3.12 Gastro-intestinal diseases

Last updated: May 2020

Suggested citation: Purcell, K. Hurly, S and Greenhalgh E 3.12 Gastro-intestinal diseases. In Greenhalgh EM, Scollo, MM and Winstanley, MH [editors].  Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2020. Available from  http://www.tobaccoinaustralia.org.au/3-12-gastrointestinal-disease


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 reported having some sort of peptic ulcer in 2001.2

Smoking increases the risk of peptic ulcer disease in people who are infected with Helicobacter pylori.3 In Australia, about 13% of peptic ulcer disease in men and 9% in women has been attributed to smoking.4

Smoking affects the gastrointestinal tract in several 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 may be 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 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

A complex interaction between genetic factors and environmental factors, including smoking, influences the risk and prognosis of inflammatory bowel disease.8-10

The 2014 US Surgeon General’s report conducted a meta-analysis on 24 studies of smoking and Crohn’s disease. Smoking at or before diagnosis was associated with a 1.8-fold increased risk of this disease. The conclusion was that the evidence suggests, but is not strong enough to conclude, causation of Crohn’s disease from smoking. Smoking increases the risk of Crohn’s disease, but more evidence is needed to confirm whether it is a cause.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 Australia in earlier reports quantifying the burden of disease published prior to the 2014 US Surgeon General’s report, about 34% of Crohn’s disease in men, and about 36% in women, had been attributed to smoking.12 There was some debate whether the effect of smoking on Crohn’s disease is dose‐dependent.13)

At the time of diagnosis, smokers with Crohn’s disease report a  greater use and greater dependency on corticosteroids compared with non-smokers.14 Patients with Crohn’s disease who continue to smoke also have a worse prognosis and their symptoms are exacerbated compared with non-smokers .15 A 2016 systematic review and meta-analysis of the effects of smoking on the disease course in Crohn's disease confirmed that smokers had increased risks of a recurrence  of disease activity.16 Smokers also have a greater risk of needing intestinal surgery.10,14,16 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.15 Quitting smoking has a beneficial impact on disease related outcomes.16  

Smokers with both main types of irritable bowel disease appear to be at greater risk of manifesting symptoms of the disease in other parts of the body, including chronic skin disorders and joint problems.17 Following cessation, the risk reduced to that of never smokers between 1 and 2 years after quitting.17

In contrast to its impact on Crohn’s disease, smokers seem to have a decreased risk of ulcerative colitis by about 40% and quitting increases the risk.18 The 2014 Surgeon General’s report concluded that the evidence suggests, but is not sufficient, to conclude that smoking has a protective effect.11 Ex-smokers have an almost 80% higher risk of ulcerative colitis compared with never smokers.18 The reason or reasons for the apparent contradictory effect of smoking on the two main IBDs is unknown.7

Microscopic colitis is also a type of inflammatory bowel disease characterised by watery diarrhoea. It affects the large bowel and can only be diagnosed from a biopsy examined under the microscope. Two large prospective cohort studies of women in the United Kingdom found an association between current smoking and increased risk of microscopic colitis. The risk of microscopic colitis was greatest for heavier smokers (higher pack-years). The risk was  reduced following sustained smoking cessation of five years or more.19  The mechanism by which smoking increases the risk of microscopic colitis is not currently known.19

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%.20 Ex-smokers were found to have elevated risks for these conditions compared with never smokers, but lower risks than current smokers.

A 2019 meta-analysis of data from 26 prospective studies found that smoking appears to increase the risk of developing all biliary tract cancers except gallbladder cancer.21

A 2016 systematic review and meta-analysis of 59,530 gallbladder disease cases among 4,213,482 participants found an increased risk of gallbladder disease associated with tobacco smoking. There was a dose-dependent positive association with increasing number of cigarettes smoked per day.22

Large case-control studies in the UK and US have found that smoking increases the risk of primary biliary cirrhosis (now referred to as primary biliary cholangitis) by about 50–60%.23, 24 Primary biliary cholangitis is an autoimmune disease that results in the destruction of hepatic bile ducts. 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%.25 A 2019 systematic review and meta-analysis of nine case–control studies with 21,577 participants also confirmed that smokers were at greater risk of primary biliary cholangitis than never smokers. It has been suggested that the effect of smoking on the immune system and the cytotoxic effect of cigarettes were possible mechanisms associated with this elevated risk.26 The severity of disease is associated with greater intensity of smoking. For every pack-year increase in smoking intensity, there was a 3.2 times higher likelihood of advanced fibrosis. Smokers with advanced primary biliary cholangitis also had increased mortality rates compared with never smokers.27

