3.5 Other cancers caused by or associated with smoking

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3.0 Background

3.1 Tobacco—a leading preventable cause of death and disease

3.2 Cardiovascular diseases

3.3 Lung cancer

3.4 Respiratory diseases

3.5 Other cancers caused by or associated with smoking

3.6 Reproductive health and smoking

3.7 Pregnancy and smoking

3.8 Infant health and smoking

3.9 Increased susceptibility to infection in smokers

3.10 Eye diseases

3.11 Dental diseases

3.12 Gastrointestinal diseases

3.13 Bone density and risk of fractures

3.14 Effects of smoking on the skin

3.15 Smoking and complications in medical treatment

3.16 Smoking and diabetes

3.17 Poorer levels of general health

3.18 Smoking, motor vehicle crashes and other injuries

3.19 Burns and fires caused by tobacco use

3.20 Tobacco poisoning

3.21 Health effects for younger smokers

3.22 Genetic influences on tobacco-caused disease

3.23 Smoking, dementia and cognitive decline

3.24 Lung disease, smoking and occupational exposures

3.25 Air pollution, cigarette smoking and ill health

3.26 Health effects of smoking brands that claim to deliver lower levels of tar, nicotine and carbon monoxide

3.27 Health effects of smoking tobacco in other forms

3.28 Health 'benefits' of smoking?

3.29 Morbidity (ill health) attributable to tobacco-caused disease

3.30 Deaths attributable to tobacco by disease category

3.31 Morbidity and mortality due to tobacco-caused disease and socioeconomic disadvantage

3.32 Health effects of smoking other substances

3.33 Health effects of chewing tobacco, and of other smokeless tobacco products

3.34 Public perceptions of tobacco as a drug, and knowledge and beliefs about the health consequences of smoking

3.35 Health benefits of cessation

3.36 The global tobacco pandemic

Acknowledgments

References

Tobacco smoke contains 69 known carcinogens,35 including a number of known organ-specific carcinogens, and compounds which assist with the formation of carcinogens within the body. Carcinogens and carcinogenic metabolites from tobacco are carried through the body in the bloodstream, following absorption through the lungs. Carcinogenic by-products from tobacco have also been found in the urine, saliva and oral mucosa of smokers. Smoking also affects metabolism and enzyme activity, which may affect carcinogenesis.5

3.5.1 Laryngeal cancer

The larynx ('voice box') is the cavity within the throat that contains the vocal chords. The larynx is in direct contact with tobacco smoke as inhaled smoke passes through the glottis, the space between the vocal chords.5

Smoking is a cause of laryngeal cancer. Risk of developing cancer rises with duration of smoking and the number of cigarettes smoked, and declines with smoking cessation. Heavy smokers have up to 20 times the risk of developing laryngeal cancer compared with non-smokers.5 Alcohol use is also an independent risk factor for development of cancer of the larynx, and heavy use of alcohol and tobacco often coincide.36 Among individuals who both smoke and drink alcohol, the combined effect of the two risk factors is synergistic (multiplicative rather than additive).

Almost all cases of laryngeal cancer reflect the use of tobacco or alcohol consumption, or both. While the majority of laryngeal cancers can be treated (with a five year survival rate of 67%37), most could be prevented.5

In 2004–05, of all deaths from laryngeal cancer in people aged over 35, 71% in men and 65% in women were caused by tobacco use.20

3.5.2 Cancers of the oral cavity and pharynx

Cancers of the oral cavity (mouth) include tumours of the lip, cheek, gum, tongue and lining of the mouth (buccal mucosa). The pharynx (throat) is the cavity behind the nose and mouth, and the connecting passage to the oesophagus.

