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. 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. 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 endoglobinin 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
Relevant news and research
For recent news items and research on this topic, click here.(Last updated September 2019)
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, NationalCenter 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