Non-alcoholic fatty liver disease (NAFLD) is another important cause of chronic liver disease often associated with obesity and metabolic syndrome. While some large studies have found that smoking is an independent  risk factor for NAFLD,28,29 others have reported that the association between smoking and increased risk of NAFLD only occurred among those who did not drink alcohol.30 There appears to be a dose response association and the incidence of fatty liver disease increases significantly as the number of cigarettes smoked increased.30,31 Smoking also appears to increase the severity of NAFLD, and smokers have a higher risk of liver fibrosis compared with non-smokers.32,33,34 There also appears to be an increased risk of NAFLD associated with exposure to second hand smoke. 35

 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 was initially difficult to determine whether smoking per se increases the risk of pancreatitis independently of other risk factors.  However, the association between smoking and pancreatitis is now well-established.36-39

Smoking is associated with an increased risk of acute pancreatitis, an earlier age of onset, and more frequent recurrences of acute pancreatitis.40 Dual use of tobacco and high- risk drinking are associated with increased risk.38,41 Male smokers who consumed more than four drinks per day had a higher  risk of developing pancreatitis compared with never smokers and former smokers.38  The exact mechanism by which smoking increases the risk of pancreatitis is not well understood, although two common metabolites from cigarette smoke, (nicotine and NNK ) have been shown to induce  changes in the pancreas consistent with those seen in pancreatitis.42,43

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.44 A 2015  meta-analysis of twenty-two studies also  identified a positive association between cigarette smoking with the development of pancreatitis.37

A large population-based prospective study in the United States, confirmed that smoking was an independent risk factor for non-gallstone related pancreatitis, recurrent acute pancreatitis and chronic pancreatitis  in men and women.  Smoking was not associated with gallstone acute pancreatitis in both men and women.38 Another meta-analysis of 12 observational studies had similar findings—that smokers were at greater risk of developing acute pancreatitis but not gallstone related pancreatitis.39 A dose-response effect was observed, with current smokers having a 40% increased risk of acute pancreatitis for every additional 10 cigarettes per day they smoked.39

Another meta-analysis of twelve studies confirmed an association between  smoking and increased risk of acute pancreatitis. The risk is strongest for current smokers, but former smokers had a higher risk compared with never smokers.45 A 2019 systematic review and meta-analysis of ten prospective studies on tobacco smoking and pancreatitis found that current smoking was associated with 49%, 93% and 62%  increases in the relative risk of acute pancreatitis, chronic pancreatitis and acute/chronic pancreatitis combined compared to never smokers. Former smokers showed 24%, 30% and 29% increases in the relative risk compared to never smokers. There was a dose response effect, with an increasing risk for every 10 cigarettes smoked per day and a  an increased risk for every 10 pack-years of smoking.46

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 appendectomy by about 65%, but that this risk decreases by 15% every year after quitting.47 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 consultations in non-perforated appendicitis (see Section 3.15).48

The microbiome refers to a community of microbes residing in a location comprising of bacteria, archaea, viruses, fungi, and protozoa, together with their genes and genomes.49 Microbiome has a critical role in the development of healthy immune responses.49 Smoking causes changes to the gut microbiome, leading to various diseases of the gastrointestinal track such as Crohn's disease, ulcerative colitis and cancers. However, the exact causal relationship between smoking and microbiome alterations is still being examined.49 A 2018 study of patients undergoing an upper GI endoscopy found that mucosa-associated microbiota (MAM) of current smokers has reduced bacterial diversity compared with never smokers.50 A population based cross-sectional study of 758 males, also found the bacterial composition of gut microbia among smokers was different to that of never smokers.51 Smoking cessation has some benefits, with bacterial diversity at least partially or fully restored in ex-smokers.50,51

Sessile serrated polyps (SSPs) are associated with the development of colorectal cancer.52,53 A large cross-sectional study from Korea of more than 30,000 adults undergoing colonoscopy included both younger (30–49 years) and older ( 50–75 years) adults. Current smokers in both age groups had an increased risk of SSPs. Heavier smokers (those with the greatest pack-years) were at greater risk of developing SSPs than lighter smokers and never smokers and also had an elevated risk of larger or multiple SSPs.53

A 2016 systematic review and meta-analysis found that tobacco smoking is associated with an increased incidence of diverticular disease and related complications. There was a dose-dependent association with increasing number of cigarettes smoked per day associated with higher risk. There was also some evidence that smoking increases the risk of diverticular disease complications, but the number of relevant studies was small.54

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 January 2021)



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. Available from: https://www.aihw.gov.au/reports/australias-health/australias-health-2010/contents/table-of-contents.

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. Available from: https://www.aihw.gov.au/reports/australias-health/australias-health-2004/contents/table-of-contents.

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: https://www.cdc.gov/tobacco/data_statistics/sgr/2004/index.htm.

