death in patients with coronary artery disease. Archives of Internal Medicine 2003;163(19):2301-5. Available from: http://www.ncbi.nlm.nih.gov/pubmed/14581249
67. Christen AG. The impact of tobacco use and cessation on oral and dental diseases and conditions. The American Journal of Medicine 1992;93(1A):25S-31S. Available from: http://www.ncbi.nlm.nih.gov/pubmed /1497000
68. Mirbod SM and Ahing SI. Tobacco-associated lesions of the oral cavity: Part II. Malignant lesions. Journal of the Canadian Dental Association 2000;66(6):308-11. Available from: http://www.ncbi.nlm.nih.gov/pubmed /10927896
69. Sham AS, Cheung LK, Jin LJ and Corbet EF. The effects of tobacco use on oral health. Hong Kong Medical Journal 2003;9(4):271-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12904615
70. Banoczy J, Gintner Z and Dombi C. Effect of smoking on the development of oral leukoplakia. Fogorvosi szemle 2001;94(3):91-6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11480242
71. Johnson GK and Slach NA. Impact of tobacco use on periodontal status. Journal of Dental Education 2001;65(4):313-21. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11336116
72. Moller AM, Villebro N, Pedersen T and Tonnesen H. Effect of preoperative smoking intervention on postoperative complications: a randomised clinical trial. The Lancet 2002;359(9301):114–7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11809253
73. Hodge P and Binnie V. Smoking cessation and periodontal health--a missed opportunity? Evidence-Based Dentistry 2009;10(1):18–19. Available from: http://www.nature.com/ebd/journal/v10/n1 /full/6400632a.html
74. Wagner E, Curry S, Grothaus L, Saunders K and McBride C. The impact of smoking and quitting on health care use. Archives of Internal Medicine 1995;155(16):1789–95. Available from: http://www.ncbi.nlm.nih.gov/pubmed/7654113
75. Huxley R, Jamrozik K, Lam T, Barzi F, Ansary-Moghaddam A, Jiang C, et al. Impact of smoking and smoking cessation on lung cancer mortality in the Asia-Pacific region. American Journal of Epidemiology 2007;165(11):1280–6. Available from: http://aje.oxfordjournals.org/cgi/content/full/165/11/1280
76. Peto R, Darby S, Deo H, Silcocks P, Whitley E and Doll R. Smoking, smoking cessation, and lung cancer in the UK since 1950: combination of statistics with two case-control studies. BMJ (Clinical Research Ed.) 2000;321(7257):323–9. Available from: http://www.bmj.com/cgi/reprint/321/7257/323
77. Pelkonen M, Notkola I, Tukiainen H, Tervahauta M, Tuomilehto J and Nissinen A. Smoking cessation, decline in pulmonary function and total mortality: a 30 year follow up study among the Finnish cohorts of the Seven Countries Study. Thorax 2001;56(9):703–7. Available from: http://thorax.bmj.com/cgi/content/full/56 /9/703
78. Au D, Bryson C, Chien J, Sun H, Udris E, Evans L, et al. The effects of smoking cessation on the risk of chronic obstructive pulmonary disease exacerbations. Journal of General Internal Medicine 2009;24(4):457–63. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19194768
79. Gey D, Lesho E and Manngold J. Management of peripheral arterial disease. American Family Physician 2004;69:525-32.
80. Mishra G, Dobson A and Schofield M. Cigarette smoking, menstrual symptoms and miscarriage among young women. Australian & New Zealand Journal of Public Health 2000;24(4):413-20.