Tobacco smoking causes oral and pharyngeal cancers.5 The average risk for developing oral or pharyngeal cancer is 10 times higher among male smokers and five times higher among female smokers than among lifetime non-smokers. The risk of developing cancer rises with duration of exposure to tobacco and the amount consumed, and declines with cessation of use. Risk is halved after about five years of cessation, with further reductions apparent over a more extended period of abstinence.5 In Australia in 2004–05, about 58% of all deaths from oropharyngeal cancers in men aged 35 and over, and 50% of fatalities from these cancers in women in the same age group, were due to tobacco use.20

Alcohol use is also a risk factor for these cancers, and use of both alcohol and tobacco gives rise to a higher risk of developing cancer than that resulting from the use of either substance alone.5 The sucking or chewing of tobacco products, a practice uncommon in Australia but endemic in many other parts of the world, also causes oropharyngeal cancers. For further discussion about chewing tobacco and other smokeless tobacco products, refer to Section 3.33.

3.5.3 Oesophageal cancer

The oesophagus connects the mouth with the stomach. Smoking causes cancer of the oesophagus, the risk increasing with duration and extent of exposure to smoke.5 Smokeless tobacco use (in the form of sucking or chewing tobacco) is also implicated as a cause of oesophageal cancer. Smokers have up to seven or eight times the risk of developing oesophageal cancer of non-smokers. As with cancers of the larynx, oral cavity and pharynx, alcohol consumption is an independent risk factor, and used in conjunction with tobacco, the risk increases synergistically.5

In Australia in 2004–05, about 54% of all deaths from oesophageal cancer in men aged 35 and over, and 46% of deaths from these cancers in women in the same age group, were due to tobacco use.20

Smoking cessation halves the risk for oesophageal cancer after five years of abstinence, subsequent reductions in risk occurring more gradually.5

3.5.4 Pancreatic cancer

Smoking causes cancer of the pancreas. The pancreas is a gland situated behind the stomach that secretes enzymes that facilitate food digestion, as well as hormones, including insulin. Cancers of the pancreas most commonly arise in the cells that line the pancreatic ductules. Carcinogens from tobacco smoke reach the pancreas through the bloodstream or through refluxed bile that comes in contact with the pancreatic duct, causing irregular mutations within the cells. Metabolic activity in the pancreas may also interact with toxic chemicals in tobacco smoke to promote cellular mutations. The damaged cells replicate themselves, forming a tumour.5

The risk of developing pancreatic cancer increases with duration of smoking and the number of cigarettes smoked daily, and declines following cessation of smoking. Heavy smokers have three to five times the risk of developing pancreatic cancer compared to non-smokers.5 In Australia in 2004–05, about 25% of all deaths from pancreatic cancer in men aged 35 and over, and 20% of all pancreatic cancer deaths in women of the same age group, were caused by smoking.20

Sufferers of pancreatic cancer have a very poor prognosis, with only about 5% surviving the first five years following diagnosis.18 Reduction of smoking rates is the only known potentially effective strategy for reducing the incidence of cancer of the pancreas.5

3.5.5 Stomach cancer

Smoking causes cancer of the gastric cardia, the region where the oesophagus joins the stomach. The immediate effects of nicotine and other chemicals in tobacco smoke include duodenal reflux, and altered production of gastric secretions important to stomach function.5 In Australia in 2004–05, 14% of all deaths from stomach cancer in men aged 35 and over were caused by tobacco use. In women, the corresponding figure was 10%.20

Smoking may also be related to the development of cancers in other sites within the stomach ('non-cardia gastric cancers'), possibly by interaction with the Helicobacter pylori infection.5

Cessation of smoking is related to a lower risk of developing gastric cancer.5

3.5.6 Kidney and bladder cancers

Smoking causes cancer of the renal (kidney) cell, the renal pelvis (the area within the kidney in which urine is collected and channelled into the ureter), the ureter (the tubes connecting each kidney with the bladder) and the bladder. Many metabolised products from tobacco smoke are excreted from the body via the urine, and the urine of smokers shows increased mutagenic activity, meaning that it has the potential to alter the DNA of cells lining the organs and structures with which it comes into contact.5

