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/chapter-3-health-effects/3-5-other-cancers

 

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 liver 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 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.

Relevant news and research

For recent news items and research on this topic, click here.(Last updated November 2018)

References

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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

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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

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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

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