81. Farley T, Meirik O, Chang CL and Poulter N. Combined oral contraceptives, smoking, and cardiovascular risk. Journal of Epidemiology and Community Health 1998;52(12):775-85. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10396518
82. Hirdes J and Maxwell C. Smoking cessation and quality of life outcomes among older adults in the Cambell Survey on Well-Being. Canadian Journal of Public Health 1994;85(2):99–102. Available from: http://www.ncbi.nlm.nih.gov/pubmed/8012927
83. Mulder I, Tijhuis M, Smit HA and Kromhout D. Smoking cessation and quality of life: the effect of amount of smoking and time since quitting. Preventive Medicine 2001;33(6):653–60. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11716663
84. Sales M, Oliveira M, Mattos I, Viana C and Pereira E. The impact of smoking cessation on patient quality of life. Jornal Brasileiro de Pneumologia 2009;35(5):436–41. Available from: http://www.ncbi.nlm.nih.gov /pubmed/19547852
85. Shahab L and West R. Do ex-smokers report feeling happier following cessation? Evidence from a cross- sectional survey. Nicotine & Tobacco Research 2009;11(5):553-7. Available from: http://www.ncbi.nlm.nih.gov /pubmed/19351779
86. Australian Bureau of Statistics. 4714.0.55.001 - National Aboriginal and Torres Strait Islander Social Survey, Australia, 2002 Canberra: Australian Bureau of Statistics, 2004. Available from: http://www.abs.gov.au/AUSSTATS/[email protected]/DetailsPage/4714.0.55.0012002?OpenDocument
87. McNeill A. Harm reduction. Review. BMJ (Clinical Research Ed.) 2004;328(7444):885–7. Available from: http://www.bmj.com/cgi/content/full/328/7444/885
88. McNeill A and White P. Editorial: The case for harm reduction in smoking. Drugs: Education, Prevention and Policy 1998;59:125-27.
89. Piasecki T. Relapse to smoking. Review. Clinical Psychology Review 2006;26(2):196–215. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16352382
90. Tverdal A and Bjartveit K. Health consequences of reduced daily cigarette consumption. Tobacco Control 2006;15(6):472-80. Available from: http://tc.bmj.com/cgi/content/abstract/15/6/472 91. Godtfredsen NS, Holst C, Prescott E, Vestbo J and Osler M. Smoking reduction, smoking cessation, and mortality: a 16-year follow-up of 19 732 men and women from the Copenhagen Centre for Prospective Population Studies. American Journal of Epidemiology 2002;156(11):994–1001. Available from: http://aje.oxfordjournals.org/cgi/content/full/156/11/994
92. Godtfredsen NS, Osler M, Vestbo J, Andersen I and Prescott E. Smoking reduction, smoking cessation, and incidence of fatal and non-fatal myocardial infarction in Denmark 1976-1998: a pooled cohort study. Journal of Epidemiology and Community Health 2003;57(6):412–6. Available from: http://jech.bmj.com /cgi/content/full/57/6/412
93. National Cancer Institute. Risks associated with smoking cigarettes with low machine-measured yield of tar and nicotine. Smoking and Tobacco Control Monograph. Bethesda, MD: U.S. Department of Health and Human Services National Institutes of Health, National Cancer Institute, 2001.
94. NSW Retail Tobacco Traders' Association. The Australian Retail Tobacconist; 83.Cigarette price lists. 1-4. 2010.
95. Siahpush M, Spittal M and Singh GK. Association of smoking cessation with financial stress and material well-being: results from a prospective study of a population-based national survey. American Journal of Public Health 2007;97(12):2281–7. Available from: http://www.ajph.org/cgi/content/abstract/97/12/2281
96. Freiman A, Bird G, Metelitsa A, Barankin B and Lauzon G. Cutaneous effects of smoking. Journal of Cutaneous Medical Surgery 2004;8(6):415-23.
97. Lane B. Age, job and sex hold key to your cost of insurance. The West Australian, (Perth) 1999:Monday 17 May 45
98. Chernichko L, Saunders L and Tough S. Unintentional house fire deaths in Alberta 1985-1990: a population study. Canadian Journal of Public Health 1993;84(5):317–20. Available from: http://www.ncbi.nlm.nih.gov/pubmed/8269379
99. Chapman S and Balmain A. Reduced-ignition Propensity Cigarettes: A review of policy relevant information. Canberra: Commonwealth Department of Health and Ageing, 2004.