Heavy smoking (more than 40 cigarettes a day) doubles the risk of developing kidney and bladder cancers. The likelihood of developing cancers of these sites increases with duration and volume of cigarettes smoked, and declines following quitting smoking.5

Australian data shows that in 2004–05, 53% of all deaths from kidney cancer in men aged 35 and over were due to smoking. Forty-six percent of all deaths in women from kidney cancer were caused by smoking. The corresponding statistics for bladder cancer show that 40% of all deaths from this cause in men aged 35 and over were attributable to smoking, compared to 33% in women.20

3.5.7 Cervical cancer

After some years of debate, it has now been determined by the US Department of Health and Human Services (US Surgeon General)5 and the International Agency for Research on Cancer (IARC)35 that smoking is a cause of cancer of the uterine cervix. Infection with human papilloma virus (HPV) is understood to be a necessary precursor for initiation of the disease, and it is thought that smoking might interact with the HPV by increasing the risk for persistent infection, or by increasing the rate at which malignancy develops in women who have the infection persistently.5

Cervical mucus in women who smoke is mutagenic (that is, has the potential to cause changes in cellular DNA), and contains the carcinogen NNK. The risk of developing cervical cancer increases with the duration of smoking and the amount smoked.5

In Australia in 2004–05, 17% of deaths from cancer of the cervix in women aged 35 and over could be attributed to tobacco use.20

3.5.8 Acute myeloid leukaemia

The confirmation that smoking causes acute myeloid leukaemia (AML) has also been reported recently.5, 35 AML is a disease of the blood-forming cells found in the bone marrow. The disease causes the production of an excessive number of cancerous white blood cells, which may impair normal blood cell activity.

Tobacco smoke contains a number of carcinogens known to cause leukaemia in humans, including benzene, and the radioactive metals polonium-210 and lead-210, both of which emit ionising radiation.5 The risk for acute myeloid leukaemia increases with the number of cigarettes smoked and with duration of smoking. Smokers and former smokers have a 30–50% higher risk of developing acute myeloid leukaemia than never smokers, and heavy smokers have double the risk of developing this cancer.5

3.5.9 Liver cancer

There remains some debate about the role of smoking in the development of liver cancer, although it is agreed that smoking is at least strongly associated with this disease. In its most recent review of the scientific evidence concerning the carcinogenicity of tobacco, the International Agency for Research on Cancer has concluded that smoking is an independent cause of cancer of the liver, irrespective of possible confounding factors such as alcohol use or concurrent infection with the hepatitis B or C viruses.35 The US Surgeon General's 2004 Report has concluded that 'the evidence is suggestive but not sufficient to infer a causal relationship between smoking and liver cancer,' and that 'the global burden of liver cancer may increase if smoking increases around the world.'5 p297

The pathway for development of cancer is likely to be due to the many carcinogens in tobacco smoke which are metabolised in the liver, possibly leading to cellular damage and the eventual development of cancer. Carcinogens may act directly on the genes of the hepatocytes (the main type of cell found in the liver).5

3.5.10 Colorectal (bowel) cancer

There is increasing evidence that smoking may be one of the avoidable risk factors that cause colorectal adenomatous polyps (pre-malignant growths in the colon) and colorectal cancer.5 Recent long-term studies have shown that long-term smoking may have a role in both early and later stages of carcinogenesis.5 There is also some evidence that smokers are more likely to develop colorectal cancer at an earlier age than non-smokers, especially in combination with alcohol use.38 Tobacco carcinogens are known to affect DNA in the cell lining of the colon. However further research is needed to clarify the role of smoking in relation to other risk factors such as diet, obesity, physical inactivity and family history.5

Apart from non-melanoma skin cancers, colorectal cancers are the most commonly occurring malignancy in the overall Australian population.19 If smoking is found to be a causal factor in development of colorectal cancers, it will result in a significant increase in estimates of morbidity and mortality caused by tobacco use in Australia and globally.