4. Whetton S, Tait RJ, Scollo M, Banks E, Chapman J, et al. Identifying the Social Costs of Tobacco Use to Australia in 2015/16. Perth, Western Australia: The National Drug Research Institute at Curtin University, 2019. Available from: http://ndri.curtin.edu.au/NDRI/media/documents/publications/T273.pdf.

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=www.springerlink.com

8. Allais L, De Smet R, Verschuere S, Talavera K, Cuvelier CA, et al. Transient Receptor Potential Channels in Intestinal Inflammation: What Is the Impact of Cigarette Smoking? Pathobiology, 2016; 84(1):1-15. Available from: http://www.ncbi.nlm.nih.gov/pubmed/27388890

9. Adams A, Kalla R, and Satsangi J. Editorial: the influence of genetic factors in mediating the effects of tobacco smoke in IBD. Alimentary Pharmacology and Therapeutics, 2018; 47(2):306-307. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29265462

10. Lang BM, Biedermann L, van Haaften WT, de Valliere C, Schuurmans M, et al. Genetic polymorphisms associated with smoking behaviour predict the risk of surgery in patients with Crohn's disease. Alimentary Pharmacology and Therapeutics, 2017. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29052254

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: https://www.cdc.gov/tobacco/data_statistics/sgr/50th-anniversary/index.htm.

12. English DR, Holman CD, Milne E, Winter MG, Hilse GK, et al., The quantification of drug caused morbidity and mortality in Australia 1995: Part 1. Canberra: Commonwealth Department of Human Services and Health; 1995.

13. Yamamoto T, Shimoyama T, and Kuriyama M. Letter: deleterious effects of smoking on post-operative Crohn's disease. Alimentary Pharmacology and Therapeutics, 2016; 43(11):1247-8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/27137736

14. Alexakis C, Saxena S, Chhaya V, Cecil E, Majeed A, et al. Smoking Status at Diagnosis and Subsequent Smoking Cessation: Associations With Corticosteroid Use and Intestinal Resection in Crohn's Disease. American Journal of Gastroenterology, 2018. Available from:  https://europepmc.org/article/med/30323269 

15. Reese G, Nanidis T, Borysiewicz C, Yamamoto T, Orchard T, et al. 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=www.springerlink.com

16. To N, Gracie DJ, and Ford AC. Systematic review with meta-analysis: the adverse effects of tobacco smoking on the natural history of Crohn's disease. Alimentary Pharmacology and Therapeutics, 2016; 43(5):549-61. Available from: http://www.ncbi.nlm.nih.gov/pubmed/26749371

17. Severs M, van Erp SJ, van der Valk ME, Mangen MJ, Fidder HH, et al. Smoking is Associated With Extra-intestinal Manifestations in Inflammatory Bowel Disease. Journal of Crohn's and Colitis, 2015. Available from: http://www.ncbi.nlm.nih.gov/pubmed/26721937

18. 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: https://www.mayoclinicproceedings.org/article/S0025-6196(11)61253-6/fulltext 

19. Burke KE, Ananthakrishnan AN, Lochhead P, Olen O, Ludvigsson JF, et al. Smoking is Associated with an Increased Risk of Microscopic Colitis: Results From Two Large Prospective Cohort Studies of US Women. Journal of Crohn's and Colitis, 2018. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29370359

20. 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: https://pubmed.ncbi.nlm.nih.gov/19033524/ 

21. McGee EE, Jackson SS, Petrick JL, Van Dyke AL, Adami HO, et al. Smoking, Alcohol, and Biliary Tract Cancer Risk: A Pooling Project of 26 Prospective Studies. Journal of the National Cancer Institute, 2019. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31127946

22. Aune D, Vatten LJ, and Boffetta P. Tobacco smoking and the risk of gallbladder disease. European Journal of Epidemiology, 2016. Available from: http://www.ncbi.nlm.nih.gov/pubmed/26898907

23. 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

24. Gershwin ME, Selmi C, Worman HJ, Gold EB, Watnik M, 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

25. 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

26. Wijarnpreecha K, Werlang M, Panjawatanan P, Kroner PT, Mousa OY, et al. Association between Smoking and Risk of Primary Biliary Cholangitis: A Systematic Review and Meta-Analysis. Journal of Gastrointestinal and Liver Diseases, 2019; 28:197-203. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31204401

27. Mantaka A, Koulentaki M, Samonakis D, Sifaki-Pistolla D, Voumvouraki A, et al. Association of smoking with liver fibrosis and mortality in primary biliary cholangitis. European Journal of Gastroenterology and Hepatology, 2018. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30106760

28. Kim BJ, Kang JG, Han JM, Kim JH, Lee SJ, et al. Association of self-reported and cotinine-verified smoking status with incidence of metabolic syndrome in 47,379 Korean Adults. Journal of Diabetes, 2018. Available from: https://onlinelibrary.wiley.com/doi/abs/10.1111/1753-0407.12868