100. US Department of Health and Human Services. Reducing the health consequences of smoking: 25 years of progress. A report of the US Surgeon General. Rockville, Maryland: US Department of Health and Human Services, Public Health Service, Centers for Disease Control, Centre for Chronic Disease Prevention and Health Promotion, Office of Smoking and Health, 1989. Available from: http://profiles.nlm.nih.gov /NN/B/B/X/S/
101. Wakefield M, Freeman J and Inglis G. Chapter 5: Changes associated with the National Tobacco Campaign: results of the third and fourth follow-up surveys. In Hassard K, edn. Australia's National Tobacco Campaign: evaluation report vol. 3 Every cigarette is doing you damage. Canberra: Department of Health and Ageing, 2004 Available from: http://www.quitnow.gov.au/internet/quitnow/publishing.nsf/Content/national- tobacco-campaign-lp
102. Trotter L, Mullins R, Boulter J and Borland R. Key findings of the 1996 and 1997 household surveys. Quit evaluation studies no. 9. Melbourne, Australia: Anti-Cancer Council of Victoria, 1998 1-26. Available from: http://www.quit.org.au/downloads/QE/QE9/QE9Home.html
103. Milberger SM, Davis RM and Holm AL. Pet owners' attitudes and behaviours related to smoking and second-hand smoke: a pilot study. Tobacco Control 2009;18(2):156-8. Available from: http://tobaccocontrol.bmj.com/cgi/content/abstract/18/2/156
Copyright © 2016 The Cancer Council. All rights reserved. Chapter 3: Health Effects » 3.36 The global tobacco pandemic
3.36 The global tobacco pandemic
Last updated: April 2015 Suggested citation: Bellew, B, Greenhalgh, EM & Winstanley, MH. 3.36 The global tobacco pandemic. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/3-36-the-global-tobacco- pandemic
According to a recent review of mortality trends, world life expectancy is currently slightly above 70 years; most deaths earlier than that are avoidable, and are primarily caused by non-communicable diseases.1 Although communicable diseases, for example influenza and influenza-like illnesses, have a tendency to capture news headlines and possibly the attention of policy-makers more dramatically than many other health issues, an examination of the disease burden of influenza2-5 compared with the disease burden of tobacco6-8 leaves little doubt about the salience of tobacco as an issue in global public health. Death and disease caused by tobacco use now constitutes a pandemic; its use is the leading cause of preventable death and is estimated to kill more than five million people each year worldwide.9-11 This constitutes one death about every six seconds.12 In 2004, 12% of all deaths worldwide among adults over 30 were attributed to tobacco.12 In 2010, smoking caused about a quarter of all cancer deaths in Europe and America, and even greater numbers from other diseases. Smoking is also a major cause of death in China, India, and other countries throughout Asia.1 In several Asian and African countries, more than 25% of male deaths are now related to smoking, matching regions in Europe and North America that previously had the highest proportion of tobacco-related mortality. More than two thirds of tobacco deaths occur in low- and middle- income countries,13 with the gap in deaths between low and middle income countries and high income countries expected to widen further over the next several decades if effective prevention measures are not implemented.9 If current trends persist, tobacco will kill more than eight million people worldwide each year by the year 2030,14 and about 1 billion by the end of this century.13
By 2030, it is projected overall that there will be approximately 26 million new cancer cases and 17 million cancer deaths per year.15, 16 This compares with about 12 million new cases and 7.6 million cancer deaths estimated to have occurred globally in 2007. The projected increase will be driven largely by growth and ageing of populations and will be largest in low- and medium-resource countries. Under current trends, increased longevity in developing countries will nearly triple the number of people who survive to age 65 by 2050. This demographic shift will be compounded by entrenched modifiable risk factors such as smoking, which is the leading risk factor for cancer mortality in countries of low, middle and high income.15, 16 On the basis of current tobacco consumption patterns, it has been estimated that approximately 450 million adults will be killed by smoking between 2000 and 2050. At least half of these adults will die between 30 and 69 years of age, losing decades of productive life. Cancer and the total deaths due to smoking have fallen sharply in men in high income countries but will rise globally unless current smokers, most of whom live in low and middle income countries, stop smoking before or during middle age.17
Projections of global mortality and burden of disease from 2002 to 2030 have been undertaken by Mathers and Loncar using three scenarios–'baseline', 'optimistic' and 'pessimistic'.8 The projections highlight tobacco- related mortality and burden of disease as a major threat to public health and allow comparisons with other major threats to public health such as human immunodeficiency virus (HIV) infection18 or obesity.15,19,20 In these projections, global HIV/AIDS deaths rise from 2.8 million in 2002 to 6.5 million in 2030 under the 'baseline' scenario, which assumes that coverage with antiretroviral drugs reaches 80% by 2012. Under the 'optimistic' scenario, which also assumes increased prevention activity, HIV/AIDS deaths drop to 3.7 million in 2030. By contrast, total tobacco-attributable deaths rise from 5.4 million in 2005 to 6.4 million in 2015 and 8.3 million in 2030 under the 'baseline' scenario. Tobacco is projected to kill 50% more people in 2015 than HIV/AIDS, and to be responsible for 10% of all deaths globally.8
