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