29. Jung HS, Chang Y, Kwon MJ, Sung E, Yun KE, et al. Smoking and the Risk of Non-alcoholic Fatty Liver Disease: A Cohort Study. American Journal of Gastroenterology, 2018. Available from: https://pubmed.ncbi.nlm.nih.gov/30353055/ 

30. Okamoto M, Miyake T, Kitai K, Furukawa S, Yamamoto S, et al. Cigarette smoking is a risk factor for the onset of fatty liver disease in nondrinkers: A longitudinal cohort study. PLoS ONE, 2018; 13(4):e0195147. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29664906

31. Kim BJ, Han JM, Kang JG, Rhee EJ, Kim BS, et al. Relationship of cotinine-verified and self-reported smoking status with metabolic syndrome in 116,094 Korean adults. Journal of Clinical Lipidology, 2017; 11(3):638-645 e2. Available from: http://www.ncbi.nlm.nih.gov/pubmed/28431854

32. 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

33. Ou H, Fu Y, Liao W, Zheng C, and Wu X. Association between Smoking and Liver Fibrosis among Patients with Nonalcoholic Fatty Liver Disease. Can J Gastroenterol Hepatol, 2019; 2019:6028952. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31737583

34. Munsterman ID, Smits MM, Andriessen R, van Nieuwkerk CMJ, Bloemena E, et al. Smoking is associated with severity of liver fibrosis but not with histological severity in nonalcoholic fatty liver disease. Results from a cross-sectional study. Scandinavian Journal of Gastroenterology, 2017; 52(8):881-885. Available from: http://www.ncbi.nlm.nih.gov/pubmed/28446050

35. Akhavan Rezayat A, Dadgar Moghadam M, Ghasemi Nour M, Shirazinia M, Ghodsi H, et al. Association between smoking and non-alcoholic fatty liver disease: A systematic review and meta-analysis. SAGE Open Med, 2018; 6:2050312117745223. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29399359

36. Singhvi A and Yadav D. Myths and realities about alcohol and smoking in chronic pancreatitis. Current Opinion in Gastroenterology, 2018. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29965868

37. Ye X, Lu G, Huai J, and Ding J. Impact of smoking on the risk of pancreatitis: a systematic review and meta-analysis. PLoS ONE, 2015; 10(4):e0124075. Available from: http://www.ncbi.nlm.nih.gov/pubmed/25879541

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44. 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

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47. Oldmeadow C, Wood I, Mengersen K, Visscher P, Martin N, et al. Investigation of the relationship between smoking and appendicitis in Australian twins. Annals of Epidemiology, 2008; 18(8):631–6. Available from: https://www.ncbi.nlm.nih.gov/pubmed/18652981

48. Sadr Azodi O, Lindström D, Adami J, Bellocco R, Linder S, et al. Impact of body mass index and tobacco smoking on outcome after open appendicectomy. British Journal of Surgery, 2008; 95(6):751–7. Available from: https://bjssjournals.onlinelibrary.wiley.com/doi/pdf/10.1002/bjs.6079

49. Huang C and Shi G. Smoking and microbiome in oral, airway, gut and some systemic diseases. Journal of Translational Medicine, 2019; 17(1):225. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31307469

50. Shanahan ER, Shah A, Koloski N, Walker MM, Talley NJ, et al. Influence of cigarette smoking on the human duodenal mucosa-associated microbiota. Microbiome, 2018; 6(1):150. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30157953

51. Lee SH, Yun Y, Kim SJ, Lee EJ, Chang Y, et al. Association between Cigarette Smoking Status and Composition of Gut Microbiota: Population-Based Cross-Sectional Study. J Clin Med, 2018; 7(9). Available from: https://www.ncbi.nlm.nih.gov/pubmed/30223529

52. Crockett SD. Don't Smoke 'em if you got 'em-Tobacco Exposure Increases Risk of Serrated Polyps. Clinical Gastroenterology and Hepatology, 2019. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30743008

53. Lee JY, Chang HS, Kim TH, Chung EJ, Park HW, et al. Association Between Cigarette Smoking and Alcohol Consumption and Sessile Serrated Polyps in Subjects 30 to 49 Years Old. Clinical Gastroenterology and Hepatology, 2018. Available from: https://www.cghjournal.org/article/S1542-3565(18)31277-1/pdf

54. Aune D, Sen A, Leitzmann MF, Tonstad S, Norat T, et al. Tobacco smoking and the risk of diverticular disease - a systematic review and meta-analysis of prospective studies. Colorectal Disease, 2017. Available from: http://www.ncbi.nlm.nih.gov/pubmed/28556447