Tuberculosis (TB), HIV and chronic obstructive pulmonary disease (COPD) are burgeoning epidemics in developing countries. The link between TB and HIV is well established. Less well recognised is the strong relationship between tobacco smoking and the development and natural history of TB. These associations are of considerable relevance to public health and disease outcomes in individuals with TB. Moreover, tobacco smoking, a modifiable risk factor, is associated with poorer outcomes in HIV-associated opportunistic infections, of which TB is the commonest in developing countries. It is now also becoming clear that TB, like tobacco smoke, besides its known consequences of bronchiectasis and other pulmonary morbidity, is also a significant risk factor for the development of COPD.18 Almost 90% of COPD deaths occur in low- and middle- income countries, and it has been estimated that COPD will be the third leading cause of death in 2030 globally.13 Thus, the harmful synergistic interaction between TB, HIV, tobacco smoking and COPD in a large proportion of the world's population that deserves urgent attention in developing countries.18
International research on current smoking prevalence and behaviours among youth aged 13–15 has reported disturbing trends for the future. The Global Youth Tobacco Survey, assessing data from more than 130 countries and principalities, has found that:21 the gap in smoking rates between school-aged girls and boys is decreasing, a finding of particular importance for those countries in which smoking has previously been negligible among the female population, use of tobacco products other than cigarettes is widespread, a sizeable proportion of children who currently do not smoke are contemplating adopting the behaviour, and children are widely exposed to secondhand smoke.
Each of these findings can be expected to have a significant impact on morbidity and mortality from tobacco use in forthcoming decades.21
While the current burden of death is distributed evenly between developing and industrialised countries,22 most of the future burden of death will occur in low and middle income countries, where more than 80% of the world's smokers live.23 Smoking rates are for the most part well in decline in Western Europe, the UK, the US, Canada, New Zealand and Australia. However in some countries in Asia, South America and Africa, the prevalence of smoking is still increasing.24,25 In China, home to one-third of the world's population, the death toll from smoking currently stands at about 800 000 per year and it has been estimated that smoking will cause three million Chinese deaths annually by the middle of this century.26 Tobacco smoking rates vary; men usually smoke more than women in overall consumption and in prevalence. Current available estimates are 49% for men and 8% for women in low and middle income countries, and 37% for men and 21% for women in high income countries.27 This is reflected in the proportion of mortality attributable to tobacco, which is higher among men than women.12 A series of country profiles on non-communicable diseases made available by the World Health Organization points out that since prevalence varies greatly, these country profiles provide a useful way of examining this aspect of the pandemic and are illustrative of the importance of tobacco as a cross-cutting risk factor for non-communicable diseases.28
The global tobacco pandemic is characterised by an escalating burden of death and disease that is increasingly being borne by developing countries; efforts to promote global health equity must therefore prioritise reductions in tobacco consumption.29 The scale of this global tobacco pandemic8, 15-18, 27, 30 and the globalisation of tobacco use31 provide a clear rationale for a global response such as that set out in the World Health Organization Framework Convention on Tobacco Control (FCTC)33 and the supporting MPOWER package.33 The World Health Organization's Report on the Global Tobacco Epidemic describes some of the progress achieved as a result of the FCTC, such as 739 million people in 31 countries being afforded protected by comprehensive smoke-free laws;34 but an earlier World Health Organization report also implicitly acknowledges that much more needs to be done because it notes that less than 10% of the world's population is covered by any one of the MPOWER measures by the year 2008.14 Chapman, while acknowledging that an acceleration of policy development in tobacco-control policy has been ushered in by the FCTC, has also noted the optional nature of some aspects of the treaty and thus the particular importance of intensified strategies in harm reduction, demand reduction, denormalisation of tobacco use (especially among health workers in nations where use remains high) as well as further efforts to regulate the tobacco industry (especially plain packaging, under-the-counter retail sales and the regulation of tobacco products).35
Chapter 1 provides international prevalence comparisons while Chapter 2 gives international comparisons on tobacco consumption. The global nature of the industry is covered in Chapter 10. The WHO Framework Convention on Tobacco Control is described in detail in Chapter 18.
References
1. Norheim OF, Jha P, Admasu K, Godal T, Hum RJ, et al. Avoiding 40% of the premature deaths in each country, 2010–30: Review of national mortality trends to help quantify the UN Sustainable Development Goal for health. The Lancet, 2014. Available from: http://www.sciencedirect.com/science/article /pii/S0140673614615919
2. Shrestha SS, Swerdlow DL, Borse RH, Prabhu VS, Finelli L, Atkins CY, et al. Estimating the burden of 2009 pandemic influenza A (H1N1) in the United States (April 2009-April 2010). Clinical Infectious Diseases 2011;52(suppl. 1):S75-82. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21342903
3. Guo RN, Zheng HZ, Li JS, Sun LM, Li LH, Lin JY, et al. A population-based study on incidence and economic burden of influenza-like illness in south China, 2007. Public Health 2011;125(6):389-95. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21616513
4. Dawood FS, Fiore A, Kamimoto L, Bramley A, Reingold A, Gershman K, et al. Burden of seasonal influenza hospitalization in children, United States, 2003 to 2008. The Journal of Pediatrics 2010;157(5):808-14. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20580018
5. Simmerman JM and Uyeki TM. The burden of influenza in East and South-East Asia: a review of the English language literature. Influenza and Other Respiratory Viruses 2008;2(3):81-92. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19453467
6. Seffrin J, Hill D, Burkart W, Magrath I, Badwe R, Ngoma T, et al. It is time to include cancer and other noncommunicable diseases in the millennium development goals. CA: A Cancer Journal for Clinicians 2009;59(5):282–4. Available from: http://caonline.amcancersoc.org/cgi/reprint/59/5/282
7. Abegunde DO, Mathers CD, Adam T, Ortegon M and Strong K. The burden and costs of chronic diseases in low-income and middle-income countries. The Lancet 2007;370(9603):1929-38. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18063029
8. Mathers CD and Loncar D. Projections of global mortality and burden of disease from 2002 to 2030. PLoS Medicine 2006;3(11):e442. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17132052
9. World Health Organization. WHO report on the global tobacco epidemic, 2008: the MPOWER package. Geneva: WHO, 2008. Available from: http://www.who.int/tobacco/mpower/en/index.html
10. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: http://www.cdc.gov/tobacco/data_statistics /sgr/index.htm
11. US Department of Health and Human Services. The health consequences of involuntary exposure to tobacco smoke: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2006. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/sgr_2006/index.htm
12. World Health Organization. WHO report on the global tobacco epidemic, 2009: implementing smoke-free environments. Geneva: WHO, 2009. Available from: http://www.who.int/tobacco/en/
13. The Tobacco Atlas, Smoking's death toll. American Cancer Society, World Lung Foundation; 2015. Available from: http://www.tobaccoatlas.org/topic/smokings-death-toll/
14. World Health Organization. WHO report on the global tobacco epidemic, 2009: implementing smoke-free environments. Geneva: WHO, 2009. Available from: http://www.who.int/tobacco/en/
15. Thun M, DeLancey J, Center M, Jemal A and Ward E. The global burden of cancer: priorities for prevention. Carcinogenesis 2010;31(1):100–10. Available from: http://carcin.oxfordjournals.org/cgi/reprint /31/1/100
16. Ferlay J, Shin HR, Bray F, Forman D, Mathers C and Parkin DM. Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008. International Journal of Cancer 2010;127(12):2893-917. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21351269
17. Jha P. Avoidable global cancer deaths and total deaths from smoking. Nature Reviews. Cancer 2009;9(9):655–64. Available from: http://www.nature.com/nrc/journal/v9/n9/full/nrc2703.html
18. van Zyl Smit R, Pai M, Yew W, Leung C, Zumla A, Bateman E, et al. Global lung health: the colliding epidemics of tuberculosis, tobacco smoking, HIV and COPD. European Respiratory Journal 2010;35(1):27–33. Available from: http://erj.ersjournals.com/cgi/content/full/35/1/27
19. Withrow D and Alter DA. The economic burden of obesity worldwide: a systematic review of the direct costs of obesity. Obesity Reviews 2011;12(2):131-41. Available from: http://www.ncbi.nlm.nih.gov/pubmed /20122135
20. Kelly T, Yang W, Chen CS, Reynolds K and He J. Global burden of obesity in 2005 and projections to 2030. International Journal of Obesity 2008;32(9):1431-7. Available from: http://www.ncbi.nlm.nih.gov /pubmed/18607383
21. Warren C, Jones N, Eriksen M and Asma S for the Global Tobacco Surveillance System (GTSS) collaborative group. Patterns of global tobacco use in young people and implications for future chronic disease burden in adults. The Lancet 2006;367(9512):749–53. Available from: http://www.ncbi.nlm.nih.gov /pubmed/16517275
22. Ezzati M and Lopez AD. Regional, disease specific patterns of smoking-attributable mortality in 2000. Tobacco Control 2004;13:388-95. Available from: http://tc.bmjjournals.com/cgi/content/abstract/13/4/388
23. World Health Organization. The world health report 1999: making a difference. Geneva: WHO, 1999. Available from: http://www.who.int/whr/
24. Hammond SK. Global patterns of nicotine and tobacco consumption. Handbook of Experimental Pharmacology 2009(192):3–28. Available from: http://www.springerlink.com/content/t353k255747342h6/
25. Shafey O, Dolwick S and Guindon G. Tobacco control country profiles. Atlanta, Georgia: American Cancer Society, World Health Organization, International Union Against Cancer, 2003. Available from: http://www.cancer.org/docroot/PRO/content/PRO_1_1_Tobacco_Control_Country_Profiles.asp
26. Liu B, Peto R, Chen Z, Boreham J, Wu Y, Li J, et al. Emerging tobacco hazards in China: 1. Retrospective proportional mortality study of one million deaths. British Medical Journal 1998;317:411-22. Available from: http://www.bmj.com/cgi/reprint/317/7170/1411
27. Slama K. Global perspective on tobacco control. Part I. The global state of the tobacco epidemic. International Journal of Tuberculosis and Lung Disease 2008;12(1):3-7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18173869
28. World Health Organization. Noncommunicable diseases: country profiles 2011. Geneva: WHO, 2011, [viewed 17 September 2011] . Available from: http://www.who.int/nmh/publications/ncd_profiles_report.pdf
29. Collin J. Global health, equity and the WHO Framework Convention on Tobacco Control. Global Health Promotion 2010;17(suppl. 1):S73–5. Available from: http://ped.sagepub.com/content/17/1_suppl /73.full.pdf+html
30. Lando HA, Hipple BJ, Muramoto M, Klein JD, Prokhorov AV, Ossip DJ, et al. Tobacco is a global paediatric concern. Bulletin of the World Health Organization 2010;88(1): 2–2. Available from: http://www.who.int/bulletin/volumes/88/1/09-069583/en/index.html
31. Glynn T, Seffrin J, Brawley O, Grey N and Ross H. The globalization of tobacco use: 21 challenges for the 21st century. CA: A Cancer Journal for Clinicians 2010;60(1):50–61. Available from: http://caonline.amcancersoc.org/cgi/content/full/60/1/50
32. WHO Framework Convention on Tobacco Control. Geneva: World Health Organization, 2003. Available from: http://www.who.int/tobacco/framework/en/
33. World Health Organization. MPOWER: a policy package to reverse the tobacco epidemic. Geneva: WHO, 2008. Available from: http://www.who.int/tobacco/mpower/mpower_english.pdf
34. World Health Organization. WHO report on the global tobacco epidemic, 2011: warning about the dangers of tobacco. Geneva: WHO, 2011. Available from: http://globalink.org/redirect/www.who.int/tobacco /global_report/2011/en/index.html
35. Chapman S. Global perspective on tobacco control. Part II. The future of tobacco control: making smoking history? International Journal of Tuberculosis and Lung Disease 2008;12(1):8-12. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18173870
Copyright © 2016 The Cancer Council. All rights reserved.